The shiny new darlings of Big Pharma are the GLP-1 RAs, drugs such as Ozempic, Wegovy, and Mounjaro that were originally designed to improve blood glucose control in type 2 diabetic patients, but were serendipitously discovered to cause weight loss in diabetics and non-diabetics. Now, it seems every day brings some new malady that *might* be solved by taking a GLP-1RA.

Here’s a partial list, generated by AI, of all the purported *possible* benefits supported by research, currently being investigated, or under consideration to be:

Type 2 diabetes mellitus, obesity and overweight with comorbidities, prediabetes and diabetes prevention, metabolic syndrome, insulin resistance, polycystic ovary disease, fatty liver, renal diseases, kidney stones, cardiovascular disease, heart failure, hypertension, dyslipidemia, chronic kidney disease, obesity‑related liver enlargement and liver enzyme elevation, post‑bariatric surgery weight regain, obstructive sleep apnea, asthma, shortness of breath of severe obesity, infertility associated with obesity/PCOS, low sex hormones linked to obesity and insulin resistance (men and women), osteoporosis, psoriasis and other dermatologic conditions, rheumatoid arthritis, gout, neurodegenerative disorders (Parkinson’s, Alzheimer’s, and other dementias), epilepsy, chronic pain syndrome, migraine, depression, addictive behaviors, substance abuse and eating disorders, and finally cancers of several types.

Some of these benefits are already pretty convincingly validated in RCTs—diabetes improvement and weight loss, for instance—while others are still in the tenuous or preliminary stages.

Case in point: the last mentioned—cancer. A recent article appeared in Cure (a website devoted to issues dealing with cancer) with the following headline: GLP-1 Associated With Colorectal Cancer Prevention, Research Finds.

The article detailed observational research, presented at the 2026 American Society of Clinical Oncology Gastrointestinal Cancers Symposium and published this month in the Journal of Clinical Oncology, comparing the use of GLP-1 RAs to aspirin for prevention of colorectal cancer (CRC), with a primary endpoint of the development of CRC and a secondary endpoint development of adverse events associated with either therapy.

From the jump, this is only an observational study, and as such it cannot on its own impute causality. And to be fair, they say that up front in the title: GLP-1 associated with…prevention. A good weasel word to be sure, but unfortunately one most of the public and journalists will ignore.

So the careful reader will see right away there’s no green light here for pulling out the GLP-1RA syringes to combat colon cancer based on this data, but it might suggest hypotheses that could later be investigated with a more rigorous trial. Let’s see if there’s anything robust here.

The study subjects’ data were drawn from a 150-million-patient multicenter database (TrinetX), and the design excluded those subjects who had taken any other form of NSAID besides aspirin over a given period, any other form of diabetic medication apart from a GLP-1RA, or who had reached a primary or secondary endpoint before the study window, which was the 6 months after their first documented use of the therapy (either aspirin or GLP-1RA). These eliminations resulted in two cohorts of approximately 140,000 subjects each, comprised overwhelmingly of middle-aged participants (mean age 58), who were white (67%) and women (69%), who were matched between the cohorts using propensity scoring.

Their conclusions (and the headline that kicked this discussion off) are prime examples of inflating a minuscule, might-possibly-be-an effect into something that, in the headline, sounds like a major news story about a big medical breakthrough.

First, their conclusions:

“GLP-1RAs were associated with a 26% relative reduction in CRC incidence compared to aspirin. These results along with the favorable safety profile of GLP-1RAs could underscore a potential public health impact and warrant prospective validation in randomized clinical trials.”

Wow! Twenty-six percent! That sounds amazing, doesn’t it? But just a quick look beyond the headline and the conclusion tells a different story.

“CRC incidence was 0.13% (183/140,758) in GLP-1RA users vs 0.176% (247/140,692) in aspirin users, yielding an ARR of 0.0455% and NNT of 2,198.”

So the bottom line is that after they ended their study and crunched the numbers, the difference between the GLP-1RA users’ incidence of developing CRC and that of the aspirin users was a mere 64 cases out of 281,000 patients.

If my math is correct, it’s 0.23 cases per 1,000 more or less. That’s about one-fifth of a case per 1,000 people treated. A very weak association. Truly negligible and practically not worth mentioning. (Unless you make GLP-1RAs, that is.)

