15. Is Red Meat Actually Bad For You? Carnivore Deep Dive Pt. 5/6

TL;DR: The only evidence that red meat is bad for you stems from extremely poor and outdated science, and there is much stronger research to show that red meat actually one of the healthiest foods available, even in “blue zones”. Contrary to popular belief, high LDL cholesterol levels are good for us so long as we don’t already have insulin resistance from excessive processed carbs, which almost 90% of the population does.

This article is part of our 6 part series on the carnivore diet. For previous sections, see the links below:

Red Meat Doesn’t Shorten Your Life

There’s all sorts of weird myths surrounding meat, like that it sits in your colon for days, or it causes cancer or shortens your life. We’ve been eating meat, including red meat, for millions of years, and these claims just don’t make sense. In this section, we will cover the research supporting that not only does meat do none of these things, but is actually most likely one of the best foods to lengthen your lifespan.

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The WHO Study

Most of the myths surrounding red meat and shortened life span stem from the World Health Organization’s International Agency for Research on Cancer (IARC), which was released in 2015. It sounds like a fancy title, but let’s dive into the research to see the facts. 22 scientists from 10 countries considered 800 studies and concluded that for every 100g of red meat eaten, there is a 17% increase in colon cancer risk, and for every 50g of processed meat there is an 18% increased risk. They also classified red meat as probably carcinogenic. The media widely reported on this, and influenced public opinion.

It sounds like meat increases risk of cancer, but there were extremely questionable methods used in this mega study. For starters, a more detailed 2018 report of their findings revealed that they only considered 14 of the 800 studies in their conclusions and every one was observational epidemiology (correlation, not causation). Why were the other 786 studies not included?

Furthermore, of the 14, 8 showed no link between red meat and cancer. Only 1 of the remaining 6 showed a statistically significant link and it was on Seventh Day Adventists in America who advocate in their religion for a plant based diet. This is a big red flag because if a Seventh Day Adventist doesn’t follow the guideline of a plant based diet, it is very reasonable to conclude that they don’t follow other guidelines either. This would be an example of the unhealthy user bias – those who eat meat tend on average to engage in other activities viewed as unhealthy like smoking. In support of this point, the strongest correlation was found in the obese in this group with higher likelihood of insulin resistence. Both of these are strong risk factors for cancer by themselves [2,3 Ch.10]. So, out of the 800 studies, the only one showing any evidence that meat is unhealthy is one on Seventh Day Adventists, and it is pure correlation.

Studies Refuting the WHO Study

We can also look at other studies on correlation with meat and health outcomes. One in a population of 200,000 Asians was done over 10 years and the findings were that those who consumed the most meat had the least cancer mortality and cardiovascular mortality [4 Ch.10]. Then there is another on 60,000 people, some vegetarian and some non-vegetarian where colon cancer was found in higher rates in the vegetarians [5 Ch.10].

Then, when we look at controlled studies like interventional studies, which show causation – stronger than correlation, we see more evidence of meat being healthy. One interventional study on mice compared regular mice chow to bacon, beef, or chicken and there was no increase in colon cancer in the meat groups over 100 days. Mice are also not as carnivorous by nature as humans. Interestingly, the bacon actually showed protection against colon cancer [6 Ch.10].

Then, we can look controlled (causation) studies in humans. One includes 37 diabetics divided into two groups for 6 weeks, one on a diet with 30% animal protein as calories, and the other on 30% plant protein as calories. Gastrointestinal inflammation was measured and there was no increase on the animal protein diet, but there was an increase in a compound called calprotectin on the plant protein diet [7 Ch.10]. There was another study over 8 weeks on 60 people, one group on a normal diet and the other group had their carbohydrates from plants replaced by an 8oz piece of red meat. Multiple measures of inflammation and oxidative stress were measured and the red meat group had lower measures of both [8]. Note that according to the WHO’s study, 8oz of red meat should increase colon cancer risk by 40%, so why didn’t it show any signs of inflammation or oxidative stress? These underlying measures would show if red meat were truly unhealthy.

