Eggs and Cholesterol

Are eggs really that bad for you? i know eggs are one of the best sources of real food protein and they are also a cheap source of protein, but am i putting myself at risk by eating 6 eggs a day pretty much everyday? recently people have been saying that its the saturated fats and hydrogenated fats that are the real cause of heart problems so should cholesterol still be a concern considering i keep the rest of my diet clean (minimal hydrogenated fats, pretty much all foods from the “foods that make you look good neckid” article)?

Some like Dr. Serrano say you can eat as many whole eggs as you want and not have to worry. Sometimes he’s a little wacky though in his recommendations. I’d like to hope he’s right though!

Cut back on the yolks. I eat about twelve egg whites and only two whole eggs a day

This question comes up every few weeks…check the archives.

obviously your diet can influence your good and bad cholesterol levels. however high cholesterol levels are usually genetically predetermined. most people with cholesterol problems also have parents and other family members with the same problem. however like i said before your diet can make it worse or improve that condition. if you dont have a problem with your current cholesterol levels eat all the eggs you want.if your bad levels go up then increase the whole grain food sources.

I wouldn’t worry about it much, just try to get you’re omega 3’s in.

why the hell dont people ever do searches. this is yet another dumb question. Hydrogenated fats are poison and have no benefit. Saturated do.

I agree with p-dog in that it is all genetically determined. Some people don’t repsond too well when eating foods with high cholesterol. Unfortunately, I am one of them.

Try the eggs fortified with extra Omega-3, and with less staurated fat. Around my parts here in Pa., they’re sold as “Eggland’s Best” and “Full Spectrum Eggs”. They’re whole eggs, BTW, and I average about 20 whole eggs a week. I haven’t had my cholesterol checked in about four years though, so I don’t know how my egg consumption is affecting it.

Even though this is only anecdotal evidence, I’ve been eating 6 whole eggs every morning for a year with no negative change in my cholesterol profile. My mother who is quite a bit smaller than me has eaten two whole eggs for breakfast for 50 years and she has an immaculate cholesterol profile. There are so many variables to good health including genetics that it makes if very hard for blanket statements about fat/cholesterol to be 100% true. The best bet is to add the whole eggs to your diet for a month or two and then see if your cholesterol profile improves or gets worse, if your that worried. A cholesterol test is not the end-all be-all of heart health either.

Steve, which Dr. Serrano is that? I did a google search and found quite a few.

The Serrano comment came from one of the SWIS articles at T-mag by either Shugart or Berardi. A search from SWIS at T-mag should bring them up.

It is Dr. Eric Serrano…he works with many top athletes and bodybuilders in addition to “normal population” clients. Although many people feel some of his recommendations are a little unorthodox or unfounded, I have had the privilege of talking with him over e-mail where he has been able to go a little more in depth about some of his ideas…and believe me, the man knows what he is doing, and he gets results.

There was a study perhaps 7 or 8 years ago
on the correlation between blood lipid profiles of egg-consuming athletes and the number of eggs they consumed. Up to and including the maximum level of intake studied – a dozen eggs per day – the BETTER the blood lipid profiles were.

Doesn’t prove causation but does suggest
eggs are not a problem with regard to blood lipid levels.

One important point, so often missed: what is loosely called “cholesterol” in blood tests is NOT the substance found in eggs in the first place! The substances measured in blood are lipoproteins, and some of them are beneficial, e.g. HDL. The substance in eggs is a steroid. Two different animals.

Let me know what that study is. That is not what the literature suggests.
Though it not as important other factors, Weggemans et al. (Am J Clin Nutr 2001;73:885–91) showed increases the total-cholesterol to HDL ratio via meta-analysis with increased egg consumption.
In addition, several cohort studies, including (Shekelle RB, MacMillan Shryock A, Paul O, et al. Diet, serum cholesterol, and death from coronary heart disease—The Western Electric Study. N Engl J Med 1981;304:65–70 and
McGee DL, Reed DM,Yano K, Kagan A, Tillotson J. Ten-year incidence of coronary heart disease in the Honolulu Heart Program.
Relationship to nutrient intake. Am J Epidemiol 1984;119:667–76)found significant associations between dietary cholesterol and the risk of CAD. Data also shows that dietary cholesterol increases CAD is primates and thus it is not correct to say that dietary cholesterol does not affect CAD risk. (Stamler JS, Shekelle RB. Dietary cholesterol and human coronary heart disease. Arch Pathol Lab Med 1988;112:1032–40).

