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‚Äźincome countries, and now in middle‚Äźincome countries, creates attractive, hyper‚Äźpalatable, cheap, ready‚Äźto‚Äźconsume food products that are characteristically energy‚Äźdense, 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] Djouss√©, 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‚Äôs 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] Pa√Įss√©, 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‚Äôs 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, √°M, R. T. Demmer, and P. N. Papapanou. “‚ÄúGum bug, leave my heart alone!‚ÄĚ‚ÄĒepidemiologic 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‚Äď3¬†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¬†őľM, 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¬†őľM)… ¬†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‚Äď100 őľM….

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 ő≤1 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‚ÄĎdose aspirin and everolimus were 19.6, 33.6 and 53.7% (P<0.05) in H22 hepato¬≠carcinoma, 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 (‚Č•2 times per week) had a multivariate relative risk (RR) for colorectal cancer of 0.79 (95% confidence interval, [CI], 0.69‚Äď0.90) compared with nonregular users. However, significant risk reduction required at least 6‚Äď10 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‚Äď1.39). 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‚Äď1.18) for men who used 0.5‚Äď1.5 standard aspirin tablets per week, 0.80 (CI, 0.63‚Äď1.01) for 2‚Äď5 aspirin tablets per week, 0.72 (CI, 0.56‚Äď0.92) for 6‚Äď14 aspirin tablets per week, and 0.30 (CI, 0.11‚Äď0.81) 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‚Äď0.67; 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‚Äď0.50) and would add 900,000 people (95% CI 300,000‚Äď1,400,000) to the American population by 2036. After valuing the quality-adjusted life-years appropriately, Americans could expect $692 billion (95% CI 345‚Äď975) 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¬ģ¬†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.

Cholesterol for Brain Health

The human brain contains a high proportion of cholesterol, which is necessary for proper function. A number of scientific studies have found that higher cholesterol is associated with better brain health, and that low cholesterol is associated with worse.

The brain and cholesterol

The brain makes up only 2% of body weight but accounts for 23% of total body cholesterol. Clearly, the brain has a high need for cholesterol, which is important for the myelin sheaths of nerve cells and in neurotransmission. Insufficient cholesterol can impeded neurotransmitters.

In recent articles, we’ve seen how higher cholesterol is associated with longer life, and that much of current thinking on cholesterol and health has it backward. It seems likely, given links between long life and cholesterol, as well as the high cholesterol content of the brain, that higher cholesterol could lead to better brain health. What does the evidence say?

Dementia and cholesterol

In the elderly, high total cholesterol and high LDL cholesterol are associated with better memory function, although there was no association in APOE4 carriers. Low total cholesterol may be an early marker for cognitive decline.

In elderly people – 85 years old and up – those whose serum cholesterol levels had increased had the lowest risk of dementia.

Even among healthy middle-aged women, higher total and LDL cholesterol was associated with better memory function. The authors of this study caution, “Possible cognitive effects
of cholesterol reduction should be considered in future studies of lipid lowering agents.” What this means is that statins could harm cognitive function.

In a study of Finnish men, dietary cholesterol and egg consumption was associated with lower risk of dementia and/or Alzheimer’s disease. Each additional 1/2 an egg daily was associated with 11% lower risk of dementia. Eggs are good for the brain.

Cholesterol and violence, suicide, and depression.

Major depression, violence, and suicide have long been linked to low cholesterol.

A significant association between low or lowered cholesterol levels and violence is found across many types of studies. Data on this association conform to Hill’s criteria for a causal association. Concerns about increased risk for violent outcomes should figure in risk‚Äďbenefit analyses for cholesterol screening and treatment.”

Low serum total cholesterol level is associated with an increased risk of suicide. Those in the lowest quartile (fourth) of cholesterol levels (<162 mg/dl) had 6 times the rate of suicide as those in the highest (>224 mg/dl).

Low cholesterol is associated with increased depressive symptoms in older men. Another study found the same result.

Cholesterol levels are low in major depressive disorder.  Chart below shows the correlation between plasma cholesterol and the Beck Depression Inventory (BDI) score.

Low cholesterol and high triglycerides are associated with 4.3 times the risk of major depression, and with 5.4 times the risk of a suicide attempt, in Mexico.

Statins are associated with worse cognitive function

Statins are drugs that lower cholesterol, and if the associations between low cholesterol and poor brain health we’ve discussed above are causal, then statin use should also be associated with worse brain health.

Stains have been anecdotally associated with memory loss. Adverse cognitive effects from statins appear to be dose-related.¬†Some 90% of patients who had cognitive problems reported improvement after they stopped taking a statin, sometimes within days of stopping. “Of interest, in some patients, a diagnosis of dementia or Alzheimer’s disease reportedly was reversed.”

Statin use is associated with about double the risk of Parkinson’s disease, and high cholesterol cut the risk of Parkinson’s in half.

Large increases in dementia or other cognitive impairment have been found with statin use.


Most of the data above (except animal experiments) are association only, and do not show causation. But given what we know about how the brain uses cholesterol, there are good reasons to think that high cholesterol is good for brain health, and that low cholesterol, whether “natural” or achieved through diet or statins may harm the brain, and increase dementia risk, as well as risk of depression, violence, and suicide.

