Before I get started with this blog post, I want to emphasize that the results I am seeing here, are likely not the results you will see. N=1 experiments have value because they get people thinking about the process of personalizing health, not because they create hard and fast rules.
To you eggs are what you had for breakfast, a lovely, nutrient dense package of morning goodness. However, in the world of nutrition, things are more complicated. For us, eggs are a polarizing topic. The Vegan community, and especially Vegan physicians, will tell you that eating an egg is worse than smoking a cigarette.
All that cholesterol!
By contrast, you have the Paleo types (who in this case are probably better represented by “the science”) claiming that eating an unlimited number of eggs every day will have no impact on your health or your lipids and that the old thinking on cholesterol has been thoroughly debunked.
Both sides are wrong, for some people.
I decided to eat eggs everyday for breakfast for a month to see how an increase in dietary cholesterol would change my lipid panel, if at all, and use my results as the backdrop for a bi-partisan discussion on the heated topic of dietary cholesterol.
Note: cholesterol isn’t the whole story with eggs, TMAO is something that should also be on your radar.
The new thinking on cholesterol
The idea was hatched in our podcast episode on how to tell if eggs are good for you. On the show, we reviewed a study done by the American Journal of Clinical Nutrition which showed that eating eggs doesn’t seem to move the needle much on blood lipid markers like total cholesterol, LDL-C, Triglycerides and ApoB. 1
To quote the study authors:
Our findings indicate that moderate egg intake (1 egg/d) does not increase the risk of CVD or mortality among those with or without a history of CVD or diabetes. Also, no significant association was found between egg intake or dietary cholesterol and blood lipids.
Seeming to validate the “new thinking” on dietary cholesterol, the AJCN study still didn’t find a significant impact on blood lipids even when egg consumptions spiked to >7 eggs a week.
Of course, there are problems with the AJCN study. A large chunk of it relies on food frequency questionnaires and the subjects are international, so not all were eating eggs with the Standard American Diet.
However, the AJCN study isn’t anything new. Physicians have been sounding the alarm on some of our misguided thinking on cholesterol for quite some time now. We now know that most of us don’t absorb much of the cholesterol we eat from foods like eggs, and to the extent we do, the body regulates cholesterol levels by simply making less of it when significant amounts are absorbed. That is the rule of cholesterol homeostasis – a rule that Vegan commentators often seem to cynically ignore, or downplay.
Cholesterol homeostasis is sound science, but as with any rule, there are exceptions.
Hyper-absorbers of cholesterol
Yes, many don’t absorb much of the cholesterol they eat, but there is a tremendous range, and we do know that cholesterol “hyper-absorbers” are relatively common. Consider the quote below from John D. Griffin at Tufts.
One issue difficult to factor into dietary cholesterol recommendations is individual responsiveness. It has been clearly shown that individuals vary considerably with respect to their response to dietary cholesterol. Subsequent work has demonstrated that the distinction between hyperresponders or hyporesponders has a genetic basis, dependent on polymorphisms in the cholesterol transporters ABCG5/8 and NPC1L1, among others.
Further, not everyone’s body gets the message and stops making cholesterol once absorption picks up. This is especially true for those with one or two copies of APOE 4. 4 In this scenario, you have cholesterol from food as well as the recirculating pool of cholesterol from bile acids making its way into the blood, and simultaneously, the synthetic pathway is fully switched to green, which means your liver is making a ton of cholesterol. Add to this mix poor clearance of cholesterol and you have someone who actually is at much greater risk for heart disease when consuming loads of cholesterol.
The logical next step for anyone reading this blog is to determine whether they are a hyper absorber of cholesterol.
How do you know if you’re a hyper-absorber?
Genes and blood tests.
On a blood test, your physician will want to see levels for these three sterols as proxies for cholesterol absorption:
Animals make cholesterol, a type of zoosterol because of the fact that it is found only in animals, but all plants have phytosterols, their cholesterol equivalent.
Sitosterol, as a type plant fat, isn’t supposed to be absorbed in the gut, nor does the body want it in the bloodstream. When sitosterol does show up in the blood, it’s because it’s been absorbed. Since 80% of the cholesterol in the body is made by the body, we can’t measure cholesterol absorption straight away, so certain types of sterols serve as a proxy.
