Chris Masterjohn, PhD

TOMORROW! If you live in Kentucky, vote for this guy. If you know someone in Kentucky, tell them to go vote. If you don’t, donate to his campaign. Massie is the only good person in the House. Contrary to the view that he’s an obstructionist who gets nothing done, he successfully campaigned against the BBB getting a 10-year override on the ability of states to regulate AI, which directly protects your ability to locally keep them out of your own back yard or prevent them from starving you of electricity. His PRIME Act helped keep small innovative farms alive by taking away USDA from being too high a barrier to entry and keeping health inspections local for people who sell locally. Massie was instrumental in getting the Epstein files released. The Epstein billionaires are trying to flush out their last principled critic. Don’t let them. Photo of me and him is from October 26, 2024 at the Weston A Price Conference where he was giving the keynote address.

NEW Study: Fetuses with prenatal SSRI exposure have brain & placental alterations seen on in utero MRI (PMID: 42106476). No one will EVER make sense of this until they realize that  1) THE role of serotonin is to adjust ALL mitochondria to situations of absolute or relative hypoxia both inside the body and throughout every tissue of the body. 2) SSRIs block half of this because it requires both extracellular and mitochondrial serotonin receptors and serotonin entry into the mitochondria and SSRIs prevent serotonin from entering the cell and then into the mitochondria. 3) The placenta has the HIGHEST expression of the serotonin transporter. 4) In pregnant women THE GREATEST effect of SSRIs is to deprive the fetus of placentral serotonin transport. 5) This is because until the baby is born it is in a CONSTANT STATE OF HYPOXIA not because of absolute deprivation of oxygen but because its source of oxygen is not its lungs and therefore its oxygen delivery has to be completely rewired until this is suddenly reversed the second it is born. and  6) SSRIs are therefore drugs that induce mitochondrial dysfunction in babies.

I think more specific data will provide insights that they can use to convert the vicicous mitochondrial cycles to virtuous mitochondrial cycles and I hope and pray for Jordan’s robust and lasting recovery.

What's Wrong With Jordan Peterson's Health? Jordan Peterson’s health has been suffering tremendously. Mikhaila, his daughter, saw that what was ailing him was affecting so many systems of his body that it had to all be connected and began to wonder if it was a form of mitochondrial dysfunction. In trying to research whether mitochondrial dysfunction could be driven by the turning points in his health problems like SSRI withdrawal, benzodiazepine withdrawal, and toxic mold, she found my work and reached out to me. This is the conversation that we had: https://www.youtube.com/watch?v=MFhBq2Qlbto My hypothesis is as follows. Mikhaila shares half of Jordan’s genes and has been more detailed about her own health journey going back to childhood, so we start with her. She had juvenile arthritis symptoms starting at 2 and a diagnosis at 7. She went on Enbrel, a “biologic” (a pseudoscientific regulatory term) that opposes the action of the inflammatory mediator tumor necrosis alpha (TNF-alpha); and on methotrexate, which inhibits folate and adenosine metabolism. Methotrexate raises adenosine, which inhibits T cell proliferation. Its inhibition of folate metabolism is thought to be more relevant to cancer but its adenosine-mediated inhibition of T cell proliferation is thought to be more relevant to autoimmune arthritis. The next year, at age 8, she was diagnosed with depression and put on SSRIs. My hypothesis is that she has an underlying block in mitochondrial metabolism leading to CoA sequestration, which occurs when CoA-requiring pathways fail to complete properly. This leads to secretion of TNF-alpha as part of a cellular stress response. TNF-alpha serves to increase carnitine transport into the cell. The carnitine then trades places with CoA, detoxifying the metabolic intermediates and carrying them out into the urine, allowing CoA metabolism to continue. Blocking the TNF-alpha is a double-edged sword. On the one hand, the elevated TNF-alpha will interact with genetic predispositions to certain types of immune dysfunction and with suboptimal joint mechanics to produce an autoimmune disease. Blocking the TNF offers relief from the autoimmunity, but then in doing so makes the cells that were releasing it as a stress signal unable to mitigate their CoA sequestration. This may lead to a plethora of side effects, and for Mikhaila this was depression. I do not discount that inhibition of folate metabolism by methotrexate could have messed with her methylation system, but Mikhaila remains very intolerant of methylfolate and thrives on a low-folate all-meat diet, and I do not think any of her health problems are explained merely by a methylation deficit. Her first major advance was going on an elimination diet that eventually morphed into the red meat carnivore “Lion Diet.” T cells are fueled by glucose and glutamine during active inflammation, and when they transition to resolving inflammation a major drop in glucose and glutamine is a central hallmark of the metabolic shift. The zero-carb nature of the Lion Diet helps resolve T cell inflammation and displaces the need for methotrexate. The large amount of red meat provides carnitine, which addresses CoA sequestration from the point of carnitine supply, relieving the need of cells to secrete TNF-alpha to signal carnitine demand. The carnitine in the red meat thereby helps relieve the need for the Enbrel. Since her elimination diet gave her the first relief of depression she had experienced, it led her to go off the SSRIs. Going off SSRIs produced 2.5 years of new-onset neurological dysfunction, which I contend was new-onset mitochondrial dysfunction. This may have interacted or blended with the mitochondrial dysfunction that initially led to the arthritis, or it may have just been a completely new acquired mitochondrial disorder thrown on top of the existing problems.

