Is cholesterol the forgotten anabolic?

Cholesterol is a small, fat-like molecule that supposedly clogs our arteries and kills us. But is cholesterol really the bad guy? Or maybe it’s the opposite: a lifter’s best friend?

 

Cholesterol & your gains: the research

Riechman et al. (2007) found that cholesterol may be good for your gains. In their study, 49 elderly individuals completed a 12-week strength training program with nutritional guidelines. Retrospective analysis of participants’ nutritional logs showed a linear dose-response relationship between dietary cholesterol intake and lean body mass increases (per DEXA). The more cholesterol they consumed, the more muscle they gained. This relationship held up when protein and fat intake were controlled for. See the figure below.

 

cholesterol lean body mass

 

Most other research on the relationship between cholesterol and muscle growth hasn’t been published yet. Below is a recap of the data we currently have.

  • In a similar design as the above study, Riechman & Gasier (2007) again found beneficial effects of a high cholesterol intake for muscle growth and strength development, though the effects were more modest than in their previous study and it’s unclear if protein intake was controlled for.
  • Riechman et al. (2008) performed another replication study and found a dose-response relationship between cholesterol intake and strength development but not lean body mass. Again, it’s unclear if protein intake was controlled for.
  • In yet another replication study, Iglay et al. (2009) found no relationship between cholesterol intake and muscle growth or strength development. However, they also did not find any effect of 0.9 vs. 1.2 g/kg/d of protein, which suggests their study was statistically underpowered to research this topic.
  • Lee et al. (2011) compared a high (~800 mg/d) and a low (< 200 mg/d) cholesterol diet in young, healthy adults. The high cholesterol group had a nearly 3 times higher myofibrillar protein synthesis rate 22 hours after intense resistance exercise than the low cholesterol group. Myofibrillar protein synthesis is a measure of muscle growth, specifically how quickly your muscles are creating new proteins, so these findings again suggest a high cholesterol diet is beneficial for muscle growth.

 

Research on statins also hints at a beneficial role of cholesterol for your muscles. Statins are a type of medicine used in the treatment of various cardiovascular (heart-related) problems. Statins lower your cholesterol and a common side-effect is myopathy. Statin therapy can reduce muscle strength and functionality, induce inflammation in your muscles (myositis) and even complete muscle fiber death (rhabdomyolysis).

 

A low cholesterol intake may also be the reason why lacto-ovo-vegetarian diets tend to result in less muscle growth than omnivorous diets in strength trainees, even with the same protein intake. Cholesterol content in plant lipids is about 100-times lower than in animals. However, many other factors, like protein quality, could also explain the lesser muscle mass of vegetarians.

 

All in all, the available research suggests a high-cholesterol diet is good for muscle growth and strength development.

 

How can cholesterol increase muscle growth?

The main-stream media demonize cholesterol based on its potential effects in your blood. If you’ve been basing your perception of cholesterol around that message, you may be surprised to find that cholesterol has several potential mechanisms of action to increase muscle growth.

  • Cholesterol increases membrane viscosity, which may influence membrane stability. This may have an influence on the extent to which muscle cells are damaged during exercise and the magnitude of the inflammatory response.
  • Cholesterol seems to play a role in the muscle repair process by controlling inflammation. Muscle damage creates inflammation, which leads to the recruitment of immune cells to assist with the recovery process.
  • Cholesterol is essential for lipid raft formation. Lipid rafts assemble the components for signalling pathways and enhance signalling between pathways that play an important role for muscle hypertrophy, such as the growth factors IGF-I and mTOR. Cholesterol depletion can lead to protein missorting, which reduces the signal transduction.

 

Simply put, cholesterol can help your muscle cells resist damage and can improve their ability to repair themselves after your workouts, which is crucial for muscle growth.

 

Cholesterol can also improve your gains indirectly.

  • Cholesterol is the precursor for anabolic hormones and is crucial for their production.

 

However, simply having a high serum cholesterol level or eating a ton of dietary cholesterol doesn’t necessarily lead to increased testosterone or more lean body mass gain by itself. The limiting factor of anabolic hormone production is often the transport of cholesterol into mitochondria, where its turnover takes place, not necessarily the amount of cholesterol available in the blood stream. So increased dietary cholesterol intake doesn’t lead to increases in the testosterone level in all studies.

