Carnivore Diet Blood Work

Meal after meal for well over a year. Not one bite from a plant. Not a piece of fruit, not a serving of vegetables, not an occasional treat. Nothing but meat and some eggs. And here are the results of my Carnivore Diet Blood work.

When my test results arrived, they came with a warning from the facility to go see a doctor. And instead of seeing a doctor, I’ve been thinking about how to write this post – how to describe my carnivore diet blood work in the most helpful way.

This post has taken a long time to write. I started writing about lipids, attempting to describe the complex interplay of cholesterol and triglycerides in the metabolic machine that is our bodies.

But as I was weaving together the intricate interplay between my lipid panel, metabolic panel, and complete blood workup in an attempt to draw a coherent picture of the complex interactions of blood, hormones and lab values in the context of my carnivore diet and lifestyle, I realized what I really needed to write here. 

If I can drive home this one thing, I’ll consider this post a success.

Carnivore Diet Blood Work: The ONE Thing

Because really this post is not about my carnivore diet blood work, nor is it about understanding all the biochemistry and physiology. Rather, it’s about understanding the framework of health in order to have a clue what your picture of health actually shows.

So instead of painting a picture of my carnivore diet lab results, I want to show you the canvas and the frame, so you can be your own artist. And at the end, I will show you some paint strokes – describing my blood work – as a means to help you paint your picture.

By the end of this article, my goal is that you understand the canvas and can see the frame, so you can understand what blood work is, if and when you should get your blood work done, and what it all means.

Carnivore Diet Blood Work: What You Need to Know

Solving the Puzzle

I want to extend our canvas analogy.

If the canvas is your picture of health, imagine the painting is cut up into innumerable puzzle pieces. If you can gather all the puzzle pieces, fit them together, you can see the picture.

The first challenge in solving the puzzle is gathering as many pieces as you can. Getting blood work done gives you some puzzle pieces. Pieces that you can start to connect.

Puzzle Dynamics

This is no ordinary puzzle, however. It’s very tricky. It’s dynamic.

The puzzle pieces change size and shape continuously. And not only the pieces, but the overall picture changes with it.

And all the pieces influence all the other pieces. Just imagine one tiny puzzle piece changing shape, which then slightly alters all the puzzle pieces, and the overall final picture. If you think it sounds like an impossible puzzle to solve – you’re right.

The only way to extract meaning is to understand it as a dynamic system.

People often make the mistake of viewing blood work as a picture of the whole puzzle. When really, your blood work gives you just a few pieces of the puzzle. And if you just put these pieces together and think these pieces show the whole picture it’s easy to draw false conclusions.

With limited perception, what you think you see isn’t always what’s there. A puzzle piece (i.e. a lab value) can be an odd shape (i.e. “high” or “low”) for good reason or bad reason. That irregular shape could be just the perfect fit for that place and time. Or it could be irregularly shaped because there is a problem.

The Frame

The key to putting the pieces together, the key to actually being able to “solve” the puzzle, is to look at all the pieces in context with all the other possible pieces.

The frame that hold the canvas is context.

Context is the key.

Without context we assume your puzzle is the same as my puzzle and all our pieces should be the same.

However, your puzzle is a certain age and gender, it has certain genetics, lives in a certain area, and has a history of certain experiences, certain diets, and habits. No puzzle is the same as yours. The frame of your canvas is unique to you. The puzzle pieces that fit in your frame shouldn’t necessarily be the same shape as my puzzle pieces.

The Indecipherable Puzzle

If you just look at the puzzle pieces from your blood work you have an indecipherable puzzle.

You have this massive frame and just a few puzzle pieces. There is so much empty space in the frame that any attempt to conclude what the picture shows is not much better than a guess.

But when you add other pieces – diet, lifestyle, stress, age, gender, occupation, health and history (health, medical, diet, injuries, changes) you can start to see a more full picture. 

Now even if you gather all these pieces, you still can’t completely solve the puzzle.

The reason is that the puzzle is dynamic. It’s always changing. Puzzle pieces change shape and size with the time of day, with the season, and unless you live in a bubble these changes are difficult if not impossible to control and account for. [r]

Perhaps one of the biggest secrets to getting a good glimpse of the whole puzzle is to acknowledge the fact that the puzzle is ever-changing so at any one time you can get a snapshot, but a snapshot the next day could, and likely will, look different. 

Carnivore Diet Blood Work: When to Get Tested

Gathering Puzzle Pieces

Daily I get a message from someone who has completed 30 days on the carnivore diet, got their blood work done, and is then worried about some number on the report.

They ask me what I think.

And (after responding that I don’t/can’t give medical advice to them) I have to respond with the same “I don’t know.”

Problem #1

The first problem is all they gave me is a few pieces of a gigantic puzzle.

It’s like handing me 5 pieces of a 5-million-piece puzzle and asking me what’s the picture on the puzzle. And even if all 5 pieces seem to fit together perfectly, I’m still just seeing a miniscule part of the whole picture.

Problem #2

The second problem is getting a test so soon after a major dietary change, is like handing me puzzle pieces that morph in size and shape before my very eyes.

I can’t tell what fits with what. Or if I could, it might fit for a second, before it doesn’t fit again.

It’s not that it’s bad to get tested this earlier, it just doesn’t tell you much. But if you continue for 6 months and get more blood work, and then another year and get more, you can start connecting some dots – start to see more of the complete picture.

When to get Blood Work

For most people, I don’t think it makes sense to get blood work after 30 days after a major dietary change (unless you have the time and money – then go for it).

