Essential Oils Treat Baldness and Acne

Essential oils treat baldness

A reader commented on my post on whether fungal infection causes male pattern baldness, and says that rosemary oil is making his hair grow back:

After reading some studies about rosemary essential oil being as effective as minoxidil for hair regrowth (and without the warnings about not letting my wife and kids touch it). I’ve been doing a self-experiment of applying a few drops of a homemade hair tonic consisting mainly of rosemary and lavender essential oils suspended in a carrier of sesame oil to my scalp and beard.

At the start of the experiment, in mid-Summer, the top of my head was a cue-ball with a few stray short hairs here and there. During the first week or so after I started, it was like an unnoticed whitish, salt-like crust came up off of the top of my scalp. Then, I noticed hair growth. At first, they were short, blonde baby hairs, but now I have extensive patches of brown hair on the top that need regular trimming.

My hair seems to be coming back in the reverse order that I originally “lost” it. It isn’t fully back yet though. But the progress has been surprising. I continue to use my normal shampoos and conditioners, or whatever partially-used mini bottles my wife asks me to help finish. Sometimes I wear hats, sometimes I don’t. Sometimes I brush it, sometimes I don’t.

I haven’t used any other hair growth products or treatments during this time and haven’t tried anything else for 5+ years. I had basically resigned myself to look like my father.

Now, what is the rosemary changing on the top of my head, I don’t know. But by using it, my hair looks healthier. Also, my beard looks fuller.

He cited a couple of studies. One: Rosemary oil vs minoxidil 2% for the treatment of androgenetic alopecia: a randomized comparative trial. Rosemary oil was as effective as minoxidil (Rogaine).

“… both groups experienced a significant increase in hair count at the 6-month endpoint compared with the baseline and 3-month endpoint. No significant difference was found between the study groups regarding hair count either at month 3 or month 6.”

Rosemary oil is anti-fungal. And, it turns out, a number of essential oils are also anti-fungal.

The essential oils obtained from five commercial samples of Sicilian aromatic plants, laurel, sage, oregano, rosemary and coriander were analyzed by GC/MS and assayed for their antibacterial, antifungal and antioxidant activities. Twenty-five different genera of bacteria and one fungal species were used in this study as test organisms. The oils showed a high degree of inhibition against all the microorganisms tested.

Clove and rosemary oils in combination have synergistic effects against fungi and bacteria.

Totally makes sense, since many phytochemicals made by plants are there to be used for chemical warfare against other plants and against animal predators. In this case, fungi predate on plants, so the plants need to have anti-fungal defenses.

I don’t know whether the other essential oils besides rosemary will treat baldness, but I bet they would. In any case, the fact that rosemary oil does treat it, and is anti-fungal, adds further evidence to the cause of male pattern baldness.

Essential oils and iron chelators treat acne

I mentioned this in my article on acneThe use of iron chelators in biocidal compositions. Through the magic of SciHub, I got my hands on the full paper.  The authors show that iron chelators potentiate acne medications such as salicylate and benzoyl peroxide from 4 to 250-fold.

Could you add an iron chelator to an acne med on your own? Maybe. Green tea extract or IP6 seem likely candidates. Topically applied IP6 penetrates the skin.

Essential oils also treat acne. Tea tree oil was as effective as benzoyl peroxide.

A number of essential oils are effective in killing the bacteria that causes acne, Propionibacterium acnes. The most effective were thyme, cinnamon, and rose oils.

The beauty of essential oils in this case are that their chemical nature makes them able to penetrate skin. However, I don’t know whether they might be irritating or toxic to skin.

Rosacea, iron, and fungi

Another skin condition is rosacea, characterized by red, inflamed skin on the face. It can range from mild to disfiguring. They still haven’t figured out the cause of it. The most effective treatment appears to be topical metronidazole.

Metronidazole is an interesting drug, the only one in current use that’s effective against both protozoan parasites (like Giardia or Plasmodium) and anaerobic bacteria. It’s been thought that this drug works against rosacea by killing Demodex, a skin mite. The problem is that it appears most people have Demodex; that doesn’t mean it’s not causative; most people seem to have Malassezia too, and that causes dandruff and maybe baldness.

However, rosacea patients have higher levels of ferritin in the skin of their lesions.

Serum peroxide levels were significantly higher and serum total antioxidative potential levels were significantly lower in patients with rosacea than in healthy control subjects (P < .05). Compared with control subjects, the number of ferritin-positive cells was significantly higher (P < .001) in skin samples from patients with rosacea, especially those with severe disease.

Ferritin is made in response to free iron, so this suggests that rosacea is associated with higher iron levels in the skin, causing oxidative stress and just maybe allowing for the growth of some microorganism, such as a fungus.

I was unable to find whether metronidazole successfully kills fungi; in any case, it isn’t used for that. But its structural resemblance to the anti-fungal drugs ketoconazole and fluconazole did not escape my attention. And ketoconazole chelates iron.

So it seems possible that metronidazole is either killing fungi in the skin and/or removing iron. (Either that or I’ve been looking at PubMed for too long and starting to see things.) A wastewater treatment for removing metronidazole uses iron particles, indicating iron chelation.


In summary, baldness, acne, and rosacea may have something in common: the presence of microorganisms. In turn, these microorganisms could get a perch on the skin by access to iron.

What we need is a study to see whether blood donors have fewer of these skin conditions. Rosacea typically starts after age 30, as does baldness, which could implicate iron. Obviously multiple factors, including genetic susceptibility, must be at work in all of these conditions.

PS: Check out my books, Dumping Iron, Muscle Up, and Stop the Clock.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Why a Low-Carb Diet Is Best for Weight Loss

If you want to lose weight, you have a number of choices. The most popular is to cut calories and eat a low-fat diet. A way that’s becoming more popular, because it works much better, is to cut carbohydrates. Here we’ll take a look at scientific proof that a low-carb diet is best for weight loss.

No calorie counting

The biggest impediment to losing weight on a low-calorie diet is hunger. If you voluntarily reduce calories while eating the same foods, you get hungry, as is to be expected. Your body defends its weight, i.e. it has a set point, and makes you hungry if your weight moves away from the set point.

On a low-carbohydrate diet, you merely cut the amount of carbohydrates in the diet, and in most studies looking at low-carb diets, the dieters ate as much as they wanted. Only carbohydrates were restricted. Cutting carbohydrates lowers levels of the hormone insulin, which signals the body to store fat, and which is responsible for setting the body weight set point. The result is nearly effortless weight loss.

In the first study we’ll look at, a group of obese women were randomized to either a low-fat, low-calorie diet, or a low-carbohydrate diet that was not restricted in calories, and followed for 6 months. Weight loss result in the chart below.

low carb weight loss

The low-carb group ate 20 g of carbohydrate daily, but were allowed to increase this to 40 to 60 g after 2 weeks, so long as they remained in ketosis as shown by urinary testing. The low-fat group was restricted in calories by 30% and ate about 55% of their calories as carbohydrates.

Despite the fact that the low-carb group could eat as much as they wanted, they spontaneously reduced their calorie intake to about the same as the low-fat group. That shows the power of low-carb in reducing hunger and changing the body’s weight set point. And they still lost more weight, an average of 7.6 kg, than the low-fat group, at an average of 4.2 kg.