The widespread practice of prescribing statins to all and sundry could increase the incidence of cognitive decline and dementia.


PS: For more on how to avoid the diseases of aging, see my book, Stop the Clock.

PPS: Check out my Supplements Buying Guide for Men.

Higher Protein for Greater Weight Loss

By now we know that low-carbohydrate diets are much more effective for weight loss than standard low-calorie or low-fat diets. Usually, the effectiveness of low-carbohydrate diets is attributed to their low carbohydrate content, which leads to lower insulin, better appetite control, and spontaneous calorie reduction. But there’s something else a typical low-carb diet has that may make a big difference in weight loss: more protein.

Protein leverage and the obesity epidemic

The obesity epidemic in this country began in earnest in the mid-1970s, and it shows no sign of stopping. Researchers have postulated many reasons for the obesity epidemic, including greater consumption of calories, carbohydrates, and fat; less physical activity; even chemical toxins. Many proponents of low-carbohydrate diets have fixed upon the introduction of national dietary guidelines in the U.S., which recommended cutting saturated fat and led to increased consumption of carbohydrates, which were thought to be benign or even healthy. The following chart, from the CDC, shows how nutrient consumption changed. (Note the chart only goes up to the year 2000.)

Table 1

Most observers have focused on increased carbohydrate consumption, which went from 42 to 49% of calories. Fat consumption decreased from 37 to 33%. (These figures are for men; the figures for women are similar.) Calorie consumption also increased, from 2,450 to 2,618 calories a day.

The least attention has been paid to protein: its consumption declined from 16.5% to 15.5% in men, and from 16.9% to 15.1% in women.

Since 1) the intake of protein is lower than from fat and carbohydrates, and 2) the intake of protein hasn’t changed much throughout the obesity epidemic, it’s been thought that protein is relatively unimportant. But those two facts are precisely what gives protein the leverage to drive the obesity epidemic. These ideas make up the protein leverage hypothesis of obesity.¬†(Full paper for download at Google Scholar.)

Leverage refers to the ability of small differences in forces to cause outsize effects in outcomes. If protein has leverage, then small changes in intake could drive obesity.

Consider some evidence for protein leverage:

  1. Animals and humans given a choice of food with widely varying protein content will consume enough (or as little) as needed to meet a protein target. For humans, this seems to hover around 15% of calories. We prioritize protein.
  2. When food protein content is low, more fat and carbohydrate are necessarily ingested, leading to weight (fat) gain.
  3. Protein alleviates hunger more effectively than carbohydrate or fat.

If protein requirements increase, and if food is relatively dilute in protein, then more food – and more fat, carbohydrate, and calories – must be ingested to increase protein intake.

There are several circumstances when protein requirements as a percentage of calories increase. One is less physical activity. Yes, less.

Protein is used by the body mainly for the building and maintenance of structure, while fat and carbohydrates are used for energy. The maintenance requirement for protein doesn’t change much; a more or less constant amount is needed. But if physical activity declines, then less carbohydrate and fat are needed, and therefore the percentage of dietary protein must increase to maintain a constant amount.

Another use of protein is in gluconeogenesis, the making of glucose when carbohydrate isn’t available. Gluconeogenesis normally proceeds at a low basal rate, and insulin strongly suppresses this process. In insulin resistance, such as in the metabolic syndrome and type 2 diabetes, gluconeogenesis proceeds unabated, using dietary protein and/or breaking down muscle to fuel it. So in insulin resistant states, protein requirements increase.

Perhaps the most important point of protein as it relates to the obesity epidemic is that, if only low-protein food is available, one must increase food consumption to obtain adequate protein.

Has the protein content of food declined since before the obesity epidemic until now? Yes.

We’ve been advised to eat less meat, dairy, and eggs due to their saturated fat content. These are all high-protein foods. The following charts show changes in macronutrient consumption plotted against obesity rates. The protein-obesity correlation (a negative one) is the strongest. Countries that have increased protein intake have the lowest rate of obesity.

Many predictions of the protein leverage hypothesis of obesity have been borne out in experiments.

In mice, diets low in protein led to higher food intake and fat gain.

In humans, data collected from 38 different trials of food consumption that used widely varying intakes of protein, from 8 to 54% of energy, showed:

Percent dietary protein was negatively associated with total energy intake (F‚ÄČ=‚ÄČ6.9,¬†P‚ÄČ<‚ÄČ0.0001) irrespective of whether carbohydrate (F‚ÄČ=‚ÄČ0,¬†P‚ÄČ=‚ÄČ0.7) or fat (F‚ÄČ=‚ÄČ0,¬†P‚ÄČ=‚ÄČ0.5) were the diluents of protein. The analysis strongly supports a role for protein leverage in lean, overweight and obese humans.¬†

In obese humans, substitution of carbohydrate with protein leads to far greater weight loss, nearly twice as much.

In a human trial, decreasing the percentage of protein in food from 15% to 10% led to increased calorie intake of 12%. However, increasing the protein percentage from 15 to 25% did not affect calorie intake, which shows that humans may target a certain amount of protein, and eat no more or less when they get it.

Implications for the obesity epidemic

Protein content of food has declined in many countries since before the obesity epidemic, and protein consumption is negatively correlated to obesity rates.