I think it’s more valuable to first reach a homeostatic position with the diet and lifestyle. This is usually at least 90 days as that’s how long it takes your red blood cells to turnover. But if your weight is still fluctuating, hormones are still rebalancing, just wait.

The point of the blood work is to help get meaningful puzzle pieces. And ongoing testing, whether it’s every 6, 12, 18, 24 months can help connect dots over time, again help to draw a more complete picture.

As for what tests to get and how often is can start general but then get very individualized.

As you’ll see with my results, there are some markers that I will test more frequently, some results that caused me to order a unique test, and others that I may test less often. My subsequent testing (both the tests and the interval) will be different than yours. But getting blood work on a recurring schedule that you and your doctor determine is a good way to keep a pulse on these parts of the puzzle, and it helps you connect dots over time, and see your grand picture of health.

Carnivore Diet Blood Work: Where the Confusion Arises

Obviously, the complex nature of our individual puzzles leads to a lot of confusion. But what complicates matters even further is that everyone looks at these puzzles through different frames.

Context Clues

I spent two decades studying nutrition from the viewpoint of a bodybuilder.

When I studied, read research, and experimented it was through a lens of building muscle and losing fat.

It’s fair to say – I viewed nutrition from a different angle than say an oncologist.

Muscle vs Metastasis

Bodybuilding Frame

To build muscle there are important hormones like insulin and IGF-1 that help help pack on the pounds.

Bodybuilders will often combine carbs and protein post-workout to spike insulin and stimulate muscle protein synthesis. They maximally “turn on” mTOR which stimulates cellular growth by activating IGF-1.

All good in the context of building muscle.

Physician Frame

But through the eyes of many healthcare practitioners, insulin, IGF-1, and mTOR are all bad.

A common thread among obese and diabetic patients (and so many chronic diseases) is hyperinsulinemia – chronic high insulin levels. Insulin is bad news.

Through the eyes of an oncologist – insulin, IGF-1, and mTOR –are really bad. They fuel aging and cancer.

Longevity Researcher

Consider the dichotomy that could exist between two longevity researchers.

One researcher concludes that turning these muscle building growth factors “on” increases longevity. Greater muscle mass is consistently one of the best predictors of living a long life and lowering all-cause mortality rates. (r, r)

A second researchers sees the correlation linking mTOR, aging, and death.

So are these hormones good or bad? Who is right?

No one is wrong, per se. The context is different.

If you see insulin, IGF-1 and mTOR only from one vantage point you may miss the whole picture. One longevity researcher agrees with the bodybuilder, concluding stimulating these growth factors are essential to living a long life. The other longevity research agrees with the oncologist, concluding they fuel cancer growth and aging.

The frame you look through matters.

Carnivore Diet Blood Work: Cholesterol Context Clues

I want to look at a couple of examples of understanding labs values and nutrition in context. 

Cholesterol

If the average doctor looks at my blood work, they may have a heart attack. And they’d likely think I’m on the verge of having one with them.

But they would be missing all the context – looking through the wrong frame or only seeing part of the picture.

Cholesterol can be “high” for good reasons and high for bad reasons. I wrote this article here to specifically address cholesterol, but for now, it’s enough to know that many factors influence cholesterol levels.

Cholesterol and Metabolism

If you are lean and eat a high fat, low carbohydrate diet, the way your body distributes energy is different than someone who eats a carbohydrate-based diet. (r)

If a doctor is missing this context, or perhaps doesn’t understand how this process works, they will say things like your cholesterol is high and you need to be on a statin.

Well, they will be right and wrong. Your cholesterol very well may be “high” compared to others on a the Standard American Diet (SAD), but it is “high” only in the context of a SAD. It is the physiologic norm for this phenotype (lean, high fat, low carb). The body is functioning exactly as it should. He’d be very wrong in suggesting cholesterol lowering medication.

Measuring What Matters

One obstacle is measuring what matters. 

For example, drugs are often developed to reduce the risk of heart attack or stroke with a goal of long term survival. These are hard to measure without long-term clinical outcomes. So instead, pharmaceutical companies use indirect “surrogate” or “proxy” measures.

Proxies help get drugs to market as fast as possible.

Blood Sugar or Death

Consider the drug Avandia. It is good at controlling blood sugar. Since blood sugar is easy to measure it was used as the proxy for this diabetic medication.

The problem is that 2 out of 3 diabetics suffer heart complications. So, one of the main goals of diabetic treatment is to reduce the risk of heart problems.

Although Avandia helped control blood sugar, that proxy measurement got confused by what actually matters – death. And in Avandia’s case it increases the risk of heart attack, stroke, and death. (r, r, r, r, r, r, r)

The proxy (blood sugar) didn’t correlate with the outcome (mortality).

This happens all the time.

Cholesterol Proxy

Statins are prescribed to lower cholesterol. Cholesterol is a proxy. There are drugs like Vytorin and Zetia which are great at lowering cholesterol. But they have no evidence of lowering heart disease or stroke. But lots of evidence of adverse side effects. (r)

I bring up proxy measurements because you may have a puzzle piece that looks irregular, like my cholesterol. And if this proxy (puzzle piece) isn’t seen through the correct frame it can cause you to worry. And further, it’s important to recognize that if a puzzle piece is used as a proxy to predict what the whole picture looks like – it could easily be wrong.

It’s like saying “if this one puzzle piece is a certain shape, then we predict your whole completed puzzle looks like this.” But often that puzzle piece isn’t representative of the whole puzzle.