You can even eat more calories and still lose weight

The second study concerns weight loss in obese teenagers. A group of adolescents, average age 14, were assigned to either a low-carb diet or a low-fat diet.

The low-carb group was instructed to keep carbohydrates at less than 20 g a day for the first 2 weeks, but increasing to 40 g a day in weeks 3 through 12. They could eat as musch as they wanted.

The low-fat group was instructed to keep fat at <40 g a day. They also could eat as much as they wanted.

Here are the results.

low carb weight loss 2

The low-carb teenagers averaged 9.9 kg of weight loss, compared to 4.9 kg in the low fat group. (That’s 22 pounds vs 11 pounds.) That was despite the fact that the low-carb group ate over 1800 calories a day, while the low-fat group ate 1100 calories a day. That’s the power of lowering carbohydrate intake. Also it’s guaranteed that the low-carb group was less hungry.

You don’t even need to reduce carbohydrates much

The third study compared a low-carbohydrate to a low-fat diet in severe obesity. These people had a high prevalence diabetes or metabolic syndrome.

The low-carbohydrate group was instructed to keep carbs at <30 g a day. However, they didn’t. They could eat as much as they wanted.

The low-fat group was instructed to keep fat  at <30% of calories, and to reduce their calorie intake by 30%.

low carb weight loss 3

The low-carb group lost 5.8 kg after 6 months, the low-fat group 1.9 kg. (13 pounds vs 4 pounds.) The low-carb group spontaneously reduced their calorie intake, so that the 2 groups ate about the same number of calories, again showing the power of reducing hunger and body weight set point.

Notably, the low-carb group wasn’t very compliant, and they only reduced their carb intake to 37% of calories at 6 months, vs 51% for the low-fat group. Yet they still lost more weight.

Low-carb vs low fat and Mediterranean diets

The fourth study was a three-way comparison between a low-carb, low-fat, and Mediterranean diets. The low-fat and Mediterranean diets were restricted in calories, with limits of 1500 calories daily for women, and 1800 for men.

The low-carb dieters could eat as much as they wanted, so long as they restricted carbohydrates to 20 grams daily initially, but increasing to a maximum of 120 grams.

Here’s what happened:

low carb weight loss 4

Once again, low-carb is a clear winner. Low-fat lost 2.9 kg, Mediterranean 4.4 kg, and low-carb 4.7 kg. The low-carb group still ate a whopping 40% of calories as carbohydrates, although that was down from 51% at baseline, representing a drop of 120 grams of carbs daily.

Noteworthy is the increase in weight after the first few months of weight loss, which was greatest in the low-carb group. That group actually increased its carb intake slightly. Another explanation might be a lower metabolic rate and/or less exercise. the low-carb group did decrease the amount of exercise between 6 and 24 months; the low-fat group increased exercise.

Reviews of low-carb diets

We’ve seen above that several studies have found that low-carbohydrate diets are superior for weight loss. have I cherry-picked the studies? Nope.

Several meta-analyses (reviews of studies) have found that low-carb diets beat calorie-restricted low-fat diets.

Dietary Intervention for Overweight and Obese Adults: Comparison of Low-Carbohydrate and Low-Fat Diets. A Meta-Analysis. This study concluded:

This trial-level meta-analysis of randomized controlled trials comparing LoCHO diets with LoFAT diets in strictly adherent populations demonstrates that each diet was associated with significant weight loss and reduction in predicted risk of ASCVD events. However, LoCHO diet was associated with modest but significantly greater improvements in weight loss and predicted ASCVD risk in studies from 8 weeks to 24 months in duration. These results suggest that future evaluations of dietary guidelines should consider low carbohydrate diets as effective and safe intervention for weight management in the overweight and obese, although long-term effects require further investigation.

Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials. This study concluded:

Compared with participants on LF diets, participants on LC diets experienced a greater reduction in body weight.

What to eat on a low-carb diet

Low-carb diets vary in the degree of carbohydrate restriction. One scheme that I used in my book Stop the Clock was the following:

  • moderately low-carb: <130 grams of carbohydrate daily
  • low-carb: 50 to <130 grams daily
  • very low-carb ketogenic: <50 grams daily.

As we saw in this article, virtually any degree of carbohydrate restriction is beneficial. But, the more you restrict carbs, the better your weight loss is likely to be.

Timothy Noakes, M.D., a noted advocate of low-carb diets, recently published an article, Evidence that supports the prescription of low-carbohydrate high-fat diets: a narrative review. In it, he listed the following foods as being “green-lighted” for a low-carbohydrate diet:


This list is meant for people who are insulin-resistant. If trying to lose weight, it would be a good idea to go easy on the added oils and nuts.

You should omit the following foods entirely:

  • anything made with flour: bread, pasta, tortillas, pastries
  • anything with added sugar: soft drinks, fruit juice, candy, cookies
  • starch: potatoes, sweet potatoes

Did I miss anything? It’s easy, just eat plenty of meat, eggs, vegetables, cheese. Don’t go hungry.

For what it’s worth, I eat this way all the time. Most days my carb intake is probably 20 to 60 grams, some days rising to 100.

PS: Check out my books, Dumping Iron, Muscle Up, and Stop the Clock. And don’t forget Top Ten Reasons We’re Fat.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Podcast with Mark Baxter

I recently had a conversation with my friend Mark Baxter. We discussed iron, high intensity weight training, why young men should care about longevity, and the bnest three supplements for men. Listen to it at Mark’s site or at SoundCloud.

PS: Check out my books, Dumping Iron, Muscle Up, and Stop the Clock.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Insulin Resistance Is a Major Risk for Cancer

Insulin resistance, the condition in which a person becomes insensitive to the effects of insulin and has to produce more insulin to overcome that insensitivity, ultimately leads to diabetes if it goes on long enough. Insulin resistance is also related to cancer. In this article I’ll discuss why insulin resistance is a major risk for cancer, why this is important, and what you can do to dramatically decrease your cancer risk.

Association between insulin resistance and cancer

Insulin is a hormone, and one of its main functions is to allow cells to take up glucose from the blood to use for fuel. When more insulin than normal is required to do this, then a state of insulin resistance occurs. When insulin resistance gets to a point in which the body can’t keep glucose under control and blood sugar rises, that’s the disease of type 2 diabetes.

Both insulin resistance and diabetes are associated with many chronic diseases, as I discussed in my post on fasting insulin. Cancer is one of them.

Most people tend to think of cancer as something that strikes out of the blue and that there’s little they can do about it. (The exception being smoking.) The seemingly chance nature of cancer, as well as its often fatal outcome is what make cancer so frightening to so many.

Cancer doesn’t strike by chance, though. Many factors that are under your control can radically decrease your risk of getting it. One of the most important is insulin resistance.

Prostate cancer

Men are often told that prostate cancer is almost unavoidable, that most men will have some degree of prostate cancer as they get old, even if it doesn’t become serious or kill them.

I doubt that’s true.

Men with insulin resistance have a far higher risk of prostate cancer. Men in the highest tertile (third) of insulin resistance were almost 3 times more likely to have prostate cancer than those in the lowest tertile.

Conversely, men with the highest insulin sensitivity had a 65% reduced risk of prostate cancer.

Waist-hip ratio as a measure of obesity adds to the risk. men in the highest tertile of both insulin resistance and waist-hip ratio had more than 8 times the risk of prostate cancer.