Throughout this story, various exposures to toxic mold occurred that made her problems worse, including one in 2022 that gave her a whole new list of problems that only moving away from the mold was able to solve. Mold toxins are mitochondrial toxins, so exposure to them would cause a third layer of mitochondrial dysfunction. Jordan had been on SSRIs for over twelve years, but when he saw Mikhaila cure her depression with the early precursor to the Lion Diet, he followed her approach. Having gotten rid of his own depression, he too went off SSRIs around the same time as she did. This led to akathisia, a catastrophically debilitating movement disorder. I contend that this is SSRI withdrawal-induced new-onset mitochondrial dysfunction. He then had a terrible reaction to apple cider that had sodium metabisulfite as a preservative. This led him to be unable to sleep for two or three weeks. He became green and hunched over, and couldn’t walk. For this he was placed on clonazepam, a benzodiazepine. Sulfite has to be converted to sulfate, which requires the mineral molybdenum and the transfer of electrons from the sulfite to the mitochondrial respiratory chain. Mitochondrial dysfunction will prevent sulfite clearance. Zero-carb diets will increase endogenous sulfur production and diets that lack liver and legumes are low in molybdenum. The mitochondrial dysfunction induced by the SSRI withdrawal would inhibit sulfur clearance and the diet that helped Jordan and Mikhaila cure their depression would keep the sulfur-detoxification system maximally occupied. If sulfite is not quickly metabolized to sulfate, it converts to S-sulfocysteine, which is a neurotransmitter that activates glutamate receptors. Sulfite itself is mitochondrially toxic, so if it crosses a critical threshold it can elicit a storm of excess sulfur catabolism and impaired sulfur clearance that keeps S-sulfocysteine levels high. That vicious cycle could explain why the sleep loss lasted 2-3 weeks. Clonazepam directly opposes S-sulfocysteine in that it binds to GABA receptors making GABA more powerfully activate them, which counteracts the S-sulfocyteine’s activation of glutamate receptors. Peterson stayed on clonazepam for three years and then tried going off of it, but this caused an even worse case of akathisia than he experienced from SSRI withdrawal. It lasted three years, and it made him suicidal. Clonazepam can alter calcium signaling in mitochondria in opposite ways depending on the preexisting state of the mitochondrial function. Possible effects of withdrawal include a catastrophic energetic supply/demand imbalance and precipitation of calcium causing damaging deposits that jam up the mitochondrial infrastructure. It is very possible that the clonazepam was causing progressive mitochondrial dysfunction the entire time he was on it and that it only became apparent once the GABA breaks on energy demand were removed by withdrawal. He briefly restarted an SSRI during this time but it didn’t help and it made him so fatigued he needed four extra hours of sleep per day. Ultimately, the final version of the all-meat Lion Diet helped Jordan recover from akathisia. More recently, however, his parents died and he had been cleaning out their moldy basement preparing for a big move, and this led to an attack of pneumonia and sepsis and a return of his akathisia. The mitochondrial toxins in the mold thus became his third acquired mitochondrial disorder, the first two from withdrawal from SSRIs and benzodiazepines. Jordan and Mikhaila share a lot in their health history but her mom has none of these problems and has never been on SSRIs. Thus, it is very likely there are genetic predispositions to these problems that Jordan and Mikhaila share. The Lion Diet is overall extremely helpful but could probably benefit from specific strategies around managing sulfur metabolism. I will do what I can to help them, starting with looking at their mitochondrial function.

