Do Calorie Restriction, Fasting, and the Ketogenic Diet Have the Same Anti-Aging Effect?

Calorie restriction (CR) is the most robust and effective life-extension intervention known, and intermittent fasting shows great promise in life extension as well. (I’ve written extensively about both calorie restriction and intermittent fasting on this site.) The question, unanswered so far, is how they work, although many possible explanations have been offered. Many pieces of evidence point towards the production of ketones as being the underlying, unifying factor, in which case calorie restriction, fasting, and the ketogenic diet have the same anti-aging effect.

Ketones mimic effects of calorie restriction

Ketogenic diets extend lifespan in lab animals. Does this diet extend lifespan through the same mechanisms as CR and fasting?

Consider that a reliable outcome of CR is the production of ketones. Intermittent fasting also results in ketone production, in fact, larger than calorie restriction. Obviously, ketogenic diets produce ketones also.

Ketone bodies mimic the effects of calorie restriction. Ketone supplements do much, if not exactly, the same thing as a ketogenic diet. Ketones lower insulin signaling and blood glucose, key elements that have been shown to affect lifespan in all kinds of lab animals from yeast to C. elegans (a worm) to rats.

One of the biochemical pathways thought to be crucial in aging is mTOR (mechanistic target of rapamycin). The ketogenic diet inhibits mTOR. Whether it inhibits it to the same degree of CR or fasting isn’t known; likely much more research would be required to find out.

The ketogenic diet stimulates mitochondrial biogenesis, as does CR and fasting. It lowers oxidative stress by upregulating antioxidant defense mechanisms. The ketogenic diet stimulates autophagy.

The ketogenic diet is well known to result in loss of excess body fat, as are CR and fasting, and reduction of excess body fat is thought to be a major mechanism of CR in lifespan prolongation. This aspect gives me a little pause in the comparison, because it’s possible that, while ketogenic diets help fat loss, they don’t universally decrease it to low levels. It’s perfectly possible, although perhaps difficult, to gain fat mass on a ketogenic diet.

What accounts for effects of CR

Are the effects of CR due to reduced calories in general, or reduced protein, carbohydrates, and fat? Or maybe CR is just a form of fasting, since animals on CR eat all their food at once.

Between 70% and 100% of the effects of fasting are due to carbohydrate restriction.

The lower figure, 70%, comes from a study in diabetics in which they either fasted or ate a VLCKD (ketogenic diet) for 3 days. One could argue that had the experiment used a longer time period, the values for fasting and ketogenic diet may have converged, since benefits of zero carbohydrate intake usually take longer than a few days to manifest completely. (Although the study did show that you get instant benefits by restricting carbohydrate.)

The higher figure, 100%, comes from a study in which volunteers either fasted or fasted with a lipid infusion that gave them all their caloric requirements. There was no difference between the groups in plasma glucose, free fatty acids, ketone bodies, insulin, and epinephrine concentrations, which led the researchers to conclude: “These results demonstrate that restriction of dietary carbohydrate, not the general absence of energy intake itself, is responsible for initiating the metabolic response to short-term fasting.” However, the researchers seem to have missed the fact that neither group of volunteers consumed any protein either, so their conclusion seems premature.

Many scientists in this field place great emphasis on protein restriction as important, for instance Valter Longo and his fasting-mimicking diet. However, recent experiments have found no effect of protein restriction on the metabolic and biochemical parameters affected by CR. Some data shows otherwise, but this major series of experiments by John Speakman and colleagues, and their null results with regard to protein restriction, cast serious doubt on the idea that it will prolong lifespan. For what it’s worth, in my opinion protein could be important, but distinctly second in importance to restricting carbohydrates.


Fasting and CR have a great deal in common with the ketogenic diet, with many overlapping if not identical effects, including the extension of lifespan.

Is it even necessary to restrict calories or fast, or does one need merely to follow a ketogenic diet? While CR and fasting may offer benefits beyond the ketogenic diet, it seems probable that the ketogenic diet gets you at least ~90% of the benefits of CR and fasting.

PS: For more on extending your lifespan, check out my book, Stop the Clock.

PPS: Check out my Supplements Buying Guide for Men.

