Fiber isn't excreted unchanged as we used to think. It (esp. soluble fraction) is digested by the microbiome, which produces short-chain fatty acids (SCFAs) - butyrate, acetate, propionate
SCFAs feed our gut wall and help prevent disease
3) SCFAs regulate hormone balance and appetite/weight
Direct administration of SCFA precursors induces the gut wall to secrete hormones that signal satiety and prevent weight gain
this indicates that 2 populations with the same ApoB level would have different risk depending on what type of ApoB particles are elevated (LDLs? VLDLs? both?)
NO. the study shows all these ApoB particles are atherogenic but points to TG-rich lipoproteins as being even more so *particle for particle*. most people have many more LDLs so the risk attributable to those will still predominate
Re: heart disease in particular, we can find heterogeneity in the literature. Some studies point to a signal of risk for eggs, others find no stat sig effect.
One of the main differences between science and Social Media content is how they deal with heterogeneity.
Social Media feeds you polarization. One FB forum argues eggs are poison, and shows you only the studies reporting risk.
Another argues eggs are a perfect, risk-free superfood, and shows you only favorable studies.
over 2 months, he lost 27lbs. his BMI came down to the normal range
his LDL-C dropped 20%. his triglycerides, 39%
his anecdote illustrates a couple points:
▶️we can lose weight on almost any type of food, as long as we cut calories enough
▶️ some foods make it easier to cut calories. calorically concentrated junk food makes it easier to overconsume calories, so for most people they're not ideal. most people won't achieve the precise control on a day to day basis that the Prof exercised in his experiment
Once you understand HDL-cholesterol is not causally protective, it's straightforward to see why some of the popular ratios can be misleading
quick 🧵 using TC/HDL-c as example
to make the math easier let´say my HDL-c is 40mg/dL and my total cholesterol (TC) is 200
That’s a TC/HDL-c ratio of 5
Hypothetically, if my HDL-c doubles (and everything else stays constant), my HDL-c is now 80 and my TC is 240 (remember, TC is the sum of all serum cholesterol including HDL-c)
Does high ApoB still raise risk if I´m “metabolically healthy”?
The evidence indicates it DOES.
(thread)
The idea that cholesterol level is completely irrelevant has largely subsided.
As the public is exposed to more scientific evidence, it has become increasingly obvious that blanket denial is not realistic.
So a more nuanced idea emerged.
“it´s about context”
According to this idea, high cholesterol/apoB increases risk in “sick” people (e.g. insulin-resistant/obese/diabetic) but is harmless for the insulin-sensitive & lean