2/ “#Ketogenic diet could also prove to be a valuable measure in the
threatening situation of the current #COVID-19 pandemic” ya, no kidding... in more ways than one
3/ “These new immunological aspects of KD might contribute to the modern concept of metabolic therapy of cancer (Seyfried et al, 2017, 2020). KD not only targets the Warburg effect, but could also
strengthen anti-tumor immunity (Ferrere et al, 2021).” .@Sam_Apple1 #sugar#cancer
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2/ I feel strange about this one because I’m actually really liberal when it comes to genetic engineering. You want to crispr by brain for Apoe2, great. I’m your lab rat... but this is really appalling. I’m not even anti-plant base, but the fact that he would propose this...
3/ demonstrates an extreme example of tunnel vision and clear close-mindedness about the issue of eating sustainably for the planet and for human health. It’s like the low-fat saga but with 21st century genetic engineering tools 🛠...
1/ How robust were the instruments? Were derived from linkage disequilibrium clumping w clumping parameters of 1 million nts, including 229 SNPs 4ApoB. Stated that tool would “not be considered weak,” Can someone explain this to the Twitter lay audience please?
2/ Building on that, while they adjusted for genetic parameters, I didn’t see anything about adjusting for medications? If they’re talking biomarker data and not adjusting for meds doesn’t the analysis appear vulnerable to healthy use bias?
Public Apology Thread 1/ A couple days ago I posted a tweet that I intended to be a commentary on the state of diabetes management in the US. What I didn’t realize at the time is that the image had a lot of historical baggage and suggested a patient-blaming perspective...
2/ Maybe I should have been aware of this history or maybe it’s irrelevant. I’m not asking for forgiveness for that ignorance. The point is that it seriously offended some people. In the hours during which the Tweet is up, before I gathered how it was really hurting people...
3/ and took it down, I doubled down on it in responses. The blunt truth was that I was resistant to listening because I got caught in the heat of aggressive comments, including a few violent threats. Excuses aside, I’m sorry to anyone I hurt. The LAST thing...
Results show equally sustainable given the right conditions, but...
Researchers designed study that during first 4 weeks of each diet, food was provided & during the next 8 they had to buy their own. Baseline&followup adherence scores were also collected. All this allowed researchers to determine how sustainable diets were under diff conditions
baseline #keto adherence score was lower than Medi score. BUT during the time period when food was provided AND when they had to buy their own food, mean keto score was equal to or higher than Medi score. At the follow-up #keto score had dropped again. From this I conclude...
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.
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.