Carnivore Diet Blood Work: What is it?

A helpful way to view your blood is to see it as a delivery system (of oxygen and nutrients) and a disposal system (of wastes products).

Certain organs are stops along this system for processing before delivery or dumping – like the liver, kidneys, spleen, and lungs.

Blood work is a snapshot in time to get an idea how this system is working.

There are thousands of tests you can get. All are puzzle pieces.

Enough of the preamble. Let’s get to my Carnivore Labs…

Carnivore Diet Blood Work: My Results

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Here are my blood test results.

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I ordered three common panels – lipid panel, metabolic panel, and a complete blood count – as well as a few less common tests like insulin and hs-CRP.

This is not to say these are necessarily what you should get.

If I had signs of metabolic syndrome, I’d get my fasted blood sugar, a glucose tolerance test, hemoglobin A1c, and fasted insulin to see how they work together for a more complete picture.

If I had risk factors associated with cardiovascular disease, I’d get a fractionated lipid panel, which is a more in depth look at the lipids.

Lipid Panel

The lipid panel measures two types of fats – cholesterol and triglycerides.

The first thing that jumps out when looking at my blood work is my cholesterol. It’s “high.”

I am perfectly happy with it.

My HDL is quite high, my triglycerides are quite low. This is the ratio I care about. I have very low remnant cholesterol. Based on this, my LDL is of absolutely no concern to me. (r, r)

If you want to know what numbers are important, here’s my list.

As far as I’m concerned, I’m happy my brain and body are getting all the cholesterol they need. (r, r) And to me it’s further evidence that I’m a fat burner, which isn’t too much of a surprise as I’m eating almost no carbohydrates, I’m quite lean, and train daily. 

Metabolic Panel

The metabolic panel gives me a look at the processes in the body that convert or use energy.

Here I get information about minerals which can impact things like water balance, blood acidity, and muscular function (i.e. calcium, chloride, magnesium, phosphorous, potassium, and sodium).

I get information about organ function like the liver and kidneys through values like bilirubin and albumin.

Lots of puzzle pieces here.

To the casual observer, a couple puzzle pieces look irregular in shape.

BUN and ALT

My blood urea nitrogen (BUN) as well as my alanine aminotransferase (ALT) are high. “My liver and kidneys are failing!” No, I expected this.

In the context of a high protein diet and daily training, BUN is often elevated due to the high rate of protein metabolism and muscle turnover. (r, r) People fear metabolic acidosis but looking at my metabolic panel there just isn’t any evidence of this whatsoever.

The same goes for ALT. Elevated liver enzymes are very common in people who work out on a regular basis. ALT tends to remain elevated for 7+ days post workout. (r, r) And I workout every day.

I could have taken a week or two off…oh who am I kidding, I couldn’t do that.

There are a couple other values that I want to highlight.

Insulin

A fastest insulin test is one of the simplest, most affordable, most accurate tests to evaluate metabolic health. Hyperinsulinemia underlies so many of our modern chronic diseases – everything from heart disease to cancer to dementia. The biggest killers.

Blood glucose and HbA1c are valuable, but fasting insulin can detect problems before insulin resistance (pre-diabetes/diabetes) starts to set in.

My insulin was 2.3.

This is very insulin sensitive. For perspective, anything below 2.0 is undetectable. This is the opposite of insulin resistance.

There isn’t agreement on what is an ideal fasting insulin, but a study out of Arizona found that women with a fasting insulin around 8.0 had twice the risk of prediabetes as those with 5.0. (r) And research from the University of Washington showed “the average insulin level in the US is 8.8 mIU/ml for men and 8.4 for women.” (r) From the research I’ve done, I would say 2-5 is an ideal range.

If you are getting your blood work done, ask you doctor if you can include this test.

HS-CRP

A second test I ordered which is out of the “norm” is a high-sensitivity C-Reactive Protein test. CRP is a protein that the liver makes when there is inflammation in the body. This test evaluates inflammation and risk for heart disease. You want it below 1.0.

CRP is traditionally measured down to concentrations of 3-5 mg/L, but with hs-CRP you can now detect even low-grade inflammation down to 0.2 mg/L.

My CRP was so low it was beyond detection (less than 0.2 mg/L).

This is a good sign that I don’t have any kind of chronic systemic inflammatory problem and that I’m quite low risk for cardiovascular disease. (r)

If meat was inflammatory or if it was a cause of a chronic inflammatory reaction, like from an autoimmune response, it would be detected via CRP.

It’s important to note that CRP can be elevated by many inflammatory diseases, cancers, and infections. But if it’s elevated, it’s an important puzzle piece to investigate.

Complete Blood Count (CBC)

The CBC gives me a look into the health of my blood cells – red, white, and platelets. I can see the quantity, size, and volume as a broad screening tool to detect possible infections, allergies, or diseases like anemia or leukemia.

My blood is pretty boring, all values sitting within normal range. 

Carnivore Diet Blood Work: Values of Note

I want to point out a couple values of special note in relation to the carnivore diet.