Despite what you’ve heard, there’s no relation between testosterone and prostate cancer. In fact, testosterone replacement therapy (TRT) is associated with a decrease in the risk of prostate cancer of 40%.  I speculate that it does this by improving body composition (ratio of muscle to fat) and thus improving insulin sensitivity.

Breast cancer

Breast cancer occupies a place in the psyche of women that may be hard to overestimate. Some women have feared it so much that they have had preemptive mastectomies — they’ve had their breasts chopped off so they won’t get breast cancer.

But as with prostate cancer, breast cancer is highly associated with insulin resistance. Women in the highest quintile (fifth) had nearly 3 times the risk of breast cancer than those in the lowest. That was independent of degree of body fat.

Other cancers

Insulin resistance and diabetes are associated with a higher risk of many other cancers. These include cancers of the stomach, colon, liver, pancreas, kidney, ovaries,  and endometrium.

A recent study found that insulin resistance was associated with a 12 times greater risk of any cancer.

Metformin lowers cancer risk by lowering insulin

Metformin is a drug that lowers glucose and insulin and is the most common drug treatment for diabetics.

Metformin use is associated with large reductions in cancer relative to other diabetic drugs. New users of metformin have about a 40% decreased risk of cancer. New users have a lower risk in this study probably because they’re actually taking their metformin, whereas in other studies, results were based on any history of metformin use.

Glucose is fuel for cancer, so that’s one way metformin works.

Insulin promotes growth, and for that reason may promote cancer.

Metformin has become a hot topic in anti-aging circles, since it increases lifespan in mice. Human trials of metformin for life extension are under way.

From associations between higher insulin and increased cancer, and lower insulin (from metformin) and decreased cancer, it’s clear that insulin and insulin resistance raise the risk of cancer.

Berberine is an over-the-counter supplement that works very similarly to metformin.

Growth versus longevity

A big theme in aging is that of growth versus longevity. In general, anything that promotes growth also promotes aging, and anything that inhibits growth promotes life extension. Calorie restriction is a good example: it inhibits growth and extends lifespan. Exogenous human growth hormone promotes growth (obviously) and decreases lifespan.

Insulin also promotes growth. It causes energy storage of fat in fat cells, and is necessary for muscle growth too.

Unrestrained growth is a hallmark of cancer. Insulin and glucose promote that growth.

How to decrease the risk of cancer

There are actually lots of ways to decrease your risk of cancer, but for the moment, let’s confine the discussion to lowering insulin resistance to decrease cancer.

Low-carbohydrate diet

Low-carbohydrate diets cause insulin to decrease. Even when no weight is lost, insulin declines.

Ron Rosedale and Eric Westman studied patients put on a very low carbohydrate diet. Over the course of an average of 3 months, their insulin levels dropped about 40%, and glucose about 7%. This shows the importance of the insulin test, since the body can keep glucose within the normal range by increasing insulin, and a simple fasting blood glucose test does not detect this.


In a comparison of fasting versus a carbohydrate-free diet, fasting lowered insulin response by 69%, while the carb-free diet lowered it by 49%. This led the researchers to conclude that carbohydrate restriction alone could account for more than 70% of the insulin response in fasting. Note that this was a 3-day fast, a long one.

Another study compared a 3.5-day fast to receiving all calories via lipid infusion. Insulin dropped in both conditions. These researchers concluded that absence of carbohydrate was responsible for all of the responses to fasting. Probably hyperbolic, in my estimate, but close.

Fasting decreases insulin and improves insulin sensitivity.

Strength training

Exercise improves insulin sensitivity. Quote from this study, “The most important site of peripheral insulin resistance is the skeletal muscle, and in this tissue there are several steps involved in insulin-mediated glucose uptake in which insulin resistance might occur.”

To improve insulin sensitivity the most, exercise all muscles. So, not (or just) aerobic exercise (cardio), but strength training. Lifting weights. Resistance training improves insulin sensitivity.

It does this by depleting muscles of glycogen and increasing glucose transporters in muscle tissue.


Insulin resistance is strongly associated with cancer. In fact, I know of no other association with cancer as strong, with the exception of cigarette smoking or perhaps very toxic chemicals such as heavy metals.

To decrease your risk of cancer, improve your insulin sensitivity via

  • low-carbohydrate eating
  • intermittent fasting
  • lifting weights.

PS: Check out my books, Dumping Iron, Muscle Up, and Stop the Clock.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Fasting Insulin

A test for fasting insulin is one of the most important blood tests you can take; Dr. Joseph Mercola in fact believes that it’s the most important.

It’s important because it shows the degree of insulin resistance — the higher the number, the more insulin resistant. A really high number generally means type 2 diabetes. A number merely higher than normal means metabolic syndrome or pre-diabetes.

Insulin resistance is one of the main causes of chronic disease in the modern world, including heart disease, cancer, kidney disease, and of course diabetes. It either causes or is caused by obesity; the arrow of causation in that case is controversial. Being sedentary also leads to insulin resistance, and exercise can prevent it.

Insulin resistance is strongly associated with obesity, but normal weight people, especially those who are skinny-fat, can have it too.

My fasting insulin test

Doctors don’t routinely test for fasting insulin; they normally do so only if they suspect diabetes.

I’ve had a few tests of fasting blood glucose that were high, in the range of 100 to 110. That’s an odd result, because I eat a low-carbohydrate diet and lift weights, and have a body fat percentage that i don’t know exactly but is no doubt <15%.

It’s probably due to the so-called dawn phenomenon, or physiological insulin resistance, which is normal. When on a low-carbohydrate diet, the liver can become insulin resitant in order to make glucose for the rest of the body. To be honest, the causes of the dawn phenomenon are not fully elucidated, and experts give varying explanations. But the fact is that many people who eat low-carb report it.

Not being clear on whether I should be concerned about my high fasting glucose, I decided to get a fasting insulin test from Life Extension.

Result: 2.9 µIU/ml. Normal range is 2.6 to 24.9. (On this scale, 1 µIU/ml = 6.9 pmol/L.)  Ideal, according to Dr. Mercola and others I’ve read, is <3. The odds ratio for prediabetes rises sharply with increased fasting insulin.

My result was about as perfect as one could want. I think I’m going to live another few years.

Should I remain concerned about my fasting glucose test? Probably not; my non-fasting glucose is actually lower than my fasting glucose, which would seem to indicate, together with my insulin test, that I have no risk of diabetes. It would indeed be strange if I did have increased risk, for the reasons mentioned above: low-carb diet, weight lifting, low body fat, plenty of muscle too.

If you do have a high fasting insulin, then you need to get to work. Below are relative risks of hypertension, high triglycerides, and diabetes based on fasting insulin levels. (Source.)

Image result for fasting insulin

You can order a fasting insulin test through Life Extension; blood is drawn at no extra charge at LabCorp.

PS: Read my book, Stop the Clock, for why insulin sensitivity is important. Read my other books too.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

High Iron Means Increased Risk of Gestational Diabetes

Quick take: High iron means increased risk of gestational diabetes.

Gestational diabetes occurs in up to 10% of pregnant women, and can lead to complications for both mother and child. Complications include preeclampsia, a serious condition.

From the paper:


The aim of this study was to prospectively and longitudinally investigate maternal iron status during early to mid-pregnancy, and subsequent risk of gestational diabetes mellitus (GDM), using a comprehensive panel of conventional and novel iron biomarkers.