In which case, you can massage the numbers with a little sleight of statistical hand to show that the 247 cases of CRC in the aspirin group versus the 183 in the GLP-1RA group represents a 26% relative reduction in cancer incidence, but that’s spurious. It’s a relative risk difference, not an absolute risk difference. It has an average risk reduction of 0.0455% with a large number needed to treat. Which sounds a lot less impressive than a 26% reduction. In other words, not actually a whole lot here to crow about.

There is some very preliminary research that suggests GLP-1RAs may have anti-inflammatory and even anti-proliferative activity in colon (and other) cancers, so I would agree that they might want to look further into them with a well-designed randomized controlled trial (RCT). But even if such a trial showed that giving people these drugs reduced the incidence of colon cancer (or anything else) can you tease out whether it is a newly recognized effect of the drug or merely the effect of the drug to help patients achieve better glucose control, satiety, and weight loss—to make them metabolically fitter in general. Let’s back up to look at the target of this receptor they’re so fond of agonizing.

What is GLP-1 anyway?

Glucagon-Like Peptide-1 is a small hormone of the incretin family, produced locally by enteroendocrine L-cells in the gut in response to foods entering the distal small intestine and first part of the large intestine. Its role is to help regulate insulin and glucagon release, gastric emptying, and appetite. Its release amplifies insulin secretion if the food coming in is carbohydrate-rich and glucose is elevated, but it has minimal effect on insulin if not. It also suppresses glucagon secretion (insulin’s opposing hormone) if glucose levels are above the fasting baseline (but not if there is hypoglycemia). It acts to slow gastric emptying time creating a sense of postprandial fullness, which suppresses appetite.

And all of that action seems to be of physiologic benefit to those who have diabetes, obesity, or some other component of metabolic syndrome.

But if stimulating GLP-1 receptors (which is what GLP-1RAs do) is the biochemical mechanism behind these purportedly positive effects, why not just stimulate the release of GLP-1 with food and let it do its natural thing by binding itself to its receptors?

Dietary fat and protein each roughly double to quadruple circulating GLP‑1 after a meal, with levels peaking within a half hour to an hour and a return toward baseline over roughly two to three hours. Fasting GLP‑1 is typically around 5 to 15 pmol/L. Mixed meals generally raise total GLP‑1 about 2- to 4‑fold, regardless of macronutrient makeup, when energy is reasonably matched.

High‑protein meals can produce some of the highest GLP‑1 responses seen with physiologic feeding. In a crossover study, a 60% protein breakfast produced higher GLP‑1 levels at two hours that remained elevated for the 4‑hour sampling period than did isocaloric high‑fat or high‑carb meals.

But dietary fat is itself a potent GLP‑1 secretagogue in both humans and animals, triggering detectable GLP‑1 release within about 30 minutes that peaks around one hour.

Protein plus calcium (e.g., dairy) appears particularly effective, with human work showing some of the highest postprandial GLP‑1 concentrations reported for normal feeding when the two are combined.

When calories are matched, high‑protein and high‑fat meals both stimulate GLP‑1, but several studies show greater GLP‑1 area under the curve after high‑protein or protein‑enriched drinks compared with carbohydrate‑rich or fat‑rich comparators.

In summary, carbohydrates (especially glucose) trigger GLP‑1 quickly via proximal small intestinal sensing and this action will amplify the signal for insulin release. Fat provides strong and somewhat more prolonged stimulation as it reaches the distal bowel’s L‑cells, and protein (and certain amino acids) can produce robust GLP‑1 release that is enhanced by calcium.

So eating meals that are high in quality protein and fat, and limited in carbohydrate would seem like a recipe for doing what a GLP-1RA does. And clinical research bears out that a well-formulated, protein-rich, fat-rich, low-carb ketogenic diet can indeed control diabetes, reduce excess weight and body fat, improve cardiovascular blood lipid measures, resolve fatty liver, improve sleep apnea, and more, all without the untoward potential GLP-1RA side effects that can include such maladies as nausea, vomiting, gastroparesis, lean body mass loss, Ozempic butt, and Wegovy face.