• Homocysteine – On a carnivore diet people fear insufficient folate. Yet if I were deficient, my homocysteine would likely be high. But it’s right in the normal range. People on plant-based diets tend to have high homocysteine levels – associated with higher likelihood of cardiovascular disease and death. (r)
• Uric acid – Many people have concerns about the high purine levels in meat and gout. Not an issue.
• Calcium – I eat little to no dairy, and my calcium is in the high normal range.
• Testosterone – When I announced I got my blood work, this was the one number most men asked about (it was in the high/normal range):
  • 915 ng/dL total testosterone
  • 101.8 pg/mL free testosterone
• Estrogens – Low/normal
• Thyroid – TSH is normal
• Blood Sugar –
  • Glucose: 89*
  • Insulin: 2.3
  • Hb A1c: 4.9

*Although a blood glucose of 89 falls within the “normal” range, and I’m clearly not diabetic based on the other values, my blood glucose is higher than most would anticipate given this data. But this isn’t uncommon among low carb athletes. There is a theory called “Adaptive Glucose Sparing” in which the body preferentially uses fat for energy and resists the use of glucose, saving it for certain tissues like the brain and red blood cells.

Carnivore Diet Blood Work: Irregular Puzzle Pieces

When I got my blood work results I had two irregular puzzle pieces that didn’t make immediate sense to me. This gives me a good opportunity to explain my thinking process around irregular puzzle pieces.

DHEA Sulfate

The first puzzle piece that that didn’t seem to fit was my DHEA. It was a bit low. Not super low, but low, nonetheless.

This value was particularly curious because DHEA is a precursor of testosterone and my testosterone was quite high.

DHEA is produced by the adrenals and it does tend to be high in young male athletes. But like many hormones, it has numerous roles. It also tends to be high in people with insulin resistance and chronic high stress. It’s obviously influenced by a myriad of factors.

Testing DHEA

Doctors generally order DHEA test because they’re worried it’s too high (not because they think it’s low).

DHEA can be high for numerous reasons like stress. In stressful situations the adrenals release cortisol and DHEA. For example, it is often elevated in people suffering from PTSD. (r)

Generally, a doctor does not order DHEA because they suspect it might be low, unless checking for Adrenal Insufficiency (AI). There has been a recent trend of testing for “adrenal fatigue” though there is no evidence that “adrenal fatigue” is actually a thing. (r) To me it makes sense that there are milder forms of adrenal insufficiency that could explain many of the symptoms we face as a result of our high stress modern lives, but medical literature doesn’t support it.

Anyway, searching for low levels of androgens in healthy people without specific symptoms is not generally recommended, and treating them with androgenic hormones isn’t the standard of care.

DHEA Insufficiency

Symptoms of low DHEA include poor body composition (fat storage and little muscle), low libido, fatigue, depression, weakness, difficulty in getting up in the morning, and a weakened immune system.

I simply don’t have any clinical symptoms characterized by DHEA insufficiency.

The clinical expression of hormone function is a very important consideration. How you look, how you feel, how you perform are all parts of the puzzle.

So why is my DHEA low?

I have a hunch that it could be from maintaining too low levels of body fat, overtraining, or potentially a high level of receptor sensitivity (in other words, I don’t need much of it in order for it to optimally perform its functions).

DHEA Hypersensitivity

DHEA hypersensitivity is generally understood in the context of women who have normal DHEA lab values, but experience symptoms associated with high levels of DHEA – weight gain, hair loss, low energy, acne, irritability, infertility, deepening of voice, stress, and PCOS.

It’s an imbalance between the amount of DHEA and the receptor sensitivity.

In a balanced scenario “low” DHEA levels would correspond to “high” receptor sensitivity, and is potentially why my DHEA is low.

Hormone Receptor Sensitivity

I do think with a proper diet, exercise, sleep and general health we see efficient use of hormones (not over-production) with very sensitive receptors.

Other hormone receptors like thyroid and leptin can behave much the same way – whereby your organs don’t have to continuously pump out loads of hormone for proper function. They are efficient.

I think we should be cautious of the reactionary doctor who has an asymptomatic patient with “low” T3 and wants to put them on Synthroid. Hopefully most doctors try and see through the correct frame to make sense of the puzzle pieces.

Ferritin

The second irregular puzzle piece was my ferritin. It was quite high.

Ferritin is a measure of iron storage.

The easy explanation would go something like this: I’ve been eating a lot of red meat which is high in iron so – duh – my iron stores are high. But that would be missing a key piece.

Iron Absorption

The liver produces a hormone called hepcidin which monitors iron levels and tells intestinal cells how much to absorb.

On average we lose 1 -2 mg of iron every day – so not surprisingly – this is how much we usually absorb per day.

There are really two main causes of high ferritin levels:

1. Absorbing more than normal (hereditary hemochromatosis).
2. A reactionary response to inflammation such as: metabolic syndrome (obesity, diabetes), liver disease, daily alcohol, infections, cancers like Hodgkin’s lymphoma and leukemia, rheumatoid arthritis and systemic lupus erythematosus). (r, r, r)

The second one, a reactionary inflammatory response, explains high ferritin in over 90% of cases.

The problem is, the most typical explanations for high ferritin don’t seem to apply to me. I don’t have metabolic syndrome (see Metabolic Panel), I’m not chronically inflamed (see HS-CRP), I don’t drink, I don’t have any infections (see CBC), and I don’t seem to have any cancers or autoimmune diseases.

So perhaps I have hereditary hemochromatosis (HH)…

Hereditary Hemochromatosis (HH)

Hereditary hemochromatosis is a genetic change affecting the synthesis and/or activity of hepcidin. The result is an increase in intestinal absorption of iron and potential iron overload.

The incidence is about 1 in 200 so while unlikely, I definitely can’t just rule it out. (r)

Unfortunately, I don’t have prior blood work with ferritin levels.

But while my ferritin was high, it really wasn’t in the HH high range (>1000).