A case–control study of 107 women with GDM and 214 controls (matched on age, race/ethnicity and gestational week during blood collection) …


Hepcidin concentrations during weeks 15–26 were 16% higher among women with GDM vs controls (median 6.4 vs 5.5 ng/ml; p = 0.02 ), and were positively associated with GDM risk; the aOR (95% CI) for highest vs lowest quartile was 2.61 (1.07, 6.36). Ferritin levels were also positively associated with GDM risk; the aOR (95% CI) for highest vs lowest quartile was 2.43 (1.12, 5.28) at weeks 10–14 and 3.95 (1.38, 11.30) at weeks 15–26… 


Our findings suggest that elevated iron stores may be involved in the development of GDM from as early as the first trimester. This raises potential concerns for the recommendation of routine iron supplementation among iron-replete pregnant women.

As far as I’m aware, Eugene D. Weinberg was the first, or one of the first, to call attention to the possible relation between gestational diabetes and iron.

Increased ferritin is associated with diabetes, and iron depletion decreases insulin resistance.

The risk of those in the highest quartile of ferritin was 4 times that of the lowest quartile. This is an association of course and causation is not proven. But it does call into question the idea that all pregnant women should get supplemental iron, since that would appear to be not without risk.

An accompanying discussion states:

Gross iron overload has long been known to result in diabetes mellitus. However, it is now thought that milder levels of iron overload, possibly within the normal range, also increase the risk of diabetes mellitus. The article by Rawal et al in this issue provides further support for the relationship between mild degrees of iron overload and the risk of gestational diabetes. The purpose of this commentary is to briefly discuss the background of this relationship and the implications it may have for routine pregnancy care.

PS: Check out my book, Dumping Iron.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Iron and Fungal Infections

We saw recently that iron is involved, however unlikely it may seem, in producing dandruff, seborrheic dermatitis, and quite possibly, male pattern baldness. These conditions all have in common that a fungus, Malassezia, is involved. In this short post I want to take a look at the evidence of a connection between iron and fungal infections.


Dandruff and seborrheic dermatitis are both associated with several species of fungus of the genus Malassezia. They are specialized to live on human skin. Like all other microbial pathogens, Malassezia require iron to grow and reproduce, and they obtain iron from their hosts.

Transferrin is the protein molecule in mammals that binds and carries iron. (Ferritin is for iron storage.) Transferrin is at the center of an evolutionary arms race between microbes and primates. Primates try to withhold iron from microbes, and the microbes try to grab it. Each one of them attempts to fight their respective opponents by evolving molecules that have an ever stronger grip on iron.

Iron sequestration provides an innate defense termed nutritional immunity, leading pathogens to scavenge iron from hosts. Although the molecular basis of this battle for iron is established, its potential as a force for evolution at host-pathogen interfaces is unknown. We show that the iron transport protein transferrin is engaged in ancient and ongoing evolutionary conflicts with TbpA, a transferrin surface receptor from bacteria. Single substitutions in transferrin at rapidly evolving sites reverse TbpA binding, providing a mechanism to counteract bacterial iron piracy among great apes…  These findings identify a central role for nutritional immunity in the persistent evolutionary conflicts between primates and bacterial pathogens.

Transferrin inhibits the growth of Malassezia. Adding transferrin to a culture of the fungus withholds iron from it so that it can’t grow. Ciclopirox and salicylate, both iron chelators, also inhibit Malassezia in skin.


Candida is a genus of fungus with a number of different species and which cause a number of different diseases, including thrush (oral candidiasis), vaginal and skin infections. They can also be invasive and cause blood  and other internal infections. Naturally, Candida requires iron.

Ciclopirox, the iron chelator, inhibits Candida, and the addition of iron reverses the inhibition.

Candida albicans, the major species in this genus, is the only microorganism known to directly exploit ferritin for its iron.

Iron is an essential nutrient for all microbes. Many human pathogenic microbes have developed sophisticated strategies to acquire iron from the host as most compartments in the body contain little free iron. For example, in oral epithelial cells intracellular iron is bound to ferritin, a protein that is highly resistant to microbial attack. In fact, no microorganism has so far been shown to directly exploit ferritin as an iron source during interaction with host cells. This study demonstrates that the pathogenic fungus Candida albicans can use ferritin as the sole source of iron. Most intriguingly, C. albicans binds ferritin via a receptor that is only exposed on invasive hyphae…  Therefore, C. albicans uses an additional morphology specific and unique iron uptake strategy based on ferritin while invading into host cells where ferritin is located.

Cryptococcus neoformans

Cryptococcus neoformans is a fungus that causes an often fatal infection of the meninges and brain, especially in HIV patients. When it senses that iron is available, it grows, and elaborates its pathogenic mechanism.

Iron overload is known to exacerbate many infectious diseases, and conversely, iron withholding is an important defense strategy for mammalian hosts. Iron is a critical cue for Cryptococcus neoformans because the fungus senses iron to regulate elaboration of the polysaccharide capsule that is the major virulence factor during infection. Excess iron exacerbates experimental cryptococcosis and the prevalence of this disease in Sub-Saharan Africa has been associated with nutritional and genetic aspects of iron loading in the background of the HIV/AIDS epidemic. We demonstrate that the iron-responsive transcription factor Cir1 in Cr. neoformans controls the regulon of genes for iron acquisition such that cir1 mutants are “blind” to changes in external iron levels. Cir1 also controls the known major virulence factors of the pathogen including the capsule, the formation of the anti-oxidant melanin in the cell wall, and the ability to grow at host body temperature. Thus, the fungus is remarkably tuned to perceive iron as part of the disease process, as confirmed by the avirulence of the cir1 mutant; this characteristic of the pathogen may provide opportunities for antifungal treatment.


There are many other species of fungi that can cause infections, and this is just a quick look at three of them and how they require iron. All other microbes require it as well.

Keeping iron (ferritin) under control may stop these infections from happening. Iron supplementation is known to increase the infection rate and exacerbate their severity.

PS: For more on iron, see my book, Dumping Iron.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Does Sugar Cause Heart Disease?

Does sugar cause heart disease? Evidence points to it.

A study published in the Journal of the American Medical Association found highly positive and graded correlations between sugar intake and death from cardiovascular (heart) disease (CVD). Comparing quintiles (fifths) of sugar intake, the highest consumers had more than double the risk of dying from CVD.

In the highest consumers, who ate >25% of their calories as sugar, the risk nearly tripled. Those who consumed >10% but <25% of calories as sugar, had 30% increased risk of death.

Most adults that this study looked at, 71% of them, consumed more than 10% of calories as added sugar, and around 10% of them consumed more than 25% of calories as added sugar.

Pathetic. And we wonder why there’s an epidemic of heart disease – and obesity.

The results were adjusted for “sociodemographic, behavioral, and clinical characteristics”.

I believe that these heart disease risks may be underestimates, when you compare the risks to people who consume no sugar at all. Since over 70% of adults consume more than 10% of calories as sugar, people who eat zero sugar must be hard to find, at least enough for a study. (Maybe they could study Rogue Health and Fitness readers.)

How sugar causes heart disease


Dietary sugar is associated with hypertension – high blood pressure, and that’s independent of weight gain. This may occur due to high levels of insulin, with subsequent increase in body water. Insulin is an anti-diuretic: it increases the retention of fluid.

