2026-01-31 01:04:09
I started writing this as a reply on X to Greg Yang, co-founder of xAI, who recently stepped down from xAI to address his debilitating case of Lyme disease.
Ultimately, I decided that a blog post could provide more detail and allow proofreading by credible researchers, so here we are.
Before we dive in, a disclaimer: I’m not a doctor, nor do I play one on the internet. I was hesitant to publish this, as I know how much flak I’ll get, but the results and underlying science are just too interesting.
The following is for informational purposes only. Please consult with your doctor and read the warnings at the end.
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Growing up on Long Island (see this link), I’ve contracted Lyme disease twice. Most of my childhood friends and neighbors have had tick-borne diseases. My second case of Lyme in 2014 was incredibly severe, but it was resolved in 4–6 weeks with an unorthodox approach: strict ketosis. I’ve now been 100% asymptomatic for more than 10 years.
I have since replicated the results with four out of four friends who were effectively disabled by Lyme disease. In this post, I’ll cover some of the science, simple how-to instructions, lots of open questions, and upcoming tech options that might offer some benefits of keto in a headset, no diet required.
Am I saying the ketogenic diet will work for everyone? Of course not. I am saying that, compared to a lot of complex or questionable treatments for Lyme, ketosis is a simple “first, do no harm” approach with minimal downside for most people. Drugs often have off-target effects, and we’ve scientifically studied ketosis for more than 100 years.
Furthermore, ketosis has been a mainstay of human evolution for millennia. So perhaps it’s worth testing for a few weeks to see if you’re a responder? Lots of caveats with this, but I’ll unpack it.
Let’s begin with my personal case.
As mentioned, I twice contracted Lyme disease and co-infections on Long Island, confirmed with local testing, best-of-class lab testing in NYC, and lastly with specialists at the Stanford Infectious Diseases Clinic. I mention the three separate rounds of testing, as a lot of people are misdiagnosed with Lyme.
Many conditions have similar symptoms to Lyme disease, including Long COVID, Fibromyalgia, Chronic Fatigue Syndrome (CFS/ME), Multiple Sclerosis (MS), and Rheumatoid Arthritis (RA). Disambiguating takes proper testing from legitimate MDs, in my opinion.
There are simply too many charlatans and well-intentioned amateurs running around.
I had no rash in either instance, which is true in 20–30% of cases. Unfortunately, I believed the local folklore of “no rash, no Lyme” and, in the 2014 instance, I waited until symptoms were debilitating: severe joint swelling, slurred speech, forgetting common words and friends’ names, etc. I didn’t seek proper help until my assistant said, “Tim, I’ve seen you tired, I’ve seen you sick, and this is something else. You need to see a doctor.”
So, I did. Sadly, after proper diagnosis and courses of antibiotics, which I still believe are critical, most symptoms persisted. I operated at ~10% capacity for 9 months and was on the verge of accepting that my mind, body, relationships, business, and more might be handicapped forever. I felt like I had advanced dementia, fatigue often kept me bedridden, and arthritis-like pain wracked my entire body.
What happened at 9 months?
I started brainstorming subtraction. I’d already tried addition: adding drugs, supplements, and all manner of sketchy “alternative” options. If anything, some of them seemed to be generating more problems.
This is how I returned to the ketogenic diet.
Fortunately, I’d used the ketogenic diet in college for various sports experiments, and I decided to test whether or not picking a new fuel and harnessing anti-inflammation (more on these later) would improve things. I knew I could get into clinical ketosis within 3–4 days.
Within a week, all of my cognitive symptoms were gone.
After roughly 4–6 weeks of a strict ketogenic diet (<20 grams of carbohydrates per day), I completely and durably fixed all of my symptoms. It’s been more than a decade, and none of the symptoms have returned. It was a Hail Mary that worked.
And here is perhaps the most surprising part—I didn’t need to stay on the ketogenic diet. I went back to the slow-carb diet after 4–6 weeks of keto, and my diet has varied tremendously since. Whatever it did seemed to stick.
But there was one rub.
I had no satisfying explanation for why it worked.
I had a few plausible theories, sure, but nothing watertight. I knew the short-term effects of ketosis… but a durable fix? How was that possible?
The lights went on in late 2025 when I again interviewed Dr. Dominic D’Agostino, one of the world’s leading researchers and synthesizers of ketones.
Let’s start with the biggest missing piece he provided.
Lyme disease spirochetes (Borrelia burgdorferi) are largely dependent on glycolysis for energy production, as they lack a tricarboxylic acid (TCA) cycle and oxidative phosphorylation pathways. In simple terms, the bacteria that cause Lyme disease primarily use carbohydrates for fuel. I had no idea and simply got lucky.
But is it really as simple as starving the bacteria out?
This might not apply to all cases, as such spirochetes can also use alternate fuels like glycerol and pull off all sorts of evolved tricks. LLMs seem to raise an eyebrow at the above theory, but we have at least an N (sample size) of 5 with a 100% success rate. It’s not a Randomized Controlled Trial (RCT), but a lot of compelling science starts with a few interesting case studies.
This glycolysis-dependent piece of the puzzle seems to be critical, but might there be alternate explanations for why keto seems to work? A few possibilities come to mind, and perhaps they synergize to produce the “remission” I and others experienced.
Below are a few leads.
A ketogenic diet (KD) has a host of fascinating effects on mitochondria, the so-called “powerhouses” of the cell that generate most of your energy (ATP). This was one of my placeholder theories in 2014, as researchers started exploring this terrain seriously in the 1990s.
KDs can help you produce more mitochondria (biogenesis), increase energy production, and arguably improve mitochondrial quality by recycling and replacing them (mitophagy). Net-net, this could be a reboot of your metabolic machinery—you’re remodeling your mitochondria.
Could that address some of the fatigue symptoms of Lyme? Is 1–2 months sufficient to produce these changes and have them stick? Were my later periods of regular fasting—typically three contiguous days of water fasting per quarter—key for reinforcing what the KD kicked off? We don’t really know.
But even if 1–2 months of KD isn’t enough to overhaul your machinery, there are acute energy benefits that could explain my one-week turnaround of cognitive symptoms.
Ketones supply an alternative fuel to glucose, and in some contexts (impaired glucose metabolism) ketones are vastly superior. Perhaps this is partially why, even if not in ketosis, I will take a ketone salt or monoester before recording podcasts: I’m significantly sharper without having to mainline caffeine in the afternoon and sacrifice sleep quality later.
There are documented cases of Alzheimer’s disease (AD) patients who respond incredibly well to exogenous (supplemental) ketones (listen to 2:21 here), and I’ve heard clinicians describe AD patients who normally fail the clock test (drawing a clock) but who can succeed without any difficulty after a single 10–30-gram oral dose of exogenous ketones. Something interesting seems to be happening. Alzheimer’s is sometimes referred to as “type 3 diabetes.” Could a ketogenic diet fix part of the underlying problem, or are ketones simply working around damage (e.g., amyloid plaques and tau tangles)?
I don’t know, but here’s what I do know: every time I cross ~1 mmol/L blood concentration of ketones as measured by any commercial ketone meter (e.g., Keto-Mojo or Precision Xtra), a light switch is flipped and I have extra gears. I’ve seen this repeatedly since my first keto experiments in the mid- and late 1990s. Of course, your personal threshold will likely differ, but I can turn this on at will with exogenous ketones; a 1–2-day water fast; or a 2–4-day, low-calorie KD.
Curiously, these extra gears seem to often kick in for many people who are not obviously glucose-impaired. Why? Perhaps it relates to the next bullet.
And perhaps people who aren’t glucose-impaired at the whole-body level (i.e., as assessed by standard blood tests) can nonetheless be glucose-impaired at the brain level? I’d bet money on it.
The primary circulating ketone, beta-hydroxybutyrate (BHB), appears to dial down inflammatory signaling through multiple pathways. In other words, some ketones have direct anti-inflammatory effects.
The next paragraph is technical, so feel free to skip, but there are some juicy bits.
BHB inhibits the NLRP3 inflammasome (a molecular trigger for cytokines like IL-1β), engages the HCA2/GPR109A receptor on immune cells, and may influence gene expression through epigenetic mechanisms like histone β-hydroxybutyrylation. The claim that BHB is a potent HDAC inhibitor is debated in the literature (if true, there are significant cancer implications), but net-net, for some people, ketosis seems to reduce systemic inflammation.
Lyme-induced inflammation can produce vasoconstriction and cause a range of problems (cold hands/feet, dysautonomia), but ketones (D-BHB and L-BHB) have a remarkable effect on improving cardiac output and blood flow by reducing peripheral vascular resistance. This is of personal interest, as both I and my mom have long-standing Raynaud’s Syndrome, but we never thought of any connection to Lyme. My mom has had both Lyme and alpha-gal syndrome, which was transmitted by the Lone Star tick. Now she can’t eat mammalian protein without risk of life-threatening anaphylaxis.
For more on the anti-inflammatory potential of ketones, I suggest you listen to this segment here from my very first conversation with Dominic.
Broadly speaking, anti-inflammatories can have some very fast effects. For instance, if you have minor aches and pains that make it a little painful to walk, you might be able to take two Advil and go for a pain-free walk 60 minutes later.
By extension, how quickly could the anti-inflammatory effects of ketones on a KD translate to less painful or pain-free joints? Smoother and faster cognition? Less or no fatigue? Once again, in my personal experience, all of these and more changed within a week of tipping past 1 mmol/L concentration of BHB as measured by a finger stick with a Precision Xtra or Keto-Mojo device.
Last but not least, guess what? Neuroinflammation impairs glucose metabolism in the brain, and impaired glucose metabolism worsens neuroinflammation.
Everything in this post seems tightly interrelated. That’s good news. Ketosis might be a hammer that hits several nails at once.
This section will overlap a lot with the preceding two.
Lyme disease is sometimes called “The New Great Imitator” because its symptoms overlap with so many conditions. Some are autoimmune, but many are psychiatric, including but not limited to depression, anxiety disorders, bipolar disorder, obsessive-compulsive disorder (OCD), and ADHD. There’s also emerging data that infection is linked to these disorders and other neurodegenerative diseases.
Dr. Chris Palmer, a Harvard Medical School psychiatrist at McLean Hospital, has developed what he calls “the brain energy theory of mental illness.” In my conversation with him on the podcast, he argued that mental disorders may, in many cases, be metabolic disorders of the brain. His core insight: when brain cells are metabolically compromised, they can become either underactive (shutting down from lack of energy) or hyperexcitable (misfiring when they shouldn’t).
In his model, a ketogenic diet may help by providing an alternative fuel source to struggling brain cells.
The keto–mental health connection isn’t new. Ketogenic diets have been used clinically for 100+ years to treat epilepsy. Centuries ago, churches sometimes locked “possessed” people in a room without food, and lo and behold, the “demons” disappeared after roughly enough time to metabolically switch to ketosis.
Ketogenic diets appear to act through multiple, sometimes overlapping pathways, including those affecting neurotransmission, inflammatory signaling, and gene expression. I bolded those we haven’t directly addressed in this piece.
Furthermore, the ketogenic diet dodges some of the metabolic and off-target side effects associated with many psychiatric medications, especially antipsychotics.
For more on this, I recommend Chris’s book Brain Energy and our full conversation. I also chatted with Dave Baszucki, founder of Roblox, about how he used metabolic psychiatry to save his son, who is diagnosed with bipolar disorder.
In brief, if you’ve been diagnosed with Lyme, it might make sense to try 1–2 months of a strict ketogenic diet DURING or AFTER antibiotics but BEFORE you try speculative treatments with non-trivial or unknown downside risks.
Of course, speak with your doctors first.
ChatGPT and similar LLMs can help cover most bases and even meal plans, but be sure to specify “less than 20 grams per day of carbohydrates (CHO).” People can get cute with “net-carbs” and outsmart themselves. I prefer a wide margin of safety when stakes are high (e.g., Lyme symptoms).
If you like books, amidst a sea of terrible options, there are a few that are pretty good.
From Dr. Dominic D’Agostino:
From a CEO I can’t name, who has access to thousands of patients who’ve tried a ketogenic diet in various forms:
For the most part, I think that trying to eat keto-friendly bagels and faux-desserts is the path to disappointing results.
Especially if you’re just doing a trial run for a few weeks, I like to keep it simple. Do fool-proof first, then, if you want, layer in clever and crunchy after at least two weeks of 1 mmol/L blood readings, and only then with constant ketone monitoring.
To jumpstart keto, I personally like to first do intermittent fasting (IF) for at least a week, only eating within an eight-hour window each day. IF alone can dramatically change your blood work, OGTT, and more. Note that it can take your body 1–2 weeks to overcome the first 12 hours or so of lower energy and occasional irritation, but when you do adapt, it pays long-term dividends.
If you adapt to IF, it’ll make future keto transitions a lot easier and likely eliminate any fogginess, low energy, or “keto flu” symptoms. It helps jumpstart your ketogenic machinery without extended ketosis.
But if you’re in a rush to test keto and want to bite the bullet, you can also just start with a lower-calorie keto diet. The sub-maintenance calories will dramatically speed things up.
In my case, I default to something like the below at a bodyweight of around 175 lbs.:
• 9am Morning – Coffee or tea with 2 tbsp heavy cream (NOT half and half)
• 11am Mid-morning – For the first week of keto and sometimes longer, I’ll mix KetoSpike cocoa exogenous ketone powder into my coffee or tea. This remedies early fatigue.
• Cardio, if any Zone 2 to be done
• ~2pm Lunch – Two cans of chub or jack mackerel mixed with 2 tbsp MCT oil + 2 tbsp apple cider vinegar + salt/pepper. Cheap, fast, and surprisingly good. This will clock in at around 500–700 calories.
• 5pm Weight training, if any
• 7pm or 8pm Big dinner. This will contain the rest of my calories for the day.
Chopped ribeye on huge salad with extra virgin olive oil, plus a side of creamed spinach
OR
Chicken and cheese plus keto-friendly veggies like broccoli and cauliflower
OR
Lamb chops plus keto-friendly goulash, etc.
You can always add fat with some additional heavy cream in a beverage, as has been done successfully for more than a century with epileptic kids, or a few dollops of sour cream or a dessert of keto-friendly cheeses.
• Post-dinner – Walk the dogs and curb any glucose/insulin response from the large meal.
That’s it. Once you’re in proper ketosis, you probably won’t feel much hunger. It’s quite liberating to reorient to hunger and eating that isn’t compulsive and full of snacking. If you really want to snack, eat more at meals. If you still want to snack, it’s habit and not physiology talking.
Postscript:
Supplements: I take electrolytes (sodium, magnesium, and potassium) as pills or packets at least twice a day. Especially if you’re new to keto, this will be important for avoiding dizziness, cramping, and sleep problems. Just ensure no sweeteners, maltodextrin, etc. are hiding in the product. You’d be surprised what some popular brands do.
Fat: Don’t try to do a low-fat, high-protein version of keto. For reasons we’ll skip here, it’s very hard to make work and not worth the gamble. Aim to consume at least 70% of your daily calories from fat.
Snacks: Be careful with snack foods, even keto-friendly-ish macadamia nuts, which can add up and knock you out of ketosis. Avocados also contain more carbs than you might think. Once mildly knocked out of ketosis, some people need multiple days to regain footing and end up feeling depleted, exhausted, and awful. For beginners, treat ketosis as binary and watch your exact grams of carbs. Play it safe so you don’t end up in metabolic purgatory.
Can you get some of the benefits of a ketogenic diet without eating meat, eggs, and cheese all the time? It sure would be nice.
And, yes, you can make a KD much more appealing, eating a surprising quantity of salads and greens, but I’m always looking for tools and approaches that might make its benefits more accessible.
Here are a few that I’m tracking closely:
Intermittent fasting by itself. At least a 16-hour window of fasting. Read up on neuroscientist Mark Mattson and “flipping the metabolic switch.” Here is one oldie-but-goodie, but note that Mark suggests 16–18 hours of fasting instead of the 12-hour onramp mentioned in that publication. This is also referred to as 16:8 time-restricted eating. 16:8 or 18:6 is a goldmine and perhaps my most surprising personal change of the last two years, in addition to accelerated TMS.
The “metabolic switch” relates to depleting your liver of glycogen, requiring around 16 hours for most people, which then leads to a more ketotic state.
Bioelectronic medicine (e.g., vagus nerve stimulation [VNS]). Dr. Kevin Tracey and others have described the “inflammatory reflex,” whereby vagus signaling can modulate immune activity. Early clinical work has explored VNS in inflammatory conditions (e.g., rheumatoid arthritis). This is not a Lyme treatment per se, but it’s plausible that a VNS device, particularly implants or an ear-based transauricular VNS (taVNS), could be used to decrease inflammation-driven symptoms. There are also some potentially interesting applications to chronic pain management via HMGB1 (special thanks to Ulf Andersson).
Caveat emptor – there is a LOT of BS out there related to vagus nerve stimulation.
Listen to my interview with Kevin, and I’m hoping to help make easier auricular devices more widely available soon. For a possible alternative route, also read up on the applications of famotidine (Pepcid) to the vagus nerve and the inflammatory reflex, which has applications to COVID and more. As always, speak with your doctors before using.
Ultra-low-intensity magnetic approaches (Fareon). Stealth startup Fareon has published preclinical work suggesting microtesla-range magnetic fields can influence neuroinflammation and disease models. This is early science, not clinical guidance, but I became an early investor in this company for a lot of reasons. One of them: I’m hoping it might offer some of the anti-inflammatory benefits of keto with simple, at-home hardware. Their tech is not yet available outside of trials, but I’m hoping to help expand that. You can sign up for their email list to be the first to know.
Others?
Do you have other ideas or suggestions? If so, please let me and readers know in the comments section of this blog post.
It bears repeating: Many conditions have similar symptoms to Lyme disease, including Long COVID, Fibromyalgia, Chronic Fatigue Syndrome (CFS/ME), Multiple Sclerosis (MS), Rheumatoid Arthritis (RA), and more. Disambiguating takes proper testing from legitimate MDs, in my opinion.
It is also worth noting, however, that data suggest a ketogenic diet might help with symptoms of nearly all of the above(!):
MS → strongest early clinical evidence
Fibromyalgia → promising pilot data
CFS/ME → strong theoretical fit, weak trials
Long COVID → emerging hypothesis
RA → indirect anti-inflammatory benefit
Returning to the caveats, there is another risk lurking behind the label of “Lyme disease.” Some people go shopping for the Lyme diagnosis. If you keep seeing doctors long enough, especially once you venture into “doctors” at the fringe, I promise that you will eventually get a Lyme diagnosis. Some such patients are simply desperate for any explanation and treatment that can provide relief. Others are subconsciously hoping for an external cause for depression and lethargy caused by issues like a rocky marriage, alcoholism, social isolation, etc. It’s a lot easier to take pills or get IVs rather than fundamentally changing the tectonic plates of your life. I get it, and I’ve been there in different contexts.
In the case of Lyme disease, there are entire cottage industries that have popped up to happily take your money for endless treatment that won’t do much.
So, good to be aware and always ask: If I took Lyme off the table, what else might possibly explain this?
If you’re on insulin, sulfonylureas, GLP-1 agonists (e.g., Ozempic, Zepbound), or any SGLT2 inhibitor (the “-flozin” drugs), don’t attempt a ketogenic diet without clinician supervision, as carb restriction/fasting can trigger euglycemic ketoacidosis, and medication doses may need rapid adjustment.
In fact, please be sure to always speak with your doctor, m’kay?
Just note that you might need to offer them some reading on the ketogenic diet, as it isn’t a common intervention. This blog post or linked studies and podcasts offer a few starting points.
Also avoid DIY keto if you are pregnant/breastfeeding, have significant kidney/liver/pancreatic disease (including prior pancreatitis), or have a history of eating disorders.
All that said, overall, humans are incredibly well evolved to handle ketosis, especially for the brief periods of time necessary to notice before-and-after changes in the context of Lyme.
One final addendum from Dominic on ALS, at his request:
“FYI, my friend Deanna Tedone was diagnosed with rapidly progressing ALS 17 years ago (given 3 years to live, at most). Her dad, Dr. Vince Tedone, was a world-famous orthopedic surgeon for the Yankees. He came up with the Deanna Protocol, and we proved efficacy in mice: Metabolic Therapy with Deanna Protocol Supplementation Delays Disease Progression and Extends Survival in Amyotrophic Lateral Sclerosis (ALS) Mouse Model.
Deanna tested positive for Lyme disease, and we think this may have been the cause of her ALS. Their foundation is Winning The Fight, and they’re hoping to fund more research on the link between Lyme and neuro diseases.”
For now, that’s all, folks!
Illness and medicine can be squirrely beasts, and I myself have been tempted to give up at times. It can seem like the deck is stacked against you. But sometimes there actually is a simple light of hope at the end of the tunnel.
The ketogenic diet is not a panacea, but its applications beyond weight-loss are compelling. For some, like me and my friends, they can be life-changing.
I sincerely hope this post is helpful.
All the best to you and yours,
Tim Ferriss
Thanks to everyone who proofread this post. Any remaining mistakes are mine. If you spot errors or have corrections, please leave a comment below.
The post How I Beat Lyme Disease with The Ketogenic Diet — Science, How-To Protocols, and 10+ Years of Zero Symptoms appeared first on The Blog of Author Tim Ferriss.
2026-01-29 04:16:48
Please enjoy this transcript of my interview with Dr. Tommy Wood (@drtommywood), an associate professor of pediatrics and neuroscience at the University of Washington, where his research focuses on brain health across the lifespan. Alongside his academic work, Tommy is head scientist for Motorsport at Hintsa Performance, overseeing health and performance programs for multiple Formula 1 drivers. He also helped to found the British Society of Lifestyle Medicine, is head of research for the dementia prevention charity Food for the Brain, and serves as chief science officer for brain-health coaching company BetterBrain. He is co-host of the Better Brain Fitness podcast and author of the forthcoming book The Stimulated Mind.
Products, resources, and people mentioned in the interview
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Listen to this episode on Apple Podcasts, Spotify, Overcast, Podcast Addict, Pocket Casts, Castbox, YouTube Music, Amazon Music, Audible, or on your favorite podcast platform.
Transcripts may contain a few typos. With many episodes lasting 2+ hours, it can be difficult to catch minor errors. Enjoy!
Tim Ferriss: Tommy, Tommy, Tommy, nice to see you.
Tommy Wood: Nice to see you.
Tim Ferriss: Thanks for making the time.
Tommy Wood: Yeah. Thanks for having me.
Tim Ferriss: Absolutely. And as mentioned before we started recording, this is just going to be like our last conversation, because I wanted to reach out to you because cognition, cognition, cognition. Boy, oh, boy, is that on the mind. And pun intended on one level, but we are going to bounce all over the place, and I hope to give people, including myself, a lot of tactical, practical recommendations. Also being clear where the science is solid and where the science is maybe a little thinner ice.
Tommy Wood: Mm-hmm.
Tim Ferriss: Right?
Tommy Wood: Yeah.
Tim Ferriss: Or where something is plausible but not yet proven out. And you’ve got me chewing xylitol gum, you’ve got me looking at air purifiers, but I’m skipping ahead. Let’s go back to the beginning, and I want to give the good old Dr. Chatterjee a nod here because it came up in a conversation you had with him and I was like, “Wow, I never would have thought of that.” Why are human babies so plump? Why are they so fat compared to other species?
Tommy Wood: If you look at human babies compared to pretty much every other mammalian species, we are the only species that’s born fat, even compared to other primates. And it’s thought that the primary reason for this is that that fat is a repository for things that the brain needs in order to develop. And the two that are probably most interesting to you and seem to be particularly important are DHA, the omega-3 fatty acid, and fats as a source of ketones for the brain. When the brain is developing in particular, and I think this is also very relevant to recovery from brain injuries and other states, the preferred synthetic precursor, as in the thing that the brain uses to make structure like fats and cholesterol and that kind of stuff, which makes up a significant chunk of the brain. Ketones are the preferred source, particularly in the developing brain, but I think also later on in various states as an adult.
And so in order to support that very hungry brain, which it is particularly in humans, we’re born fat so that we can generate a bunch of ketones to support that brain developing for the first — you know? Especially for the first few weeks, but maybe even for months after that.
Tim Ferriss: Also, lots of, as I understand it, beautiful bat brown adipose tissue, to keep those little hairless —
Tommy Wood: Keep them warm. Yeah.
Tim Ferriss: — monkeys warm. Yeah. All right. So we’re going to talk about, because I think the, in a sense, the extremes inform the mean, but not the other way around. So we can talk about certain maybe edge cases, things that people might not view as immediately relevant to themselves.
But since we’re talking about newborns, I’m curious, you’ve looked at therapies, various types of research into brain injury and newborns. What do you do? What can you do? I mean, what’s the state of the art when it comes to treating brain injury in newborns or in infants?
Tommy Wood: There’s two main brain injuries of babies that I study, and they’re probably also the two main brain injuries that are most broadly studied, just because of their impact. And so the first is preterm brain injury. So that’s a baby’s born early, the earlier you’re born, the greater the risk of neurodevelopment of impairment or some other kind of neurological disorder, cerebral palsy, other impairments later in life. And the other is something that we call hypoxic ischemic encephalopathy, which is essentially you get to normal full term, something happens —
Tim Ferriss: Not enough oxygen? Exactly.
Tommy Wood: Exactly. Not enough blood flow, not enough oxygen gets to the brain. Something happens, usually during childbirth, and people think about the cord is wrapped around the neck or you can get placental abruption, right? The placenta kind of tears off the inside of the uterus or the uterus can completely rupture. But sometimes we don’t know what happened, the baby just comes out and something has happened. In that scenario, the second one, HIE, as we call it, those babies are cooled down. So this is something that I studied a lot in my PhD. You take that baby, and as long as you start within a few hours of birth, you cool them down to 33.5 degrees Celsius for 72 hours. And that significantly reduces death and disability.
Tim Ferriss: That’s 92.3 degrees Fahrenheit for yankees out there.
Tommy Wood: Although even in the US, many of the cooling machines are made in Europe, so they still run on Celsius. So those babies get cooled down, and that’s really the state of the art. Although now we’re starting to figure out that there are still a whole bunch of injuries where that doesn’t help, including preterm babies. So if you’re born preterm, cooling doesn’t help, actually it can be detrimental. And in that scenario, one of the things that they found recently, which is probably most beneficial, is caffeine.
Tim Ferriss: Really?
Tommy Wood: Yeah. Caffeine is not given for neuroprotection. It’s given because babies who are born preterm don’t breathe as well. They have this thing called apnea prematurity. So they don’t have a normal respiratory drive. So you give caffeine to stimulate that, but the trials that used caffeine to treat apnea prematurity, saw significant improvements in cognitive function.
Tim Ferriss: And those were durable improvements, or just during treatment with caffeine?
Tommy Wood: Yeah. So when you do these kinds of trials, usually you follow those babies up to something like two or three years old. That’s mainly because an NIH funded trial or an NIH grant lasts five years. So if you’re going to do a full trial in five years, then you can only follow — You have a year or two to enroll and treat, and then you have two or three years to follow them up. And so they see significant improvement at that age, but then also going into childhood, which is ideal. You really want to look out as far as you can. So then there’s now a renewed interest in caffeine and other brain injuries in babies, and that’s something that we’ve tested in my lab. There are some trials now starting in other brain injuries. But beyond that, in both groups, really the biggest impact on later outcomes is the home environment that kid goes back to.
So yes, my colleagues who are practicing neonatologists do a whole bunch of amazing stuff to keep these babies alive and keep their brains in good shape as much as they can when they’re in the intensive care unit, but actually the home environment is where the biggest impact happens, and so then that means that even if you have an imperfect start to life, there’s probably a lot that you can do as a parent, to help that brain to develop and grow as normally as possible.
Tim Ferriss: All right, we’re going to continue to talk about brain injury for a little bit, and then we’re going to talk about a whole lot of multifactorial prisms around cognition and whether or not you can intervene with the fates to preserve or enhance cognition as an adult. So we’re going to get to that. But if we make the hop from infant to adult, right, if you slipped on the ice and hit the back of your head and suffered a severe concussion, what would you personally do after that?