Vitamin C can increase iron absorption, but on a meat-only diet, and without supplementing Vitamin C, this isn’t a likely suspect. If I don’t have HH and I don’t have reactionary inflammation, it turns out we really don’t know the cause of mild elevations in ferritin. (r)

This leaves me in an interesting situation. I have an irregular puzzle piece with no immediate explanation.

What to do – How I think about “irregular” puzzle pieces

So here’s what I’ll do and how I think about this.

• I will likely get another iron panel – this time including TIBC (total iron binding capacity). This way I can re-check ferritin and see if TIBC >45% (which is an indication of HH).
• If TIBC is greater than 45% then I’d get a genetic test to rule out hereditary hemochromatosis.
• If it is less than 45% and the ferritin is still around where it is, I’ll likely monitor over time.

As the current research recommends, observation below 1000 ng/mL is standard procedure in this case. But if ferritin elevates towards or above 1,000 ng/mL, I will likely get further testing. (r)

I tell you this to show you my train of thought when it comes to blood work.

• What it is – A process of understanding / putting puzzle pieces together.
• What it’s not – A reactionary response to an elevated value and immediate medication/treatment/jumping to conclusions.

Understanding vs. Justifying

There is a big difference between understanding the puzzle pieces in the big picture frame and trying to justify puzzle pieces that don’t look good.

For example, I can understand why my cholesterol, BUN, and ALT are high. And not only understand but expected this in the context of my life. It makes sense in how it fits with the other pieces of the puzzle.

But this is not to say that if I see puzzle pieces outside of normal shapes and sizes to justify them with theories.

It justifies just the opposite, to dig in, further evaluate, find some more pieces to see if it fits or if there might be a problem. 

This is exactly what I did and am doing with the ferritin and DHEA numbers. I’m digging in to possible reasons. I will monitor and test over time. I’ll keep an eye out for issues and explanations. And seek out more informed experts and opinions if called for.

Carnivore Diet Blood Work: 2024 Update

Fast-forward. It’s now 5 years later. And after about 7 years of carnivore eating, I got my blood work done again. Yes, this is longer than I would have recommended. But the whole 2-year Covid thing derailed a lot of things with blood and needles.

However, the context around this blood work is different than last time.

This blood work was done after 18 months of a “Carnivore Bulk” where I was eating mostly just 3 foods: beef, eggs, and raw milk.

The 2 big differences were the hypercaloric diet (thus increasing weight/body fat) and raw milk.

Important things to note about this blood work

• Raw milk has carbohydrates, and at my peak, I was eating ~100 grams of carbs from lactose per day
• My weight went from 151 to 186 pounds and my body fat from 12% to 19%
• I got this blood drawn January 31st 2024, in the depth of St. Louis winter

The last important piece of context to this blood draw: The night before I was hit with a personal issue that provoked a lot of stress and a sleepless night before my 7:30 a.m. blood draw. I didn’t get my cortisol taken, but I’m pretty sure it would have been at the highest level possible. I was even having anxiety about the anxiety and how it would impact these results. Did this impact my results? Probably to some degree, but what and how much…who knows.

Now to the blood work.

Lipid Panel

My lipids in 2018 were:

• Total Cholesterol: 313
• LDL: 185
• HDL: 111
• Triglycerides: 72

I was a borderline Lean Mass Hyper-responder (LMHR).

But between the carbs (lactose from the raw milk) and the extra body fat (from the bulk), my cholesterol this time should be down according to the Lipid Energy Model, which is the theory that explains LMHRs.

Could putting on body fat and adding in one of the most cholesterol-rich foods (raw milk) actually decrease my cholesterol?!?!

It turns out the answer is “yes!”

My 2024 Lipids (vs 2018): 

• Total Cholesterol: 205 (down 108)
• LDL: 110 (down 75)
• HDL: 82 (down 29)
• Triglycerides: 72 (same)

With the raw milk and added body fat, I’m no longer a LMHR.

My LDL is just outside the “normal” range and my HDL and triglycerides are still solid.

The question now is: if you’re on a very low-carb diet, and your cholesterol goes up, is that going to cause cardiovascular disease?

Should you just add 50-100 grams of carbs/day which can dramatically decrease your LDL to mitigate this risk if you are a LMHR? Maybe.

The truth is that we don’t know.

But a recent study by Dave Feldman and colleagues sheds light on this…

They compared 5 year keto LMHRs to a matched control group.

Results: There was no relationship between LDL levels and arterial plaques. (r)

Metabolic Panel

The metabolic panel was quite similar to 2018.

I’ve addressed BUN above, but one thing to address here is blood sugar. I think the glucose was on the higher end because of the stress/sleepless night/elevated cortisol. This is an easy one to re-test (but I’m not too concerned about it).

My blood sugar over the last 90 days and insulin help fill in the picture.

Both my A1c and insulin are in a healthy range. Compared to 2018, they are higher, which is what I’d expect having put on about 35 pounds and pushing my body fat percentage to the higher end of the “healthy” range (19%).

In fact, having more “insulin resistance” at this body fat level is what you want to see. It means the body is resisting the further storage of energy.

A problem occurs when people have higher body fat and are still too sensitive to insulin whereby the body stores excess and beyond. This is what happens with excess polyunsaturated fatty acids like linoleic acid (i.e. “seed oils”) in the diet. This is a long discussion for another post, but in essence, lower body fat should result in higher insulin sensitivity and higher body fat more insulin resistance within a physiologic norm.

C-Reactive Protein

My hs-CRP is still quite low, indicating general inflammation is low.