Salt is only minimally related to hypertension. The correlation between processed foods and hypertension arises not from salt, but sugar.

Increased triglycerides

Sugar causes levels of triglycerides to increase, and triglycerides are associated with CVD. Sugar also causes HDL cholesterol to drop. In truth, since we don’t believe in the lipid hypothesis of heart disease around here, those are probably just markers for increased insulin resistance.

Increased inflammation

Sugar increases the levels of inflammatory markers, which are associated with CVD.

Insulin resistance

It’s likely that all of the above mechanisms and effects are due to insulin resistance.

Sugar (sucrose) is a molecule made of a fructose and a glucose molecule linked together. Hence, sugar is 50% glucose, 50% fructose. High-fructose corn syrup, which is increasingly used in place of sugar, is 45% glucose and 55% fructose – it’s not that different.

Fructose seems to be the bad element here. A high intake of fructose leads to hyperlipidemia (high fat in the blood) and to insulin resistance.

Some time ago, Gerald Reaven, M.D., of Stanford University, studied a group of men and classified them according to tertiles (thirds) of insulin resistance. (I discussed that study here.) He then followed them for a number of years and looked at the type and number of diseases they got, including hypertension, CVD, diabetes, cancer, and stroke. Results are in the chart below.


In the lowest tertile of insulin resistance, no one got sick.

Those in the lowest third of insulin resistance remained perfectly healthy, those in the highest third developed all kinds of nasty things, and those in the middle had an amount in between the others.

This likely explains how and why sugar is associated with heart disease.



Added dietary sugar is associated with cardiovascular disease.

So don’t eat sugar.

PS: You can support this site by purchasing through my Supplements Buying Guide for Men.

How a Low-Carbohydrate Diet Slows Aging

Low-carbohydrate, high-fat diets (LCHF) have many health benefits. They can cause weight loss in overweight people without hunger, and improve insulin resistance and dramatically improve diabetes. Even more, LCHF diets greatly improve lipid markers of cardiovascular disease risk. Besides the beneficial effect on cardiovascular markers and weight loss, I’ll show here how a low-carbohydrate diet slows aging.

Glucose shortens lifespan in C. elegans

Carbohydrates are long chains of sugar molecules; in the case of common foods like wheat, rice, and potatoes, the carbohydrates are long chains of glucose, the same type of sugar as in the blood. The influence of glucose as a food source has been studied in aging research.

In the worm C. elegans, dietary glucose shortens lifespan. One of the most important ways it seems to do this is through the production of advanced glycation end products, or AGEs. These molecules result from the attachment of glucose to proteins (hence glycation), and they are implicated in diabetic complications. AGE’s may also be important in the buildup of irremovable cellular junk (lipofuscin), resulting in the garbage crisis of aging.

On the other hand, glucose restriction increases lifespan in C. elegans. Restricting glucose activates the equivalent of AMPK, the cellular energy sensor, which in turn inhibits mTOR and increases stress defense mechanisms, notably Nrf2. Essentially, it acts as a form of hormesis.

Important to note that the biochemical pathways involved in C. elegans lifespan extension are evolutionarily conserved mechanisms, so these results are of relevance to humans, though how much is a different question.

Glucosamine extends lifespan by reducing glucose metabolism

Glucosamine is an over-the-counter supplement, and it extends lifespan not only in C. elegans, but in mice too. (Important because that gets us closer to human physiology.) Mice who got glucosamine

show an induction of mitochondrial biogenesis, lowered blood glucose levels, enhanced expression of several murine amino-acid transporters, as well as increased amino-acid catabolism. Taken together, we provide evidence that GlcN [glucosamine] extends life span in evolutionary distinct species by mimicking a low-carbohydrate diet.

So, this is further evidence: reducing glucose metabolism increases lifespan. You could take glucosamine, or you could just cut out the middleman and reduce your carbohydrate consumption.

Calorie restriction extends lifespan and reduces glucose metabolism

Calorie restriction (CR), that is, the reduction in food given to lab animals or humans, is the most reliable and robust life-extension intervention there is, extending lifespan in rodents as much as 50%. The greater the restriction, the longer the life extension.

As one might expect, massive amounts of research has been done on CR attempting to pin down the means by which it counteracts aging. CR effects many biochemical/physiological changes, and some or all of these may be important to its benefits. One thing CR does is to decrease the metabolism of glucose, and to increase fat burning.

A key metabolic change during CR is a shift from carbohydrate metabolism to fat metabolism.

Once again, AMPK is involved, which coordinates a series of biochemical effects, including the shift to fat metabolism.

Carbohydrate restriction lowers insulin and IGF-1

CR lowers levels of both insulin and IGF-1 (insulin-like growth factor), and this is thought to play a large role in lifespan extension. Animals that have modified insulin signaling live longer, and IGF-1 is important in the development of cancer.

Humans that eat a carbohydrate-restricted diet see a large drop (50%) in plasma insulin, and about a 30% decrease in plasma IGF-1. This happened on a diet that contained 5% carbohydrate, as opposed to 60% before. Of interest, protein is thought to be important to IGF-1 levels, and this diet increased protein, to 35%, and IGF-1 still dropped, although muscle IGF-1 increased.

To what extent does carbohydrate restriction mimic calorie restriction? Probably a fair amount: restricting carbohydrate alone is responsible for about 70% of the benefits of intermittent fasting.

Conclusion: Burning fat instead of glucose increases lifespan

The evidence above suggests that less metabolism of glucose and more of fat increases lifespan.

If you want to implement a low-carbohydrate, high fat diet, here’s what you can eat (source):



PS: For more on fighting aging, read my book, Stop the Clock.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Deadlifts for Reps

Here’s a video shot today. I’ve been concentrating not on increasing my max load lifted, but on increasing the number of reps. By the end of a 10-rep set, even 245 pounds feels like a lot – anyway, to me it does.

Deadlifts for reps, 245 x 10.

A video posted by P. D. Mangan (@pdmangan) on

Higher Heart Disease Risk in Post-Menopausal Women Is Due to Iron

One of the key pieces of evidence leading to the implication that iron causes heart disease is the differential incidence of heart disease between men and women. Men have far higher rates of heart disease, and they have much higher iron levels, since women lose iron via menstruation. When women cease menstruation at menopause, their risk of heart disease goes way up, and this is not due to hormones, as both of the pieces below note.

That’s the topic of two letters just published in JAMA Cardiology, one by Luca Mascitelli, M.D. and Mark Goldstein, M.D., the other by Virginia Mary Hayes, M.S., Ralph George DePalma, M.D., and Leo Zacharski, M.D., all of them experts on the relation between iron and health. I know a couple of these people, and Dr. Mascitelli kindly sent me these letters, which I’m publishing here because otherwise the public won’t get to see them due to a paywall.




Iron (ferritin) levels above the minimum serve no purpose; it’s merely storage. (Admittedly, if you lost a lot of blood, didn’t die from it, and had no medical care, you might return to health faster if you had more iron stores, but that’s about the only example I can think of where more iron might be better.) Basically, there’s no downside to keeping ferritin within a low normal range, and it could save you from a heart attack.

Premenopausal women have naturally low levels of iron, and this almost completely protects them from heart disease.