Then, we see studies directly confronting the WHO’s study:

“These [IARC] recommendations are, however, primarily based on observational studies that are at high risk for confounding and thus are limited in establishing causal inferences, nor do they report the absolute magnitude of any possible effects. Furthermore, the organizations that produce guidelines did not conduct or access rigorous systematic reviews of the evidence, were limited in addressing conflicts of interest, and did not explicitly address population values and preferences raising questions regarding adherence to guideline standards for trustworthiness.” [9 Ch.10]

This same group confronting the WHO’s study then did a meta-analysis on 12 randomized controlled trials (causation, not just correlation) including a total of 54,000 participants and found no effect on risk of cardiometabolic outcomes or cancer mortality, and found that vegetarians had worse muscle development and less anemia than vegetarians https://pubmed.ncbi.nlm.nih.gov/31569236/.

The suggestion that meat causes cancer is extremely weak and is based on very questionable research. Out of 800 studies “included” in the WHO’s study, only one showed a correlation between red meat and cancer while 799 did not, and from this they claim that 100g of red meat increases colon cancer risk 17%. Furthermore, a large number of independent and much more rigorous studies show no effect of red meat on cancer, and some show increased risk in vegetarians. Other researchers seriously question the quality of research of the WHO’s study, and when you look at their methods it’s easy to see why. Then, when we consider that we’ve been eating meat for millions of years and evolved quickly while doing so, combined with all of the evidence thus far indicating that meat is the most nutritious category of food, it is much more compelling of an argument that red meat does not cause cancer and is healthy.

Check out our article on some of the most nutritious foods for more.

The Molecular Growth Switch: mTOR

mTOR is a molecule that makes you grow, including muscle. It is involved in turning on the anabolic pathways – a bodybuilder’s heaven. It is most active during childhood and puberty, and after resistance exercise like weight lifting. Some say meat causes cancer because it stimulates mTOR too much and makes cancer cells grow faster – we see an mTOR mutation in cancer cells that causes excessive growth [20,21 Ch.10]. However, carbs actually stimulate mTOR in a stronger way than proteins do. Carbs release more insulin than proteins do, especially on a carnivore diet, and insulin stimulates mTOR for 3-4 times as long as from amino acids that are rich in meat like leucine [25 Ch.10] – a BCAA often used by bodybuilders. We also know resistance exercise is good for us, and that stimulates mTOR so it also doesn’t really make sense to say things that stimulate mTOR are necessarily bad.

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In addition, there is an opposite pathway to mTOR called the AMP kinase pathway, which is triggered by lack of nutrients and growth signals, like what happens during fasting. When AMP kinase is triggered, it breaks down cells and increases catabolic pathways, so it balances out mTOR. We know resistance training and eating food is good for us, and these trigger mTOR and make us grow. We know fasting is good for us and that triggers AMP kinase, which balances out mTOR. What makes the most sense is that we balance anabolic or growth pathways like mTOR with catabolic, or “clean-up” pathways like AMP kinase.

Lastly, in ages below 65, higher protein intake is correlated with increased cancer, but in ages over 65, it is correlated with reduced cancer and longer lifespan. Could it be that as we age, we need more growth stimulation and more mTOR? As we noted earlier as well, in Asian studies, higher meat intake is correlated with longer lifespan. Low protein diets are also correlated with muscle wasting and sarcopenia, which are major risk factors for death [23,24 Ch.10].

High Protein and Kidney Damage

Some people think eating a lot of protein damages your kidneys. Multiple studies on high protein diets show that this doesn’t happen, including a meta-analysis (a study compiling many controlled studies) [26,27 Ch.10].

There is also an argument that higher protein increases the acidity of our blood, which causes our bodies to release minerals like calcium from our bones to neutralize it. This may be a reason why some say high protein may cause osteoporosis – weakening of the bones. However, our bones are made up of ⅓ protein [3], and higher protein diets also increase absorption of calcium in the digestive tract. Furthermore, high protein diets are actually correlated with increased bone density and lower risk of fractures [30,31,32 Ch.10].