Folate

Prior to the blood draw, several people asked that I check my folate. It looks to be all good, in the upper half of the reference range.

Over the last 18 months, I have had some beef liver (that which came with the cow I bought) and I have had eggs, usually 3/day, which are two good sources of folate.

Thyroid

My TSH was a bit lower than in 2018, which is expected due to the increase in food consumption and body fat.

Testosterone

Testosterone is nearly identical to 2018, in the upper end of the reference range.

Free testosterone is normal, but ideally would be a bit higher. Perhaps some getting bound up in SHBG (more in this in a second).

DHEA

DHEA is a bit higher than 2018, still on the low end.

This time I can’t say it’s because of the low body fat, as I got up to 19% body fat. But perhaps overtraining and over stress are keeping it down, or as discussed above, the potential for sensitive receptors.

Sex Hormone Binding Globulin (SHBG)

Unfortunately, I didn’t previously test SHBG, so I don’t have a comparison. But it’s often tested if someone is having symptoms of low testosterone.

SHBG binds up testosterone, thereby decreasing free testosterone. So, to increase free testosterone, people try and lower SHBG.

But there’s some problems with this…

The first problem is that the best way to lower SHBG is to be obese. That’s obviously not our goal.

SHBG tends to go up as insulin goes down. But insulin sensitivity is generally a good thing. I don’t recommend trying to become diabetic to lower SHBG in order to try and increase free testosterone.

Next, and related, is that polyunsaturated fatty acids (PUFAs), high in vegetable oils, turn down SHBG. (r) But I wouldn’t turn to these to turn down SHBG as they are obesogenic (among other detriments).

Eating the least healthy foods and getting fat in order to increase free testosterone seems counterproductive to me.

Lastly, low SHBG is not only associated with obesity but overall mortality as well. So the goal isn’t really just to lower SHBG, but to get it in the right range, which if it’s high, can mean increasing free testosterone.

My SHBG is in the higher end of the reference range, and perhaps ideally would come down a bit.

If you’re SHBG is high and free testosterone is symptomatically low, one thing that could help is some extra boron, although the effects seem to be transient.

My biggest sources of boron are milk and coffee. To get more (~1 mg/day) you’ll likely have to reach outside of the animal kingdom with foods like prunes, raisins/grapes, peaches, apples, pears, or avocados (which also provide a good magnesium punch which can help). However, fiber tends to lower testosterone and increase SHBG…

If you’re no / low carb and have high SHBG, adding in carbohydrates would likely help bring it down as carbs move your physiology more from the “fasted state” to a “fed state” which can turn down SHBG.

For me, I think my biggest issue which is likely impacting some of these sex hormones is this next number…

Vitamin D3

My vitamin D is low.

Prior to getting this blood work done, I predicted by cholesterol would come down (it did), that my ferritin would come down (see next section), and that my vitamin D might be low.

Why low vitamin D?

The first obvious reason is that prior to this blood work, I’d gone months with little sun due to winter. The second, less obvious explanation, is that I’ve put on body fat during this time too. Vitamin D is a fat-soluble vitamin. I hypothesized that less sun exposure with concomitant increasing fat reserves would result in lower vitamin D. Alas, I was right. Granted this is lower than I hoped.

At the time of this writing, I am starting my Carnivore Fat Loss phase and I’ll be doing this in the spring/summer of 2024. I predict the vitamin D levels will come up with this combination (fat loss + sun). I’ll have to re-test toward the end of summer and see.

These lower levels of vitamin D can impact sex hormones like testosterone, DHEA, and SHBG.

I know many people will say, “Just take a vitamin D supplement!” But I’m not a big vitamin D supplement advocate (another long discussion for another post). But maybe. We’ll see what the summer fat loss results bring.

Iron / Ferritin

The number I was most keen to see — ferritin.

In 2018 it was high. I re-tested to verify and it was confirmed high (600-700 range).

Now…it’s in the normal range, even in the lower half of the reference range.

I anticipate this for a few reasons.

First, over the last 5 years, I’ve donated blood 13 times. That’s roughly 6L of blood.

Second, I’ve been drinking milk. Calcium competes with heme-iron, thus inhibiting its absorption.

Third, I’ve continued to drink coffee and eat eggs both of which can inhibit iron absorption. (r)

Lastly, I have a theory. Prior to carnivore I had an iron poor diet. Hormones (i.e. hepcidin) did their best to maintain homeostasis with low iron intake. But with a rapid switch to an iron-rich diet, my body didn’t have time to re-calibrate, resulting in excess iron absorption and thus high iron storage (ferritin).

I’m not sure how much of a role each of these played, but I’ll likely continue to donate blood 1-2X/year and perhaps keep some milk in the diet (but I’m planning on reducing this quite a bit).

It’s great to know that my iron is under control and I can still eat pounds of red meat per day 🙂

Now I have to go get out in the sun, so I’ll see you later!

Carnivore Diet Blood Work: 2024 Update (Part 2)

Fast forward again. It’s now been 6 months since my previous labs and I got my blood drawn again.

This time under (almost) the exact opposite circumstances.

Over the last 6 months, I’ve lost the 30+ pounds of the weight I had gained during the previous 18 months. Instead of it being the end of winter, it’s the end of summer, and I’ve gotten to catch some rays!

The one thing that hasn’t changed is the food. I’ve continued to eat just beef, milk, and eggs. Just less.

It concludes my 2 year experiment of eating just 3 foods — beef, milk, and eggs — to build muscle and lose fat.

