Top Tweets for #LCL6

You have no reason to be in this discussion, frankly... you jumped into a conversation where someone claimed food “doesn’t contribute” to obesity. That’s why I brought up losing 150 pounds and keeping it off, and our published average of 43 pounds lost. Not to talk about my self, as you are suggesting.... those outcomes literally don’t explain the national trend. They DIRECTLY challenge the claim that food is irrelevant.... why did you ignore that? Yes, obesity prevalence has fallen as GLP-1 use has risen. I’m not disputing that. I’m disputing the leap from “these trends track together” to “GLP-1s caused the entire decline.” Let alone by someone who literally doesnt understand nutrition. How do I know he doesnt, here is a study showing seed oils blunt GLP response compared to olive or lard. How inconvenient for the peptide maxxers https://t.co/v0pLRt4lxr Also in same timeframe, people have also been questioning nutrition dogma, and low-carb diets have gained recognition in diabetes care in 2019. CDC stopped pushing carbs in 2022. The new dietary guidelines emphasize real food in 2025. None of those trends, on their own, tells us how much each contributed. And a drug working does not prove the disease is caused by a deficiency of that drug. Antibiotics treat sepsis. Sepsis is not an antibiotic deficiency. GLP-1 drugs act on appetite pathways; that doesn’t mean food sits downstream of a “broken hypothalamus.” THATS literally STUPID and the reason I wrote the post NOT to talk about myself as you accused me of. Literally to point out a gap in knowledge... which I did quite bluntly. The problem here is people talking about shit they dont understand pretending to be an authority when they arent. Your solution, accuse me of being selfish? Get over your ignorance and help him get over his.

Linoleic acid intake has more or less monotonically risen over time. However, the *mixture* of all dietary fatty acids has also changed over the same time span. This trend in intake, coupled with the fact most human studies quantify fatty acids as a percent of total (rather than measuring actual concentration), has caused many people to draw erroneous conclusions about how linoleic acid affects health biomarkers. People have basically taken relative measurements (left column below) and how they correlate with various health biomarkers at face value... without even realizing that they weren't looking at actual concentrations. By doing that, you would be tempted to draw conclusions like, "Seed oils lower total cholesterol and lower triglycerides. See, the correlations are negative!" But when you look at actual linoleic acid concentrations, rather than relative abundance, the correlations go in the opposite direction. This is one example of why understanding methods and mechanisms is so important. Without that kind of knowledge, you are more easily duped by human studies with methodological flaws or serious caveats - studies which are often blindly held up as "superior" to all other forms of evidence. More info on linoleic acid/PUFA consumption over time: https://t.co/AAEZRBUn20

“Keto works, but you have to be able to never eat potatoes again.” People would genuinely rather live with type 2 diabetes than give up potatoes. That’s the bit I can’t get my head around. We’re talking about a condition that can affect your eyes, kidneys, nerves, heart and blood vessels. And the dealbreaker is a potato. What matters more, your health or eating potatoes?

A just about 100% overlooked piece to the calorie restriction=health span myth is that it works when one is swapping out processed food. When animals are feed something akin to a species appropriate diet, this signal vanishes and CR+appropriate diet= early death. I dug into all this a number of years ago: https://t.co/32F2SiXene

This graph proves nothing but it does show that we complied when told to eat more chicken and less beef because it was healthier. Chicken availability more than doubled, beef availability fell roughly 28% and diagnosed diabetes prevalence more than doubled since 1980. Availability is a proxy for consumption that the USDA is fond of using.

There's been a lot of talk about a new study claiming that ketogenic diets promote intestinal cancer. Here's what you need to know: This was an animal study in mice genetically predisposed to developing cancer that were fed a diet containing starch, sucrose, food dyes, lard, and soybean oil. That was the "ketogenic diet." Oh, and the paper was explicit that the effect was not due to ketone metabolism.

It may be time to change how we talk about GLP-1 medications. One of the standard principles we hear is that they help with weight loss by slowing digestion. Well, results from a new study challenge this (https://t.co/rODMwDxDNi). Among people on the drug, how slowed their stomach emptied had basically no link to how much they actually ate. When comparing people on the drug vs. placebo, delayed emptying explained only 4–6% of the difference in food intake, and the link disappeared entirely when they limited the comparison to the people on the drug alone. So the popular "it just parks food in your stomach so you feel full" explanation doesn't explain the reduced appetite. The appetite effect looks like it's coming from somewhere else, most likely the brain controlling hunger/cravings and possibly changes in how the body burns fuel (with glucagon agonists).

They just announced a gene therapy that permanently lowers LDL cholesterol. One shot. For life. They are calling it the future of heart disease prevention. Before you celebrate, look at this chart. The Women's Health Study. 27,939 women. 21 years. JAMA Cardiology. Every cardiovascular risk factor ranked. Diabetes: 10x risk. Metabolic syndrome: 6x. Inflammation: 2.98x. LDL cholesterol: 1.4x. Dead last. They just built a permanent gene edit to solve the 1.4x. Nobody is building anything for the 10x. 🧵