In fact the list of possible adverse side effects—from the common to the rare—is longer than the list of proposed targets for treatment:

Nausea, early satiety, post‑prandial fullness, vomiting, diarrhea, constipation, abdominal pain, cramping, bloating, dyspepsia/heartburn, fatigue, dizziness, headache, injection‑site reactions (erythema, pruritus, nodules, mild pain), hypoglycemia when combined with insulin or insulin secretagogues (e.g., sulfonylureas), mild resting tachycardia, possible orthostatic symptoms (low blood pressure on standing from volume depletion of GI fluid losses), biliary, pancreatic, and GI motility slowing, gall stones and inflammation, gall bladder colic, acute pancreatitis (rare but clinically important), worsening or unmasking of gastroparesis, rare bowel obstruction or ileus, acute kidney injury from volume depletion, electrolyte disturbances secondary to GI fluid loss, boxed warning for thyroid C‑cell tumors (medullary thyroid carcinoma) in rodents; contraindication in patients with personal/family history of MTC or MEN2, systemic allergic reactions, very rarely anaphylaxis, development of anti–drug antibodies, transient visual blurring related to rapid glycemic shifts, worsening of pre‑existing diabetic retinopathy when glucose control improves very rapidly (not uniformly seen, but enough to be on warning labels for some agents), optic neuropathy and other visual events with some agents (causality not fully established), hair loss (alopecia) reported anecdotally and in some pharmacovigilance datasets, mood changes and rare reports of suicidal ideation are being actively surveilled but not definitively linked.

So, if you want to rid yourself or those you love or care for from the specter of that long list of diseases at the start while avoiding that long list of adverse side effects above, the best nutritional advice comes back to this: eat real food. Eat meat, fish, poultry, eggs, dairy, green leaves and vegetables, nuts and seeds, little fruit, some starch, and no sugar.

I’ve seen it, and so have you. We coach the same workout all day. Some athletes thrive on the challenge, and others don’t look as good. We second-guess ourselves: “Did I scale them right?” “Was that the right workout today?” But sometimes the answer is simpler. It’s not the workout that needs a closer look, it’s the athlete who is struggling. This is where mitochondria enter the conversation.

MetFix is the only commercial entity concerned with the care and feeding of the mitochondria.

I’ll admit that line didn’t land at first. Mito-what? It sounded like textbook science, not a coach’s job. But experience has taught me that when Coach Glassman makes a claim that doesn’t make sense right away, it’s worth listening to. If I don’t understand it yet, it usually means there’s something big I’m missing. That’s why, when I heard Pete Shaw’s lecture at the first Foundations Course, the line finally clicked: capacity lives or dies inside the mitochondria. What we call fitness is really mitochondrial function expressed on the gym floor.

If we’re going to talk about fitness and health, we have to care about mitochondria, because talking about performance without them is like talking about a drag race without talking about the engines.

So let’s look under the hood. Nearly every cell in your body is built around these engines. Mature red blood cells and lens cells of the eye are the exception. Red blood cells carry oxygen, but they do not have mitochondria. Most tissues do. The mitochondria you “see” in performance live mainly in skeletal muscle, the heart, and the nervous system. Those are the engines that move the load and keep output steady. But mitochondria in organs like the liver, pancreas, and gut set the fuel mix and metabolic signals that determine whether those performance engines run clean or overheat. At the cellular level, each mitochondrion fires like a cylinder, turning the fuel you eat into ATP, the cell’s universal energy currency. Mitochondria turn fuel into ATP. That’s where we get the horsepower. Nutrition sets the fuel mix, and training controls how hard the engine has to work. This tiny engine explains what coaches see every day: elbows drop, midlines soften, footwork gets sloppy, while someone right beside them stays crisp and in control. Mitochondria determine who has the power to do the work, who adapts, who fades, and who can show up again tomorrow. Performance and health share the same mechanism: when these engines adapt, athletes get fitter; when they run on the wrong fuel for too long, dysfunction isn’t far behind.

The mitochondria don’t care about food brands or nutrition fads; they care about substrates. Everything—fat, carbohydrate, and protein—gets broken down into acetyl-CoA, the molecule they burn to produce ATP. Fat enters through beta-oxidation. Carbohydrate runs through glycolysis and pyruvate oxidation, and amino acids contribute during fasting or excess intake. In metabolic terms, fat is the long, clean burn; carbohydrate is the fast, hot flame. With oxygen, a molecule of fat yields roughly three times more ATP than a molecule of glucose. That difference shows up on the gym floor, where fat supports steady output and repeat efforts, while glucose is powerful but limited—one feels sustainable, the other urgent.

Metabolic flexibility is the capacity to burn the right fuel at the right time. When mitochondria are efficient and abundant, fat supports the easy gears and glucose is reserved for speed. When they’re limited, so too is the capacity to burn fat. The engine runs too hot, too soon. More glucose is burned without oxygen through glycolysis. Coaches see the result: athletes who look in distress instead of control, faces flushed, breathing panicked, pace collapsing long before the clock demands it, recovery slowing to a crawl. Without metabolic flexibility, training becomes futile suffering instead of driving adaptation.