Some also claim that red meat causes gout, which is caused when uric acid deposits in the joints. A component in meat called purines break down into uric acid, so some think this means more meat causes more uric acid which causes gout. However, when fasting, uric acid levels increase in the blood perhaps due to cellular breakdown, but gout flare ups do not happen during fasting. This indicates increasing uric acid in the blood is not enough to increase risk of gout. When we eat more meat, we simply excrete more uric acid and blood levels remain stable [35 Ch.10]. Gout is mainly correlated with insulin resistance, which reduces uric acid excretion [33 Ch.10]. Gout is strongly linked to diabetes, an insulin problem [34 Ch.10], as well as alcohol and fructose [36 Ch.10] consumption.

Blue Zones Were Interpreted Incorrectly

Many have heard of the blue zones, which are areas of the world with a high concentration of people who live a long time. Some examples include:

Okinawa, Japan
Sardinia, Italy
Loma Linda, California
Nicoya, Costa Rica
Ikaria, Greece

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Blue zones were popularized by work done by Dan Buettner published in National Geographic in 2005 where he said the commonalities between these places were: low rate of smoking, social engagement and focus on family, frequent moderate physical activity, and a plant based diet. The problem is that many locations of long-lived people were left out of his sample, including Hong Kong, with one of the highest life expectancies in the world at 85 years, and also third highest consumption of meat per capita at 1.5 lbs of meat per day.

Furthermore, when you look at a larger sample size of countries and plot their life expectancy vs. the % of calories they consume from animal protein, you get a more comprehensive look:

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Again, this is a correlation above, so it doesn’t necessarily mean eating more meat makes you live longer, but it does lend some evidence to that hypothesis. The healthy user bias actually favours meat in this case to some degree since wealthier people tend to eat more meat, and wealthier people are healthier in general to begin with.

When we keep looking into correlations, we see other studies like the NHANES III Project, a study of 17,611 individuals showing that white meat reduced mortality and red meat had no impact [38 Ch.10]. Similarly, in Australia, no correlation was found in 243,096 vegetarians, pescatarians, or semi-vegetarians and mortality [39 Ch.10], and another large study in the UK found no correlation between vegetarian diets and mortality [40 Ch.10]. So, it seems that there isn’t a correlation between plant based diets and longevity, and there might be with animal protein and longevity.

We should also be skeptical that blue zone areas are even plant based. Here is some evidence refuting this finding reported by Buettner:

Nicoya, Costa Rica only has a long life expectancy for males and they are well known to eat a lot of meat and cook in animal fats. They have high levels of male sex hormones as well [43 Ch.10]
Sardinia, Italy treasures the “Sarda pig” raised on open range in the forest, and it plays an important role in their diet. [44 Ch.10]
Okinawans consume more meat than the general Japanese population [45 Ch.10] perhaps because they were not influenced by Buddhist vegetarianism, and consumed a lot of pork and goat. “Unexpectedly, we did not find any vegetarians among the centenarians” [4]
Ikaria, Greece have lamb and goat as a central part of their diet. In one study, no plant food was associated with longevity, but those who ate more calories lived longest [46 Ch.10]
Loma Linda seventh day adventists encourage plant based diets and no smoking or drinking. Half are lacto-ovo vegetarian and a small percentage are vegan. They live longer than average by about 7 years compared to California on average [47 Ch.10], but so do other religious groups like Mormons who discourage smoking and drinking but don’t discourage eating meat [48,49 Ch.10]. Interestingly, the lacto-ovo vegetarians had much worse sperm quality than non-vegetarians, and vegans had even worse [51 Ch.10]. Really driving this point home is a study at Harvard showed men who ate the most fruit and vegetables had the worst sperm quality [50 Ch.10].

Lastly here, longevity genetics play a role here, and Okinawans and centenarians such as those in New England have better genetics for longevity [52,53 Ch.10].

So, it seems Blue Zone areas weren’t plant based to start with, and many countries were not included in the Blue Zones study who also ate large amounts of meat and lived a long time.

Telomeres: The End-Caps of DNA

There’s more on the longevity point here, let’s keep going!