 

However, we do have indirect evidence from the literature on saturated fat that a typical high cholesterol diet increases testosterone production. Saturated fat is a building block for cholesterol, which in turn is used for testosterone production.

 

Saturated fat cholesterol testosterone

 

A low saturated fat intake is associated with reduced testosterone production. For example, men going from a 40% fat diet with a high saturated fat intake to a 25% fat diet with a low saturated fat intake experienced a decrease in total and free testosterone levels; going back to their original diet caused testosterone levels to increase again (see graph below if you’re interested in the details). Several other studies have also found that diets low in saturated fat reduce circulating testosterone levels.

 

Fat intake testosterone

In fact, in the first study of cholesterol’s effect on lean body mass, the authors also found a significant correlation between saturated fat intake and lean body mass growth. Many diets with a high cholesterol content are also rich in saturated fat, so this is not too surprising, but it leaves open the possibility that cholesterol is actually irrelevant and it’s all about saturated fat instead. To find out, the Bayesian research team contacted Dr. Riechman, the principal investigator of the above study on cholesterol. He confirmed that they controlled for the total fat intake (and protein and energy intake) in the analysis on cholesterol, strongly suggesting cholesterol plays an independent role for muscle growth.

 

The cholesterol conspiracy theory

Before everyone starts eating 10 eggs a day, we feel the research is a bit suspect: only about 1 in 3 studies on the relation between cholesterol and muscle growth have been published, even though the research was conducted several years ago already. And most of the published research mentioned above was performed by the same principle investigator, Dr. Riechman, who received research grants totaling roughly $2.7 million (that we could find) from sources including the U.S. Poultry & Egg Association.

 

However, it’s just a fact that scientific research is expensive, so people willing to put a lot money into it, often have something to gain from it. Individuals like Bret Contreras and Menno Henselmans that pay for scientific research out of their own pocket are very rare. The scientific industry is set up so that the integrity of the researchers should prevent the sponsors’ conflict of interest from deceiving the public. And this generally works. Food industry funded nutrition research does not have significantly different outcomes than research with other funding. Plus, Dr. Riechman also received funding from the American Heart Association and the US Army. Not to mention, it’s pretty damn far fetched to pour millions of dollars and risk your career and reputation to promote – of all things you could sell – cholesterol specifically for – of all possible markets – individuals interested in muscle growth. Us meatheads are a tiny part of the population. Us meatheads interested in scientific research tinier still.

 

Ok, let’s take the tinfoil helmets off and assume there’s no major conspiracy theory going on. That begs the question…

 

But isn’t cholesterol bad for your heart?

Nope. The mainstream media portrayal of cholesterol’s health effects is about as accurate as the claim of most Olympians that they’re natural. The media will have you believe all that cholesterol you consume ends up clogging your arteries, but the reality is, for most people how much cholesterol you consume in your diet does not even influence how much cholesterol is in your blood. Cholesterol is so important for the body that it is highly regulated. If your diet does not contain much cholesterol, your intestines will increase their absorption to compensate. If that’s not enough, your body will produce its own cholesterol. 

 

Some people, around 20%, have a genetic variation that makes them absorb or synthesize so much cholesterol that their diet does influence their blood cholesterol level. Even in these hypperresonders, however, a high cholesterol diet does not generally negatively influence their cholesterol profile. If total blood cholesterol increases at all during a high cholesterol diet, both ‘good’ HDL and ‘bad’ LDL cholesterol generally increase in the same proportion.

 

A review paper on the heart-related health effects of cholesterol concluded: “Epidemiological data do not support a link between dietary cholesterol and cardiovascular disease.”

 

A review on egg consumption concluded that “the evidence suggests that a diet including more eggs than is recommended (at least in some countries) may be used safely as part a healthy diet in both the general population and for those at high risk of cardiovascular disease, those with established coronary heart disease, and those with type 2 diabetes mellitus.