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Dietary Carbohydrates Promote Aging

Dietary carbohydrates are usually thought of as healthy or at worst benign, and current dietary guidelines suggest eating plenty of carbohydrates, especially grains. But are carbohydrates really healthy or benign, or do they harm health and promote aging? As we’ll see below, dietary carbohydrates promote aging.

Whole grains: no evidence for benefits

Dietary guidelines specifically call for eating whole grains, and we’ve been bombarded with messages that eating them is the healthy thing to do.

However, there’s little evidence that whole grains provide any benefits.

The evidence that does exist is mostly epidemiological, that is, the evidence consists of associations between better health and the use of whole grains. (Overview of the evidence here.) As with other studies showing associations, causality cannot be shown. People who eat whole grains are likely to smoke less, exercise more, be more health conscious, have higher IQ and higher conscientiousness, have lower prevalence of obesity – in short, to be motivated to be healthy and take steps to be so. This is the healthy user effect. It’s difficult to separate any effects of whole grains from the other factors.

Randomized controlled studies are the gold standard for showing causality. And meta-analyses done by the Cochrane group are the gold standard for ascertaining the validity of scientific evidence.

A recent Cochrane meta-analysis of randomized controlled trials of whole grains in relation to cardiovascular disease risk found:

There is insufficient evidence from RCTs of an effect of whole grain diets on cardiovascular outcomes or on major CVD risk factors such as blood lipids and blood pressure. Trials were at unclear or high risk of bias with small sample sizes and relatively short-term interventions, and the overall quality of the evidence was low. There is a need for well-designed, adequately powered RCTs with longer durations assessing cardiovascular events as well as cardiovascular risk factors. [Emphasis added.]

If whole grains have no effect on cardiovascular risk, it seems likely that other health effects would be minimal to non-existent.

In truth, whole grains may have some benefit depending on what they displace in the diet. For example, whole grains have a lower glycemic index than refined grains, so if a person ate whole instead of refined grains, that could be beneficial.

But, since whole grains increase insulin response and raise blood sugar, cutting them out of your diet entirely would make more sense.

In any case, the lack of evidence of benefits for cardiovascular disease in controlled trials makes a travesty of the allegedly “evidence-based” dietary guidelines. Health authorities should not be subjecting the American people to a massive dietary experiment without extremely good evidence that what they recommend is healthy. Instead of healthy, we got the obesity epidemic.

Dietary carbohydrates are associated with increased death rates

The PURE study, recently published, showed an association between dietary carbohydrates and increased death rates, and it is not the first study to do this.

High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.

The charts below show associations between the amount of energy in the diet from total fat, different types of fat, and carbohydrates, in relation to total mortality and cardiovascular mortality.

Large image of Figure 1.

Fat was protective, carbohydrates were harmful. To be fair, one must point out that the percentage of carbohydrate that showed higher death rates was very high, above 65% of calories. Currently, Americans eat about 50% of calories as carbohydrates. In the PURE study, more than half the subjects ate 60% or greater carbohydrate, and one quarter ate more than 70%.

These results, like other similar studies, show an association only, but in this case the association shows the opposite of what health authorities believe.

Dietary carbohydrates promote aging

Most carbohydrates consist of long chains of glucose molecules, which means that when broken down by digestion, glucose results. Carbohydrates raise blood sugar and insulin levels, and this process is related to aging and greater mortality.

Taking the body of preceding evidence both from model organisms as well as human epidemiology into account, we therefore believe that current nutritional recommendations in regards to macronutrients, but most importantly in regards to refined carbs and sugar, should indeed be fundamentally reconsidered.

Lowering blood glucose, either through carbohydrate restriction or via drugs like metformin and acarbose, increases lifespan.

Ketogenic diets extends lifespan

Ketogenic diets are characterized by very low to zero carbohydrate intake, which results in the production of ketones.

Ketogenic diets extend lifespan in lab animals, and even ketone supplements do so. More recent studies have found the same: ketogenic diet extends longevity and healthspan in mice.

Ketogenic diets may extend lifespan because they generate ketone bodies, or because they lower blood sugar and insulin, or because of all of these, or conceivably because of other additional factors. The fact that ketone bodies mimic calorie restriction, the most potent lifespan-extending intervention known, argues that ketone bodies themselves are the magic ingredient.


