In my odyssey of reading and writing about fat science I have stumbled on the new idea that the epidemic of obesity may be caused by eating too much protein. The low fat fiasco is well known and there are still a lot of experts on the it's-the-carbs-stupid bandwagon. But what if it's been the proteins all along? Wouldn't that be a kicker.
That's all there are, just those three possible food suspects in the crime of obesity - protein, fat, and carbohydrates. However only protein is necessary to prevent you from dying. You will die if you don't eat anything. But you could probably survive if you don't eat any fats or carbohydrates. Maybe that's why protein has been flying under the radar.
In this essay I try to cobble together and organize multiple of my substack articles about this idea.
Feeding muscles protein
“If you keep muscle healthy, you’ve got a good shot at avoiding obesity, avoiding diabetes, avoiding cancer, etc.” —Don Layman
Don Layman is an illustrious Food Science and Human Nutrition Department maven at the University of Illinois Urbana-Champaign. He sees the world of human welfare through the proteins in our bodies and diets. I recently listened to a Peter Attia podcast that interviewed him.
Firstly there are some nifty basic science things this podcast added to the background of protein nutrition.
How much protein you need to eat is apparently very hard to figure out and the recommended dietary allowances (RDAs) are based on gross approximations and then doubled just to be safe. Professor Laymen says that the building blocks of proteins in the body, the 21 amino acids, 9 of which are essential and have to be eaten because they can't be made by our metabolic chemistry, should be thought of as like vitamins. It's not just a matter of total protein. The body needs to have available every amino acid building block for a necessary protein or the body doesn't make that protein. He argues we probably need to eat more and better proteins than recommended. But I would quibble that since the RDA of protein is so sloppy and mysterious it could be that the converse is true.
He points out that all the proteins in the body are in constant flux and turnover. Why are proteins so fragile that we have to keep throwing them out and making new ones? Part of it is about reacting and adjusting to life's vicissitudes, I guess. He does not mention any estimates of the proportion of amino acids that derive from recycled proteins and how many have to be eaten because they are totally lost or disposed of. That may be a flux that is mostly unknowable but that would affect how much protein we need to be eating, in the absence of growing or being pregnant or losing blood etc..
Professor Layman said that all amino acids are originally made by bacteria. Some are made in the soil and are used by plants. But plant proteins may be deficient in some of the amino acids that animals are more made of. Animals either have to eat a wider variety of plants, that is inefficient and requires a lot of eating and disposing of the unnecessary redundant incomplete proteins or they have to eat other animals. Or coolest of all, they can brew the plants they eat in a bacterial soup in their stomachs, like cows do, to fortify the amino acid mix. This is called up-cycling. Ruminants are animals, mostly cows, that have this magical chemical factory in their stomachs which they also help by contemplatively regurgitating and chewing more. Turns out steaks and milk are highly processed foods. If bacteria were lost from God's earth so would be the rest of life.
Some amino acids, like leucine, are also signals, hormones, like insulin, that tell muscle cells when to take advantage of what we just ate.
Muscles are the biggest and most changeable reserve of protein in your body. Muscles like bone and brains and fat are built at an early age that can effect the rest of our lives. Even though the number of muscle cells don't change, their size can change through life. Exercise is the signal to make bigger muscles. Muscle mass is so important then not exercising is deadly. That's why little kids are always exercising insanely. Layman's bottom line is that if we take proper care of our muscles we'll be healthy.
So Layman's group has done multiple studies demonstrating his dietary prescription of increased dietary protein in weight loss diets. (2,3,4) They consistently demonstrate that high protein/low carb vs. high carb/low protein diets causes the same weight loss. But more importantly to his way of thinking higher protein relative intake caused more fat loss and less muscle loss.
Another of his groups findings is that there is more satiety when dieting which is to say eating fewer calories overall, with a higher protein percentage of calories. That would be expected to improve compliance and maintenance when trying to lose weight. One of their studies that added exercise to the mix showed that the exercise was additive for improving body composition.
How does this jibe with the protein-is-the-new-culprit idea? Well,.... I'm not sure. All of Layman et als. subjects were calorie restricted. What would happen if you ate too many calories at different protein/carb/fat ratios?
1. https://peterattiamd.com/donlayman/
2. Layman DK et al. A Moderate-Protein Diet Produces Sustained Weight Loss and Long-Term Changes in Body Composition and Blood Lipids in Obese Adults. The Journal of Nutrition, Volume 139, Issue 3, March 2009, Pages 514–521, https://doi.org/10.3945/jn.108.099440
3.Layman DK et al. A moderate-protein diet produces sustained weight loss and long-term changes in body composition and blood lipids in obese adults
J Nutr. 2009 Mar;139(3):514-21. doi: 10.3945/jn.108.099440. Epub 2009 Jan 21. PMID: 19158228 DOI: 10.3945/jn.108.099440
4. Layman DK et al.Dietary protein and exercise have additive effects on body composition during weight loss in adult women. J Nutr. 2005 Aug;135(8):1903-10. doi: 10.1093/jn/135.8.1903. PMID: 16046715 DOI: 10.1093/jn/135.8.1903
5. Ferraz-Bannitz R. Dietary Protein Restriction Improves Metabolic Dysfunction in Patients with Metabolic Syndrome in a Randomized, Controlled Trial.