What we see as poor performance is often early metabolic disease. The same engines that decide who holds form in a workout also decide who drifts toward chronic disease. When mitochondrial oxidative capacity is limited, athletes rely more heavily on glucose and fatigue sooner. Chronic overexposure to refined carbohydrate and industrial seed oils drives the overload, increasing oxidative stress and eroding the ability to adapt. First, performance breaks. Then health breaks. Diabetes, fatty liver, cardiovascular disease, and cancer—many of them begin with the same failing engine. Research in cancer metabolism, insulin resistance, and cardiometabolic disease increasingly identifies mitochondrial dysfunction as an upstream driver of metabolic disease. Workout performance is the first test of metabolic health, and coaches administer it every day. Doctors use a similar principle with exercise stress tests, unmasking cardiovascular problems that are silent at rest. Long before fasting insulin climbs above 5 µIU/mL or the triglyceride-to-HDL ratio rises past 2.0, coaches can see the engine struggling on the gym floor.

Back to what we see all the time—one athlete keeps mechanics sharp and breathing steady, while the other fades early: red face, slumped posture, confusion in the eyes. What you’re noticing is the engine beginning to fail. One engine is responsive; the other is overheating and struggling to convert fuel into power. Scaling won’t fix a failing engine; you have to change what goes into the tank.

When adaptation stalls, it’s usually a fuel problem, not a programming problem. Fasting can help restore insulin sensitivity and reset energy signaling. If you want mitochondria that make power and recover fast, you need adequate protein, sufficient total energy, and food that supports stable blood sugar so training can stay consistent. The principle is the same moving from sick to well as it is from well to fit, but the dose changes: total intake, macros, training load, and recovery have to be fitted for the athlete in front of you.

This is the care and feeding of mitochondria. In MetFix terms, mitochondria are the biological engine behind work capacity across broad time and modal domains. Mitochondria drive metabolism and control capacity—and they’re trainable. Give them a consistent signal and they expand, giving you more capacity to make energy, hold output longer, and recover faster between bouts. Remove the signal and they diminish. The same workout feels harder, breathing spikes sooner, and recovery slows. Coaches measure it with a stopwatch and record it with a whiteboard.

Coach the mitochondria, and you coach both performance and health.

A recently published study in Neurology, titled High- and Low-fat Dairy Consumption and the Risk of Dementia, reached what the authors may have felt was a somewhat startling conclusion: high-fat dairy and cheese consumption appeared to reduce the risk of developing dementia, even that variant related to atherosclerotic cerebrovascular disease. (I suspect at the outset the researchers assumed they’d find the precisely opposite outcome.)

The research is a prospective epidemiological study (therefore weak evidence) from Sweden that identified and then intermittently followed a cohort of 27,670 people over the course of 25 years seeking to uncover a link between dairy intake and dementia risk, trying to elucidate the effect of what they felt was an easily modifiable risk factor. The primary endpoint was development of dementia of any sort, which befell 3,208 of the subjects, and then they further teased out a secondary cohort of those with a diagnosis of Alzheimer’s disease or atherosclerotic vascular-related dementia from the larger all-cause dementia group.

The dietary intake data was collected via 7-day diet diaries, food frequency questionnaires (both notoriously unreliable), and a single in-person dietary interview lasting about 45 minutes to an hour. One caveat here is that extrapolating these few data points to what the person consumed over 25 years can lead only to vague and speculative quantification of dairy intake at best. So, a bit of a grain of salt there.

The conventional wisdom in neurology is that a diet high in saturated fats is toxic to the brain because (so they say) it promotes insulin resistance, puts stress on the endoplasmic reticulum, and leads to neuronal mitochondrial dysfunction. And that a dysfunction in insulin signaling in the neurons impairs cognitive function. Ergo, put simplistically, a diet chronically high in animal fats leads to dementia. But does it?

Earlier studies had seemed to contradict this Swedish study’s beneficial conclusions, suggesting instead that eating a higher fat diet worsened the progression from mild cognitive impairment to outright dementia. The fly in the ointment, however, is that in most of this research the subjects studied were individuals already beset with systemic metabolic dysfunction (metabolic syndrome, insulin resistance, diabetes, obesity, etc.). But a body (or a brain) doesn’t get into that shape by eating saturated fat alone; it’s usually the typical Standard American Diet (SAD) containing saturated fat, to be sure, but also filled with sugar, refined flour, seed oils, and additives. And yet the researchers all seem to zero in on the saturated fat component and tag it as the proximate cause.