Tommy Wood: There are a few things that I think we can probably do, and we actually wrote a paper about this, came out last year, that covered various nutritional strategies, and most of the strategies would be nutritional supplements that I would probably lean on. And assuming that I didn’t have any control over what happened beforehand, ideally I do lots of things to improve the health of myself, because I think that’s going to affect how my brain and body then respond to the injury. But after that point, then there’s a couple of things that I would do. One, is I would manage fevers. So this goes back to the hypothermia that we talked about in babies. Lots of trials have tried hypothermia for traumatic brain injury in older humans and adults, and they haven’t really shown any benefit. What does seem to be beneficial is preventing hyperthermia.
So if you have significant trauma, one of the things that happens as the immune system gets activated is you get a fever. And that fever increases this gap between the metabolic demand in the brain and the supply of energy, because the mitochondria become damaged during the injury. So if you increase that gap because the higher metabolic rate, because you’re hotter, that seems to make that injury worse. And this has been found in some animal models, but also in some human data. So the most important thing to do is to prevent fevers.
Tim Ferriss: So, get your flu shots, et cetera, other things?
Tommy Wood: Well, so in this scenario, if you need to take Tylenol to prevent a fever —
Tim Ferriss: I see, take acetaminophen.
Tommy Wood: Right. Yeah, yeah.
Tim Ferriss: Right.
Tommy Wood: Yeah, acetaminophen, paracetamol, depending on where you are in the world.
Tim Ferriss: Yeah, where you are. Yeah.
Tommy Wood: Maybe even there are some devices where you can do some neck cooling or head cooling. They probably don’t have as much of an effect as some people think they do, but whatever you can do to maintain your body temperature. And so, antipyretics, so things that help prevent fevers, are going to be helpful. I would then also manage blood sugar. The main thing being probably avoiding things that are going to cause large glucose spikes. So avoiding refined carbohydrates, and —
Tim Ferriss: Why does that matter acutely after you whack your head?
Tommy Wood: So you see, again, in multiple studies, and we have to do this experimentally. So some of this comes from animal models, but if you create diabetes or the hyperglycemic during the injury or immediately afterwards, and some of it is driven by the injury, if you have an acute injury, you’re going to get higher blood sugar. So some is cause, some is effect, but it seems that these high glucose spikes are, again, stressful in that setting of an acute brain injury. So just minimizing that as much as possible. That doesn’t mean that you shouldn’t eat carbohydrates, but just I would avoid refining carbohydrates. When I worked with athletes at high risk of concussions, if you’re being taken off the field, a low risk thing is just to not chug Powerade as you’re being taken down the tunnel.
Other things that are going to become important with varying degrees of evidence, but still good enough that there’s a high positive asymmetry, right, high possibility of benefit with low risk, creatine supplementation. Creatine is probably more beneficial if you have it on board beforehand, but there’s at least one trial in pediatric TBI that showed creatine enhanced recovery. Omega-3 fatty acids are the same, would certainly include those as well. And then the next thing I would do is I would take exogenous ketones. I have them at home, there are things I’ve played with. I don’t use them regularly, but in this setting, again, I think there’s enough promise to suggest that they’re worth taking. I didn’t include that in this paper because we don’t have good evidence for it, but if I had a brain injury, I would take exogenous ketones.
Tim Ferriss: I would too.
Tommy Wood: Yeah.
Tim Ferriss: I would too.
Tommy Wood: And then there were a few other things that have an increasing amount of evidence for them. So there’s some studies on some B vitamins, particularly riboflavin, branch chain amino acids seem to be beneficial, and that seems to be by improving sleep. Then if you have sleep issues, melatonin has some evidence for it as well. I would avoid caffeine actually in this scenario. There’s a little bit of evidence that says that again, it’s probably due to increasing brain metabolic rate in that sort of early window, similar to high temperature. So I would avoid caffeine particularly early on. And then probably the most important thing that we have evidence for, is early return to physical activity. So low level aerobic exercise, as soon as you can tolerate it at a level that doesn’t make symptoms worse, and then increasing that over time as you get better, that’s going to be an important part of recovery as well.
Tim Ferriss: What’s the supposed mechanism of action with the return to physical exercise and the impact that has on the recovery from, say a concussion?
Tommy Wood: Yeah, there’s probably a few different mechanisms, and to be honest, I don’t think anybody really knows. Again, the evidence is best in pediatric brain injury, particularly pediatric sports related concussions, that’s where they’ve done most of these like randomized controlled trials. But there’s a few things that are going to be happening. You’re going to be improving cerebral blood flow, probably going to get a whole bunch of myokines, exokines that get released during physical activity. We know many of those can have a beneficial effect on the brain. And then you may also see improvements in sleep, right? We know that physical activity helps support sleep. So many of those could be going on at the same time, as long as you’re not doing a level of activity that’s then making symptoms worse.
Tim Ferriss: Mm-hmm, right. So we’re going to take a moment, not for a commercial break, but just for a topical break, to ask a very important question, which is, when you came in second at Washington’s Strongest Man in 2024, and then when you came in the top 20 in the world’s first ever fully off-road Ironman triathlon, what were your weights? What was your body weight in both of those cases?
Tommy Wood: So those two competitions were more than a decade apart, I will say. So in 2012 was when I did the world’s first fully off-road Ironman. It was initially called X-Man, and then Marvel sued the company. So it ended up being called X Tri ’24.
And so when I did that, I think I was probably something like low, 80 kilo, 82, 83 kilos, so like 185 pounds, something like that. And then fast-forward a decade, when I was competing in Washington’s Strongest Man, I was in the middleweight class, and to get into that class, I had to basically diet down and then do a water cut to get under 198 pounds. So I was just under 90 kilos on the day, although normally I’d hang out like 15 pounds higher than that.
Tim Ferriss: Yeah. Okay, super interesting. We may come back to that. Certainly going to talk about your own personal routines and tricks of the trade that you apply. Before we do that, I want to tie up a couple of loose ends, specifically infant baby, this thing you mentioned, DHA, and why that, and/or omega-3s more broadly speaking are important, right? And I, for instance, I’d say one meal a day is probably right now two cans of sardines, or chub mackerel mixed with some type of oil, like olive oil or MCT oil, with a splash of apple cider vinegar. It’s shockingly good, it sounds like cat food. It’s actually better than it sounds, with some salt. But could you explain why this DHA, et cetera, is important? You also mentioned the omega-3 in the context of recovery from brain injury. So why is it important and what is the prescription, so to speak? How can people translate that into something they actually do?
Tommy Wood: When you think about, again, sort of the structure of the brain, and you’re trying to develop the brain in the first place, then —
Tim Ferriss: Big pile of fat.
Tommy Wood: Big pile of fat. And a lot of that fat is DHA. And actually brain, if you don’t mind eating brain, brain is a great source of omega-3s.
Tim Ferriss: I tried it, I tried cheap brain in Turkey. I’m going to tell you, the presentation could have used some work. It was just like straight out of the formaldehyde jar plopped onto a plate. It was a bit much for me, to be honest, but, yeah.
Tommy Wood: You can fancy it up if you want, but equally, brain consumption is not required. So DHA tends to concentrate at the synapses of neurons. It seems to be really important for helping to regulate the release of neurotransmitters, like being part of the structural component of those synapses. It also tends to accumulate in mitochondria, and the DHA content of mitochondria is positively correlated with their capacity for energy production. Some of it could be due to some weird physical, as in physics properties of DHA, like how electrons move through it differently from other fats.
But anyway, it seems that particularly for mitochondrial function as well as synapsic function, DHA is critical, and so it sort of preferentially accumulates in those areas. Very important during brain development, so much so that the mother will sacrifice her own DHA stores so that the baby gets enough if she’s sort of borderline in terms of DHA levels. And it’s also why women in general tend to be better at converting shorter chain omega-3 fatty acids like ALA to DHA and EPA. It’s thought that that’s because that’s going to be needed for a baby one day, more so than in men.
Tim Ferriss: So eat brains or find someone you can breastfeed on. Am I hearing this correctly?
Tommy Wood: Yeah.
Tim Ferriss: I’m just kidding.
Tommy Wood: Are those the only two options? I’m not sure.
Tim Ferriss: I’m kidding. Oh, wait, I forgot about the fish. I forgot about the fish, yeah.
Tommy Wood: Or you could eat some fish. Optional third. Then we also know that DHA in particular, but also EPA, these are both the long chain omega-3 fast acids, they’re important precursors for various signaling molecules that are important as it pertains to brain function, but also recovery from brain injury. So —
Tim Ferriss: What is an example of a signaling molecule?
Tommy Wood: Yeah, so actually a lot of the various molecules that have various functions in our body activating receptors, turning genes on and off, are derived from different fats. And so in this setting, the ones I’m thinking about, are called like resolvins, maresins, protectins, that are derived from these unsaturated fatty acids. And so neuroprotect in D1 is one that people are very interested in, it’s being tested as, you know, you give it exogenously after different brain injuries. We’re not at a point where I would recommend that people take it, but that’s something that’s being studied right now. And neuroprotection D1 is derived from DHA. In the setting of brain injury, these resolvins and protectins seem to be really important for regulating the immune response, in particular switching off the immune response. The immune response is important, but we also need to be able to switch it off.
And that’s probably part of the role that they’re playing. When you look at long-term omega-3 supplementation, there was a study that was done in football players, where they randomized them to different levels of DHA across the season, and they found that those taking one to two grams of DHA a day saw less of an accumulation of a marker of brain injury in the blood, called neurofilament light, across the season. The thought being that all these small sort of subconcussive impacts that the kids experience on the field is generating this sort of low level of injury that accumulates across the season, and omega-3s or DHA seem to protect against that. So all of those to say that if you want to maintain brain function, and we see if you’re omega-3 deficient, you’re at higher risk of dementia, cognitive decline, that’s dependent on other things like methylation status, but it’s going to be an important component of maintaining brain structure and function.
So I think that kind of level, one to two grams a day on average, at least this is going to — you know? If you get two or three good servings of seafood a week or a reasonable supplement, that’s going to be probably enough to consistently hit those levels.
The other part of it is that your body will actively sequester extra up to a point. So when people are talking about different forms of DHA, like should you take your omega-3s as a phospholipid form or a triglyceride form. And the triglyceride form is more common in seafood. The studies that look at these over long periods of time, what happens is if you consume a lot of the triglyceride form from seafood, your adipose tissue is used as a storage place. So it cycles through the adipose and then it gets released and the brain can use it afterwards. So that probably requires you to spend periods of time where you’re accessing your adipose tissue, right? You’re not constantly eating. So exercise or periods of fasting may help you access that depot, but that depot allows us to then use these other forms of DHA that can sort of accumulate on our bodies over time and then we use them as we need them.
Tim Ferriss: All right. I’m wondering if there’s anything else, and it may end up circling back around as well, but is there anything else related to omega-3 specifically that you’d like to comment on? And I could be hallucinating here, it’s not just AI that does it, but omega-3, does that have — oh, no, it was B complex, which you’d brought up before perhaps. Or maybe there is an interaction with omega-3 and homocysteine.
Tommy Wood: Yes.
Tim Ferriss: I’m trying to figure out where homocysteine fits into the picture with respect to cognitive health.
Tommy Wood: Yeah. So there absolutely seems to be this interaction between omega-3 status and B vitamin status, particularly the B vitamins that are involved in methylation, so they affect the level of something called homocysteine. And this is something you can get a blood test for. And those who have inadequate B vitamin status or inadequate methylation status, have an elevation of homocysteine. There have been multiple trials that happened two or three decades ago, maybe even in the last decade, where people thought, “Oh, omega-3s are going to be the answer to dementia prevention, or B vitamins and homocystine are going to be the answer to dementia prevention,” and then they would give people B vitamins or omega-3s and then they didn’t see much of an effect.
What we found out later, I mean, the scientific we, was that both are required in order to see benefit. So this was probably first seen in the VITACOG trial, which was run by David Smith at Oxford, and they found in individuals with elevated homocysteine, so that was a level above 13, giving B vitamins to reduce homocysteine significantly improved rate of brain atrophy and cognitive function, only in those who had an adequate omega-3 status.
And the same thing was seen in the B-Proof trial subsequently, and then the opposite, which was seen in the omegaAD trial where they gave omega-3 fatty acids, but they found they only saw benefit in individuals who had a low enough homocysteine. It’s thought to be because if you want DHA to be in a membrane in a cell in your brain, it needs to be attached to some kind of phospholipid, right? Fats don’t just float around, they’re part of these phospholipids that sit inside the cell membrane. And that requires it to be attached to a head group, these head groups are usually derived from choline or an ethanolamine, although those can be converted from one to the other. And in order to do all of that kind of biochemical attaching and placement, requires methylation. It’s very methylation dependent. So it’s thought that in order for DHA to do its job, you need adequate methylation status so that all those processes can run. And if you only have one or the other, then you won’t see benefit.
Tim Ferriss: Got it. Yet another reminder for long-term listeners, this will come as no surprise, but you’ve got to get blood tests, comprehensive blood tests, and really track this stuff with trend lines over time. But that’s a much longer conversation, but suffice to say, you need the orchestra, right? Or you need multiple legs of the stool.
Tommy Wood: Yeah. Yeah.
Tim Ferriss: It’s not just one leg of the stool.
Tommy Wood: Mm-hmm.
Tim Ferriss: All right. So let’s maybe return to, I’m going to use a term that’s a little dangerous to throw around, but kind of first principles or fundamentals maybe is a better way to phrase it. I’m terrified as many people are of this thing called Alzheimer’s disease. And you could throw in dementia, cognitive decline in general, right? And conversely, very interested in extending health span. I’m not totally convinced that we’re going to get to 150 years, 200 years —
Tommy Wood: Yeah, me neither.
Tim Ferriss: — like all the tech billionaires might want to have us believe, but it does seem, certainly if I look at my own health span, kind of local maximum right now for myself, there’s just capacity right now compared to prior generations, I feel very good about it. So I feel like I can extend that runway. And cognition for me is just one of the most, maybe the most important pillars of that. Because having seen multiple people disintegrate cognitively, they don’t just lose their ability to remember. They basically lose their identity, right? They lose their ability to emote. It’s a loss of the self. I mean, it’s a death before death almost in a way. So really would love to do anything possible with the right risk benefit ratio, to avoid it. But fundamentals. Should we talk about, I’m going to fuck this up, Auguste Deter, Auguste Deter? Deter? How do you say this name?
Tommy Wood: Auguste Deter, I think.
Tim Ferriss: There we go. Yeah. All right. Who is this person? Because I’m guessing most folks will not recognize the name. Certainly I didn’t recognize the name. Hadn’t seen it until I got a couple of notes from you, prior to hopping on.
Tommy Wood: Yeah, so Auguste Deter, or if you read some of the original papers, Auguste D, was Alzheimer’s index patient. So Alois Alzheimer, that Alzheimer’s disease is named after, was a psychiatrist in the early 20th century, and he took a particular interest in individuals who had sort of rare or unusual cases of presenile dementia. So what now most of us call Alzheimer’s disease, which is sort of a late onset dementia or what was called a senile dementia, which just meant that it occurred after 65 years old, that was not what Alzheimer studied. He studied unusual dementias where people who were quite young in their 40s or 50s experienced significant cognitive decline and dementia, and Auguste Deter was one of them. He then, after studying them as a psychiatrist or working with them as a psychiatrist, after they died, he then looked at their brains under a microscope.
So he was the first person to see amyloid plaques, tau tangles, that are now sort of pathognomonic. They’re like what we consider to be required as part of Alzheimer’s disease. But it’s just interesting that what we have now is not what he studied. So over time, people thought that the brains of individuals who had this sort of early onset Alzheimer’s or these early onset dementias that Alzheimer’s studied, and those who have these late onset dementia that we now call Alzheimer’s disease, those brains looked very similar under a microscope, so they were kind of lumped together. Although we do still have two kind of broad forms. The early onset Alzheimer’s, which is usually a single genetic mutation in something like a precinct gene or the amyloid precursor protein gene, that then creates a picture that’s much more like what Alzheimer’s studied, or the late onset Alzheimer’s, which is what most people think about when they think about Alzheimer’s disease is probably somewhere between 95 and 99 percent of cases of Alzheimer’s.
And there is a genetic component to risk, but it seems to be much more tightly tied to lifestyle and the environment and other lifestyle factors that we have some control over, hopefully. And the reason why Auguste Deter is interesting to me is because I don’t think she actually had Alzheimer’s disease as we would now think of it. So there have been groups that have taken sections of her brain from Alzheimer’s old collections, and they’ve done genetic studies, and she didn’t seem to have any of the genes that cause early onset Alzheimer’s disease, or any of the mutations that cause early onset Alzheimer’s disease. She wasn’t an APOE4 carrier. I think she was 3-3, if I remember correctly. So she didn’t have any of the genetic risk factors. And so what caused this and caused this so young, I think she was in her 50s, is still actually unknown.
There have been some recent retellings of the story. Some people think that she may have had neurosyphilis, and neurosyphilis actually causes amyloid accumulation, it looks very similar to Alzheimer’s disease.
Tim Ferriss: Neurosyphilis, meaning she had syphilis and she just —
Tommy Wood: It got into her brain.
Tim Ferriss: Got it, mm-hmm.
Tommy Wood: Yeah. And that can look very similar under a microscope, especially 100 years ago or more than a hundred years ago when we just sort of first starting to look at brains under microscopes. And then others suggested that it could have been more psychiatric. Nutrient deficiencies, certainly very common, could have been just like the other components of her environment. She was by all accounts like a downtrodden housewife that maybe didn’t get much engagement or stimulation or wasn’t particularly well treated at home, and that could have sort of precipitated it. And we don’t actually know, but many of these things, it just seems interesting that it’s probably quite likely she didn’t have Alzheimer’s disease at all.
Tim Ferriss: Wild. All right. So I’m going to take this in a few different directions, and as per usual, turn it around to be self-serving for yours truly. But I’m going through some of the notes that I had for our conversation and I’m sure I will have mentioned this in the bio and intro at the very top of this show, but I have this bullet in front of me and I just want to make sure this is something you feel is defensible. 45 to 70 percent of dementia is preventable through lifestyle. Is that a defensible statement?
Tommy Wood: Yes. As far as we think it can be defensible.
Tim Ferriss: Yeah. I’m not trying to put you in the hot seat. I’m just saying, I don’t know where that number comes from.
Tommy Wood: So I can tell you where that number comes from.
Tim Ferriss: That sounds great, right? That seems like a ray of sunshine and a pretty gloomy possible conversation where people think you’re just like, “Okay, there’s genetic determinism. You got this thing and you’re screwed. If you have a bunch of it in your family, you’re also screwed, et cetera.” But it seems like there’s a lot you can do to right the ship for a period of time. Okay. So where does 45 to 70 percent of dementia is preventable from lifestyle? Where does that number range come from?
Tommy Wood: So 45 percent comes from the most recent edition of the Lancet Commission Report on Dementia Prevention, which is overseen by Professor Gill Livingston and brings together all these different experts in dementia and its risk factors. And they sort of scour the research for observational studies and then as much as possible, interventional studies. So a lot of it is epidemiological data. Looking at different risk factors that have a consistent relationship with dementia risk. And then, you do these sort of statistical calculations to look at something called population attributable risk.
Which is essentially saying, if I eliminated this risk factor entirely from the population, what percentage of dementias would I expect to no longer happen? That’s essentially what it means. And all of these different percentages add up to 45 percent. So it’s a couple of percent for smoking, it’s 7 percent for a low level of earlier education. It’s like a percent for alcohol. Then there’s hypertension, hearing loss — or sorry, high blood pressure. Hypertension is the fancy medical word. High blood pressure, hearing loss, obesity, low physical activity.
And all these different percentages add up to 45 percent. There are some things that were on that list or that aren’t on that list that I think should potentially be included. So like sleep loss or poor sleep and insomnia is not included. Late life physical activity was discussed in the report but was not included even though there seems to be some good evidence there. So actually that suggests that there may be more than 45 percent that are preventable. And there are other studies, like there was one big study done from the UK Biobank data by Professor Jin-Tai Yu that estimated that up to 72 percent of dementias were preventable.
If this was going to happen, this would require a complete societal overhaul because a lot of this risk comes from low socioeconomic status, low educational and work opportunities, like all these other things that are kind of baked into societal risk for dementia. But others are things that we have more control over, like level of physical activity, whether we smoke, whether we drink. So some is directly under our control. That’s probably something like 15 to 20 percent, maybe more.
And some is kind of driven by these maybe bigger kind of societal risk factors. But if you did all of that and we managed to completely change how everybody lives and all of these risk factors, the idea is that maybe even up to three quarters of dementia cases could be entirely prevented. Now, that’s very different from saying that I could guarantee that you will not get dementia, right?
That’s not the same thing. We’re talking about this stuff at the population level. And I have to say this because if I talk about physical activity or sleep or nutrition, and these are really important for dementia risk, somebody will always say, “Well, my family member did all that stuff and they still got dementia.” And so we’re talking about probabilities. We’re not talking about, I can definitely guarantee that somebody will avoid dementia, but I think we can definitely say you can stack the deck massively in your favor through a whole variety of actions that should decrease risk long term.
Tim Ferriss: All right. So part of the reason that I make this very self-interested is because I’m self-interested. The other part is that I think the personal is very easy for people to concretize for themselves so they can interrogate how they’re behaving, what they might do differently, what they might add, what they might subtract. So let me tell you some of what I am observing and then some of what I’m doing. And I would love for you to identify or maybe speak to things that are low hanging fruit or like reasonably accessible that are missing, right?
All right. So a few things. Lots of folks in my family currently who I’m caring for in one way or another deteriorating very quickly with what has been called Alzheimer’s — again, kind of a tricky diagnosis, not sure how much they’re actually looking at, whether it’s beta amyloid, tau or anything else, but certainly in some cases, these blood relatives are APOE33. So I’m like, “Huh.” It also raises the question of, is there an undiagnosed infection? Maybe it’s an STI. Who knows? I don’t know what the answer is to that.
I mean, it’s kind of another line of testing perhaps. And so, I’ve been trying to do a few things for myself, recognizing that if someone starts to really show obvious symptoms that can’t be easily explained away in their 70s, let’s just say, the process probably started, what, decades earlier? I mean, things have started, like the cars have started to pile up, the machinery has started to break a lot sooner. So it would seem like the earlier you intervene with better lifestyle changes, et cetera, the better off you’ll be.
So I’ve got the fasting and the ketogenic diet and all of that stuff, which I do regularly. They’ve got the exogenous ketones, which like you, I use sparingly. I don’t use them all the time because particularly like before this conversation, I took 11 milliliters of a ketone monoester. But I think once all is said and done, it’s basically 51 percent, 1,3-Butanediol. And I have some concerns around 1,3-Butanediol specifically in chronic use or at sufficiently high doses, say 30 plus per day.
So I tend to use it for special occasions like this, toast, have a glass of champagne, have some exogenous ketones and off to the races. All right. So there’s the ketone piece, which I think is non-trivial. There’s the — I would say for the most part, avoiding crazy glucose spikes all the time. Occasionally I’ll have Christmas, sure, had a bunch of cookies. Who cares? It’s Christmas. It’s fine. Had a bunch of pie. But I have a CGM on right now. I had a continuous ketone monitor on at the same time for about 28 days.
I’m really interested to look at all of that, but I’m generally following like a slow carb diet or Mediterranean style diet. I am getting enough omega-3. I know that because of fish intake and also when needed supplemental intake. I do seem to be a poor methylator. So I’m taking B vitamins, L-methylfolate, all of that stuff. Tracking blood once a quarter. So I’ve got super comprehensive stuff on that side. Zone three training, I do find it as boring as watching paint dry. Even when I’m listening to a podcast or watching a Netflix mini-series or something.
But probably doing two to three sessions a week, let’s call it 30 to 60 minutes, walking every day, lots of walking and we’ll come back to that because actually, I can’t resist. We probably will come back to it, but walking 4,000 plus steps a day reduces dementia risk 25 percent optimal, 10,000 steps daily, and then reverses hippocampal shrinkage, two percent increase versus expected one to two percent decrease. That’s the bullet that I highlighted. And then, weight training a couple of times a week. I could keep going. I’m not going to bore people to death with this Dr. Evil life story.
But I will say that I’ve also wanted to get a snapshot of what things look like. So I’m going to be having a call. I won’t mention the company by name because I haven’t done all of my due diligence. They have some scientific advisors who I think are very credible, but have done brain MRI. I’ve done the blood draws, the DNA tests, everything else, because I’m APOE34. And looking at the brain MRI, I mean, I’m a muggle, right? So I probably shouldn’t be allowed to sort of grab the wheel when driving on the MRI reading.
But I wanted to look at the data. It seems like, and who knows how defensible this is, but my MRI predicted brain age based on hippocampal volume, et cetera, et cetera, et cetera, is 46 instead of 48. So I wasn’t thrilled about that. I’m like, “Well, all right, not sure what else I can do. Maybe a flood dose of ibogaine.” That’s pretty interesting data around that from Nolan Williams, but not something I would recommend to most people, including myself. So there’s that. Did a whole battery of cognitive testing through this startup.
Now that came in at brain age of 20 years predicted, 28 years younger than your chronological age, but you can kind of beat the test. There’s some gamification, so I don’t know how heavily to weigh this, right? So brain age of 20 years, man, sounds great. There are certain aspects that are harder to game, like reaction time testing. Okay. So I had like 267 milliseconds basically versus 406 milliseconds. Okay, great. There could be some training effect, like learned training effect, but then there’s like number span, focus.
I won’t bore everybody with that, but word pairs, names, and face pairing. With mnemonic devices, if you train yourself, you can really sort of game the test. And TBD on like proteomics, I’m getting all sorts of stuff drawn to try to get an accurate baseline of where I stand now so that I can measure all of the effect hopefully of these interventions over time.
What would you say are like, there are 20 things I could mention, but like here are three or four that I would also pay attention to.
Tommy Wood: So first, a couple of comments on all the stuff that you mentioned about what you’re currently doing. I’ve already mentioned that I think that there’s a lot of promise for ketones. I’m not sure that ketones necessarily have to have a place in prevention and I’m not sure that you would necessarily need them from a prevention standpoint. There are some reasonably good data. So like the medium change regulatory work from Stephen Cunnane’s lab, is quite compelling in the Alzheimer’s disease taking MCT oil seems to increase acetoacetate uptake into the brain.
This is associated with improvements in cognitive function and this is overcoming what looks like an energetic deficit in individuals who have Alzheimer’s disease. And this is something that, again, is one of those things that are pathognomonic. We think that we see this and this is kind of like part of the picture of Alzheimer’s. We see that like this is Alzheimer’s.
Tim Ferriss: Yeah. Can I pause for one second?
Tommy Wood: Yes.
Tim Ferriss: Real quick, don’t lose where you are. We’re talking about MCT oil. Number one, if people want to play with MCT oil, be close to a bathroom when you start. And if you combine it with double espresso and creatine, definitely have some depends around. The second is the ketogenic diet for me, just to briefly provide a little more context, is also for its, I think, plausible anti-cancer effects and just kind of all cause mortality plus mental acuity. I just think a lot faster when I have more metabolic flexibility with something like intermittent fasting.
That’s another thing I do a lot of, where my body has just got the machinery to produce ketones. But yes, I hear you. Okay. MCTs.
Tommy Wood: So the thought being here, right, there’s a difference between what you find works really well for you versus what the listener thinks they should have to implement for themselves. And so, I’m now going down the road of why I don’t think we all need to be in ketosis to prevent dementia. So I think from a therapeutic standpoint, it seems to be beneficial overcoming this energetic deficit that we see in Alzheimer’s disease, particularly early Alzheimer’s disease, or maybe it’s easier to overcome earlier on.
And one of the ways we look at this is with something called a PET scan, right? So you do an FTG PET, you give a labeled glucose molecule, you inject that, you see how much gets into the brain in individuals with Alzheimer’s disease, less glucose is getting into the brain. Now, we’ve traditionally come at it from the point of that glucose can’t get in, right? There’s some kind of metabolic disease, instant resistance. This is where the idea of type three diabetes has come from, insulin resistance in the brain, that glucose isn’t getting in.
