The headlines are once again filled with advice to reduce egg and cholesterol consumption based on a study that found an association of egg and cholesterol consumption with increased risk for cardiovascular events. Sounds scary and persuasive, doesn’t it? After all, nearly 30,000 people were tracked over 17 years and the authors authoritatively declare that this proves that eggs and cholesterol are risk factors for heart disease.
There are several problems with this assessment. It is emblematic of the studies that confuse people, yield wildly conflicting conclusions, are used to craft absurd and ineffective dietary guidelines, and provide tantalizing headlines for media. And it is virtually all untrue.
Problems:
1) This is an observational study, meaning people are asked a few questions, then followed for many years, i.e., they are observed. Over and over again, observational studies that do not involve any sort of intervention (i.e., people purposefully advised to eat, say, 3 eggs per day vs. people advised to eat no eggs, as would be done in a real clinical study—much more difficult and costly to conduct) cannot be used to generate cause-effect relationships. See this Undoctored Blog post about the fictions generated by such observational studies. 4 times out of 5, the conclusions drawn by observational studies are disproven by prospective randomized clinical trials, i.e., the real way to prove or disprove a cause-effect relationship. Or, stated differently, 80% of the conclusions drawn through observational analyses are false. In other words, the majority of conclusions drawn by observational studies are complete fictions.
If we were to believe observational studies, we would have to believe that Premarin is good for women’s health, since proven to increase endometrial cancer, breast cancer, and cardiovascular death despite the observational evidence suggesting the opposite; red meat causes colon cancer; coffee consumption leads to extended longevity, etc., all the absurd proclamations based on the fictions of observational studies and nutritional epidemiology.
2) Observational studies are unreliable because they are plagued by confounding factors—That is, people who eat eggs also do other things differently than people who don’t eat eggs. Perhaps they eat cured bacon, exposing them to nitrosamines like N-nitrosodimethylamine. Or perhaps they eat at restaurants that use soybean or corn oil to prepare the eggs. In other words, the nature of observational analyses is that you cannot untangle the oodles of other factors that can influence outcome and cannot say that one factor—egg consumption—is the cause. This is the reason why, by the way, the vegetarian community declares that being vegetarian is healthier: Being vegetarian is not healthier; being vegetarian is associated with a constellation of other behaviors such as less cigarette smoking, less alcohol, more exercise, more overall health consciousness, etc. that can improve health, but health has nothing to do with avoiding animal products.
3) That all said, observational studies can occasionally lead to firm conclusions if the association is overwhelming powerful. This happened with cigarette smoking: The increase in heart disease and lung cancer was so large that even the observational data proved conclusive. The very small increment in risk suggested by this study (17% increased cardiovascular disease, 18% increase all-cause mortality) is essentially no difference at all—much too small to be conclusive.
Observational studies have been the basis of all manner of nutritional misinformation. It is the basis for cutting total and saturated fat, increasing consumption of “healthy whole grains,” “move more, eat less,” all the fictions that have created the worst epidemics of obesity, heart disease, type 2 diabetes, gastrointestinal and autoimmune diseases ever in the history of humankind. Dietary guidelines have gotten it wrong for 50 years and I am not hopeful that they will ever get it right in our lifetimes.
What I find most shocking is that most of us in healthcare know that observational studies are virtually worthless and cannot be used to generate cause-effect conclusions, yet the authors of this study state authoritatively that their study should be used to resurrect the advice to limit dietary cholesterol. I cannot decipher their motivations beyond garnering attention and headlines. But don’t fall for it: This is yet another example of how far wrong dietary conclusions can be when drawn from the fictions of nutritional epidemiology.
Debra
March 16, 2019 at 11:29 amThanks you Dr. Davis!
R. Taylor
March 16, 2019 at 11:50 amI totally agree with Dr. Davis’ post but am a little confused when I stopped my daily breakfast of organic steel-cut oatmeal for 2 eggs a day and 3 months later re-tested my cholesterol levels my total cholesterol went up 70 points and LDL-C went up about 60 points. I’m guessing it had nothing to do with the eggs but the lack of the daily fiber/beta glucan from the oatmeal? The ratios with the latest cholesterol tests were all still pretty good but certainly not ideal. Just makes me wonder if I should cut down on the eggs despite the positive outlook on them.