Aging can be defined as a tendency to worse health

Carbohydrates, at least in sufficient amounts, worsen health. Ergo, carbohydrates promote aging.

While ketogenic diets are beneficial, any carbohydrate restriction is beneficial, so you don’t need to go ultra-low to zero carbohydrate to reap the benefits, although it certainly appears that very low carbohydrate ketogenic diets offer the most benefit.

Sugar is arguably the worst carbohydrate for health, so eliminate that first.

I discussed a very low carbohydrate diet as a cornerstone in fighting aging in my book, Stop the Clock.

PPS: Check out my Supplements Buying Guide for Men.

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The Risks of Excess Medical Treatment

Medical treatment by a doctor is not risk-free. In an ideal world, medical diagnosis would be perfect and treatment would be appropriate for the patient’s condition, and without adverse side effects. In the real world, the risks of excess medical treatment arise from the fallibility of the healthcare system both to properly diagnose illnesses and to provide appropriate care.

The Rosenhan experiment

In a recent article on the ineffectiveness and potential harms of health screening, we saw that imperfect diagnosis can lead to medical treatment that carries health risks. False negatives – a failure to find a real disease – and false positives – “detecting” a disease that isn’t really there – make the screening of healthy people much less safe and effective than most people realize. The diagnosis or even suspicion of a non-existent cancer, for example, can lead to further extensive testing including biopsies, chemotherapy, and surgery, all of which carry risks from anxiety to death.

Back in the early 1970s, a Stanford psychologist, David Rosenhan, sent 8 volunteers, one of whom was himself, to a number of different mental hospitals around the country. All of the volunteers were completely normal. They made appointments at these hospitals and claimed that they had been hearing voices which said “empty”, “hollow”, and “thud”. All were diagnosed as schizophrenic and admitted to hospital. This became well-known as the Rosenhan experiment.

After the “patients” were admitted, they ceased pretending to hear voices, acted normally, and told the staff that they were fine. In all cases, it took days to weeks to a couple of months before they were released, all with a diagnosis of schizophrenia in remission. Meanwhile, they were prescribed anti-psychotic drugs (which they didn’t take) and confined to the hospital.

The false positive rate was 100%.

After Rosenhan published a paper on this experiment, psychiatrists were outraged that they had been tricked, and the head of a mental hospital challenged Rosenhan to send his volunteers to his hospital, where he said he would readily detect them. Rosenhan agreed. Out of about 200 people over the subsequent several months, the hospital’s doctors decided that 41 of them were definite fakes and another 42 were suspected fakes. However, Rosenhan had sent no one.

False negative rate was maybe 20 to 40%, depending on how you measure it, that is, assuming the people were really mentally ill but deemed to be faking it.

Do you suppose psychiatric diagnosis has improved much since the early 1970s? I’ve no idea.

People diagnosed with a mental illness can get lots of mind-altering and toxic drugs, including antipsychotics, antidepressants, tranquilizers, etc, which kill people.

It may be thought that a group of people faking psychiatric symptoms may not be relevant to psychiatric treatment, but normal people often think something may be psychologically wrong with them and seek treatment for it. Psychiatrists and psychologists should be able to detect normality, to simply say “there’s nothing wrong with you”; many people are placed on SSRIs or other drugs, and it’s a good bet that some fraction of them have little wrong with them.

Doctors aren’t infallible

A recent economics paper was written by some economists who sent a patient with healthy teeth to 180 different dentists in Switzerland.

Of those dentists, 50 recommended that the patient get at least 1 cavity filled. The economists found that the patient was considerably more likely to get a recommendation for treatment when the dentist needed the money.

If you can’t trust a Swiss dentist, who can you trust?

Imagine what happens when you go to a doctor. You could end up with toxic medications, surgery, chemotherapy.