But a PET scan cannot differentiate between the glucose can’t get in versus the brain isn’t asking for that glucose in the first place. And there are actually some very nice studies that looked at brain activation and glucose uptake in response to cognitive stimulus in individuals with Alzheimer’s disease. And what they see is that yes, at baseline, there’s less glucose being taken up into the brain of individuals with Alzheimer’s disease, but if you stimulate that brain cognitively, it can take up glucose just fine so that you get into the range of a normal healthy brain in early Alzheimer’s disease.
Once you get to like advanced stage dementia, it’s too late. But at that early stage, I think part of the reason why we’re seeing less glucose uptake is because those parts of the brain are less active because we’re just not using them as much. And just like glucose uptake into the muscles, which is demand driven, right? You work your muscles, they ask for more glucose, they take more up. The brain seems to be the same, at least early on. So I think we think a lot about the supply side, the energetic supply side, but I don’t think we think enough about the demand side.
How do we create energetic demand in the brain such that we are maintaining glucose uptake, maintaining energetic state, and then doing that also maintains all the metabolic machinery that you really care about in terms of long-term function.
Tim Ferriss: Can I just muggle translate for a second?
Tommy Wood: Yeah.
Tim Ferriss: All right. So if I’m hearing you correctly, this is something I’ve chatted with Dominic D’Agostino about, but I’m wearing this CGM, right? So I’ve got this device on my arm that tells me what my glucose levels are at any given point in time with whatever, three minute sampling or something like that. You’ve got to calibrate that with a fingerprint, by the way, folks. But if I eat a meal and then I don’t go for a walk, my glucose spikes and I might conclude, “Wow, my muscles are really not accepting glucose.”
My muscles are bad at accepting glucose, but that’s not actually true in my case, right? If I go for a walk or I do some light exercise, I guess it’s like GLUT4 transporters or whatever, get all jazzed up and help that glucose to be better disposed into muscle tissue, right? And like you said, in the case of the brain and people referring to Alzheimer’s as type three diabetes, it’s like, “Wow, the brain can’t use glucose,” or it’s very bad at using glucose. But if I’m hearing you correctly, the additional question that they should be asking is, is it just that or is the brain not asking for glucose, right? The equivalent of the GLUT4 transporters, right?
Tommy Wood: Yep.
Tim Ferriss: Is the brain basically offline? It’s a car up on blocks, but if you take it down, yeah, it’s going to use gasoline just fine. So if that’s the case, I guess it’s just a call to action for more stimulation of the brain. And when I was first just coming across your notes that you sent prior to this conversation, I went on ChatGPT and I was like, “What are the most glucose intensive activities for the brain?” And they gave me a bunch of mental exercises, which isn’t exactly what I was looking for, but I could have prompted it better.
And it said, “But even still, the sort of improvement or increase might be plus, less than 10 percent in terms of the total.” And then I was like, “Well, are there other activities such as physical activities that might increase glucose uptake in the brain?” And it gave me a whole list, but rather than regurgitate that, are all types of stimulation created equal or are there some sort of 80/20 analysis like, okay, there are some tools that are better for the job.
Tommy Wood: Yeah. So when looking at this purely in relation to glucose uptake, those data don’t exist, right? So I’m going to have to extrapolate further than that. And I think that’s important because a decrease in glucose uptake is just a signal that that area of the brain isn’t as metabolically active, which means we’re not just not using it as much at the simplest level. So then if you think about various activities that we could use to stimulate the brain, which do seem to be protective in various different ways, both they can enhance cognitive function in the short term.
And then protective against dementia in the long term. Actually, this ties very nicely into the comment that I was going to make about your physical activity routine, because this is where I think some things could be layered on.
When you look at the different physical activities or exercise and how they affect the brain, different types of exercise affect the brain differently. So you certainly need a smorgasbord of all of them to kind of get a global support for the brain. But something that seems to be particularly beneficial is coordinates of exercise or open skill exercise, plus or minus things that have a navigational component.
And these are essentially sports or activities where you’re constantly having to respond to the environment and adapt. That’s what makes them open skill rather than closed skill or unimodal exercise like going for a jog or sitting on a bike or something like that. So when they compare sports or activities that have the same amount of physical challenge, but a different amounts of cognitive challenge because of the open skill nature, you see greater benefits in terms of brain structure, improvements in cognitive function.
Tim Ferriss: And open skill just means high level of unanticipated variety or variety. What is it?
Tommy Wood: So both. So it basically has a greater amount of complex motor skill required. Some of it can be learned. So dancing is one example, right? So because you learn the steps of a dance, but some —
Tim Ferriss: Single strongest activity for dementia prevention. Am I overstepping there?
Tommy Wood: Yeah, probably. So if you look at physical activity and the effect that it has on cognitive function and also —
Tim Ferriss: Or one of mental health.
Tommy Wood: Yeah, but in terms of both mental health, so studies in depression, as well as studies looking at different activities that people do and the risk of dementia, their risk of dementia, and studies where they randomize people to different types of activity, including dance, dance seems to have the highest sort of effect size compared to other types of physical activity. But there’s multiple components to dance, right? So you have to learn the steps, but there’s also a social component, there’s a music component, right?
All these things are probably part of the magic source together, but open skill sports also include board sports or ball sports or team sports where you’re having to react to the environment and other people around you.
Tim Ferriss: Do you say bull sports like rodeo? What are we talking?
Tommy Wood: No. Ball.
Tim Ferriss: Ball. B-A-L-L.
Tommy Wood: B-A-L-L.
Tim Ferriss: Awesome. It’s not going to be good for the TBI to get people on top of bulls, but okay, got you.
Tommy Wood: I think bull sports would probably be good if you could avoid the TBI, actually probably right up there. Similarly, martial art is also good as long as you don’t get punched in the head a bunch or kicked in the head a bunch —
Tim Ferriss: Or choked out too much.
Tommy Wood: Or choked out too much. So these — beyond the physical strain that these exercises have, they seem to have an additional aspect of requiring reaction speed, challenging processing speed, learned complex motor skills, those — they seem to have an outsized effect in terms of cognitive function. Something else, just to — this is kind of an aside, but just based on the physical activity component, when you’re looking at more aerobic or even like closed skill, unimodal, running, cycling kind of sports.
The benefit seems to be intensity dependent. So yes, if you’re not doing anything, then going for a walk and walking a certain number of steps a day is going to be great, beneficial, decreased dementia risk, absolutely. But looking at hippocampal structure and function, for instance, which you mentioned, right? You’re talking about measuring your hippocampus on an MRI scan. Higher intensity activities seem to be better.
So probably the longest study where they ever did something like this, they had people, this was an Australian study where they had people do the Norwegian 4×4 protocol, three times a week for several months.
Tim Ferriss: My God.
Tommy Wood: And so for anybody who doesn’t know what this involves, it’s four sets of four minutes on a treadmill at 85 to 95 percent of your maximum heart rate with four minutes rest, you do that four times. It is miserable.
Tim Ferriss: I mean, that’s like, pretend like you’re being chased by wolves through the snow for four minutes. And then take a four minute rest and then do that. Yeah.
Tommy Wood: Four times.
Tim Ferriss: Yeah. Okay. Right.
Tommy Wood: But they saw significant improvements in hippocampal structure and function that were maintained for several years after the end of the trial.
Tim Ferriss: Several years.
Tommy Wood: Several years after trial.
Tim Ferriss: So a few months and then sustained for several years.
Tommy Wood: Yeah. I think they followed them up for five years after the end of the trial.
Tim Ferriss: That makes it much more interesting.
Tommy Wood: I think a lot of this is driven by lactate. So when we talk about the various things that support the brain through exercise, we often talk about BDNF, brain derived neurotrophic factor, which has increased with exercise. But the BDNF that you can measure in the blood, that’s produced by the muscles during exercise doesn’t really get into the brain very readily. Most of the BDNF we have in the brain is produced locally and it’s actually driven by things like lactate. So lactate does get into the brain.
The more lactate you have in the blood, the more it gets into the brain. And then that acts as a histone deacetylase inhibitor that activates the blood and the BDNF ketones do the same thing. Osteocalcin, which is released when we sort of load the bones structurally, it’s released from bones, seems to do something similar. So generating lactate seems to be beneficial — probably because one of the things it’s doing is it’s generating more BDNF that then is associated with improvements in hippocampal structure and function.
So as long as you’re doing sports that have some high degree of intensity, so you’re regularly producing lactate and then, either in the same sport or separately doing these sort of high skill, high reaction time, open skill kind of sports, that’s probably going to be beneficial from an exercise standpoint.
Tim Ferriss: I’m still completely stuck on the three times a week, basically VO2 max training, right?
Tommy Wood: Yeah.
Tim Ferriss: For a few months. Is a few months like three or four months, or how many months was it?
Tommy Wood: The study was either six or 12 months. I can’t remember the intervention period. It was one or the other.
Tim Ferriss: And with durable effects over a follow-up period of five years.
Tommy Wood: Five years.
Tim Ferriss: Something like that.
Tommy Wood: Yeah.
Tim Ferriss: That is a great investment. That makes it a much more compelling sales pitch for me. And like I’ve done plenty of VO2 max training in the past, but it’s not necessarily fun, right?
Tommy Wood: No.
Tim Ferriss: I mean, I will say, if you can, again, avoid getting your arms snapped, exhibit A right here with my elbow surgery, but if you can avoid the breaking limbs and getting choked out too frequently, something like jiu-jitsu is actually fantastic because you might have three to five minute rounds and then, you take a break for a round and then you go back in and chances are, depending on who you’re rolling with, it’s going to be pretty intense. Obviously, it depends on how competitive the gym is, but the durability is just remarkable. That is really, really, really, really interesting.
Now, is the threshold for sufficient intensity, I imagine it varies tremendously from person to person, depending on lactate threshold, right?
Tommy Wood: Yeah.
Tim Ferriss: But like for you, do you need to do something approaching the Norwegian 4×4 to cross the threshold sufficiently in your mind or does something less suffice?
Tommy Wood: Yeah. The problem with having just one — I mean, it’s one very good study, but just having one study on this is that we get really focused on the protocol, but I think that anything that is regularly producing, you’re getting above your lactate threshold, you’re generating significant — several millimoles of lactate. I don’t think people need to measure it, but if you’re getting six, seven plus, something like that, you’re definitely going to be in that range.
Tim Ferriss: Is there something, like people use a talk test, for instance, Peter Attia talks about this for zone two training, where you can kind of have a conversation and be labored short sentences, but you don’t really feel like it, as an indicator that you may be roughly sort of in zone two. Is there an equivalent for that range of lactate?
Tommy Wood: Not that I know of.
Tim Ferriss: 10 percent from puking into a bucket.
Tommy Wood: Yeah, it’s definitely going to be like misery related. So if I think about a lot of the training that I did as a student, I was a rower. And this is something that —
Tim Ferriss: Brutal. You love misery.
Tommy Wood: Actually, I don’t love misery enough, which is why probably I wasn’t as good a rower as I could have been. But there are lots of protocols where you’re doing relatively short sprints with relatively long rest periods that still generate large amounts of lactate. And so in studies where they’ve done this, you’re talking about 30 seconds flat out on a bike or a rowing machine with several minutes of rest times six, eight, 10 rounds. By the end, you can generate a lot of lactate without having to do something continuously for several minutes at a time.
I was just reading that one of the favorite training protocols for one of the world champion rowers was 45 seconds, flat out, completely flat out on the rowing machine, within six minutes of recovery, but doing that several times. And then at the end, you’re generating several millimolar of lactate. So I think anything like that, that’s going to get you in that zone, it just requires maximum effort for even just like 20 to 40 something seconds, even with several minutes break in between, you’re going to be hitting that.
Tim Ferriss: So I imagine the gold standard, do you have some guy in a lab coat with a clipboard who pricks your finger or something and does these blood draws to determine the millimolar concentration of lactate? Is there a breathable option as there is with ketones, right? Where you can measure acetone through something that looks like a breathalyzer as opposed to a finger prick for BHB? Does anything like that exist and make it a little —
Tommy Wood: No, they’re working on continuous lactate monitors just like you would have — and some people do sort of have those, because they’re right near being commercially available. So some people do have access to those already. But equally, I would argue that it doesn’t matter that much. Just like go and do something really, really hard for a short period of time and do that a few times over and do that relatively regularly. That’s probably enough majoring in the minors that you need to do to get that benefit.
Tim Ferriss: Sounds like my sled assignment. I do love my sled pushing and pulling. You can definitely wipe yourself out with that stuff.
Tommy Wood: Okay. All right.
Tim Ferriss: Without necessarily the impact of me trying to run from wolves on a treadmill or something. Okay. So I do want to take a brief commercial break, but it’s not for any sponsor. It’s just to mention that, and then we’re going to kind of dive straight back into the programming and discussion. But you have a book that is coming out shortly called The Stimulated Mind. It goes through all the stuff we’re talking about and a lot more. People should pick it up, that’s Dr. Tommy Wood, obviously, but The Stimulated Mind. There’s so much horseshit and charlatanism floating around out there in the world of anything related to cognition and memory. It’s part of the reason — segue is a little awkward, but I was like, that’s part of the reason I wanted to have you on is not to highlight necessarily that, but the antithesis of it, which is someone with real clinical expertise, research credentials, who is also a practitioner. It’s like you walk the walk.
And I wanted to ask you, you mentioned supplements earlier, and of course everybody loves to hear about supplements. But what are some that may not be on the usual list of suspects, so to speak? One, I would love to hear you speak to is CDP choline. People might not think of xylitol as a supplement, but certainly you could argue that maybe there’s a place for it. Do you want to add anything to that and just expand on those?
Tommy Wood: Sure. I can expand on those. I think that the supplements that we have the best evidence for they start with those core nutrients that we could get from the diet, but if we don’t, then we definitely should supplement. So we’ve mentioned omega-3s, B vitamins, especially those involved in methylation. So that’s vitamin B12, folate, which is B9, riboflavin, which is B2 and then B6. Vitamin D, obviously critical. Iron supplementation, particularly if people are anemic. So that requires a whole assessment for why are you anemic in the first place, but often particularly more common in women. And many of the symptoms that women may experience around perimenopause are associated with inadequate iron status. So getting your iron status checked and addressed is really important. Magnesium, certainly critical as well.
If we’re thinking about other things that do seem to have both an acute and long-term benefit in terms of cognitive function, then all the kind of antioxidant polyphenols are very interesting, particularly those that come from berries, but related ones in coffee, tea, on the skins of roasted nuts and seeds, they have similar effects. And so you mentioned choline, and right at the beginning when we were talking about omega-3s, I think choline is critical because of its importance as a head group for fats to be attached to in membranes. That’s maybe one of the reasons why it’s important for the brain. And various estimates suggest that we’re becoming increasingly choline deficient as we stop eating things like eggs and liver, which are our richest sources of dietary choline. But there are randomized controlled trials in two different settings that we’ve talked about already. So one in older adults already experiencing some degree of cognitive decline where supplementing with CDP choline, which is also called citicoline, seems to improve certain aspects of cognitive function.
And then again, after traumatic brain injury, there are meta analyses that show that supplementing with CDP choline can improve some neuropsychological outcomes, in particular after TBI. So I think most of us can probably get choline from the diet. But in some of these cognitively degraded states, we might call them something like 500 to 1,000 milligrams a day of choline seems to be beneficial.
Tim Ferriss: Do you take it or do you just get it from eggs and salt?
Tommy Wood: I get it from eggs and liver. And some seafood, sardines have some choline in. As do some whole grains, like oats have some, quinoa has some, so all of it kind of adds up.
So I don’t supplement the choline. I do supplement with creatine. I don’t have the perfect trial that creatine is going to prevent dementia, but I think we’ve seen enough interesting data across depression. Again, sleep deprivation —
Tim Ferriss: Sleep deprivation. How many grams do you take daily? What’s your standard daily dose?
Tommy Wood: I take 10 grams every day.
Tim Ferriss: Single dose or divided, doesn’t matter?
Tommy Wood: So I take it all in one go in the morning. There’s some evidence that suggests that once you get above five grams, you probably start to saturate creatine uptake transporters, so maybe you don’t take all of it up. But the reason why I take it all in one go is because I remember to take all of it in one go. Another reason is that I find creatine to be quite cognitively stimulating for me. So you took your ketones. I took my creatine before I got on this call.
Tim Ferriss: I took five grams of creatine too.
Tommy Wood: And so if I take creatine later in the day, I don’t sleep as well. It’s very noticeable for me, but that’s not the case for everybody. Some people take creatine and they don’t notice the cognitive effect. It doesn’t affect their sleep, so it’s very different from person to person. And so those are the reasons why I just take it all in one go in the morning. But especially if you’re going to take over 10 grams, 20, 30 grams, you’re probably best splitting it up into several doses so that you absorb more of it.
Tim Ferriss: Yeah. Or 30 grams at one go also is tempting the gods to smite you with a really, really bad bathroom situation.
Tommy Wood: So yeah, a lot of people do mention GI side effects from creatine. I think some of that is due to the quality of the supplement that you’re taking.
Tim Ferriss: Yep, I agree.
Tommy Wood: So if you’re taking like Creapure Creatine Monohydrate, that’s what most studies that have tested creatine have used. And there was actually a systematic review meta analysis that just came out that found that across all the studies they could find compared to placebo creatine, didn’t have any additional GI side effects. But also those studies use high quality creatine. Also, not all those studies use 30 grams. So you could certainly get to a point where you’re going to start to have GI effects based on those.
Tim Ferriss: Yeah. I think it also has to do with the fact that my polypharm in the morning when I’m just getting booted up, it’s like I might be having the coffee plus the creatine plus the sardines. Yeah, there’s a lot going into the cocktail of potential disaster, which you do acclimate to. Quick question before I forget, on lactate. Is there any argument to be made for anything that you would ingest or otherwise put into your body, not to avoid doing the intense exercise but to increase the amount of lactate that you uptake into the brain? Or is that something that people have looked at or is that just risky business and to be avoided because you’ll end up in like — I don’t know, like some type of acidosis or some other problem?
Tommy Wood: So people have looked at exogenous lactate itself, usually as lactate salts, just like people have looked at ketone salts. You can bump up blood lactate a little bit, but similar to ketone salts, you don’t get nearly the increases you do with other compounds. You don’t need to do anything to increase brain uptake of endogenous lactate because the brain will generally just take up as much as you’ve got, similar to ketones.
Tim Ferriss: Yeah, I think I misspoke when I was asking the question. I guess it was just increasing the amount of circulating lactates, so your brain just sucks it up like a vacuum.
Tommy Wood: Yeah. No, I think you can make plenty of lactate yourself. So another way to do it, blood flow restriction is another great way to produce lactate with low load. And there were some studies where — well, they have them do leg presses, but like sets of 20 leg presses wearing blood flow restriction cuffs, but that will get you up there as well. Again, several millimolar of lactate. It’s not fun.
Tim Ferriss: I think I’d rather do the Norwegian 4×4. Yeah. Oh, wow, that’s intense.
Tommy Wood: So that’s another way to do it. So if you, for whatever reason, don’t want to do sprints on a row machine, you can probably get up there with some blood flow restriction under low load and high rep. But no, I don’t think there’s anything that I would take to increase lactate, just because you can make it so easily yourself.
Tim Ferriss: All right. So I want to hop on the low flow restriction because I have — what make and model do you use? What’s your kind of tool of choice for the BFR stuff?
Tommy Wood: I use the B Strongs. So they have —
Tim Ferriss: Excuse me?
Tommy Wood: The company is called B Strong.
Tim Ferriss: B-E Strong?
Tommy Wood: No. Capital B Strong.
Tim Ferriss: Okay, got it.
Tommy Wood: I have no real —
Tim Ferriss: Affiliation.
Tommy Wood: I have no affiliation with them other than I know some of the guys who work there, but I paid for my device myself. So it has leg and arm cuffs, but it comes with like a Sphygmomanometer. One of those blood pressure things to kind of pump it up to get the pressure. And those are the ones I use.
Tim Ferriss: Yeah, nice and simple. I’m testing a few different ones right now. So when you travel, people think of exercise as this thing that involves potentially all sorts of machines and you need your kit. There can be a lot of excuses or things that people imagine as obstacles that are not in fact obstacles. So talk to me about your exercise when traveling with blood flow restriction. What does it look like?
Tommy Wood: So as my wife calls it, I have my gym in a bag, which I take everywhere I go when I travel. And it is a set of blood flow restricting cuffs and a set of bands. I use the Black Mountain products bands, which come with handles. And I like them because they come with a lifetime warranty. I break them and snap them all the time and you just email them and be like, “Hey, this broke.” And they just send you a new one and they cost 40 bucks or something like that, so super cost-effective.
Tim Ferriss: Can I pause you for a second?
Tommy Wood: Yeah.
Tim Ferriss: Just for people who are not looking at Tommy, you’re freaking gigantic. You look gigantic. You’re wearing a very thick sweatshirt and I can still see your pecs moving around for God’s sake. What are your dimensions here? Not to turn you into like a Playboy Playmate or something.
Tommy Wood: So I’m 6’2″. I’m usually 220 pounds. I usually hang out somewhere around 12 percent body fat.
Tim Ferriss: Yeah, strong unit. Okay. The reason that I brought that up is not to flirt with you, although I’m not against that.
Tommy Wood: Oh, I appreciate it. I’m not against it.
Tim Ferriss: No, the reason I wanted to bring it up is people might think there’s somebody out there who’s like an internet keyboard jockey on Reddit who’s living in a basement and squats 135 and is like, “Oh, that guy must be some pencil neck dweeb.” And it’s like, no, actually not. He’s pretty big. And yet you can get, sounds like a decent workout with bands that cost 40 bucks and blood flow restriction. How’s that possible? What do you do?
Tommy Wood: And when I travel, because I’m usually at work, conferences, I’m doing podcasts or whatever, like I don’t have two hours to go to the gym, which I like to have if I’m at home. So I might do 10 to 15 minutes and you put on the cuffs, legs and arms, I’ll do some lunges, like body weight lunges, squats, presses, pushups, and then bicep coals and tricep extensions, and that’s probably it. So a pretty standard protocol, which is essentially in three to four minutes, you accumulate somewhere between 75 and 100 reps. So 30, 20, 20, 20, or 20, 15, 15, 15, 15, something like that, with 30 seconds of rest in between. Try and do one body part at a time, but you can superset them if you’re kind of short on time. That’s it.
And kind of to your point, when we moved into this house, this was now eight years ago, I built my own gym here. But for a long period of time, I didn’t have a gym and I was working from home and all I had was bands and BFR cuffs. And then it wasn’t even the B Strongs. It was like these really cheap ones that kind of look like something that somebody would use to kind of like draw your blood.
Tim Ferriss: Trainspotting, yeah.
Tommy Wood: Yeah, exactly. It looks like a tourniquet to tie up your leg if you’ve blown off your foot. And again, they cost like 20 bucks. They’re probably not the best. But anyway, so I had some of those and some like 40 buck bands and that was all I used to work out for like four or five months. And I didn’t lose any muscle mass or strength. I just got straight back into it afterwards. So you can maintain and gain pretty well as long as you have to do some hardware. BFR can be a little bit painful if you sort of push it, but also very, very safe. It’s been used in rehab, right? All these other things that frail images.
Tim Ferriss: Just for people who are like, “What the hell are they talking about?” I’ll use an analogy. This isn’t exactly what’s happening. But imagine you had a small belt, tiny belt that you put around your upper arms under the shoulders, right at the top of the biceps, let’s just say keep it simple. And then I guess close to the hip on the legs?
Tommy Wood: Yeah, right up in the leg.
Tim Ferriss: And you’re partially occluding blood flow. So you’re not totally cutting off blood flow, but you’re making it a lot harder for blood to get to your arms and your legs.
Tommy Wood: It’s mainly blood to get out.
Tim Ferriss: Blood to get out, okay.
Tommy Wood: Yeah. You’re not compressing the arteries where the blood gets in. You’re stopping the blood from coming out.
Tim Ferriss: The venous return.
Tommy Wood: Yeah, exactly.
Tim Ferriss: Okay, got it. Yeah, and the net effect is if you’re like Arnold Schwarzenegger and you’re like, “Ah, the pump, I feel like coming.” Yeah, if you want to take that to a 20X extreme and feel very, very, very uncomfortable, BFR is a great way to do it. And again, for people who are like, “Oh, come on man, I squat 315 or whatever.” I’m guessing you probably squat at least 315 or more. And what do you squat? I’m curious now.
Tommy Wood: As of a couple of years ago, 405 is my best squat, better deadlifter than I am a squatter.
Tim Ferriss: What do you deadlift? What’s your PR for deadlifting?
Tommy Wood: 550.
Tim Ferriss: Yeah, that’s up there. All right. And I think you would probably agree, if you put somebody in leg cuffs and you’re like, “Yeah, do proper lunges like knee to the ground and go for a 100 yards and come back.” I don’t even think most people could do that, but it’s just like, you’re going to feel it. You are absolutely going to feel it.
Tommy Wood: Yeah.
Tim Ferriss: All right. Gym in a bag. We’ll link to all this stuff in the show notes as well. So I want to list off a couple of things here and then talk about — we can keep bouncing around a lot. Well, on the supplements, I’m going to kind of cut this short and we’ll put things in the show notes, but the periodontal health, mouth health and dementia, the connection there, hence the use of xylitol. Whether that’s the gum, Epic, KaiGum, or air purifiers, mouthwashes. We’ve got all this stuff. So I’m going to link to that in the show notes just in the interest of time and certainly feel free to chime in.
I wanted to talk about cognitive stimulation. So we spoke about dancing earlier. Could you speak to language learning and music? Because I’m realizing, I think accidentally I might have really helped my brain a lot early, which is great as a surprise. But also have next to me an ohana ukulele, which was gifted to me, that has basically just been gathering dust. And after doing prep for this and then looking into it, I’m like, “You know what? I should spend a couple of minutes a day just screwing around with this.” It seems like a great use of time, but could you speak to music and language learning?
Tommy Wood: Yeah. So this actually, if we include dance, this comes back to something that we started talking about earlier, which is what are these experiences or what are these activities that you can do with the brain that kind of maximally activate it or increase glucose uptake. And there was a really interesting study that came out recently called Creative Experiences and Brain Clocks. And what it did was —
Tim Ferriss: Creative Experiences and Brain Clocks.
Tommy Wood: Yeah.
Tim Ferriss: Okay.
Tommy Wood: So I’ll break that down, there’s different components. So kind of like when you did an MRI scan for your brain, and all those other tests you did, there are various different ways that people can sort of like estimate how old the brain looks, right?
Tim Ferriss: Right. And I don’t know if that’s hugely BS or not. I don’t know. Yeah.
Tommy Wood: It’s a bit of both.
Tim Ferriss: Yeah.
Tommy Wood: But in this context, I think it’s kind of useful because when you think about what happens to the brain as it ages, there are a few things that happen. The structure changes, different parts of it gets smaller, you lose volume, but then functionally also changes. The different networks that we have in the brain that have different functions and activities, they become less discreet and they become more distributed. So you get less of these kinds of very functions, specific, tightly knit networks and connections. And then everything just becomes a little bit more sort of like loose and different areas of the brain get connected together and there’s a bit more of a mismatch. You get this increase in entropy. Initially what we call it is brain entropy. It’s not as discreet. And entropy then decreases again as we get towards the end stage of dementia, just because there’s not much going on in there, unfortunately anymore.
Sorry, that’s the best way I could put it. And so when you look at different ways to quantify how old this brain looks, one way is to look at the structure and the connectivity of the networks and how discreet they are. Things like the frontier parietal network, the salience network, the attention network, like these parts that are really important for executive function, focus, attention, all this kind of stuff. And they tend to lose function as we get older. And the easiest way to do this is with EEG, so electro encephalogram where you basically measure the electrode activity in the brain. And so in this study, what they did is they took a whole bunch of different studies and they looked at these different creative experiences. So one was tango dancing, one was language learning, then there was musicians, they had artists, and they also had video gamers, and they had an interventional study where they had people learn the video game.