Telomeres are like aglets on the end of our shoelaces, the main thing they do is protect the rest of the shoelace from falling apart. Many of us have probably heard the news that telomere length is correlated with increased lifespan, and longer telomeres generally means that a cell is further from programmed cell death, called apoptosis. Unhealthy activities have actually been shown to decrease our telomere length, and healthy activities thankfully can increase it [41 Ch.10].

Only one food is correlated so far with longer telomere length: red meat. Cereal, poultry, dairy, vegetables, fruit, and beverages like tea did not make a difference. In addition, the biggest difference in telomere length was found between the ‘never’ eats red meat group and the ‘eats meat 1-2 daily’ group. This shows that going from no to some red meat jumps up the length of our telomeres the most providing more evidence that meat is a strong factor for telomere length. This evidence is from a study in 28 subjects followed for 3 years to see their eating habits [28 Ch.10]. More research is needed here.

What About Scurvy and Vitamin C?

Some species make Vitamin C in their bodies, and others don’t. Humans stopped making Vitamin C about 60 million years ago [54 Ch.10]. Vitamin C is essential for many functions including making collagen for our joints, tendons and ligaments so we need to get some in our diet. When we don’t get enough, a major symptom is joint pain, and when developed far enough it can turn into the notorious scurvy within 2 months of zero intake.

One thing people think when they hear carnivore is that you won’t get any Vitamin C, and you will eventually develop scurvy. When you enter any meat into a nutrition tracker, you’ll notice 0% for Vitamin C. Funnily enough, researchers never thought to actually measure the amount of Vitamin C in meat because they assumed there wasn’t any. Turns out there is. In 1 pound of meat, there is approximately 15 mg of Vitamin C, and fresh meat is a well known antiscorbutic, which means it cures scurvy. Organ meats like kidney, liver, thymus, and brain have about 30-40mg per 100g serving. Even when cooked, it has enough Vitamin C, and it appears more heat stable in meats than in plant foods.

Some argue that even though meat has enough Vitamin C to meet our needs, more is better. There only appears to be correlation studies to indicate this. Interventional, or causation studies, show no benefits on total mortality, cardiovascular disease, blood pressure, or incidence of common colds [58,59 Ch.10]. Supplementing Vitamin C shows no changes to markers of oxidative stress or DNA damage, and doesn’t show benefits for colorectal cancer, skin cancer, breast cancer, or non-Hodgkin’s Lymphoma [60,61,62,63 Ch.10]. Even in one study where the blood levels of Vitamin C increased 35%, there were no changes in antioxidant capacity, DNA damage or vascular health [64 Ch.10]. This is strong evidence that extra Vitamin C doesn’t really do much for us.

Furthermore, too much Vitamin C can result in kidney stones, nausea, bloating, acid reflux, B12 deficiency and increased oxidative stress [65,66 Ch.10]. 500mg – 1000mg of supplemental Vitamin C have been linked to increased rates of kidney stones [54,67 Ch.10].

Another interesting point is that insulin resistance reduces blood levels of Vitamin C, and decreases its absorption, and its utilization. Also, flavonoids covered earlier compete with Vitamin C for absorption [69 Ch.10]. These and other factors indicate that those on the carnivore diet have less need due to less insulin spikes and other compounds that reduce absorption and utilization. More carbs and plant foods would thus increase the requirement for Vitamin C.

Lastly, no one on the carnivore diet ever gets scurvy, ask the carnivore forums in the more resources section above the references below.

Red Meat Is Not Bad For Your Heart

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Cholesterol is good for us

We make 1,200 mg in our bodies every day, it’s needed for every cell membrane, and to make many hormones and other steroids like estrogen, testosterone, cortisol, progesterone, and aldosterone as well as to make bile acids to digest fats and it is a precursor to Vitamin D made in the skin. That’s a lot of important functions. For cells to make these things, they need cholesterol to be delivered by LDL (the “bad” cholesterol) since the 1,200 mg made in cells is not enough alone. Cholesterol is moved around by lipoproteins like low density lipoprotein (LDL), and high density lipoprotein (HDL).