The function of ABCG5 and ABCG8 genes are supposed to help kick sterols that do get absorbed out of the wall of the gut (the lumen) and back into the intestine where we can get rid of them in our stool (also how we rid the body of excess cholesterol).
I am someone who carries mutations in my ABCG5/8 pathways and, as a result, see greater absorption of both sterol and cholesterol, both of which are there in plain view on my lipid panels. My sitosterol numbers are especially high when I eat a lot of almond butter, avocados, and nuts and seeds. Based on both my genetics, as well as my blood work over a number of years, it’s fair to identify me as a hyper-absorber. This is why I’ve experimented with Zetia in the past.
It was against this backdrop that I went into the egg experiment that follows.
Where is the best place to get a sterol panel done?
Boston Heart’s exclusive Cholesterol Balance test directly measures the major production markers (lathosterol and desmosterol) and absorption markers (beta-sitosterol, campesterol and cholestanol) for circulating plasma cholesterol. The levels of these markers are indicators of LDL-C lowering response to treatments (e.g., statins or ezetimibe).
If you’re wondering whether there is a physician in your area that can run these tests, Boston Heart staff is friendly and will do a search for you in your area for partnered medical offices.
My egg experiment
I kept things simple (and yes, I realize that this is 100% anecdote and wouldn’t withstand troll review, let alone peer review) .
Instead of my usual bowl of oatmeal with banana, I made eggs. Three eggs every morning to be exact. Some of the time, it was eggs over easy with a side of roasted potatoes, most of the time it was scrambled eggs with some low carb accompaniment, maybe grape tomatoes, beans, or sprouts.
Total and LDL Cholesterol
Score one for Peter Attia, the AJCN, and cholesterol homeostasis.
I didn’t see huge changes here, but there was movement. My LDL-C was up about 20%, but at 108 mg/DL it’s not too far out of range where major red flags go off.
My total cholesterol went from 167 mg/dL –> 183 mg/dL after the egg experiment.
You wouldn’t think adding eggs to the diet would increase fasting triglycerides, and things held true to form with only a small move from 112 to 115.
I did give up all sugar during this period for Lent, which is a big part of why my ALT numbers looked so good.
My small LDL-P was 308 nmol/L, well into the green.
At < 1.5 nmol/L my VLDL-P was so low as to be unmeasurable.
Here is why I am worried, and why as a hyper-absorber, I ultimately decided to scale back my egg consumption.
My Lp(a) shot up when I ate a lot of dietary cholesterol.
Lp(a) goes to its highest ever
And now finally we arrive at the key takeaway for me after this experiment – dietary cholesterol seems to drive my Lp(a) numbers higher.
If you’re new to Lp(a), I suggest a quick detour to my recent podcast interview with Dr. Joel Kahn, author of Lp(a): The Heart’s Silent Killer.
Lp(a) is a genetic type of bad cholesterol. The particles themselves are Frankenstein combination of an LDL particle with an Apo(a) protein tail.
Long story short, you want your Lp(a) lower, not higher, and the bad news is that since these particles are genetically determined, there isn’t a ton you can do with diet to move the needle, especially when Lp(a) is severely elevated.
However, in my case, I am one of the lucky ones. I have elevated Lp(a), but only modestly, and I have had it measured where it fell in the green at 72 nmol/L. By contrast, after this egg experiment my Lp(a) hit 113 nmol/L, which is higher risk.
Since Lp(a) is a cholesterol rich particle, it seems that my egg intake plays a role in my serum levels of Lp(a). The combination of hyper-absorbing cholesterol, combined with a genetic predisposition to elevated Lp(a) leaves me more cautious with how much dietary cholesterol I consume.
In my past blood draws, I have seen Lp(a) moving incrementally lower when I have been more hawkish with cholesterol.
John's Lp(a) progress
- Many of us don’t absorb dietary cholesterol, and even when we do, our bodies simply make less of the stuff to keep cholesterol levels in balance. That rule goes the other way as well. When we make more cholesterol, less is absorbed.
- There are exceptions to this rule. People who tend to absorb more of the cholesterol they make (which is 80% of cholesterol in the body) and the cholesterol they eat, are known as “hyper-absorbers.”
- While eating eggs might not have much, if any, impact on lipids for many people, those of us who are hyper-absorbers need to exercise extra care.