By the way, another possible explanation as to how lower iron decreases heart disease risk concerns microbes: iron allows them to grow, and they may cause heart disease.

PS: For more, read my book, Dumping Iron.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Does Fungal Infection Cause Male Pattern Baldness and Heart Disease?

Quite the rabbit hole I’ve been down with my research. Does fungal infection cause male pattern baldness and heart disease? There’s an iron link to fungal infection too.

This started when a reader told me that he had started donating blood after reading this site and my book on iron.

He said that he had had seborrheic dermatitis of many years standing. (Click here if you want to see what that looks like.) It’s basically something like really terrible dandruff, but can be on any part of the body. He had tried both anti-fungal medication and topical steroids, and nothing worked. Since it didn’t bother him much, he quit worrying about it.

After his first blood donation, it started clearing up, and after his third donation, it completely disappeared.

What in the world? It turns out that both dandruff and seborrheic dermatitis are linked to a fungal infection by the fungus Malassezia. So is tinea versicolor, a skin infection; when I lived in Sierra Leone, virtually everyone had it to some degree.

In this report, we show that dandruff is mediated by Malassezia metabolites, specifically irritating free fatty acids released from sebaceous triglycerides.

Dandruff is caused by a fungal infection.

All microorganisms that invade man and cause disease require iron. (Every living thing requires iron.) Withholding iron from microbes is at the center of an evolutionary arms race. It stands to reason that donating blood can treat fungal infections of the skin by lowering skin iron levels. (Donating blood will also make you look younger.)

Shampoo that contains salicylate and ciclopirox effectively treats dandruff. Ciclopirox is an iron chelator (attaches and removes iron). So is salicylate. By attaching and removing iron, they deprive fungus of required growth material, it dies, and dandruff is treated.

Ketoconazole, an anti-fungal chemical that works by inhibiting fungal steroid synthesis, also treats dandruff.

Male pattern baldness

Male pattern baldness has been linked to fungal infection as well, and the antifungal drug ketoconazole treats male pattern baldness just as well as minoxidil (Rogaine).

Comparative data suggest that there may be a significant action of KCZ [ketoconazole] upon the course of androgenic alopecia and that Malassezia spp. may play a role in the inflammatory reaction.

If this holds true for many or all cases of male pattern baldness (androgenic alopecia), then our notions of why some men go bald (that it’s due to testosterone metabolites) may be all wrong. Curiously, folklore has it that hats cause baldness — perhaps by giving fungus a warm, moist environment in which to grow?

Male pattern baldness is also associated with heart disease. Severe baldness was associated with a 2.5 fold greater risk of death from heart disease. Huge increase.

If fungal infection in the skin causes both male pattern baldness and dandruff, then iron is implicated, because all invasive microorganisms must take iron from their hosts.

High iron (ferritin) is also associated with heart disease. The mechanism usually postulated is increased oxidative stress of the walls of arteries; iron is a very reactive metal capable of damaging biological structures.

But another mechanism might be the stimulation of fungal growth. “Occult fungal infection is the underlying pathogenic cause of atherogenesis” (from the journal Medical Hypotheses):

Atherosclerosis is the underlying cause of coronary heart disease (CHD). Atherogenesis is supposed to result from response to injury and is considered an inflammatory condition. A variety of infectious agents have been investigated as the underlying risk factor for atherogenesis, however, none have been proved to be causally linked. Also several interventions against these agents have not been proved to be of benefit in trials. The role of fungal infection, however, has not been explored in sufficient detail. Baldness particularly male pattern baldness and coronary artery disease have been linked in several epidemiological studies. There is some evidence that this type of baldness could be due to fungal infection and this link is being established even though traditionally male pattern baldness was associated with androgen effect. Seborrheic dermatitis and Pityrosporum [Malassezia] infection have been causally linked and the benefit derived from antifungal shampoo in male pattern baldness, gives further credence to the link with fungal infection. Here it is being hypothesized that fungal infection is the underlying risk factor for both baldness and CHD. Several interventions, which have proved beneficial in CHD like statins and drug coated stents, also have antifungal effects, lending further credence to the present hypothesis.

Fungal elements have been detected atherosclerotic plaques (27% of those examined). Fungal DNA has also been found in plaques.

Male pattern baldness is also strongly linked to insulin resistance and metabolic syndrome. The Japanese have both a lower prevalence of diabetes and obesity, and male pattern baldness in Japan develops a decade later and less frequently than in the West.

Hemochromatosis, or hereditary iron overload, causes hair loss in the majority of cases, though apparently mostly body hair.


Admittedly that’s a lot of information. Here’s where we are:

  1. Fungal infections of the skin cause dandruff and seborrheic dermatitis. Fungi, like all microorganisms, require iron to grow.
  2. Blood donation as well as iron chelators lower iron in the skin, depriving fungi (Malassezia, in this case) of a required nutrient. They then die off. Dandruff and dermatitis cured.
  3. Male pattern baldness may very well be caused by fungal infection, together with other factors, such as androgens and genetic susceptibility.
  4. The common link between male pattern baldness and coronary heart disease might be fungal infection, in turn caused by too much free iron.
  5. Bladness is associated with insulin resistance, and this in turn associates with coronary heart disease.

Conclusion: What to do

  • If you have male pattern baldness, anti-fungal shampoo may fight it. Blood donation or iron chelators might also.
  • If you have male pattern baldness, you’re at higher risk of heart disease. If the fungal/iron connection holds true, getting your ferritin (iron) lower could lower your risk. In fact, even if the fungal connection isn’t solid, lowering your ferritin still lowers your risk.
  • Male pattern baldness is strongly linked to metabolic syndrome, which if not taken care of, often ends in diabetes. Taking care of yourself with a low-carbohydrate diet and exercise treats metabolic syndrome. It might make your hair grow back too.

Male pattern baldness is usually discussed in terms of cosmetics only, and is thought to be caused by androgens in the skin. But it could be caused by fungi that feed on iron, and a sign that something deeper and unhealthy is going on.

PS: Read my book, Dumping Iron.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Muscle, Fat, and Weight Loss

The best thing you can do to get and keep a trim body is to pay attention to your body composition, the proportion of muscle and fat your body has. Unfortunately, hardly anyone knows or does this. This article will show the scientific truth behind muscle, fat, and weight loss.

Low-calorie diets don’t work

The most common way that people try to lose weight is through eating less, in other words, a low-calorie diet. This approach has a number of problems:

  1. Eating less can only be pulled off over relatively short time periods; hunger eventually sets in and the person usually returns to eating more. Evolution made hunger a powerful drive, for good reason.
  2. Weight loss by eating less is virtually always accompanied by muscle loss, which is bad for health and leads to greater disease risk.
  3. Eating less lowers the metabolic rate — the amount of calories you burn at rest. A lower metabolic rate, besides making you feel fatigued and cold, also means that weight loss stalls, since the body has adjusted its burn rate lower to match the number of calories taken in. Evolution also made this happen for a good reason, namely to prevent you from starving to death.

Eating less, often combined with “moving more” (more exercise), is an all-around lousy way to lose weight and has repeatedly been shown to be ineffective in the long run.

Recently we discussed the group of people who lost tremendous amounts of weight via eating less and moving more on the TV show The Biggest Losers. The dirty secret of this show is that most of the people who lose weight regain it, and often end up weighing even more than when they started.