Most physicians, through no fault of their own, don’t know how much of what they practice is not based on high-quality evidence. John Ioannidis et al. write:

Most physicians and other healthcare professionals are unaware of the pervasiveness of poor quality clinical evidence that contributes considerably to overuse, underuse, avoidable adverse events, missed opportunities for right care and wasted healthcare resources. The Medical Misinformation Mess comprises four key problems. First, much published medical research is not reliable or is of uncertain reliability, offers no benefit to patients, or is not useful to decision makers. Second, most healthcare professionals are not aware of this problem. Third, they also lack the skills necessary to evaluate the reliability and usefulness of medical evidence. Finally, patients and families frequently lack relevant, accurate medical evidence and skilled guidance at the time of medical decision-making. Increasing the reliability of available, published evidence may not be an imminently reachable goal. Therefore, efforts should focus on making healthcare professionals, more sensitive to the limitations of the evidence, training them to do critical appraisal, and enhancing their communication skills so that they can effectively summarize and discuss medical evidence with patients to improve decision-making. Similar efforts may need to target also patients, journalists, policy makers, the lay public and other healthcare stakeholders.

Medical treatment comes with risks.

Unnecessary surgery

A number of patients consulted a neurosurgeon for a second opinion on whether they should have spinal surgery.

The surgeon determined that 17.2% of them had been scheduled for unnecessary spinal surgery.

From the physician perspective, overtreatment is common. In a survey of physicians, they themselves thought that

20.6% of overall medical care was unnecessary, including 22.0% of prescription medications, 24.9% of tests, and 11.1% of procedures. The most common cited reasons for overtreatment were fear of malpractice (84.7%), patient pressure/request (59.0%), and difficulty accessing medical records (38.2%). 


Polypharmacy occurs when people take too many prescription drugs, and when those drugs are inappropriately prescribed. Polypharmacy is a significant problem, especially among older people.

In one study at a Veterans Administration hospital, 65% of patients were taking at least one drug that was inappropriate.

Virtually all drugs have adverse side effects, some of them serious ones.


The practice of medicine is as much art as science.

Physicians are not infallible, and medical treatment, whether surgery or drugs, carries risk.

Solving this problem isn’t easy, but one of the main things patients can do is to educate themselves.

Fear of malpractice may drive many of a physician’s decisions, which means your best interests may not always be in mind.

PS: You can stay a lot healthier and avoid excess medical treatment if you train for strength, as I write in my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

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Iron-Induced Cell Death: Ferroptosis

As I wrote about in my book Dumping Iron, excess body iron stores are implicated in many diseases, including heart disease, diabetes, and cancer, as well as in aging itself. Among the other diseases that excess body iron is implicated in are Alzheimer’s and Parkinson’s diseases, which are characterized by (among other things) neuronal cell death. A process that causes cell death has recently been elucidated and this is iron-induced cell death, ferroptosis.

Programmed cell death

Programmed cell death occurs when cells initiate actions that lead to cell suicide, or apoptosis. This is thought to be done as a safety measure that ensures the integrity of the organism. When cells die in a non-programmed way, necrosis occurs, which presents problems for the organism, so cells have ways of killing themselves in the face of certain stimuli.

Programmed cell death is also essential in embryogenesis, tissue homeostasis, and immune response.

Ferroptosis is a newly discovered mechanism of programmed cell death, and as its name makes evident, iron is involved.

Much research has gone into elucidating the specific biochemical reactions that take place in ferroptosis, but for now, I’ll stick to basics. Three different chemical entities are involved in ferroptosis:

  1. iron
  2. polyunsaturated fatty acids
  3. glutathione.

Polyunsaturated fatty acids are necessary components of cell membranes, but they are readily oxidized. Free iron, that is, iron that is not bound by proteins such as ferritin or transferrin, react with the polyunsaturated components of the cell membranes to form highly toxic lipid peroxides.

Glutathione, the cell’s most important and abundant internal antioxidant, is used to detoxify these lipid peroxides. If enough glutathione is not present, then lipid peroxides accumulate to critical levels, at which point the cell executes its cell death program, ferroptosis. Schematic illustration, below. (Source.)


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Cystine, the dimerized form of the conditionally essential amino acid cysteine, enters the cell to be used in the production of glutathione. When it’s blocked, or when enough isn’t available, glutathione decreases, lipid peroxides cannot be detoxified and therefore accumulate, at which point ferroptosis occurs.

There are a few important points here as this process relates to health – this isn’t just a bunch of dry biochemistry, and in any case, I’ve greatly simplified it.

Iron chelators – molecules that bind and remove iron – prevent ferroptosis. This is important because it shows that free and not bound iron initiates the process. If the iron were bound – to ferritin, transferrin, hemoglobin, or any of a number of other iron containing molecules – iron chelators would be powerless to stop it.