Nutrients 2022, 14(13), 2670; https://doi.org/10.3390/nu14132670
Extra calories increase fat while extra proteins increase lean body tissue
In this study from 2012, head-authored by Dr. George Bray, a heavyweight in fat science, looked at the effect of overeating a diet containing 3 levels of protein content in a group of 25 normal weight volunteers who were brought into a controlled hospital setting for 10 weeks.(1)
First they established how many calories the volunteers were eating while their weight was stable for 2 weeks. That was about 2000 Calories. Then they were overfed by 40% which was about 1000 extra Calories per day for 8 weeks. There were 3 groups during this overfeeding phase. One group got 6% of their calories as protein, the low protein group. Group two got 15%, the normal protein group, and the third group got 26% of their intake as protein, the high protein group. The rest of their diets were fats and carbohydrates to make up the total increased calorie count. So the low protein group got more, and the high protein group got less, as carbohydrates and fats.
The low protein group gained only half as much weight as the other two groups, 6 1/2 lbs. vs 13 lbs., but all 3 groups gained the same amount of extra fat, 9 pounds. So the normal and high protein groups gained more weight proportionally, as lean body tissue and the low protein group lost some lean body tissue. The low protein group also had no increase in resting energy expenditure or total energy expenditure, while the normal protein and high protein groups increased their energy expenditure significantly. This part of the project was the stated finding of the study although the double weight gain in the high protein diet was the more amazing result to me.
This must mean that extra calories as protein are different from extra calories as carbs or fat. They increase your weight, your lean body tissue, and your energy expenditure. This also means that BMI is not very useful as a measure of what's going on and increased energy expenditure did not help for weight losing. The low protein group that lost weight had a lower energy expenditure.
So pretty counter intuitive, right? I wonder how long they would have kept gaining weight. The fat weight gain was still steeply upward while the lean body mass was plateauing for all all protein intakes by the end of the 8 weeks. So would they have gained even more weight with more time. Or would they have just gotten sick and refused to keep eating the excess calories? Since they adjusted the carbs and fats to make up the difference between the 3 different protein groups to maintain the Calorie intakes the same, maybe that's all that matters rather than the proteins. But eating more carbohydrates and fats didn't cause any more fat gain. These authors extrapolate that we're all eating too much because there's this obesity epidemic thing. But in the real world our weights are stable for long periods. So maybe not so fast.
In an editorials about Dr. Brays study two experts from Los Angeles, California seem to be missing the evidence here. (2) They say standard things like,
"This study demonstrates how low protein foods with hidden sugars or fats may be contributing to the obesity epidemic. Sugars such as sucrose, fructose, and high fructose corn syrup are converted efficiently to fat with calorie excess. Carbohydrates and protein elicit different signaling pathways for muscle and fat cells. Therefore, when individuals consume excess carbohydrates out of proportion to protein, the body may gain less weight than when protein is consumed in adequate amounts. The study by Bray et al demonstrated that the lesser added weight consists largely of fat mass rather than lean body mass when excess calories were the same. Moreover, added fat calories (including hidden fat in processed foods) consumed in excess will also lead to weight gain contributing to the obesity epidemic."
Ok the high protein group gained less relative fat since they also made more lean body mass but they put on just as much fat. Eating more protein also increased energy metabolism so they were burning up calories faster. But they put on just as much fat. Maybe the fat distribution was better - smaller bellies - but that was not looked at.
I think the message might be - we should eat less protein. Sugar and fat are not to blame here. They didn't make anybody more fat in total.
These editorialists did make one more valid point, and another report and editorial in this same issue of JAMA (3,4) also showed, that BMI is not telling you what is going on in terms of weight and fat gain.
1.Bray GA, et al. Effect of dietary protein content on weight gain, energy expenditure, and body composition during overeating. JAMA 2012;307(1):47-55
2. Li Z,Heber D. Overeating and Overweight. Extra Calories Increase Fat Mass While Protein Increases Lean Mass and Overweight. JAMA. 2012;307(1):86-87. doi:10.1001/jama.2011.1959
3. Sjöström L et al. Bariatric Surgery and Long-term Cardiovascular Events. JAMA. 2012;307(1):56-65. doi:10.1001/jama.2011.1914
4. Livingston EH. Inadequacy of BMI as an Indicator for Bariatric Surgery. JAMA. 2012;307(1):88-89. doi:10.1001/jama.2011.1950
Methionine restriction causes weight loss in mice
Everybody has been talking about the new fad of intermittent fasting that might have some of the benefits of calorie restriction on longevity and good health without the pain of being hungry all the time, just part of the time. But that part of the time is still hard. Could there be an even better way? How does this form of torture work? Methionine restriction might be at least part of the answer to these questions.
Methionine is almost always the first amino acid in the chain of amino acids that make up all the proteins in your body. The protein making machinery does not even start if there is no methionine available. It is one of the essential amino acids that you can't make from scratch. So it has to come from what you eat. That means you can't remove methionine totally from your diet or you will die. Methionine is also one of the two amino acids, together with cysteine (cysteine is not an essentially amino acid), that contains sulfur. It has been observed, in the short term at least, that removal of only methionine from the diet can reverse diet-induced obesity and promote insulin sensitivity in mice. Methionine restriction also protects mouse models from obesity and diabetes.
