ok, that's just 1 study. who cares. maybe there was something weird about those students...
RCT fed people egg or egg substitute. they were able to do it double-blind: neither the volunteers (similar taste) nor the experimenters knew who was on eggs academic.oup.com/ajcn/article-a…
indeed cholesterol rose from baseline when people were on eggs
here's the genius part. they switched the groups mid-way (cross-over study)
adding egg bumps cholesterol ~20points, removing them makes it drop again. on and off like a rollercoaster
ok but those were free-living subjects. who knows. maybe they changed their diet and it confounded the results
we need to keep the volunteers at the research center for the whole study and control every bite of food they take
lucky for us, that's been done dozens of times
meta-analysis of >70 metabolic ward studies on effect of dietary cholesterol and saturated fat on blood lipids
tl,dr: swapping 10% cals from sat fat with whole carbs drops cholesterol by 20 pts; cutting 200mgs cholest (~1 egg) drops another 5 pts
in fact the effect of saturated fat (and secondarily, dietary cholesterol) on blood lipids is one of the most reliable observations in nutrition science
you know something is reproducible when there's a mathematical equation for it
ok so we have a very specific question, experimentally very tractable (so much so people can do the experiment themselves) and has been addressed ad nauseam in the literature
then why does this appear so controversial??!!?
it helps to understand the full breadth of the effect
the effect of food on blood lipids is dependent on context (more specifically, your baseline)
i.e. the higher your blood levels, the smaller the effect of a dietary increase in sat fat/cholest
this is not specific to cholesterol. many parameters work like that
that dynamic means that specific values will vary depending on baseline
so if we take hypercholesterolemic individuals (typical western diet, high sat fat/cholest) and add a bit more (e.g. 1 extra egg), a small or no difference is expected
this is routinely done in egg industry-funded studies
the problem is not the experiment, it's the interpretation
seeing no sig. change means an extra egg makes no difference *in that specific context*. not that "eggs don't affect serum cholesterol". yet this is often what you'll see implied in the paper and esp. in the media blurbs
the (predictable and, indeed, desired) result is confusion
other ways to manipulate experimental design and thereby confuse include
1) the choice of comparison foods (compare eggs to butter and they look pretty good)
2) a more sophisticated approach: acknowledge eggs raise LDL-c but argue that's fine bc some other parameter "makes up for it" (HDL-C, particle size etc)
(preponderance of evidence indicates neither is likely to do much to offset a LDL-c/apoB rise)
neither. they have substantial SFA and cholest but overall dietary pattern >>>> individual foods
this means a dietary pattern can include some eggs AND be healthy (or unhealthy)
and vice versa
so how much can we get away with? depends (on your lipids, overall health, family history etc etc etc). some people can handle more than others. that's life
e.g. if your lipids are stellar, chances are you have more leeway. if they're iffy, you have less room to play
PS. some will say 'sure, dietary cholesterol/SFA raises LDL-C/apoB, that's established. but do those markers translate to higher risk of CVD? that's the question'
and yes, preponderance of evidence overwhelmingly says they do. covered it here:
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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