The Five Laws of Mitochondrial Health Living in accordance with these laws keeps us on the path to vibrant health. We defined health. We’ve put our sights on the North Star. We know how to know when we’re healthy. But what do we do to get there? If we have arrived at the promised land, how do we stay there? How do we explore it more deeply to discover the riches of its treasures? What Everyone Should Be Doing For Their Health is a collection of “the basics” that everyone should check in on from time to time to make sure they aren’t missing any of the foundational health strategies. But what if you’re missing many of the basics? Where should you start? How should you narrow in your focus? Or what if you’re hitting them all and you need a more advanced health strategy? How do you guide your search? The Five Laws of Mitochondrial Health The Five Laws of Mitochondrial Health are the compass you need to keep you following your North Star. They are the lenses with which you should view the basics. They are the guardrails that keep you on solid footing as you search for your next advanced strategy. These are the Five Laws of Mitochondrial Health: The First Law: Always start with your mitochondria. The Second Law: Put food first and pharma last. The Third Law: Never put tech before nature. The Fourth Law: Remember your needs are your own. The Fifth Law: Observe your needs as they change with time. Applying these five laws will require specific mitochondrial strategies and a plethora of mitochondrial tactics. Our purpose in this article, however, is to understand the laws so that when we seek to apply them using strategies and tactics we do so from a position of wisdom and understanding. This is educational in nature and not medical or dietetic advice. See terms for additional and more complete disclaimers. This is a fundamentally philosophical article, so it focuses on articulating the philosophy rather than on substantiating claims with evidence from scientific literature. The 1st Law: Always Start With Your Mitochondria Mitochondria extract usable energy from the food you eat so you can use it to fuel the production, maintenance, repair, and distribution of everything in your body. The amount of cellular energy your mitochondria produce drives the dial of health and disease. As you produce more energy, the dial drives to the right and points to health. As you produce less energy, it falls back to the left and points toward disease. Within each range, the amount of cellular energy drives how ill we are or how healthy we are. There are thousands of genetic variants and uncountable experiences and exposures that can drive what disease or health looks like for each one of us. For one person, disease is diabetes. For another, it’s heart disease. For another, it’s cancer. For yet another, it’s a neurological disease. And for yet another, it’s chronic fatigue. For one person, peak health is athletic achievements. For another, it’s business. For yet another, it’s leadership and the formation of harmony within a community. And for yet another, it’s contemplation of eternal truths and their articulation in art or writing or speech. But whether we experience health or disease and how much of each we experience comes down to how much usable energy we can extract from food and to what extent we can use the top layer of abundant energy to fuel the commitment of the bulk of the energy toward our health and highest purpose. Living in accordance with the first law can be achieved at many levels: one level applies to how we manage our own health; another applies to how a physician may manage the health of others; yet another applies to the scientists who study how the many things we could be exposed to impact our health. For example, using or prescribing mitochondrially toxic antibiotics for acne before giving the skin enough vitamin B5 to allow its mitochondria to clear away the fatty acids that are fueling the growth of those bacteria violates the first law. Consider high cholesterol.

Training the liver’s mitochondria to produce abundant energy through fasting and intense exercise will improve the ability of the liver to fuel the energy-intensive clearance of cholesterol from the blood. To do this before resorting to strategies focused exclusively on micromanaging the production of the cholesterol transporters with fiber, ezetimibe, seed oils, and statins is to live in accordance with the first law. A scientist trying to solve the protracted withdrawal syndromes of benzodiazepines and SSRIs by focusing exclusively on neurotransmitters does not walk in the way of the first law. To walk in its way, the scientist must consider how these drugs distribute through the entire body, entering cells in every tissue and altering their mitochondria. Read the full article here: https://chrismasterjohnphd.substack.com/p/the-five-laws-of-mitochondrial-health