A recent report shows some of how this works and some of how it probably doesn't work in mice. (1) The data shows that wild type male mice who are induced to be obese by a high fat diet and who are then fed a methionine restricted diet lost 45% of their body weight. Otherwise similar mice continued without methionine restriction gained 8% at 8 weeks after stopping the high fat diet. They also repeated the experiment with the same results in mice with genetic manipulations that prevented the rise of adiponectin and fibroblast growth factor 21 that was seen during methionine restriction. So these were two things that were not causal factors in this process.
It was also seen that methionine restriction promotes a futile lipid cycle and apoptosis and autophagy in fat and other body tissues.
-Futile lipid cycle means that calories are burned without making energy that can be used in the body apart from simply heat production. This happens in brown fat. This is a way for animals to stay warm.
-Apoptosis is the programmed death of cells.
-Autophagy is the process of getting rid of some of a cell's internal structures to conserve energy and to trigger the rebuilding of new proteins.
Methionine restriction extends lifespan and health-span across different species. The same benefits we saw with calorie restriction and intermittent fasting.
If you kids want to try this at home most fruits and vegetables contain very little methionine. Beef has the highest content of methionine at 0.680 g/100 g. Poultry, lamb, veal, game, finfish, shellfish, pork, dairy and egg all contained more than 0.4 g/100 g. Most legumes, though protein dense, are lower in methionine. (2) Maybe those vegan diet eaters are on to something. But in practice it is very hard to deeply restrict methionine by itself without restricting all protein because it is everywhere.
1. Cooke D. et al. Weight Loss and Concomitant Adipose Autophagy in Methionine‐Restricted Obese Mice is Not Dependent on Adiponectin or FGF21. Obesity April 20,2020. https://doi.org/10.1002/oby.22763
2. Ables GP, Johnson JE. Pleiotropic responses to methionine restriction. Experimental Gerontology 2017;94:83-8. https://doi.org/10.1016/j.exger.2017.01.012
Rabbit starvation
At the meeting of the American Society of Bariatric Physicians (ASBP) in 2006 there was a lot of talk about the low or no carbohydrate diet. There is a group of evangelists dedicated to this proposition and they have a professional organization called the Nutrition and Metabolism Society that coordinated their symposium with this annual ASBP one. Their point of view, made famous by Atkins, says that carbohydrates are poison and the root of all evil in our diets and responsible for the epidemic of obesity that we are having. There is actually some merit in what they are preaching and we've talked about the pros and cons of this idea in many previous columns but one thing that they have shown definitively is that you can survive and do just fine, aside from craving carbs if you lose weight, eating no or very little carbohydrate. They've also convinced us that a low fat diet is not so great, especially if you eat more carbohydrates instead.
There are certain fatty acids called essential fatty acids that cannot be made in the human body and so these fatty acids are like essential amino acids or vitamins. Essential fatty acid deficiency can cause rashes and there have been a lot of other things attributed to essential fatty acid deficiency but it is not really clear how dangerous it would be to eat no fat forever. Anyway you could survive eating just a little of the essential fatty acids, like taking a fatty acid supplement pill that represents a tiny portion of your total calorie intake.
We also know you cannot survive without eating any protein. That's called kwashiorkor. Even if you're not a growing child or recovering from surgery, there is a certain amount of indispensable turnover and repair that goes on. But it requires a surprisingly tiny and unknowable bit of protein in the diet to replace.
What about staying away from that whole hornet's nest of carbohydrates and fat and eating just protein? There are some weight loss diets and there were some speakers who were pushing diets that provide way more protein. People with bad kidneys have to eat a low protein diet because it strains their kidneys further and we know that if you have normal kidneys they will swell to accommodate a high protein diet but you seem to remain otherwise healthy.
Then there is a thing called rabbit starvation that is said to arise if you eat nothing but rabbits which have hardly any fat in their bodies. This disease comes from hoary tales of wilderness expeditions where people had nothing but rabbits or other lean meat to eat for prolonged periods and apparently got sick and died of it. Some authorities say that you should not eat more than 35% of your calories as protein. (1) Other authorities do not mention an upper limit of protein proportion in the diet or a maximal load of protein that can be tolerated. The issue remains unclear but I would not recommend eating only protein.
1. Bilsborough, Shane; Neil Mann (2006). "A Review of Issues of Dietary Protein Intake in Humans". International Journal of Sport Nutrition and Exercise Metabolism (16): 129-152.
Eureka
This revelation came to me from David Allison's ObesityandEnergetics.org listserv (July 29, 2022). I plagiarize it for you by the brute force cut and paste of the reference and abstract. You should read the entire article which I have cast in bronze and put on my mantel.
