349 karma · joined October 5, 2022
And why would your body go out of its way to preserve metabolically more expensive tissue during longer periods of deprivation?
Absolutely wrong: https://news.ycombinator.com/item?id=38194372
Longer fasting periods, including 16/8 TRE and alternate-day fasting, have been shown to cause a disproportionate amount of lean body mass loss: https://jamanetwork.com/journals/jamainternalmedicine/fullar...
>In this RCT, a prescription of TRE did not result in weight loss when compared with a control prescription of 3 meals per day. Time-restricted eating did not change any relevant metabolic markers. Finally, there was a decrease in ALM in the TRE group compared with CMT. Together, the results of this study (1) do not support the efficacy of TRE for weight loss, (2) highlight the importance of control interventions, and (3) offer caution about the potential effects of TRE on ALM. Future studies should be aimed at understanding the effects of early vs late TRE and protein intake or timing as a means to offset the loss in ALM.
ALM = Appendicular (i.e., limb) Lean Mass.
One of the authors of this study, Ethan Weiss, is a cardiologist and was a big proponent of TRE, but after the results of his own study came in showing drastic loss of LBM in TRE group (to the point that most of the weight lost was LBM) and no added benefit, he completely stopped doing TRE, stopped recommending it, and went to Twitter and the news media to publicize the harm, eg: https://www.insider.com/new-research-finds-intermittent-fast...
X isn't showing his Twitter thread, but there's a copy of it here: https://old.reddit.com/r/ScientificNutrition/comments/j1fav8...
>In the in-person cohort, the average weight loss in the TRE group was 1.70 kg. Of this, 1.10 kg (~ 65% wt lost) was lean mass; only 0.51 kg of weight lost was fat mass. Loss of lean mass during weight loss is normal but typically accounts for 20% to 30% of total weight loss
>So in summary: 1) no matter how you slice it, prescription of TRE is not a very effective weight loss strategy; 2) There was no advantage to TRE when compared to a proper control group; 3) What weight was lost looked to come more from muscle mass than fat mass
> Both groups gained 1.6 kg in weight; however, the MRI assessment showed that the SFA group gained more liver fat, total fat, and visceral fat, but less lean tissue compared with subjects in the PUFA group (Table 2).
And even without weight gain, it seems to impair insulin sensitivity: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291812/
> A diet very high in fat and saturated fat adversely affects insulin sensitivity and thereby might contribute to the development of type 2 diabetes.
> Over 5,483,981 person-years of follow-up, we documented 22,761 T2D cases. Intakes of total, processed, and unprocessed red meat were positively and approximately linearly associated with higher risks of T2D. Comparing the highest to the lowest quintiles, hazard ratios (HR) were 1.62 (95% confidence interval [CI]: 1.53, 1.71) for total red meat, 1.51 (95% CI: 1.44, 1.58) for processed red meat, and 1.40 (95% CI: 1.33, 1.47) for unprocessed red meat.
> Conclusions: Current evidence suggests that whole, fresh fruit consumption is unlikely to contribute to excess energy intake and adiposity, but rather has little effect on these outcomes or constrains them modestly. Single-meal RCTs, RCTs lasting 3–24 weeks, and long-term observational studies are relatively consistent in supporting this conclusion. Whole, fresh fruit probably does not contribute to obesity and may have a place in the prevention and management of excess adiposity.
> Conclusions: Current evidence suggests that whole, fresh fruit consumption is unlikely to contribute to excess energy intake and adiposity, but rather has little effect on these outcomes or constrains them modestly. Single-meal RCTs, RCTs lasting 3–24 weeks, and long-term observational studies are relatively consistent in supporting this conclusion. Whole, fresh fruit probably does not contribute to obesity and may have a place in the prevention and management of excess adiposity.
Yet the obesity and Type 2 Diabetes epidemics have only gotten worse, with the diabetes epidemic reaching what appears (in this graph) to be an inflection point around the time sugar consumption started to decline (which makes sense when you realize it entails a shift to more fat consumption, including saturated fat): https://www.ncbi.nlm.nih.gov/books/NBK568004/figure/ch3.fig2...
I'm amazed that here we are, in the third decade of the low-carb era, with the obesity rate now hovering over 40% despite a decline in sugar consumption, and this nonsense is still being taken seriously, let alone by people (like HNers) who think they're well-informed.
BTW go look at photos of Johnson and Lustig: they're both fat, unlike Barnard, McDougall and other doctors who advocate ultra low-fat, whole food, plant-based diets.
She benefited from the January Effect: https://www.investopedia.com/terms/j/januaryeffect.asp
RT = resistance training, PI = protein intake. While total protein intake is most important, protein timing and distribution still matters for muscle (contrary to what's propounded in fasting and time-restricted feeding circles), and according to this study, even if the distribution is spaced out, if it's skewed toward dinner, that appears to be sub-optimal.