For example, suppose you are lifting weights. Your numbers keep going down. It is certainly possible that you have a new health problem and that’s to blame, but the rational thing to do in response is to vary your total effort expended in weight lifting by varying your volume, frequency, intensity, duration, or exercise selection. If increasing total effort leads to better results, you weren’t getting enough stimulus. If decreasing total effort leads to better results, you were doing too much. Suppose you determine you were in fact doing too much, but you believe in your heart of hearts that you should be able to do more. You might be right, in which case you should make being able to do more a goal of your health and enter an optimization cycle to achieve that goal. But you should hone your expectation management skill by discussing this with experts and peers and by doing a little research to see if you are framing the issue the right way. For example, you might start out thinking you should be able to do more volume in the gym, but through dialogue you might arrive at the conclusion that you really want to be stronger, or faster, or be able to hike with your friends and not get tired, and that doing more volume is not the best way to achieve your true goal. Having clarity about your problems, challenges, and goals can help improve your interpretation of your North Star. Vet Everything Against Your North Star All your other markers should be vetted against the North Star. Sleeping more? That is often excellent. The way you know it is excellent is you start feeling more energetic during the day, more clear-headed, and less anxious. If you start feeling progressively more tired during the day as you sleep more, however, you’re probably sleeping more because you need more sleep, and the underlying reason could be a drop in your health. Did a strategy increase your energy? Great — but did it lower your anxiety? If the energy-to-anxiety ratio didn’t improve, the North Star isn’t necessarily looking better. Did a strategy lower your ApoB? Great — but what happened to the North Star? Perhaps you notice nothing and you improved a proxy marker covering one aspect of your longevity. But if it hurts more to move, something is going wrong that takes precedence. If your North Star is shining brighter in every respect, you may be genuinely on to something fantastic. Never Forget the North Star Carry on in your journey as far as you yearn to go. But never forget to look up at the sky to let the North Star guide you.

I define “health” like this: The Definition of Health Health, noun, The ability to meet the demands of your life with abundant energy, to rest and recover fully, and to be as adaptable as needed to how demands may change over time outside your control, or to how you may choose to willfully change the purpose of your life. But how do you know you are healthy? What are more specific things you look out for to verify you are on the right track? Many of us can get lost in tactical details and proxy markers, looking at our weight, waist circumference, sleep metrics, HRV, testosterone, estrogen, ApoB, VO2max, microbiome testing, and so on. While proxy markers are necessary in some respects and tactical details matter greatly when we are in the weeds of optimizing something, we need a North Star to govern the constellation of markers we are tracking, or to check in on when we aren’t tracking anything. This is your North Star: You are meeting the demands of your physical and cognitive pursuits with abundant energy and clarity, high libido, low anxiety, and pain-free ease of movement. We can derive some guiding rules from this. You Should Rarely get Sick For example, you should rarely get sick. You can regard each sickness as docking a chunk off your energy score: You were likely missing energy and resources to defend against the illness. Your body may have purposefully become inflamed to calm you down because it didn’t have the energy to do what you were trying to make it do. Regardless of why you got sick, recovering from the illness will take a considerable chunk out of your energy budget. The downtime associated with the illness has to be counted against your healthfulness through taking points out of the energy score. The Energy-to-Anxiety Ratio Another rule you can derive from this is that you want a high energy-to-anxiety ratio. A state that is abundant in energy is one in which the top layer of that energy is used to direct the bulk of the energy into the right places and toward the right uses. As you start to lose energy, often the first thing you may notice is that what energy is left goes into the wrong places because you lost the energy that you needed to control the rest. If your energy is spent on worrying about things you cannot control, this is a lower energy state than if it is spent on taking charge of the things you can control. It may feel like the same amount of energy is buzzing through your body in each case, but that is because the additional energy it takes to direct the flow of the bulk of your energy doesn’t feel like a buzz. It silently flows through you, increasing the gracefulness of the bulk energy. You may not feel more energy. You may instead feel that your energy burns more cleanly, flows more calmly, and is more available to your purpose. Libido and Life Force Energy You can take a broad view of “libido” to think of it as life force energy. If you are purposefully directing your life into pursuits that do not involve sex, I am not arguing that you have to be tortured with sexual desire to be healthy. But you should feel that this underlying life force is abundant and under your purposeful direction. Pain-Free Ease of Movement You should feel comfortable in your own body, and appear to others that you are comfortable in your own body. It shouldn’t hurt to sit still or to move, and your movement should reflect your intention. Expectation Management Properly interpreting the North Star requires some skill in expectation management. If you feel overwhelmed and totally unable to meet your goals, is it possible that you are just trying to do too much? There is always an easy way to find out if you are doing too much: do a little less and see if everything gets better.