"Dietary Protein Restriction Improves Metabolic Dysfunction in Patients with Metabolic Syndrome in a Randomized, Controlled Trial
by Rafael Ferraz-Bannitz
Nutrients 2022, 14(13), 2670; https://doi.org/10.3390/nu14132670
Abstract
Dietary restriction (DR) reduces adiposity and improves metabolism in patients with one or more symptoms of metabolic syndrome. Nonetheless, it remains elusive whether the benefits of DR in humans are mediated by calorie or nutrient restriction. This study was conducted to determine whether isocaloric dietary protein restriction is sufficient to confer the beneficial effects of dietary restriction in patients with metabolic syndrome. We performed a prospective, randomized controlled dietary intervention under constant nutritional and medical supervision. Twenty-one individuals diagnosed with metabolic syndrome were randomly assigned for caloric restriction (CR; n = 11, diet of 1420 ± i64 Calories per day) or isocaloric dietary protein restriction (PR; n = 10, diet of 2010 ± 564 Calories per day)+ and followed for 27 days. Like CR, PR promoted weight loss due to a reduction in adiposity, which was associated with reductions in blood glucose, lipid levels, and blood pressure. More strikingly, both CR and PR improved insulin sensitivity by 62.3% and 93.2%, respectively, after treatment. Fecal microbiome diversity was not affected by the interventions... Protein restriction is sufficient to confer almost the same clinical outcomes as calorie restriction without the need for a reduction in calorie intake. The isocaloric characteristic of the PR intervention makes this approach a more attractive and less drastic dietary strategy in clinical settings and has more significant potential to be used as adjuvant therapy for people with metabolic syndrome."
Professor Allison, me, some Brazilians, and now you are among the first to know about this. So far I haven't seen breaking headlines on CNN or in the New York Times that say, "Stop eating so much protein!" and "Excess protein eating is the cause of obesity!" and "New weight loss miracle without starvation!."
Obesity Risk of infant formula
The nefarious operation on our shape of eating too much protein might start early in life. Could lower protein intake possibly prevent childhood obesity? That is the contention of some authors from Amsterdam. Their recent report (1) finds that the increased protein in baby formula compared to breast milk may be a smoking gun.(Why do they have to write in English. They must resent that.)
It is widely acclaimed that breast milk is the best way to feed babies. But I thought that among the benefits of breast milk cited by these authors, prevention of obesity was a largely discredited idea. I'll have to go back and rehash that argument again later. But the observation that cow's milk based formulas have higher protein, and so proportionally less fat and sugar, and the fact that the protein concentration in breast milk decreases over the weeks of lactation, while the protein concentration of infant formulas obviously remains constant, make you wonder what God intended. It has been shown that protein intake during the first 6 months of life is up to 66–70% higher in formula-fed infants compared to breastfed infants.
It has also been reported that premature babies fed fortified formula, fortified with both protein and calories, does result in faster weight and head circumference gains during the first and second year of life. Premature babies are the ones we want to gain the most weight. However there is evidence that even though they grow faster on fortified formulas they eat less of it and so they don't actually eat more calories, just more protein. Or it could be that eating more concentrated calories saves on the energy of eating.
Whether or not breast feeding really prevents obesity this contention about protein remains contentious. Among the problems are the fact that the studies are short term. Will it lower the rates of obesity in adults to feed them lower protein as infants? Exclusive breast or formula feeding mostly only happens before 6 months of age. After that the diets of kids get way more complicated and uncontrollable. Will this tiny window of opportunity really make that much difference? We really have to be careful manipulating the diets if innocent tiny babies, as opposed to the huge uncontrolled experiment foisted on us all since baby formula feeding became popular in the 1950s. Back in the really olden days if you couldn't breast feed or if you were rich, you got a wet nurse for your baby. That must have been some kind of slavery to be a wet nurse.
In 1988 The American Academy of Pediatrics (AAP), being American, had promulgated that the weight gain rate is the single most valuable component of the clinical evaluation of infant formula. We have traditionally esteemed weight gain in babies. However, the higher weight gain rate in formula-fed infants during the first months of life compared to breastfed infants might be the cause of higher weight-for-length, BMI, and obesity risk in later life. Therefore, it might be desirable to lower the weight gain rate of formula-fed infants. And there is movement afoot in Europe to recommend lower protein in formula to do that.
Or you might just avoid his whole sticky wicket and breast feed your babies. There are lots of other good reasons to breast feed - it’s cheaper - it’s easier - it’s more fun… They discuss lots more intriguing aspects of these questions in this very readable article. Find it and read it.
1. Kouwenhoven SMP, Muts J, Finken MJJ, Goudoever JBV. Low-Protein Infant Formula and Obesity Risk. Nutrients. 2022 Jun 30;14(13):2728. doi: 10.3390/nu14132728. PMID: 35807908; PMCID: PMC9268498.
Protein leverage
There is this thing, called the protein leverage hypothesis, that is being examined as a possible contributor to our obesity epidemic. Protein leverage is the innate drive to eat more if you are not getting enough protein. Your body needs protein to grow and repair. So if the diet is lacking in good protein, that is a complete protein with all the essential amino acids that are the building blocks of protein, then you are hungry to keep eating more stuff and more total calories. It is protein hunger, like hunger in general and thirst. An example of the understanding of this sort of thing is the folklore about how pregnant women want to eat strange things, even dirt, in order to get certain vitamins and minerals that they must be lacking in order to feed the cookie monster in their uterus.
The terms “protein leverage” (PL) and the “protein leverage hypothesis” (PLH) were invented in 2005 and these ideas were reviewed by the inventors of those terms in the journal Obesity in August of 2019. (2) They explored some of the implications of this thing as a possible cause of the obesity epidemic. It has been shown that all kinds of animals have a drive to keep eating whatever is available to them in order to get enough protein. Part and parcel of this idea is that they may wind up over eating certain things that they will need to get rid of or waste.
