Prodrome Science™ — Webinar Series
Muscle health and condition are better indicators of longevity than mere body weight. Muscles are what build bones through flexion; mobility correlates with cognition and brain health. In this webinar, Dr. Goodenowe explains and demonstrates through global research why muscle building through resistance training creates a physical reserve you can hold for the rest of your life.
Excerpt — full video on Dr. Goodenowe’s website.
Dr. Goodenowe gives this lecture in sweats and a T-shirt rather than his usual suit, and the wardrobe is part of the argument. He calls the topic “immortal strength.” He is fifty-seven. He has not been inside a gym in more than thirty-five years. “When people say, don’t have time to work out, I go, You’re telling me this?” His view is that most people never start because they have built the entrance too tall — the right clothes, the right shoes, the right gym, and the question of how they will look in it.
What he proposes instead is a concept he uses across all of his work: reserve capacity. He describes building it in your physical strength “the same way you create a reserve capacity in your bank account, the same way you take a reserve capacity in your biochemistry.” The target is not performance. It is a margin wide enough that ordinary life — a flight of stairs, a gallon of milk, getting out of a chair — never approaches your limit. And underneath the physiology, he says, the real subject is “the mentality of accepting or not accepting that the loss of physical vitality is something that is inevitable as you get older.”
He opens with the pet peeve: that most people are told the wrong things about fat, and then worry about the wrong number. The study he builds on followed 12,563 people and looked at body mass index alongside fasting insulin, C‑reactive protein, and mortality. Its conclusion, in his reading, is that inflammation and insulin resistance confound the relationship between BMI and death — that BMI is largely a proxy for problems it does not itself measure.
According to Dr. Goodenowe, BMI alone shows very little association with all-cause mortality in women at all. In men there is a familiar U‑shaped curve, low and high both carrying risk. But correct for inflammation and glucose control, he argues, and the U‑shape flattens out. “Healthy fat people with low inflammation and retained glucose metabolism live the longest,” he says. His summary line is the one worth keeping: “What you weigh doesn’t matter. How you weigh what you weigh matters.”
And the reason it matters, in his framing, is muscle. Moving mass requires muscle to move it — so a heavier person who is functioning well is, by definition, carrying the muscle to do it. His warning about weight loss follows from that: “You have to be very careful when you lose weight to maintain your muscle density. Otherwise, you will lose your muscle faster than you will lose your fat.”
Worth reading precisely: this is an argument about what BMI fails to capture, not a case for gaining weight. The confounders he highlights — inflammation and insulin resistance — are themselves driven by excess adiposity in most people, which is exactly why the two usually travel together in the first place. His point is that the marker is crude and the underlying metabolism is what matters. It is not that body fat is protective, and he does not claim it is.
The pivot of the lecture is that muscle mass turns out to be the lesser variable. “It’s actually really not your muscle mass that matters; it’s your muscle strength that matters.” He presents grip strength by quartile, and the shape of the finding is what makes it striking: “When you talk about strength, there’s no U‑shape. Unambiguously, the stronger you are, the longer you live.” Unlike weight, there is no such thing as too much.
Grip strength is a stand-in, and he says so — scientists need something they can measure the same way in everybody. The chair-stand test, counting how many times a person can rise and sit in a fixed period, is the other one, and it is the measure used in his own clinical work. Alongside it he shows skeletal muscle mass across five groups of a roughly twenty-thousand-person cohort, with deaths falling steadily from the lowest muscle group to the highest. Toward the upper end the odds of death run well under half those of the least muscular group — an odds ratio in the neighborhood of 0.44 — and the pattern holds independent of BMI, age, or sex.
To his credit, he then spends several minutes dismantling one of his own charts. The skeletal muscle index appears to lose its benefit in the very highest group — and he explains why that is an artifact: the index divides muscle mass by height, so short people score disproportionately high on it, and height carries its own independent association with mortality. “Details matter. And this is what happens when people make conclusions based on limited information.” It is a useful demonstration of the reading habit he is asking for.
From there he moves to cognition, and this is where the lecture becomes relevant to the rest of this site. “Muscle mass goes hand in hand with cognition and longevity,” he says, presenting data in which lower appendicular muscle mass tracks with lower cognitive scores in seniors, and sarcopenia — the clinical term for muscle wasting — tracks with cognitive impairment.
His explanation for the link is almost too simple to notice: “What moves your muscles? It’s your brain that moves your muscles… So if your muscles are moving, your brain is moving.” He takes a detour to dispose of the dumb-athlete stereotype on the same grounds — moving a body well through space is a cognitive act, not a mechanical one.
Then he offers a biochemical mechanism, and it is the part of this webinar that connects most directly to everything else on this site.