Through this very same mechanism, however, it has the strongest ability to silently poison the ability to switch it on in people who already have a major deficit in mitochondrial function. Diazepam (Valium) has the strongest ability to support the transport of cholesterol into mitochondria for the production of conventional steroids in the adrenal and reproductive glands and the production of inflammation-cooling and energetically calming neurosteroids in the brain. Through this very same mechanism, however, it also has the strongest ability to hurt the mitochondrial conversion of blue light to red light during energetic crisis and to hurt the ability of mitochondria to defend themselves against oxidative stress. In This Article: Benzos Are Whole-Body Drugs Benzo Use and Withdrawal: Not A Clean GABA Picture Benzos Are Mitochondrial Drugs Messing With the Mitochondria’s Gas Pedal Benzodiazepine Withdrawal as an Energetic Supply/Demand Imbalance Benzodiazepine Withdrawal as Dramatic Energetic Failure Red Light, Blue Light, and Oxidative Stress What Concentrations Are Needed For These Effects? The Deadly Physiological Trap Read it all here: https://chrismasterjohnphd.substack.com/p/benzodiazepine-withdrawal-is-mitochondrial

Benzodiazepine Withdrawal Is Mitochondrial Dysfunction Part 1 out of 2: How We Know Benzodiazepines (“benzos”) are drugs used to treat anxiety, insomnia, seizures, spasms, alcohol withdrawal, and related forms of overstimulation. Widely believed to regulate the ability of the brain to relax by increasing the power of the neurotransmitter GABA, they are actually whole-body drugs with specific mitochondrial targets. Using them and quitting them both have the potential to cause mitochondrial dysfunction. About four percent of populations in the modern West use benzos, and as many as ten percent of the US population uses them. They include drugs like alprazolam (Xanax), diazepam (Valium), lorazepam (Ativan), clonazepam (Klonopin), temazepam (Restoril), midazolam (Versed), and oxazepam (Serax). They also include Rohypnol (flunitrazepam), known as “roofies” or “the date-rape drug,” which is illegal in the United States and several other countries. There are also a number of benzodiazepine “designer drugs” that are broadly illegal or controlled substances in most modernized countries, including clonazolam and flubromazolam, which can be found in preparations with names like “Xanax bars” or “liquid Xanax.” Benzos are thought to act primarily by increasing the potency of GABA, the primary inhibitory neurotransmitter. GABA calms and relaxes us, though it plays other roles such as suppressing our attention to distractions, which helps us focus. GABA is the primary counterbalance to glutamate, which excites our nervous system. People who use benzodiazepines are 60% more likely to die over a given period of time than those who don’t use them, but people who quit them are 60% more likely to die than those who stay on them. Correlation is not necessarily causation and these data do not necessarily show that using and withdrawing from these drugs causes the excess mortality, but they raise the possibility that using them is a deadly physiological trap. As we will soon see, their use and withdrawal can both cause mitochondrial dysfunction, and since maintaining healthy mitochondrial function is the single most important driver of all health and disease, the possibility that they do create a deadly physiological trap must at least be considered. This is educational in nature and not medical or dietetic advice. See terms for additional and more complete disclaimers. Withdrawal from benzos often causes rebounds of the conditions the drugs were originally treating that are worse in magnitude than they had been prior to treatment. It can also cause new-onset symptoms that are unrelated to the original reason for treatment. These can include digestive problems and food intolerances; trembling in the limbs, skin, or whole body; difficulty driving or walking; problems with balance, muscle spasms, heart palpitations, and blood pressure; difficulty swallowing; new-onset seizures; hallucinations; and akathisia, a neuromuscular disorder that can produce an inner unbearable restlessness and uncontrollable non-productive movements that persist without any relief. While the available data seem to imply that most people get over these symptoms in a matter of weeks, some people experience a “protracted withdrawal” syndrome that can last for at least as long as one to five years. For example, in a survey of just over 1200 people who were active on internet sites about drug withdrawal, many reported symptoms lasting over a full year: over 50% reported these including digestive problems and muscle weakness; almost 50% reported trembling in their limbs or skin, head pain, and difficulty driving or walking; over 40% reported problems with their balance, muscle spasms, heart palpitations, or blood pressure problems; 38% reported difficulty swallowing; 36% reported akathisia; 26% reported uncontrollable whole-body trembling; 22% reported seizures; and 20% reported hallucinations.