The main theory as to why these people regain their weight and then some is that they have permanently damaged their metabolism by consuming less food. Let’s call it, appropriately, the permanent metabolic damage theory. They then get in a situation where it’s virtually impossible to eat less than they burn, and gain weight no matter how hard they try.

Evolution isn’t that stupid.

There’s no such thing as permanent metabolic damage.

My theory is that the Biggest Losers and others who lose weight by eating less and moving more have lost lots of muscle along with the fat. In fact, unless you lose weight the right way, muscle loss is inevitable and comprises between one fourth and one third of all weight lost. That’s a disaster.

Losing muscle is a disaster not just for health, but for maintaining a normal body weight. Muscle is the most metabolically active tissue. Loss of muscle translates into a lower metabolic rate.

This is precisely what happened to the Biggest Losers when they regained weight. (Also, trying to use a low-fat, high-carbohydrate diet for weight loss and maintenance is a contributory factor.)

No such thing as permanent metabolic damage

A new review of the literature on weight loss, regain, and metabolism shows that “body composition [relative amounts of muscle and fat] is the most critical factor in determining absolute RMR [resting metabolic rate] in neutral energy balance.”

Furthermore, ” the theory of permanent, diet-induced metabolic slowing in non-obese individuals is not supported by the current literature.”

In simpler terms, the more muscle you have, the higher your metabolic rate — the rate at which your body burns calories for energy.

Permanent, diet-induced metabolic damage, or a permanently lower metabolic rate due to weight loss, does not exist.

Retaining muscle with age

Obesity is said to be a characteristic of aging, and empirically, it is. But is it an inevitable aspect of aging. No, it is not.

One reason for increasing obesity with age is said to be muscle loss, which almost always occurs when people get older.

Why do we lose muscle with age? One reason is anabolic resistance. When someone is anabolically resistant, muscle does not respond as well to either resistance exercise or protein.

Anabolic resistance is not an inevitable consequence of getting old. It is closely connected to insulin resistance.

So to retain youthful levels of muscle anabolism, get insulin sensitive. Do this by avoiding refined carbohydrates and sugar, and eating a paleo diet. Add weight lifting into the mix.

That will keep your metabolism in good running order, and you’ll feel better and will be much less likely to gain body fat.


There’s no such thing as permanent metabolic damage. There’s only muscle loss.

Anabolic resistance as a phenomenon of aging is way oversold. It’s connected insulin resistance and nothing more.

PS: For how to build muscle, get my book Muscle Up.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

The Truth About the Blue Zones

The so-called Blue Zones are regions where there’s a high proportion of very old people, nonagenarians and centenarians.  Is that really the truth about the Blue Zones?

The number of Blue Zones depends on whom you ask, but on the “official” site, there are five:

  • Barbagia region of Sardinia
  • Ikaria, Greece
  • Nicoya Peninsula, Costa Rica
  • Seventh Day Adventists – Highest concentration is around Loma Linda, California.
  • Okinawa, Japan

Do Blue Zones even exist?

That’s a strange question to ask, one might think, but given past hype about allegedly long-lived people that turned out not to be true, it might pay to be skeptical.

How much do the Blue Zones have in common with gerrymandering or redistricting? In the United States, a ruling political party often redraws congressional and other districts to make them full of people who will elect that political party. It’s easy to do, just by drawing lines on a map. Have researchers drawn lines on a map that includes high numbers of centenarians and then dubbed them Blue Zones?

I have no evidence that they did that, but it reminds me of how numerous, above-average cases of leukemia or other cancers have been found in certain locations, only to find out later they were statistical flukes.

A problem, as I see it, in this research, is that people tend to see what they want to see.

Why are some groups included and not others?

Take the Adventists of Loma Linda, California; male Adventists live about 7 years longer than other white Californians, and this is ascribed to their lifestyle. The Adventist church recommends being vegetarian, although not all Adventists follow that stricture.

But Mormons in California and Utah appear to have about the same increase in life expectancy as the Adventists, and they are not vegetarians. So why aren’t Mormons on the Blue Zone list? Is it because of an agenda? Not sure what that might be, since Adventists are looked at as almost equally “weird”  — not by me, just saying that’s the perception.

Maybe there are other places in the world where people live a lot longer, but because they don’t fit an agenda, they’re not included. I’m not accusing anyone of cooking the books, just noting that biases are everywhere, and our own biases are the hardest to see.

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The above chart shows differences in life expectancy in the U.S. by religion. (Source.) Why not Jews in the Blue Zones? I’ll speculate that it’s because Jews have no special health practices (that I’m aware of), but live longer because of intelligence, education, and income. You can’t really point out a long-lived group and say “be like them” if being like them is impossible.

The Blue Zones are not in Western Europe

The Blue Zones all lie outside Western Europe, and except for the Adventists, none of the people inhabiting them are Western European. To a great extent, the factor that unites all of these groups is either being less touched by modernity, or actively rejecting it.

Western Europe is characterized by the nuclear family, which consists of parents and children to the exclusion of other relations. Outside Western Europe, households are more likely to include grandparents, aunts, uncles, cousins, etc., or in any case they all live quite near each other.

Observers have noted that social cohesion is a common factor in the Blue Zones. Even among the Adventists, who are mainly of European origin, their minority religious status ensures that they stick together. Church attendance is also associated with longer life.

How would social cohesion make people live longer? Probably by giving older people a sense of purpose and belonging, leading them to actively participate in family and society.

The average American over the age of 65 watches television more than 7 hours a day. What would that do to their sense of belonging and purpose, much less the amount they spend in physical activity? Television viewing time independently raises the risk of death; each 1 hour of viewing associates with an additional 4% risk of death. Whether that’s due to lack of physical activity, decreased social cohesion, genetic confounds, or demoralization from crap TV shows, can’t be determined. But it seems doubtful that people in the Blue Zones are watching TV that much.

Food and the Blue Zones

What you eat is undoubtedly important for health, but whether it’s important enough to get a larger fraction of people to live to very old ages is another matter. Most non-scientific commentary on the Blue Zones emphasizes that they eat a lot less meat than others.

The Okinawan diet has been perhaps the most studied. Okinawans in 1949, representing the cohort that was long-lived, ate a high-carbohydrate diet, low in fat and protein, and low calorie too. Okinawans ate about 15% fewer calories than in mainland Japan. Of interest, most of their diet consisted of sweet potatoes, and they only ate half as much rice as in Japan. They ate about 1% of calories as fish, and < 1% as meat, compared to 4% and < 1% respectively for mainland Japan.

So what’s the magic ingredient for Okinawan longevity?

They ate the same amount of meat as in Japan, although quite a bit less fish. Hard to see how meat could be a factor.

They ate a lot less rice, a food with a high glycemic index.  Nearly 70% of their calories came from sweet potatoes, compared to 3% for mainland Japan. The sweet potatoes look like this:

Image result for okinawan sweet potato

Looks very high in beneficial polyphenols.

In animals, calorie restriction is the most robust lifespan-extension intervention. And the Okinawans ate a lot less.

Here’s how the Okinawan diet has been characterized:

  • Relatively high consumption of unrefined, low GI carbohydrates: principally vegetables, legumes, and fruits. 
  • Moderate fish and marine food consumption. 
  • Lower intake of meat with emphasis on lean meats. 
  • Liberal use of medicinal plants, herbs, spices or oils. 
  • Regular tea consumption and moderate alcohol consumption.

