Meat, Saturated Fat, and Long Life

Mainstream health authorities have told us for decades that we should eat less meat, and replace it with carbohydrates, but are they right? Let’s take a look at the relation between meat, saturated fat, and long life.

Countries that eat meat, and those that don’t

Meat consumption varies tremendously by country.

Hong Kong

The country with the world’s highest meat consumption appears to be Hong Kong, according to the National Geographic. (Although Hong Kong isn’t a self-governing nation, but an administrative district.)

From National Geographic:

Hong Kong consumes more meat per person – both calorically and in weight – than any other nation. At 695 grams per day, people in Hong Kong eat 60% more meat than the next-highest meat eaters in New Zealand.

Hong Kong is also number three in the world in per capita beef consumption, so their meat isn’t just chicken or seafood.

Together with China and Macao, Hong Kong is fourth in the world in per capita pork consumption.

If our health authorities are right, then people in Hong Kong should be dropping like flies from heart disease and cancer.

But they’re not.

The WHO lists Japan as having the world’s highest life expectancy, at 83.7 years. But as noted, since Hong Kong is not a country, it doesn’t appear on their list.

But Hong Kong now has a life expectancy of 84.3 years – 81.3 for men, and 87.3 for women. It appears to be the world’s highest.


India has the second lowest per capita meat consumption in the world. The only country lower for which there’s data is Bangladesh.

Yet cardiovascular diseases are epidemic in India. They accounted for 32% of adult deaths from 2010 to 2013. The figure for the U.S. is 23.4%.

India has a life expectancy of 68.3 years.

Now, there are obviously lots of differences between countries like Hong Kong and India, mainly wealth and poverty, which leads to widely differing standards of medical care.

But if meat were the cause of cardiovascular disease, it seems unlikely that India would have a high rate, while Hong Kong has the world’s longest life expectancy.

India should have a low rate of cardiovascular disease, given its low meat consumption.

What could be causing high CVD rates in India? In addition to higher rates of smoking (22% among Indian men, compared to about 17% in U.S. men):

The epidemic of sedentariness has penetrated rural households with rapidly increasing use of labor-saving technologies. Dietary habits have undergone a see change with greater consumption of fats, saturated fats, trans fats, and processed foods. Calorie-dense fast foods (comfort foods) are easily available and both Indian-style and Western-style fast foods are being consumed widely. (Source.)

So, less physical activity might be one cause.

But also, greater consumption of processed foods, high in sugar, seed oils, and refined carbohydrates.

None of these have anything to do with meat consumption, which is low in India.

This is some evidence for my contention that the main causes of cardiovascular disease are cigarettes, seed oils, and sugar. Not meat or saturated fat.

In addition, carbohydrates are associated with cardiovascular disease, and saturated fat is not.

France has the highest consumption of saturated fat, and has the lowest rate of cardiovascular disease. Switzerland has the second highest consumption of saturated fat, and has the second lowest CVD mortality.

Switzerland also has the second highest life expectancy of any country. France stands at number 7.

The PURE study, which tracked data from countries that spanned a great range of income, including India and Pakistan, as well as countries like Canada and Sweden (high income) and Poland and Turkey (middle income), found the results presented below.

The more saturated fat people ate, the lower their rates of CVD and the lower their total mortality. The more carbohydrates they ate, the higher their rates of CVD and total mortality.

In Europe alone, the situation with regard to saturated fat and CVD death rates is as follows (source):

The more saturated fat that Europeans ate, the lower their rate of cardiovascular death.

Another European study found that total animal fat and protein intake were highly and negatively correlated to cardiovascular mortality. (Source.)


Saturated fat consumption is not associated with increased cardiovascular disease rates or death rates, but lower rates.

Hong Kong has the world’s highest meat consumption, and the highest life expectancy. The people of India eat little meat, and have a high rate of cardiovascular disease.

While the evidence presented above is illustrative or associational only, and not 100% conclusive, it pokes a serious hole in the mainstream “plant-based” dogma that meat is unhealthy.

Meat is in fact healthy, as is saturated fat.

The real dietary culprits of our current epidemic of bad health and obesity are seed oils, sugar, and refined carbohydrates.

Why don’t scientists and doctors see this?

Perhaps they do see it, but don’t change their opinions or practices because:

  1. Money: statins are a multi-billion dollar business, and doctors have been trained to prescribe them. Lowering cholesterol has become the focal point for much of modern medicine.
  2. Saving face: they’ve preached the benefits of low-fat, low-meat, and high carbohydrate diets for decades now, and to admit they’re wrong would mean losing face, and prestige.


The Number One Cause of Chronic Disease

The Western world, along with an increasing fraction of the rest of the world, is facing a health crisis. With a combined overweight and obesity rate of 80%, epidemics of diabetes and depression, and heart disease and cancer as the most important causes of death, understanding the roots of our problem is critical. To avoid becoming a health statistic, understand the number one cause of chronic disease.

Diseases of Civilization

The diseases of civilization are those that people living in civilization get, and that people living a primitive or hunter-gatherer lifestyle do not get. They include:

  • coronary heart disease
  • obesity
  • hypertension
  • type 2 diabetes
  • cancer
  • autoimmune disease
  • osteoporosis

These diseases are “rare or virtually absent in hunter–gatherers and other non-westernized populations”.

We could add a few others to that list:

  • depression
  • sarcopenia
  • ADHD
  • male hypogonadism (low testosterone and erectile dysfunction).

A huge fraction of Americans live with chronic disease

The diseases of civilization are chronic diseases, and a large number of Americans have them.

According to the Center for Disease Control (CDC), 78% of Americans 55 years and older have chronic diseases.

These diseases include arthritis, asthma, cancer, cardiovascular disease, COPD, and diabetes.

For Americans age 55 to 64, the percentage that have a chronic disease is 70%.

For Americans 65 and over, the percentage is 86%.

Much of this is avoidable.

Much of this is correctable too.

The top 1% have no chronic disease

A small fraction of people age 85 and up have no chronic diseases. Zero.

These people have been called super seniors. They represent the top 1% in health for their age.

While 1% is a low number, it shows what’s possible. You can get older without falling victim to chronic disease.

Or, you can be like almost everyone else and look forward to a great deal of pain and suffering.

The number one cause of chronic disease

What’s the mysterious factor that leads to chronic diseases in the developed world, but leaves hunter-gatherers alone?

Processed food. Specifically, foods that contain hefty amounts of seed oils, sugar, and refined grains. (See these links for citations.)

Humans are not genetically adapted to eating modern, ultra-processed foods. We’ve been around for hundreds of thousands of years, and our predecessors for millions. Yet agriculture began only about 10,000 years ago, and we began to eat ultra-processed food in large quantities only in the past few decades.

The diseases of civilization are better called the diseases of processed food.

When people living a traditional lifestyle begin to eat processed foods, their health declines and they get chronic diseases. This phenomenon has been seen over and over.

The rise of cheap fast food and other ultra-processed foods in the past few decades is arguably responsible for the obesity epidemic.

Despite what conventional health wisdom claims, animal foods have nothing to do with chronic diseases, including obesity. The main offenders are all plant-based foods: seed oils, sugar, and refined grains.

Americans ate huge amounts of meat in the 19th century and before, and didn’t have chronic diseases. So did many other people in many other nations.

“Heart-healthy” isn’t

Ever since the dawn of the cholesterol hypothesis of heart disease, animal products have been demonized.

They urged us to replace animal products with “healthy whole grains” and “heart-healthy” oils like corn oil.

As a consequence, obesity rates exploded.

They started an uncontrolled experiment on the American people, who never gave their consent. Even when they began, there were many dissenting voices, but of course they were ignored, or had their careers ruined.

Mainstream health authorities are being dragged, kicking and screaming, away from their dogma, but most will never admit that they’ve been wrong. If they do, it would mean taking responsibility for the horrible state of health of most Americans.

Another consequence is that most people now consider processed foods as healthy, or at least benign.

Processed foods now make up 70% of the American diet. The answer is staring us in the face.

If someone sees a doctor about a chronic illness, in all likelihood the doctor won’t advise lifestyle changes. Some do, but most don’t know what the right changes are.,

Instead, the doctor will prescribe drugs, which are often toxic or at best ineffective.

To reliably produce obesity, metabolic syndrome, and fatty liver in lab animals, just feed them processed food.

Other lifestyle factors

Certainly, other lifestyle factors are involved in chronic disease. Among the most important are:

  • exercise
  • sunshine
  • circadian rhythms
  • sleep
  • social connection.

It’s difficult if not impossible to assign ranks of importance or the degree to which these things are responsible.

But I do argue that processed food is a huge factor, and if you stop eating it, you could make huge gains in health.

Eat whole, minimally processed food.

PS: Exercise is important for avoiding chronic disease, and resistance training should be a big part of your exercise program. See my book Muscle Up for details on why, and how to do an effective resistance training program.

PPS: Check out my Supplements Buying Guide for Men.

The Most Important Lipid Panel Marker

Many people regularly get tested for cholesterol, and the test usually includes other markers and is known as a lipid panel. There’s a lot of confusion about which of these markers are important, so let’s look at the most important lipid panel marker as documented by biomedical science.

What’s a lipid panel?

Lipids are fats, and a lipid panel measures levels of different types of fat in the blood.

More specifically, it measures lipoproteins, which are proteins that transport lipids in the blood.

A lipid panel includes:

  • total cholesterol
  • LDL cholesterol
  • HDL cholesterol
  • VLDL
  • triglycerides

Up until a few years ago, doctors focused most on total cholesterol.

Now, the focus is more on LDL, the so-called “bad” cholesterol. (A dumb name if you ask me.)

Why the focus on LDL? Most doctors and scientists believe high LDL causes atherosclerosis, which leads to heart attacks.

More importantly, they focus on LDL because there are expensive drugs that lower LDL, and patients must take them for a lifetime. Statins. The pharmaceutical companies coach doctors at conferences, and buy influence via medical journals, to convince medical gatekeepers that they must prescribe statins. “In 2011, US doctors wrote nearly 250 million prescriptions for cholesterol-lowering drugs, creating a US$18.5-billion market”. The preceding sentences are probably not cynical enough though.

However, LDL really doesn’t correlate very well with cardiovascular risk compared to other tests.

LDL cholesterol

First, LDL, the one doctors focus on the most.

In a large cohort of people hospitalized for cardiovascular disease, a total of 136,905 hospitalizations, “almost half have admission LDL levels <100 mg/dL”. Their LDL was normal, yet they had heart disease.

The following graph, put together by Ivor Cummins from data from this study, shows that LDL only matters in the context of low HDL. If you have high HDL, then high LDL is barely a risk factor.



If you have low HDL, however, watch out.

Triglyceride/HDL ratio

The triglyceride/HDL ratio appears to be the most powerful marker for heart disease risk. The lower the better.

Consider the following chart, which I discussed here, and which comes from data from this study.

Those in the top quartile (fourth) of the ratio of triglycerides to HDL had 16 times the risk of heart attack as those in the lowest quartile.


Pretty much explains cardiovascular risk.

This relationship has been found in other studies too.

A high ratio of triglycerides to HDL predicts extensive coronary artery disease. Of all the lipid markers, “only TG/HDL-c and HDL-c were useful for detecting extensive coronary disease, with the former more strongly associated with disease.”

Let me repeat, of all lipid markers, only the triglyceride/HDL ratio and HDL were associated with coronary disease, and the ratio was a stronger marker. No significant relationship was found between total cholesterol or LDL.

Men with a low ratio of triglycerides/HDL had a low risk of ischemic heart disease, even when they had other risk factors.

“Men with conventional risk factors for IHD have a low risk of IHD if they have low TG–high HDL-C levels.”