And it was StarCraft was the game that they used just in case anybody was wondering. Although if we’re talking about video games as a cognitive stimulus, the one that has the best evidence is Super Mario 3D World, just in case you were interested. Lots of studies with that actually. And what they did is that they compared amateurs to experts, and then they also looked at the effect of an intervention where people actually were trained in this thing. And as you increase in expertise in these different creative, complex arts, you see improved structure and discreteness of these really critical networks that are susceptible to aging as we get older. But the effect was similar in tango dancers versus those who are bilingual versus those who are artists versus video gamers. So there’s some core effect of these complex multisensory stimuli that require us to gain significant expertise and skill in order to perform them that seem to have this broad effect.
So part of this is probably because we’re training our brains to be able to focus and learn, and then part of it is just like the actual engagement in this complex task. And so when you look at, say, languages, two very good colleagues of mine at the University of Washington, Andrea Stocco and Chantel Prat, they study individuals who are bilingual. And what they see, they’ve done this from both measuring brain activity and different types of cognitive function, and then trying to model what’s actually going on. And what it looks like is that those who grew up bilingual perform better on tasks requiring executive function. So things like response inhibition, which is you kind of want to do something but you stop yourself just in time. Normally when I talk about it’s like, you know when you have these thoughts of like, “Oh, well, what would happen if I just opened this window and jumped out?” Or you think something and you stop yourself just before you say it, because it’s a really bad idea because it’s like your boss —
Tim Ferriss: How do they test that? Are you using like a Stroop test as a — I’m just throwing something out there.
Tommy Wood: Yeah, So often it’s like a go no-go task. So you’re presented with different stimuli and it’s whether you react to it or not, but like a Stroop is partly an example of that, which is where people don’t know what Stroop is.
Tim Ferriss: You should explain it. Yeah.
Tommy Wood: Yeah. So you get shown words that spell a color and they are also colored. And then you have to respond based on whether the word spells the color you’re looking for or is the color you’re looking for. And so it like requires you to juggle these multiple things. And so yeah, they use tests like that. But basically it seems that because you spend your entire life having to suppress one language while you activate another and then move back and forth, your brain becomes better at suppressing these different — but at the same time, interestingly, it seems that you become less good at other things. So none of this is good or bad, but people who are bilingual seem to be less responsive to what’s immediately happening around them in the outside world. And that’s probably, again, just because of how their brains have adapted to these different stimuli.
But you do see that those who grew up bilingual have a decreased risk of dementia, or if they do get dementia, they get it later. But you also see improvements. If you train in a language, even like using an app on Duolingo, they’ve shown that, in older adults, you use Duolingo, and of course you have to actually move through it, not just stare at it for 30 minutes a day, but that you see significant improvements in executive function and you see the same thing with music learning. So there is something to these complex, very human kind of skills that have these carryover effects into these kinds of core components of cognitive function.
Tim Ferriss: Yeah. I’d never heard about the response inhibition with subjects who are bilingual. But it might explain in a totally separate battery of cognitive testing that I did, which was much more rigorous, I think, than what I did a few days ago. My digit string memorization, despite all my mnemonic trickery, is very bad because it’s only flashed for a second and then you have to do your best. If you gave me a bunch of time, I could use all my trickery.
But if it’s just a flash and it’s kind of relying on, I guess, my hardware, then I’m very bad to the point where people might have some concern, but I’ve always been like that. Conversely, with something like this, there was a test that was pretty much exclusively the Stroop test, but it had a few things that were very similar. And I was like, I’m exaggerating, but tense standard deviations outside of the norm. I was so much better that they were like, “Why are you so good at this? We’ve actually never seen something like this.” And it could be studying all these different languages. I don’t know, maybe. Who knows?
Tommy Wood: So do you know what? I’m actually the same, and we’re kind of convincing ourselves that this is real, just because it’s the case for us. So I often do cognitive function tests on people we work with in studies and that kind of stuff, and we do this full battery, all the things that you mentioned. And on every test, memory, all these other things, I’m just like, I’m perfectly average. And you always think that, oh, I’m so smart, so therefore I should be at what X standard deviation. But no, I’m perfectly average on everything except for response inhibition tests or the Stroop test. And I also grew up speaking multiple languages, so maybe that’s the thing. We don’t know.
Tim Ferriss: Which languages do you know?
Tommy Wood: So I speak Icelandic because my mom’s Icelandic, so half my family were in Iceland. And then I lived in Germany and France when I was a kid for various periods of time. And then I did my PhD in Norway and I taught in the medical school, so I had to learn Norwegian so that I could teach Norwegians medicine.
Tim Ferriss: Wow, that’s hardcore. Yeah, there’s quite a few. And for people out there who are like, “Well, I wasn’t raised bi or trilingual.” I didn’t really even get started until I was 15, 16. Always assumed I was very, very bad at languages for reasons that were mostly related to the schooling and not to any inherent ability. But I’m also thinking about tango as an example, because I spent a lot of time doing tango. I’m not sure if you have any familiarity with this chapter in my life, but in 2004, basically spent like six to eight hours a day doing tango in Argentina. And competing ultimately going to the world championships and all this craziness. But you have the physical component, but like you said, it’s actually a pretty complex cocktail. And in my case, sure you have the dancing, but you also have Spanish. I was learning Spanish at the same time. And then you have the music, and I’m wondering if studies have been done looking at the effect of listening to or having to track different types of music versus producing music. Has anyone looked at that?
Tommy Wood: Not as much. Certainly frequent music listening is associated with a lower risk of dementia and cognitive decline as much as you can get rid of all the sociological pieces of that. There are some studies looking at training adults in musical theory, which requires actually listening to music and then pulling out the different components that seem to be, again, associated with similar benefits to say learning to play a musical instrument. So I think even some of that attentive listening and actually engaging with the music as a listener seems to have some of the benefits in addition to producing the music yourself.
Tim Ferriss: Yeah, because with dance, obviously, if you actually have a hope of dancing well, you have to listen very, very carefully to the music. And in particular, you could have choreographed dancing, but what interested me about tango which I didn’t realize in advance of getting to Argentina, is that the vast majority of it, tango de salon is improvised. So if you’re going to compete in that particular style of tango, salon tango, you don’t know what music’s going to be played and then they just serve up whatever the songs happen to be. So you’re not only responding to the music, but you’re memorizing music. And in any case, makes me want to give back to Argentina.
Tommy Wood: Maybe it’s all that time off, that’s why your hippocampus has been catching up with you.
Tim Ferriss: Yeah, exactly. Oh, add that to my litany of complaints. So I wanted to highlight something. You’ve mentioned this. I don’t think we need to spend a lot of time on it right now, but sensory loss, hearing, vision, getting aids/surgery as soon as possible since those seem to be so correlated to increased risk or onset of dementia. I want to mention two things and then I’ll let you rip. The second one is — now, I’m kind of paraphrasing here, but error detection triggers adaptation. So the importance of failure, because with a lot of the hand wavy, pseudo-scientific games and this, that, and the other thing that are sold for supposedly helping people with memory cognition, et cetera, a lot of them don’t seem to check that box. So maybe if you could speak to the sensory loss and then the kind of error detection and defining that and the importance of it.
Tommy Wood: Yeah. So there are several studies that suggest that sensory loss, particularly vision loss through cataracts and hearing loss through age-related hearing loss, presbycusis are associated with an increased risk of dementia and that this risk is reversible. So, if you have cataract surgery, then that increased risk is no longer there. And if you get hearing aids, again, that risk is no longer there. Only of those two randomized controlled trials have only been done with hearing aids and they only showed significant benefit in those who were at an increased risk of dementia for other reasons. So, like poor health, cardiovascular disease, these other things.
So, it may be that it’s exacerbating other underlying risks, but equally we can think about two broad reasons why sensory loss might lead to cognitive decline and why often as people get older, they’re like, “I don’t want to get hearing aid because then I’m old,” right?
Tim Ferriss: Conceited defeat.
Tommy Wood: Yeah. And so, this happened with my mom actually and she recently got hearing aids and I encouraged her. I was like, “As soon as there’s a thing that you need, you should get it.” And it’s had a dramatic effect on our quality of life. And so, we know that if you lose an input to an area of the brain, that area of the brain is going to decrease function as a result, right? It’s no longer being used and with the process of allostasis or constantly adapting to the demands that are placed on you, that part of the brain is going to diminish its function. So, that’s part of it. But I think a bigger part is that when you lose senses, you no longer engage in the world in the same way that you did previously.
You go out of the house less, you socialize less, you do less tango dancing because you don’t feel like you can engage with it in the same way. So, I think there’s a lot of benefit from recovering lost senses that’s not the same as, so if you are born or if you never had sight or you never had hearing, that’s not associated with increased risk because you learn to engage with the world in other ways, right? So, it’s the loss of that engagement that I think is important. Then the error part, the easiest way to think about this is that if we’re trying to improve function and structure of certain parts of the brain, that allows us to have greater reserve, greater total capacity.
And therefore if we do lose some volume or some capacity as we get older, we have more to lose. So, we’re less likely to get to the point where we have significant deficits. In order to drive improvements in structure and function, we need to drive these processes that we call neuroplasticity, right? New connections, new branches, all the supporting machinery, the other cells that are necessary. We think a lot about neurons, but there’s a whole bunch of other cells and stuff in your brain that are really important as well that are part of this response to stimulus.
But to drive neuroplasticity, you essentially have to have a difference between capacity and expectation, right? So, the best way to uncover that is with mistakes or errors. If you —
Tim Ferriss: Kind of like muscular training to failure or —
Tommy Wood: Exactly. Yeah. So, if you don’t ever get to the point where you’re no longer capable of doing the thing that you want to do, nothing needs to change. You can already —
Tim Ferriss: Yeah, exactly. Your body doesn’t need to adapt.
Tommy Wood: Exactly. Yeah. So, that’s essentially it. And this is what becomes important in dancing, learning languages, learning music, is that you’re having these opportunities to fail to get beyond your current capabilities and that’s what drives the processes of learning and plasticity.
Tim Ferriss: What else do you have in your personal regimen of non-negotiables? Obviously, you’re lifting weights, you’re doing your blood flow restriction torture every once in a while. I don’t know if you’re much of a ballroom dancer.
Tommy Wood: I was a field raver in my youth, but I was never much of a ballroom dancer.
Tim Ferriss: Get that man some glow sticks. So, a big part of the reason I got elbow surgery was to get back into rock climbing, which I think is just a phenomenal, phenomenal sport for mental and physical development. I mean, it’s just a kinesthetic puzzle on a wall. I mean, and was really inspired over the last two years seeing people in places like Colorado, Idaho, Utah, where I’d go into these gyms and you see people in their ’60s and ’70s who are doing stuff that I can’t even imagine doing physically. And they meet a couple times a week and I was like, “Wow, okay. If you can have that kind of longevity in this sport, that seems like a great investment.” Plus I just really, really enjoy doing it.
But what are some other non-negotiables, right? If you look at all the possible things you could do, all the things you do and you’re like, “All right, these are the things that are meaningful and that I stick with consistently, what falls in that bucket?” Because a lot of people will get these like 27 things, 47 things you can do to improve your brain health lists or whatever. And even if they want to do all those things, there’s no way they’re going to. So, there’s a question of sustainability or adherence as well, right? So, yeah, what are some of the other non-negotiables for you?
Tommy Wood: Yeah. So, I think the one that we haven’t talked about that really as non-negotiable is sleep.
Tim Ferriss: Yeah, let’s talk about it.
Tommy Wood: Yeah. And I think this is the major thing that’s missing from these studies looking at dementia prevention as a risk factor. And I think inadequate sleep, really seen in so many studies now that’s associated with increased risk of dementia. So, that’s something that I very consistently make sure that I get enough of. That’s like the one thing that really is non-negotiable. I don’t mind if my diet gets a bit crappy for a few days or I don’t mind if I can’t get to the gym for a few days. This stuff integrates over months and years, but if I can only focus on one thing, then sleep is really critical for me.
But I will say one thing that I noticed a lot was that historically, I used to really get in my head about my sleep, and I know this is going to be the case for many people who have tracked their sleep or used wearables or thought about the importance of sleep, right? And so, something that changed recently, particularly because I spent a lot of time looking at the research, and this also affected me at home because my wife was like, “If you don’t sleep and then you don’t get your coffee, I don’t want to be around you because —
Tim Ferriss: Picked up a moderate heroin habit?
Tommy Wood: A lot of it was honestly self-induced because I thought I didn’t sleep well, therefore I’m not going to function well. I’m going to be grumpy, like all this kind of stuff, right? And we know that this is influenced by outside factors, this is influenced by our own thought processes. There are studies that have shown this, randomizing people to be told by their wearable they didn’t sleep well even though when they slept just fine, right? And what you see in the short term, long term, sleep is critical, right? Absolutely. And any sleep you can get more than you are having now, the better, right? So, if you sleep six hours a night, you can get six and a half, great. Don’t think that you have to sleep eight hours.
If you can get an extra half an hour, that’s amazing. But in short periods of time, actually sleep deprivation doesn’t have as much of a negative effect on cognitive function as we think. And this is just important so that we can go about our day-to-day lives and perform well when we don’t sleep well. So, what happens
Tim Ferriss: Especially when you have a chalkbag full of creatine at your desk.
Tommy Wood: So, the creatine helps, but equally like we travel, we have kids, all this kind of stuff. Sometimes, you’re just not going to sleep well. But in short periods of time over a few days, what happens is that processing speed slows down, but accuracy doesn’t. So, the quality of your work is just as good. It just might take you a little longer and mood is affected much more than performance. So, actually we don’t perform less well. We just feel more grumpy about how we performed. And so, actually, knowing this, I then just completely changed how I approached my sleep. So, if I didn’t sleep well, I’m like, “Do you know what? I’m actually going to be fine.” And then it turns out I am fine.
So, that’s like, yes, sleep is critical, but how we think about these things I think is really important. And then another thing, so like important factors are going to be like avoiding excessive alcohol, don’t smoke. But then two things that you’ve mentioned we haven’t touched upon fully, I’ll like briefly talk about. One is air quality and air pollution, which is a significant risk factor for dementia. A lot of these studies are quite recent looking at say wildfire exposure and things like that. But even living near roads, like in the short term is associated with greater cardiovascular risk, higher blood pressure, which you can improve with having an air filter.
And of all the different like metabolic type risk factors for dementia, high blood sugar and high blood pressure are the two most important, lipids and other things are important as well, but those are consistently the highest risk factors. So, managing blood pressure is really important. And if so you live near somewhere with a lot of air pollution, then air filters certainly seem to help there. And then oral health was the final one. So, the reason I say this because I appreciate that I’m British and I’m going to tell you you should go to the dentist. So, historically when I lived in the UK, I did not go to the dentist very, very frequently.
And actually, the first time I went to the dentist here in the US, I had this one metal crown from back when I was a medical student and my dentist looked at it and he was like, “You didn’t get that done in the US.” That was his first comment. But gum disease, so gingivitis, especially if it advances the periodontitis, is significantly associated with an increased risk of dementia. This is probably both due to an increased like systemic inflammatory effect, plus those bacteria can get into the bloodstream. They’re found in atherosclerotic plaques in heart disease. They’ve been found in amyloid plaques in the brain. So, treating gum disease is really important, whatever that requires.
And that’s why I mentioned xylitol to you because there are several studies showing that xylitol gum or xylitol mouthwash can improve the oral microbiota, decrease some of these like cavity and periodontitis causing bacteria like Strep mutans and Porphyromonas gingivalis. So it’s just like a really low risk kind of thing. There he is with this gum.
Tim Ferriss: A low risk in my pocket.
Tommy Wood: A low risk thing to consider. And I don’t think they’ve looked at it by APOE4 genotype, but things that have an anti-inflammatory effect or decreased inflammatory burden seem to have an outsized benefit for those who are APOE4 carriers. And so, gum disease would obviously be one of those that’s worth keeping an eye on.
Tim Ferriss: That’s part of the reason not to keep banging on this drum because I know it’s not the shoe that fits everyone, but that’s another reason for my fascination with ketones, just remarkably anti-inflammatory on a couple of different levels. So, for folks who might be wondering, and we’ll put these in the show notes as well, air purifiers, do you mind if I just read from this email that you sent to me?
Tommy Wood: Sure.
Tim Ferriss: Because of course I’m such a stickler. I’m like, “What exactly make and model?” So, yeah, I’ll just read from this. The blood pressure study I mentioned — this is I equals Tommy — use the HealthMate, that’s one word. JSPR is good, that’s J-S-P-R. As are most of the Blueair, one word, Blueair models tailored to the size of the room. The Coway, C-O-W-A-Y Airmega is a good budget option. So, we’ll link to all these in the show notes. This is one, God with travel, such a pain in the ass, although I think it was James Nestor who wrote the book Breath, who was giving me just some horrifying quantified self data related to looking at like CHO2 concentration in various hotels around and airplanes and so on.
And so, I don’t think he’ll stay in a hotel that has sealed windows. I think it’s part of his policy because —
Tommy Wood: Yeah, high CO2 really negatively impacts sleep. So, like lots of people in a small room that’s not ventilated, that can definitely negatively impact sleep. So we always have a window open or something for that reason.
Tim Ferriss: Anything else that you do for sleep besides not becoming too orthorexic about it and like freaking out on the wearables and stuff, which is a real thing for sure. So, besides recognizing that you’re going to be fine, humans have been dealing with this for a long time, what else would you say, right? I would imagine there’s things people have probably heard like keeping the temperature, whatever it might be, 65 to 70 degrees Fahrenheit, et cetera. Other things that you find particularly helpful?
Tommy Wood: Yeah. So, things that have helped me a lot, I stop work before dinner. I don’t do work after dinner unless I really, really have to. And that helps a lot because I find I ruminate a lot more if I do work late into the evening. A basic shutdown routine, I put on the blue light blocking glasses, they’re probably just placebo at this point, but I put them on and my brain is like, “Oh, it’s bedtime.” And then I read fiction before I go to sleep. Quite a recent purchase was an eight sleep, which has been amazing because I tend to get quite hot when I sleep, so that’s helped a bunch. So, I just helped stay cool. And then I wear an eye mask, which I really like for blocking out light.
And there were also some very nice studies on that. One of my favorite studies looking at eye masks, you ever see this one where in the control group, they had them wear a Zorro mask? So they were still wearing a mask, but the eyes were cut out.
Tim Ferriss: No.
Tommy Wood: And this was during the summer when light would come in early in the morning, would disrupt sleep and they saw significant improvements in cognitive function in those wearing the regular eye mask versus like the Zorro mask.
Tim Ferriss: The Zorro?
Tommy Wood: Yeah, it was hilarious. I think that’s probably my list.
Tim Ferriss: Got it. I’m going to ask you something specific about sleep, but just because I have it in front of me to ask you, vitamin K2, do you supplement K2 or do you get it from something else?
Tommy Wood: I do generally supplement just like a few micrograms a day, maybe 15 or 20, but that’s mainly because it comes with my vitamin D that I was supplementing particularly in the winter. In the summer, I get plenty of sun exposure on bare skin, but in the winter, can’t do that in Seattle. But I also don’t mind a little bit of natto or some fermented foods that would have K2 in as well. So, don’t need to supplement, but certainly
Tim Ferriss: Stinky spiderwebs. If anybody likes the sound of stinky spiderwebs, try natto, N-A-T-T-O. It’s the one that Japanese people like to give foreigners to watch the face. Some people like it. I can handle a little bit. I can handle a little bit.
Tommy Wood: I mean, I grew up eating rotten shark in Iceland.
Tim Ferriss: Oh, that stuff is so fucking bad. I went to this place called Hotel Ranga, I think it’s Ranga, to bring my family. My mom had always, her whole life wanted to see the northern lights. And so we went there in the middle of the winter. By the way, folks, not a whole lot of light. It’s like twilight for a few hours. That’s all you get. But there was some fermented shark celebratory day and we drove to what looked like, and I think it was a gas station, but had a restaurant attached to it and ate this fermented shark. How would you describe it?
It was like, I mean, fermented shark as you would imagine, but like eating something soaked in like ammonia, like the pungency when it hits your sinuses is like smelling salt. I mean, it’s so —
Tommy Wood: So it is ammonia. So to make Greenland shark, which is the type of shark edible, so Greenland sharks don’t have kidneys. So their tissue, just their body accumulates urea, because they don’t pee it out. So in order to make it edible, that urea has to break down to ammonia and then it becomes “edible” in quotation marks. And so, it is ammonia that you’re tasting, but it’s like it’s got the texture of tuna and the taste of a really, really, really strong blue cheese that you peed on.
Tim Ferriss: I will say, I wasn’t really hankering for a return trip to that particular gas station to eat fermented shark, but watching my brother try to eat it was one of the most entertaining moments I’d had in a long time.
Tommy Wood: So, you know you’re supposed to alternate shark with Brennivín, which is Icelandic aquavit. And so, like you use the shark, you eat the shark, then you use the aquavit to take away the taste of the shark, you use the shark, take away the taste of the Brennivín, and then you just continue that until —
Tim Ferriss: You just get hammered enough that you don’t care that you’re eating fermented pissed sharks?
Tommy Wood: Exactly. So, actually, I don’t mind the shark that much. There’s one thing that’s much, much worse. If you ever have a chance to try Surströmming, which is a Swedish fermented herring in a can, that is the worst thing I’ve ever put in my mouth. It’s terrible. Actually, if you look it up, there are all these YouTube videos of people who get it in the US and they open it and the smell comes and then they immediately throw up. It’s like you open the tin and you take out these rotting bones of herring that you put on bread. Highly recommended.
Tim Ferriss: Yum. All right, I know what I’m doing for New Year’s. All right. So, sleep, do you have a position on the DORAs on the dual orexin receptor antagonists because I’ve chatted with folks, including Matt Walker, who’s very credible in the space with respect to sleep research, the potential that DORAs could help with the clearance of beta amyloid, what is it? pTau217, et cetera, and possibly be of some help in preventing the accumulation of things that later contribute to Alzheimer’s. I mean, it’s not like the vote is in and it’s 100 percent, but there seems to be a couple of interesting publications around it, including in humans. Do you have a position or any thoughts on it?
Tommy Wood: Yeah. So, very quickly, we know that sleep quality and quantity affect amyloid accumulation in the brain. That can be seen over short periods and long periods. And some of that work is from Matt Walker’s lab. And he’s even done studies that show that later in life, if you can improve the amount of sleep that you get, then that’s associated with a lower overall amyloid burden. I think that some of this, we get very focused on amyloid. It’s a part of the picture of Alzheimer’s dementia, just like you said, it’s not the full picture. But I think we look at it and it’s a marker for all the things that you should be clearing out of the brain when you sleep that you aren’t, right? Amyloid is one of those things.
There are probably many other things as well. So, the DORAs have now several studies in different states within insomnia, in sleep apnea, these states where we know people are getting lower quality sleep and they certainly seem to improve that. I think that in individuals who have some kind of sleep issue, be that insomnia, something else that’s going to prevent high quality sleep, then improving that is certainly going to be beneficial. Right now, the DORAs are now the best option. Previously, people recommended trazodone, which is like, we talked previously, the least worst option because it doesn’t negatively affect sleep architecture, unlike many of the other sedatives that people might use to help sleep.
But if you’re sleeping fine, or you manage to maintain high quality sleep, as you get older, I don’t think we need to start taking DORAs to prevent Alzheimer’s because I think your sleep is probably already doing the job that it’s doing. And there are studies that show that increased cognitive stimulation in older adults improves sleep quality, or that engaging in cognitively stimulating activities helps to offset some of the potential increased risks that we would have with poor or less good deep sleep, which is when a lot of this clearance happens.
So, I think a lot of the other things that we mentioned already, physical activity we know improves sleep quality. So, I wouldn’t jump straight to DORAs, but in somebody who does have insomnia and say CBTI, so CBT for insomnia doesn’t help them, or some of these other things that we can do to improve sleep and those don’t work, and you’ve ruled out anything sinister, then I think they’re now our best option to help support sleep.
Tim Ferriss: All right. We have covered a lot. I want to know why you decided to do something very difficult, which is write a book, The Stimulated Mind. What was the driver behind this and who is the book for?
Tommy Wood: I like to joke that the book is for anybody with a brain. The subtitle is about preventing dementia, but really a ton of it is just about cognitive function and cognitive performance in general. So even people who are younger and aren’t thinking about dementia yet, although like you said, it’s worth thinking about it earlier than you think.
So I think for most people who think about how their brains work or want their brains to perform better and/or want to prevent or minimize their risk of dementia long term, it’s got what I think are the big rocks and the tactics for how to address those that we know substantially increase dementia risk, all those things we talked about earlier that contribute to those dementias that are potentially preventable. And the reason I wrote it is because I didn’t think that book really existed. People might focus on one particular area or they might focus on everything, right?
There are books on dementia prevention that are just like endless tables of blood tests and supplements and this stuff that just like most people are never going to do, right? It’s not going to be sustainable. I didn’t really see a middle ground, but equally, I wanted it to be very heavily referenced. So if people want to get into the references, I have a reference list. It’s going to be 2,000 papers, all in humans, and it’s cited in the text, right? I have like little super script citations in the text.
Tim Ferriss: You teased the subtitle a little bit. It’s a good subtitle. So, I want to give it some real estate here. So, The Stimulated Mind subtitle, Future Proof Your Brain from Dementia and Stay Sharp at Any Age. I’m looking at the Amazon page for the first time. I hadn’t looked at it. I had no idea that you know Kelly and Juliet Starrett. Those are two very close friends of mine and you got a very nice quote from Dr. Kelly and Juliet for the book. That’s fantastic.
Tommy Wood: So, I only really connected with them about a year ago, but they’ve been so, so helpful. What do you do when you wrote a book and how do you get it out there and how do you get people to read it? They’ve given me so much of their time and help. They’ve been amazing.
Tim Ferriss: Yeah, they’re fantastic. All right. So, “Dr. Wood,” that’s you, “explains that a brain that improves with age is the result not of expensive pills, far off discoveries or strict lifestyle optimizations, but rather of actions within our control, diet, sleep, physical activity, social connection, and stress tolerance.” And obviously it goes on and on. But clearly, you have a lot of very practical, specific advice that people can implement.
And what else makes this book different?
Tommy Wood: So I think those things that I mentioned make it different. I think it’s very practical and approachable, but very science driven. And if people want to dig into the references, those are available. And then I think, like towards the end, there’s all these different areas where we talked about nutrition, sleep, physical exercise I give, like how you would approach each of those things in terms of supporting cognitive function and minimizing dementia risk. But then I bring them together in a model of how I think people can implement this in their daily lives. How do I just pick one thing?
And actually, does picking just one thing help to support like the overall function of the brain? And the answer is yes, it does because when you sleep better, so say if you focus on improving sleep, you’re more sociable, you’re more likely to engage in cognitively challenging tasks. Your blood sugar improves, your blood pressure improves, right? So, just changing one area, suddenly the whole network shifts in your favor. And that’s the case from almost anywhere where you approach it. And I think that means that people are much more likely to actually start doing this stuff and realize that it doesn’t require a ton of work to start moving the needle and then these things compound over time.
Tim Ferriss: Mm-hmm. All right. The Stimulated Mind, folks, go grab a copy. Obviously, I hate when people say obviously, but I’m going to say it. Obviously, Dr. Tommy has the credentials, has the expertise, has the bonafides with respect to research in humans and has provided a lot that you can use in this conversation and a lot more is in The Stimulated Mind. So, check it out. Why on Earth is your X account called Dr. Ragnar?
Tommy Wood: So I first started blogging around the time you first started podcasting. And I remember listening to your first interviews with Don D’Agostino back in the day when I was in my PhD chair writing blog posts. But my middle name is Ragnar, so I created a website. It was Dr. Ragnar. That was initially where I did my stuff.
Tim Ferriss: So let me think about this for a second. I’m going to make myself probably regret asking this question, but does Ragnar mean anything? Because now I’m thinking of Ragnarok and if those two have any connection. Does it mean anything in particular?