It turns out that eating breakfast cereal, bagels, and pasta may have a serious downside that no one considered before they placed us all on an unregulated, non-consensual national experiment.

Implications for weight loss

The lesson here is obvious: if you want to lose weight (fat), then eat more foods that are higher in protein, and less of those that are lower.

High protein foods include meat, eggs, fish, and dairy products (not including butter and cream).

Ditch the pasta and breakfast cereal and donuts.

Higher protein foods during weight loss have an additional and very important benefit, they help preserve muscle. An unfortunate by-product of fat loss is muscle loss, which ranges from a quarter to a half of all lost weight, and is greatly to be avoided. Higher protein, along with resistance training, can completely abolish this effect, so that all lost weight is fat weight.

Update: Someone expressed a concern about possible harmfulness of high-protein diets, which is a common idea that floats around. In young, healthy, resistance-trained men, one-year of a high protein diet at 4 times the RDA of protein resulted in no effects on kidney and liver function or on blood lipids.  Also of interest, the men who ate high protein gained no body weight, despite eating a significantly higher number of calories.

PS: For the other, no less important half of weight loss, see my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Older People with High Cholesterol Live Longer

High cholesterol among older people is associated with longer life. In Japan, high cholesterol is associated with longer life at all ages. More recent evidence indicates that the relation of high cholesterol to longevity is as robust as ever, and that older people with high cholesterol live longer.

Consider the following an “out of sample” study in which results are verified, associations confirmed, and the risk of data mining undercut.

Cholesterol and mortality

A newly published study looked at 3090 adults aged 60 and up in the Swedish National study on Aging and Care. Baseline date was 2001-04. The study followed the subjects until the end of 2011.

The results:

Compared to normal total cholesterol (<5.18¬†mmol/l), borderline-high (5.18‚Äď6.21¬†mmol/l) and high (‚Č•6.22¬†mmol/l) total cholesterol were associated with a decreased risk of all-cause mortality, with the multiple-adjusted hazard ratio (95% confidence interval, CI) of 0.71 (0.61‚Äď0.83) and 0.68 (0.57‚Äď0.80), respectively (P¬†for trend <0.001)…¬† reduced all-cause mortality associated with high total cholesterol (‚Č•6.22¬†mmol/l)) was mainly due to the reduced risk of non-cardiovascular mortality (hazard ratio‚ÄČ=‚ÄČ0.67, 95% CI‚ÄČ=‚ÄČ0.51‚Äď0.88). These associations were statistically evident only among individuals without use of cholesterol-lowering medications.


The inverse association between high total cholesterol and reduced all-cause mortality in older adults is primarily due to non-cardiovascular mortality, especially among those who are not treated with cholesterol-lowering medications.

Graphs showing survival curves shown below. Those with the highest cholesterol, >240 mg/dl, lived the longest, those at 200-240 mg/dl were in the middle, and those with cholesterol <200 had the highest death rate. (To convert cholesterol from mmol/L to mg/dl, multiply by 38.67.)

Noteworthy, those who had high cholesterol but took cholesterol-lowering drugs such as statins had no survival advantage.

The reduced risk of death seen in those with high cholesterol was mainly due to lower risk of non-cardiovascular death. High cholesterol was associated with a ~30% lower mortality rate.

The authors speculate that higher cholesterol may modulate inflammation, or that low cholesterol is a sign of frailty and poor health. Proponents of the harmfulness of cholesterol argue the latter case, but even if true, why would you want your cholesterol in the range of unhealthy, frail people?

In men aged 85 or more, who are described as “very elderly”,

total mortality in the low-TC [total cholesterol] group was 1.7-fold higher than that in the high-TC group. Mortality, adjusted for the same factors, decreased 0.9% with each 1 mg/dL increase in the serum TC concentration and decreased 0.8% with each 1 mg/dL increase in the serum (low-density lipoprotein) LDL-cholesterol (LDL-C) concentration. Our results indicate an association between lower serum TC concentrations and increased all-cause mortality in a community-dwelling, very elderly population. Mortality decreased with the increases in both TC and LDL-C concentrations, after adjustment for various confounding factors. These findings suggest that low TC and low LDL-C may be independent predictors of high mortality in the very elderly.

Survival curves for all participants (A), men (B), and women (C), shown below.
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When I’m 85 years old or more, I don’t plan on being described as “very elderly”. I’ll still be doing deadlifts and won’t be trying to lower my cholesterol.

Should the elderly take statins?

In a review of studies on cholesterol and statins in the elderly – greater than 80 years old – found two basic conclusions:

  • total mortality was highest at the lowest cholesterol levels: “Low TC (<5.5¬†mmol/l) [total cholesterol <212 mg/dL] is associated with the highest mortality rate in 80+-year olds.”
  • no benefit of lipid-lowering in this age group: “There is not sufficient data to recommend anything regarding initiation or continuation of lipid-lowering treatment for the population aged 80+, with known CVD, and it is even possible that statins may increase all-cause mortality in this group of elderly individuals without CVD.” [Emphasis added.]

Hemodialysis patients

In hemodialysis patients, who are quite ill indeed, higher levels of LDL were associated with reduced risk of infections, and no increase in cardiovascular risk.