It has indeed been shown that free range humans eat more calories when they eat less protein. From 1961 through 2013 as we were experiencing the obesity epidemic we were eating more calories but about the same amount of protein. But since we need only very little dietary protein, unless we are growing or pregnant or recuperating from surgery or trauma, why would we be so hungry for protein? But if the protein as a percentage of total calorie intake goes down, maybe that hunger of protein leverage still drives. But if you do more math it still can't explain all of the increase in obesity. It's complicated. For more analysis using differential equations and further commentary and further discussion see 3,4,5.
It would seem that the best candidates for examining the protein leverage hypothesis would be in children who are growing and need the most protein. An investigation of the protein hypothesis was done and published in February, 2023, by Christoph Saner and colleagues examining kids in Finland. They carefully found that their kids did eat ate more calories if they ate less protein as a proportion of their total calorie intake, but those extra calories did not correlate at all with their shape. "Increased energy intake on diets with lower protein content was counterbalanced by increased energy expenditure and therefore did not translate into increased adiposity." (6)
They forgot or neglected to conjecture about that amazing fact. Why or how do they think that eating more calories but less protein makes them burn more calories? But that won't inhibit me from wildly surmising. Maybe it has to do with the autophagy thing whereby you recycle your own proteins if you eat less proteins and that costs more energy. Furthermore that contradicts Layman. Remember he said more protein causes more energy expenditure. Maybe it's a different thing in kids.
They did conjecture however, contrary to their own evidence, that children and adolescents who are chronically exposed to a diet containing high quantities of ultra-processed foods could still be more adipose by the protein leverage thing. I think they say that because Finns are not as obese as the rest of the world and eat a more healthy diet. Perhaps they are not the best ones to test the ultra-processed food liability on.
1. https://conscienhealth.org/2019/07/protein-leverage-coming-at-us/
2. Raubenheimer D, Simpson SJ. Protein Leverage: Theoretical Foundations and Ten Points of Clarification. Obesity. 2019;27(8):1225-38.
3. 4. Hall K D. The Potential Role of Protein Leverage in the US Obesity Epidemic Obesity 2019;27(8):1222-4.
4. Hill CM, Morrison CD. The Protein Leverage Hypothesis: A 2019 Update for Obesity Obesity. 2019;27(8):1221.
5. https://qz.com/1669418/the-problem-with-americas-protein-diet-obsession/
6. Saner, C. et al. Evidence for protein leverage in a general population sample of children and adolescents. Eur J Clin Nutr (2023). https://doi.org/10.1038/s41430-023-01276-w
High carb diet makes mice live longer
It's going to upset people on the low-carb bandwagon but recent evidence shows that high carb diets can make you live longer, maybe even longer than calorie restriction.
Calorie restriction (CR), eating less of every kind of calorie, improves cardiometabolic risk factors, generic hallmarks of aging, brain function and makes all kinds of animals live longer. But being hungry all the time is one of the few things that are worse than death. We need to find a better way to get those benefits.
Mice consuming a low-protein, high-carbohydrate, low-fat diet (LPHC, protein/carbohydrate ratio ~1/10) lived longest and were healthier in old age, even when compared to calorie restriction achieved by dilution of chow with non-digestible no calorie fiber. The beneficial effects of LPHC diets on lifespan are conserved across a range of organisms from invertebrates to mice. The observation that eating as much as you want of this diet is beneficial for lifespan and late-in-life cardiometabolic health suggest that it may also delay brain aging. (1)
Lean body mass and overall body mass was the same in both diets but body fat was lower in the CR diet. Insulin metabolism and cholesterol was the same. Fibroblast Growth Factor 21 is a regulator of energy metabolism in the liver and fat tissue. It was much higher in the most protein restricted diet.
It seems like protein is the poison. The lowest percentage of protein, along with plenty of carbs works the best. There is a high protein bandwagon that's going to be upset with this information.
Looking at what genes are regulated up or down by these diet manipulations will help us zero in on the mechanisms of these observations. A very low-protein, high-carbohydrate diet may be a more feasible nutritional intervention to delay brain aging than hunger. Maybe it's not how much you eat but what you eat after all. But it won't fix your body shape.
You have to eat some protein because your body, besides water, is mostly made of protein. But not very much.
1. Wahl D. et al. Comparing the Effects of Low-Protein and High-Carbohydrate Diets and Caloric Restriction on Brain Aging in Mice. Cell Reports 2018;25(8):2234-43. https://doi.org/10.1016/j.celrep.2018.10.070
Measuring protein
Remember the protein Alamo? I snatched two articles from OES (1) that add two more wrinkles to the protein problem. The first one is well written and understandable that explains important basic science about how the standard published protein content estimates of our food is highly inaccurate. It actually contributes a quarter to a third of its wrongness. (2) So there's that. When you remember the other black box - that proteins can be burned as calories or recycled by processing old worn out proteins into making new proteins according the availability of proteins and carbs and fats in the diet we are in a state of major obfuscation. How objective are quantitative measures and any recommendations about food protein? Signifying nothing.