Tommy Wood: So, no. So, you’re right. Ragnarok is like the final battle for Valhalla, right? And actually, there were some online gaming accounts where I used the name Ragnarok. No, I think what it means, the translation for the old Norse is like “wise counselor.” I think that was another reason why I picked it, because it was very self-important as a 30-year-old health blogger, but it was my grandfather’s name and then these names get passed down in the family. Technically, because I was the firstborn grandson. It should have been my first name, but my dad was English and it was like, “People are just going to make fun of him at school. He’s going to get bullied if he’s called Ragnar.”
It’s very cool now, because of Vikings and all these other TV shows where Ragnar now appears. But yeah, that’s —
Tim Ferriss: I mean, you could make it work, but Dr. Ragnar Wood also has a strange combo one, two to it. All right, got it. @drragnar. R-A-G-N-A-R on X for people who want to check it out.
Tommy Wood: To be honest, I don’t use X. So, you can follow me on X, but you won’t see anything.
Tim Ferriss: But people can find, presumably there’s something at drtommywood.com, drtommywood.com. So, that’s the home base online.
Tommy Wood: Instagram.
Tim Ferriss: Instagram?
Tommy Wood: @drtommywood. Again, drtommywood.
Tim Ferriss: @drtommywood. All right folks. So, you got it. Check out The Stimulated Mind. I’m a huge fan of what you do. I am going to try to improve my and arm situation with more use of BFR and bands. And is there anything else you would like to say before we wind this to a close? Anything you’d like to ask of the audience, point them to, requests, complaints, anything that comes to mind?
Tommy Wood: No. Other than if you do happen to pick a copy of the book and you do have any complaints, do send them to me. One of the reasons why I wanted to make it so that every statement that I have in the book has a citation, you can go, you can read that paper. If you disagree with my interpretation of it, I want to know. I can’t promise that I have all the answers. So, that will help me learn more. So, yeah, if you have a complaint, just tell me about it.
Tim Ferriss: All right, Tommy. I really appreciate all the time, man. This was great. Took tons of notes for myself, which is always a good sign. So, thanks for carving out a bit of time to be on the show. Really appreciate it.
Tommy Wood: Thanks so much. Thanks so much for having me. This is so much fun.
Tim Ferriss: And for everybody listening as per usual, we’ll provide copious links and show notes at tim.blog/podcast, tim.blog/podcast. And until next time, be just a bit kinder than is necessary to others and also to yourself. As Jack Kornfield says, if your compassion does not include yourself, it is incomplete. Thanks for tuning in.
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2026-01-28 22:40:54
Dr. Tommy Wood (@drtommywood) is an associate professor of pediatrics and neuroscience at the University of Washington, where his research focuses on brain health across the lifespan. This includes therapies for brain injury in newborns, prevention and treatment of adult brain trauma, and the factors that contribute to long-term cognitive function and cognitive decline. Tommy received an undergraduate degree in biochemistry from the University of Cambridge, a medical degree from the University of Oxford, and a PhD in Physiology and Neuroscience from the University of Oslo.
Alongside his academic work, Tommy is head scientist for Motorsport at Hintsa Performance, overseeing health and performance programs for multiple Formula 1 drivers. He also helped to found the British Society of Lifestyle Medicine, is head of research for the dementia prevention charity Food for the Brain, and serves as chief science officer for brain health coaching company BetterBrain. He has also trained and competed in multiple sports, coming in the top 20 in the world’s first ever fully off-road ironman triathlon, and 2nd at Washington’s Strongest Man in 2024.
Tommy is co-host of the Better Brain Fitness podcast and author of the forthcoming book The Stimulated Mind.
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“If you look at human babies compared to pretty much every other mammalian species, we are the only species that’s born fat, even compared to other primates. And it’s thought that the primary reason for this is that that fat is a repository for things that the brain needs in order to develop.” — Dr. Tommy Wood
“There are actually some very nice studies that looked at brain activation and glucose uptake in response to cognitive stimulus in individuals with Alzheimer’s disease. And what they see is that, yes, at baseline, there’s less glucose being taken up into the brain of individuals with Alzheimer’s disease, but if you stimulate that brain cognitively, it can take up glucose just fine so that you get into the range of a normal healthy brain in early Alzheimer’s disease.” — Dr. Tommy Wood
“Dance seems to have the highest sort of effect size [on mental health and risk of Alzheimer’s] compared to other types of physical activity.” — Dr. Tommy Wood
“What it looks like is that those who grew up bilingual perform better on tasks requiring executive function—so things like response inhibition, which is you kind of want to do something but you stop yourself just in time.” — Dr. Tommy Wood
“As you increase in expertise in these different creative, complex arts, you see improved structure and discreteness of these really critical networks that are susceptible to aging as we get older. But the effect was similar in tango dancers versus those who are bilingual versus those who are artists versus video gamers. So there’s some core effect of these complex multisensory stimuli that require us to gain significant expertise and skill in order to perform them that seem to have this broad effect.” — Dr. Tommy Wood
“How do I just pick one thing? And actually, does picking just one thing help to support the overall function of the brain? And the answer is yes, it does. … If you focus on improving sleep, you’re more sociable, you’re more likely to engage in cognitively challenging tasks. Your blood sugar improves, your blood pressure improves, right? So just changing one area, suddenly the whole network shifts in your favor.” — Dr. Tommy Wood
Want to hear another episode about preventing Alzheimer’s disease and optimizing for longevity? Listen to my conversation with Dr. Peter Attia, in which we discussed longevity drugs, Alzheimer’s disease prevention, the three most important levers to pull for health span, VO2 max optimization, blood testing protocols, and much more.
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The post Dr. Tommy Wood — How to Future-Proof Your Brain from Dementia (#851) appeared first on The Blog of Author Tim Ferriss.
2026-01-26 22:00:00
Bill Gurley (@bgurley) is a general partner at Benchmark, a leading venture capital firm in Silicon Valley. Over his venture career, he has invested in and served on the boards of such companies as Nextdoor, OpenTable, Stitch Fix, Uber, and Zillow. He earned his Bachelor of Science degree in computer science from the University of Florida and then his MBA from the University of Texas at Austin. For more than two decades, Bill has written about technology and other subjects on his popular blog Above the Crowd and on his social media accounts.
I interviewed Bill for the second time recently, and we got into his new book Runnin’ Down a Dream: How to Thrive in a Career You Actually Love, which will come out next month and is now available for preorder.
To give you a taste, I asked Bill if we might reprint a chapter on the blog, and he and his publisher kindly agreed.
If you want to start a tech company, go to Silicon Valley. If you want to be in movies, go to L.A. Geography still matters.
—Brian Chesky, cofounder and CEO of Airbnb
By the time Tony Fadell graduated from the University of Michigan, he already had more entrepreneurial experience in his field than virtually all of his peers. As a teenager in the mid-1980s, he created a semiconductor company that sold parts to Apple. He had another company that sold mail-order software for the Apple II, and he also started a third company, with one of his professors, that sold educational software for Mac computers. He skipped his first week of college classes to man a booth at the Applefest in San Francisco.
Tony had spent years reading everything he could about the computer industry, mostly in Byte Magazine and MacWorld. In story after story, he read about companies based in the Valley. Studying the ads in the magazines, he noted that most of the company addresses were also in Northern California.
He flew out to Silicon Valley a few times a year for meetings, all on his own dime, and he absolutely loved it. On one trip, he rented a car and drove to the original Fry’s Electronics in Sunnyvale—“a superstore, like Costco, for everything under the sun in the world of electronics.” For a kid who grew up obsessed with computers and building technology—in elementary school he rigged his clock radio to put a headphone jack in it so he could listen to music all night without his parents knowing—this journey felt more like a pilgrimage.
“I was like ‘Ho-ly shit!’” he told me. Decades later, you can still hear that original awe in his voice.
Tony knew that when he graduated, he needed to move to Silicon Valley, the epicenter of the industry he loved. At first he thought he wanted an internship at Apple, which was run by John Sculley at the time. The company flew Tony to Cupertino and put him up in a nice hotel with a fruit basket waiting in the room. But when they offered him the internship, Tony declined.
To his surprise, they offered him a full-time job, working at a joint venture Apple was doing with IBM. But again, stunningly, Tony turned them down. He had his eye on a different job. “I said, ‘No, I don’t want anything to do with that,’” he told me. “I wanted General Magic.”
At the time, Tony didn’t even know what General Magic was doing, but a few years earlier he read about Silicon Valley computer engineer legends Bill Atkinson and Andy Hertzfeld in a Rolling Stone story profiling the Mac team. As Tony was flying to the West Coast, doing these interviews, he read in the back of one of his tech magazines that some of these big names had begun a secretive spinoff from Apple. “I’m like, ‘Whatever it is,’” Tony told me, “‘that’s where I want to be.’”
Despite his remarkable résumé and network of contacts, Tony was told that there weren’t any openings at General Magic—but that just made him want it more. So on one of his trips to California, Tony decided to go to the General Magic building, in downtown Mountain View, and present himself unannounced. He found the address in the Yellow Pages and drove over at 8:30 a.m. He wore a jacket and tie and a big, naive midwestern smile. But when he got to the building, it was mostly empty. Security dogs roamed the halls, ready to attack any intruder. When he found the right floor, he walked up with his résumé in his hand. The office door was open. Inside, he found—nothing. “It was just cube wall after cube wall, a desolate cube area,” he says.
As he walked through the rows of cubes, he thought he was completely alone. But then he spotted two men in a cube and they looked like they’d been up all night. Undaunted, Tony made sure that this was indeed the General Magic office—they said it was—and offered up his résumé. Without even looking at it, the two men told him the company wasn’t hiring. So Tony left and went back home to Michigan.
At this point, leaving the Valley gave him something akin to withdrawal symptoms. Michigan seemed bleak. “I went back to Ann Arbor and it was literally a frozen tundra,” he told me. “I kept asking myself what I was doing there.”
It is different now, but at the time Michigan did not have a community of technology enthusiasts like those in the Valley. There were no startups. It felt like people there barely spoke the same language. So he was even more convinced that he needed to be in California— and more specifically, he needed to be at General Magic.
First, he racked his brain to think of anyone he knew at Apple, anyone who might be able to open a door there for him. He made some calls, pleading his case, and it took a few months, but eventually he got a call back from a woman at General Magic named Dee Gardetti. Tony didn’t know it at the time, but Dee was the fourth employee at the company and she was the head of HR. She told him she was impressed with his résumé and she would see what she could do. She told him to be patient.
But Tony is not a particularly patient person. He started mailing letters to the company. He estimates that he sent between fifteen and twenty old-school letters, pleading for a job. As time went by, he graduated from Michigan and moved back in with his parents. He sold his educational software company. He turned down numerous other jobs—much to the chagrin of his parents. He was relentless, but he was also charming. When he called Dee, he was able to make her laugh and win her support. Then, in November 1991, nearly seven months after that original unannounced visit, Tony was invited back for an interview.
He flew back out to the Valley, put on his jacket and tie, and showed up to General Magic’s new office in Mountain View. “There were no dogs this time,” he jokes.
But now, after all this time and this relentless pursuit, Tony began to feel something all of us have felt at one point or another: imposter syndrome. “I’m like, ‘What am I doing here?’ I’m totally melting. I’m seeing these people that I’ve idolized, my heroes, they’re interviewing me. I’m just a little kid.”
He was told to take off his tie and his jacket. He was told to sit on the floor like everyone else, around an arcade machine in the middle of the office. As he got more comfortable, Tony showed the General Magic team his senior project: a portable touchscreen computer— something most people had never heard of in 1991.
Well, it turned out that General Magic, this top-secret company of superstars, had been working on a portable device with a touchscreen, the earliest iterations of what would become the smartphone. Some of their partners and investors included Sony, Motorola, and AT&T.
Tony thought the interviews went well, but he left without a job offer. He went back to Michigan, where the chill of autumn was morphing into the bitter cold of winter. More than two weeks later, he finally got the call from Dee.
“I want to let you know you’re going to be a diagnostic engineer on the hardware team at General Magic,” she told him. “And you can start right away.”
Tony still remembers running around and screaming when he got the call. His salary was $28,000, below the cost of living in the Valley at the time, but he didn’t care. He packed up his car, said goodbye to his parents, left his mother crying in the driveway, and headed to California.
Tony is a good friend of mine, and we’ll discuss some of his incredible accomplishments later, but I want to highlight this part of his story for a reason. He made the audacious decision to move, not just to the geographic center of the industry he wanted to work in, but to the one company where so many of his idols had come together.
It’s a hard decision and often a hard pursuit, but if you have the chance, put yourself in the center of the action.
As your dream job journey evolves, you may eventually confront a decision with enormous consequences: Should I physically relocate in order to maximize my chance of overall success?
Of course, many of us move away for the first time to attend college. And that is not the end of the world. We meet new people, we meet new friends, we are exposed to new cultures and experiences. We learn and grow. Making that decision a second time can and will have a profound impact on your chances of dream job success. It may seem incredibly intimidating, but it may also be the best decision you make in your entire life.
Your journey may not be as dramatic as Bob Dylan hitchhiking from Minnesota to Greenwich Village. I relocated twice in my career— first to New York and then to Silicon Valley—partly because I saw how my dad benefited from moving from Virginia to Houston to work at NASA.
The truth is, different industries are bigger and more prominent in different places—for all sorts of reasons. The tech industry and a disproportionate number of start-ups are in the San Francisco Bay Area. For finance and banking, it’s New York City. New York is also the center of the book publishing world and America’s theater scene. But for television and film, the epicenter is Los Angeles. Government and policy? Washington, D.C. Biotech and pharma? That’s Boston. Oil and energy? Houston. The automotive industry is still largely based in De- troit. If you want to make it as a singer-songwriter, you’ll probably have to spend some time in Nashville, regardless of your genre.
A few industries have multiple hubs, which means you’ll have more choices. The fashion industry, for example, is big in Milan, Paris, New York, and L.A. If you want to make it in esports, you can probably pick between Tokyo, Seoul, or Los Angeles—though you’ll have a ton of other factors to consider as you decide.
Being in these places puts you in the flow of the industry. You are surrounded by people who speak the language. You are closer to decision-makers, mentors, collaborators. You are able to learn faster, move faster, be seen more quickly. And sometimes, most importantly, you are simply reminded that this is real—that there are people who are doing the thing you want to do, every single day.
Regardless of the geography, there are at least ten ways relocating can help your career.
1. More jobs—There are just more opportunities where the industry is dense.
2. More networking—You’re greatly increasing the chances you’ll bump into people in your field.
3. More mentors and more peers—The best in the business are often just a coffee shop away.
4. More events—Meetups, panels, workshops—they’re happening much more often in the industry’s epicenter.
5. Exposure to trends—You’re first to see what’s next.
6. Résumé credibility—“She’s based in L.A.” or “He worked in New York” carries weight.
7. Faster advancement—Your chances of moving up go up when you’re where things are happening.
8. Higher pay—It’s more competitive and often more expensive, but these places also come with higher compensation.
9. Serendipity—The breakthrough meeting, the unexpected connection—it’s more likely to happen when you’re immersed. You create your own luck.
10. Fun and energy—You’re surrounded by people who care about the same things. That matters. If you truly love your chosen field, that will excite you.
I saw this in Silicon Valley. I watched people have lunch with billionaires, go to talks by start-up founders who had just IPO’d, meet cofounders over coffee. People in the Valley take time to respond to authentic requests for learning and advice. I felt it on the way up, and I have tried to reciprocate and continue the tradition. It is a vibe you don’t necessarily see in other places. I have heard plenty of similar stories about musicians in Nashville. They move there with no guarantees. But they know one thing: The best people are here. I want to be around that.
That’s the idea. You want to roll around in it. If the idea of being immersed in your industry doesn’t appeal to you, you might need to go back to the first principle and reconsider whether this is truly your passion. You should want to be so steeped in your craft that large parts of it become second nature.
Immersion isn’t passive—it’s transformative. When you’re fully submerged in the culture of your field’s epicenter, learning accelerates. Opportunities multiply. Your network organically expands. Immersion creates a powerful osmosis effect, exponentially accelerating your growth and visibility.
All of this can seem intimidating, I know. Maybe it sounds too competitive. Being nervous about a step like this is totally understandable. My advice: Try your best to remove those thoughts from your mind.
So what if you just really can’t relocate? We live in an era where physical relocation is not the only option. Virtual epicenters can also propel your career. You can engage deeply with Reddit groups and Twitter/X communities. You can consume or even participate in Twitch streams, podcasts, LinkedIn groups, virtual courses on almost any subject.
You can establish yourself with an online presence through content curation, expert interviews, and consistent digital engagement. If you have something interesting and thoughtful to say about a subject on a regular basis, you will build an audience eventually.
To be clear: These are all things you should be considering whether you have already relocated or not. This is part of the learning process, part of building a peer network, and part of seeking out mentors. Physical proximity will likely give you an extra advantage, but in today’s world you should be utilizing every tool available.
There are also industry epicenters that seem to bubble up, sometimes in surprising locales. In the 1970s, northern Florida became a hub of Southern Rock, producing a stunning lineup of bands that included Lynyrd Skynyrd, the Allman Brothers Band, and 38 Special—all from Jacksonville. Tom Petty and the Heartbreakers formed around the same time down the road in Gainesville.
A few years ago, comedian Ron White encouraged Joe Rogan to relocate to Austin. For more than two decades, Rogan lived in Los Angeles, one of the two or three big hubs for top-tier stand-up comedy, along with New York and Boston. Rogan was a staple at The Comedy Store on the Sunset Strip. For years, he went several nights a week. He honed his act with two or three short sets in a night and spent the rest of his time hanging out with his fellow comedians in the venue’s legendary green room.
In March 2023, Rogan opened his own club, Comedy Mothership, on Sixth Street in downtown Austin. He named the bar Mitzi’s, after Mitzi Shore, the woman who owned The Comedy Store until her death in 2018. Rogan brought Adam Eget, one of The Comedy Store’s bookers, to Austin to help launch the business. Around the same time, other prominent national comedians relocated from both Los Angeles and New York. Within a few years, the Austin comedy scene included Tom Segura and his wife Christina P, Tony Hinchcliffe, and Shane Gillis. They are all regulars at the Mothership, and now nearly every big comic has to stop in Austin a few times a year.
But something else happened, too. Other smaller comedy clubs started popping up all over town. There were more open mics and more paying gigs. As Tony Hinchcliffe’s podcast, Kill Tony, got more popular, more and more aspiring comics migrated to Austin instead of New York or L.A. Austin has officially become a comedy hub. Though they tour a lot, comedians still need a quality base to sculpt and workshop their material.
Of course, some professions are itinerant by nature. Some industries don’t have traditional hubs. Think about sports. If you want to be a college or professional coach, you will probably need to relocate several times. That is true whether you are an assistant or a head coach. It is certainly true for athletic directors. Chances are your next job will not be in the same place as your last one. This is true of journalists, too. As you come up in the industry, you will likely have to move a few times.
But even these itinerant occupations have industry events, reasons to come together in the same place. There are annual conferences, key networking events that function as temporary epicenters. In these industries, it’s even more important to seek out and connect with mentors and experts and to stay in touch with peers.
I know this is not easy. Moving is expensive and stressful. Most of us are not nomadic by nature. We crave stability. Relocating is one of the single most disruptive things you can do in life. Maybe your parents live nearby, and you are the one they lean on. Maybe your kids love their school and your weekends are filled with soccer games and birthday parties. Maybe you have built a close-knit community over years, or decades, and the idea of leaving that feels like tearing something sacred.
Moving also means facing more intense competition. You might know more about a subject than anyone else in your graduating class, but once you move to an industry hub, you are suddenly the lowest person on the totem pole. But careers are not zero-sum games. Competition is a tide that raises all boats. Sure, for a while everyone you encounter will know more than you, but that just means you will have the opportunity to learn infinitely faster than you would if you stayed at home.
You might also need a “support job” while you grind. Plenty of struggling actors found other gigs to pay the rent—sometimes for years—before landing a breakthrough role. Some of the best musicians in America spent substantial portions of their lives busking on sidewalks or playing for free in grimy bars. That perseverance can pay off. Sometimes the first job will not be the big career winner. It may just be a critical stepping-stone.
That is what happened with Tony Fadell.
After he finally got that job at General Magic, he worked there for three and a half years. But the company was not a success story. General Magic’s failure has become one of the most important legends in the history of Silicon Valley. (It’s also the subject of a great documentary that I would highly encourage everyone to watch.) However, joining General Magic put Tony squarely in the epicenter of the Valley. And the connections he made there were part of an amazing foundation that would help launch him to greater and greater heights.
After leaving General Magic, Tony continued his pursuit and passion for designing breakthrough portable computing devices. His next stop was building the Philips Mobile Computing group, where he assumed the role of CTO at the age of twenty-five. After four years there and a brief dance with Real Networks, he started his own company in 1999 called Fuse, which aimed to be the “Dell of Consumer Electronics.” That timing was not ideal, as the dot-com crash made it difficult for Fuse to raise its second round of financing. Tony kept grinding.
After ten years, Apple hired Tony through an eight-week consulting contract to develop a new MP3 music player. Tony’s nine years in Silicon Valley, and the learning he had done through nearly a decade of working on mobile computing products, were finally about to pay off. After a successful consulting gig, Apple hired Tony internally. Within a year, Apple would launch their first MP3 player, the iPod, which would eventually sell over 450 million units. After that, Tony assumed the role of head of engineering for the iPhone. We all know how that turned out. Apple has sold 2.3 billion iPhones, making it the most successful mobile computing device of all time.
Tony wasn’t done. He later left Apple to build yet another mass consumer product via Nest Labs. Nest launched a breakthrough product—the Nest Learning Thermostat—which would revolutionize the home automation industry. If you don’t have one, you’ve probably stayed in an Airbnb with a Nest thermostat.
Google eventually acquired Nest for $3.2 billion. Since leaving Google, Tony has become a prolific angel investor and has authored a bestselling book that I would recommend to everyone dedicated to finding their own unique career pathway—Build: An Unorthodox Guide to Making Things Worth Making.
Think of your dream as a seed. The epicenter of your industry is the fertile soil that allows that seed to flourish. Embrace the challenge—not as an end in itself, but as the necessary step toward meaningful growth. If the idea of moving ignites something within you, trust that instinct. You already have your answer. Go where the action is.
From Runnin’ Down a Dream: How to Thrive in a Career You Actually Love by Bill Gurley, available for preorder, to be published on 2/24/2026 by Crown Currency, an imprint of The Crown Publishing Group, a division of Penguin Random House, LLC. Copyright © 2026 by Bill Gurley. Reprinted with permission.
The post Go Where The Action Is appeared first on The Blog of Author Tim Ferriss.
2026-01-22 14:48:49
Please enjoy this transcript of my interview with Dr. Michael Levin (@drmichaellevin ), the Vannevar Bush Distinguished Professor of Biology at Tufts University and director of the Allen Discovery Center. Dr. Levin is primarily interested in how intelligence self-organizes in a diverse range of natural, engineered, and hybrid embodiments. His lab has developed new applications in birth defects, organ regeneration, and cancer suppression and produced synthetic life-forms that serve as exploration platforms for understanding the source of patterns of form and behavior in a wide range of natural, artificial, and hybrid embodied minds.
Products, resources, and people mentioned in the interview
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Tim Ferriss: Mike, very nice to finally connect.
Michael Levin: Yeah, wonderful.
Tim Ferriss: Thanks for making the time.
Michael Levin: Of course. Yeah, thanks for having me. Yeah.
Tim Ferriss: We have lots of ground to explore, and I thought we would begin with a book that had a spot on my bookshelf when I was a kid. It seems like you and I may have found it at the same time, but you did a lot more with it than I did. The author is Robert O. Becker. Is that enough of a cue to tee it off?
Michael Levin: Yeah, I think it is, I think it is.
Tim Ferriss: All right. What is the book, and why is it relevant?
Michael Levin: I’m going to guess it’s The Body Electric.
Tim Ferriss: That’s right.
Michael Levin: Yeah, yeah, yeah, yeah, it’s very relevant. I discovered it in an old bookstore that my dad and I visited when I was in Vancouver, Canada, for the World’s Fair in ’86. And I found this thing, and it’s a patchwork of a number of different things. He was into applied field of dangers and things like that. But I was just stunned with all the references to prior work that revealed to me that the kinds of things I’d been thinking about were actually real and that people had investigated it.
Tim Ferriss: And that book, I guess Dr. Becker was an orthopedic surgeon, and he was effectively penning a scientific memoir, describing experiments involving salamanders and other animals, exploring the role of electricity and many, many different aspects of biology. How would you define, for folks, bioelectricity? What is a helpful way to define that term? And then we’ll probably hop to the video in a sense that introduced me to your work, which I will not be alone in citing, but let’s begin with the definition. Bioelectricity. What is that?
Michael Levin: Well, bioelectricity, in general, is the way that living systems exploit physics, in particular, the physics of electricity, to do the amazing things that living systems do. And there are, roughly speaking, two kinds of bioelectricity. There’s the familiar kind, which is studied by neuroscience. And so this is the electrical activity of the cells in your brain. And I think everyone has a rough understanding of the fact that the reason you know things that your individual neurons don’t know and that you have beliefs and the preferences and so on that are more than just any of the neurons in your head is through this amazing cognitive glue that electricity provides. It binds your neurons into a collective intelligence that underlies our mind. And so that’s the bioelectricity that everybody’s familiar with.
And then there’s the other kind, also called developmental bioelectricity, which you can get to by asking about, but where did the brain come from, and where did it learn those amazing tricks? And very quickly, you realize that, wow, some of these things have been around for a very long time, long before we had brains and neurons. And that the question of what does your body think about, and before it has a brain, how does it use electricity is the study of developmental bioelectricity.
Tim Ferriss: The video that I was referencing, you will not be surprised to hear, was an older TED Talk and then subsequent interview on stage, and that was sent to me by Adam Goldstein, who’s now at Softmax. And that was probably several years ago, I would say at this point that it was sent to me. Could you perhaps — and I know a lot has happened since, but could you describe some of the experiments that you covered at TED to give people an idea of how this becomes tangible, this conversation of bioelectricity becomes tangible?
Michael Levin: When we look at biology, we see lots of amazing things. For example, in a salamander, if they lose a limb, they regenerate the limb, and they stop when it’s complete. And in fact, there are many other interesting, these kinds of things that when anybody looks at it, the first thing they ask is, “How does it know to do that?”
And one of the things I discussed in that video was if you scramble the craniofacial organs of a tadpole, they still make a pretty normal frog. They sort themselves out, they move in new paths until they get to a normal frog face, and then they stop. And so anybody sees that, and immediately the question is, “Okay, but how do they know what a proper frog face looks like? And if you do know, then how do you know how to get from here to there? How do you navigate?”
So the way we’re all taught in biology is that that’s a bad question. We are told none of these things know anything. They are mechanical machines that roll forward according to rules of chemistry. And in the end, some cool stuff happens, and we’ll call it emergence and things like that, and complexity science will catalog them, but don’t worry, none of these things actually know anything, that’s just what they do.
And so what I was trying to describe in that talk is this idea that, well, actually, the idea that chemical processes can in fact know things, it’s not magic, it’s not mysterianism. We are chemical processes that know things, and we’ve had, for many decades, mature science of — including cybernetics and control theory and things like that — a mature science of figuring out how it is that machines of all different kinds can know things and they can have goals and so on.
So what I tried to show in that talk are some examples by which the living tissues, for example, flatworms that are cut into pieces and every piece has to figure out “How many heads should I have? Where do the heads go? What should the shape of my face be?” These kinds of things, that in fact they do know, and the way they know is because they store memories, and maybe not shockingly, although it’s certainly shocking to a lot of folks, the way those memories are stored is in an electrical network that is very similar to the way that we store our goal-directed behavioral repertoires in our brain and that these things are widely spread. And so regeneration, cancer suppression, and cancer repair and remodeling, birth defects and birth defect repair, all of these things are extensively using electrical pattern memories, and we now have a way to rewrite those pattern memories.
Tim Ferriss: I’ve been so excited to have you on the show because I am an intrepid muggle, blindly, half blindly exploring science to the extent that I can. And every once in a while, I’ll share a resource like I did recently, this multi-part series called The Gene. This is a Ken Burns-produced documentary about genetics, the history of genetics, starting with Mendel and so on, working all the way up to modern biotech. But the underlying framework for that entire series is DNA as master copy, let’s call it, then RNA, then protein. And that’s kind of how it works, right? You have this blueprint that is executed upon, and that produces what we see in the world on some level.