This builds on previous reports of isolated cases of tinnitus lasting 6 months to two years and one case of it lasting over five years, and on cases of numbness and burning lasting two to four years. Most studies do not adequately follow people up in the long-term and and we have no reliable data on how common protracted withdrawal is. The possibility that going on these drugs raises the risk of mortality by 60% and quitting them raises it another 60%, however, hints at the possibility that some degree of long-term physiological damage could be relatively common. These data make much more sense when we realize that benzos are mitochondrial drugs and benzodiazepine withdrawal is a form of mitochondrial dysfunction. It is never the case that what we think a drug does is exactly what it does, nor is it ever the case that our present understanding of a drug encapsulates everything it does, and it is quite often the case that whatever we think a drug does is not even its primary mechanism of action. Psychiatric drugs, though, are unique in the degree to which they are claimed to do one thing but have powerful effects no one talks about. The reason is that psychiatry systematically claims that its drugs target the brain, yet it is totally implausible that a drug taken orally primarily goes to the brain. Human autopsy studies show that benzos have the second lowest accumulation in the brain out of any tissue measured. As a proportion of tissue mass, their highest uptake is in the adrenal gland. As a proportion of total benzodiazepine, their greatest accumulation is in muscle and fat. GABA receptors themselves are strongly enriched in the nervous system, but they are found ubiquitously throughout the body on the surfaces of many different types of non-neuronal cells where they carry out signaling activity just like in neurons. Many but not all of these are sensitive to benzodiazepines. It was in the two papers outlining the very first discovery in 1977 of the ability of these drugs to impact GABA signaling in which a second receptor was discovered embedded in the mitochondrial membrane. At that time, it was wrongly thought to not be present in the brain and was named “peripheral” for its abundance outside the brain. Thus, the very birth of our mechanistic understanding of benzodiazepines brought forth twins: a brain-dominant GABA receptor-binding site; and a mitochondrial membrane receptor dominantly distributed outside of the brain. Somewhere in the translation of pharmacological science into the practice of psychiatric medicine, there were people who consciously buried the knowledge that benzos are whole-body mitochondrial drugs. Presumably they did this because they considered it unrelated to the reason psychiatrists would use them to treat people’s anxiety and insomnia. Or perhaps they buried it because it was an obstacle for promoting the use of benzos for these conditions. We now know that benzos have two independent mitochondrial targets. The GABA receptor target lies on the surfaces of cells and is accessible to the extracellular fluid. But benzos are relatively fat-soluble and their transport into the brain is proportional to how fat-soluble they are. Once there, they primarily accumulate in cellular and intracellular membranes. While the drugs obviously distribute into synapses to carry out their GABA-enhancing activity, their accumulation in membranes puts them in much closer vicinity to their mitochondrial targets than to their GABA receptor targets. Their impacts on GABA absolutely impact mitochondrial function through GABA signaling itself. Withdrawal from this effect would be expected to create a severe crisis of imbalance between the supply and demand for cellular energy. Each of them, however, has different abilities to act on the two mitochondrial targets. Clonazepam (Klonopin) has the strongest ability out of any to assist in “switching on” mitochondrial energy production in people who need a moderate boost.

The Definition of Health Health, noun, The ability to meet the demands of your life with abundant energy, to rest and recover fully, and to be as adaptable as needed to how demands may change over time outside your control, or to how you may choose to willfully change the purpose of your life. This is my definition of health. What is yours?