> A high-fat, high-saturated fat diet decreases insulin sensitivity without changing intra-abdominal fat in weight-stable overweight and obese adults
https://diabetesjournals.org/diabetes/article/63/7/2356/3433...
> Despite comparable weight gain after 49 days, this double-blind trial showed that overeating energy from PUFAs prevented deposition of liver fat and visceral and total fat compared with SFAs. Excess energy from SFAs caused an increase of liver fat compared with PUFAs. Further, the inhibitory effect of PUFAs on ectopic fat was accompanied by an augmented increase in lean tissue and less total body fat deposition compared with SFAs. Thus, the type of fat in the diet seems to be a novel and important determinant of liver fat accumulation, fat distribution, and body composition during moderate weight gain. We also observed fatty acid–dependent differences in adipose tissue gene expression. The significant decrease in pancreatic fat in both groups during weight gain was an unexpected finding that needs confirmation due to the low amounts of pancreatic fat in this lean population.
Apparently none of you have heard of Dr. Panda, which means you've done barely any research into any of this, and yet you're still smugly confident that TRF/IF are safe and healthy? Enough to nit-pick the studies saying otherwise, and downvote and flag those posting them?
Meshes with all of the other studies that show no benefit to TRF or IF unrelated to weight-loss (which can be achieved without TRF/IF), and the studies showing harm, like this one:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9182756/
and this one:
https://www.researchgate.net/publication/368542960_Insulin_r...
What was the obesity rate in 1993 vs. 2023?
Canola is primarily monounsaturated.
> Saturated fat is essential for health.
Saturated fat is literally not essential.
> Cholesterol is nutritious
> All of that bullshit advice against saturated fat and dietary cholesterol has been completely debunked many years ago. It was fraudulent science.
You're spouting dangerous, pseudoscientific nonsense.
Where's the evidence? I linked to a study, one that isn't confounded by weight-loss (unlike the studies you people like to cite) demonstrating that as the fat (especially saturated fat) content of the diet increased to an absurd degree (55%!), insulin sensitivity tanked. Why would insulin sensitivity, when measured by an Oral Glucose Tolerance Test, suddenly improve if you restricted carbohydrate even further? Yeah, at some point your intake will be so low that you can "game" an HbA1c or fasting BG test, but underlying insulin sensitivity will be trash (which an OGTT would show), unless maybe you lose enough bodyfat to offset it.
Why do so many people on keto develop "physiological insulin resistance?" Why does all of the epidemiological evidence show strong inverse correlations between low-fat carbohydrate consumption (like whole grains and fruits) and T2DM, but the reverse for high-fat "carbs" like cookies or pizza?
The most reasonable interpretation of the data right now is that high-fat diets make you less insulin sensitive.
I think you misread my post, or misread the study. Whole grains are some of the healthiest foods you can eat, especially when it comes to reducing your risk of T2DM, while the person I was replying to implied the opposite:
> Thirteen studies with 29,633 T2D cases were included in the high vs. low intake meta-analysis (overall intake range: 0–302 g/day). Comparing extreme categories, a strong inverse association between T2D and whole grain intake was observed (RR: 0.77; 95% CI 0.71–0.84, I2 = 86%) (Supplementary Figure S1). Each additional daily 30 g of whole grains was inversely associated with T2D risk (RR: 0.87; 95% CI 0.82–0.93, I2 = 91%, n = 12 studies) (Supplementary Figure S2). The inverse associations and heterogeneity persisted in additional analyses stratified by sex, age, follow-up length, geographic location, number of cases, dietary assessment, and outcome assessment (Supplementary Table S14). Evidence of heterogeneity between subgroups in stratified analyses was observed for geographic location, dietary assessment method, and outcome assessment. There was significant evidence for small study effects in the high versus low meta-analysis, but not in the dose–response meta-analysis. Visual inspection of the funnel plot suggests that small studies showing positive association may be missing (Supplementary Figure S25). There was evidence of a non-linear dose–response association; the risk of T2D decreased by 25% with increasing intake of whole grains up to ~50 g/day. Small benefits for increasing intake above this value were observed (Fig. 2).
Telling people to eat fewer, not more, whole grains to prevent T2DM and cancer is peak HNism:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506108/
https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.31198
and high-fat, high-saturated fat diets actually make insulin sensitivity worse:
Really? I'm old enough to remember when Google bought Deja, and with it suddenly came the ability to search the entire Usenet archive going back to its inception, through the Google Groups interface. Being able to search the archives of comp.lang.whatever was a great educational and productivity booster, like Stackoverflow before SO.
I made the mistake of visiting the (archived) page linked to by the second Tweet from that (archived) feed announcing the conviction of someone of interest to them on several criminal counts, and what I read there was nightmare fuel potent enough that if these are the kind of people the site "stalks," I can't say I'm sympathetic. (Seriously, don't read it.)