But as I understand it, you, by manipulating bioelectricity, have produced, for instance, animals that have two heads that that trait persists over generations, and maybe I’m getting the specifics wrong, but that is not by virtue of manipulating DNA. And I’m just wondering if I’m, first of all, getting that right, but secondly, what that says about how we might be revising our understanding of biology and what the textbooks might look like five or 10 years from now or further out.
Michael Levin: Yeah, you’re not wrong. I could list any number of scenarios that we and others have studied in which the genetics not only don’t tell the whole story, but in fact, tell a fairly misleading story. And the way that I would describe it, and there are two pieces to this, and I’ll do the simpler piece first, and then we can talk about the other piece. The simpler piece is really we can get there by thinking about the distinction between software and hardware.
And by the way, I should preface this because some people get really upset about this. I am not saying that the current way that we think about software and hardware is sufficient to get everything we need from biology. It does not cover all of biology; it covers one important piece of biology. Reprogrammability is really critical. And so if you wanted to make that same movie about computers, for example, you could make a movie that basically goes electric fields, silicon and germanium, and transistors, and the flow of energy through circuits, done, right? That could be your movie.
And it’s not an unimportant part of the story; it’s a very important part of the story, but the critical part that that doesn’t get to is that’s the hardware. And in fact, that’s what the genome does. So the genome tells every cell what the hardware is going to be. So the genome gives every cell the little, tiny protein-level hardware that it gets to have. But now comes the other interesting part, which is the reprogrammability. And we’ve known for a very long time now that if your hardware is good enough, and the biological hardware is more than good enough, then that hardware is reprogrammable.
So what happens, just as an example, what happens in these flatworms, these two-headed flatworms that you were referring to, the standard — the flatworm has a bioelectric memory in it that says — and we can see it. I’m saying these things because we can now see these memories and we can rewrite them at will. So this is now actionable in the lab. It has a bioelectric memory that says one head.
That memory is not genetically encoded. What is genetically encoded is a bunch of hardware that when you first turn on the juice, it basically acquires that memory as a default. When you buy a calculator from the store and you turn on the power, they all say zero. Reliably, 100 percent of the time, they all say zero. Great. But that zero is not the only thing that that circuit can do. As you find out very quickly, they can store memory and do all these things. The genetic hardware of the worm is very good at making sure that every worm starts out with a very specific — it’s a little bit, I think, related to instinct and how certain birds are born knowing how to make nests and things like that. The hardware has defaults, and by default, one head, but the hardware is reprogrammable.
So what we were able to do is go in and identify the memory that actually says how many heads, and we can change it. And when you change it, you don’t need to change the hardware, you don’t need to change the genetics any more than when we form new memories, you don’t need to change the genes in your brain to form new memories. I always say to people, “On your laptop, if you want to go from Photoshop to Microsoft Word, you don’t get out your soldering iron and start rewiring. It’d be laughable if you had to, but that’s how we used to do it. In the ’40s and ’50s, you programmed a computer by pulling and plugging wires, but you don’t do that anymore because it’s reprogrammable. And that’s what the biology is.” And so that’s the first thing.
And the second thing, just very quickly, and we can get into it if you want, is that the cellular intelligence that exists not only is reprogrammable, but it is actually creative in the sense that it interprets the DNA. And we can talk about this. It doesn’t blindly do what the DNA says, and this is a deep thing because it’s the way our cognition works too, it interprets memories in a way that is improvisational. It does not simply follow what they say, counter to what we all learn.
Tim Ferriss: All right. So I’m going to come back to how the textbooks might be revised question in a minute. But before we get there, you said we can see memories. So this is empirically demonstrable in the lab. What does it mean to see those memories? What does that actually mean and look like? And then secondly, with the flatworms with the two heads, why does that persist if it does into future generations?
Michael Levin: What we can see directly are the bioelectrical properties of tissues. And we’ve developed tools using voltage-sensitive fluorescent dyes. And so that means you take your embryo or your tissues or whatever you’ve got, and you soak it in this special chemical that glows different degrees or different wavelengths depending on what the local voltage is.
And so back in the olden days in electrophysiology, you had an electrode, then you would have to poke a little needle, and you would poke every cell, and you would get the voltage reading. We don’t need — I mean, of course, we still do that for certain purposes, but what you can now do is get a full map of the whole tissue all at once. And in fact, you can make movies of it and watch it change over time. And we have these amazing videos of embryos changing their electrical activities over time. It’s basically like what neuroscientists do when they do imaging in brains, but we can do it in the rest of the body. So there, what you see are the electrical patterns.
Now from there, you have to do a lot of experiments to prove that what you’re looking at are in fact memories. And there are many different kinds of things we do, but functionally what you have to show is that you can decode the electrical pattern that you’re seeing and show that what it encodes is the future set points towards which the cells will work. In other words, I can take a one-headed worm, I can change the voltage pattern. It’s still a one-headed worm, but it’s internal representation of what a correct worm should look like now says two heads. You don’t see it because it’s a latent memory, but when you cut the thing into pieces, now what the cells do is consult the memory, and they say, “Oh, two heads,” and then they build two heads, and you get your two-headed worm. So you don’t know right away. When you’re first looking at it, you don’t know that that’s a memory. You have to do experiments to prove that that’s what it actually is.
Tim Ferriss: And then the persistence, the durability over generations?
Michael Levin: The process of regeneration and repair in general is a kind of homeostatic process. So it’s like a thermostat. You have a set point. If the temperature gets too low, it tries to go up, if it gets too high, it tries to come down, it tries to keep a certain — that is exactly what happens in the body, which is anatomical homeostasis. So cells come and go all the time. So we’re a ship of feces in many ways. So cells and materials come and go. Sometimes drastic kinds of injuries for animals that regenerate past them. Embryogenesis, I mean, look, half our population can regenerate an entire body from one cell. I mean, that’s amazing. That’s an amazing development. Embryonic development is an incredible example of regeneration, the whole body regenerating from just one egg cell.
And in all of those cases, what needs to happen is just like a thermostat has to remember what’s the right set point, there has to be a memory mechanism that stores it. And so the electric circuits in the body that store these patterns, they have a memory property as well, such that when you change it, it stays.
Now sometimes there are multiple memories. And so we’ve done things like, for example, in these flatworms, there are different species that have different shaped heads: round ones, triangular ones, flat ones. We’ve shown that you can take a worm, change the bioelectrical signaling and get it to grow a head of a different species. But the fun thing about that is it grows the head of a different species. You haven’t touched the genetics, by the way. Again, the genome’s totally wild type.
Tim Ferriss: It’s so wild.
Michael Levin: Right, but right, but it’ll grow the head of a different species, and it’ll stay there for about 30 days. And then it goes back to its origin, it’s not permanent. The two-headed thing is permanent, that never changes. But the head shape, after about 30 days, they go back. And so clearly there are multiple, there’s more than one. There’s some kind of metacognitive thing that says, “Yeah, I know you thought that was your memory, but actually that’s wrong.” So it overwrites some kind of error-correction thing, which, that one, we haven’t cracked yet. So there are layers upon layers.
Tim Ferriss: All right. So for people who are listening and wondering how this translates or might translate to humans, I want to get there, but I’m going to bridge to that simply by saying that this topic of bioelectricity has long been interesting to me. I mean, it’s been interesting to humans for a very long time, going back to slaves in ancient Rome, stepping on electric eels and finding relief from gout, but in a more modern incarnation, I had Dr. Kevin Tracey on the podcast some time ago who was — he’s incredibly well-sited, played a part after his experiences with patients with septic shock, identifying TNF-alpha and a lot of subtleties around that and has developed hardware in this case. I mean, they’re programmable, but for vagus nerve stimulation, predominantly for, at this point, autoimmune disorders like rheumatoid arthritis and so on. But you can see some incredible, incredible clinical effects, and we’re just touching the tip of the iceberg.
So I’m wondering, it took a long time to get here though, even with something that is relatively, I would say, straightforward to identify, which is the vagus nerve, AKA vagus nerves, these intercontinental cables running down either side of the neck with 100,000 fibers on either side. So in this case, we’re talking about flatworms. We could certainly talk about other species that are known for regeneration, but broadly speaking, what might this mean for humans? How might this be applied to humans? Do humans have this programmable layer just as some of these other species do? What might therapeutics or morphoceuticals or otherwise look like?
Michael Levin: Yeah, yeah, yeah, no, and that’s a great connection. Yeah, Kevin’s work is amazing. I was just talking to him a couple of weeks ago.
Tim Ferriss: Oh, nice.
Michael Levin: It’s awesome stuff, yeah.
Tim Ferriss: Great guy, great guy.
Michael Levin: Yeah, he really is. Right. So a couple of things to explain why this is relevant to humans, and then I’ll give you three broad areas of application. The reason it’s absolutely relevant to humans is that we are all basically built on fundamentally the same principles. People have this idea that, well, frogs are a lower creature, but we’re mammals. And once you get past yeast and things like that, we are all roughly the same. As far as this stuff goes, these kind of electrical signals were — evolution discovered them around the time of bacterial biofilms, very long ago. And so this is all very well-conserved.
And for that reason, for example, there are human mutations in ion channels that are birth defects. So if you mutate ion channels in humans, you get birth defect just like we see in frog and chicken, zebrafish, and things like that. So those are all well-conserved.
And with David Kaplan, who’s a collaborator of mine at Tufts, we’ve done a bunch of work on bioelectrics of human mesenchymal stem cells. So this stuff works, for humans as well. It is not some frog or flatworm specific thing. This is very, very broad.
I should say, this is a disclaimer I always have to do, you mentioned morphoceuticals. So there are a couple of spinoff companies that have licensed some of this technology, so I need to say that as a disclosure. So one is specifically called Morphoceuticals. This is a company that is pushing forward our limb regeneration work in bioelectrics. And then there’s also this other company called Astonishing Labs that is doing some of this stuff in aging and so on.
So having said all that, I firmly believe that these things are heading for clinical application in humans, and probably not that far off, I hope. Here are the three applications. So the first application is birth defects. So we have shown that we can repair a number of different birth defects of the brain, the face, the heart, what else, the gut, these kinds of things by restoring correct bioelectrical patterns in vivo. And so this is now in animal models. We are moving, of course, to more clinical kinds of things. And I hope in the future this will absolutely be of human application. So birth defects is one. Regeneration is another.
The name of the game here is communicating with the cells. This is not about stem cells or gene therapy or scaffolds made of nanomaterials. Those are all tools that might be useful, but the real trick here is to communicate to a group of cells, what do you want them to build? And that’s what the bioelectric code is all about; it’s about communicating to the collective, to the cellular collective. And so we’ve done work on limb regeneration, we’ve done work on inducing whole organ formation, eyes and things like this. So I think there are going to be massive applications hopefully clinically in restoring damaged and missing limbs and other structures like that.
And then the third thing is going to be cancer, so something else, and we can get into what the more profound aspect is, but the bottom line is that cancer fundamentally involves an electrical dysregulation among cells. I’ll just say it and we can unpack it later, but it’s basically a dissociative identity disorder on the part of the cells. It’s literally a disorder of the cognitive glue that binds individual cells towards large-scale purpose where large-scale purpose, I mean building organs and tissues and things like that, as opposed to being amoebas and doing amoeba-level things. So cancer is another thing.
And we’ve shown again in these animal models, both that we can detect incipient tumor formation and we can prevent, and normalize tumors after they form by restoring, not by fixing the DNA if there is any DNA issue, which doesn’t have to be, not by killing the cells with chemotherapy, but by electrically reconnecting them to the group such that they can form, again, a memory of what they’re supposed to be doing. So those three things, regeneration, birth defects, and cancer, I think are going to be of great value in humans.
Now there’s also issues of aging. So we also have an aging program in our lab and looking at why it is that over time cells forget how to upkeep a proper organism. And we have some interesting thoughts about that as well.
Tim Ferriss: Well, let’s dive in. I’d love to hear more about the interesting thoughts on aging. And then we’re definitely going to get to cognition, which is — I mean, that can go in a lot of directions, but let’s start with the aging piece. What are some of the implications or experiments or just maybe conceptual frameworks that are due as a revision of what we’ve thought to date?
Michael Levin: First of all, one of the things that we’ve seen is that, and, by the way, this is fairly recent work. So this is in no way is this the final story. This is just what we know now. I’m sure this will be updated. Over time, the electrical pre-patterns that tell the cells and tissues what large-scale structure we’re supposed to look like, they get fuzzy, they degrade over time. And so much like what we do with birth defects is we try to reinforce the correct patterns. And this is one of the ways we’re addressing aging as well, is by reinforcing these patterns.
Now one question you might ask is why over time are these things getting fuzzy, what’s going on? And there are a couple of schools of thought. One is that this is the consequence of accumulated noise and damage, so molecular damage entropy, basically. Over time, you just accumulate damage, and everything gets degraded over time. And then there’s also these kind of — what they call programmatic theories where basically the idea is that you’re programmed to age. For whatever reason, evolution has favored a decline and death.
So we have an interesting third alternative to offer, which is the following. And we did a simulation experiment where we had a virtual body where the cells cooperate together to build an embryo, and so they work really hard to work together. They build to a particular pattern memory, so this thing I’ve been telling you about, they build. And then I said, “Let it run. Just leave it alone, and let it run.”
And so what you see is something very interesting. They work really hard together, and they make the correct body. Then it stays that way as they defend it, and then it falls apart, and it begins to degrade.
Now what’s interesting is that in our simulation, there was no evolution for a limited lifespan, there was no noise, there was no damage; it was perfect, everything was perfect, and still, it degraded. Why would it do that? I had this interesting thought, and I’ll back into it this way: just imagine this standard Judeo-Christian version of Heaven. So you get to Heaven, and you get there, let’s say you, your pet snake, and your dog get to Heaven. So okay, everything is great, there’s no more damage, there’s no decay, nothing is damaged, everything is great, everything’s fantastic. For the next trillion years, what happens?
So the snake may be fine doing snake things for every day is the same as every other day, may be fine. The dog, not sure. Probably okay chasing rabbits on the farm, may be fine for forever, basically. The human though, what do you think? I’d be interested in your thoughts. What are the odds that a human cognitive system can be sane for an infinite — okay, I’ll keep myself busy for the first 10,000 years, maybe 100,000 years, but a billion years in, are we still sane? What happens? What do you think? What do you think would happen?
Tim Ferriss: That’s interesting. Well, if I’m hearing you correctly, I don’t really have a passing through the Pearly Gates timeline prediction for the half life of sanity, but if I’m hearing you correctly, that the biological programmed, I mean, death, I suppose, is basically to — intended to ensure biological death before insanity. Am I mishearing that?
Michael Levin: Well, so maybe. That’s not the claim I was going to make, but it’s not impossible.
Tim Ferriss: Not a claim, but I guess I’m trying to squint and look through the exercise.
Michael Levin: What I took away from that work that we did was the following: you have a goal-seeking system that has met its goal. It’s achieved the goal. It made the body was supposed to make. The error falls to zero, everything is great, hangs out there for a while, but what does a goal-seeking system do when there are no new goals? Because we’re looking at a system that may or may not be able to give itself new goals. I mean, cognitively, I think we can, but it’s not clear yet that this system can do that. And so what we were able to do is we were able to give it new goals by having interventions and going back in and saying, “Okay, now this is your new pattern,” and it will do that.
But I think part of the, you could call it the boredom theory of aging, basically, not cognitively, somatically. If your body cells over a long period of time, they’ve completed their job, they’ve created a body during adulthood, but at some point they start to degrade. The cells don’t degrade; the collective does, the cohesion, the alignment between them because there’s no longer a common goal. I mean, this is what makes for an embryo or a body as opposed to just a billion independent cells, is they’re all aligned towards the same set point, towards the same goal.
And so when that isn’t there, regeneration, repair, maybe remodeling becomes something else. I don’t know how. Maybe you need to change up the body every once in a while. That’s also a possibility. Planaria do it. Planaria are immortal.
Tim Ferriss: And planaria are the flatworms we were talking about earlier?
Michael Levin: Yeah, the flatworms. Yeah, yeah, they’re immortal. Every two weeks, they rip themselves in half and regenerate, so they give themselves a challenge every two weeks. And so they’ve been that way for half a billion years or so. And I think that we can see evidence of this.
For example, if you look at — there’s a way to look at the age of certain genes, the evolutionary age of genes to see when did they show up. The gene expression of a young person, all the cells are in — all the different tissues have the same idea of what evolutionary stage they are, meaning in a human. When you look at old tissue, and this is something we just published recently, when you look at, we call it atavistic dissociation, when you look at the tissues of old age, the genes that they express start to float backwards in evolution. And they’re discordant, they’re out of sync. So your liver versus your neurons, they may all start to get different ideas in terms of the genes they express, of where on the evolutionary tree they are. So again, it starts to float off. In the absence of a compelling set point or goal state, all the subunits start to sort of float off and do their own thing. And this is, I think, an important component of aging.
Tim Ferriss: So if you were put in charge of, for lack of a better term, the Manhattan Project style initiative related to aging, that was your sole directive, was to really do a deep dive with the intention of developing some type of therapeutic for humans, what might that look like? I mean, for all intents and purposes, infinite funding, but you have the resources, you can get the talent. Where would you take it, if you had a similarly pressing deadline? And I’m not asking for the impossible, but if you had a reasonably tight deadline by which you needed to try to come up with something, where would you take it? How would you think about it?
Michael Levin: Tight deadlines for aging are tough, because you’re not going to know for decades whether your thing works.
Tim Ferriss: Yeah, right.
Michael Levin: No, but I get the idea. This is what I would say. I think that fundamentally, I think that aging, cancer, birth defects, lack of regenerative repair throughout our lifespan, all of these kinds of things are downstream of one fundamental pressure point, that if you solve that, all of these things get solved by side effect. And that is regeneration.
More specifically, that in turn is, everything there hangs on the cognition of groups of cells. In other words, how do groups of cells know what to build, when to stop? How do we communicate with them, and what kind of intelligence do they have? And I’m being very specific about this. When I say they have intelligence, I don’t mean complexity. I don’t mean some sort of linguistic project where I’m going to take things that are beautiful and fascinating, and I say, “Well, that’s the intelligence of life.” That’s not what I mean. I’m using a very specific definition of intelligence, which is what behavior scientists use, which is problem solving, memory, different degrees of a cognitive light cone of goal-directed, the size of your goals, things like that.
So specifically, figuring out what are the competencies of the living material that we’re made of and how do you communicate new goals to them? There are lots of amazing people in the aging field doing interesting things and that’s cool. If I had a lot of money specifically for aging, I would put everybody on that question. I would say, you’re not studying aging. What you’re studying is the goal-directedness of multicellular systems. Figure out how they know what to do and how we communicate goals with them. If you solve that, all of these other things get taken care of as a side effect.
Tim Ferriss: What might an example or sample new directive be? To give human cells or groups of cells a new goal, what might that new goal look like?
Michael Levin: I’ll give you an example, and then we can talk about what the human case might look like. What we can do is, we can take a frog embryo and induce a particular electrical pattern somewhere in the body that we already know, that pattern codes for make an eye. That’s how the other cells interpret that pattern. It means make an eye. Very interesting in the sense that we don’t have to say which cells do what. We don’t have to say which genes you need to turn on. These are all micro level details. We don’t need to worry about them, because the material is competent. Just like when I’m talking to you, I don’t need to worry about how your synaptic proteins are going to — you’re going to take care of all of that. All I need to do is give you the prompt, and vice versa, and we’re having this amazing conversation. But our hardware takes care of all the molecular details. And the same thing here.
So, we provide a bioelectrical pattern that says make an eye here, and the cells make an eye. Now, the first thing that happens, it’s interesting. The first thing that happens is, there’s a battle of worldviews that takes place. The cells try to get — we inject a few cells. They tell their neighbors, “Let’s make an eye.” The neighbors actually say, “No, we’re supposed to be skin or gut. Don’t do it.” And sometimes they win and sometimes we win. And so the goal of regenerative medicine is to be as convincing as possible, so that you win 100 percent of the time.
But in the cases where we are convincing, and we have amazing videos of cells like convincing each other to have different voltages and whatnot, they make an eye. And so, what you’ve done is, you’ve taken a bunch of cells that were going to be, for example, gut, and you’ve now pushed them to be an eye. At a very high level, I don’t know how to build an eye. I don’t know all the genes that have to be turned on. You do that. I’m telling you something at the level of organs, this is going to be an eye. The eye is of the right size. It has all the right layers to it. It is functional. So you can see out of these ectopic eyes, it’s really, really amazing.
And so that is an example of giving these cells a new goal. How do I know it’s a goal? Because I did not micromanage you to do it. I was not there saying, “Turn on this gene, turn on that gene.” I gave you a far off set point, by the way, in a wild space that no individual cell knows anything about, the anatomical space of organ structures. No individual cell knows what an eye is, but the collective does. And they stop when it’s done. I don’t need to be there to tell them to stop. They stop when it’s done.
And so, this is autonomous goal-directed activity, and it’s a navigation of anatomical space. And so, we can do this. And we can’t make everything. We can make portions of the brain. We can make eyes. We can make, in some cases, limbs. We can make some other structures.
So, in the human, you could imagine two ways to go, and I don’t know which is going to be correct, and we need to do a lot of experiments in mammals to nail this down. One possibility is that it might be enough to simply reinforce the existing human pattern. Every so often, you would get like a tuneup that reminds all the cellular collectives what we’re supposed to look like. That’s one possibility.
There’s another possibility, and I don’t know which is correct. I hope the first one is right, but I think it wouldn’t be the end of the world if it’s the latter. Maybe it really does get too boring with the same pattern, meaning that, okay, you can go a few hundred years with this reminding of the standard human pattern, but eventually you have to do something unique. Now, the planaria are telling us that actually, it’s hundreds of millions of years that you can make the same thing, so I’m kind of optimistic that you can do that. But let’s say that’s not the case.
If that’s not the case in humans, maybe you have some number of hundreds of years or whatever of the standard human body plan. But then if you want to keep going, you got to make some changes. What does that mean? Maybe you wanted some wings. Maybe you want some tentacles. Maybe you want a third hemisphere to crank your IQ. Maybe you want, I don’t know —
Tim Ferriss: A third eye. Who knows?
Michael Levin: Sure, sure, sure. Infrared vision out the back of your head. I don’t know. People email me all the time asking for all kinds of weird peripherals. So maybe, maybe at some point, it means that you’ve really got to change things up a little bit, caterpillar, butterfly style. Maybe.
Tim Ferriss: Wow. And just to come back to a piece that we covered through the thought exercise of the pet snake, the pet dog. Do you think we have evolved to die, or to age? I mean, if so, why? What might be a straw man argument for that? I’m just curious. Yeah.
Michael Levin: There certainly are reasonable theories of why evolution wants you dead, and there have been a number of them. Overall, I think there may well be trade-offs of the kind that, for example, we’re not going to put a lot of — evolution would not put a lot of effort into maintaining something if something else is going to go off and you’re going to die anyway. So there are these ecological trade-offs.
I’ll give you an example of something like that. People ask, “Hey, why can’t humans regenerate their limbs the way that axolotls can, and things like that?” Nobody knows, but here’s a plausible theory. Imagine, you’re an early mammal, you’re running around the forest, somebody bites your leg off. Now, you have a high blood pressure, you’re going to bleed out. If you don’t bleed out, you’re going to walk around and grind that thing into the forest floor. It’s going to get infected. You’re never going to have time to regenerate. What you might do is scar, seal the wound, inflammation, so that you might live to fight another day, but you’re definitely not going to have time to regenerate the way that an axolotl might, sort of floating around in water for three weeks or whatever.
So basically, what you might say is that evolution just kind of decided that it’s not worth it. It’s never going to work. It’s not worth it. And by the way, deer antlers. Deer antlers are the one amazing mammalian example of regeneration, plus the liver. I mean, liver regenerates. But deer antlers, it’s a large adult mammal that regenerates this huge structure of fast —
Tim Ferriss: The rate of regrowth is just incredible.
Michael Levin: Crazy. Yeah. Centimeter and a half per day of new bone.
Tim Ferriss: So nuts.
Michael Levin: That’s bone, vasculature, innovation. And you don’t put weight on it. It’s not load bearing. It’s the one appendage that’s not load bearing. So anyway, why I’m saying that is because you can imagine evolutionary trade-offs like that, where evolution just didn’t bother optimizing for long age. You can imagine that. But fundamentally, I do not believe that we are inevitably mortal. I think that at some point, if we knew what we were doing, if we had appropriate regenerative medicine, I don’t see any particular reason why we have to age and die.
And then you face interesting questions about, for example, mental plasticity. We all know with advanced age, people get a little less plastic mentally, that kind of stuff. Is that a hardware problem or a software problem? We don’t know. If you had somebody with a physically young brain at 100, would they be like an 18-year-old in terms of their ability to take on new ideas and focus and pay attention, whatever? Would that still stay? Or is there some kind of a cognitive, I don’t know, a tiredness that happens, that is not a hardware issue? I don’t think we know, but we need to find out.
Tim Ferriss: So I was going to ask you about computer science and AI and concepts that you would like biologists to learn. Well, let’s start there. And then I’m going to ask a question that might destroy any shred of respect that you have for me, but I’ll save that for after this one. Do any concepts come to mind, because you certainly have spent a lot of time in computer science, that you wish you could require biologists to become familiar with, or to study? I’m wondering about cross pollination between disciplines within which you’ve spent a lot of time. It could go the other way as well, and this could be concepts from developmental biology or biology writ large that you think computer scientists should pay more attention to. But does anything come to mind for either of those?
Michael Levin: My original background is in computer science. Computer scientists are amazing, generally, at compartmentalizing, course graining, sort of modularizing, like hiding details and asking, “Okay, but what’s actually important here?” And like black boxing things. Biologists generally think everything is important, and if you ask biologists, you’ll get a list of 30 genes. And these are hard-won details, right? They’re all important. But a computer scientist is like, “Okay, but what is that actually doing?” And that’s really important. The most basic thing is this issue of reprogrammability, is that understanding that you get — and certain kinds of hardware is reprogrammable and why. That, I think, is really key.
The other thing that I wish, and there’s not really time, unfortunately, for almost any biologist to do this, but one thing I really love for my students to do, if they can, is to take a course in programming languages, and here’s why. Not so they could code, that doesn’t matter. It’s not the coding aspect. What happens in a typical course of programming languages is that you spend — so let’s say in a single semester, you’ll spend three weeks doing different languages. And the thing about those languages, and maybe this is true of some human languages as well, but it’s definitely true of computer languages, is that each language is a different way of looking at the world. You start off with something that makes sense and you’re like, oh, step by step, you sort of tell it what to do. Okay. And then all of a sudden, bam, now there’s this other thing where every piece of data — there’s this language called LISP where every piece of data is also instructions, and you can execute any piece of data. Like, what? And then you get into this other thing, and it’s functional programming. Now there are no variables. You don’t get to have any variables. Everything is just a function call.
And every time you do this, it sort of rips the foundation of your world out from under you, and it says, this universe works in a very different way than you thought before. Forget everything you knew before. Now you got to do this. And how are you going to solve this problem? Now there’s recursion, or now there’s no global variables, or whatever. And every time, and what it’s really good for is that mental plasticity that reminds you that the way you think things are and the tools you think you have are not the only things in town. And so, when you do that in a lightning, and you have to get, things go fast and then the final exam comes and it’s this other thing you’ve never seen before. Being able to do that quickly, I think is super valuable, and I would love that to be more known in biology.
But the final thing I’ll say is, and this is, I think this is true, but just to be clear, this is very controversial and almost nobody else thinks this is true, so who knows? But the interesting thing that a lot of people, not just biologists, but a lot of people think is something like this. Okay, there’s something going on with humans, maybe other animals, where biochemistry does not tell the whole story. You read the biochemistry textbook and you say, okay, that’s cool, but there’s something about my mind and my ability to solve problems in abstract spaces and my inner perspective and all this stuff. It’s just not captured in these low level details. And so, that’s a little disturbing. It’s like, but what is that then, if it’s not captured in the chemistry? Wait, where’s that coming from?