The following chart, taken from this paper, shows that men with a low triglycerides/HDL ratio had a low risk of heart disease even when LDL levels were high.

Incidence of ischemic heart disease (IHD) according to lipid categories and level of low-density lipoprotein cholesterol (LDL-C). P value represents statistical significance between the 2 groups. TG indicates triglycerides; HDL-C, high-density lipoprotein cholesterol.

These are of course markers, and not necessarily causative. Raising HDL artifically with drugs has been shown to be ineffective against CVD.

What are good numbers for the triglyceride/HDL ratio?

Last time I checked, mine was 0.5, and it’s hard to get lower than that. Dr. Stephen Sinatra suggests that below 2.0 is ideal.

What does all this mean?

The old model of atherosclerosis and heart disease suggested that arteries were like pipes, and cholesterol clogged them.

In reality, atherosclerosis is an inflammatory disease.

Triglycerides and HDL are markers of insulin resistance, which raises inflammation.

Is there a simple way to identify insulin-resistant individuals at high risk for cardiovascular disease? Yes, a triglyceride/HDL ratio of >3.5 identifies them.

Risk factors for heart disease also raise insulin resistance and inflammation:

  • smoking
  • obesity
  • lack of exercise
  • poor diet of processed foods containing sugar and seed oils.


The ratio of triglycerides to HDL is the most important blood lipid marker.

It predicts cardiovascular risk much better than other markers, such as total or LDL cholesterol.

PS: High iron is an overlooked risk factor for heart disease and a number of other diseases. Find out why and what you can do about it with my book, Dumping Iron.



PPS: Check out my Supplements Buying Guide for Men.

Interview with Kickboxing World Champion Andrew Tate

Three-time kickboxing world champion Andrew Tate, 31, has outspoken views on success, what it takes to make it in the world, and the current culture of victimhood and excuses.

This interview turned out beyond my expectations. Anyone, and I mean that literally, can learn from Andrew’s attitude of persistence and grit and making no excuses for yourself or your failures, no matter what area of life they may be in.

Beginning as a chess player, Andrew entered the kickboxing ring at age 16, determined to win.

(Note a few audio problems here and there but Andrew comes through loud and clear.)

High Iron Leads to Low Testosterone

High levels of iron in the body can, as we know, lead to some serious health problems, as I documented in my book, Dumping Iron. Among these problems, high iron leads to low testosterone. If you have low testosterone, it’s possible that the simple fix of lowering an abnormally high iron level could solve your problem.

Hemochromatosis and low testosterone

Hemochromatosis is the genetic condition which leads to high body iron levels. Ferritin, the most reliable measure of body iron, may be very elevated in hemochromatosis, up to thousands of ng/ml, compared to the normal range of 20-500 for men and 20-200 for women, according to the Mayo Clinic.

Men who have hemochromatosis often have hypogonadism, a condition of low testosterone, low sex drive, and infertility.

Iron depletion, via phlebotomy (blood removal), can cure hypogonadism, leading to normal testosterone, sex drive, and fertility.

But if you don’t have hemochromatosis, but just slightly high iron levels, could that lead to low testosterone? Maybe you wouldn’t have full-blown hypogonadism, but could your testosterone be lower than you’d like, resulting in low T symptoms, like low energy, low sex drive, and erectile dysfunction?

It appears that the answer is yes, high iron could be causing low testosterone.

I’m hearing anecdotes from my network that lowering iron in men has resulted in higher testosterone levels.

Normal iron isn’t normal

As mentioned above, the Mayo Clinic defines normal iron for men as 20-500 ng/ml. However, the upper limit of that range is far too high for good health.

For optimal health, men should have a ferritin no higher than 100.

In men with iron levels within the normal range, that is, less than 500, iron is inversely correlated with testosterone.

The men in this study had an average iron (ferritin) level of 318 ng/ml, high by our standards but well within the Mayo Clinic’s normal range. Their average testosterone was 627 ng/dl, quite respectable, although they were in young middle age, average age 37. Normal range for testosterone is 264-916.

The higher the men’s ferritin, the lower their testosterone, even though none of the men had pathologically high levels, as mainstream medicine defines them.

While the inverse correlation of iron and testosterone didn’t rise to the levels seen in pathologically high iron – hemochromatosis and hypogonadism – it seems entirely possible that getting iron to a healthy normal, 100 ng/ml or below, could be good for a decent increase in testosterone, say 100 points or more.

If so, then the anecdotes I’m hearing about men raising their T levels by lowering their iron are not only true, but show causality.

Testosterone lowers ferritin

When men supplemented testosterone, their ferritin declined.

The reason: testosterone caused an increase in hematocrit, which is the percentage of the blood that is composed of red blood cells. Low testosterone can lead to anemia, and increasing testosterone can treat that anemia. (There are many causes of anemia, so testosterone doesn’t necessarily treat every type of anemia.)

When you make more red blood cells, iron is required. By drawing from body iron stores, increased red blood cell production therefore decreases ferritin, or body iron. Red blood cells represent the single biggest repository of body iron.

The interplay of ferritin and testosterone is complex, and it appears they both affect each other.

High ferritin levels also lead to oxidative stress and chronic inflammation, both of which are death to testosterone.

Since testosterone increases the absorption of iron via the hormone hepcidin, iron in turn negatively regulates testosterone. Boom.

“Crosstalk between testosterone and iron has significant implications in testosterone deficiency and therapy. Additionally, the regulation of testosterone by iron may indicate a significant role for iron in the development of the hypogonadotropic hypogonadism of aging and chronic disease.”

Older men are more likely to have low testosterone, and they are also more likely to have increased ferritin.

Paradoxically, high ferritin levels are associated with lower hemoglobin and hematocrit, as Dr. Zacharski and colleagues found in both normal people and diabetics.

Some of this relation between higher ferritin and lower hemoglobin could be mediated by testosterone. That is, higher ferritin -> lower testosterone -> lower hemoglobin and hematocrit.

Therefore getting ferritin into the safe range of 100 or below could not only increase testosterone, but improve exercise capacity by increasing hematocrit.


Very high iron levels as seen in hemochromatosis can lead to low testosterone, low sex drive, and infertility.

But iron that is only slightly high and within the conventional normal range may also decrease testosterone.

If you have lower testosterone than you’d like, your iron (ferritin) level may be one place to look for an answer.


PS: For how excess body iron harms health in many other ways, see my book, Dumping Iron.

PPS: Check out my Supplements Buying Guide for Men.

Why Decreasing Saturated Fat May Be Harmful

U.S. dietary guidelines have called for people to decrease their intake of saturated fat, on the grounds that saturated fat causes cardiovascular disease. The theory that saturated fat causes heart disease is now known to be false, and evidence now shows why decreasing dietary saturated fat may be harmful.

What saturated fat is

Fat can be classified according to its degree of chemical saturation; thus we have:

  • polyunsaturated,
  • monounsaturated
  • saturated fat.

Polyunsaturated and monounsaturated fat are most associated with plant fats and oils, although there’s plenty of both in animal foods also, and plant foods can contain saturated fat. Seed (vegetable) oils are high in polyunsaturated fat, while olive oil is high in monounsaturated fat.

Decreasing the amount of saturated fat in the diet generally means decreasing the amount of meat, dairy, and eggs that we eat.

However, when we decrease the amount of saturated fat that we eat, we need to replace it with something, usually either a different type of fat, or with carbohydrates.

Replacing saturated fat with carbohydrates increases heart risk markers

If you replace saturated fat with carbohydrates, it could make you diabetic.

The increase in carbohydrate consumption in the U.S., especially that of corn syrup, closely parallels the prevalence of type 2 diabetes.

Protein and fat were not associated with diabetes prevalence when energy intake was taken into account.

While most know that corn syrup (such as high fructose corn syrup, HFCS) is harmful, recall that mainstream health organizations and the U.S. government issued virtually no warnings about possible dangers of HFCS and sugar. It was all about the saturated fat and cholesterol.

They had most people believing that eggs would kill them. Food companies produced thousands of “low-fat” products that were loaded with sugar.

Restricting carbohydrates, on the other hand, produces a unique metabolic state that improves lipid markers.

LDL cholesterol, the so-called “bad” cholesterol, can be composed of small, dense particles, or large, fluffy particles, and it’s the small dense particles that are associated with heart disease risk. A high fasting insulin, together with small, dense LDL particles, was associated with about a 6-fold increased risk of heart disease.

Higher intake of saturated fat means an increase in LDL particle size.

Yes, more saturated fat could decrease heart disease risk, while replacing saturated fat with carbohydrates could increase risk.

Replacing saturated fat with vegetable oils raises the death rate

Dietary guidelines called for using seed (vegetable) oils in cooking and dressing food.

They called for replacing fats such as butter, tallow, and lard with seed oils such as safflower, soybean, and corn oils.

That was a bad move.

It turns out that whenever any improvements were seen in heart disease or death rates, they’re due to an increase in omega-3 fatty acids., according to a recent meta-analysis.

Seed oils are largely composed of omega-6 fatty acids, and when only omega-6 fatty acids are increased, heart disease rates and death rates rise.

“Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.”

Another study noted, “… there was no indication of benefit from the replacement of saturated fat with vegetable oils rich in linoleic acid, with either a composite outcome of myocardial infarcts plus death from coronary heart disease or non-fatal myocardial infarcts alone. Thus, although limited, available evidence from randomized controlled trials provides no indication of benefit on coronary heart disease or all cause mortality from replacing saturated fat with linoleic acid rich vegetable oils.”

A re-analysis of data from the Sydney Diet Heart Study found increased death rates in men who replaced saturated fat with vegetable (seed) oil.

Use of these data from the Sydney study incorporated into an updated meta-analysis found that increasing linoleic acid with seed oils was associated with about a 30% increased risk of death from heart disease.

Way back in 1971, they found that men who used seed oils in place of animal fats died of cancer at about twice the rate as those who did not use seed oils.

They knew.

But they kept recommending seed oils anyway. Probably to save their beloved cholesterol hypothesis of heart disease.

Is the traditional diet-heart hypothesis of heart disease correct?

The diet-heart hypothesis says, in brief, that certain foods, mainly animal foods with saturated fat, raise your cholesterol, which then clogs your arteries.

Is it correct?

There is no benefit to decreasing saturated fat intake if it’s replaced with carbohydrate or polyunsaturated fat from seed oils. There’s no benefit from decreasing intake of animal foods.

So, as traditionally formulated, it is incorrect.

But it appears they just got the food wrong. Food can cause heart disease, as long as the food contains the processed food trifecta:

Consumption of seed oils, sugar, and refined carbohydrates is sky high

The chart below shows the consumption of linoleic acid, the main component of seed oils, in the U.S.


American diets of 1909, as well as pre-agricultural diets, were lower in linoleic acid than what about 90% of Americans now consume. Most of that is due to the consumption of soybean oil.

Americans consume about 58% of calories as ultra-processed foods. A large number of Americans get over 20% of their calories as sugar, and few get less than 10%.

Americans consume about 50% of their calories as carbohydrates.

Conclusion: Cutting down on saturated fat may be harmful

If you cut back on saturated fat, you must replace it with something.

Replacing it with seed oils or carbohydrates worsens health.

A meta-analysis published in 2014 said this about saturated fat:

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

If current evidence, with its thousands of studies and trials, does not support lowering saturated fat consumption, it seems unlikely that any new studies will change the balance of the evidence.

Demonizing saturated fat was a mistake. A big one.

Since saturated fat does not cause heart disease, there’s be no need to cut back on it anyway. Since humans have been consuming saturated fat in large quantities for a long time, it makes no sense that it would suddenly start to cause heart disease in the 20th century.

What did cause the heart disease spike in the 20th century? Cigarettes, seed oils and their products such as margarine and shortening, and sugar, are the most likely suspects, in my opinion.