Cholesterol-lowering insanity

When will the cholesterol-lowering, statin-prescribing insanity end? Probably not any time soon, since Big Pharma has a large influence on medical practices. There’s huge money in prescription drugs including statins.

Cholesterol is a natural molecule synthesized by the human body, and is critical for the function of cell membranes and hormones.

If higher cholesterol is associated with longer life in the elderly, and in all ages in Japan, then that casts considerable doubt on cholesterol as a cause of cardiovascular disease. Since age is a risk factor for CVD, if high cholesterol caused it, we would expect to see higher death rates in the elderly with high cholesterol. But we do not.


PS: For how iron can cause cardiovascular disease, see my book, Dumping Iron.

PPS: Check out my Supplements Buying Guide for Men.

Guest Post: Is CrossFit a Good Way to Exercise?

I’ve been skeptical about CrossFit as an optimal form of exercise, so we’ve got an experienced CrossFitter to tell the other side of the story. – P. D. Mangan

Is CrossFit a good way to exercise?

by Carl Turner

Today it is difficult to walk around town without passing by a CrossFit gym, or listening as someone enthusiastically promotes the benefits of their Crossfit workout. There is a pretty good reason for this too: Crossfit has become one of the most popular workout programs worldwide.   

You might be wondering, what is it about CrossFit that has so many people hooked? Is CrossFit a good way to exercise? Let’s take a closer look. 

What is CrossFit?  

CrossFit is best understood as a multidisciplinary workout regimen that targets all of the major areas of physical fitness and health. CrossFit members engage in strength, endurance, and flexibility exercises, while targeting important attributes like balance, agility, speed, power, and coordination.   

This multidisciplinary approach provides several benefits, which have helped to catapult the CrossFit name to international fame. First of all, by actively targeting several areas of fitness during the workout, participants can attend to their overall fitness and health in a broad and powerful way.   

For example, stronger muscles make endurance and flexibility training easier, and they contribute to better joint and bone¬†health. Endurance ‚Äď or aerobic ‚Äď exercises make strength and flexibility training easier, and aerobic exercises improve circulation, heart and lung health. Finally, flexibility and balance training¬†allows¬†for easier strength and endurance training, while cutting down on stress and injury.¬†

Besides the potent health benefits, constantly switching up the workout schedule has another powerful effect: it cuts down on boredom and tediousness. CrossFit members say they enjoy that every day they come in, the workout is different. And the workouts change at a fast pace, which makes for exciting workout sessions.  

For an idea of what to expect in a Crossfit session, common workouts include power-lifting with weights, push ups, sit ups, pull ups, running, squats, thrusts, stretches, climbing ropes, lifting kettlebells, working with medicine balls, jump roping, using a rowing machine, body exercises with weighted bars, and much more.   

File:District Crossfit Class Warfare-28 (15160360945).jpg

Why CrossFit May Be the Right Workout 

If vigorous exercise and participation in a welcoming community sound good to you, you’re probably a perfect fit for Crossfit. As mentioned above, each Crossfit workout tends to be short, but each workout is also very intense. Crossfitters enjoy the constant movement in and out of various exercises: you’re constantly moving and there is little time for rest.   

As you can imagine, the intensity and variety of the CrossFit workouts help to get participants extremely fit in many different areas quickly.

Expect better flexibility, greater endurance, increased strength, weight loss, elevated moods, better metabolism, reduced stress, improved body image, and a host of other benefits.   

Most importantly, one of the biggest draws for dedicated Crossfitters is the strength of the Crossfit community. Crossfit gyms tend to be full of dedicated, passionate, and welcoming members who are quick to motivate newcomers. The strong group dynamics behind Crossfit are highly encouraging for those looking to advance physically, and members are highly motivated to compete with each other and help each other reach higher levels of physical attainment.   

CrossFit: Possible Downsides 

There are a couple of Crossfit limitations that are worth considering if you are trying to decide on whether you are going to join a CrossFit gym. Because CrossFit is a general workout program that has highly varied exercises, you are likely to become very fit, but not necessarily better at any given specialized discipline. For example, if you are interested in Olympic weightlifting, gymnastics, or a specific sport, you may supplement your training with CrossFit activity, but CrossFit will not make you proficient on its own.   

Another issue that Crossfit has is the intensity of its workout program. Because of the speed and vigor of each exercise, it becomes more likely to get injured, especially the more fatigued you get. And yes, it is possible to get too much exercise, which is a risk inherent in the CrossFit program.  

If you have an existing health issue to work with, CrossFit may not be the right fit for you. Choosing a good CrossFit gym with credentialed and knowledgeable trainers is a good way to cut down on injury risks and develop an exercise program that is right for you. Finally, if you’re more into a solo exercising experience, and you don’t necessarily want to share your goals and progress with other people, then CrossFit’s community focus may turn you away.  [Probably the case with me. Рed.] 