But don’t worry, we have this other thing over here, which are machines. Dumb machines. Dead matter, dumb machines, algorithms, computers, and those things do only exactly what the algorithm tells them to do. They are perfectly captured by our formal model. So we have a formal model of chemistry and the rules of chemistry, and that we think does not capture what it is to be an entire, full-on human. But we have these other formal models of Turing machines and programming and code and mechanics, and those things capture exactly what the machines do. Those get the whole thing.
I think, and this is the part that’s very sort of controversial and not a widely shared opinion, I think that’s false. I think our formal models never capture all of what’s going on, and some of the craziest stuff coming out of our lab recently is showing how much, even in very simple sorts of machines, how much interesting novelty, not just complexity, not just unpredictability, but things that any behavioral scientist would recognize as some kind of a protocognitive capacity, shows up in even minimal systems where you don’t expect it.
And so, what I’d like the biologists to sort of eventually, once we can show this widely, the biologist to understand is that the biological systems are amazing and awesome, but it’s a kind of a larger degree, not kind, of what’s already going on in inanimate systems. And for this reason, this is also kind of a crazy claim, is that I think the circle, if you make a circle of cognitive things and living things, I think cognition is wider than life. I think cognition predates life and I think it’s bigger than life.
Normally people do that the other way around. They say, here’s the inanimate universe. Some chunk of that is living and some tiny piece of that is intelligent. I think that’s exactly backwards. And that’s something we need to understand, both on the biology and on the computer science end, is like, is there a distinction between what people commonly think of as living things and machines? Are there any actual machines in the sense that we like to think that there are? That’s a deep set of questions for both fields in the future.
Tim Ferriss: All right. That’s a super tempting opening to take, and I might come back to it, but I wanted to take the opportunity, as promised, to destroy any credibility I might have with you and my audience.
Michael Levin: Great.
Tim Ferriss: All right, so I’m going to try to give myself some air cover by going back. Sorry to drag you into it, Kevin, but to go back to Kevin Tracey, and also, actually, years before my interview with Kevin, one with Martine Rothblatt. And in both cases, Martine is just an incredible polymath on a lot of levels. People should look into Martine.
But we were chatting, Martine and I, about a transauricular stimulation of the vagus nerve. And there’s quite a bit of mechanistic debate around this. How many fibers are you hitting? Is it actually possible to do through the skin? Et cetera. But suffice to say, the clinical outcomes of certain types of placement, of certain types of currents on the ear, seem to produce pretty dramatic anti-inflammatory effects.
And so, then that raised the question for me of, wait a second, do those maps I’ve seen in Chinese medical offices have anything to them? Now, chatting with Kevin, he’s like, “Well, funny thing about that is that it was a Frenchman who actually put that together after taking a ballpoint pen and pressing on patients’ ears, and then it made its way back to China.”
I don’t know the full history, but as we’re talking about bioelectricity, I have to ask, and again, this might be a dead end, but if you look at traditional Chinese medicine — I went to two universities in China and took a pretty close look at this at the time, in 1996, but is there anything to Meridians, Chi? Did they get anything right, or was it just coincidence? Is there really nothing defensible to it? I’m just wondering if there’s any overlap.
Michael Levin: Yeah. I was wondering how wild you were going to get that with that question, like where that was going to go. That’s not too bad. Okay, I don’t know the epidemiological data on acupuncture and how it works in clinical trials or any of that stuff. I don’t know. What I do know is that I personally, I know an amazing, there’s a guy in Boston called Tom Tam, and I’ve known him since the ’80s, my whole life, since I was a kid. And he’s treated me, he’s treated my family. I’ve seen people, advanced cancer patients in his clinic. Don’t know anything about the wider epidemiological aspect of it. To me, as someone who’s interested in practical results, I would say, I can’t say anything other than 100 percent that I think there’s something very powerful here, very significant.
So the next question is, what are those meridians, and do they have any functional overlap with the bioelectricity that we’re talking about? I don’t know. We actually had, back in 2006, I think, we had a little bit of a collaboration with the New England School of Acupuncture to try to figure that out. I wanted an animal model. I wanted to see if we can do a frog model of acupuncture or something, and so on. It didn’t work, for a number of reasons.
The real answer is I don’t know. But if I had to guess, what I would say is that whatever it is that acupuncturists are managing with their treatments are — it has the same relationship to the bioelectricity that the bioelectricity has to the chemical signaling. In other words, chemical physical protein signaling pathways, bioelectrical state, there’s some other informational state. Maybe it has to do with the biomechanics of tissues. And again, disclaimer, I still get acupuncture. Vanessa Grimes here in Beverly, every month I get a tune up. I think it really works, so take it all with a grain of salt.
But I don’t think they’re managing bioelectricity directly. I think they’re managing something else, which is no doubt relevant to the bioelectric layer, because it then has to transduce through that to the rest of the body. But I suspect it’s not bioelectricity per se. I suspect it’s something additional. That’s a guess on my part.
Tim Ferriss: Yeah. Cool. I’m glad I asked. Thanks for answering, too. On the acupuncture side, I don’t get a whole lot of acupuncture. And you can look at sham studies and so on where, yes, in the case of, for instance, one of my PTs in Texas, you can use something called dry needling instead for muscle spasms, and it’s very, very effective. But then you can also conversely look at data in, say, canines, or pain control in animals, where, as far as we know, placebo is going to be pretty tough to defend.
Michael Levin: Well —
Tim Ferriss: Well, maybe. I guess, you tell me. Maybe not. Or surgery with, I mean, this is probably not the right term, but sort of anesthesia via acupuncture, also pretty interesting. So, I don’t know where to take that. I don’t have any domain expertise, but it continues to be interesting, I suppose. And also, pregnancy data, acupuncture for conception, which may intersect with vagus nerve stimulation. Who knows?
Michael Levin: Yeah. I mean, the deal with placebo, I don’t see placebo as a confound. I mean, it can be if you’re trying to calculate certain things, but I think it’s kind of the main show in a lot of ways. And some of the placebo research, like Fabrizio Benedetti is one of my favorites, and he has a talk where he says, “Words and drugs have the same mechanism of action.” And it’s amazing, because he actually does the experiments of giving patients drugs that he tells them what they are, and then he looks at molecular markers in their blood and in their cells, and yeah, they turn on the downstream, except that they didn’t get any of the drug.
So there’s something very interesting going on here, and we already know — I mean, okay, if I were to come here and tell you that, “Hey, did you know that with the power of my mind alone, I can electrically depolarize up to 30 percent of the body?” You’d say, “What is that? Yoga, mind matter? Mind, body, what kind of thing is that?” I’d say, “No, it’s voluntary motion. We do it every day.” So it’s an amazing thing that nobody talks about.
Think about this. You wake up in the morning, you have these very abstract, high-level goals. You have social goals, financial goals, research, whatever. And in order for you to do any of that, you have to get up out of bed. So what has to happen is these incredibly high-level, abstract intent has to change the way that calcium and potassium ions go across your muscle cell membranes. These abstract mental things have to change the chemistry of your body cells. We know that’s true. Every time you lift your arm up or you take a step, voluntarily, that is what’s happening. So we know that works.
So if that works, why is it so bizarre to think that our other mental states might not affect, either through the electrical transduction of the nervous system, or through other non-neural bioelectricity or through other pathways yet, could affect ways that other cells act? It doesn’t seem weird to me at all. It seems like it would have to be that way. But what we need to figure out is how it works and how to communicate. I think that’s an incredibly powerful — if acupuncture is some kind of entry point into figuring that out, great. It’s not a confound, it’s a feature.
Tim Ferriss: Yeah. I totally agree with the placebo not necessarily being a confound, as you mentioned, depending on what you’re optimizing for measuring and so on. I mean, as someone who’s funded a lot of basic science and clinical research involving psychedelic compounds, which are just notoriously difficult to blind. It’s like, yeah, give someone a megadose of niacin plus X, Y, and Z or Ritalin or something like that. But generally, the control group knows that they are the control group. But that doesn’t invalidate the research, right? It just points out maybe some methodological revision or tweaking that might be helpful. I want to —
Michael Levin: Well, sorry, just to add it, there’s something else here that’s really interesting, and I haven’t seen anybody in the field, maybe you know folks that have looked at it. A lot of times, at least what I understand in some of Fabrizio’s data, both for the efficacy and for the side effects, because there’s the nocebo effect. People, they start, oh yeah, definitely headache or whatever. But what’s interesting is, to me anyway, is that unless, if you’re a scientist and I tell you that, okay, I just gave you an SSRI, you may know what the downstream steps are going to — if you’re a regular person off the street participating in this study, now how do you know what the actual —
Tim Ferriss: That’s the wild part, right?
Michael Levin: Yeah.
Tim Ferriss: How do you actually implement the instructions?
Michael Levin: That’s right. That’s right. And I think actually, I think animal studies should actually be very — this is how we got here, is talking about animal placebo, because there are studies in experimental effects in animals, where — there are whole books on this where you do, in behavioral science, you do these experiments on rats, and whatever the experimenter believes is what the rats end up doing. They don’t need to understand the placebo. They’re going to do it anyway if the experimenter believes it, right? So, trying to understand some of these subtle cues and influences, and how does your body know things, I think, is like super, super interesting.
Tim Ferriss: Okay, I can’t let that one go. So, what do you think is actually happening there between the experimenter and the rats? I mean, is it just the subtle body language, et cetera, that’s being transmitted to an animal who’s perceiving that? That seems like a stretch, even as I say it, but I don’t know what the alternative explanation would be.
Michael Levin: Yeah.
Tim Ferriss: What might be a theory or two for what is actually happening?
Michael Levin: Yeah, good question. I don’t have a theory, but I will mention some things to think about. One of the remarkable things that living systems are good at is in credit assignment, in selective attention. So for example, there’s this old work on biofeedback from, I think, the ’70s, where they can show that a rat can generate a temperature difference of a few degrees Celsius between its ears if you reward for that. And so now, just think. And it doesn’t take years of practice, it’s pretty quick. And just think, you’re a rat, you just got some reward. So let me see. While my tail was pointing north and my whiskers were kind of vibrating and my gut was doing this and my toes were — what the hell did I just get rewarded for?
You would think, and this in computer science is called the frame problem, because trying to get robots and AIs to focus on the important thing. There’s an old — I forget who did this example, but imagine there’s a robot, and it’s in a room with a bomb, and the robot says, “Oh, there’s a bomb. I’ve got to get out of here.” And it leaves. Except the bomb was on a cart that was connected to the robot, so it goes with him, and of course, he blows up. So what does the next robot do? Maybe Dan Dennett, I don’t remember. So the next robot is like, okay, okay, we have to have them consider all the options. So now this robot he goes in, so the robot’s like, “Well, let me see. The walls are pretty vertical and the paint is dry, yeah, and it’s a 90 degree angle. Cool.” And so by the time it’s considered all these things, of course it blows up again. So that’s no good. And so biologicals are amazing at knowing what to pay attention to, “What was I just rewarded for? What was the thing I did, which I’m never going to do again which turned out poorly?” We don’t know how that works. And that I think is going to be a major part of that puzzle that you’re asking about.
And I’ll just give you an example from our work, flatworms. Again, planaria. We put planarian in a solution of barium. Barium is a non-specific potassium channel blocker. It blocks all the potassium channels. So that makes it very hard for cells to do their physiology, especially the neurons freak out. Their heads explode. Literally overnight, their heads explode. But as it turns out, so it’s called deep progression is a way to put it, but basically the cells just explode.
Tim Ferriss: It’s a very polite way to put it.
Michael Levin: Yeah, yeah. It sort of deprogresses. But what we found is that —
Tim Ferriss: Net negative treatment in special ops assassination. “Oh, yeah. It’s just a negative treatment, yeah.”
Michael Levin: Yeah, yeah. Basically it’s a deprogression. But here’s the amazing part. So you take the part that’s left, the tail and the mid-body, you leave it in the barium. And within about 14 days, they grow a new head and the new head doesn’t care at all about the barium, no problem whatsoever. So the new head is fine. So how is this possible?
So what we did was a very simple-minded experiment. We took all the genes that a normal head expresses, all the genes that — and for sure, this doesn’t have to be in the genes. This is just a simple thing we did to start with. And what genes does the barium-adapted head express? And we found less than a dozen genes that make the difference. Now think about this. planaria don’t normally see barium in the wild. You don’t have an evolutionary response to what happens when I get hit with barium. You’re sitting there, I view that you have something like 20,000 genes. You’re hit with this new stressor that you’ve never seen before. How do you know which of those 20,000 genes are going to help?
I always visualize this as you’re sitting in one of those nuclear reactor control rooms, there’s buttons everywhere, the thing’s melting down. You don’t have time to start flipping switches sort of randomly. You’ll be dead long before that. How did they zero in on the correct 12 things out of a space of 20,000 dimensions that they could have? It’s a very high dimensional search problem. We don’t know. Nobody knows.
And that aspect of it, biology, finding solutions to problems they haven’t seen before, knowing what’s salient, figuring out what to pay attention to. There are aspects here that we haven’t even come close to replicating in our engineering technologies. I think it’s going to be part of all that.
Tim Ferriss: Well, this is a pretty close hop to — and this is a term that has very specific meaning for you, so it may not be the right term for me to use, but cognition. Let’s talk about human cognition in the way that most people would think about it. We have this big, big ball of fat inside our skulls. A bunch of magic seems to happen and we’ve got these amazing tools. We’ve got these MRIs, PET scans, et cetera, that we can — EEGs and so on that we can use to try to study the brain and what’s actually happening. And my question is, and not to belabor this type of question, but it’s just a forcing function for conversation, 10 years out, 10 years from now, how the textbooks, and textbooks may or may not even exist at that point, but how the teaching of neuroscience might have fundamentally changed as it relates to cognition.
Because I look at, for instance, funding a lot of neuroscience over the last 10 years. And it’s like, okay, sometimes the scientists are attracted to whatever the fanciest tools might be. There’s some prestige in that. They produce a lot of beautiful images. You can slice and dice the data from a single study 15 different ways and get a lot of publications. And this is not something I could technically defend. I’m left feeling, as a lot of people do, that there’s something missing. It’s not quite capturing the full picture, pun intended, not just with the MRIs, but with a lot of these tools that we’re using.
And I’m bringing this up because of the comment you made about the gap between the biologics and current engineering. And this certainly relates to AI and so on, but I don’t have the technical chops to understand quantum effects, but if I think about some of the cursory reading I’ve done about quantum effects in olfaction, let’s just say, smell. I’m just left wondering what we might be missing fundamentally about how cognition works and also ties into, not to turn this into my own TED Talk, I’ll try to wrap this up in a second, but having conversations with my friend, Kevin Kelly, who’s the founding editor of Wired Magazine, who’s an avid beekeeper and about just the collective memory of hives and properties that you would never be able to predict and that I’m not entirely sure you can, at least at this point, engineer from the ground up. But how do you think our view of cognition, thinking, mind might change in the next five, 10 years?
Michael Levin: Yeah. Okay. I want to talk about two things, one of which I’m pretty sure is going to be very different in that timeframe, and another thing which is more fundamental that may take longer or may not.
The one thing that I think for sure is going to change is that there’s a thriving emerging field out there now called diverse intelligence. And this is the idea that biology, and as I’ve been pushing it also non-biology, has been doing intelligence of different kinds long before brains and neurons appeared. It’s been solving problems, navigating spaces, having memories, anticipating the future long before neurons appeared. The biggest barriers to this are these ancient categories that we got saddled with from pre-scientific times, this idea that everything is binary. People ask, “Is it intelligent? Is it conscious? Is it this or…” That binary framing has been holding everything back for a really long time.
Tim Ferriss: Is it holding it back because it’s bifurcated between inanimate and animate? Or is it something else?
Michael Levin: It’s the idea that it hides and it obscures the fact that we don’t have a good story of scaling. Just two quick examples. When you go to court, there’s this notion of an adult. We all know if you really think about it, nothing happens on the night of your 18th birthday, literally nothing, and that’s A. And B, we don’t actually have a good story of a scientifically grounded story of what does it mean to have personal responsibility? How does that change over time? How is it impacted by neurotransmitters, brain tumors, Twinkies, society, whatever? We don’t actually have those questions answered, but you’ve got to get traffic court done, or whatever. And so we’ve just decided we’re going to have this thing called adult and we’re going to clock it on the 18. The car rental industry actually does better because they look at statistics and they’ll say, “No, actually it’s 25 is when you’re more fully cooked is when you can rent a car,” and so they do a little better, but regardless, the idea is that we — and we all say it’s an adult.
And so what those binary terms do is they obscure the fact that, yeah, but underneath, we actually still don’t have a proper understanding of what’s going on. And so by saying that something is or isn’t intelligent, what you’re basically assuming is that somewhere, some developmental biologists can tell you what happened from the time that you were an oocyte, a little blob of chemicals that presumably was well handled by biochemistry and physics, and then eventually, well, now you’re the subject of physiology, and then eventually you’re the subject of developmental biology. And then, oh, look, now you’re the subject of behavior science. Oh, wait, psychoanalysis. So each of us made that journey. It’s a smooth, continuous journey. Developmental biology offers no support for this idea that somewhere there’s a bright light, flash of light and that, okay, now you used to be just chemistry, but now you’ve got a real mind. That never happens.
Because here’s the other thing they do. If I were to say that it’s a continuum, if cognition is a continuum from the most primitive passive matter to humans and above, what I could say is, “I’m going to take some tools from behavioral neuroscience and I’m going to apply them to all kinds of weird things and see how that works out for me and that’s how we’re going to know what’s cognitive and what’s not.” And this in fact is what my lab is doing. That project is very disruptive and there are a lot of people who really think that’s crazy because what they will say is, “Look, it’s a category error.” Brains and humans think. Cells and tissues can’t think. How do you know? Well, because the way the word is defined.
So what they’ve done is they’ve taken something that’s actually should be an empirical experimental science, take the tools and see where they give you benefits and where they don’t, but instead they’ve made it into a philosophical or a linguistic project where these ancient categories that we got saddled with, “Oh, don’t make a category error.” That kind of thing, so I think it’s very disruptive.
So I think what’s going to happen in the future is that all of the applications now that are coming out from Active Matter Research, from basal cognition, from work in slime molds and single cells and materials with learning capacity and all this stuff, we’re going to realize, I think, this is again one of these claims, I think that neuroscience is — we’re going to realize neuroscience is not about neurons at all, and that what neuroscience is really about is cognitive glue. Neuroscience is the question of what kind of architectures add up to larger-scale minds from aligned simpler components? Now, neuroscience has a lot to teach us about that because that’s basically what they’ve been studying, but I think the majority of them, not everybody, because we have all kinds of collaborators in this field who are doing something else, but the vast majority of traditional neuroscience think they’re studying neurons, that this is something unique to these cellular systems that they’re studying.
And I think this field of diverse intelligence combines artificial intelligence and engineering and cybernetics and evolutionary biology and AI and exobiology and the search for alien life. All of these things are together asking what are actually the common threads of being an agent? No matter what your origin story, whether you were designed or evolved or engineered or evolved, or whether you were made of squishy proteins, or whether you were made of silicon or something else. Yeah, I don’t know. I think science fiction prepares you for that nicely and for that kind of stuff to really have a broader conception of it. And so I think really understanding what neuroscience is actually about, I think, is going to be a massive change.
And the final thing I’ll say is, and this, I don’t know how long it’s going to take to, hopefully not that long, but you might remember this story that at one point I think in the late 1800s, I think it was Lord Kelvin who said that, “Yeah, physics is kind of done. There’s just these two black clouds or something, but mostly it’s just about more digits past the decimal point, but there’s these two clouds.” And the two clouds basically became quantum mechanics and relativity and all of that.
And so I think neuroscience has a couple of black clouds, and I’ll just describe one of them. We did a, Karina Kofman and I, she’s amazing, she started as a high school student working with me remotely, we just did a review of this, clinical cases in humans of normal or above normal IQ while having very minimal brain volume. I’m sure you’ve heard some of these cases, but there are many to look at. Now, it’s not that you can’t add a bunch of epicycles to standard neuroscience and somehow try to squeeze these things into the mainstream paradigm. Maybe you can. But to me, the most important thing is that it doesn’t predict that that should be possible. There’s nothing we learn, at least that I’ve ever seen in neuroscience courses that tells you that, “Oh, and by the way, yeah, you should be able to do all this with less than a third of the brain volume of a chimpanzee.”
So there’s something going on here, which I think is really fundamental. It’s one of these observations that you can try to sweep under the rug, but I think it’s actually telling you that we have some very, very seriously wrong assumptions somewhere in the theory.
Tim Ferriss: Yeah. It’s exciting. It’s super exciting. I mean, I’ve looked at some of that research, or in some cases brain adaptations around severe injury, and they just raise a lot more questions than we can currently answer.
This could be a quagmire I’m about to create, but I’m going to take a stab at it anyway. A lot of people talk about consciousness maybe in the same way that people argue about God without defining it very well, but then even the best intentions to define it can end up slipping on banana peels. But I am curious, you’ve spent time with Daniel Dennett, who I think you mentioned a little bit earlier. We’re talking about, and I think you can keep most people probably on the same page when you’re talking about intelligence as very carefully defined in a specific way. And I’m paraphrasing here from memory, so I apologize if I get it wrong, but goal seeking systems that maybe can satisfy those goals in multiple ways, maybe this is kind of along William James lines. Feel free to fact check that. But I’m wondering where you go from there or how you think about consciousness. If you do at all, maybe that’s just one of those terms that’s like, well, it’s like success or happiness. It’s so poorly defined I don’t spend a lot of time thinking about it because it’s a dead end. But if that’s not the case, how do you think about consciousness? Because as you’re talking, and some people may have been thinking of this, they’re like, “Well, wait a second, is Mike a panpsychist?” Where are we going here?”
Michael Levin: Yeah. I’m a, I don’t know, some sort of super panpsychist or something. Okay, I don’t think it’s unimportant. I think it’s a very important question. Big picture, I think it’s really important. I’m not a consciousness researcher and in my lab, we haven’t done pretty much any experiments on consciousness, so I want to preface everything I’m about to say by saying that, first of all, this is not something I typically work on. And the reason I don’t work on it right now, and I do have some stuff cooking, but it’s not ready yet for public consumption, the reason I don’t focus on it now is that there’s so much that can be done without delving into that, with a third person perspective on observable problem solving, cognition. And even that has been such a slog. I’ve been at this for now 20 years and it’s been so difficult to get people to shift in that way, that I don’t need to get into consciousness to do the things that I need to do now. Nevertheless, and so for that practical sort of strategic reason, I haven’t been talking about it except for when people ask.
And so if you ask, I would say that for the purposes of defining what we’re talking about now, I would say simply something like: first person perspective of the kind that makes my toothache really quite different in import than anybody else’s toothache. There’s something about my toothache that’s quite different than when other people — it’s terrible when other people have a toothache, but there’s something different when I have it. And so that’s, I think, the kind of thing that we’re talking about here.
So here’s what I would say about it. First of all, again, I really can’t understand how anybody can maintain a binary view about this, both on an evolutionary scale and on a developmental scale. If you think you are conscious, and I realize that some people don’t even think that, but let’s assume that we think that we are conscious, you have to tell me when that showed up in development. Development is slow and gradual and either the oocyte had something that got scaled up in some way, and then what we really owe is the story of scaling, which is what I think. Or some sort of people will say phase transition. And that’s a fine hypothesis. You have to show me what the phase transition is and why I can’t zoom into it because the nice thing about those graphs that goes like this, is that if you just stretch the horizontal axis, they all become smooth and flat eventually. So what exactly happened that you weren’t conscious and then you became? I think that’s a total nonstarter.
So I think the question about consciousness is: what kind and how much, right? So let’s just start there. And then I would say that there are roughly four reasons why people give each other the benefit of the doubt about consciousness. So the problem of other minds, how do I know that you’re conscious? And there’s usually four types of reasons that people give. What I can say is that if you like any of those reasons, for any of those four reasons, you should take very seriously, for example, the idea that other organs in your body have their own consciousness for those exact same reasons. For the same reason, we can dive into it if you want, but for the same reasons that you and I think each other is conscious you should take very seriously the idea that there are other parts of your body that are.
Now, at this point, people usually say, “Well, that’s weird. I don’t feel my liver being conscious.” Right. Your left hemisphere that’s verbal puts up a very nice story about how it’s the only one that’s conscious. And of course you don’t feel your liver being conscious, you also don’t feel me being conscious. That’s because you are not that consciousness. But that doesn’t mean that there aren’t any number of other consciousnesses inhabiting your body and you would not have primary access to them. And some people disagree, but that’s what I think.
So I think that we should take very seriously the idea that certainly all kinds of other minimal biologicals have some degree of, I’m not saying every cell is sitting there having hopes and dreams like we are, but little ones, little tiny ones. And so that I think I can say reasonably strongly.
The thing that is a total conjecture is the following. Something that I’ve said more recently, just this year I’ve started talking about this notion of this Platonic space. And if you want to talk about that, we can get into it. But I think that in many ways, all the things that we are looking at, so bodies, computers, robots, embryos, the biobots, all of those things are in an important sense, thin clients. They’re front-end interfaces for patterns, patterns of behavior, patterns of information processing, patterns of form and so on for patterns that come from a different space. They don’t come from this physical space and we can dig into that.
If that’s the case, then what you could say is, and again, this is not something that, this is just conjecturing here. I’m not saying this is useful in the lab yet or anything like that. I like to keep those things separate. But if you have to say something about consciousness, what you might say is that consciousness is, it’s the point of view of the pattern projecting into the physical space. In other words, third-person observable behavior problem solving like normal science is what we see with each other doing within the space, but consciousness is the viewpoint of the pattern that is fundamentally, like you and I on that view and many other things are fundamentally patterns that live in this other space and we sometimes project through various interfaces, like physical bodies, robots, androids, whatever, machines, embryos. We sometimes project through these physical interfaces and consciousness is what it is like, the experience that it is like, to be one of those patterns projecting into space. That’s one way you might think about it.
Tim Ferriss: Could you explain that again as if I’m a smart sixth grader very interested in technical stuff? And I suppose what I’m trying to triangulate on is: are you getting into Donald Hoffman territory of reality as user interface? I’d love to hear you explain the other space or not coming from physical space, just maybe to put it a different way.
Michael Levin: Sure, sure. Okay, let’s run through it. So I think Don’s work is very interesting. For the purposes of what I’m about to say, we don’t need to worry about it. Let’s assume a perfectly conventional physics. I think Don’s onto something I think for sure, but let’s assume that we don’t need to worry about that. A perfectly conventional physics. One thing that scientists nowadays like is a view called physicalism. Physicalism says that, “Look, there’s only one realm that we need to worry about. It’s this physical realm. Physics tells us everything you need to know about this realm, and there it is.” A lot of people like that. But I actually think that view is a non-starter for the following reason: there are all kinds of important facts that are simply not facts about physics. They are not discovered by physicists. They will never be discovered by physicists. They are not changed by anything we do in physics. And those are certain facts of mathematics.
So for example, the exact value of E, the natural logarithm, the fact that complex numbers behave differently than quaternions that behave differently than octonions under certain — the truths of number theory, certain facts of topology and the distribution of prime numbers, you can’t just dissolve the math department and hope that, “Don’t worry, the physicists will figure out why this is. This is not what they will ever do.” The math department does things that are different and additive to what physics does.
And both in physics and biology, and I think in cognitive science too, there’s an interesting phenomenon, which is that if you’re like a five-year-old and you do that thing where you keep asking, “But why? But why?” If you keep asking “But why?” long enough, eventually you always end up in the math department. It’s the damnedest thing. Imagine.