LDL Isn’t “Bad” Cholesterol

We hear LDL is bad cholesterol, but this doesn’t appear to be true. Lipoproteins like LDL and HDL serve an important role mentioned above in moving around essential cholesterol to cells, as well as protecting us from infections. It’s not bad to have more of them, what is bad for heart and artery health is actually insulin resistance.

Bacteria secrete molecules in our bodies that signal to other bacteria when to coordinate and attack our bodies, and LDL binds to these molecules so they can’t communicate. When mice are altered to have higher levels of LDL, they take much longer to die from infections of gram negative bacteria (the other type being gram positive, usually less dangerous) [6 Ch.11]. Rats with lower LDL genetically die more often and have higher inflammation levels when injected with endotoxin (a toxin from bacterial cell walls released when the cell is killed), but supplementing LDL fixes this. [7 Ch.11] LDL actually binds to endotoxin and neutralizes it. LDL blocks bacteria from signalling to each other giving us a much better chance of fighting them.

Many studies show that LDL is protective for our health and actually keeps us young, especially as we age, and especially to keep our immune system strong. Here are multiple studies to back this claim up:

A large meta analysis (causation) including 68,406 people showed that higher cholesterol correlates with lower death rates from gastrointestinal diseases and respiratory diseases, most of which are infectious in nature [23 Ch.11].
In a 15 year study of over 120,000 patients, those with the highest total cholesterol had the lowest rate of being admitted to the hospital for an infectious disease, including urinary tract, viral, musculoskeletal, skin, respiratory, and gastrointestinal. [24 Ch.11]
- Replicated with another study of 100,000 patients which showed those with the highest cholesterol had the lowest risk of pneumonia or the flu [25 Ch.11]
In those with HIV, higher total cholesterol is associated with reduced AIDS mortality [26 Ch.11]

As we age, we become more vulnerable to infection and death. LDL seems to be especially protective of older people likely related to a strengthening of the immune system [10-20 Ch.11]. Here are even more studies to back up this claim:

A study of 105 people over 80 in Iceland showed the correlation that those with highest total cholesterol had less than half the risk of dying as those with lower levels [21 Ch.11]
In another study of 347 individuals over 65, low total cholesterol was correlated with a much higher risk of dying from non-vascular causes – those with elevated cholesterol had half the risk of dying as the reference population [10 Ch.11]
A study of 724 elderly living in Netherlands measured over 10 years showed the correlation that a 38mg increase in total cholesterol corresponded with a 15% decreased risk in all cause mortality [22 Ch.11]
Elevated LDL does not increase mortality or cardiovascular mortality in the elderly [9 Ch.11]
An interesting fact is that many people prior to death from cancer have a drop in lipid levels. Rates of cancer death are lower in those with higher cholesterol.

These studies are in direct contrast to popular opinion that LDL is bad for us and causes heart disease and other problems. If anything, it is very clear that LDL is very protective due to improving our ability to get cholesterol to our cells essential for cell membranes, creating hormones, making bile acids to digest fats, creating vitamin D, and strengthening our immune system.

So Why Do People Say LDL Is “Bad” Cholesterol?

When we hear about coronary artery disease, atherosclerosis, heart disease, and cardiovascular disease, they all generally refer to plaque formation in the arteries.

The reason people say LDL is bad is because in some studies it is correlated with higher rates of heart disease. A famous one is the Framingham Study following 5,129 people for 14 years with total cholesterol measured twice per year. LDL was found to be associated with heart disease [27 Ch.11]. When plaque was analysed, LDL was found, but not just ordinary LDL. It was ingested by immune cells called macrophages and stuck in the arterial wall [28 Ch.11]. When the macrophages eat the LDL they form what is called foam cells and this is what blocks our arteries. The idea Saladino gets across is that LDL is in plaque, but does not cause it by itself. There are other important factors at play here.

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LDL moves into the artery walls, like HDL does, to deliver some cholesterol to the cells in the wall since all cells need cholesterol. The problem is that sometimes it gets stuck in a part of the artery wall called the tunica intima. When it does, it can become oxidized and immune cells called macrophages come in and eat the LDL to try to get rid of it, but they become too filled with fat and expand into what is called foam cells. This is why people say that more LDL is bad, because more LDL in the bloodstream means more foam cells will form right?

