"Has it backwards"... What? No, absolutely not. Fasting absolutely eats muscle. Your body requires EAAs to function and they come mostly from skeletal muscle when dietary intake is inadequate. Oliver Owen did the classic fasting research on this and found that 21 days of fasting in obese men led to half of their weight loss coming from lean mass, of which 60% was structural protein (PMID: 9665093). And yes, his research showed it takes about 5 days for protein sparing mechanisms to kick in (see first image), but even at max capacity your skeletal muscle is never "protected" or "spared" in the sense that you can prevent muscle loss. And muscle loss is substantially worse the leaner you get. Abdul Dulloo did a lot of work on this with data from the Minnesota Starvation Experiment and others, finding that the ratio of protein losses to non-protein losses increase exponentially with lower levels of body fat (PMID: 10673906; see second image). Another study observed the same thing and found that protein contributed 2-3 times more energy in normal weight vs obese adults during prolonged fasting (PMID: 10574520). In fact, they didn't even really observe an adaptation in normal weight people like they saw with obese people, with oxidation being consistent for up to a month of fasting.

I'm highly skeptical of this finding. Need to see the full-text when published, but a few issues pop out to me based on the conference abstract (screenshots included for convenience). First, how is reverse causality accounted for? One of the primary indications for TRT in women is sexual dysfunction, and a 2024 meta-analysis of nearly 150,000 participants found that cardiovascular diseases are themselves associated with sexual dysfunction in women (PMID: 38297501). Second, what was the testosterone exposure? There's no info about formulations, doses, duration of treatment, serum levels, etc. Third, composite cardiovascular events increases statistical power to detect differences between groups, but they aren't interchangeable. This isn't necessarily a bad thing, but I'd want to see the individual outcome rates and whether any association was driven by less severe diagnoses. Fourth, how is surveillance bias accounted for? Women on hormone therapy are more likely to be part of the medical system than those not receiving it, so the likelihood of documenting something is higher by this alone. Fifth, what is going on with their data table? There were supposedly 3164 women in each group (testosterone vs control), but in the second row, 305 events at 3.2% would be over 9,000 participants in the group. Maybe they meant to put 105. Could just be a simple error. Anyway, these are just some things off the top of my head. Might be more. Sucks that such findings can make the rounds and strike unnecessary fear before any meaningful review of their study is even possible.

I'm disappointed to see Speth publish a piece on rabbit starvation with so little empirical evidence investigating the issue (DOI: 10.1016/j.qeh.2026.100120). I've written about the upper limit to protein metabolism, which I'll ink to in a follow-up comment, and the available evidence indicates that no such upper limit has yet been found. In fact, no limit is observed even at doses of amino acid infusions that cause participants to vomit. Speth, to my surprise, relies on the old Bilsborough and Mann 2006 review which itself relies exclusively on an old 1973 publication by Rudman, who himself later acknowledged his study was properly designed to test the concept. As such, Speth makes bogus claims like the upper limit being about 300 grams per day, and then further puts the limit "typically between about 5.0–6.0 g/kg/d or even slightly higher," without any references. He basically just took the 300 grams and divided it by the average hunter-gatherer / forager body weight of 50 to 60 kg. Everything after that is historical accounts of "rabbit starvation", but none of these indicate that protein intake per se was the issue. Rather, as I state in my article, rabbit starvation is just a term used to describe the predictable consequences of sustaining on exceptionally lean and nutritionally limited foods, particularly when super active with a high energy expenditure. - High thermic cost of metabolizing protein, meaning that people needed more total food to obtain the same net energy. - Difficulty consuming enough lean meat to meet high energy demands. - Inefficient use of protein when nonprotein energy was scarce - Nutrient deficiencies (essential fatty acids, fat soluble vitamins, and minerals)

Obesity is driven by a number of interacting factors that all converge to affect its proximal cause: chronic energy surplus. Beliefs, priorities, and preferences are the biggest factors. Most people simply have no desire to be healthy or to put in the effort required to be healthy in the modern environment. And appreciating this truth and the agency that people possess is not mutually exclusive with everything else that follows. Hyperpalatable food supply is next, defined by food options rich in combinations of added sugars, refined grains, added fats, salt, and flavorings. None of these things is obesogenic on its own. Inactivity comes third. People don't want to be active, and the modern environment is great at allowing people to live their lives with very little physical activity being needed. Then you have things like genetics, sleep and circadian disruption, chronic stress, medications, socioeconomic factors, alcohol, toxicants, and the microbiome. Key thing is figuring out what the biggest levers are for a particular person. But energy balance remains king, and encouraging personal agency over behavior is essential (e.g., no food will ever compel you to eat it).

As someone who is a huge fan of supplements in general, it really irritates me to the core to see companies sell products with complete bullshit claims like this. You cannot tell me with a straight face that 100 mg of your collagen product is equivalent to 10 grams of another.

One of the only studies to ever investigate a reasonably high protein intake in people with overweight and obesity (PMID: 26817506).

I have no problem locating the paper, but I'm not going to pay to view it, hence my question to you. At the very least, can you please share the effect estimates and confidence intervals for the non-significant results (HDRS, HARS, POMS)? I recommend including those in your article as well, since writing "no statistically significant effect" actually doesn't tell us anything about the data's compatibility with a benefit or harm. Plus, you included them for the BDI and BAI.

Was an absolute honor to join you in this discussion.

@ADM_Christine @MensHlthNetwork

Had a great time talking with Admiral Brian Christine (@ADM_Christine) and Ronald Henry (president of @MensHlthNetwork; not shown) on the Men's Health panel discussion at the Heritage Foundation event: Restoring Men's and Women's Health Summit.