Important things to note about this blood work

• My weight went from 186 to 154 pounds and my body fat from 19% to 7%
• I got this blood at the end of summer, September 5th 2024.

The last important piece of context to this blood draw: It was scheduled the week before, but I moved it due to having caught a cold (asymptotic besides 1-2 days of down energy), and I decided to move the appointment in order to minimize variables that could impact the results (see “ferritin”).

I generally don’t recommend getting blood work when “bulking” or “cutting” as it can distort results. But I was curious about how fat gain and loss could impact blood markers.

Prior to getting the blood work, I made predictions in my Saturday 7 newsletter.

Below, I will summarize the predictions with their rationale and compare with the actual results.

Now to the blood work.

Lipid Panel

Six months ago, I predicted that my cholesterol would be in line with the Lipid Energy Model (LEM) and it was more-or-less correct.

So, based on this model, I thought my cholesterol would rise this time, compared to 6 months ago, but not to “Lean Mass Hyper Responder” (LMHR) levels.

My rationale was that 6 months ago I had more body fat and was consuming more carbs from milk lactose. Now having lost 30+ pounds and dropping 7% body fat, I’m leaner and consuming fewer carbs, so according to the LEM, I should have higher cholesterol.

The caveat is that my overall fat intake (and likely metabolic rate) is lower, which would mean less “fat turnover” which could decrease LDL, and is why I don’t think I’ll measure as high as LMHRs. 

Previous (6 months ago):

• LDL: 110 
• HDL: 82 
• Triglycerides: 72 

Prediction for this time:

• LDL: 140
• HDL: 90
• Triglycerides: 68

Actual Results:

• LDL: 136
• HDL: 86
• Triglycerides: 98

Not a bad prediction!

Even though I’m much leaner, it seems the raw milk and lower fat consumption, is keeping my cholesterol down from LMHR’s but “higher” than SADs.

Per the above on cholesterol, I’m totally good with these numbers.

Metabolic Panel

For the metabolic panel I predicted:

“I don’t expect anything crazy with the metabolic panel beyond the standard expected higher values for BUN and creatinine.”

This was also mostly right on target:

I’ve already addressed much of this above like BUN/Creatinine (as well as in other articles, like here).

One interesting thing of note is that blood glucose came back down.

Regarding calcium, it is ever-so-slightly elevated, which is not a concern for me. If I were forced to rationalize this, I’d say there’s a couple possible explanations.

As you’ll see under “Vitamin D” below, it went up. A lot.

Vitamin D plays an important role in calcium metabolism, increasing absorption. Combine this with the fact I was still drinking milk and eating high protein (which also increases absorption), and it’s not crazy to see why it’s on the higher end.

Calcium is also regulated by parathyroid hormone, which I didn’t test, but my guess is that it’s likely trending down to decrease calcium a bit (decreased osteoclast activity, kidney reabsorption/downregulating calcitriol), all of which is good for bone health.

Beyond the increase in vitamin D, another possible explanation is slight dehydration which can increase the concentration of calcium in the blood due to reduced volume of fluid in the bloodstream. And I was fasted 12+ hours.

Insulin

Over the last 6 months I more than cut my body fat in half, and thus I predicted my insulin sensitivity would double.

• Previous Result: 5.6
• Prediction: 2.3
• Actual Result: 3.6

I would grade this as an accurate prediction without giving myself full credit 🙂

Insulin sensitivity increased but closer to 1.5X than 2.0X.

Contrary to popular opinion, I think the fact that I’m less insulin sensitive than I predicted is a good thing. Being overly insulin sensitive (i.e. overly low basal insulin levels) can cause electrolyte issues as well as cause more rebound fat gain.

Thyroid

My TSH prediction was wrong because I misspoke. I meant to say that I expected my T3 (active thyroid hormone) to go down a bit with the fat loss and energy restriction. This is a metabolic adaptation to conserve energy, which results in TSH increasing.

Although TSH rose slightly, I didn’t have symptoms of low T3, besides the fact I wasn’t as hot this summer as I was during the previous summer when I was piling on the body fat.

Testosterone

Testosterone — I was right, yet very wrong in my prediction.

I was keen to see what would happen to my testosterone with a 6 month diet to low levels of body fat.

Testosterone is notorious for tanking when cutting down to low levels of body fat because it creates physiologic stress that impairs testosterone production and use.

However, even though I had dropped to 7% body fat, I thought there were factors that could have saved it a bit.

Because I anticipated a rebound in my vitamin D and felt good, I thought perhaps my testosterone wouldn’t drop that much. And that was partly correct…

• Previous: 891
• Prediction: 860
• Actual Result: 615

My overall testosterone dropped from 891 to 615, which is a significant drop. But 615 is not low.

What is low is the free testosterone.

It’s all getting bound up in SHBG…

Sex Hormone Binding Globulin (SHBG)

SHBG binds up testosterone, thereby decreasing free testosterone.

I expected my SHBG to go up because low levels of body fat and low insulin cause SHBG to rise. Basically, it goes like this:

Low body fat ➡️ perceived threat to survival due to a lack of energy reserves ➡️ increase in SHBG ➡️ decrease in free testosterone ➡️ signals the body to downregulate anabolic processes (like muscle building) to prioritize survival functions.

In essence, low body fat levels trigger a cascade of hormonal adaptations that reduce free testosterone, increase SHBG, and signal the body to conserve energy and prioritize fat storage as a survival mechanism.

I anticipated this cascade. I just didn’t think it had gone as far as it did because even though I tipped the InBody scales at a low of 6.6% body fat, I felt good.