It’s not so simple. Why does LDL in some people get stuck, but in others it causes no problems and no heart disease? We all have LDL in our blood, yet some people’s arteries are spotless.

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Why do so many studies also show that higher LDL is just fine, and even is highly protective against infection and disease? Check out the following:

Epidemiology studies of women, Canadian and Russian men, Maoris, and Asians do not show associations between total cholesterol or LDL levels and incidence of heart disease or all-cause mortality. [23,35,36,37,38 Ch.11]
Furthermore, vegetarians display similar heart disease rates even though they have lower LDL levels [39 Ch.11]
In statin trials, there is no correlation between reduced LDL and reduced plaque formation [40,41,42 Ch.11]
In studies with statins and PCSK9 inhibitors (which lower LDL levels to below 40mg/dl), the majority still continue to develop cardiovascular disease despite the low LDL levels [43 Ch.11]

Here comes another interesting factor affecting the Framingham study: insulin resistance, which is essentially pre-diabetes, where insulin doesn’t work properly to regulate blood sugar. HDL, the “good” cholesterol, is very directly inversely correlated with insulin resistance – aka more HDL less insulin resistance. With insulin resistance, HDL levels fall, and triglycerides rise. This phenomenon is known as dyslipidemia.

When you separate out those with low HDL (insulin resistant) from those with high HDL (healthy insulin response) in the Framingham study, you get a much different graph than the one above:

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Here we can see that when LDL rises, it doesn’t matter unless a person is insulin resistant. So, we have to ask ourselves, is the LDL the problem or it is insulin resistance?

Furthermore, when we look at a few more factors, the picture is pretty clear here. Firstly, non-oxidized LDL does not contribute to coronary artery disease [52 Ch.11]. Only when it gets stuck and oxidized does it contribute. Next, when we look at the amount of LDL moving around our bodies, it outnumbers our cells 1000 to 1. If this ubiquitous little guy were really the problem, our arteries would be clogged in seconds. Plus, why would we have so much of it in our bodies if it were so dangerous?

As a side note, HDL carries more cholesterol than LDL, hence the name high density lipoprotein. HDL outnumbers even LDL by 10 to 1, but doesn’t have the same molecule (APOB100) on its surface that causes it to stick to the arteries. It doesn’t appear that high cholesterol in our blood is the problem here, it’s the “stickiness” of the LDL in some people. What causes stickiness of LDL? If you said insulin resistance, you guessed it – those with insulin resistance have stickier LDL that gets stuck in the intima of the arteries [54,55,56,57,58 Ch.11]. Arteries in diabetics, which is basically advanced insulin resistance, show changes in something called the proteoglycans in their arteries, which make them have a higher affinity to stick to APOB100 on LDL. So the arteries themselves can become stickier to LDL as well, again caused by insulin resistance or diabetes.

Another question is why do veins not get clogged when they have the same amount of LDL circulating around, just arteries? Plaque formation happens most around high pressure blood flow areas. When veins are transplanted into these high pressure areas, they also develop plaques just the same. It is proposed that LDL is there to help cleanup damage to artery walls from any sort of damage that occurs, whether from high pressure, insulin resistance or other causes, and just like a fireman shows up to a fire, they’re not to blame for it. All placental mammals in fact develop LDL deposits in the artery wall including herbivores, omnivores, and carnivores [66,67,68,69 Ch.11]. Herbivores don’t consume the “bad” saturated fats we do yet still have plaque build up.

In summary, higher LDL is good for you, but insulin resistance and diabetes makes your arteries more sticky to LDL, which causes them to get stuck, get oxidized, get eaten by macrophage immune cells and turn into foam cells which block your arteries. To make matters worse, 88% of the American population has some form of metabolic dysfunction, including insulin resistance [61 Ch.11]. We should look to insulin resistance, not cholesterol numbers if we want to protect our heart.

Insulin Resistance: A Root Cause?