The Incredible, Edible Easter Egg https://chrismasterjohnphd.substack.com/p/the-incredible-edible-easter-egg

The Oura ring designers made a huge mistake by introducing little green lights into the gen 3 and 4 rings. The most fundamental, non-negotiable rule of design is NO LITTLE GREEN LIGHTS IN THE BEDROOM. While the lights introduce features such as blood oxygen sensing and activity-induced heart rate tracking, you can toggle these off in the apps and the little green lights reduce their activity but do NOT turn off. Putting the ring in airplane mode does NOT stop the little green lights. The little green lights can light up a blacked-out bedroom like a flashlight! Green and blue light are anti-sleep. The purpose of tracking your sleep is to gain insights that will improve it. If your tracking involves lighting your room up with anti-sleep blue or green light you are shooting yourself in the foot from the start. I thought I lost my gen 2 ring and opened up a backup gen 3 ring I had bought two years ago but never used and quickly saw how intolerable these little green lights are. Thankfully I found my gen 2 ring the next morning. Oura MUST introduce the ability to COMPLETELY DISABLE the little green lights within the app. You should be able to toggle on automatic disabling that lasts for 11 hours starting 2 hours before your scheduled bedtime, and you should be able to manually toggle on and off the little green lights at will. Until that happens, DO NOT buy a gen 4 oura ring. Get a used gen 1 or gen 2 ring. Ebay is a good place to look for a used ring your size.

Are the Seed Oil Trials Confounded by Trans Fats? Part 1: The LA Veterans Administration Hospital Study The randomized controlled trials of seed oils done in the mid-20th century in net showed that seed oils are not good at preventing heart disease and probably raise the risk of cancer. The idea behind these trials was that the polyunsaturated fatty acids (PUFAs) in seed oils will lower cholesterol levels in the blood and thereby prevent heart disease. Detractors from this idea focus on PUFAs making our tissues highly vulnerable to oxidative damage — very similar to the rust that accumulates on metal objects kept outdoors over time — and maintain that these fats could worsen the risk of heart disease by making the lipoproteins that carry cholesterol in the blood, such as LDL, more vulnerable to oxidative damage. The failure of the seed oil trials to show a convincing reduction in heart disease and their worrisome finding that they may increase the risk of cancer suggests that this vulnerability to tissue damage is the mechanism that wins out in the long run. One of the criticisms of these trials is that they are confounded by the use of trans fats in the seed oil groups. While there are some trans fatty acids that occur in nature, such as in beef or dairy fat, there are specific trans fatty acids that occur in massive amounts in partially hydrogenated vegetable oils that do not occur in nature. Hydrogenation itself is done to make liquid oils harder. When carried to completion, it turns all of the monounsaturated and polyunsaturated fatty acids to saturated fatty acids. However, the path from a polyunsaturated fatty acid to a saturated fatty acid involves a monounsaturated fatty acid as an intermediate. The definitional chemical characteristic of a saturated fatty acid is that it contains only single bonds and no double bonds, whereas monounsaturated fatty acids contain one double bond and polyunsaturated fatty acids contain more than one. The path from a natural double bond found in an unsaturated fatty acid to the single bond of a saturated fatty acid involves the formation of an unnatural trans double bond. Thus, partial hydrogenation causes a loss of PUFA, but an increase in both monounsaturated and saturated fats, and the unique production of unnatural trans fats that are not found in any other foods. Partially hydrogenated oils have been effectively banned in the United States and various other countries, but were widespread during the time of the classic seed oil trials. Were these trials truly confounded by these unnatural trans fats? We start our analysis with the longest seed oil trial ever conducted, the eight-year LA Veterans Administration Hospital Study. The claim that it is confounded by trans fats relates to the use of a margarine in the seed oil group. There were actually two margarines used, one which was free of trans fats and one which contained trans fats. Here, we dig into historical sources such as advertising materials, preserved boxes with ingredient labels, patent infringement lawsuits, and scientific papers of the era. We blend this with direct analyses of the margarines and foods made with them and physiological biomarkers of trans fat consumption to narrow in on the best answer. But first, why was this trial so incredibly important? Read the full article here: https://chrismasterjohnphd.substack.com/p/are-the-seed-oil-trials-confounded

Sick? Worried about getting sick? Your go-to source of info is my guide, How to Not Get Sick: https://chrismasterjohnphd.substack.com/p/staying-immune-through-the-winter Covered in it: * Stocking your cabinets * Nutrients to focus on for immunity * At the first sign of a suspicious sneeze * If you get sick, what to do: week 1, week 2 If you’ve gotten sick and are not recovering like you should, go to my guide on “How to Finally Get Rid of Your Lingering Cough” https://chrismasterjohnphd.substack.com/p/finally-get-rid-of-your-cough For the science on how to leverage nutrients to keep from getting sick, see my course, Nutrition and Immunity: https://chrismasterjohnphd.substack.com/p/nutrition-and-immunity