Getting Started  

If¬†Crossfit¬†sounds like the right activity for your lifestyle, it’s not difficult to get involved. Today there are¬†Crossfit¬†gyms from coast to coast, whether you‚Äôre looking for the¬†best¬†Crossfit¬†gym in Southern California or Camden, Maine. Just make sure you seek out a gym with knowledgeable and credentialed instructors, and you really like the community presence there. This way, you can get the most out of the¬†Crossfit¬†experience, and ultimately, get the most optimization for your overall fitness, health, and well-being.¬†¬†¬†

Author Bio:  Carl Turner is a personal trainer and freelance lifestyle writer from Los Angeles, California. With over 10 years of experience, he has trained many clients and has helped them to reach their personal fitness goals. 

PS: For my favored form of exercise, see my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Who puts a sprig of parsley in their scrambled eggs?

The Conventional Wisdom on Cholesterol Is Full of Holes

I’ve argued against the conventional wisdom on cholesterol many times on this site. The conventional wisdom on cholesterol is full of holes.

Questions on atherosclerosis

Someone who believes in the conventional wisdom, namely that cholesterol clogs arteries, pointed me to an article called Twenty questions on atherosclerosis, by William C. Roberts, M.D. Roberts is the Executive Director of the Baylor Heart and Vascular Institute, and the Editor-in-Chief,¬†The American Journal of Cardiology¬†and¬†Baylor University Medical Center Proceedings. In other words, a cardiologist’s cardiologist. He writes:


Is atherosclerosis a disease affecting all animals or only certain animals?

Atherosclerosis affects only herbivores. Dogs, cats, tigers, and lions can be saturated with fat and cholesterol, and atherosclerotic plaques do not develop. 

I was easily able to find that “Dogs with atherosclerosis were over 53 times more likely to have concurrent diabetes mellitus than dogs without atherosclerosis”. Diabetes increases the risk of atherosclerosis greatly, 53 times more in dogs. So, not only do dogs get atherosclerosis, against what Dr. Roberts says, when they do it appears to have nothing to do with cholesterol.


Are human beings herbivores, carnivores, or omnivores?

Although most of us conduct our lives as omnivores, in that we eat flesh as well as vegetables and fruits, human beings have characteristics of herbivores, not carnivores (). The appendages of carnivores are claws; those of herbivores are hands or hooves. The teeth of carnivores are sharp; those of herbivores are mainly flat (for grinding). The intestinal tract of carnivores is short (3 times body length); that of herbivores, long (12 times body length). Body cooling of carnivores is done by panting; herbivores, by sweating. Carnivores drink fluids by lapping; herbivores, by sipping. Carnivores produce their own vitamin C, whereas herbivores obtain it from their diet. Thus, humans have characteristics of herbivores, not carnivores.

There’s a lot to unpack there, so I’ll just leave the following chart:

Image result for humans carnivores groves chart

Humans look far more like carnivores than herbivores.

Update: Several people have pointed me to the above chart at various times, which was compiled from a series of articles by the late Barry Groves. That said, I don’t know who actually made the chart. So, as additional support for the idea that humans are not natural vegetarians, see this article, How Humans Became Meat Eaters.


Is atherosclerosis a consequence of aging and therefore a degenerative disease?


Another chart (source), which shows that age is a major, perhaps the major, risk for atherosclerosis:

Effect of age and gender on the degree of atherosclerosis in the human aorta. Autopsy studies measured the area of the human aorta exhibiting raised atherosclerotic lesions as a function of the age and gender of the subject. Adapted from Supplementary data in Vihert (1976) 

What risk factors predispose to atherosclerosis?

Risk factors include hypercholesterolemia, systemic hypertension, diabetes mellitus, obesity, low HDL cholesterol, cigarette smoking, and inactivity.

This is perhaps the most interesting of Roberts’ answers. He listed 7 risk factors, and only one of them is high cholesterol. If high cholesterol causes atherosclerosis, how can diabetes or hypertension or smoking be risk factors? They have nothing to do with cholesterol and show that cholesterol either doesn’t cause atherosclerosis or is a relatively unimportant factor.


Of the various atherosclerotic risk factors, which one is an absolute prerequisite for development of atherosclerosis?

The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL 

As I wrote about here, the typical heart attack patient has a normal cholesterol level, but is glucose intolerant. So high cholesterol isn’t required for atherosclerosis, but glucose intolerance may be.


What evidence connects atherosclerosis to cholesterol?

The connection between cholesterol and atherosclerosis is strong.

He says herbivores get atherosclerosis when fed cholesterol. Humans aren’t herbivores, who don’t normally consume cholesterol, since it’s not found in plant foods.

He says atherosclerosis increases at cholesterol levels above 150 mg/dl. I already showed above that the typical heart attack patient has normal cholesterol; also, high cholesterol is associated with longer life.

He says the higher the LDL cholesterol, the more atherosclerosis. But in people over age 50, the lower the cholesterol, the greater the risk of death: 11% increased risk of death, and 14% increased risk of death from cardiovascular disease, with each 1 mg/dl decrease in cholesterol.

Roberts goes on to praise the efficacy and safety of statins. However, more recent trials of statins have been less than spectacular, and many found no benefit.


Is it important to lower elevated serum triglyceride levels?


Triglycerides are not cholesterol, and if it’s important to lower them – and it definitely is – then that shows that something besides cholesterol causes atherosclerosis. Elevated triglycerides are seen in diabetes and insulin resistance.