The secret to Okinawan longevity could be

  • less food overall
  • less fish
  • less rice
  • more sweet potatoes
  • hormetic phytochemicals
  • something else or a combination of the above.

I can state for a fact that Okinawans in 1949 watched zero television.

Many but not all of the Adventists are vegetarians, and the residents of other Blue Zones appear to eat less meat than others.


Metals in plasma of nonagenarians and centenarians living in a key area of longevity. This study shows that in one of the Blue Zones, in Sardinia, nonagenarians and centenarians had much lower levels of iron than middle-aged controls — almost 40% less. The important health risk factor of iron may be a key point in longevity in the Blue Zones.

No one discusses this. Few people know it. See my book, Dumping Iron.

Adding longevity factors

An article about the Adventists in JAMA Internal Medicine, Ten Years of Life: Is It a Matter of Choice?, says that the average Adventist man lives 7.3 years longer than other men in California. The article looks at the risk factors to see what are the most important driving the difference. See chart below.


Expected ages at death (95% confidence intervals) in men with jointly high- or low-risk values for the risk factor in a particular column and those to its left (other variables at medium-risk values). BMI indicates body mass index.


Smoking and body weight are by far the most important risk factors, and curiously, the next most important is eating nuts. That’s followed by exercise, with vegetarian status being the least important.

Risk factors for Okinawans could be similar when compared to mainland Japan. Okinawans probably smoked a lot less, since they were poor, and they probably weighed less, since they ate less. They may have been more physically active, since many of them were farmers or fishermen.

Conclusion: How to Live Long, and the Truth About the Blue Zones

The factors that make for a long life in the Blue Zone people could be one or a combination of

  • less smoking
  • lower body weight
  • less food
  • lower body iron stores
  • less meat eaten
  • less refined carbohydrates eaten
  • more plant foods eaten
  • higher social cohesion
  • religious attendance
  • importance of family
  • greater physical activity
  • less modern life (TV, cars, alienation)

My money would be on the first four: smoking, body weight, food, and iron.

Although the Okinawans eat substantially less food than in Japan, the other Blue Zones may not be similar.

In Nicoya, Costa Rica, men at age 60 have a life expectancy of 24 more years, reportedly the highest in the world currently. Male Nicoyans apparently have the same rate of cancer as other Costa Ricans; their mortality advantage is due to less heart disease. If that statistic is true for those in other Blue Zones, then that helps us zero in on the important factors. Of course, cancer and heart disease have lots of overlapping causes.

I’m skeptical that eating less meat has much if anything to do with it, although lower iron levels may point to it as a factor.

The truth about the Blue Zones, as I see it, is that there’s a lot more here than meets the eye.

Living a long time requires a confluence of factors coming together.

Even though I see certain risk factors as more important, I don’t dismiss any of them. For example, it seems clear to me that being well-integrated with your own family as you get older is very important for health, and so is being well-integrated with society and with a church.

PS: See my books for more on how to live a long time.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Social Dominance Increases Testosterone

Testosterone and social dominance

Testosterone, the hormone primarily responsible for male sex characteristics, is known to increase social dominance and aggressiveness in animals, including man. In turn, social dominance increases testosterone.

The male sex characteristics that testosterone (T) changes in men include body mass (higher), muscle mass (higher), voice (lower), body and facial hair (more).

Since men compete with other men either directly, such as in fights or combat, or indirectly, such as the achievement of higher status, and since the results of these competitions determine mating success to a large degree, it might be expected that T affects psychological characteristics that play a role in male-to-male competition.  Indeed it does.

In rodents, T increases aggression, or physical violence directed at other animals. But it doesn’t necessarily do so in humans. Humans win competitions in the status hierarchy less by aggression with intent to cause harm than by dominance — placing others in submission or on a lower level of the hierarchy.

In competitions for status, T rises in the winners and declines in the losers. T also rises in anticipation of the competition, regardless of who ultimately wins or loses.

Dominance and T affect each other, reciprocally. That means that acting dominant can raise T levels.

Sports cars, testosterone, and the Handicap Principle

Conspicuous consumption is a type of status display. Flaunting a large display of wealth (or other resources) is a signal that one has such high status that one can afford to do so.

Conspicuous consumption could be said to be an example of the handicap principle; essentially, you have so much wealth (or power, strength, or other resources) that you can afford to waste some of it on your conspicuous displays. The peacock’s tail is the classically cited example: he is so strong, his genes are so great, that he can afford this costly tail which attracts predators and hinders his flight, all just to attract a mate.

Luxury cars are an example of both conspicuous consumption and the handicap principle.

Can luxury cars, or sports cars, raise T levels?

Indeed they can.

Scientists had men drive either a Porsche 911 Carrera, worth over $150,000, or a “a dilapidated 1990 Toyota Camry wagon having over 186,000 miles that was borrowed from a friend of the second author”.

When they drove the Porsche, T levels rose, about 5%; T levels dropped about 5% when they drove the old Toyota, but only when it was driven downtown, and not the highway, presumably because there was more of an audience downtown.

A display of dominance, that is, showing that one occupies a high rung on the ladder of the status hierarchy, raises T.

Fake it ’til you make it? Social dominance hacks

The evidence from this study, along with others that show that winning, either directly or vicariously, increases T, shows that a perceived jump up the status hierarchy can increase T. The sports car study shows that the jump doesn’t even have to be real.

That leads to the idea that you might be able to fake social dominance or higher social status to raise T. In turn, higher T increases the chances that phony social dominance could become real.

Posture: It’s been my observation that many men, most of them in fact, have poor posture. I attribute this either to laziness or ignorance of how they appear to others. Many of them, if they knew what it looked like, would stand and walk a lot more upright. Social signals like good or poor posture register subconsciously to most observers; I’m probably among the minority who sees them more directly, since I’ve become very aware of it.

Probably the first and easiest social dominance “hack” is improvement in posture and other body language. “Power poses” may increase T and lower cortisol, but this particular research has been disputed and may not be valid. Nonetheless, as social dominance increases T, this seems very unlikely to hurt. By standing and walking upright and not bent over, one signals pride in oneself, and others get the message.

Sports cars: You can get an actual sports car. If you can’t afford one, get a well-maintained used one — hardly anyone will know the difference. (Personal communication with the author.) Getting rid of my sensible Japanese compact car and buying a 2-seater sports car was definitely a social dominance hack.

Dress for success: This adage is well-known, and even has the distinct message of faking it ’til you make it. If you dress like you’re successful, others think you are, and then you’ll become successful. These days, it doesn’t take much either: merely dress like you haven’t just been shopping at Wal-Mart and you’ll look more socially dominant than most men out there.

Conclusion: Attitude matters

The research presented here shows the connections between mind, body, and society. Physical health is not merely a matter of diet and exercise and other physical inputs, but of one’s own outlook and attitude.

Taking pride in oneself and acting like it could reap big benefits.

PS: To get a dominating body, read my book, Muscle Up.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men.

Interview with Aaron Grossman, M.D.

I recently did an interview/podcast with Aaron Grossman, M.D. We discussed iron, body composition, and even Schopenhauer.

You can download an MP3 podcast version at Dr. Grossman’s site. Or get it from iTunes.