Mainstream dietary dogma over the past several decades has been harmful, and as we see in this article, not even necessary in the first place.



For more reasons why a low-carbohydrate diet may help you live longer, see my book, Stop the Clock.

PPS: Check out my Supplements Buying Guide for Men.

Why a Plant-Based Diet Is Not the Answer for Health

You’ve probably seen lots of recommendations that we eat a “plant-based” diet to improve our health. A plant-based diet allegedly improves heart health and prevents cancer. But there are a number of reasons why, despite superficial plausibility, this is misleading. Here’s why a plant-based diet is not the answer for health.

What is a plant-based diet?

You might think that calling a diet “plant-based” is simple and straightforward. It means based on plants, right? But the reality isn’t so simple.

Most people eat plants in some form or another – other than pure carnivores, who probably number less than 1% of the population. I eat plants.

At what point does a diet go from “meat-based” or “animal food-based” to plant-based?

If you get greater than 50% of your calories from plants, is your diet now plant-based? You could still be eating 49% of your calories from animal foods, such as meat, eggs, fish, and dairy, but now most of your calories come from plants, so that must be plant-based.

Or if you get greater than 50% of your food by weight from plants, maybe that’s plant-based. That would be easy to do. Vegetables like broccoli and cabbage have low caloric density, and therefore weigh a lot compared to the amount of calories they provide. A pound of cabbage provides only 112 calories, so you could be eating lots of it and still get most of your calories from animal food.

The designation “plant-based” leaves a lot to be desired. It’s ill-defined and obscures more than it illuminates. I might go so far as call it useless.

“Plant-based” seems more a euphemism for “vegetarian” or “vegan”. Those who use the term plant-based know it would be significantly less popular if they called it vegetarian or vegan.

Why a plant-based diet isn’t the answer for health

A number of vegan doctors claim that eating a plant-based diet, whatever that might turn out to be, greatly reduces the risk of heart disease and cancer.

Maybe it does. Caldwell Esselstyn, and others such as Dean Ornish and John McDougall, claim success for their diets in actually reversing heart disease. For the sake of argument, let’s accept that at face value.

The question is, does eating more plants or fewer animal foods confer the benefits of these diets, or is it something else?

Dr. Esselstyn claims that the events that lead to coronary heart disease are “set in motion, and worsened, by the Western diet, which consists of added oils, dairy, meat, fish, fowl, and sugary foods and drinks—all of which injure endothelial function after ingestion, making food a major, if not the major cause of CAD”.

Note that added oils and sugary foods and drinks are not animal foods. In fact, they’re plant-based.

Also note that eating fish is associated with less coronary artery disease and death, not more.

These facts about oils, sugar, and fish cast great doubt on the claim that animal foods are uniquely harmful. Added oils and sugar may indeed be creating all of the harm, for all we know – and in fact that’s probably the case.

Some of the other studies Esselstyn cites in support of a plant-based diet also changed other lifestyle factors, such as smoking.

Ornish: The Ornish study was “without added oil”. Right there is an important change that has nothing to do with animal foods. Vegetable oil is a plant food. The Ornish study also utilized smoking cessation, exercise, and stress management. Thus there are no grounds for concluding that a low-fat vegetarian diet, which Ornish used, had anything to do with better outcomes.

Norway: “Strom and Jensen reported a profound decrease in circulatory diseases in Norway during WWII when the Germans confiscated the country’s livestock, forcing the Norwegians to subsist mostly on plant food.”. During the German occupation of Norway, many things changed.

The paper by Strom and Jensen notes that, “there was a considerable decline in the consumption of meat and meat products, whole milk, cream, margarine and other fats (but not butter), cheese, eggs, fruit and berries, sugar, and coffee. On the other hand, there was a rise in the consumption of fish, skimmed milk, cereals, potatoes, and vegetables.”

So, during the war, the Norwegians ate more fish, and less margarine (an industrial product made from seed oils) “and other fats” (hydrogenated fat and/or vegetable oils?) as well as less sugar.

They also must have smoked a lot less, as tobacco was rationed or scarce in wartime Europe. Gasoline was also rationed, so the Norwegians undoubtedly walked more.

All of these, more fish and exercise, and less smoking and margarine, could account for the decline in circulatory diseases. Did they lose weight? Maybe calorie restriction caused lower mortality.

Thus there’s little to no basis for concluding that less animal food had anything to do with what happened in Norway during WWII.

Finland: Finland, at one time the heart disease capital of the world, decreased its heart disease rate by 80%. The methods cited included smoking cessation and reduction in blood pressure, both of which have nothing to do with a plant-based diet. Both smoking and high blood pressure are large risk factors for heart disease.

Is medical treatment any better?

Here’s where I’m completely on board with Esselstyn: we should focus efforts on prevention, not treatment:

In overlooking disease causation, we implement therapies that have high morbidity and mortality. The side effects of a plethora of cardiovascular drugs include the risk of diabetes, neuromuscular pain, brain fog, liver injury, chronic cough, fatigue, hemorrhage, and erectile dysfunction. Surgical interventions are fatal for tens of thousands of patients annually. Each year approximately 1.2 million stents are placed with a 1% mortality rate, causing 12,000 deaths, and 500,000 bypass surgeries are performed with a 3% mortality rate, resulting in another 15,000 deaths. In total, 27,000 patients die annually from these two procedures.

What really works to prevent heart disease

Vegetable (seed) oils, sugar, and refined carbohydrates are all plant-based foods. Eating more of them will damage our health, so “plant-based” isn’t the answer.

Wait, you say they mean unprocessed plant foods? Bingo, there’s your answer.

Dr. Esselstyn uses the term “whole food, plant-based nutrition (WFPBN)“.

The “whole-food” aspect is the important part.

By eliminating processed foods, you eliminate seed oils, refined carbohydrates, and added sugar. You eliminate pizza, Coke, potato chips, and donuts.

The more important distinction for health is not between animal and plant foods, but between whole, minimally processed food, and ultra-processed food.

Virtually anything you eat is healthier than the Standard American Diet (SAD), so long as it’s whole, minimally processed food.

That’s why (in my opinion) “plant-based” diets, however defined, have shown some success in preventing or reversing heart disease. They eliminate the processed garbage that passes for food in America and much of the developed world today. In addition, they come packaged with smoking cessation, exercise, and treatment for high blood pressure.

Are “plant-based’ diets optimal?

No, they are not.

But if they are based on whole foods, and force you to give up processed junk, they may do a lot of good.

Ultra-processed food contributes significantly to most chronic disease, including coronary artery disease and obesity. Some have even proposed that the “diseases of civilization” be renamed the “diseases of processed food”.

Moral of the story: eat, whole, minimally processed food. If your food was made using an industrial process in a factory, beware.

Update: Here’s the talking head version:


PS: Another way to sharply lower your disease risk is through strength training, so you may want to get a copy of my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

How to Choose a Healthy Cooking Oil

Oils for cooking and dressing are common food items, yet some are unhealthy and definitely to be avoided, and others are healthy. Which oils and fats should you consume, and which should you avoid? Here’s how to choose a healthy cooking oil.

Why some oils are unhealthy

I’ve written quite a bit on this site about why you should avoid vegetable oils, which are better known as industrial seed oils. It’s easy to see why they use the term “vegetable” since it makes them seem healthy, when in fact they are not. It’s PR.

Vegetable Oils Cause Insulin Resistance

Vegetable Oils Cause Obesity

Do Vegetable Oils Raise Heart Disease Risk?

Vegetable Oils Promote Aging

Vegetable Oils Promote Male Infertility

Vegetable Oils Are Dangerous to Health

I can’t think of any reason you would want to consume vegetable (seed) oils.

Problem is, they’re added to almost all processed and fast foods, so avoiding them entails eating minimally processed food that’s as close to natural as possible.

The most important reason why these oils are unhealthy is because of very high amounts of omega-6 fatty acids, which are harmful both in themselves, and because they lead to a very unbalanced omega-6/3 ratio in body tissues. (See articles above for more detail.)

Some oils may contain other chemicals that cause ill health. Canola oil, for example.

In all cases, the unhealthy oils are industrial seed oils, aka vegetable oils.

Which oils you should avoid

What these oils have in common is that they’re made by an industrial process from seeds that normally don’t yield much oil. Hence they need a way to process massive amounts to get that oil.

Ever wonder how they get oil from corn? There’s not a lot there to begin with.

Here’s a video on how they make canola oil. Doesn’t look too appealing if you ask me.

In general, then, avoid the following oils:

  • corn
  • safflower
  • sunflower
  • soybean (the most common processed food additive)
  • peanut – something of an exception since peanuts have a lot of oil, but it’s high in omega-6 fats
  • nut oils
  • cottonseed
  • canola or rapeseed.

And I shouldn’t need to add, but I will

  • margarine
  • shortening.

Wikipedia lists an astounding number of vegetable (seed) oils, so the above isn’t an inclusive list.

If an oil wan’t used before the late 19th or early 20th century, then a good rule of thumb is to avoid it. Fats and oils that our ancestors used are, in general, healthy.

Healthy fats and oils

Fats and oils that come from sources that are not seeds or nuts are generally healthy. “Generally”, because as noted there are many different types of fats and oils, so I’ll only discuss the most common.

These are healthy for cooking and dressing food:

  • olive oil
  • lard
  • beef tallow
  • butter
  • ghee
  • coconut oil
  • avocado oil
  • palm oil

These fats and oils are healthy because they contain much lower levels of omega-6 fatty acids. In the case of animal fats, very little to none. (Lard has some.) They’re composed mainly of saturated and mono-unsaturated fat.

Olive oil has of course been consumed for thousands of years. There are a couple of concerns about olive oil.

The main problem with olive oil is that much of it, maybe most of it, may not really be olive oil, but adulterated with soybean or other seed oils.  There are a few ways to discover whether the olive oil you buy is pure or adulterated (which you can find online), but probably the most important is to get it from a reputable source. Unfortunately, Italy doesn’t appear to be a reputable source, and even big, well-known companies have been caught red-handed adulterating their olive oil.

Olive oil from other countries appears to have much better odds of being pure. Countries like Greece, Spain, Argentina, and even the U.S.A (California). But that’s not a guarantee.

The second concern with olive oil is in cooking. It has a lower smoke point than some oils, and high heat may cause it to break down. The concern that cooking with olive oil is in some way unhealthy appears to be lacking in evidence. Nevertheless, some fats or oils may make better choices for cooking.

Lard and beef tallow may be better for cooking at high heat, since they’re largely composed of saturated and mono-unsaturated fat. Leftover animal fat may also be suitable here. One concern about lard or tallow is that some of it in supermarkets may be hydrogenated, so definitely avoid those.

Butter is perfectly healthy but also suffers from the high heat angle. Works great for cooking eggs though. Ghee is clarified butter and more suitable for higher heat. Coconut oil also.

Avocado oil may be in the same league as olive oil here for cooking.

Lastly, palm oil. Palm oil was demonized for years due to its saturated fat content. Now that we know that saturated fat doesn’t cause heart disease, that concern appears moot. On the other hand, its saturated fat content makes it good for cooking. When I lived in West Africa, they cooked all the food in palm oil and it tasted great, although it left an orange residue on the plate. Palm oil may have a few other issues however, so unless you live in West Africa and have nothing else to cook with, other choices may be better.

Why cook at high heat?

Possibly a more fundamental question when it comes to fats, oils, and cooking, is: why cook at high heat? What are you using these fats and oils for?

Now, I’m not much of a cook. Happily, someone else cooks for me most of the time. If I had to cook for myself, I’d be eating Vince Gironda style most of the time.