The second article sensationally and alarmingly proclaims that, "Given the long-term association between height and phenotypic IQ, the lower quality of nutrients in children’s diet may also seriously affect intellectual potential and future civilizational development. In light of these findings, current nutritional strategies should be seriously reconsidered and recommended protein intakes for children must be urgently reevaluated." (3)
This single author hangs this momentous emergency on the FAOSTAT database, which abbreviation I had to google. It's the Food and Agricultural Organization of the United Nations. He does explain, "These statistics are computed by combining the total quantity of foodstuffs produced in each country with the total quantity imported and are further adjusted to the quantities exported, fed to livestock, used for seed, put into manufacturing for food use and non-food uses, and losses during storage and transportation. The obtained amount of each food item that is actually available for human consumption is then divided by the country’s population......." He concedes there are many, numerous, uncountable by me..., potential inaccuracies like it doesn't count wasted food. He explains many reasons why we should be able to trust this basis before he comes to the dire conclusion that we are killing ourselves by not eating enough protein.
There are way too many weeds in this jungle and my machete is getting dull and I'm tired. But I'm skeptical.
1. Dr David Allison et al. Obesity and Energetics Offerings list serve. https://obesityandenergetics.org/subscription
2. Pferdmenges, L. E., Colombani, P. C., Hauger Carlsen, M., Pajari, A. M., Poulsen, A., Dias, M. G., … Schweiggert-Weisz, U. (2025). Toward harmonizing protein data in food composition databases: evaluating perspectives, methods and implications. Critical Reviews in Food Science and Nutrition, 1–14. https://doi.org/10.1080/10408398.2025.2503461
3. Grasgruber, P. (2025). Back to the pre-industrial age? FAOSTAT statistics of food supply reveal radical dietary changes accompanied by declining body height, rising obesity rates, and declining phenotypic IQ in affluent Western countries. Annals of Medicine, 57(1). https://doi.org/10.1080/07853890.2025.2514073
The heartbreak of sarcopenia
Now that I am old I need to wrap my head around one more part of the protein problem before I die.
Of the multiple insults to you as you get older perhaps the worst is that your muscles fade away. Muscle mass loss is called sarcopenia from the ancient Greek for "poverty of flesh." The German word "fleisch" means meat. So sarcopenia is loss of muscle. While you can slow the speed and details of sarcopenia with exercise it is still inexorable. You might have already noticed the difference between the motors of kids and the old people who sometime have to babysit them. Being sick and bedridden and flying in space are other causes of sarcopenia.
Given that most men and women gain weight from age 25 years to 65, it is apparent that they must be replacing muscle with fat. Under conditions where there is loss of muscle, total body weight will not be telling you what is happening to body composition.
Sarcopenia affects the ability to lead an active lifestyle but also contributes to reduced quality of life, osteoporosis, and worsening metabolic health. And it goes both ways, these things also contribute to sarcopenia. A recent review of these issues discussed some of the implications that sarcopenia has for the development of obesity and the other indignities of aging. (1)
Besides the decrease in exercise energy expenditure, the loss of muscles leads to decreases in the two major components of the energy expended by our bodies. There is resting energy expenditure (REE) the energy expended by doing nothing. REE is the majority of expended energy. It is decreased by loss of muscle mass. Then there is non-exercise activity thermogenesis (NEAT), the energy expended for everything we do that is not sleeping, eating or sports exercise. It ranges from the energy expended walking to work, typing, performing yard work, undertaking agricultural tasks and fidgeting. Even trivial physical activities increase metabolic rate substantially. It is the cumulative impact of a multitude of actions that add up to an individual's daily NEAT. So NEAT explains a vast majority of an individual's non-resting energy needs. Brain centers have been identified that specifically and directly increase NEAT in animals. By understanding how NEAT is regulated we may come to appreciate that spontaneous physical activity is not spontaneous at all but carefully programmed.
People have two general types of skeletal muscle fibers. Skeletal muscles are the muscles attached to bones as opposed to the heart muscle and the muscles in your intestines called smooth muscles. The 2 types of skeletal muscles are: slow-twitch (type I) and fast-twitch (type II). Slow-twitch muscles are for long-endurance feats such as distance running, while fast-twitch muscles get tired faster but are used in powerful bursts of movements like sprinting. Depending on the parts of your body and what kind of an athlete you are, you generally have about 50-50% type I and type II skeletal muscle fibers. With aging we seem to lose more type II than type I muscles. Aerobic exercise (running) may improve this relative shift of type II to type I and it uses 2-3 times more calories for any given time spent and it is better for maintaining metabolic health which means reduced oxidative stress and inflammation, increased insulin sensitivity, decrease in blood pressure, and improved blood lipid profile. That, in turn, strongly and independently increases longevity. But only resistance training (weight lifting) can increase skeletal muscle mass and slow (but not stop) the loss of muscle as we age.
It is the contention of these authors that "the combination of aerobic and resistance training will slow sarcopenia development, decrease fat mass accretion (especially the harmful visceral fat), and decrease the risk of developing a number of metabolic diseases throughout the lifespan." But you're still going to get sarcopenic and forgetful and old.
1. Hunter GR et al. Sarcopenia and Its Implications for Metabolic Health. J Obes. 2019; 2019: 8031705. Published online 2019 Mar 6. doi: 10.1155/2019/8031705
Why do we lose muscle strength as we age?
A new article with this title by Peter Attia reviews the 4 reasons we lose muscle power as we age. (1)
1. We lose total muscle mass.
2. The muscles we do have get weaker. That is they are weaker to a greater degree than explained by the loss of muscle mass. There is degradation of the mitochondria, the respiratory energy sources inside of the cells, and the moving parts of muscle fibers gum up to some extent.
