Another thing to consider is that in man, endogenous production of cholesterol far exceeds the largest dietary intake – I don’t recall but I think it is by a factor of 10 or 20 – so it would be odd for changes in dietary intake to be able to make much difference. Correlations may have been seen, but it will take persuasion I haven’t yet read (doesn’t mean it’s not out there though) to make me think there is causation of any substantial adverse effect from cholesterol per se.
On the 12 eggs per day point, while I wouldn’t say they were like steroids for me, when training naturally, those periods when I had a dozen eggs per day definitely seemed to owe something substantial to the eggs. Nothing definitely measured, but a clear impression. I do think they are excellent P+F food for bodybuilders and athletes.
True vegetarian diets do not lead to atherosclerosis. This is different than the “Americanized” vegetarian diet, high in refined sugar.
Also, rats do not get atherosclerosis, in part, due to lack of CETP, the enzyme which moves cholesterol esters from HDL to LDL. Thus rats carry most of their cholesterol in HDL which can only be taken up by the liver and steroidogenic tissues. Age 3 in a rat would not correspond to age 3 in a human, actually closer to age 70-80.
And yes, endogenous production is greater than intake, but in individuals that do not supress HMG-CoA reductase to a level equal to intake will therefore see a rise with dietary intake.
I think its important to remember that the response, as with most metabolic parameters, depends ont he interaction between genetic and environmental factors, so I’m sure there are many, in whom dietary cholesterol has little or no effect at all.
To Goldberg, no offense but your statement is an uninformed one.
No offense taken but that is what i was taught in my exercise science classes. My professor also said that when he was at LSU they did a mini study where they took blood samples and sent them to three different labs. all three labs showed an enormous difference in the measurements. so how can there be a correlation when a reliable measurement cannot even be taken.
Wait a second: those on vegetarians never
get any atherosclerosis? Is this really a fact? If so I’m quite surprised, though as
I said it’s not my field and there will be things I don’t know. This is really proven?
Secondly, saying 3 years in a rat corresponds to 70 or 80 years in a human really doesn’t follow. A lot of processes don’t work that way. Just because an animal dies quickly for
other reasons, does not mean it would not
develop other conditions if it didn’t live
longer. Using rats as a model to understand processes in humans that take many years to develop could reasonably be doubted for reliability.
Goldberg, he is incorrect. Come take my course :). Search Pubmed. I always recommend people see the data for themselves. Also look at lipids online. They have slide shows you can view.
You are correct that there is variability - like anything else - for example if I measure your testosterone, and aonther lab does, it eaily could be 10-20% different, but that doesn’t detract from the relationship between plasma cholesterol and CAD. Look at the MRFIT trial. You’ll note that atherosclerosis is non-existant is individuals with a cholesterol <150.
Also if the same lab always measures yours, using the same assay, changes in the value will be a reliable reliable indicator.
Bill - Atherosclerosis is pretty nonexistant in vegetarian eating countries (not referring Americanized vegetarian diets of course). Regarding the rat model, the rats life span is about 3-4 yrs. It reaches maturation after a few months and goes through "menapause" around 12-16 months.
Find some of the readings on some of the early signs of atherosclerosis. THey are really interesting. Napoli et al (reference is in a big box of papers at the moment) found that stillborn children have atherosclerotic plaques, and the level of these is related to their mothers cholesterol levels (specicially hypercholesterolemic mothers), others have found for the plaques to increase the childs cholesterol has to be raised.
Cholesterol doesnt ‘cause’ chd, but its a pretty good risk factor (blood not dietary intake)
There are other potential factors, especialy with the new theorys on inflamation and chd prevalence etc.
Ok i went and talked to him and here is what he said. the correlation between HDL levels and CAD is high. The lower the levels of HDL the higher the risk CAD. He wouldnt budge on the total cholesterol argument though. And i have to agree there. My moms cholesterol is over 200 but her HDL is over 100. On her last test she had a little greater than a 1 to 1 ratio of HDL to LDL.
Yes, the correlation between HDL levels and CAD is high. It is also high between LDL or total cholesterol and yes it depends on the ratios as well. But this has been overemphasized in the US, as countries with low total cholesterol and low HDL in fact have less CAD than those with high total and high HDL for reason you mention, that is the ratio HDL to LDL is higher.
One thing most don’t know also is that the level of HDL itself can be misleading since it is the function of HDL that is important, not the total amount. This means that someone can have high HDL but this HDL may not be protective if the HDL-associated enzymes don’t function optimally. Conversely, if you have low HDL, but he enzymes work better, you are more protected than would be predicted. For example, in your mother after menapause her HDL may drop and the enzyme activity will as well. Good luck.
Prof., I’m not as current on the literature as you seem to be, so I’ll ask your opinion here. I remember reading, back in the 80’s when all those scary studies about how bad cholesterol is for you came out, that people with a high level of strenuous physical activity (say, for example, a well-designed weightlifting program) basically showed none of the adverse effects of eating a lot of eggs that others did.
Since pretty much everyone on this board is probably engaged in such a program, do you think that it’s really worthwhile for us to be worrying about the number of eggs eaten per day? Or am I just totally off here?
Char - I don’t know if you are referring to dietary or blood cholesterol. I’ll assume dietary. Dietary itself isn’t as important as factors like saturated/trans fats, fiber and insulin. Also coming form eggs isn’t worse than other sources. Exercising will lower TG and some studies show a reduction in LDL, so some will see a total cholesterol with training. HDL generally increases with training. Exercise will also better CAD risk by other means which I’m sure you’re aware of.
I think you should monitor dietary cholesterol, egg on not. If you currently eat a lot of cholesterol, keep doing so for a while and get a lipid panel. Then stop, and after a few months get another, keeping the rest of your diet the same and see if it changes. If you don’t eat eggs and you want to, do this in opposite order.
I usually recommend if you want eggs, have 5 whites for each yolk. If the rest of your diet in low in saturated fat, refined sugar and trans fats, and high in fiber, 1-2 yolks a day for “most” who read the site is fine.
I also recommend, if you are worried about CAD down the road, to get a CRP test if you find a lab that will do it for you. Its a marker of inflammation, which atherosclerosis is a disease of. Look at Ridker’s papers.