Since in my house we eat whole, unprocessed and mostly low-carbohydrate food, there’s not a lot of need for frying or cooking at high heat. Eggs get cooked in butter, but meat gets cooked in its own fat. But we’re not frying up batches of potatoes. Chicken, which we hardly eat anymore due to its high omega-6 content, gets cooked in the oven or broiler. Likewise, pork or tri-tip is cooked in the oven. You get the idea.

My point is, if you need some kind of oil that needs to stand up to high heat, ask yourself what you’re cooking and do you really need to eat it. (Admittedly since I’m not a cook and have little imagination as well, there may be foods I’m missing here, so feel free to let me know.)

Conclusion: Industrial seed oils

Vegetable oil is a euphemism, and these oils are better called industrial seed oils, since they’re made from seeds via a modern, industrial process.

Seed oils form one leg of the processed food trifecta, which also includes sugar and refined carbohydrates.

Seed oils illustrate a rule of thumb about healthy eating: if your great grandmother (or her great grandmother) wouldn’t recognize it as food, best avoid it.

Other oils and fats, such as olive oil and animal fats, are healthy for cooking and dressing.

The go-to fats and oils in my house are butter, olive oil, and coconut.


PS: My most recent book is Best Supplements for Men.


PPS: Check out my Supplements Buying Guide for Men.

Today’s Workout

Here are a couple of very short videos of me deadlifting today. Might as well post them here, even though they’re not as earthshaking as Kanye.

A couple more:

Other exercises I did today included T-bar rows, like so (from an earlier date):


A post shared by P. D. Mangan (@pdmangan) on

I did a drop set on the rows, like I do on most exercises – squats and deadlifts being exceptions.

I also did:

    • cable crossover (chest)
    • chest press
    • weighted dips, Gironda dips
    • triceps pulldown, overhead triceps pulldown
    • preacher curls, hammer curls


A post shared by P. D. Mangan (@pdmangan) on

Metabolic finisher was deadlifts, 155 lbs x 15.

PS: Don’t forget to Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

The Modern World Causes Obesity

Scientists, doctors, dietitians, and amateurs of all stripes have suggested many factors that may lead to obesity and that have lead to the obesity epidemic. But what are the odds that all of these factors just happened to change in the same direction, towards causing more obesity, at the same time? The odds are astronomically low, which leads one to the conclusion that the modern world causes obesity.

Factors involved in obesity

In our last article, we saw that, while processed and high-carbohydrate foods are associated with obesity, that has not always been the case. Americans used to eat plenty of obesogenic food, but didn’t become obese.

Let’s take a look at some of the factors that have been plausibly suggested to lead to obesity. Many of these have scientific backing of some form or another, either animal or human experiments, or epidemiological evidence.

  1. Sleep
  2. Light
  3. Medications
  4. Sugar
  5. Refined carbohydrates
  6. Vegetable (seed) oils
  7. Less physical activity or exercise
  8. Decline of tobacco use
  9. Low-fat food
  10. Less protein
  11. Large portion sizes
  12. Sugar-sweetened beverages
  13. Constant food availability, snacks
  14. Cheap food and greater wealth
  15. Environmental endocrine disruptors
  16. Changing social norms
  17. Hyper-palatable processed food
  18. Food fortification with iron and folate
  19. Microorganisms
  20. Increasing maternal age
  21. Epigenetics
  22. Heating and air conditioning

In my opinion, many or most of these are valid causes of the obesity epidemic. There’s just too much evidence for many of them. I’ve probably missed a few too.

For the sake of argument, assume that the above is a comprehensive list of the causes of obesity, or of the obesity epidemic, and that each one of them contributes some fraction to the effect. What are the odds that each of these factors changed, and all in the same direction – towards causing more people to gain fat – all at the same time?

If the odds were 50/50 that a factor could go one way or another (as in a coin toss), the odds of all 22 factors going in the same direction are 1 in 4.194 million. (Calculator here.) I could probably use some help on these statistical assumptions from Nassim Taleb. But we’ll just go with these.

Something caused all factors to move in the same direction. Even though a lot of assumptions are embedded in that calculation, our ballpark estimate shows that the odds of this being due to chance are low.

What is that something that changed all of those factors?

The modern world.

The modern world and obesity

The key difference between the so-called developed countries and the underdeveloped countries is that the former are more modern. They’re wealthier, and the average person in a developed country doesn’t need to work as hard or struggle as much for a given level of wealth. In short, life is easier.

Life is easier because our wealth allows us to isolate ourselves from nature.

  • We don’t have to stop activity at dusk, because we have electric lights, as well as televisions and computers.
  • We don’t need to walk; we have cars.
  • We don’t let our bodies heal themselves; we have drugs for almost everything.
  • We don’t need to eat bland food; we have sugar.

The list goes on, but the idea is that living closer to nature imposes limits on us. And we had to work hard and endure much in trying to overcome those limits.

For a long time, hundreds of thousands or millions of years (depending how you define “human”), we’ve lived much closer to nature. Suddenly, we are not.

Our biological and social inputs are more artificial, controlled by ourselves.

We were shaped by evolution to be adapted to the older, more natural world. Our genes are not adapted to the modern world.

That’s why we have an obesity epidemic. Many environmental factors have changed, and some are sure to be more important to obesity than others, like 24/7 availability of cheap, processed food. But the modern world changed these factors in the direction of causing obesity, and at about the same time.

We’re insulated from stresses. We never go hungry and physical activity levels are low.

We’re not forced to conform to natural rhythms, so we don’t sleep as much or as well. We insulate ourselves from heat and cold much more than before.

We don’t force our bodies to deal with adversity, we take drugs.

We eat highly artificial foods. Children don’t play in the dirt.

We need the stresses and the rhythms of nature to be lean and healthy.

Control your environment

When I discussed the Deep Soy State, I pointed out the myriad ways in which our environment conspires to make us fat and unhealthy.

The points outlined above show the same.

If you want to be lean and healthy, or to become so, you must control your environment to the extent possible.

You must seek out normal stressors like hunger and exercise. Virtually all discussion of health, fitness, and obesity focuses on diet and exercise, and indeed they’re very important. But you also have to pay attention to all the other factors in your environment.

For example:

  • determine whether you need the medications you take, or whether they may be doing more harm than good;
  • use a light filter or app that dims electronic devices at night, so you can sleep better;
  • go hungry for 16 to 20 (or more) hours a few times a week;
  • lift weights, do some sprints;
  • don’t consume foods or beverages radically different from anything found in nature – pizza and soda qualify here; eat meat and eggs and vegetables, like humans are meant to;
  • take a cold shower and learn what actual cold feels like;
  • walk, preferably among the trees and nature, not on a treadmill.

All of these are a few ways of changing your environment to be more in tune with a natural environment. They involve discomfort and suppression of impulses. Hopefully we can use the modern world to get the best of nature – more trees and fewer infectious diseases, for example.

You’re going to have to avoid many features of our modern environment too. The shortest rule of thumb here is: whatever you see unhealthy and/or obese people doing – don’t do those things. For example;

  • Don’t shop in the middle aisles of the supermarket.
  • Don’t eat at fast food restaurants.
  • Don’t watch television.
  • Don’t eat every few hours.
  • Don’t be sedentary.


Food and physical activity are obviously important for staying lean and healthy. But there are many other factors. Our ancestors didn’t always eat right, but for the most part they didn’t get fat.

That’s because they didn’t live in the modern world, and they weren’t comfortable and coddled at all times, like us.

Be aware that the modern world has changed a multitude of factors that are important to health. That’s why we got the obesity epidemic.


PS: One way to get and stay lean is by adding muscle. See my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Processed Food and Obesity

Are processed food and obesity linked? There are many reasons to think so, but some may be more subtle than we think.

Processed food: what it is

First of all, processed food must be distinguished from unprocessed, or “normal” food. The scientific literature normally designates what we normally call processed food as “ultra-processed”, since almost all foods must be processed in some way, whether by cutting, cooking, preserving, or packaging.

Ultra-processing is “a type of process that has become increasingly dominant, at first in high‐income countries, and now in middle‐income countries, creates attractive, hyper‐palatable, cheap, ready‐to‐consume food products that are characteristically energy‐dense, fatty, sugary or salty and generally obesogenic.”

Another paper defines it as “nutrient-deficient foods in the form of refined white flour, added sugars, vegetable oils, and artificially created trans fats.”

Processed foods are things like donuts, cookies, french fries, soda pop, pastries, candy, protein bars, and almost all fast food.

Unprocessed food means meat, eggs, fish, fruit, vegetables, nuts, dairy products.

Processed food and the rise of obesity

The obesity epidemic in the U.S. began in the mid-1970s, and increased consumption of processed foods accompanied it. Graph below gives an example of the increase in processed food consumption in one country, Canada, and the decrease in unprocessed food.

There’s no doubt that sugar, refined carbohydrates (at least in excess), and vegetable oils are bad for health and weight control but there may be other and more important reasons for why processed food causes obesity.


The inspiration for this article came from the following chart, posted by Stephan Guyenet on Twitter. It shows Americans’ consumption of carbohydrates, protein, and fat from 1909 to 2009, using USDA data.

As can be seen, Americans ate as much carbohydrate in 1909 as they do today, yet there was no obesity epidemic then. Most low-carb advocates (including me) point the finger at carbs for causing obesity. Can that be reconciled with this graph?

Fry cakes and ranch hands

Consider a traditional food eaten by many, especially lower income, people: fry cakes or fry bread.

The recipe for fry bread contains flour, baking soda, salt, and vegetable oil. In the old days, they would have used lard in place of vegetable oil. Fry cakes are the same, but with sugar added, basically unleavened, plain donuts.

Note, I’m not saying these won’t make you fat. They will. Not saying that they’re healthy, because they’re not. But lots of people used to eat this ultra-processed food, and there wasn’t an obesity epidemic.

Here’s what’s billed as a ranch hands’ breakfast:

Image result for ranch hands breakfast

Who knows how much or often actual ranch hands ate this, but there weren’t too many fat ranch hands.


Ranch hands worked out on the range all day, factory and construction workers hauled around heavy stuff all day, housewives didn’t have labor-saving devices, and people walked to work or to the store. No one belonged to a gym. They might have played baseball or football as exercise.

Whether we have lower physical activity than them is an open question. One study found that modern Westerners expend the same amount of energy as hunter-gatherers. I’ve cited that study before, but I have my doubts.

However, even on Wall Street, where they sat in offices, they weren’t fat.

Image result for early wall street


Cost and frequency of processed food

Here we come to the crux of the matter (as far as this article is concerned).

The cost of food has gone way down. People used to spend a significantly higher fraction of their income on food. Restaurants were an infrequent luxury. The following graph shows food expenses starting in 1960.

Related image

Poorer countries – and the U.S. used to be much poorer than today – spend a much greater fraction of their incomes on food.

Image result for fraction of income food

We now have constant, 24/7 food availability, one reason being because it’s cheap and convenient. The idea that you can go more than a few hours without eating is foreign to most Americans. They refer to fasting as “starvation”.  They actually believe that “grazing”, which basically means eating all the time, is healthy.

Foods that are made of sugar, flour, and vegetable oil also don’t repress hunger as much as high-protein, whole foods, so people get hungrier more often and can’t resist eating. Processed foods may also override hunger; they’re a supernormal stimulus.

What’s the answer?

I don’t think I’ll be ending the obesity epidemic any time soon, but I could possibly offer some advice to the individual who wants to lose fat or maintain leanness.

1: Avoid processed food. This rule comes with a caveat: if you’re lean, and you expend as much energy as a ranch hand, and you only eat 3 meals a day with no snacks, you might be able to get away with eating processed food. It’s still not healthy, but if you satisfy those conditions, maybe it won’t make you fat.

2: Don’t eat all the time. The time between dinner and breakfast, perhaps 12 hours, was made for digesting and sleeping, not more eating. If you want to lose weight and/or get healthier, go longer without food by doing intermittent fasting.