Bob Niland
March 16, 2019 at 1:28 pmR. Taylor wrote: «…am a little confused…»
What diet have you been on, and for how long?
re: «…stopped my daily breakfast of organic steel-cut oatmeal…»
Sound move on the oats.
re: «…later re-tested my cholesterol levels my total cholesterol went up 70 points and LDL-C went up about 60 points.…»
Those are the two least useful numbers on a standard lipid panel. What were the numbers/changes for the more useful TG and HDL? If you get re-tested, get an NMR advanced lipoprotein panel, and check Lp(a) at least once.
Was that LDL-C actually measured (Direct LDL-C, aka DLDL) or one of the fictional calculations (and if so, were you even told which one)?
re: «I’m guessing it had nothing to do with the eggs but the lack of the daily fiber/beta glucan from the oatmeal?»
That’s why I asked about your wider program. Anyone following Undoctored or 2014+ Wheat Belly would presumably be getting ample prebiotic fiber from other sources.
________
Blog Associate (click my user name for details)
R. Taylor
March 16, 2019 at 4:34 pmHi Bob,
The test I did have was the NMR which includes the standard calculated lipid panel. My Triglyceride level was 70 and my HDL level was 71. Shortly before that I had an LP(a) level of 6 nmol/L from a reference range of <75 (that "range" was what was shown). The NMR test was done at LabCorp. Without boring one with details I will say that the total LDL-P nmol/L was 1354 (yes, pretty high) but the Small LDL-P were <90 nmol/L which apparently just accounts for maybe 2% of the total particles. Cardiac CRP was .64 mg/L with range of 0.00 – 3.00. Apparently even if all these labs were in the perfect ideal range from what I have read the CAC calcium score (had one test 15 months ago) was 542 and totally cancels out all great lab blood tests that are good. Been trying to follow Dr. Davis's protocol and hope for the best. What's discouraging is reading stuff on YouTube regarding heart disease that if your score is over 400 "make sure your will is in order". Gives you that confident feeling. Not!
Bob Niland
March 16, 2019 at 7:13 pmR. Taylor wrote: «The test I did have was the NMR which includes the standard calculated lipid panel.»
When you have that, it’s what we need to discuss, in particular the LDL-P Particle Number, and Small LDL-P, as you are now doing.
re: «My Triglyceride level was 70 and my HDL level was 71.»
TG is slightly elevated per program target. Although this could be due to recent/on-going weight loss, or merely failing to do the lab draw fasting, it suggests that net carb intake is higher than ideal (and to confirm that, needs to be cross-checked against HbA1c, fasting BG, then sleuthed with postprandial BGs).
re: «…LP(a) level of 6 nmol/L from a reference range of <75…»
That pretty much eliminates that as a complication.
re: «…total LDL-P nmol/L was 1354 (yes, pretty high) but the Small LDL-P were <90 nmol/L which apparently just accounts for maybe 2% of the total…»
The Small LDL-P fraction is comfortably below program target. Although the program has a target for P#, I’m getting the impression that it’s not worth chasing per se, unless, with all other markers optimal, it remains sky-high (and yours is not really sky high).
re: «…CAC calcium score (had one test 15 months ago) was 542 and totally cancels out all great lab blood tests that are good.»
No such thing. It indicates past problems for sure, but the key going forward is to slow, if not arrest, and ideally reverse any annual score increase. Perhaps you have seen on the blogs: How to Reduce Your Heart Scan Score
re: «What’s discouraging is reading stuff on YouTube regarding heart disease that if your score is over 400 “make sure your will is in order”…»
For someone remaining on a consensus diet, and with or without Standard of Don’t Care stuff like a statin, the score may be expected to grow at 25% per year, and is a real hazard (on which those dire statistics are based). With remediation of diet, score growth can be slowed so that event risk increase is nil. If arrested or reversed, event risk overall can be mitigated.
Also, if all you have is that one CAC (Agatston) score of 542, you have no idea what the current trend is. If it was 436 last year, that’s standard risk. If it was 542 last year, your risk is now substantially lower. If it was 600 last year, your risk now is near zero.
________
Blog Associate (click my user name for details)
R. Taylor
March 17, 2019 at 10:38 amThanks Bob, much appreciate your comments.
Philippa
March 18, 2019 at 10:05 pmI can’t help thinking a more interesting result could be obtained if the study measured how many eggs per capita were purchased by each household studied. I’d be interested in knowing how many eggs were cooked from scratch, vs. (for example) people who frequently ate eggs at a diner – without excluding toast and hash browns (very few people only eat eggs when they eat out), it’s impossible to know what effect the eggs had on their own.