When we look even deeper, we see links between insulin resistance and general systemic inflammation. There is a strong correlation between autoimmune conditions like rheumatoid arthritis, lupus, ankylosing spondylitis, polymyalgia rheumatica, depression, and schizophrenia. [79 Ch.11], and heart disease [80 Ch.11]. There is a strong link between the diet and gut inflammation as well, as we see earlier in the Leptin section. Damage to the gut has a strong link to diabetes [81 Ch.11].

The commonality here is insulin resistance. The cause behind it seems to be mitochondria. Mitochondria are the engines in our cells, and they burn carbs, fats, and proteins to generate ATP, which we use as fuel. They have a limited capacity though, and when there is too much fuel to burn from too many calories consumed [70,71,72 Ch.11], they release signalling molecules called reactive oxygen species (ROS), which tells the cell it’s full. The cell then refuses to take in more glucose and nutrients. This is why insulin stops working, and why the cell becomes resistant to insulin; the cell is simply full.

Very interestingly, glucose and fat in the bloodstream seem to cause this problem when eaten together, but not separately. Another interesting point is that when fat and carbs are eaten together, we tend to overeat much more than if they are eaten separately. The only known food in nature that has both is breast milk, and perhaps babies are signalled to consume a lot of this to grow quickly – something food scientists picked up on long ago. It seems a big culprit then for many diseases is junk foods with both fats and carbs combined. Processed carbs like breads, pastas, flours, and sugars also raise our blood sugar much faster than unprocessed carbs.

Some indigenous people eat a high carb diet and are healthy [90,91 Ch.11], but in others like the Pima Indian, it leads to an 80% rate in diabetes [92,93 Ch.11]. The type of carbs and how fast they release causing stress on our insulin system may play a role. Also, how much plant defense compound is in a carb containing food may be a factor. Genetics may play a big role here too.

Either way, having stable blood sugar by not overconsuming carbs, and by getting into a ketogenic state by fasting or not eating carbs all day is a good idea for our general health.

Statins

Stains are extremely widely prescribed for lowering cholesterol because they are said to decrease the risk of heart attack, which we see above is misguided. The reason they are said to be effective is because in some trials, statins slightly decrease the rate of heart attack [43,110 Ch.11]. Statins do decrease cardiovascular mortality slightly, but not from reducing LDL. There is no dose-response relationship between LDL reduction from statins and mortality. Also, other drugs that reduce LDL do not decrease CV mortality.

Statins also have negative side effects. They reduce production of other essential nutrients like CoQ10, which when depleted can lead to mitochondrial dysfunction – mitochondria are particularly dense in the heart and other muscles so this is bad news for our heart. Statins are associated with increased rates of heart failure and diabetes [102,103 Ch.11] and cognitive impairment [104 Ch.11] because of reduced cholesterol, which is especially essential in the brain. In large trials with statins, rates of death by violent crime rises and mood worsens [105-108 Ch.11] indicating a negative impact on mental health perhaps due to reduced cholesterol to the brain.

TMAO

Some claim since red meat causes higher amounts of a compound called TMAO, which some say is bad for us purely from some studies which show a correlation, not a causation, with increased rates of diabetes and cardiovascular disease [112,113 Ch.11]. TMAO is formed in the liver with the help of bacteria from choline and carnitine, nutrients both high in red meat as discussed earlier.

Another fun fact no one likes to mention on the anti-meat train is that fish contain more pre-formed TMAO than would be formed from eating the same amount of red meat [114 Ch.11] and fish have never been associated with increased diabetes and cardiovascular disease. TMAO can also be formed by bacteria in our gut from vegetables [115,116 Ch.11]. In fact, higher levels of TMAO have been found in those eating fish and vegetables than those eating red meat [117 Ch.11], so the claim that red meat is a problem because it creates TMAO in our bodies makes no sense.

TMAO has some benefits too. In rats, doses of TMAO at 4-5x normal levels show benefits leading to improvements in models of hypertension with no harmful effects on the circulatory system [118 Ch.11].