Cicadas, they come out after every, whatever, 13 and 17 years or something they come out and you say, the biologist, you say, “Hey, why is that?” “Ah, because that way they don’t time their predators. Because if it was every 12 years, then every two year, three, or four years, sixth year a predator would get you, right? So 13 and 17.” “Okay, but that’s cool. Why are those numbers so special?” “Ah, they’re prime numbers.” “But why 13 and 17? Why isn’t there one in between?” “Now you’ve got to go to the math department because they’re the only ones that understand why that is.” So it’s like this with everything. With physics, you keep digging, but why do the fermions do this or that? “Oh, because this amplitude has this symmetry group or whatever.” So there’s something interesting going on where even from the basic, most basic math that you learn in high school up through these very complicated things, there are a bunch of facts that are simply not facts of physics. Now, okay, so this I think is just how it is.
Now from here, you have a choice to make. You could say, “Well, these are just random regularities that are true in our world. It’s just a random grab bag of interesting things.” Mathematicians don’t treat it that way. They think it’s an ordered structured space that they are exploring. They think they’re, especially Platonist mathematicians think they are discovering, they’re not inventing. You don’t have a choice. You start with set theory, eventually you find out the value of E. You didn’t have a choice about that. That’s what you found out. You discovered that.
So I think more optimistically that this is not a random grab bag of stuff. This is some kind of structured space of patterns, mathematical patterns.
Now you can take one other step and you say, “Interesting. How do we know that these patterns are only of relevance to math? Is it possible? Well, we know they’re of relevance to physics because they constrain how physics go. What about biology? Well, biology is interesting.” Imagine that there’s some planet and on this planet, the highest fitness belongs to a triangle of a very specific shape. So here comes evolution and it cranks a bunch of generations and it finds the first angle. Cool. And it cranks a bunch more generations, finds the second angle. Does it need to do it again to find the third angle? Why no? Because once you know two angles of the triangle, you know the third one. Why did evolution just get to save one third of the time that it would take to figure this out? Well, you get a free gift from mathematics.
And so I think that physics is what we call things that are constrained by these patterns. Biology are the things that are enabled or facilitated by these patterns. I think biology uses the hell out of these things and we’ll talk about what they are momentarily. But now you say, “Okay, so they’re relevant in physics, they’re relevant in biology, what kinds of patterns are there?” Well, there are passive things, like the value of E and some fractals and things like that. But could it be that there are other patterns in this space that look a lot like things that are not studied by mathematicians? Maybe they look a lot like things that are studied by behavioral scientists. Could they be patterns that have some capacity for memory or patterns that have capacity for problem solving? Could they be recognizable as kinds of minds?
And so maybe, and so this is the kind of crazy claim that I’m making, maybe the relationship between the mind and the body is exactly the same relationship as between the truths of mathematics and physics. So this is an old idea. Descartes, for example, in the West is associated with this that, okay, the mind is this non-material thing somewhere. And then of course immediately the princes of Bohemia and other people immediately nailed him on this idea, but how does the interaction happen? How do you have a non-physical pattern making the brain sort of dance like a puppet? Energy conservation laws, how could that possibly work? And I don’t think he said this, and I don’t know why he didn’t say this because he was a mathematician. He could have said, I think, “You already have this problem. Since the time of Pythagoras you have this problem that you have these immaterial truths of mathematics are constraining the physics of our universe. We already have this interaction.” This is not new. This has been around for forever. This is a kind of interaction where some of these truths that come from a different space of facts absolutely constrain and enable things that happen in the physical world.
So one thing you might think about is whether some of these patterns, and we have right now, if anybody’s interested, I give you a link to it, we’re having this thing I organized called the Symposium on the Platonic Space. And we’ve got about 26 people. I initially thought it was going to be three people, me and these two other groups, it turned out there’s like 26 people who gave awesome talks about this stuff talking about this notion, I think it’s going to be huge. And I think it has all kinds of very practical implications because what do you get? Well, maybe you get static patterns, but maybe you get dynamic patterns that are more like behavioral policies or even competencies, but maybe you also get compute.
And if you get compute, and we can talk about this because we’ve actually done some experiments on this, if you actually get compute this way, maybe the way we’ve been totally adding up the cost of computation isn’t right because we’ve been looking at the front end. And I actually think this is what’s happening here, is that the theories of computation that we have are mostly about the front end interface, and they’ve kind of been neglecting some stuff that happens on the backend. And we’ve just begun, we published a couple of things on it. There’s lots more coming. So I think that’s an exciting new area that may have all kinds of implications for cognition and behavioral science more generally.
Tim Ferriss: All right. So people will definitely be interested in the Symposium on the Platonic Space, so we’ll include links to that for sure.
Separately, lots of things I want to ask you offline that relate to this. But I will say just a confession briefly, which is one of my biggest regrets is that in 10th grade I and my brother had very different experiences with math. I was very good at math up to that point. My brother also, he had a great math teacher in 10th grade. I had a really, let’s call her abusive teacher in 10th grade. I at that point retired from mathematics. My brother went on to get a PhD in statistics and has done computer science and data science. And it’s to this day one of my biggest regrets that I stopped. It’s wild to have these inflection points. Same school, two different teachers.
Michael Levin: Wow. Amazing.
Tim Ferriss: Yeah. So, never too late, I guess, to go pick up a textbook. I wanted to ask you to expand on the compute piece that you alluded to at the end. Could you say more about that?
Michael Levin: Yeah. There are two pieces to this that people should know about. One is this idea called polycomputing. And this is something that Josh Bongard and I, and his student who’s now a postdoc in my group, Atoosa Parsa, has taken on. And it’s this idea that when there’s a physical event, something is physically happening. It might be current going through a logic gate in your computer, or it might be something else like that. The question of what is it actually computing is in the eye of the beholder. So, multiple observers could be looking at the same exact physical thing going on and seeing different things being computed, okay?
And I can go into details, but I’ll give you a very simple example of this. And this was a paper that my group put out about a year and a half ago. There are these things called sorting algorithms. And these are very simple sets of rules. They’re usually about six lines of code, something like that, that are designed to — they’re recipes that you follow. It’s an algorithm, so you follow the steps. And the idea is you’re handed a list of numbers, and these numbers are all jumbled up. They’re out of order randomly. And the algorithm is designed to sort them so that everything is sorted. You might think of the way — if somebody gives you a bunch of names and you need to do a phone book, you want to put them alphabetical like that, or numbers, that kind of thing. These sorting algorithms, they have a couple of features. One feature is that they’re short, they’re fully deterministic, meaning that there’s no randomness, there’s no question about what to do. You just follow step by step, that’s it. And people have been studying them for about 80 years.
Every computer science 101 student has had to deal with these sorting algorithms. Okay. So, what we showed, long story short, is that if you actually watch what they’re doing, yeah, they’re sorting numbers, but if you watch carefully, and apparently nobody has actually looked, and I think this goes back to the thing I said earlier. If you’re completely convinced that these things are dumb machines that only do what you ask them to do, why would you look, and at what else they’re doing while they’re sorting? And that’s exactly this kind of thing where the paradigm that you’re using or the formalism that you’re using constrains what experiments you do or what you can see, right? Like this matters.
So, if you’re not so sure, as I wasn’t, that these things are only doing what you asked them to do, what you find is two general classes of things. One is that the way they do them has extra behavioral competencies, things like delay gratification, things that a behavioral scientist would recognize, that you never coded in the algorithm. You know, because it’s not some big, hairy, like three billion parameter neural net or whatever, it’s six lines of code. You can see all the code. You know what is there. Unlike biology, there’s no new mechanisms to be discovered. There it is. It’s all there. That’s why I picked this for the shock value of exactly that, that no one could say that, “Well, there’s probably some mechanism that you just haven’t found yet.” So, that’s the first thing.
And the second thing is that while they are sorting the numbers, which of course they do, they are also doing some other stuff that again, you never asked them to do. And these other things, I’ve called them side quests. They’re like these little side quests. You can also call them intrinsic motivations, because like with any system, like with a kid in school, as you were saying, there’s things you force them to do. And then within that, within the space in between that, the time they have or whatever, you get to find out what they really want to do, right? If you don’t overdo it, if you give them a little bit of room, you find out that, but what is the intrinsic, what is their sort of inner nature or their — you get the idea, that kind of thing.
So, basically what we found is that there is a simple, minimal version of that even in the most dumbest, fully deterministic — this is nothing about determinism or randomness or indeterminism. This is the idea that our view of what an algorithm is and how much of what the thing is doing it captures is incomplete.
It captures very well the thing you asked it to do, but it does not provide a good view of, but what else does it want to do? And apparently, in a very minimal way, even extremely simple systems have this. Andrea Morris wrote a really good story for Forbes about all of this. It’s like, I think very generally understandable. And, on my blog, I have a couple of pieces about trying to explain this in a very simple way.
The bottom line is this. One observer likes the sorting, and you pay for the steps of the algorithm. Of course, every step you do, you pay for it, so you pay for the sorting. But all the other stuff it’s doing, that’s all free, because there are no extra steps. You didn’t have to do the other steps. It does it while it’s doing the other thing. So, if you had a different observer that’s interested in the other thing, they got it for free. And so now the question is, how much of that. These, I call them ing…—well, this is a word that exists—ingressions into the physical world of some of these patterns, like how many of them actually are there? And how much extra oomph do you get when you don’t know that you got it? And in some cases that might be great, because that might be facilitating things you want to do.
In other cases, you might have a machine that has this going on where you don’t want that happening. You’d rather that not be happening. And we have a very active research program right now trying to figure out basically better ways to detect it, better ways to facilitate it, and ways to suppress it, because there will be situations where you don’t want this thing doing other stuff.
And so, that’s the question, what are we getting? Are we getting free compute here? Are we getting something else? I’m not even sure we have the vocabulary for it yet, because that’s just not been the way people have thought about these things.
Tim Ferriss: So, to dig a bit deeper on that, as you develop the vocabulary, the better understanding of how to measure, understand, inhibit, or facilitate this type of off-gassing isn’t the right term, but sort of like —
Michael Levin: That’s cool.
Tim Ferriss: — secondary activities. Well, I’m thinking of this technology, I think it’s called [Remora], which is this device, the hardware device they throw on long haul trailers and so on to basically take the exhaust and convert it into something useful. It’s not the best metaphor for what you’re mentioning. But as that, as we flash forward five years or however long it is, I mean, compute is a very pressing problem, right? So there are tremendous incentives. If there were a pot of gold at the end of the rainbow, so to speak, with this, if it were even five percent possible that the Metas of the world and so on would need fewer fission, let alone fusion reactors to produce the power they need, then this is of great commercial interest, right?
Michael Levin: Correct.
Tim Ferriss: Intellectual, certainly. But what might, and I know I’m asking for some real speculative leaps here probably at this point, but what might that look like in the future for compute within, just for the time being, compute within the context of hyperscalers who are like, “Okay, we need 20X the capacity of the current power grid or whatever to do what we want to do.”
Michael Levin: A couple of things. So first, this is very late breaking stuff, so take everything I say here with a grain of salt, right? We’ll see how it shakes out. But I think you’re right. I think this is going to have massive implications. Oh, and first of all, the off-gassing actually thing is important, because one thing about that metaphor, the Lamprey metaphor, is that there is a main thing that it’s doing, and then there are these side effects. But what’s interesting about polycomputing is that you actually don’t know which is the main thing. So I look at this and I say, “It’s a sorting algorithm, and oh my God, it does this other thing we call clustering.” Aliens come down, they look at it and they go, “Well, that’s a cool clustering algorithm. Wait, it sorts too? Holy crap.”
So, it’s important that it’s not obvious at all, which is the main thing. Okay. So, let’s just say we have a set of things that it does. There’s two possibilities how it could come out. I think one possibility is that multiple of these are useful as they are. And people can sort of siphon off actionable information, valuable utility out of them how they are. We’re certainly investigating that, how to do that. That’s one possibility.
Another possibility is that there is the thing you forced it to do, but there’s also a bunch of other stuff, which is much more whatever it “wants to do.” And that stuff may not actually be what you ever wanted or needed. In other words, there is no guarantee, right? So, you have a student and you’re making them study math or whatever, something useful, accounting, like you got to get a job or whatever. And then while in my spare time I make, I don’t know, figurines or something. And there is no guarantee that this other thing is ever going to be commercially valuable.
It might be really important in understanding the true nature of what you have, but there’s no saying that whatever it actually wants we would find commercially valuable, right? I don’t think you can guarantee that. I think it’s going to be a combination of both of these things, but this latter thing has an implication for AI. And the implication is this, that when we are looking at a language model, for example, and people are debating, “Is it this, is it that? I asked it how it was feeling and it told me that it had an inner world and all of this.” Okay. But what we don’t know is whether the talking, right, the language use is at all related to what the actual intelligence is in this thing. Maybe, but I’ll just say that in our sorting algorithm the additional thing it’s doing is not sorting, it’s something else.
So, it’s entirely possible that in these AIs, the thing we have forced them to do, which is to talk, and the thing that we’re all obsessed about or the things it says could be a complete red herring as far as what kind of intelligence is actually there, what does it want? How do we communicate with it? The verbal interface that we’re all sort of so glued in on might not be the interesting part of that equation. And so, that’s my only thing is that some of this may very well be commercially viable, but some of it may have implications that are very different, that are not about the utility of the compute, but about teaching you about what do you really have when you have a system like that. And I think that’s where a lot of surprises are coming.
Tim Ferriss: Yeah. Folks can go back and watch Ex Machina, but I do want to ask you about sci-fi in a moment and your most recommended sort of sci-fi books or films, favorites. But before we get there, this is me just ruminating, and I’m going to apologize in advance for anthropomorphizing. But thinking about the school child example, studying math or accounting and making the figurines, I wonder if the “unproductive side activities” in some cases might prove to be really critical to the forced function in the sense that that student who’s studying math needs to let off some steam and do something different in order to have the endurance and periods of focus to actually do the mathematics. So, if you split the baby and get rid of the figurine, do you accidentally handicap the main function at the same time? I don’t know.
Michael Levin: That’s a great question. And that is exactly what we are studying right now. I have people working on this exact question. And specifically, what is the relationship among the different things that are happening here? Are they living in completely parallel universes such that they don’t really touch each other, or are they entangled in a way that when you mess with one you’re going to have implications somewhere else? We don’t know. That’s a great question. I don’t know the answer to that yet.
Tim Ferriss: I’m tempted to chew on that word “entangled” with you, but that’s probably another two-hour conversation. Sci-fi. I mean, sci-fi, as I believe you do, I just think it’s so powerful in so many ways. Do you have any books, movies, anything at all, essays that are just favorites of yours or that you recommend to students or friends?
Michael Levin: Let’s see. Okay. Well, I grew up on all classic sci-fi from the ’50s, ’60s, ’70s, that kind of stuff, so all the favorites. One particular author that I love is Lem, Stanisław Lem, L-E-M.
Tim Ferriss: Oh, I’ve never read Lem.
Michael Levin: Oh, he’s amazing. So, Solaris was his, but also he has a ton of very humorous short stories, like really funny stuff. So, I like him a lot. He’s a master of the absurd and kind of releasing the assumptions that we all have in ways that kind of illustrate how narrow thinking and things like that is just beautiful. I’ll give you two stories that I, short stories that I like. One is They’re Made Out of Meat by Terry Bisson.
Tim Ferriss: Yeah, that’s a great one. Very fast read for people.
Michael Levin: Yeah. Yeah. Very fast read. It’s like a page and it just reminds us all how silly some of our preconceptions are. There’s another one I like, which I’m going to butcher it, because I use this example, but I’m sure I’ve added on things that weren’t really there. I think that it’s The Fires Within by Clarke. And the version that I have in my head, which probably isn’t really close, is the following, but I think it’s valuable. Imagine there’s some creatures that live in the core of the earth and they come out to the surface, so they’re incredibly dense. They’re hot, they’re incredibly dense. They use gamma rays for vision, whatever. They come up to the surface, what do they see? Well, everything that we see here that’s solid is like a thin gas to them. This isn’t solid to them. They’re walking through. It’s like walking through a garden of smells that you like, you walk right through, disturb everything, you don’t even know what’s there.
And one of them is the scientist and he says, “You know, there’s like this thin plasma around the surface of our planet.” And they go, “Oh, yeah.” And he says, “Yeah, and it’s got little patterns in it. And I’ve been watching these patterns with my instruments, and these patterns, they almost look agential. They almost look like they’re doing things, right? They almost look like they have little lives. They move around.” And, “Well, how long do these patterns stick together?” “Well, about 100 years.” “Wow, that’s stupid.” And “Nothing interesting can happen like that.” And I have a story on my blog based around this. He says, “We are real beings. We are real agents where physical agents, patterns in the gas can’t be anything.
So, you get the idea. The point is that even the distinction between an agent and the patterns within their cognitive system, thoughts versus thinkers, as William James said, and what’s data and what’s the machine like, all of this to me is a continuum, a very observer dependent continuum, and you can get there with a science fiction story.
Tim Ferriss: What fun. You mentioned the blog a few times. You’ve got some great stuff on the blog. I’ve shared some of your writing in my newsletter before, specifically your advice to students, which has some fantastic advice in it. And for folks who are listening, even if you are not in the world of science and academia, there’s a lot in that piece that they can recommend it. But where would you suggest people start? If they’ve enjoyed this conversation, within the landscape of your blog, are there one to three articles you might suggest they start with?
Michael Levin: Yeah. I have a starter pack article and things like that. I can provide some links, for sure. Yeah.
Tim Ferriss: Great. Okay, we’ll put those in the show notes, folks, as per usual. We’re going to land the plane, because I know you’ve got another engagement coming up, but I’ll tell you what, I’m going to make it dealer’s choice, but in this case you’re the dealer. So, you can pick which question you want to tackle, and then we’ll wind up.
Michael Levin: Sure.
Tim Ferriss: But super curious what you picked up from the late Daniel Dennett. I have a bunch of his books, really fascinating guy. Option number two is, this is a quote from the New Yorker piece in 2021, but this is a congratulatory toast from Clifford Tabin, if I’m pronouncing that correctly. “You are the most likely to crash and burn and never be heard from again. You’re also the most likely to do something really fundamentally important, that no one else on earth would have done, that will really change the field.”
So, I’m curious about that first part, especially “most likely to crash and burn, never be heard from again” and why that hasn’t happened. And I suppose last, and you can answer more than one of these too, but if you could put a giant billboard out in front of, and this is metaphorically speaking, just to get a message in front of a lot of people. In front of departments of biology, or just even more broadly for lots of people to see and understand what that might be. So, I’ll leave it to you to pick how you want to choose.
Michael Levin: Wow. Yeah. That last one, it’s hard, because if there’s just one billboard, I don’t know. There’s a lot to choose from. I’ll say —
Tim Ferriss: You can have more than one if you want.
Michael Levin: Well, yeah. I mean, that’s basically the blog and the website and everything, but I’ll say just a couple of things about the first two, I guess. Dan was an amazing person. We agreed on a lot. We disagreed on a lot of stuff. I think he was always an incredibly generous thinker. One of the great things that he always insisted on was steel manning. And this is the idea that if you’re going to shoot down somebody’s viewpoint or disagree with it, you first need to articulate the absolute strongest version of it that you can.
Tim Ferriss: And for people who don’t have context, I suppose we should just establish who Dan Dennett was. Just how would you describe him in brief? Philosopher, cognitive scientists?
Michael Levin: Yeah.
Tim Ferriss: Understatement.
Michael Levin: Yeah. He passed away, I think, in the last year. And before that, I think he was widely written about as maybe one of the most important living philosophers today. I think I’ve seen that. And yeah, he was a professor at Tufts where I am, and he was just an incredible thinker and he wrote many interesting and popular books and so on. Yeah. So, it’s the opposite of straw man, this idea that there’s no point critiquing a bad argument. You should be critiquing the best possible version of an argument that you can. And so, I think that’s extremely valuable, is to take the view and understand it so thoroughly that you can give it a really strong defense. And then if you want, go back and shoot it down after that. But first you got to do the first part. So, I thought that was really, really, really important.
And I guess the second part, so Cliff Tabin is a great scientist. He’s a geneticist. He was my PhD mentor. I did my PhD with him at Harvard. And yeah, I mean, I don’t know. I’m getting old now, getting into retirement. At some point we got to call it which way it’s going to be. I don’t remember how long ago it was that he said it, but it could still happen. It could still crash and burn, I suppose. Why not?
Tim Ferriss: Did he say that just because of an intrinsic intensity that you have? What would lead him to say something like that?
Michael Levin: I don’t want to put words in his mouth, but what I hear him saying is that. I mean, I’m very strategic in what I say when, but I don’t really have a filter on what I think.
Tim Ferriss: No halfway measures.
Michael Levin: Yeah. I’m just not very constrained as far as what I’m willing to think and eventually say if I think there’s good reason to say it. And I think that’s what he was talking about. That’s a very dangerous thing, because let’s face it, in science most of what we say is wrong. And I’m clear on that with people all the time. I’ll say what I think now, and I’ll say it as strongly as I possibly can, but I’m under no illusions that we have the right answer to any of these extremely difficult questions. So, most of it is probably wrong in some important way. And I think he was just commenting on the fact that I say a lot of things that are counter paradigm and not in agreement with what the mainstream thinks. Occasionally that goes well, usually that goes very poorly, which is what I think he was pointing at.
Tim Ferriss: Mike, thank you so much for the time.
Michael Levin: Thank you so much.
Tim Ferriss: I’ve had so much fun in this conversation. I want to make sure we point people to the right places. I’ve got a few websites in front of me here, thoughtforms.life, that’s one. We’ve got Dr, D-R, michaellevin.org as well. Are there any other websites or profiles you’d like to point to? Are you active on X or any other platforms?
Michael Levin: I have, yeah, @drmichaellevin on X. Yeah. The thoughtforms.life is the blog. That’s my personal blog. So, I say things there that I wouldn’t put on the website, which is my official lab website. And you can sign up for updates on the book and all that kind of stuff. The drmichaellevin.org is the official lab website. So, that has all of our papers, all of the software, you can download the data. So, that’s like all the stuff to back up all these crazy things that I’m saying. All of that is on drmichaellevin.org. There are also lists of books that I recommend to my students and things like that.
There is a YouTube channel, which also has some conversations. I’ve b
een for the last, I don’t know, five or six years I’ve been hitting record on some meetings I’ve had with some amazing people. So, some really interesting collaborators, and all of that is there for you to sort of be a fly on the wall. So, that’s fun too.
Tim Ferriss: And the YouTube channel is linked to from thoughtforms.life?
Michael Levin: Probably. I’ll send you the link. I don’t even know if I remember what exactly the URL is, so I’ll send you the link.
Tim Ferriss: Mike, thank you so much. I hope this is not our last conversation.
Michael Levin: Absolutely.
Tim Ferriss: And for people listening or watching, we will link to lots of things, everything that we can possibly link to from this conversation and more at tim.blog/podcast as per usual, just search Michael Levin or probably Levin. I think you might be the only Levin, L-E-V-I-N, and it will pop right up. So, you’ll have plenty of resources to do more digging and more thinking, more assumption testing, assumption bending in a lot of ways. And until next time, as always, be a bit kinder than is necessary to others, but also to yourself. Thanks for tuning in.
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The post The Tim Ferriss Show Transcripts: Dr. Michael Levin — Reprogramming Bioelectricity, Updating “Software” for Anti-Aging, Treating Cancer Without Drugs, Cognition of Cells, and Much More (#849) appeared first on The Blog of Author Tim Ferriss.
2026-01-21 23:08:16
Dr. Michael Levin (@drmichaellevin) is the Vannevar Bush Distinguished Professor of Biology at Tufts University and director of the Allen Discovery Center. His background is in computer science and biology, and his group works at the intersection of developmental biophysics, computer science, and cognitive science. He is primarily interested in how intelligence self-organizes in a diverse range of natural, engineered, and hybrid embodiments. Levin has been developing a framework for recognizing and communicating with unconventional cognitive systems.
Applied to the collective intelligence of cell groups undergoing morphogenesis, these ideas have allowed the Levin Lab to develop new applications in birth defects, organ regeneration, and cancer suppression. His lab also produces synthetic life-forms (e.g., Xenobots and Anthrobots) that serve as exploration platforms for understanding the source of patterns of form and behavior in a wide range of natural, artificial, and hybrid embodied minds.
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Personal Blog | Lab Website | Thoughtforms Life Podcast | YouTube | Twitter
So what I tried to show in that talk are some examples by which the living tissues—for example, flatworms that are cut into pieces and every piece has to figure out: ‘How many heads should I have?’ ‘Where do the heads go?’ ‘What should the shape of my face be?’ these kinds of things, that, in fact, they do know… And the way they know is because they store memories. And, maybe not shockingly, although it’s certainly shocking to a lot of folks, the way those memories are stored is in an electrical network that is very similar to the way that we store our goal-directed behavioral repertoires in our brain and that these things are widely spread. And so regeneration, cancer suppression, and cancer repair and remodeling, birth defects and birth-defect repair, all of these things are extensively using electrical pattern memories, and we now have a way to rewrite those pattern memories.” — Dr. Michael Levin
“I always say to people, ‘On your laptop, if you want to go from Photoshop to Microsoft Word, you don’t get out your soldering iron and start rewiring. It’d be laughable if you had to, but that’s how we used to do it. In the ’40s and ’50s, you programmed a computer by pulling and plugging wires, but you don’t do that anymore because it’s reprogrammable. And that’s what the biology is.'” — Dr. Michael Levin
“The name of the game here is communicating with the cells. This is not about stem cells or gene therapy or scaffolds made of nanomaterials. Those are all tools that might be useful, but the real trick here is to communicate to a group of cells, what do you want them to build? And that’s what the bioelectric code is all about; it’s about communicating to the collective, to the cellular collective.” — Dr. Michael Levin
“We can detect incipient tumor formation and we can prevent and normalize tumors after they form … not by killing the cells with chemotherapy but by electrically reconnecting them to the group such that they can form, again, a memory of what they’re supposed to be doing.” — Dr. Michael Levin
“Just imagine this standard Judeo-Christian version of Heaven. Let’s say you, your pet snake, and your dog get to Heaven. Everything is great, there’s no more damage, there’s no decay, nothing is damaged, everything is great, everything’s fantastic. For the next trillion years, what happens? The snake may be fine doing snake things for every day, is the same as every other day, may be fine. The dog? Not sure. Probably okay chasing rabbits on the farm, you know, may be fine for forever, basically. The human, though, what do you think? What are the odds that a human cognitive system can be sane for an infinite… Okay, I’ll keep myself busy for the first 10,000 years, maybe 100,000 years, but a billion years in, are we still sane? What happens?” — Dr. Michael Levin
“If you make a circle of cognitive things and living things, I think cognition is wider than life. I think cognition predates life, and I think it’s bigger than life.” — Dr. Michael Levin
“It’s entirely possible that, in these AIs, the thing we have forced them to do, which is to talk, and the thing that we’re all obsessed about, or the things it says, could be a complete red herring as far as what kind of intelligence is actually there. What does it want? How do we communicate with it? The verbal interface that we’re all sort of so glued in on might not be the interesting part of that equation.” — Dr. Michael Levin
“This field of diverse intelligence combines artificial intelligence and engineering and cybernetics and evolutionary biology and AI and exobiology and the search for alien life. All of these things are, together, asking, ‘What are actually the common threads of being an agent, no matter what your origin story—whether you were designed or evolved or engineered or whether you were made of squishy proteins or whether you were made of silicon or something else.‘” — Dr. Michael Levin
“If you’re like a five-year-old and you do that thing where you keep asking ‘But why? But why?’—if you keep asking ‘But why?’ long enough, eventually, you always end up in the math department.”— Dr. Michael Levin
Want to hear another episode with a pioneer of bioelectric medicine? Listen to my conversation with neurosurgeon and researcher Dr. Kevin Tracey, in which we discussed stimulating the vagus nerve to tame inflammation, treating rheumatoid arthritis and autoimmune disorders without drugs, the FDA-approved SetPoint Medical device, credible vs. bogus vagus nerve stimulation approaches, the inflammatory reflex, auricular therapy, heart rate variability, the connection between depression and inflammation, and much more.
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The post Dr. Michael Levin — Reprogramming Bioelectricity, Updating “Software” for Anti-Aging, Treating Cancer Without Drugs, Cognition of Cells, and Much More (#849) appeared first on The Blog of Author Tim Ferriss.
