MS Nutrition | Researcher 10+ Years | Scientific Communicator
Arizona, USA
Joined December 2018
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This really just seems like a classic Motte-and-Bailey.
Your original post implied that fasting-induced muscle loss wasn't really a concern because of growth hormone.
Now you're defending a much weaker claim that protein losses decline as fasting progresses due to adaptations.
You basically wrote the original to be more sensational yet preserve an element of plausible deniability when challenged.
This doesn't engage with my rebuttal of your claim: "the worry that fasting eats muscle has it backwards... growth hormone... spares protein."
The body losses substantial muscle during fasting regardless of growth hormone or ketones.
It's not the case for anyone.
xitter.cf/Alexleaf/status/211439…
"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.
Rightly so.
xitter.cf/Alexleaf/status/211439…
"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.
Absolutely not. Growth hormone is released to help mobilize fatty acids, not to spare protein, and muscle loss is substantial during prolonged fasting.
xitter.cf/Alexleaf/status/211439…
"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.
"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.
The worry that fasting eats muscle has it backwards, because the body raises growth hormone during a fast to spare protein. By day five of a fast in one study, 24-hour growth hormone was about three times higher than on a fed day, and between day one and day five free fatty acids rose almost fourfold and the ketone acetoacetate rose about fourteenfold. That's a body moving to its own fat for fuel while it protects muscle, and in my view it can do that because insulin has fallen low enough to allow it.
There's nothing about a night of poor sleep that leads to accumulated sleep debt. That's just a silly assumption that one will continuously engage in that behavior rather than treating it as a one off thing that happens infrequently
Because the body requires essential amino acids to function and survive, and skeletal muscle is the primary reservoir when dietary intake is too low.
Sounds like we agree on pretty much everything then. Food companies just want to make money, so of course they make food as appealing to our neurobiology as possible.
The people eating their products are the ones who fundamentally need to change their beliefs and habits, because the food companies would follow suit. But that will never happen and instead people will just make excuses about how food is addictive or something.
Yeah, so the entire presentation basically made the case that ultraprocessed foods are tasty and people like eating them, and then twisted that into the conventional brain disease model whereby the foods compel people to eat them and make people lose control, which is all bogus.
I think we need to stop calling foods, substances, and behaviors "addictive" because it carries some really erroneous conotations.
Like, what does addiction even mean in these situations?
1) It's rewarding and people want to keep using. Okay, that's a meaningless definition that accompanies all pleasurable activities.
2) People want to use despite negative consequences. Okay, this can again apply to virtually anything and is also completely subjective in terms of what constitutes a consequence.
3) It changes the brain in ways that compel people to continue regardless of conscious intent. This is basically the brain disease model of addiction, which has been largely discredited in addiction research.
Food companies try to engineer foods that taste good and provide pleasure to those eating them. That's it, and that pleasure contributes to motivation for many to continue eating them.
There is no circumstance where one's brain becomes "hijacked," and I actually find such wording to be quite defeating for those struggling to change their behaviors. It essentially tells people that they have no control and are victims to their food, drug, or behavior or choice.
@doctortro is right, the food environment we live in today is literally engineered to be as addictive as possible.
Turns out there's big money in hijacking our neurology.
All that said, can anyone explain how Berry's response is relevant... at all?
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.
No, because his ceiling would rise whereby he could sustain higher-intensity speeds without relying on glycolysis.
My baseline assumption would be that he was working above his first ventilatory threshold, but since it is him, I assume he's tested his lactate throughout training to find his personal threshold and just has a strong aerobic base.