Like other organ systems, the brain can develop insulin resistance, and when it does, it can’t effectively use glucose for energy. The energy deficit impairs not only cognition but the other energy-requiring brain functions, such as removal of waste products and senescent brain cells. On a high-carb, sugar-filled, bad-fat-laden diet, if the brain can’t efficiently use glucose as its main fuel, it must turn elsewhere. Fatty acids and ketones are that elsewhere.

The truth is that the brain needs fat. In fact, it is mostly made of fat; after adipose tissue, it’s the fattiest organ in the body with about 60% of its dry weight made of lipids. Phospholipids, cholesterol, long-chain essential PUFA fatty acids, such as DHA (important for neuroplasticity and synaptic function) and arachidonic acid (critical for synaptic plasticity, especially in gray matter – i.e., the thinking brain), are rich particularly in the myelin layers that insulate the axons (the long extensions of the nerve cell body that carry signals away from the nerve center). Myelin is critical to facilitate efficient, smooth, static-free communication between the neuron and its neuron neighbors, muscles, and glands.

Cell membranes, especially neuronal cell membranes, require both a degree of stiffness for integrity and a degree of fluidity or flexibility to allow for movement of receptors and transfer proteins and the like. Saturated fats play a key structural role, especially in myelin, with palmitic acid being the most abundant one. It serves to anchor the phospholipids and sphingolipids (structural membrane lipids built on glycerol or sphingosine backbones that line up in bilayers to form the membranes of neurons, axons, dendrites, synapses, and organelles, such as mitochondria). The palmitic acid keeps the bilayers tightly packed to optimize the insulation capability required for rapid signal transmission across long distances. Remembering, of course, that the length of an axon could extend from the brain to the big toe.

It’s not accidental (though it may come as a surprise to some) that human breast milk is almost 50% saturated fat, which the infant’s brain needs in plenty to build the enormous numbers of new cells and connections and all the insulating myelin attendant to that during the first few years of life.

But as the need to feed the brain for proper growth and cognition doesn’t end with cessation of breastfeeding, neither should the intake of good quality fats, including saturated fats. This is but one of the reasons the new HHS directive to give growing children full fat milk and dairy is such a boon to their nutrition and health. What they don’t need is processed junk full of sugar, concentrated refined starches, seed oils, and additives.

And, if the suggestive data from the Swedish study is any indication, the need of the brain for quality fats (including saturated animal fats) doesn’t stop throughout life. Dietary fat (from natural whole food) will provide the building blocks to keep myelin sheaths in good repair, to build new mitochondrial and cell membranes and keep them fluid but with integrity, and the raw materials to make important signaling molecules. Good fat makes good brains, so it should come as no surprise that eating it would reduce the development of dementia as we age. This study is observational and thus can only suggest hypotheses and avenues for future investigation, but it’s intriguing. Those kinds of ‘further’ studies would be difficult (and expensive) to undertake, if they could reasonably be done at all.

The brain is not a low-fat organ, and it was never designed to be fed like one. From the first months of life, when myelin is being laid down at a furious pace, to the last decades, when its maintenance determines whether the mind stays sharp or fades, fat is not the enemy of the brain — it is its substrate. Demonizing dietary fat, particularly saturated fat from whole food sources, while the modern diet drowns the brain in sugar and industrial oils, has been one of the more consequential misdirections in nutritional science. The Swedish study is one small corrective signal in a long-overdue recalibration.

Friday, Feb. 20th, 6 p.m. GMT / 1 p.m. ET

Live Q&A with MetFix Head of Education Pete Shaw and Academy staff Karl Steadman for a direct conversation about the MetFix Foundations Seminar, what it is, who it’s for, and why it matters.

Pete and Karl walk through what’s actually taught at Foundations, how it differs from other continuing education, and how it fits into the broader MetFix method.

The MetFix mission is one focused on improving the health and fitness of its members (regardless of where they begin their journey) through regular performance of constantly varied functional exercise and the consumption of a nutrient-dense diet of real foods that provide plenty of quality complete protein and good fats, absent much starch or sugar. Particularly in people who start out distinctly unfit metabolically, who have been sedentary and eating a typical diet of processed foods, high in starch, sugar, and industrial seed oils for some time, the changes brought about by adopting the MetFix methodology can be stunningly rapid, especially improvements in metabolic measures, such as triglycerides, blood sugar, blood pressure. Early on people will typically notice improvements in energy, sleep quality, and mood (exercise is a great antidepressant). Weight loss, fat loss, and muscle gains take a bit more time, but will follow suit with perseverance and consistency.