3. There is a decrease in type 2 fibers relative to type 1 as mentioned above.
4. Another reason the muscle fibers we do keep get weaker is the deterioration of the nerve connections that signal the muscles to contract. Those nerve connections are constantly remodeling throughout life according to the amount of use the muscles get.
This last one, number 4, is the only one we can influence by exercising. "In particular, endurance and power training appear to contribute significantly to neuromuscular remodeling, and data from life-long athletes indicate that regular exercise in our later years is effective in improving muscle strength and function."
But there is a fifth cause of sarcopenia, aching joints that cause loss of ease and efficiency of movements that also further conspires to decrease NEAT in old people and make them relatively fatter even if they lose weight.
My knees and back hurt and it's making it even less fun for me to run.
1. https://peterattiamd.com/why-do-we-lose-muscle-strength-with-age/
What about eating more protein?
Not so helpful according to this summary of the evidence from a meta-analysis of studies assessing the effects of protein supplementation combined with resistance training on body composition and muscle strength in the older population. (1)
Protein supplementation associated with resistance training induces greater increases in lean body mass compared with resistance training alone. But, it is suggested that the use of protein supplementation enhances gains in muscle mass but does not promote greater increases in muscle strength.
In one of the studies that contributed to the meta-analysis (2) there was no change in weight, a little increase in fat free mass (not all of that weight is muscle), and a little decrease in fat mass, with the high protein diet plus exercise compared to less protein plus exercise. But the changes were small.
Eating more protein is overrated.
1. Vieira, A.F., Santos, J.S., Costa, R.R. et al. Effects of Protein Supplementation Associated with Resistance Training on Body Composition and Muscle Strength in Older Adults: A Systematic Review of Systematic Reviews with Meta-analyses. Sports Med (2022). https://doi.org/10.1007/s40279-022-01704-0
2. Campbell, W.W., et al., Effects of resistance training and dietary protein intake on protein metabolism in older adults. Aging, 2(9), pp.10-19.
The protein eating debate
There is a roiling debate these days about the benefit versus harm of increasing protein in our diets. I am a lurking participant in this debate. Here are three articles debating this not including me.
I guess the first issue to sort out is that benefits and harms are two different things. But if there is benefit to eating a higher protein diet, then not eating more protein is harmful and conversely, or it just doesn’t matter either way.
The first article, French SJ et al. (et Allison DB) that is also cited by Peter Attia who explicitly thanks Dr. Allison, is about the woeful lack of evidence for any harm in eating too much protein. Their bottom line review of 74 references is that there is plausibility but not adequately demonstrated evidence in the case of harm to diabetics and implausible evidence in the case of shortening longevity or increasing mortality from eating a surfeit of protein. So this article is only about the harms of a higher than whatever amount of protein eating, not benefits.
Then there’s Peter Attia’s entry into this fray in his weekly email newsletter of August 23, 2025. He is an important pro-mucho mas-protein popularizer. He starts out like everybody else explaining how the RDA (recommended daily allowance) of 0.8 mg/kg of protein intake based on nitrogen equilibrium - the intake where nitrogen in equals nitrogen out - is bunk. He makes the estimable plea of using hard science to answer these questions. I don’t think there is presently as much attack on high protein diets and supplements as there is a popular craze. Though he says this trend has prompted some backlash, “the sheer variety of protein-fortified foods that have made their way onto grocery store shelves attests to the growing number of individuals seeking to increase their intake of this macronutrient.” But it could be bunk too that “..the data reveal that the majority of Americans are not achieving a level of intake that would best facilitate muscle mass gain and optimize health.”
Thirdly there was Eric Topol’s substack article of August 31, 2025 counter to one and two above. Eric Topol MD deservedly has 186,000 subscribers to his substack Ground Truths while there are 20 non-paying subscribers to fat science. He strives to answer 3 questions:
1. What is driving the protein obsession? He quotes The New York Times’ Daily podcast, “How America Got Obsessed With Protein” on this.
2. What are the data for high protein intake health benefits? For this he “pulled together all the published meta-analyses and systematic reviews that I could find on the topic of high protein intake” which was 5 of them. And “Simply put, there are no data to support more than 1.6 g/kg/day of protein.” Which is 2 times the RDA we mentioned above.
3. What are the safety concerns regarding high protein consumption? Concerns yes, but it’s epidemiological and theoretically plausible but not proven as per David Allison et al above. But David Allison is a notorious stickler, devil’s advocate, nay sometimes almost quibbler.
In his concluding remarks Dr. Topol points out that there is no way to store protein in the body like you can store fat and a few hours worth of glycogen. Any protein you don’t use that day to repair or build your body is burnt for energy and the nitrogen has to be processed and peed out. In a way he is right even though your body, except for the more than half that is water, is mostly made out of protein. That’s where the whole autophagy benefit comes in.
Pop quiz - how do I come down on this whole sticky wicket.
1. French SJ et al. The harms of high protein intake: conjectured, postulated, claimed, and presumed, but shown? The Am. J. of Clinical Nutrition. 122(2025) 9-16. https://dot.org/10.1016/ajncnut.2025.05.003
2. https://peterattiamd.com/determining-optimal-protein-intake/
3. https://erictopol.substack.com/p/our-preoccupation-with-protein-intake
Precarious proteins
Life is a crapshoot. It’s a miracle that life, which in it’s simplest form, that is the lives of single celled bacteria, is impossibly complicated. So much can and often does go wrong.
