nature.com/articles/s4159…
Some thoughts on why these results don't mean much to me 1/ It was 2 weeks, which is short term and not enough time for adaptation (see point 8 and others on this)
2/ "Both diets were low in ultra-processed food" is a misrepresentation....
...the low-carb diet was, IMO, unfairly weighted by processed foods and oils including mayo that I assume was made with soybean oil (correct me if I'm wrong), processed cheeses like "American cheese", and so on. It was also weighted towards meats and A1 dairy
3/LC diet appears far more palatable, and both diets were designed by the investigators, not freely chosen by the participants. If my snack options were unlimited roasted salted nuts sitting in front of me or dry edamame, apricots, and raisins, I'd eat more kCal of nuts too.
4/ Tied to the prev comment, that's a complication of the metabolic ward. In free living population u seek food when u're hungry rather than having it presented. Plus, you have things to do and are less likely to eat out of habits that haven't been broken bc again it was 2 weeks
5/ there was no washout period, which is very odd for a crossover trial
6/ low-fat diet decreased energy burned at rest and while sleeping
7/ AND...
7/ AND... the low-fat group did not lose more weight. they trended to lose less wight. if the investigators want to pin that on water loss the study should have been >2 weeks.
8/ back to 1, energy intake decreased in the low-carb group in week two. Do I smell adaptation?
Concl. could go on but y? Any clinician who has tried low-fat vs low-carb for overweight patients in free living w real people over a reasonable period of time (wwell-formulated diet plans) that overall low-carb is more effective
-25:30
Colleague and I had this RCT thrown in our face bc suggested a #ketogenicdiet option. Arguement was this RCT shows LCHF ⬆️LDL, therefore bad. Here's a thread about what I think...
(Spoiler, LCHF = good)...
1/ The LDL increase in the LCHF group may not itself be an adverse outcome. There was no subfractionation and it’s likely the increase in LDL and ApoB was driven by large fluffy healthy LDL particles. This assumption is supported an improvement in HDL levels in the LCHF group.
2/ HDL increased on the LCHF group, not the control group. When HDL is high and triglycerides are low, CVD risk is not meaningfully increased. See figure attached from Framingham. Furthermore, HDL (and waist circumference, below) are markers of metabolic syndrome. LDL is not.
Today's FoD is being substitued by a thread of quotes from the below article
Explains how, in 1965, The Sugar Research Foundation (SRF)/Sugar Industry bought off scientists to promote sugar+demonize fats. ncbi.nlm.nih.gov/pmc/articles/P…
A Must read
Cred to .@ProfTimNoakes lecture
The Sugar Research Foundation (SRF) became concerned with evidence showing that a low-fat [high-carb] diet high in sugar could elevate serum cholesterol level…
The SRF’s vice president and director of research, John Hickson, started closely monitoring the field…
Hickson proposed that the SRF “could embark on a major program” to counter “negative attitudes toward sugar.” …
In 1965, the SRF asked Fredrick Stare, chair of the Harvard University School of Public Health Nutrition Department to join its SRFs scientific advisory board