And, unfortunately, for some people, so will hair loss.

Shedding pounds of fat is a welcome benefit of making a positive lifestyle change; shedding hair not so much. But over years of caring for people following a well-formulated low-carb diet, I’ve seen it happen to men and women alike.

Why, they ask, when they’re eating better, living cleaner, and working harder are they now a few months into their new program suddenly losing hair? And I can assure you that seeing a shower drain full of hair is cause for considerable consternation. The natural human tendency is to link such a phenomenon to some deficiency in the newly adopted nutritional program – “I started this new keto thing and now my hair is falling out!” Quite often they’ll blame and even abandon their new diet. So, this is something coaches should be aware of, and if it happens, be prepared to reassure a client who experiences it that it’s nothing to worry about.

The likeliest explanation is telogen effluvium—the medical moniker for it.

(One word of caution: the likeliest cause of hair loss doesn’t mean only cause, so persistent cases merit a visit to the dermatologist to search for other causes.)

What is Telogen Effluvium?

Sudden loss of hair can accompany a wide range of systemic conditions. Illness and high fever can cause it. Anesthesia, radiation, some medications, and surgery can as well. Pregnancy, too. And so can marked weight loss, from dieting, GLP-1RA use, obesity surgery, or whatever cause. Paradoxically, changing your lifestyle positively by exercising properly and eating right can even cause it.

The explanation lies in the physiology of hair growth.

Humans are born with about 5 million hair follicles on their bodies, with between 100,000 and 150,000 of them residing on the scalp. The number is fixed before birth and doesn’t change, at least it doesn’t increase (though in the case of genetic baldness, the number can decrease when some of them simply quit functioning). Each hair shaft grows out of a single follicle that throughout the course of its life will cycle repeatedly through various growth stages. These are:

• Anagen: the active growing stage (usually lasting years) in which the stem cells and matrix in the follicle base are actively dividing and producing keratin, elongating and thickening the hair shaft. Normally about 85 to 90% of the 100,000 or so hairs on the average human head are in this growth phase at any one time.
• Catagen: a brief transition phase (lasting a few days to weeks) when a small percentage of the active hair follicles begin to slow down the cell division and keratin production that elongates and maintains a hair shaft in preparation to rest a while.
• Telogen: a phase following catagen, lasting 2 to 4 months, when the follicle is completely at rest. The hair shaft it’s built remains anchored to it, but the hair is no longer growing. Normally only about 10 to 15% of the follicles on a human scalp are in this dormant state at any one time, a feature designed to prevent synchronous shedding and over-thinning of the hair.
• Exogen: the shedding of dormant hair shafts.

Major metabolic stressors, such as those listed above, or sudden metabolic changes—even positive ones like making a major beneficial dietary shift—can throw a much larger percentage of active follicles suddenly into telogen, the dormant state.

After making the big switch, for example, from the Standard American Diet to a low-carb/ketogenic structure, at first there’s nothing much to see, because the ‘old hair’ is still anchored in place, even though the hair follicles have been put into telogen. Everything seems to be going well for a few months, but that resting stage will pass in two, three, four months, and when it does, the dormant follicles will re-activate. The old hair shafts of those re-activating follicles are finis, caput; the follicles can’t add onto them any longer. They can, however, build brand new healthy hair shafts from the ground up. And that’s what they do.

As the tiny new hair begins to form in the base of the follicle it ultimately pushes out the old, dormant hair shaft, and the scalp loses that hair. When 25% or 30% or 50% or more of the active follicles have been thrown into telogen by the sudden systemic stress or metabolic change, they will start to be pushed out in rapid succession, causing telogen effluvium—the flood of shedding hair caused by a large number of follicles coming out of their resting phase at once.

If inspired by the metabolic changes wrought by switching to a nutrient-dense diet, be assured, everything is in place to ensure new shafts are growing. They’ll ultimately be visible as fine new hairs around the edges of the hairline if you look with care. Certainly it will take many months of active shaft growth for a tiny new hair to replace a longer one that’s been shed, but the person will in time recover their normal head of hair. Or maybe even a shinier, more vibrant one.