For those of you who may have forgotten what happened billions of years ago, bacteria figured out how to stay alive, grow and reproduce about one billion years after the sun and the earth came into existence around 5 billion years ago. Those single celled bacterial animalcules then some how managed to survive and proliferate for a billion years despite tumultuous bombardment by asteroids, toxic solar radiation, world wide volcanic activity, total frozen earth snowball ice ages and no oxygen in the atmosphere. Incredibly they did cling to life all alone but together. Along the way these single celled troopers managed to invent photosynthesis, another still not fundamentally understood mess of inefficient metabolic machinery that makes sugar and oxygen out of CO2 from the air and light energy from the sun and water. Then they got the idea of banding together into eukaryotes and then multicellular creatures. Eukaryotes have organelles, tiny organs, like a nucleus, that separates the genetic machinery of DNA, instead of just letting the DNA float around free-range in the cell. Two other organelles, the mitochondria that have the energy machinery of the and the chloroplasts that specialized in photosynthesis. The mitochondria and the chloroplasts have their own DNA. This specializing of organelles within each cell is called symbiosis. Finally after that “boring” billion years the symbiosis trick developed into multicellular plants and animals like us. That happened just a blink of the eye - a half a billion years - ago.
This symbiosis tactic is like an ant colony or a bee hive where organelles/single cells/organs/ant colonies/human societies/computers/the internet.... kept generalizing the same pattern of ever more complicated specialized structures that in turn lead to emergent characteristics that could not have been predicted from the underlying basic building blocks but in retrospect seem inevitable. First it happens slow and then it happens faster and faster and ever more miraculously and surprisingly.....
According to an essay (1) I found on obesityandenergetics.org we added a further jeopardy to our lives by deciding to mostly relinquish the cost of making most of the the 20 amino acid building blocks of proteins. These amino acids are called essential amino acids because we have to eat other life forms who can make them, to survive. This situation seems to have happened all at once when multicellular animals first evolved during the Cambrian explosion one half billion years ago as I mentioned. How foolhardy was that? Proteins are kind of important to us. Why let that capability of making the building blocks of proteins go and decide to just mooch off of the single celled bacteria that predated us. Why did God let us get away with such irresponsible behavior? Somehow, at least so far, we seem to be doing just fine. Benjamin Pickard of Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow U.K. speculates on the origin of the this essential amino acid making delinquency, and what this means for us animals.
The essential amino acids that we can’t make for ourselves are valine, isoleucine, leucine, lysine, histidine, methionine, phenylalanine, tryptophan, and threonine. Some animals also lack the ability to make a tenth amino acid, arginine. A further six, the conditionally essential amino acids, can be synthesized by us but, in times of stress, proliferation, development, or illness, these will also require dietary supplementation. So effectively only five, a quarter of the twenty, are non-essential amino acids that can be adequately provided through onboard biosynthesis. This phenomenon has been nicknamed the “Great Genome Deletion.” So the first question confronted is, why these particular amino acids? The simplest answer is that we are all descended from a single cell that became the ancestor of multicellular organisms because there do exist a very few single celled species that have these very same deficits in amino acid making ability. But did they happen all at once? These are multiple pieces of machinery that require multiple disparate genes. Are these the hardest amino acids to make? Do they require the most energy?
Just as all your proteins are made from 20 amino acids, all of your genes are made from just 5 nucleotides. In DNA just four, abreviated A,T,G,and C and in RNA U substitutes T. So those are the only letters in the language of genes. It is widely seen that often just one wrong substitution of a single letter in these small respective alphabets can be very impactful/disastrous. Professor Pickard points out some patterns in the collection of essential vs nonessential amino acids and their gene nucleotide bases that could have happened by just a few mishaps or starvation of just a few amino acids or nucleotides in the lives of the founder of all multicellular life forms. That’s his first possible hypothesis.
His second hypothesis is, “Ultimately, however, it is an organism’s behavioral responses to amino acid shortage that dictate survival. Most immediate is the organism’s need to actively seek out food sources.” So the essential amino acid composition of proteins in multicellular beings has evolved to integrate with hunger and reproductive physiology. More important and immediate to cheating death is getting enough energy. But tagging along with those most pressing hungers is getting enough of everything else - water, minerals, amino acids... whose lack will also eventually kill you and your species. Pickard presents evidence that key protein regulators of hunger and reproductive physiology have gained functional sensitivity to the essential amino acid nutritional state by evolving sequences enriched in those essential amino acids.
Is there any pattern in the gross numbers of amino acids used by bacteria vs eukaryotes?
On the other hand, why make any amino acids? Why not just eat them all?
In addition to the risky business of outsourcing essential amino acid production are multifarious other cop outs like energy production and multiple vitamins and, in the special particular case of us humans, developing extravagantly expensive big brains. But God takes care of the birds of the air and the lilies of the field.
1. Pickard BS. Five hundred million years of hunger: how animals evolved to survive essential amino acid scarcity. Emerg Top Life Sci 24 December 2025; 9 (6): ETLS20253009. doi: https://doi.org/10.1042/ETLS20253009