 

Take-home messages

  • The available research indicates a high cholesterol diet may be advantageous for muscle growth and strength development by increasing muscle cell integrity and signalling for muscle growth. The beneficial cholesterol intake seems to be at least 7.2 mg dietary cholesterol per kg of lean body mass and more than 400 mg in men.
  • Since your body autoregulates your blood cholesterol level, a high cholesterol intake generally does not increase your serum cholesterol level. Even in hypperresonders, cholesterol intake does not generally change the ratio of ‘good’ HDL to ‘bad’ LDL cholesterol or cause heart-related problems.

 

Here’s how much cholesterol is in various foods according to the USDA.

FoodServing sizeCholesterol content
Egg yolk1 egg yolk (18 g)195 mg
Whole egg1 large (60 g)222 mg
Butter1 tbsp. (14 g)30 mg
Cheese1 slice (17 g)

100 g

19 mg

114 mg

Whole milk1 cup (230 ml)

100 ml

24 mg

10 mg

Whole milk yoghurt100 g13 mg
Red meat100 g72 mg
Poultry100 g58 – 84 g (lower end for lean protein)
Giblets (kidney, liver)100 g275 – 515 mg
Fish100 g43 – 65 g (higher end for fatty fish)

 

Since only animal foods contain significant amounts of bioavailable cholesterol, vegans may want to compensate for their low cholesterol intake by consuming more (saturated) fat so the body can produce enough of its own cholesterol.

 

If you liked this article, you’ll love the Bayesian PT Course. It takes a deep dive just like this article’s into every facet of muscle growth & fat loss. 

 



27 Comments

  1. Zack says:

    So it doesnt matter how much of my daily fat is saturated for the aspect of health?

  2. Eric says:

    Hi, Menno. Great article as usual. I have a question. My doctor suggested that I consider taking a statin since I have borderline high cholesterol (210 mg/DL total, 155 mg/DL LDL, and 55 mg/DL HDL). I’m otherwise healthy, thin, and I’ve started weight training 6 months ago. Would you skip the statin, take it, or reevaluate after a period of time passes?

    • I can’t provide medical advice based on only a snippet of information. However, if your cholesterol and particularly your HDL-total cholesterol ratio is within the reference range, I’d be skeptical of using statins.

  3. Eric says:

    Thanks, Menno. I understand it would be irresponsible to provide medical advice with such limited information. However, I appreciate the response and am glad your thoughts align with what I was already thinking.

  4. Alex says:

    Hey, Menno.
    Given that the research suggests the usage of statins could augment hypertrophy, do you think it would work out in practice for someone using them solely for that purpose?

  5. James says:

    I’d love to see a similar article for Fructose or Sucrose, both of which have been demonised by the mainstream for reasons that don’t hold up under scientific scrutiny.

    In practise, we can use fructose or sucrose to keep cholesterol synthesis high without the need for saturated fat. This should be good news for those cutting since they can omit the fat calories without negatively affecting their cholesterol levels, plus they potentially get the benefit of keeping their metabolism up (sucrose maintains T3 levels during a calorie deficit).

    https://www.ncbi.nlm.nih.gov/pubmed/3740086
    https://www.ncbi.nlm.nih.gov/pubmed/2276854

  6. Ben says:

    The evidence actually suggests that a reduction of LDL levels correlate with a reduction of incidence of cardiovascular disease, independent of HDL. This is highlighted by a meta-analysis of 14 trials containing over 90,000 participants published in the Lancet, and this is certainly reflected in evidence-based best practice treatment guidelines by numerous national cardiology bodies in including in America and Australia.

    Additionally, we know that heart disease and stroke are the number 1 and 2 top causes of death world wide, respectively. The majority is atherosclerotic-related disease, of which LDL has a well known role in its pathophysiology. Given this widespread disease burden, increases in LDL in 20% of this population, the so-called ‘hyper responders’, would certainly be considered significant.

    Further, family history is a non-modifiable risk factor of atherosclerotic disease . Given it’s very high incidence, to reduce an individual’s overall risk, it would certainly be pertinent to err on the side of caution in regards modifiable risk factors, of which hypercholesterolaemia is one.

    http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)67394-1/abstract
    http://circ.ahajournals.org/content/early/2013/11/11/01.cir.0000437738.63853.7a
    http://www.heart.org/idc/groups/ahamah-public/@wcm/@sop/@smd/documents/downloadable/ucm_480086.pdf

    • That meta-analysis is specifically about statins and does not cover HDL cholesterol, so it is not relevant for the average lean strength trainee that isn’t on medication. See the sources in the article for more relevant papers.