The main takeaway is to recognize telogen effluvium is not an uncommon event. It may occur in anyone 2 to 4 months out from surgery, major illness, pregnancy, and sometimes just from making the transition from a lousy diet and sedentary lifestyle to the MetFix methodology. It doesn’t happen to everyone, but occurs often enough that a coach will want to be aware and step in with reassurance that this, too, shall pass. The explanation of what’s going on is usually enough to keep that person traveling their road to metabolic rehabilitation.

Streams live, Tuesday Feb. 17, 11 a.m. ET / 8 a.m. PT

Listen in as Brett and Lexis talk about what it’s like running a MetFix gym as a married couple. You’ll hear about all the incredible programs they run out of their affiliate for their local community.

This series is built for coaches, owners, and leaders who want to expand their impact in their community. We’re talking with coaches who are redefining what it means to serve outside the standard class model.

In this interview at a MetFix Foundations Seminar in Seattle, Bruce Edwards—who served for several years as Chief Operating Officer of CrossFit Inc. —reflects on his long relationship with Greg Glassman, the evolution of the fitness movement, and what drew him to MetFix as an attendee. Edwards describes himself as an average athlete who nonetheless experienced profound improvements in health and strength through training and community, but admits that longstanding struggles with sugar addiction and deteriorating biomarkers persisted despite decades immersed in fitness culture. He explains that MetFix resonated because it connects behavior change, chronic disease, and aging to mitochondrial energy systems, offering the biochemical understanding he believes is essential for both coaches and individuals. In conversation with Emily Kaplan, Edwards points out that loss of metabolic health and mobility—not aging itself—is what ultimately erodes independence and quality of life, drawing on personal family experience. He frames MetFix not as a replacement for movement-based training, but as its nutritional and metabolic foundation: a complementary entry point that empowers people to make informed choices, restore health, and improve the human condition through education, community, and practical application.

Hot off the press, Bob Kaplan’s new paper explores the metabolic nature of hereditary cancer syndromes. His paper makes a case for the metabolic theory of cancer as it relates to the precise mutations many cite as proof for the somatic mutation theory.

Featured paper:

• • Hereditary cancer syndromes linked to oxidative phosphorylation insufficiency

Special for this month, the Journal Club meeting is free for anyone to watch via YouTube. BSI Medical Society Members and MetFix affiliates can still access all the past meeting in their Dashboard.

It’s not breaking news that medicine in the US today needs a makeover. We’ve become a nation of far too many overweight, out-of-shape, and chronically ill citizens, both young and old; a trajectory that is non-sustainable. One reason for this sad state of affairs is the near-complete financial capture of everything that touches health care: the media, academia, research, medical journals, and the governmental regulatory agencies, all of which has led to a misguided groupthink that the solution to all diseases lies in finding another pill, injection, or vaccine.

Americans already spend twice (or more) as much per capita on health care as Europeans and Canadians do, and yet have poorer average health and longevity to show for it.

A MedScape Scenario

The issue was exemplified by a MedScape quiz sent out recently concerning the proper next steps to address the persistently elevated blood pressure of a patient named Thelma. Her history was described in the introduction thus:

“Thelma has had check-ups every 1 or 2 months for 5 months now, and her hypertension continues to be an issue. Her workup for secondary hypertension was negative. Her daily regimen now includes losartan (100 mg), hydrochlorothiazide (25 mg), and amlodipine (10 mg). However, her blood pressure remains elevated. Her office blood pressure is 144/90 mmHg, and she completed an ambulatory blood pressure monitor test which showed an average blood pressure of 138/84 mmHg, with less than 10% dipping at nighttime. Her pulse rate ranges from 68 to 83 beats per minute.

She remains asymptomatic and adherent to her medications. She has tried to eat a more plant-based diet and has lost 1 kg in the past 5 months. An estimated glomerular filtration rate completed 2 weeks ago was 48 mL/min/1.73 m² (reduction of four units from 5 months ago), and her potassium level is now 4.2 mEq/L.”

The slight drop in her eGFR (an estimated measure of kidney filtering capacity based on the person’s creatinine measurement) is likely not all that significant. The eGFR can vary a fair bit due to lab imprecision, the person’s hydration status, diet, other concurrent illnesses that may be present, and day‑to‑day creatinine fluctuation, even when true kidney function is stable.

In a nutshell, this lady’s story is that she has been worked up for causes of secondary hypertension with none found, put on three prescription medications to control her pressure, told to ‘eat a more plant-based diet’ which she’s tried to do, and been followed monthly for 5 months. And despite this standard of care treatment she’s lost but 1 kg and her pressure is still not where her physician would like to see it, even though it is not outrageously higher than the 130/80 the ACC and AHA now recommend as ‘controlled’ hypertension.

So the dilemma is what to do next. And the first question of the MedScape quiz offers the clinician four choices as to what that should be. Choices 1, 2, and 3 are each the addition of a fourth pill to control her pressure—add atenolol 25 mg a day, add hydralazine 25 mg three times a day, or add spironolactone 25 mg a day. And the fourth choice is outrageous – refer her for evaluation for renal denervation, basically a procedure to destroy the sympathetic nerve input and output from her kidneys. Pretty extreme for a pressure mildly above what you’re aiming for and what looks to be stable kidney function.

This quiz exemplifies the kind of not-so-subtle brainwashing that passes itself off as continuing medical education. And it’s unconscionable. Why?

To begin with, she’s asymptomatic, they say and has ‘remained so’ which suggests that she was asymptomatic from the jump, and perhaps her high pressure reading was discovered incidentally. But medical management has abandoned the notion of looking at and treating the whole living person; too often it’s become an exercise in number chasing—whatever it takes, however many pills or shots need to be piled on to get a cholesterol under 200 mg/dL, get an LDL under 70 mg/dL, get a blood pressure under 130/80 mmHg.

And it’s illuminating to point out that not so very long ago a blood pressure reading of 140/90 was considered normal, and it still is considered normal in Europe and Japan where general health and longevity is better than ours. Now in the US, however, it’s been codified as a cause for three (or four) medications a day and a possible renal denervation procedure. How did that happen? Pharma capture of the narrative is how.

What could we do to help Thelma?

The introduction doesn’t tell us anything about Thelma’s physical state or other lab values. Is she overweight? (probably) Sedentary? (probably) Is her insulin elevated? (probably) Are her glucose or triglycerides high? (probably) Does she have a high waist circumference, reflective of excess storage of visceral fat and fatty liver? (probably). And if so, all of that points to underlying Metabolic Syndrome (MetS). Did they look at these things in that light? We don’t know, but they should have.

When secondary causes of hypertension have been eliminated, as they tell us they have been with Thelma, the likeliest root cause is MetS – i.e., insulin resistance – and its effects that cause the kidneys to hold onto sodium and excess fluid, among many other physiologic changes that may result in blood pressure elevation as a manifestation of the metabolic dysfunction.

And fortunately there’s a simple fix for that, but it doesn’t come in a gelatin capsule, tablet, or syringe, so there’s no corporate profit in it. It comes in a ‘Box’. It’s a whole food, protein-and-fat-rich, low-carb, ketogenic diet plus functional movement (aka MetFix methodology). Instruct Thelma to eat meat, fish, poultry, eggs, dairy, nuts, seeds, fresh vegetables, little fruit, little starch, and no sugar for a month. Have her keep a careful journal of what she’s eating every meal, because doing so increases the chance of success in implementing a lifestyle change. Get her off the couch and into the Box, and watch what happens. This approach will most assuredly reap more than a 1 kg weight loss in 5 months and countless other benefits to her health and longevity.

But changing Thelma’s diet and adding resistance training and functional exercise was nowhere to be found on that approved list of correct next steps, even though a low-carb/ketogenic diet has been shown in repeated clinical trials to improve or resolve most of the symptoms of MetS. It predictably offers quick reduction of elevated triglycerides, blood sugar, and insulin. HDL typically rises (and not much else does that but exercise). There will be weight loss and girth loss. If present, GERD improves. And in many cases (though not all, but about 80 to 85% of them) it markedly reduces blood pressure as well.

As a colleague once said to a group of physicians not yet acquainted with the power of the right nutritional structure: nothing in your experience will prepare you for how quickly this diet will work.

In fact, if her hypertension responds to the diet, it could drop her pressure so quickly that she will need to be weaned off her pills or risk falling on her face when she stands up! In our clinical practice we removed diuretics immediately upon commencing the diet and tapered other antihypertensives that might cause rebound in the pressure if removed abruptly. Our goal was always to get rid of pills, not to add another.

Sadly, this scenario isn’t rare. The country is filled with Thelmas. And all of them deserve a chance to get off the add-a-pill carousel and reclaim their health and fitness with good nutrition and proper exercise. And that’s where MetFix comes in. It’s not always easy, but it’s simple. And amazingly effective.