3: Eat, whole unprocessed foods. If it comes in a box or bag, don’t eat it.

4: Don’t go near fast-food restaurants, or almost any other restaurant for that matter.

I still believe that cutting carbohydrates and eating whole, unprocessed food is the best way to a lean physique for most people, but the considerations outlined above show that the causes of obesity may be more complicated than simply eating too many carbs.

PS: If you want to lose fat or stay lean and retain muscle, strength training is a must: Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Could the Health Benefits of Moderate Alcohol Consumption Be Due to Its Bactericidal Effect?

Note to the reader: I published this piece recently elsewhere, but since it probably won’t be seen by many people, I’m publishing it here.

Moderate alcohol consumption is associated with better health

Moderate alcohol consumption is associated with better health and lower mortality, particularly with regard to cardiovascular disease. Moderate drinkers, those who consume 1 to 2 drinks (14 to 28 grams of ethanol) daily have about a 25% lower mortality rate than non-drinkers.[1] While this relationship shows association only, a number of mechanisms have been postulated as to why alcohol might benefit cardiovascular health, such as better insulin sensitivity, lower platelet adhesion, lower levels of PAI-1, and higher HDL cholesterol.[2] The protection of alcohol against cardiovascular disease is mediated in part by an inhibition of atherogenesis.[3]

Moderate alcohol consumption also shows an association with lower risk of Alzheimer’s disease and vascular dementia, with light to moderate drinking associated with a 42% lower risk of any dementia, and a 71% lower risk of vascular dementia.[4]

Women who consumed more than 3 drinks weekly had a 52% lower risk of rheumatoid arthritis.[5]

Alcohol consumption may protect against Parkinson’s disease, with ever-drinkers having about a 40% lower risk compared to never-drinkers.[6]

Moderate alcohol consumption is associated with a 30% lower risk of type 2 diabetes.[7]

Current alcohol consumption is associated with a lower risk of incident amyotrophic lateral sclerosis.[8]

All of these diseases for which alcohol is associated with lower risk are diseases of aging.

Alcohol (ethanol) is known to be an effective bactericidal agent, at least at high concentrations, and this may be related to its presumptive health benefits.

Microorganisms may be a cause of the diseases of aging

In recent years, it’s been demonstrated that bacteria are present in the blood of a large fraction of otherwise healthy people.[9] These bacteria include species known to cause infections. A diverse microbiome exists in the blood of healthy blood donors, most of it residing in the buffy coat fraction, which consists of white blood cells.[10]

These bacteria, and other microorganisms, may be implicated in chronic diseases, which are outside of what are normally considered infections, whether acute or chronic.[11] They may be wholly or partially causative of cardiovascular disease, Alzheimer’s, Parkinson’s, type 2 diabetes, and rheumatoid arthritis.

Fungal elements have been found in the brains of Alzheimer’s patients; species included Candida species, Malasezzia species, and Saccharomyces cerevisiae, among others.[12] Fungal infection may be involved in causing amyotrophic lateral sclerosis as well.[13]

Bacterial components have major involvement in rheumatoid arthritis, and recurrent infections are a risk for that disease.[14]

Higher levels of bacterial lipopolysaccharides (LPS) are found in type 2 diabetes.[15]

Periodontal disease, in which bacteria may be shed into the bloodstream, is associated with atherosclerosis.[16] Infection with Chlamydia pneumoniae may contribute to atherosclerosis.[17]

Any agent or intervention that kills or inhibits these bacteria and/or fungi may also prevent these diseases.

Alcohol, even at very low concentrations, inhibits microorganisms

Alcohol is known to be a powerful antiseptic, but at concentrations much higher than can be obtained through moderate drinking. However, even very low concentrations of alcohol (ethanol) can inhibit certain bacteria, for example the pathogen Staphylococcus aureus.[18] Very low concentrations of ethanol (0.1%) inhibit bacterial utilization of specific amino acids, such as glutamate, proline, and ornithine, and also affects the cell walls of E. coli. At a concentration of 0.1% (vol/vol), S. aureus growth is significantly inhibited. Concentrations of ethanol as low as 0.2% prevents fungi from growing in food.[19]

A concentration of 0.1% ethanol is similar to the blood alcohol concentration after ingesting two standard drinks, or ~30 g ethanol, depending on the body weight of the person drinking.[20]

Someone who drank moderate amounts of alcohol might be ingesting enough to inhibit or kill bacteria and/or in the blood, and therefore help to prevent the degenerative diseases that have a connection to bacteria.


[1] Ronksley, Paul E., et al. “Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis.” BMJ 342 (2011): d671.

[2] Djoussé, Luc, et al. “Alcohol consumption and risk of cardiovascular disease and death in women: potential mediating mechanisms.” Circulation 120.3 (2009): 237-244.

[3] Kiechl, Stefan, et al. “Alcohol consumption and atherosclerosis: what is the relation?: prospective results from the Bruneck Study.” Stroke 29.5 (1998): 900-907.

[4] Letenneur, Luc. “Risk of dementia and alcohol and wine consumption: a review of recent results.” Biological research37.2 (2004): 189-193.

[5] Di Giuseppe, Daniela, et al. “Long term alcohol intake and risk of rheumatoid arthritis in women: a population based cohort study.” Bmj 345 (2012): e4230.

[6] Ragonese, P., et al. “A case-control study on cigarette, alcohol, and coffee consumption preceding Parkinson’s disease.” Neuroepidemiology 22.5 (2003): 297-304.

[7] Koppes, Lando LJ, et al. “Moderate alcohol consumption lowers the risk of type 2 diabetes: a meta-analysis of prospective observational studies.” Diabetes care 28.3 (2005): 719-725.

[8] De Jong, Sonja W., et al. “Smoking, alcohol consumption, and the risk of amyotrophic lateral sclerosis: a population-based study.” American journal of epidemiology 176.3 (2012): 233-239.

[9] Damgaard, Christian, et al. “Viable bacteria associated with red blood cells and plasma in freshly drawn blood donations.” PLoS One 10.3 (2015): e0120826.

[10] Païssé, Sandrine, et al. “Comprehensive description of blood microbiome from healthy donors assessed by 16S targeted metagenomic sequencing.” Transfusion 56.5 (2016): 1138-1147.

[11] Kell, Douglas B., and Etheresia Pretorius. “No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases.” Biological Reviews (2018).

[12] Pisa, Diana, et al. “Different brain regions are infected with fungi in Alzheimer’s disease.” Scientific reports 5 (2015): 15015.

[13] Alonso, Ruth, et al. “Evidence for fungal infection in cerebrospinal fluid and brain tissue from patients with amyotrophic lateral sclerosis.” International journal of biological sciences 11.5 (2015): 546.

[14] Pretorius, Etheresia, et al. “Major involvement of bacterial components in rheumatoid arthritis and its accompanying oxidative stress, systemic inflammation and hypercoagulability.” Experimental Biology and Medicine 242.4 (2017): 355-373.

[15] Jayashree, B., et al. “Increased circulatory levels of lipopolysaccharide (LPS) and zonulin signify novel biomarkers of proinflammation in patients with type 2 diabetes.” Molecular and cellular biochemistry 388.1-2 (2014): 203-210.

[16] Kebschull, áM, R. T. Demmer, and P. N. Papapanou. ““Gum bug, leave my heart alone!”—epidemiologic and mechanistic evidence linking periodontal infections and atherosclerosis.” Journal of dental research 89.9 (2010): 879-902.

[17] Filardo, Simone, et al. “Chlamydia pneumoniae-mediated inflammation in atherosclerosis: a meta-analysis.” Mediators of inflammation 2015 (2015).

[18] Very Low Ethanol Concentrations Affect the Viability and Growth Recovery in Post-Stationary-Phase Staphylococcus aureus Populations

[19] Dao, Thien, and Philippe Dantigny. “Control of food spoilage fungi by ethanol.” Food Control 22.3-4 (2011): 360-368.


Processed Food Is Associated With Higher Cancer Risk

One of the best things you can do for your health, in my view, is avoid processed foods and eat only minimally processed, whole foods. Besides helping you stay lean, they may help you avoid cancer, since processed food is associated with higher cancer risk.

Ultra-processed food and cancer

A new study found that consumption of ultra-processed food is associated with greater risk of cancer.

First of all, what are “ultra-processed foods”? Virtually all food that we eat is processed in some way; even if you hunt for your food, meat must be cut and cooked. Most of our food has seen the inside of a processing plant of some kind. Dairy products are pasteurized, some are fermented. Etc.

Ultra-processed foods are those that we would normally deem just “processed”. The study defines ultra-processed foods as:

mass produced packaged breads and buns; sweet or savoury packaged snacks; industrialised confectionery and desserts; sodas and sweetened drinks; meat balls, poultry and fish nuggets, and other reconstituted meat products transformed with addition of preservatives other than salt (for example, nitrites); instant noodles and soups; frozen or shelf stable ready meals; and other food products made mostly or entirely from sugar, oils and fats, and other substances not commonly used in culinary preparations such as hydrogenated oils, modified starches, and protein isolates. Industrial processes notably include hydrogenation, hydrolysis, extruding, moulding, reshaping, and pre-processing by frying. Flavouring agents, colours, emulsifiers, humectants, non-sugar sweeteners, and other cosmetic additives are often added to these products to imitate sensorial properties of unprocessed or minimally processed foods and their culinary preparations or to disguise undesirable qualities of the final product.

These are basically what you find in the middle aisles of the supermarket or in a fast-food restaurant.

Relative amounts of each type of food in the study:

Fig 1

They found that each 10% increase in the proportion of ultra-processed food consumed was associated with about a 10% increase in cancer risk. While that may not sound like a lot, I reckon many people eat a large proportion of their food as ultra-processed food, so they may have a much higher cancer risk.

The study showed association only, and causation is not proven.

The study’s authors suggested several mechanisms by which this food may cause cancer, including, additives and poor nutritional quality. Other ways they suggested that ring true (to me) are that they cause obesity, which raises the risk of cancer, and they cause a greater glycemic response, with higher blood glucose and insulin, which likely also raises the risk of cancer.

Here’s an example of whole, unprocessed food, one demonized by the health establishment:

Image result for steak

Here’s an example of ultra-processed food, one promoted by the health establishment:

Boost Original Complete Nutritional Drink, Chocolate Sensation, 8 fl oz Bottle, 24 Pack

In my opinion, you should do the opposite of what the health establishment recommends here.


PS: Another way to avoid cancer is to Muscle Up.


Aspirin, a Life Extension Drug

One of the most commonly used over-the-counter drugs, aspirin, has considerable potential as a life extension drug. While this has been known for awhile, at least in theory, some recent research adds support.

Aspirin deters the diseases of aging and civilization

In previous articles, we’ve seen that aspirin prevents cancer, including lung and prostate cancer. Cancer strikes mainly older people, and some 90% of cancer deaths are in people 65 years old and up. Cancer is therefore a disease of aging, and since aspirin prevents cancer, it might qualify as an anti-aging drug if it prevented the other diseases of aging and civilization.

Heart disease / atherosclerosis is another big killer that increases in incidence with age. Aspirin prevents heart attacks when used in primary prevention, that is, in people who have never had a previous heart attack, but, “In primary prevention without previous disease, aspirin is of uncertain net value as the reduction in occlusive events needs to be weighed against any increase in major bleeds.” Worth noting here is that “the main risk factors for coronary disease were also risk factors for bleeding.” Aspirin is of greater value in secondary prevention.

In diabetics, aspirin at high doses dramatically decreases glucose (-25%) and triglycerides (-50%), and improves glucose tolerance and insulin sensitivity.