Vince Gironda writes in his books that while he was bulking he had best results when he ate twenty eggs a day. He said that it worked almost like steroids for him and his trainees.

Although it sounds odd to say that a study
was “done” by the American College of Sports Medicine, that is my recollection, and it was probably in 1993 or 1994. I read only the abstract of it.

Any Stamler paper showing effect of dietary cholesterol on primates, was not to be found on Medline. As it happens I’m going to the library today so I will pull the paper while there.

Egg contains things other than cholesterol
and so whether adding cholesterol to the diet with no other changes (were that done!) and finding an adverse effect on blood lipids would not prove or even strongly suggest that eggs would do this.

Lastly, all the Shekelle papers I was able to find on Medline, or rather the abstracts of them, showed no indication of ever examining what happened when nothing but cholesterol was changed. Sorry, but when cholesterol differs greatly due to a substantially different diet of foods commonly consumed, there are a lot of changes going on besides the amount of the specific compound cholesterol, and in my opinion performing statistical regression and attempting to isolate the effect of cholesterol itself has approximately zero validity. It can be shown to have validity only if other experiments where variables are separately controlled in different manners support the model, which I really doubt was done here. Was it?

Maybe it was in abstract form. Nothing came up on eggs in MSSE.

I suggest looking at the Weggemans paper, as it has some refs there and yes, whether it is due to egg consumption per se or simply dietary choelsterol requires further study and other factors may be contributing, as it is well-known than saturated fat and insulin upregulate HMG-CoA reductase.

Also run a search on monkeys and dietary cholesterol. You’ll find some interest work done early on (1970’s) and more recent work, for example Eur J Pharmacol 415(1):79, 2001, showing that dietary cholesterol absorption inhibition mitigates diet-induced hypercholesterolemia.

On further thought, it was probably an
abstract presented at an annual meeting.

The Stamler paper was interesting but
somewhat of a disappointment, neither to
me proving its point or being an obvious
failure to be dismissed out of hand either.

It turns out that it and the many Shekelle
papers are all rehashes of the same thing:
further grinding out of statistics from
data obtained back in the 1960s. Now, that
in itself bodes ill. I’d be hard pressed
indeed to name a single thing that’s ever
been done that sort of way that really gave
good findings. Not that it could never happen
but…

If I’d been smart I would have photocopied
the paper and read it later. Instead, being
interested, I read it at the time, and then
was too pressed for time to make a copy. Duh!
Anyway, it was less than clear. The paper
was not a presentation of work done by the
authors (other than their analysis of the data) and how the data was obtained seemed
poorly described. If I got it correctly,
those in the study were on some sort of
staple diet to which for example butter and
two eggs per day were added, or hydrogenated corn oil
and eggs, or something with no eggs, etc.
and then some differences that seemed small
in total cholesterol were reported.

This alone, I have a hard time taking as
meaning much.

The part you mention about it being shown in primates
that cholesterol causes atherosclerosis wasn’t
shown in the paper. Rather it was said that others had shown it.

This also is problematic. While at first glance it may sound impressive that it was
shown in “primates,” which sound close to
us, actually other primates and man aren’t
that similar in nutritional requirements.
A gorilla for example really does not eat
like a man, and if a man tried to eat like
a gorilla (a diet heavy in leaves) I don’t
think it would work too well. So there certainly could be differences in dietary
response of man to cholesterol as opposed
to primates.

The paper also made a statement that
dietary cholesterol was “absolutely required”
for development of atherosclerosis, or if not those exact words, words meaning the same. But this is very problematic. If I’m not mistaken, vegetarian diets have no cholesterol, but is it true that vegetarians cannot develop atherosclerosis? While not my field, I think that is not true. So if an animal model, for example with a rat, showed that dietary cholesterol was absolutely necessary for development of atherosclerosis, that it did not develop without dietary cholesterol, then this shows that that animal is quite different from man since man, if I’m not wrong, develops it without dietary cholesterol.

Also, a laboratory rat usually won’t live past age 3, and how many humans have really apparent atherosclerosis at age 3?

Overall, there’s obviously something to look
at here and I look forward to seeing this
other paper you mention, but I can’t get
too convinced from a 1980s series of papers
rehashing a seemingly not well controlled or measured experiment from the 1960s (incidentally, at least one of the Shekelle
papers seems to be basically an erratum of how some conclusions previously drawn from the data can’t be supported after all due to other things not being constant, so even the author seems ready to admit problems with the data set.)

how bout the fact that cholesterol and CAD have a very low correlation so it doesnt really matter anyway.