Can niacin and fibrates be used effectively and safely in combination with the statin drugs?




No incremental benefit to niacin.

“Any potential reduction in cardiac mortality from fibrates is offset by an increased risk of death from noncardiovascular causes.”


Dr. Roberts is wrong in most if not all of his assertions and conclusions. Cholesterol doesn’t appear to cause cause atherosclerosis.

Yet this is the conventional wisdom used by doctors to treat patients right now.

Yet another instance in which mainstream medicine got it wrong.

PS: For excess iron as a cause of heart disease, see my book, Dumping Iron.

PPS: Check out my Supplements Buying Guide for Men.

Can a Low-Carbohydrate Diet Prevent or Treat Cancer?

Several lines of evidence point to the idea that restricting dietary carbohydrates may have beneficial effects in the prevention or treatment of cancer.

Cell cultures

Scientists often grow human or animal cells in lab dishes in order to study their reactions to various stimuli, such as nutrients or drugs. Cell cultures give us reliable information on how cells work, and their relative cheapness and short time frame of experiments make them a great resource, but since they don’t represent a whole organism animal or human, results must be cautiously interpreted.

In cell culture, increased uptake of sugar (glucose) increased important pathways linked to initiation of cancer and growth of cancer cells. Reduction of glucose uptake in cancer cells suppressed cancer-promoting pathways.

This makes sense due to the Warburg effect, which was discovered nearly 100 years ago by Otto Warburg. Cancer cells preferentially use glucose for energy in a process called anaerobic glycolysis. The PET scan, used to detect cancer, makes use of this effect by looking at tissues with increased glucose uptake, thus detecting cancer.

Curiously, Warburg‚Äôs original hypothesis that aerobic glycolysis itself could be the ‚Äúorigin of cancer cells‚ÄĚ had not been proven directly. Our findings provide a hitherto-undescribed direct role of increased aerobic glycolysis in inducing the cancer phenotype, in which increased glycolytic activity regulates the canonical oncogenic pathways dynamically and reciprocally. These results may provide additional evidence for how hyperglycemia in diseases such as obesity and diabetes could provide a microenvironment that results in higher risk of some cancers. Additionally, our findings may explain how small molecules, such as metformin (used for treatment of diabetes and known to lower blood glucose levels), decrease the risk and mortality of several types of cancers.¬†


Animal studies

In mice, a low-carbohydrate, high-protein diet slows tumor growth and prevents cancer initiation. Mice that were implanted with tumor cells and fed the low-carbohydrate diet had slower tumor growth, and lower blood glucose and insulin. In mice bred for higher rates of spontaneous cancer, tumor incidence and insulin were lower on the low-carb diet.

Of interest, adding celecoxib, an anti-inflammatory drug, to a low-carbohydrate diet, markedly reduces metastasis. This may be for the same reasons that aspirin use is associated with less cancer.

A very low-carbohydrate ketogenic diet increases lifespan in mice. Among the changes noted in the mice fed the ketogenic diet was much lower tumor incidence; either the absence of carbohydrate in the diet, or the presence of ketones, meant less cancer.


Cancer has consistently been reported as rare to non-existent in peoples living in accordance with their traditional lifestyles, including Africans, American Indians, and Eskimos. Modern hunter-gatherer peoples eat far fewer carbohydrates, from 20 to 40% of calories, than do modern Americans, who eat 50% of calories as carbohydrates, on average. Hunter-gatherers also don’t eat highly processed carbohydrates, such as flour and sugar, which have been suggested to be uniquely involved in promoting cancer.

Insulin and IGF-1 (insulin-like growth factor) promote cancer, and a Western diet with high intake of refined carbohydrates, of the kind that promotes high blood sugar, in turn promotes insulin and IGF-1 signaling.

Obesity and diabetes are both associated with higher rates of cancer, and both obesity and diabetes are also associated with diets high in refined carbohydrates and sugar.

Thus, there are several reasons to think that a diet high in refined carbohydrates and/or sugar could promote cancer in humans.

Do low-carbohydrate (ketogenic) diets benefit cancer patients? This topic has engendered lots of controversy, with one side claiming that they could work wonders, the other side claiming a lack of solid evidence.

A review of human and animal studies on the ketogenic diet and cancer found:

The majority of animal studies (72%) yielded evidence for an anti-tumor effect of KDs. Evidential support for such effects in humans was weak and limited to individual cases, but a probabilistic argument shows that the available data strengthen the belief in the anti-tumor effect hypothesis at least for some individuals. Evidence for pro-tumor effects was lacking completely.

Good evidence in animal studies, weak evidence in humans, and no evidence of a pro-cancer effect.

Conclusion: A good case, but more evidence needed

If the reports of low to non-existent cancer among peoples living a traditional lifestyle without Western foods holds true, then that gives us reason to believe in the refined carbohydrate and cancer hypothesis. (I say “if”, because many of the reports are older and non-systematic, but still a phenomenon remarked upon by many doctors who lived among these peoples.)

Animal studies are another brick in the evidence wall, but of course rodents aren’t humans.

The fact that cancer cells feed on glucose, and that insulin promotes cancer growth, lead to the belief that cutting dietary carbohydrates can only help prevent or treat cancer. Certainly, there’s no evidence that cutting carbohydrates is harmful in that respect – or indeed, in any other respect.