The fact that aspirin affects all of these diseases of aging and civilization suggests a common mechanism that may be involved in life extension.

Aspirin recapitulates features of calorie restriction

Autophagy, the cellular self-cleansing process that breaks down and recycles proteins and cellular components, is critical to maintaining a youthful state. Normally, autophagy declines to basal levels when an animal or human eats (is in the fed state) and increases when no food is available (in the fasted state). As we age, levels of autophagy decline and the process becomes more difficult to induce, and as a result, damage accumulates and cellular processes don’t work as well. Arguably, the increase in malfunctioning components just is aging, with the body increasingly susceptible to breakdown and infection.

Calorie restriction and intermittent fasting strongly up-regulate autophagy. Since calorie restriction has been found to be the most robust and effective life extension intervention known to science, increasing the rate or frequency of autophagy extends lifespan. In fact, mice that are genetically engineered to have higher rates of autophagy live longer than wild-type animals.

Autophagy plays an essential role in lifespan extension, and may be not only necessary, but sufficient, for lifespan extension.

It turns out that the effects of aspirin resemble those of calorie restriction, including the induction of autophagy.

The age-associated deterioration in cellular and organismal functions associates with dysregulation of nutrient-sensing pathways and disabled autophagy. The reactivation of autophagic flux may prevent or ameliorate age-related metabolic dysfunctions. Non-toxic compounds endowed with the capacity to reduce the overall levels of protein acetylation and to induce autophagy have been categorized as caloric restriction mimetics (CRMs). Here, we show that aspirin or its active metabolite salicylate induce autophagy by virtue of their capacity to inhibit the acetyltransferase activity of EP300… Altogether, these findings identify aspirin as an evolutionary conserved CRM.

EP300 is a cellular protein which functions as “a master repressor of autophagy”. By binding to EP300, aspirin de-represses autophagy.

When aspirin is ingested, it is rapidly (minutes) deacetylated and converted to salicylate. and in this case, the salicylate inactivates EP300, leading to increased autophagy.

Salicylate is one of the main components of willow bark, an ancient medicine. An extract of willow bark has been shown to be the most powerful life extension substance known to science.

So far, aspirin and/or salicylate look like potent life extension drugs.

One problem with using aspirin or salicylate for this purpose is the dose. Aspirin can cause stomach bleeding and bleeding in general, especially at high doses. While some patients such as those with rheumatoid arthritis may take large doses of aspirin, 3 grams or more daily (about 10 standard tablets), no one is going to recommend that to the general population. Many doctors even have misgivings about people taking low-dose (81 mg) aspirin due to its promotion of bleeding.

The above article states that “in patients taking up to 3 g aspirin/day, salicylate reaches 1–3 mM concentration in plasma, a dose range in which this molecule exhibits EP300 inhibitory and pro-autophagic properties, salicylate thus likely represents one of the principal metabolites responsible for aspirin activity.”

Given that we need a 1 mM concentration of salicylate to  see any degree of EP300 inhibition, and that level isn’t reached unless someone is taking a lot of aspirin, does the knowledge that aspirin is a calorie-restriction mimetic do us any good?


Possibly. A different study found that salicylate inhibits p300 (same as EP300 above) at about the same concentration, above 1mM. The study also found that diflunisal, a prescription anti-inflammatory drug and a salicylate derivative, inhibits p300 at much lower concentrations. Diflunisal showed activity at 100 μM, and at 1 mM it cut the activity of p300 in half. Difunisal appears to be a relatively safe drug given in doses of 500 to 1000 mg and doesn’t appear to have the bleeding risk that aspirin does.

Both salicylate and diflunisal blocked the growth of cancer cells by inducing apoptosis, or programmed cell death, but diflunisal did so at concentrations less than 1/10 as high.

How else could the relatively high concentrations of salicylate required for life extension be overcome?

One way is potentiation.

Metformin potentiates aspirin, activates AMPK

Salicylate, the metabolite of aspirin, activates AMPK, the master regulator of lifespan, and it does this in common with exercise, fasting, metformin, polyphenols, and other interventions. Metformin, the anti-diabetes drug that extends lifespan in lab animals (and likely in humans), potentiates the effects of salicylate.

Aspirin, the pro-drug of salicylate, is associated with reduced incidence of death from cancers of the colon, lung and prostate and is commonly prescribed in combination with metformin in individuals with type 2 diabetes. Salicylate activates the AMP-activated protein kinase (AMPK) [with] a mechanism that is distinct from metformin… A hallmark of many cancers is high rates of fatty acid synthesis and AMPK inhibits this pathway…  Salicylate suppresses clonogenic survival of prostate and lung cancer cells at therapeutic concentrations achievable following the ingestion of aspirin (<1.0 mM); effects not observed in prostate (PNT1A) and lung (MRC-5) epithelial cell lines. Salicylate concentrations of 1 mM increased the phosphorylation of ACC and suppressed de novo lipogenesis and these effects were enhanced with the addition of clinical concentrations of metformin (100 μM)…  Pre-clinical studies evaluating the use of salicylate based drugs alone and in combination with metformin to inhibit de novo lipogenesis and the survival of prostate and lung cancers are warranted.

Clinically achievable concentrations of salicylate and metformin killed cancer cells and activated AMPK.

Salicylate alone at clinically achievable levels, <1mM, activated AMPK and inhibited the growth of cancer cells, by blocking lipogenesis, the synthesis of lipid (fat) molecules necessary for growth of cancer. Metformin greatly potentiated the effect, such that, in my estimation, someone taking perhaps 2 standard aspirin tablets along with a standard metformin dose would achieve concentrations of these drugs that would kill cancer, as well as promote life extension.

A major caveat of many studies which have utilized metformin to inhibit cancer growth is that millimolar (mM) concentrations have been used, despite maximum concentrations observed clinically being 50–100 μM….

At clinical concentrations of salicylate achievable through the intake of regular strength aspirin (<1.0 mM) salicylate inhibited the survival of prostate and lung cancer cells by greater than 50%.

These data indicate that the salicylate-induced suppression of lipogenesis, taking place at clinically relevant doses of the drug, is mediated via the AMPK β1 subunit…

We found that the IC50 for clonogenic survival was dramatically reduced in all cell types when metformin and salicylate were used in combination.

We find that salicylate at concentrations as low as 0.25 mM inhibited de novo lipogenesis in prostate and lung cancer cells and this was associated with the inhibition of clonogenic survival.

A dose of .25 mM might be achievable with a standard aspirin tablet or two.

Metformin and aspirin together also significantly inhibit pancreatic cancer cells.

Aspirin inhibits mTOR

The mammalian (or mechanistic) target of rapamycin, mTOR, regulates growth and aging, and is repressed by AMPK. Many consider the deactivation of mTOR as the Holy Grail of anti-aging, and it certainly seems about the most potent anti-aging mechanism that we know about currently.

Aspirin inhibits mTOR, although the concentration here was 5mM, which is not clinically achievable.

Again, aspirin and metformin together hold promise in treating pancreatic cancer by targeting AMPK and mTOR.

A study that gets to the heart of the matter regarding mTOR and aspirin directly compared aspirin’s ability to inhibit mTOR with everolimus, an analog of rapamycin, the prototypical mTOR inhibitor. This study used tumor-bearing mice that were given low-dose or high-dose aspirin, or everolimus, or no treatment. Low-dose aspirin was 100 mg/kg, high-dose was 400 mg/kg.

The tumor growth inhibition rates induced by low and high‑dose aspirin and everolimus were 19.6, 33.6 and 53.7% (P<0.05) in H22 hepato­carcinoma, and 25.7, 40.6 and 48.7% (P<0.05) in S180 sarcoma….

We have demonstrated that aspirin may inhibit mTOR signaling associated with anti-angiogenesis and promoting autophagy on the protein expression level. We intend to continue with further experiments on the genetic level. Our study has significant clinical reference value and may potentially lead to therapeutic treatment options for hepatoma or sarcoma and other types of cancer.

According to my calculations, the human equivalent dose for the high-dose aspirin given to the mice is about 2.3 grams for a 70 kg man. (Divide mouse dose by 12 to account for higher mouse metabolism.) Still, not many people (including me) want to take 2 grams of aspirin daily, although some people with pain do so. Metformin and aspirin appear to potentiate each other in deactivating mTOR.

Atenolol is a beta blocker, a cheap, widely used anti-hypertensive drug which also promotes lifespan extension. Of interest, atenolol, aspirin, and metformin together all potentiate each other and target cancer cells by deactivating mTOR. Use of beta blockers is associated with lower rates of cancer.

Aspirin promotes nitric oxide production and reduces erectile dysfunction

Aspirin promotes endothelial function. Endothelial cells are those that line the insides of blood vessels, and their dysfunction is important in promoting atherosclerosis. Part of the protective effect of aspirin on endothelial function is due to its promotion of nitric oxide production, which relaxes blood vessel walls.

Possibly also due to increased nitric oxide production, low-dose aspirin can help treat erectile dysfunction. Men who took 100 mg of aspirin daily for 6 weeks showed significant improvement in erectile function.

Aspirin inhibits cellular senescence

Cellular senescence occurs when cells reach their growth limit (the Hayflick limit) and cannot divide any more. They go into a senescent state and emit inflammatory cytokines, which may be responsible for many of the ills of aging, and may promote cancer. Getting rid of senescent cells may actually reverse aging.

Perhaps even better than eliminating senescent cells is preventing cellular senescence in the first place. Aspirin delays endothelial cell senescence, increases nitric oxide, and reduces ADMA, a marker of atherosclerosis.

Aspirin: dose matters

Daily low-dose aspirin substantially decreases cancer risk. However, what got me onto the line of thinking leading to this article is the following: Aspirin Dose and Duration of Use and Risk of Colorectal Cancer in Men.

After adjustment for risk factors, men who regularly used aspirin (≥2 times per week) had a multivariate relative risk (RR) for colorectal cancer of 0.79 (95% confidence interval, [CI], 0.69–0.90) compared with nonregular users. However, significant risk reduction required at least 6–10 years of use (P for trend = .008) and was no longer evident within 4 years of discontinuing use (multivariate RR, 1.00; CI, 0.72–1.39). The benefit appeared related to increasing cumulative average dose: compared with men who denied any aspirin use, the multivariate RRs for cancer were 0.94 (CI, 0.75–1.18) for men who used 0.5–1.5 standard aspirin tablets per week, 0.80 (CI, 0.63–1.01) for 2–5 aspirin tablets per week, 0.72 (CI, 0.56–0.92) for 6–14 aspirin tablets per week, and 0.30 (CI, 0.11–0.81) for >14 aspirin tablets per week (P for trend = .004). Conclusions: Regular, long-term aspirin use reduces risk of colorectal cancer among men. However, the benefit of aspirin necessitates at least 6 years of consistent use, with maximal risk reduction at doses greater than 14 tablets per week. The potential hazards associated with long-term use of such doses should be carefully considered.

The higher the dose and the longer the duration of use, the less colorectal cancer risk these men had, with 14 tablets a week conferring a 70% decrease in risk. While that’s a large risk decrease, that’s also a lot of aspirin, a dosage that no one will recommend to healthy men who don’t need pain relief.

The other studies noted above suggest that lower doses can be effective, especially when used with metformin and/or beta blockers.

Aspirin: the risk

Aspirin can cause gastrointestinal ulcers and it increases bleeding risk by acetylating the COX-1 enzyme in platelets, the small blood cells that promote blood clotting. Platelets are incapable of generating more COX-2, hence aspirin permanently disables them; platelets have a life of about 10 days. For the cardiovascular protection effect of aspirin, it must be taken daily.