The Father of Evidence-Based Medicine: Why N=1 Trials Top the Evidence Hierarchy I just interviewed Gordon Guyatt, watch it here. Gordon Guyatt coined the term "Evidence-Based Medicine" in 1991 and together with David Sackett and others he founded the EBM movement, formally proclaimed in the Journal of the American Medical Association (JAMA) in 1992. He cofounded the GRADE Working Group in 2000, which has now become embedded in the World Health Organization, Cochrane, and other institutions as the authoritative distribution of EBM's influence in the world's institutions. He started the authoritative textbook on EBM, Users Guide to the Medical Literature, in 2001, which reached its third edition in 2014 and remains the authority of the field. As such there is no one else alive who speaks more authoritatively on what Evidence-Based Medicine truly means. You may then be surprised that the familiar "pyramid" of the "evidence hierarchy," which appears to have been created by an entirely unknown reference librarian at SUNY Downstate in 1997, is, according to Guyatt "totally confused." Among other reasons, properly conducted n=1 self-experiments belong at the TOP of the hierarchy, where they have appeared in the EBM textbook since 2001, remaining so in the 2014 edition. Guyatt told me that if he ever produced a fourth edition, n=1 trials would remain right at the top. We looked together at my own randomized n=1 self-experiment comparing the impact of corn vs quinoa on my sleep and energy. You may also be quite surprised at how Guyatt described the importance of mechanistic reasoning in interpreting the generalizability of human outcome studies. In some cases, it's "crucial." We talked about how I synthesize mechanistic reasoning, animal studies, and human trials to interpret the way choline status should impact the effect of seed oils on fatty liver and Guyatt weighs in with his verdict on my reasoning. In this interview, Guyatt and I discuss how to apply the principles of EBM to medicine, health and nutrition, and daily life, paying special attention to the less appreciated aspects of EBM, like the importance of individual values and choice, recognizing what we don't know, understanding the limits of generalizing from RCTs, weighing mechanistic reasoning against observational studies as means of navigating uncertainty, and how Guyatt responds to critiques from public health and to John Ioannidis's claim that EBM has been hijacked. youtu.be/xFQdiCQ5FD0

To argue that anecdotes aren’t valuable data is to argue against being a human being. Your own experience does not necessarily generalize to anyone else’s, nor are your past results a guarantee that you will obtain the same results in the future. Yet, to not use your own anecdote to generalize from your past experience to your potential future experience is to not learn from experience. Learning from experience is essential to being human. As to whether sharing your anecdote is valuable, it is, and this is why in medicine it is valuable to publish case reports and why humans as a collective love sharing stories. Again, to argue against the value of telling a story is to argue against being human. What the anecdote shows (to the extent it can be verified or trusted) is that its contents are possible. And if it was true for one person, it could be true for another. Sharing a story allows people to hear what worked for others and try it for themselves. If many people document the same thing, it becomes more possible that the thing observed is not only possible, but maybe even common. You of course cannot claim anything precise about the commonality of the experience until you have surveys based on random population samples but you can begin to get an idea. You also cannot be very confident in cause-and-effect relationship unless you can observe them repeatedly, ideally in a randomized context. But the anecdote shows the possibility of something happening that in many cases is consistent with a cause-and-effect interpretation, putting the possibility on the table. The plural of datum is data. An anecdote is a datum. The plural of anecdote is anecdotes. Anecdotes are data. A single anecdote is valuable.

Elevating randomized controlled trials over your own personal experience is not evidence-based. It’s a violation of what you would learn in the first week of Statistics 101, that randomized controlled trials do not apply to individuals. It’s the opposite of evidence-based. Clearly, generalizing from your own experience to the average person is a worse violation. The proper interpretation of the evidence is to take systematic synthesis of randomized controlled trial results to indicate the most probable outcome for the population, and then to study yourself or any other individual as a member of that population to whom those results *might* generalize, but to use the experience of the individual as the final say. That doesn’t mean that everything you believe from personal experience is true. But perfect truth is unknowable. You can conduct randomized controlled trials on yourself for much more definitive evidence, but it often isn’t worth it. Ultimately you seek the evidence you need from your experience to arrive at results you are happy with.