PS: For more on how to live longer and healthier with strength training, and avoid cancer the same way, see my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Multivitamins Prevent Heart Attacks

Chelation therapy has been used to treat heart disease, and a randomized, placebo-controlled trial of chelation therapy showed that it works, which I wrote about in Heavy Metals and Heart Attacks. Further analysis of the results from the chelation trial have shown another interesting result: in patients who do not take statins, multivitamins prevent heart attacks.

The TACT Trial

Chelation therapy, the process in which doctors infuse EDTA into a patient with the aim of removing metals, has been practiced for decades mainly by alternative practitioners. The Trial to Assess Chelation Therapy, or TACT, was designed to rigorously test this therapy, and was originally thought of as a debunking study that would finally put the idea of chelation therapy to rest and confirm the mainstream proclamations of its uselessness. Unfortunately, or fortunately, depending on which side of health care you stand on, the trial found that, contrary to expectations, it worked.

TACT used a factorial protocol, viz:

  • 1.¬†Active intravenous (IV) chelation infusions + active oral MVM [multivitamins and¬† minerals].
  • 2.¬†Active IV chelation infusions + placebo oral MVM.
  • 3.¬†Placebo IV chelation infusions + active oral MVM.
  • 4.¬†Placebo IV chelation infusions + placebo oral MVM.

Patients on double active treatment had 26% fewer cardiovascular events than those on double placebo, and diabetic patients had 51% fewer. See charts below for event rates.

Large image of Figure 1.

Note that the first chart shows a non-significant reduction in cardiovascular events in patients on placebo infusions, but taking the multivitamin/mineral supplement.

The group running the trial looked at the data using “a prespecified subgroup analysis of participants not on statin therapy”. “Prespecified” is important here because it means the reseachers did not use data mining to find their results.

Most of the patients in the trial, 73% of them, were taking statins, since these drugs are considered standard of care for heart attack patients. But 27% were not on statins, and this group was analyzed separately.

The group taking vitamins, as opposed to placebo, had 54% fewer events, a composite of cardiovascular mortality, stroke, or heart attack. See event rate chart below.

The researchers were flabbergasted:

“These findings were unexpected and have to be viewed with appropriate skepticism…¬†The TACT investigators did not expect the OMVM regimen to produce clinically important benefits independent of the chelation treatment. The findings reported here were serendipitously discovered. The relative treatment effect seems quite large and this, in the presence of substantial noncompliance and what we think we already know about OMVM, makes these results seem implausible. However, implausible does not mean wrong. Under these circumstances, it is prudent to view these results skeptically and await TACT2 replication before any serious consideration is given to the potential clinical value of these findings.”

The MVM supplement

Previous trials have found no benefit of vitamins in cardiovascular disease, but most of them used either single vitamins or different formulations with much smaller amounts of vitamins and minerals.

In the study discussed here, the only reason they used vitamins is because chelation practitioners told them that they should, because that has been their practice. The ingredients of the MVM supplement can be found here. What jumps out are much higher amounts than in the Physician’s Health Study, as well as high amounts of vitamin A, C, B vitamins, and a hefty 500 mg of magnesium. Lots of other vitamins and minerals too.

In addition, the infusion used for chelation contained EDTA Рbased on kidney function, with a maximum of 3 grams Рand  2 grams of  magnesium chloride, 7 grams of vitamin C, potassium, and three B vitamins.


My bet is on magnesium as the main component of the supplement that lowered the risk of cardiovascular events.

The patients got large doses of magnesium, 2 grams in the infusion once a week, and 500 mg daily in the supplement. That alone could have seriously good benefits for cardiovascular health, since subclinical magnesium deficiency is a principal driver of cardiovascular disease.

Huge numbers of people do not get enough magnesium, as much as 50% of the population, and that figure is using the official RDA. At a more realistic intake of magnesium, many more are deficient. And magnesium deficiency is not readily detectable with standard lab testing. Magnesium deficiency can lead to hypertension and atherosclerosis.

Many magnesium supplements aren’t absorbed well. While the study doesn’t specify what type of magnesium the MVM contained, the fact that the patients got an infusion of 2 grams of magnesium chloride weekly guarantees that body magnesium levels increased.

Magnesium citrate is the best absorbed form of magnesium. I take this one. Don’t even bother with magnesium oxide, the kind found on drugstore shelves, as the body can absorb next to none of it.

Of course other vitamins and minerals may have contributed to the lower incidence of cardiovascular events. Maybe most of them together synergized. Of note, the supplement contained no iron.


Of interest, patients taking statins got no benefit from the vitamin/mineral supplement. That could mean a couple of things.

  • Statins cancel the benefits of vitamins and minerals on cardiovascular disease risk, or
  • Statins confer the same benefits as vitamins and minerals, and the addition of vitamins and minerals conferred no extra benefit.

By eyeballing the charts, my bet is on the first option: statins negate the benefits of vitamins and minerals.


What can we conclude, or at least conjecture, about these results?