      • Ben says:

        The CARDIA study is a landmark study investigating cardiovascular risk in young people that showed, among many other things, that even modest elevation of LDL at a young age (18-30 years old) is associated with higher risk atherosclerotic disease when you’re older.

        “Young adult levels of modifiable risk factors predict the odds of developing heart disease in middle age as well as or better than levels of risk factors measured in middle age”

        Since being a lean strength athlete doesn’t discount a person from having a raised LDL, this population would still be at increased risk of cardiovascular disease when middle-aged.

        http://www.cardia.dopm.uab.edu

        • I don’t see the full text, but the point of this article is that the LDL-HDL ratio is what is generally important. As long as HDL rises along with LDL, this compensates and doesn’t seem to increase cardiovascular risk.

  7. Rdmkr says:

    This article is another strike for “food nihilism”, isn’t it? Summing up everything you’ve concluded on this blog, sugar is not that bad, cholesterol is good, you don’t need that much protein, you can gain muscle in a deficit… what exactly is there left to scrutinize in one’s food intake? Are we at the point yet where you can just say “eat whatever you like, it’ll all be fine”?

    • James says:

      I see this as a strike _against_ ‘food nihilism’ because you can’t ‘eat whatever you like’ if you want to effectively reach your fat loss/muscle gain goals. You want to get enough cholesterol, protein, sugars etc to effectively build muscle/lose fat — all the conclusions of this blog should tell you that what you eat is very important.

      This post should help dispel the silly practise of dumping the egg yolks and only using the whites.

    • I’d say this article rather emphasizes a part of nutrition that you should pay attention to – cholesterol intake- rather than just having to worry about your macros.

  8. Toro Do says:

    I am going to respectfully disagree here. Eating a diet in high cholesterol (high fat in general) will lead to significant unbalanced omega 3 to omega 6 ratio, which can lead to cardiovascular issues. Unless you’re eating pasteur eggs, grass-fed beef, poultry, and butter, you’re looking at an omega 3: omega6 ratio well into the double digits. You see this all the time with people who are on poorly constructed Keto diet.

  9. AAG says:

    From examines article on red-yeasy-rice (lovostatin):
    “1.3. Hypertrophy
    One study (otherwise healthy men aged 60-69) that noted that cholesterol was linearly associated with more lean mass gain in older individuals on a standardized diet and given resistance training noted that usage of lovastatin (in the recommended range) was associated with more muscle building than persons not using statins;[28] this study noted comparable increases with lovastain and pravastatin, both of which outperformed atorvastatin and simvastatin which comparatively outperformed no statin usage.[28] The authors hypothesized this was a recompensatory effect from the known ability of statin drugs to augment exercise-induced muscle injury as assessed by marathons[18] or downhill treadmill walking[19] and when measured 48-72 hours after (intense exercise is also an independent risk factor for myopathy from statins, suggestive of augmenting muscle damage or attenuating the rate of repair[20]).

    One study suggests that chronic usage of statin drugs and pairing statins with exercise can increase lean mass accrual from exercise, apparently synergistic with dietary and serum cholesterol. Although statins during exercise are not well studied, they appear to reduce the rate of muscle regeneration

    Do you have a comment on this?

  10. sam koumertas says:

    Hi Menno,

    Nice article, I just want to add my experience. I’m 51 and have been training 5 times per week, 15 reps per set. workout takes around 1.25 hours.
    Over the last 3 months I have lost body fat and significantly increased muscle mass while undertaking a low saturated fat/cholesterol controlled calorie diet. My serum blood Lipid results threw me. My HDL and triglycerides were the same (i.e same levels as 3 months ago) however my LDL was elevated by 20 %! WOW I was expecting reduced levels or no change at a minimum. Having read the literature it is now clear to me that my body to facilitate muscle growth increased its cholesterol production, amazing.
    It’s a fine line to walk with CVD risk on one side and positive strength/muscle growth on the other.

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