The most serious possible consequence of taking aspirin is bleeding into the brain, which can be fatal or severely disabling. This is known as a cerebral hemorrhage, and accounts for 5-10% of all strokes. Most cerebral hemorrhages are caused by aneurysms in the brain, and it turns out that aspirin could be protective against them. “… patients taking aspirin at least three times weekly had a significantly lower risk of SAH (OR, 0.27; 95% CI, 0.11–0.67; P=0.03) compared with those who never took aspirin.”

What about in the population in general and in other forms of bleeding risk, such as gastrointestinal bleeding? The title of a study tells the story:  Systematic Review and Meta-Analysis of Randomised Trials to Ascertain Fatal Gastrointestinal Bleeding Events Attributable to Preventive Low-Dose Aspirin: No Evidence of Increased Risk. Key to this is the word “fatal”.

Aspirin has been shown to lower the incidence and the mortality of vascular disease and cancer but its wider adoption appears to be seriously impeded by concerns about gastrointestinal (GI) bleeding. Unlike heart attacks, stroke and cancer, GI bleeding is an acute event, usually followed by complete recovery. We propose therefore that a more appropriate evaluation of the risk-benefit balance would be based on fatal adverse events, rather than on the incidence of bleeding…. The majority of the adverse events caused by aspirin are GI bleeds, and there appears to be no valid evidence that the overall frequency of fatal GI bleeds is increased by aspirin. The substantive risk for prophylactic aspirin is therefore cerebral haemorrhage which can be fatal or severely disabling, with an estimated risk of one death and one disabling stroke for every 1,000 people taking aspirin for ten years. These adverse effects of aspirin should be weighed against the reductions in vascular disease and cancer.

The conclusion to the article:

Gastrointestinal bleeds constitute the majority of the adverse events caused by aspirin. The increase is about 60% overall, but there appears to be no increase in fatal GI bleeds attributable to low-dose aspirin, indeed prophylactic aspirin appear to be associated with a reduction in the fatality of GI bleeds. The undesirable effect of prophylactic aspirin which is of a severity comparable to a vascular disease event or a cancer is a bleed that leads to death, and low-dose aspirin appears to be associated with one death and one disabling haemorrhagic stroke per year in every 10,000 people taking low-dose aspirin. The available evidence makes it seems likely that these cerebral events would be reduced if hypertension is identified and adequately treated.

In addition, there will be one or two non-fatal GI bleeds per 1,000 people each year, but the frequency of these bleeds appears to fall rapidly, and there is no evidence of any increase in GI bleeds attributable to aspirin after three or four years of prophylaxis

All these conclusions are relevant to the risk-benefit balance of aspirin prophylaxis and should be communicated to subjects at risk of vascular disease and/or cancer, to enable them to make an informed decision about the protection of their own health.

Aspirin may not even really cause bleeding, hard as that may be to believe after the evidence laid out above. The bacterium Helicobacter pylori, which causes stomach ulcers, could be the true culprit.  If H. pylori is eradicated via antibiotics, then possibly no bleeding would occur, and studies are ongoing to find out.

A number of people (on the Ray Peat Forum) appear to believe that taking vitamin K2 will mitigate the bleeding risk of aspirin. Unfortunately, anyone with actual knowledge of blood clotting (hemostasis) knows that won’t work. Aspirin promotes bleeding by deactivating platelets, and vitamin K2 works by activating clotting factors, which are proteins, and the lack of which are responsible for disease like hemophilia. One won’t mitigate the other.

Aspirin may be under-used

One question about aspirin is whether there’s a basis in reality for the near paranoia among doctors about promoting its use. After all, the same medical establishment is still reluctant to promote a reasonable dose of vitamin D for fear of toxicity, a reluctance which appears to me to have little basis.

A study sought “to determine the long-term economic and population-health impact of broader use of aspirin by older Americans at higher risk for cardiovascular disease.”

These data reveal a large unmet need for daily aspirin, with over 40% of men and 10% of women aged 50 to 79 presenting high cardiovascular risk but not taking aspirin. We estimate that increased use by high-risk older Americans would improve national life expectancy at age 50 by 0.28 years (95% CI 0.08–0.50) and would add 900,000 people (95% CI 300,000–1,400,000) to the American population by 2036. After valuing the quality-adjusted life-years appropriately, Americans could expect $692 billion (95% CI 345–975) in net health benefits over that period.

Expanded use of aspirin by older Americans with elevated risk of cardiovascular disease could generate substantial population health benefits over the next twenty years and do so very cost-effectively.

The average increase in life expectancy if everyone who should use aspirin did use it is only 0.3 years, but that figure is for the entire population, i.e. everyone, even those who don’t take aspirin. You can be sure that if aspirin prevents a cancer or fatal heart attack, the number of years that life is lengthened will be longer, measured in years more likely.

At one time, the then oldest living person credited his long life to taking aspirin. He was 112 at the time.


Aspirin is staring us in the face as a cheap life extension drug. In combination with metformin and/or beta blockers, it may have great potential against cancer and in promoting longer life.

Aspirin is not without risks, and long-term use should be done in consultation with a physician to determine whether the benefits outweigh the risks for a given individual. For the record, I’m not promoting indiscriminate use of aspirin.

The noted scientist Mikhail Blagosklonny mentions aspirin in his list of proposed anti-aging drugs, along with rapamycin, metformin, beta blockers, and PDE5 inhibitors.

PS: If you found this article of value, consider buying one of my books. Click on image below.


PPS: Check out my Supplements Buying Guide for Men.

Hit the tip jar.

Non-Aspirin NSAIDS Can Cause Heart Attacks

Not long ago, the FDA issued a warning that non-aspirin NSAIDs such as ibuprofen could cause heart attacks and strokes. Does this mean that we should never take these drugs, and how serious is the harm that they cause?

Non-aspirin NSAIDs

NSAID stands for non-steroidal anti-inflammatory drug. This group of drugs treats pain, fever, and inflammation, and includes ibuprofen, naproxen, diclofenac, and celecoxib. Aspirin is also an NSAID, but is not included in the FDA warning. Acetaminophen (Tylenol) is not an NSAID, although this drug has problems of its own, and is responsible for huge number of ER visits due to overdose.

The FDA (U.S. Food and Drug Administration) states:

  • The risk of heart attack or stroke can occur as early as the first weeks of using an NSAID. The risk may increase with longer use of the NSAID.
  • The risk appears greater at higher doses….
  • NSAIDs can increase the risk of heart attack or stroke in patients with or without heart disease or risk factors for heart disease. A large number of studies support this finding, with varying estimates of how much the risk is increased, depending on the drugs and the doses studied.
  • In general, patients with heart disease or risk factors for it have a greater likelihood of heart attack or stroke following NSAID use than patients without these risk factors because they have a higher risk at baseline.
  • Patients treated with NSAIDs following a first heart attack were more likely to die in the first year after the heart attack compared to patients who were not treated with NSAIDs after their first heart attack.
  • There is an increased risk of heart failure with NSAID use.

The main evidence that these drugs cause heart attacks and strokes had come from epidemiological studies, but a meta-analysis of randomized controlled trials found the same link.

Celecoxib and related drugs increased the risk of a heart attack by 76%, and of all cardiovascular events by 37%.

Ibuprofen doubled the risk of heart attack.

All NSAIDs together approximately doubled the risk of heart failure.

Naproxen seemed to be relatively safe.

All NSAIDs greatly increased the risk of gastrointestinal complications such as bleeding and ulcers; for instance ibuprofen quadrupled the rate of GI complications. That’s ironic considering that one of the reasons these drugs are touted so much more than aspirin is because of aspirin’s ability to cause bleeding.

Noteworthy from the above is that these drugs can increase the risk of heart attack and stroke almost immediately, which means that even occasional use could increase risk. Many people, including myself, have been in the habit of taking an ibuprofen or other similar drug for minor aches and pains. I will no longer do this. If needed, I’m going to use aspirin.

Why non-aspirin NSAIDs increase heart attack risk

NSAIDs decrease pain and inflammation by inhibiting cyclooxygenase, or COX, of which there are two variants, COX-1 and -2. The form that primarily but not exclusively affects pain is COX-2, while COX-1 is associated with GI side effects.

All NSAIDs affect both COX isoforms, but to different degrees. Ideally, a drug would affect only pain and have no adverse effects, but the search for such a drug has proved fruitless. The chart below (previous link) shows the relative degree to which each of these drugs inhibits COX-1 vs COX-2 at a given concentration.

From this chart, it appears that the more a drug inhibits COX-2 without affecting COX-1, the more dangerous it is in terms of heart attack risk.

Note that aspirin, which prevents heart attacks, has the lowest ratio, meaning that it inhibits COX-1 much more strongly than COX-2.


One reason that aspirin prevents heart attacks may be because of unique metabolic products that it creates, resolvins, which are anti-inflammatory molecules produced from the omega-3 fatty acid DHA. Resolvins are potent regulators of immune function and appear to have many beneficial effects, for example against cancer, and infection.

Resolvins are protective against cardiovascular disease.

Aspirin prevents heart attacks

It’s been known since 1950, or at least suspected, that aspirin prevents heart attacks. In that year, Dr. Lawrence Craven, a general practitioner in Southern California, published the first report on aspirin and heart attacks.

In the midst of a heart disease epidemic that was cutting down millions of middle-aged men, the search for a preventative was urgent. Dr. Craven had noted that some of his patients who took aspirin had excessive bleeding during surgery, and he also thought that platelets were involved in heart attacks. (He was right.) So, putting those together, he urged hundreds of his middle-aged male patients to take aspirin, and a lot of it, a minimum of 2 standard aspirin tablets daily, or 650 mg.

Craven eventually treated over 1,500 male patients with daily aspirin, and reported than not one of them suffered a heart attack.

This of course was not very scientific, since there was no control group, and his sample of patients wasn’t necessarily representative of the wider population. Still, at a time when men were dropping like flies of heart attacks, his results were remarkable.

Craven experimented on himself to get a handle on how aspirin increased bleeding risk, and reported,

Ingestion of 12 aspirin tablets daily resulted after five days in spontaneous profuse nosebleed. In order to check on the reliability of this observation the test was repeated twice over, with precisely the same results. The proof seemed to be all the more convincing as the author had not experienced nosebleed for more than fifty years.

Confirmation of NSAID risk

A study published last year in BMJ reaffirms the risk of heart attack with NSAID use.

All NSAIDs, including naproxen, were found to be associated with an increased risk of acute myocardial infarction. Risk of myocardial infarction with celecoxib was comparable to that of traditional NSAIDS and was lower than for rofecoxib. Risk was greatest during the first month of NSAID use and with higher doses.

Does this mean that taking a single dose on an NSAID could cause a heart attack? If you were at high enough risk, yes, probably. If you’re at low risk, even short-term use could increase risk, however.

With use for one to seven days the probability of increased myocardial infarction risk (posterior probability of odds ratio >1.0) was 92% for celecoxib, 97% for ibuprofen, and 99% for diclofenac, naproxen, and rofecoxib.

So, be careful with NSAIDs.

PS: I discuss aspirin extensively in my most recent book, Best Supplements for Men.

PPS: Check out my Supplements Buying Guide for Men.

Free Weights vs Machines For Strength Training

Is there any difference in results using free weights vs machines for strength training? You will get wildly varying answers to that question, depending on whom you ask.

Free weights, machines, and skill

Free weights are comprised of barbells, dumbbells, kettle bells, and similar devices. They require some level of training and skill to handle well; in some cases, say learning to curl a dumbbell or barbell, the level of skill needed is minimal; in others, such as performing a heavy squat or deadlift, the practitioner must become very skilled at what he’s doing in order to a) complete the lift and b) do it without injuring himself.

The types of lifting that require the most skill are powerlifting and Olympic weightlifting, since these modes of training and competition actually use barbells.

Strength-training machines use a weight stack or other means of providing resistance, and the weight is manipulated using a cable, bar, or something else, often via pulleys. Machines require little skill to learn, and along with that goes a lower propensity to get injured.

Strength and hypertrophy

Different people have different reasons to train for strength.

Athletes want to become stronger and better skilled at their sport. In the case of weightlifting as a sport, the connection is obvious. In the case of American football and other sports that reward size and strength, greater strength helps them, but skill at, say, squatting a barbell has a less than obvious connection to better football playing.

Bodybuilders want to improve their body composition, and as such aren’t particularly interested in cultivating weightlifting skills, apart from the bodybuilding results they get from them.

Ordinary people, like myself, are interested in both better body composition – more muscle and less fat – as well as the better health that comes with it. Personally, while I enjoy doing deadlifts, whether I use a machine or a barbell to increase my strength and health is a matter of indifference to me – I just want to do what works.

Do strength-training machines work as well as barbells for increasing muscle strength, power, and hypertrophy?

The preponderance of the evidence says that they do, according to Dr. Ralph Carpinelli’s paper on free weights vs machines.

Ralph Carpinelli

The key is that free weights and machines increase strength and hypertrophy in the exercise that’s trained for. For example, from the paper:

The free-weight group showed significantly greater strength gains than the Nautilus group when tested on the equipment used for training: 1RM bench press (24.5 and 15.3%), behind-the-neck press (22.3 and 10.9%), and leg sled (15.5 and 11.2%), for free-weight and Nautilus groups, respectively. The Nautilus group showed significantly greater strength gains than the free-weight group when tested on the Nautilus machines: bench press (47.2 and 23.3%), lateral raise (46.8 and 19.4%), and leg press (28.2 and 17.1%), for the Nautilus and free-weight groups, respectively. Overall, the average strength gain in the free-weight group was 20.4% (Nautilus and free-weight equipment combined), while the Nautilus® group increased 26.6% (Nautilus and free-weight equipment combined).

So, if you want to train for the barbell bench press, or win a bench press competition, you should train with barbells. That’s not to say that training in other ways, such as with machines, might not help you, but it seems clear that to train for specific moves and to develop the skills that go with that move, you should train with that move. Obvious.

What if you don’t care about anything more than training for strength, endurance, and hypertrophy? Then machines should be fine. Muscles don’t know whether they’re pushing against a barbell or a machine.

Mike Mentzer.

Gravity and nature

One disadvantage of barbells is that they can only be used in one direction, up or down, since the force against which the muscles work is gravity. Machines, in contrast, can be arranged such that force can be applied from other directions.

For example, using barbells or dumbbells, rows can only be done by lifting the weight. A rowing machine allows rowing from a seated position. There’s likely less propensity to hurt one’s back using a rowing machine.

Does this matter? Barbell aficionados will tell you that humans are complex, that lifting weights is about more than growing or training muscle, and that the nervous and endocrine systems play a role.

No doubt, humans are complex, but it’s hard to see what barbells have to do with this. To be sure, you develop the skill of the barbell bench press by doing it, but whether that translates into better skill in other areas, or better health, seems debatable.

Behind this argument seems to be that barbells are somehow more natural, and that the human body is more suited to using them, or that because they’re allegedly more natural, they make us healthier or better in some other way.

Lifting a heavy barbell is no more natural than using a machine. Squatting 250 pounds for reps is not a natural movement, and humans did not evolve doing it. Of course, they didn’t evolve using the leg press either.

That’s not to say that free weights and machines are exactly equivalent either. They’re not. Aside from the level of skill, squats exercise muscles differently than does a leg press machine.

Barbell enthusiasts also use the supporting muscle argument, namely that when you, say, perform a squat, you use muscles other than the quads and glutes for support and balance, and thus you train them too. You do, but that doesn’t mean you train them optimally.

Machines and free weights are clearly different, but for increasing strength and hypertrophy, it just depends on which exercise you choose and which muscles you work, not whether you’re using a machine or a barbell.

Personally, I use both. I’m relatively indifferent to developing powerlifting or Olympic lifting skills. I’m in the gym for strength, gains, and health.

Some of the argument about the alleged superiority of free weights reminds me of the argument that learning Latin helps you with English skills. No doubt it does, but learning English better is a lot more direct route to that goal than learning another language. If you want muscle gains, use the most direct route.

Arnold training his back.

PS: For more on strength training, see my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Still No Obesity Paradox

In some studies of large numbers of people, researchers have found that people with the lowest death rates had a body mass index (BMI) solidly in the overweight range. This finding has led to the so-called “obesity paradox”, meaning that while we generally think that being overweight is unhealthy, being a little overweight might be healthier than being of normal weight. A new study shows that the obesity paradox can’t possibly be true.

A paradox means your theory is wrong

When researchers declare something a paradox, it means that some piece of data doesn’t agree with their theories. For example, the French paradox refers to the fact that the French eat a diet high in saturated fat, yet have low rates of cardiovascular disease. The French paradox is easily solved if you discard the idea that saturated fat causes heart disease.

A paradox is nature’s way of telling you that you’re wrong.

The obesity paradox can be characterized as follows:

… numerous studies have documented an obesity paradox in which overweight and obese people with established CV disease, including HTN, HF, CHD, and peripheral arterial disease, have a better prognosis compared with nonoverweight/nonobese patients.

The paradox can be resolved either by concluding that being overweight isn’t really unhealthy, or that the data showing that is wrong.

What could explain the obesity paradox

The main confounding factor in the obesity paradox is likely to be reverse causation, meaning that in this case, poor health causes weight loss. If it did, then the category of normal BMI would include people who were in worse health than people who weighed more.

And we do know that poor health can cause weight loss. Smokers also weigh less than non-smokers, and are in worse health.

New study refutes the obesity paradox

The study looked at over 296,000 people in the UK Biobank database. Only people non-smokers who were healthy at baseline were included.

Result: no obesity paradox. Risk of cardiovascular disease rose starting at a BMI of about 22. Other studies have found that a BMI of about 22 or even lower is the healthiest, so this latest study adds evidence.

Of interest, being underweight had a higher risk than being overweight/obese. That’s likely due to low muscle mass.

The obesity paradox is due to confounding due to smokers and those with ill health being included in the category of normal BMI.

Maximum BMI

Another way to investigate the obesity paradox and to clarify the dangers of obeisty is through the use of lifetime maximum BMI, rather than BMI at time of enrollment.

Using lifetime maximum BMI, not only is there is no obesity paradox, but risks of overweight/obesity are much higher.

Using BMI at survey, an estimated 5.42% of deaths were attributable to the combination of overweight and obesity, whereas using maximum BMI, the attributable risk was substantially greater, at 32.58%.

Being even a little overweight is unhealthy

Well-controlled studies, which exclude smokers and other unhealthy people at baseline, show that the health risks of being overweight rise monotonically with increasing weight. There is no obesity paradox, and being overweight is bad for health. Full stop.

Other studies using maximum lifetime BMI substantially increase our estimates of the detrimental effects of overweight/obesity on health.

For those few people who have a BMI >25 due to a high muscle mass, rest assured that the aspect of high BMI that causes problems is not muscle, but fat, especially visceral fat.

Stay lean, my friends.

PS: For how it decrease body fat and increase muscle mass, see my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Your Life Expectancy May Be Greater Than You Think

Your life expectancy may be greater than you think, among the reasons the fact that you read this website. And that’s not only or even mainly because of the information I’ve written about – even though I’d like to think it is – but also because of who you are.

Life expectancy at birth

According to the CDC, life expectancy, which is the average age at which most people die, is 78.7 years for the non-Hispanic, white population. However, when broken down by sex, men have a life expectancy at birth of 76.4 years. (Data here.) Data are from 2011.

Life expectancy of ~76 years seems pretty dismal for a guy like me, as that’s only 13 years away. However, we must make several adjustments to the data to get a true picture of how long someone will live.

For one, the longer you live, the better your odds improve of living longer on a relative basis. This is especially so once you make it to adulthood, since infants have a high mortality rate – odds of dying before age 1 are about 0.5%.

According to the Social Security Administration, at age 63, I can expect to live just over 19 more years, so my current life expectancy is 82. (Which I wrote about here.) However, that figure is an average. Most men my age don’t practice a healthy lifestyle, and are overweight, eat processed junk food, and don’t exercise much – and they figure into the averages.

What happens to your life expectancy if you aren’t average – like the typical reader of this site?

Life expectancy for the above average

According to an interesting book I’ve been reading, The Life of Riley: Mastering the five secret habits to enjoy a longer and healthier life, by Phil Riley, four simple conditions greatly subtract from longevity, and if you keep yourself free of them, you’ll live a lot longer. The conditions are about what you’d expect:

  1. Heavy drinking
  2. Smoking
  3. Overweight/obesity
  4. Sedentary lifestyle

According to Riley’s calculations, if you refrain from being in any of those categories, life expectancy for a man is 89 years (using UK data). Women can expect to live to 91 if they don’t fit any of those categories. You can see some of the author’s calculations here.

Riley defines heavy drinking as more than 2-3 daily drinks for a man.

Smoking is obvious; however, even “social smoking” or casual smoking is a risk factor too, such that if someone smoked a few cigarettes a week, he’d be at higher risk of early death.

Overweight is a BMI of 25 or more, obesity of 30 or more. Generally, the leaner the better when it comes to health.

Sedentary lifestyle can be avoided by fairly minimal exercise, such as walking briskly for 30 minutes on at least 5 days a week.

Pretty simple, and my guess is that most readers of this site aim for far more than avoiding those 4 factors.

The point, however, is that average life expectancy calculations can be very misleading. No, the reader is not going to die at age 76; he’s likely going to live much longer, even without putting a lot of effort into it.

What other interventions will do for life expectancy

Here’s the bad news: since aging and the chance of death accelerate as you get older, it takes a lot to increase life expectancy. Josh Mitteldorf ran some numbers, and found, for example, that a 6% decrease in mortality translates into only 7 months of extra life. See table below.


So you need strong interventions to increase life expectancy beyond 89 years for a man.

Exercise is one of them. Men who have high levels of exercise capacity, as measured by VO2max, live a long time. Exercise capacity is a powerful factor in health risk, with those men in the highest quintile (fifth) of VO2max having a death rate about one fifth that of men in the lowest quintile. If the decrease in mortality is about 80%, then that should give you about 15 extra years of life, according to Josh’s chart above. However, that increase is only above the average (if I’m not mistaken), so 76 +15 makes only 91. In other words, not all that much above the 89 years that Phil Riley calculated.

If exercise capacity is the most powerful mortality reducer, then we can expect other interventions to do less. Furthermore, as Josh Mitteldorf has been at pains to point out, many life-extension interventions are not additive – you get the same or similar life extension even if you add them. For example, a calorie restriction mimetic, such as resveratrol, berberine, or metformin, or a ketogenic diet, may not add much to your life expectancy if you are already lean, exercise, and practice intermittent fasting.

What if you make a lot of money? Your life expectancy is already up there around 89 years old, and raising it further might be a tough proposition. See chart below.

More powerful anti-aging treatments will be needed for the average person to live longer, things like telomere lengthening. Much more research into aging will be required.

If someone were to continue to lift weights into old age, as well as watch their iron levels, take aspirin – how additive are those interventions?

My plan is to keep doing what I’m doing.

You can see lots of feeble old people around, and it seems clear that most people who live longer than average got there by luck, or by avoiding the four Riley factors noted above. No one really knows how much you can increase lifespan if you put your mind to it, and practice intense exercise, eating right and being lean, intermittent fasting, or other interventions, simply because almost no one has done it.

So we’re entering uncharted territory in extending lifespan.

PS: See my book Muscle Up for more on how strength training leads to longer life.

PPS: Check out my Supplements Buying Guide for Men.