Throughout the cut I had great energy, motivation, and drive. Alas, according to these labs, my body doesn’t feel safe being this lean.

To me, the obvious solution is to not be 6.6% body fat.

When you hear people say being too lean isn’t healthy, this is what they mean, it can really affect hormones in non ideal ways.

DHEA

Based on my low free testosterone and high SHBG, I would have guessed my DHEA would have been low too.

However, it wasn’t. And it was exactly as I had predicted:

• Previous: 100
• Prediction: 150
• Actual Result: 150

I predicted my DHEA would go up to 150 because I thought it was likely low because my vitamin D was low. And since I anticipated my vitamin D would go up, I guessed my DHEA would follow. And it did.

Perhaps, the low vitamin D played a preponderant role in it being on the low side.

Vitamin D3

Six months ago, my vitamin D was the biggest “red flag”. It was low. But it kind of made sense. The blood work was done after a long winter and significant fat gain (less exposure, more sequestration into adipose).

With the summer sun and decreased body fat, I expected my vitamin D to be significantly higher. I had half the body fat and had gotten twice the sun, so I guessed my vitamin D would double.

• Previous: 22
• Prediction: 45
• Actual Result: 52

This prediction was pretty much right on the money.

This result made me think about how I’m likely doing my “bulks” and “cuts” backwards.

Ancestrally speaking, you would be more likely to “bulk” in the summer and through the fall with food abundance and in preparation or winter. Winter months would have been natural “cuts” with less food abundance. Nature’s clock would have you gaining fat while getting plenty of sun exposure, and losing fat when you’d have less access to sun.

I do it backwards. I tend to bulk to the winter, and then cut during the summer, but I hypothesize that if I more closely mimicked nature, my vitamin D would be better regulated throughout the year.

Iron / Ferritin

I’d say my ferritin was the most unexpected number.

To recap, in 2018 it was high. I re-tested it and verified. It was indeed high (600-700 range).

Then, 6 months ago, after 13 blood donations over 5 years, it dropped into the normal range (128).

I hypothesized that the early high ferritin was a result of a iron poor diet prior to going carnivore. I thought the hormones hepcidin was downregulated and with the rapid switch to an iron-rich diet, my body didn’t have time to re-calibrate, resulting in excess iron absorption and thus high iron storage (ferritin).

I had a hunch that after 7 years of massive beef consumption that my ferritin wouldn’t rise to previous levels even if I stopped donating blood.

But I was (perhaps) wrong.

Over the previous 6 months, I did not donate blood and my ferritin shot back up to 481.

There are 3 potentially confounding factors here.

1. H63D Gene

I’m heterozygous for the H63D mutation.

This can result in excess iron absorption. So it’s not “carnivore” or “red meats” fault. It’s my genetics which likely mutated based on the iron poor diets of my ancestors post-Agricultural Revolution.

2. Liver

During my 6 month cut, I ate about 0.5 oz of liver per day. The thought was I wanted to maximize nutrition while I consumed less food. Liver is a nutrient powerhouse. But it is very high in iron. So even the tiny dose of 0.5oz/day can add up (potentially more so due to #1’s H63D polymorphism).

My plan is to greatly reduce / eliminate my liver consumption.

3. Sick?

I originally scheduled my blood work a week earlier, but I postponed it a week because I felt off (low energy for 1-2 days and thought I might have caught a cold), and I didn’t want to skew these lab results. If I was indeed sick, it can cause the body to sequester iron and boost ferritin. While I don’t think this is the mostly likely cause, it can’t be ruled out as a potential variable.

My Next Steps

Based on these lab results, my next steps are to continue my reverse diet where I’ll increase my body fat (13-15%) which I believe will get my testosterone and SHBG back in a good place.

I’m going to continue to put an emphasis on getting adequate sun exposure, and am considering altering my “bulk” and “cut” phases to more closely align with Mother Nature.

And I plan to align my diet more closely with what I believe is my ancestral diet.

I’d argue all our ancestral diet’s are meat-based. So beef will remain at the center of my diet. But as Homo sapiens dispersed from Africa and settled in different locations, different foods became more/less of people’s ancestral diets, especially at the turn of the Agricultural Revolution.

Based on my H63D polymorphism, I’ll likely limit or eliminate liver from my diet (this is also congruent with my vitamin A toxicity hypothesis). Based on my tolerance to dairy (lactase persistence), I’ll likely keep some dairy in my diet as this genetic mutation spread rapidly throughout Europe during the Agricultural Revolution indicating the likely importance on dairy as a survival advantage and daily staple of my ancestors. And after 90 months of carnivore eating, I’m considering testing some of the hypercarnivore spectrum, but that’s TBD, as I feel great, happy with how I look and perform, and with a few modifications, I’m confident the labs will look like I want them to. So stay tuned 🙂

Carnivore Diet Blood Work: Conclusion

As I hope I made clear – lab values are just a few pieces of a very complex puzzle that needs to be put together in the right frame.

Since you are reading this you are probably like me, you self-educate, you’ll try putting your puzzle pieces together, and try making sense of your frame.

But please, please, please don’t take this to mean doing it alone.

Work with your doctor. This, as I hope you know, is not medical advice, rather this is advice to get medical advice, to work with your doctor and specialists and whoever you need to so that you can make the most informed decisions regarding your health.

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If you’d like to learn more about how to do a meat-based diet (and what to watch out for), I’d highly recommend checking out The Ultimate 90-Day Carnivore Challenge: