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I Ate 21 Eggs a Week for One Month: This is What Happened to my Cholesterol

eggs cholesterol

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.

Some absorb only 25% of the cholesterol they eat, while others absorb as much as 80%. 2 3

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 genetics panel, which we report on in our nutrition plans, the ABCG8 and ABCG5 genes are important for reasons I’ll touch on in a moment.

On a blood test, your physician will want to see levels for these three sterols as proxies for cholesterol absorption:

  • Cholestanol
  • Campesterol
  • Sitosterol

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 (along with LXR) 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?

To my knowledge, Boston Heart Diagnostics is the only lab running full sterol panels for patients. 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 saw very little change here. 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, at least for me.

My total cholesterol went from 167 ——-> 183 after the egg experiment, so nothing out of the ordinary there either.


You wouldn’t think adding eggs to the diet would increase 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.

Note that my Gene Food diet type is California Coastal. In our scoring algorithm, this is a diet that we predict would be predisposed to higher levels of triglyceride, perhaps sdLDL, VLDL, and elevated blood sugar when consuming a diet higher in simple carbohydrate and sugar.

While my triglycerides, at 115, are still in the green zone on the Cleveland Heart Lab panel, and yes, while it’s actually my LDL-C, and as we will see in a moment, cholesterol rich particle that may be most at issue, I still give wiggle room to maintaining triglycerides at a level higher than most low carb enthusiasts would like to see for a few reasons:

  1. I have rarely seen elevated VLDL, sdLDL (only one time after a deliberate binge and blood draw)
  2. My insulin numbers are usually good to excellent
  3. My strong preference is to avoid factory meat, which sometimes means adding in more complex, and yes, even simple carbs, than may be ideal for my metabolism, so I have some “ethical triglycerides” floating around;
  4. Lp(a), one of my big focal points, is inversely associated with elevated triglycerides in several studies and my personal best Lp(a) ever came at a blood draw where the rest of my results were an utter disaster. 5

Breaking down particle count

Was I showing discordance between LDL-P and APOB?

First some brief background.

LDL-P is the total number of LDL, Lp(a), and IDL particles.

There is one apolipoprotein (b) (“APOB”) for every LDL particle, BUT APOB also reside on VLDL particles. Since VLDL particles confer increased risk, the total picture of APOB, rather than just the LDL particles is preferred by some physicians.

So, to make it more basic: APOB is LDL + VLDL +IDL.

You’ll notice that my APOB marker is in the “green” at 87 mg/DL and my LDL-P is in the “yellow” as higher risk at 1443 nmol/L.

The risk levels assigned by Cleveland Heart Labs would indicate a slight discordance (risk levels don’t match), but this could be attributable to “moving the goal posts” as more insulin resistant patients come to the lab with high VLDL that skews what we consider a normal APOB count, thus the lab adjusted upwards so more people could feel good about their lipids.

As I dug in and read further, both my LDL-P and APOB were about at the 50th percentile, according to the Framingham study, with the exact 50th percentile numbers being:

  • 88 mg/DL (APOB)
  • 1459 nmol/L (LDL-P)

Cleveland Heart Lab does have 935 nmol/L as seemingly the equivalent APOB of 90 mg/DL, but I will go with the Framingham and read these two numbers as essentially concordant.

Will large fluffy cholesterol reduce my risk for heart disease?

I started with the nerdiest issues, which is the possible discordance between LDL-P and APOB, but of more interest for many people is simply the elevated particle count. An LDL-P of 1443 nmol/L is not a great number. However, as I touch on below, my lipid markers of insulin resistance (sdLDL, VLDL, TG) were all in range. As such, I theorize that the particle count was elevated with large fluffy cholesterol rich LDL.

Some say large fluffy LDL are better for heart health than are the small dense LDL particles, and maybe they’re correct. My understanding is that the triglyceride rich, small dense particles are particularly atherogenic when they express greater levels of APOC3 proteins, which increases residence time, which allows for more oxidation of the particles. 6 Even if that is true, it doesn’t mean an LDL-P count of 1,400 is desirable.

The subject is beyond the scope of this blog, but if this is an issue that is of interest, I would recommend the recent consensus statement from the European Atherosclerosis Society which makes the case, once again, that LDL is one of the major factors in the long progression towards advanced heart disease.


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.

Although to my knowledge, there is no way of knowing exactly what is inside of each lipoprotein, these tests, which when elevated are associated with insulin resistance, tell me that my elevated LDL-P of 1443 nmol/L is cholesterol rich. The particles are the large fluffy type that the Paleo camp tells us not to worry about.

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.

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) 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 not where I want it.

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.

I fully get that this experiment is less than scientific, however, I have seen the reverse pattern, with Lp(a) moving incrementally lower when I have been more hawkish with cholesterol in past times.

John's Lp(a) progress

Total cholesterol
August 2016
February 2017
November 2017
September 2018
November 2018
April 2019
72 nmol/L
June 2019
80 nmol/L
March 2020
113 nmol/L

Closing thoughts

  • 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.

John O'Connor

John O'Connor is the founder of Gene Food, host of the Gene Food Podcast and a health coach trained at Duke's Integrative Medicine Program. Read his full bio here.

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