A muscle contracts because a nerve tells it to, and that instruction crosses a synapse called the neuromuscular junction. The neurotransmitter carrying it is acetylcholine — the same neurotransmitter system implicated in Alzheimer’s disease, and the one the first-line Alzheimer’s drug donepezil is designed to boost. “The way our muscles work is the same way our brain works,” he says. “The reason why there’s a muscle activity association with Alzheimer’s is because the biochemical system being affected is the same place.” If you have read our Alzheimer’s and dementia page, this is the cholinergic argument arriving from the other direction.
His evidence that plasmalogens are required for that junction to form properly comes from a rare genetic disease he has studied for years: rhizomelic chondrodysplasia punctata, which affects roughly one child in a hundred thousand and is caused by a genetic inability to make plasmalogens. The clinical picture is shortened, malformed bones, profoundly reduced muscle, and growth failure after the first months of life. In animals bred with the same ether-lipid deficiency, he reports, reduced muscle strength comes with altered development and function of the neuromuscular junction — the nerve densities never form correctly.
This is an argument for necessity, not for reversal. RCDP demonstrates that plasmalogens are required to build normal bone and muscle in a developing child. It does not by itself establish that supplementing plasmalogens restores muscle or bone lost to ordinary aging — a different claim requiring different evidence. Dr. Goodenowe is using the disease as proof that the pathway is load-bearing, which it fairly does; the step from there to adult supplementation is one he supports separately, with the trial described further down.
The bone section turns on an image from the prairies. “A tree can’t get strong without wind… The wind is what makes plants strong. The muscles are what make your bones strong.” Bone is living tissue that responds to load, and the load comes from muscle pulling on it. “You cannot have bone density without muscle density,” he says — and offers astronauts as the natural experiment, losing bone in low gravity because their muscles are no longer working hard enough to flex it.
The data he shows follows the same line: as grip strength falls, the odds of osteopenia and then osteoporosis rise. And resistance training specifically, across multiple studies of total hip bone mineral density, produces more mineral density than not training. He is candid that these trials run four, twelve, eighteen weeks — “but we’re here to talk about longevity. We talk in the terms of years” — and that the mismatch between trial length and human lifespan is a genuine limitation of the evidence.
He also draws a distinction worth carrying away: resistance training and cardiovascular training “do two very, very different things and they build two different parts of your body, both of which you want reserve capacity in.” Walking is not a substitute for loading. Neither replaces the other.
The most arresting slide in the lecture compares 150 people with Alzheimer’s to 150 without. Serum calcium is essentially unchanged between the groups. Vitamin D is markedly lower in the Alzheimer’s group, and osteocalcin lower. And the bone mineral density scores diverge sharply: by his figures, 52% of the Alzheimer’s group had osteoporosis, against 16% of the reference group.
He pairs the data with an observation from visiting memory care facilities — that compared with Parkinson’s or stroke wards, Alzheimer’s units are full of people in wheelchairs. “The lack of mobility is a very common association with Alzheimer’s disease… Bone health goes hand in hand with cognition.”
This is association, and the direction is not established. Immobility can as easily follow cognitive decline as contribute to it — people who stop moving because they are declining will lose bone either way — and both could follow from a third cause, including the poor nutrition and low vitamin D visible in the same data. The pattern is real and worth taking seriously. Which way the arrow points is not something these numbers can tell us.
Everything above rests on a single mechanism: bone is built by the muscle that pulls on it. Dr. Goodenowe places muscle and bone health as integral to the biochemical processes he describes — not downstream of them, but part of the same system. The vitamin D and the osteocalcin and the leucine all matter, and they are supplying a process that only runs when muscle actually contracts against resistance. No load, no signal to build.
Which is where structural practitioners do their work. Reserve capacity cannot be built by a joint that will not accept it. A spine that will not tolerate compression rules out the dumbbell work. A knee that gives way rules out the deep knee bends. A shoulder that will not take overhead load rules out the presses. The routine he describes below is deliberately modest — no gym, no equipment to speak of — but it still assumes a body that can be asked to work, and for a great many people over sixty that assumption is exactly what has failed.
So chiropractic, osteopathic, and physical therapy care are not an alternative to what Dr. Goodenowe is describing. They are what puts it within reach. Their contribution is mechanical rather than biochemical — restoring range of motion, load tolerance, and freedom from pain — and that is precisely the contribution his own argument requires somebody to make. The chiropractors, osteopathic physicians, physical therapists, and naturopathic doctors in our practitioner directory work that side of it, alongside the biochemistry rather than in place of it.
The section Dr. Goodenowe flags as most often missed is that training is downstream of nutrition, not parallel to it. “Exercise only works as good as your body’s able to take advantage of it,” he says. His illustration is severe childhood malnutrition making elite physical training impossible no matter how the training is designed — the raw material has to be there first. “Training alone will not get you healthy. Training has to always be consistent with the proper diet.”
He argues this is precisely where aging research keeps failing: even well-trained older people continue losing muscle and bone, more slowly but not never, and he attributes that to nutrition rather than to insufficient exercise.
The specific molecule he builds the case around is leucine, an amino acid found in ordinary protein. He cites immobilization studies in which bed rest causes predictable muscle loss — but bed rest with leucine supplementation does not, preserving both muscle activity and contractile force. The reason, in his framing, is a storage problem most people have never considered: fat cells store fat, glycogen stores glucose, but there is no protein depot in the body except muscle itself. So any period without eating — including every night’s sleep — draws amino acids out of muscle. Supply them directly and the body has no need to take them.
Around that he places the rest of what he calls muscle support: creatine at five grams a day or more, which he describes as “a big deal, cheap as dirt”; magnesium, which he thinks nearly everyone under-takes; beta-hydroxybutyrate as mitochondrial fuel; and a group of ordinary nutrients — trehalose, zinc, vitamin D, inositol, and B vitamins — that he argues are difficult to reach through diet alone.
A caution on the doses. Some of the amounts discussed in this lecture are well above dietary levels — high enough to behave like medication rather than nutrition, with real effects on liver enzymes, blood glucose, and bleeding risk depending on the nutrient. Creatine at five grams daily is well studied and unremarkable for most healthy adults. Others in the list are not in that category, and the difference is not obvious from the outside. If you are on a statin, or living with diabetes, liver disease, gout, or a bleeding disorder, treat any high-dose supplement plan as a prescription-level decision made with your physician, not a shopping list.
The human data Dr. Goodenowe brings to the muscle question comes from a study conducted in Santa Monica and published in 2022: 22 participants, ages 37 to 84, given escalating monthly doses of plasmalogen precursors. Blood plasmalogen levels rose in proportion to dose, as expected. Cognition improved. But the finding he highlights is that physical mobility improved more than cognition did — chair-stand counts rising from 11 to 16, and 12 to 15, in participants with a clinical dementia rating of 2, which is moderate dementia rather than a borderline case.
The caveats here are substantial and worth stating plainly. Twenty-two participants is a small study; it was open-label, with no placebo group; and it was conducted by the company that makes the product. Independent reviewers have characterized it as preliminary and not a demonstration of benefit. It is also worth knowing that a larger placebo-controlled trial — 276 people with mild cognitive impairment or mild Alzheimer’s — found no significant cognitive benefit, though that study used a scallop-derived plasmalogen at roughly a thousandth of the dose used here, so it is not a direct contradiction so much as evidence that the field is unsettled. The mobility result is genuinely interesting precisely because nobody was looking for it. It is also exactly the kind of result that most needs a control group before it means much.
The last third of the lecture is Dr. Goodenowe demonstrating his own routine, and the point of it is achievability rather than ambition. “Your body is very, very lazy. It’s only going to do what you ask it to do. If you don’t ask it to do anything, it’s not going to do anything.” He owns dumbbells and nothing else.
Described in the webinar as what he personally does, not as a prescription. Start from where you actually are — and if you have a structural, cardiac, or bone-density concern, start with a practitioner instead.
His closing instruction is a reordering of priorities rather than a workout: “Don’t worry about how fat you are. Worry about your muscles. Worry about your biochemistry. Make sure that your blood work is right, make sure your inflammation is down, and make sure your diet is right. If you do those things, your weight will take care of itself.”
As with the rest of Dr. Goodenowe’s lectures, this one spans several different levels of evidence, and it is worth separating them. The associations between grip strength, muscle mass, bone density, cognition, and mortality are large observational epidemiology, well replicated, and not seriously disputed — though observational studies cannot settle which way the causation runs. The effect of resistance training on hip bone mineral density comes from controlled trials, short ones. The plasmalogen requirement for neuromuscular development rests on a rare human genetic disease and on animal models, both solid for what they show. The human protocol evidence is a small open-label study conducted by the company, and he says so.
That mixture is normal for a field in progress, and it is why this page points you to the full lecture rather than standing in for it — so you can see the slides, the citations, and the Q&A yourself, and take the parts that matter to you to your own physician.
Dr. Goodenowe presents the complete muscle and bone lecture — the full BMI and mortality analysis, the grip strength and skeletal muscle data, the osteoporosis and Alzheimer’s comparison, the leucine and niacin studies, his demonstrated routine, and an extended Q&A on body composition testing, vitamin D, weighted vests, and blood-flow restriction training.
Watch on DrGoodenowe.com ↗Opens in a new tab · Free to watch
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