  1. For starters, it’s important to be well-nourished, as that can prevent or treat heart disease.
  2. Multivitamins and minerals in supplement form may treat CVD.
  3. Many people with cardiovascular disease may be malnourished – in fact, that’s a certainty in my opinion.
  4. Statins may cause harm.
  5. The medical establishment may once again be wrong about causes and treatments of cardiovascular disease.
  6. Chelation therapy with a MVM supplement works in the treatment of cardiovascular disease.


PS: For more on the benefits of vitamins and minerals, see my book, Best Supplements for Men.

PPS: Check out my Supplements Buying Guide for Men.

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Vitamin K2, Heart Disease, and Cancer

Emerging evidence indicates that vitamin K2 plays a large role in the prevention of heart disease and cancer, as well as other conditions. Vitamin K2 is likely one of the vitamins that people are most deficient in – the other being vitamin D – and therefore it may be worthwhile to supplement with it: vitamin K2, heart disease, and cancer.

Vitamin K2 – what it is

Vitamin K refers to a group of fat-soluble vitamins, K1 and K2. Somewhat confusingly, there are several different forms of K2 as well.

Vitamin K1, or phylloquinone, is found in plant foods, mainly green leafy vegetables. K2, or menaquinone, is found in animal foods, mainly dairy.

Vitamin K2 is involved in calcification, hence it’s important for bone density, a big concern for the elderly. Lack of vitamin K is associated with osteoporosis, and supplementing it can prevent it.

Of importance to men, who suffer from higher rates of heart disease in middle age than women, a deficiency of vitamin K2 can lead to calcification of arteries.

One way to look at K2 is that it causes calcification of the correct tissue: bone, and not arteries or other tissues and organs.

The evidence

A study done in The Netherlands found huge differences in heart disease mortality, all-cause mortality, and aortic calcification among subsets of people grouped by vitamin K2 intake: Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study. 

The relative risk of death from coronary artery disease in the highest tertile (third) of vitamin K2 intake was nearly 60% lower than those in the lowest tertile. I’ll take that degree of risk reduction any day of the week.

Risk of all-cause mortality was ~25% less, and the risk of aortic calcification was only about half that of the lowest intake group.

Of importance, intake of phylloquinones, or vitamin K1, was not associated with any of these outcomes.

Another study found that each 10 őľg/d intake of vitamin K2 was associated with ~10% lower risk of coronary artery disease. A high menaquinone intake reduces the incidence of coronary heart disease. The highest quartile of vitamin K2 intake in another study had about a 20% lower risk of coronary artery calcification, in line with the other study‚Äôs 25% lower rate of aortic calcification:¬†High dietary menaquinone intake is associated with reduced coronary calcification.

These studies of course show associations and not causation, but there are good reasons to believe that causation is involved.

  1. Vitamin K2 is involved in calcium metabolism; therefore reduced calcification of arteries by vitamin K2 is likely to be causal.
  2. Since vitamin K2 comes mainly from animal foods, a healthy user effect might be ruled out. People conscientious of their health have reduced their consumption of animal foods over the past several decades, following mainstream advice.

There may also be a relation between vitamin K2 intake and less prostate cancer, though results are only suggestive.

The inverse association between vitamin K2 consumption and lower rates of heart disease makes sense, since one of the functions of vitamin K2 is in calcium metabolism. Calcification of the arteries is a cause of coronary heart disease. Essentially, vitamin K2 gets calcium into the right places, bones instead of arteries.

Vitamin K deficiency may be involved in Alzheimer’s disease too:¬†Low Vitamin K Intakes in Community-Dwelling Elders at an Early Stage of Alzheimer’s Disease.

Types and sources of K2

Given the above evidence – and there’s a lot more – I want to be sure I get adequate vitamin K2.

If you supplement with vitamin D – which I do – you should also be sure to get adequate K2; both are important for calcium homeostasis, so you shouldn’t get one without the other.

Pasture-raised meat and dairy are the best sources of vitamin K2. However, they’re expensive, most people never eat them, and I only seldom do. Feedlot meat and dairy doesn’t have much. Kerrygold butter from Ireland, sold here in the U.S., is a good source, although amounts of K2 also appear to be dependent on the season of the year, so you can’t be sure.

Given all of this, I supplement with K2. It’s the only vitamin I take besides D. Heart disease runs in my family, and I don’t feel like getting it.

I’ve been supplementing with a form of K2 known as MK-4, but I recently switched to the MK7 form. Here’s why:

Comparison of menaquinone-4 and menaquinone-7 bioavailability in healthy women.

The study compared the administration of MK-7 to that of MK-4, and found that “MK-7 was well absorbed and reached maximal serum level at 6 h after intake and was detected up to 48 h after intake. MK-4 was not detectable in the serum of all subjects at any time point..”

We conclude that MK-4 present in food does not contribute to the vitamin K status as measured by serum vitamin K levels. MK-7, however significantly increases serum MK-7 levels and therefore may be of particular importance for extrahepatic tissues.

I immediately bought an MK7 form of vitamin K2. There are many brands and sizes, and this one seems to be the best value.


Vitamin K is important to the health of your arteries. Atherosclerosis is one of the leading causes of death in the developed world.

Therefore, I take a vitamin K supplement. The MK7 form is the one to get.

PS: See also my book, Best Supplements for Men.

PPS: Check out my Supplements Buying Guide for Men.

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