There’s another factor here, our friend the unhealthy user bias is causing problems again. An enzyme called FMO3 in the liver converts TMA to TMAO, and insulin makes this enzyme go faster. Insulin sensitivity (present in 88% of Americans) and diabetes increase insulin levels in the blood, which upregulates (speeds up) conversion of TMA to TMAO, and “it’s much more likely that rising insulin levels are driving the production of TMAO rather than TMAO leading to disease.” It’s like chicken and egg here except it’s clearer which came first. Correlation and bad science strike again and insulin resistance keeps rearing its ugly head.

Saturated Fat Doesn’t Cause Heart Disease

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The idea that saturated fat is unhealthy originated in the 1960s from Ancel Keys’ 7 Countries Study on the relationship between diet and heart disease in the U.S., Japan, Yugoslavia, Greece, Italy, the Netherlands, and Finland. He found a correlation between the amount of saturated fat in the diet with cholesterol in the blood and rates of heart disease. This idea was espoused by the American Heart Association in the 1960s and then made its way into mainstream health and now some people say “red meat clogs your heart!”.

Interestingly, it wasn’t always this way, and studies even as far back as the 1930s show no correlation between cholesterol levels and degree of atherosclerosis (clogging of the arteries) [120 Ch.11].

There are some other fishy things going on here too. Firstly, Ancel Keys excluded countries that did not fit the hypothesis. Why? Secondly, millions of dollars were donated to the AHA by food industries who produced vegetable oils and low fat, high grain foods. There are conflicts of interest here.

Then we have other points that refute this finding. If saturated fat really causes heart disease, then all why do high saturated fat ketogenic diets show that they reverse diabetes and insulin resistance [121,122 Ch.11] along with weight loss and improved inflammatory markers, hypertension, dementia, polycystic ovarian syndrome and more [123-131 Ch.11]? We already know insulin resistance greatly increases risk of heart disease.

There is another interesting finding that when saturated fat in the diet is decreased, and polyunsaturated fat (found in plant fats like soybean oil) is increased, levels of oxidized LDL increase [133 Ch.11] – we saw before in our section on LDL that oxidized LDL is what causes it to get stuck in our arteries, otherwise it’s no problem.

Then, just like Ancel Keys’ correlations, there are opposite correlations, so there must be more to the story. Many recent epidemiological studies (correlation) have been done showing no correlation between saturated fat and cardiovascular disease:

A large meta analysis of 43 studies in 2019 showed no connection between total fat or saturated fat with Cardiovascular Disease [134 Ch.11], but did with processed trans fats and heart attack
A large trial of 42 countries in Europe from 2016 found high fat and animal protein consumption was the most significantly correlated dietary factor with low Cardiovascular Disease. The strongest correlation with high CVD was carb consumption from potatoes, grains and alcohol [135 Ch.11]

Saturated fat does not appear to cause heart disease.

The Environment

Another angle of attack on the carnivore diet is that it causes greenhouse gas emissions from cow methane production.

However, just take a look at the amount of greenhouse gases that animals actually produce: 3.7%. That is not very much.

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Furthermore, grazing animals like grass fed cows actually increase nutrients in soil, which increases carbon sequestering ability of plants [6,7 Ch.14]. Putting cattle on depleted grasslands revitalizes that ecosystem. Many farms now like White Oak Pastures in Georgia result in a negative net carbon effect on the atmosphere [8 Ch.14]. Yes, when cows are raised properly they are actually greenhouse gas negative.

Then there is the argument that killing animals is wrong. First of all, this is highly subjective, and second of all Saladino points out that farming single crops in big fields as is common for wheat, corn, soy, and other plant foods kills a lot more animals than regular animal farming does because machines like combines mow through fields and kill small rodents and other animals. Monocrop farming also disrupts the ecosystem by turning over topsoil, which exposes microbes to sunlight, killing them and disrupting the ecosystem they support.

The only environmental argument against animal farming that makes sense is that there is limited space to farm them. The world can’t produce enough meat for everyone to be a carnivore, even though it does appear to be the healthiest option, and most people culturally would not want to anyway. At the end of the day, you have to try things for yourself to really determine what will work for you. Everyone will have a different way of eating that works for their tastes, health, budget, and convenience.