Adding iron to the cell culture medium increases ferroptosis. Again, free iron is the cuplrit

Autophagy, specifically ferritinophagy, the breakdown of ferritin, is required for ferroptosis. That’s where the free iron comes from, the breakdown of ferritin.

Polyunsaturated fatty acids in cell membranes come from the diet. The membrane phospholipids that become peroxidized are composed of arachidonic acid, which is made from dietary linoleic acid, the most abundant fatty acid in seed oils. Since polyunsaturated fatty acids (PUFAs) compete for enzymatic conversion and subsequent space in cell membranes, excessive consumption of seed oils means a greater fraction of peroxide-capable arachidonic acid compounds in the cell membrane. Thus, diet can be linked to ferroptosis. One study says that the lipid peroxidation is specific for two omega-6 fatty acids only, arachidonic and adrenyl derivatives.

Lack of glutathione is also critical in ferroptosis, and this can also be linked to diet. Cysteine, the rate-limiting amino acid in glutathione synthesis, is found in all protein-containing foods; whey protein is especially abundant in cysteine. Diabetics and others suffering from oxidative stress have low levels of glutathione, and it’s said that aging could be (in part) a cysteine deficiency syndrome.

It appears that the high iron content of cancer cells can be exploited by making them enter ferroptosis, for example with the drug artemisinin or with vitamin C.

The process of ferroptosis provides another mechanism by which excess body iron, polyunsaturated fats in seed oils, and the absence of sufficient protein, can harm health.

Excess body iron in the form of high ferritin means that abundant ferritin is available to be broken down via ferritinophagy, leading to free iron inside cells. As I wrote in my book, ferritin is like stored dynamite: in theory, it’s safe, but you don’t want a bunch of it lying around your house. The more you have, the more likely an accident can happen.

Consumption of seed oils leads to a high proportion of the kind of membrane lipids that lead to ferroptosis.

Low dietary protein, or oxidative stress brought on by diabetes or other conditions, leads to low glutathione, which promotes ferroptosis.

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

PPS: Check out my Supplements Buying Guide for Men.

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The Myth of 8 Hours Sleep

How much sleep do you need? Probably less than you think, or were given to believe. Let’s examine the myth of 8 hours sleep.

Sleep and death rates

Lack of sleep causes health problems, ranging from weight gain to fatal accidents.

Sleep times have allegedly decreased in recent years, leading to increases in obesity and diabetes and many other health problems. Is that true?

Contrary to popular belief, in a state of nature, hunter-gatherers sleep only about 6.5 hours, much less than the 8 hours that we think of as the norm. They don’t go to sleep at sundown either, as has been assumed to be the case, but typically stay up about 3.5 hours after it. They don’t take naps, and some of their languages have no word for insomnia. They also suffer little from the diseases of civilization.

Looking at the modern, developed world, it appears that sleep duration has not declined over the past 50 years. This finding challenges “the notion of a modern epidemic of insufficient sleep.”

In summary, it is beyond dispute that disrupted and inadequate sleep are highly prevalent and associated with significant risks, and that experimental sleep deprivation has myriad negative effects. Thus, the notion of a recent epidemic of insufficient sleep, and speculation that this is a primary contributor to modern epidemics of obesity, diabetes, metabolic syndrome, etc., rests largely on the question of whether sleep duration has declined in the last few decades. Consistent with recent reviews of subjective data, this review does not support this notion, at east not in healthy sleepers.

There is no epidemic of too little sleep.

The best data point to determine the optimal amount of sleep is not anecdotes or mainstream news reports, but death rates associated with hours of sleep.

Numerous studies have found that 8 hours of sleep is not only not optimal, but associated with higher death rates.

A prospective study found that sleeping less than 6 hours, and more than 7 hours, was associated with increased death risks. The odds ratio for sleeping 5 hours was 1.15, for 8 hours 1.12, while for 9 hours or more, it was 1.42. “These results confirm previous findings that mortality risk in women is lowest among those sleeping 6 to 7 hours.”

There’s a U-shaped relation between amount of sleep and death rates. See graph below.


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The lowest death rates were seen in from 300 to 390 minutes, or from 5 to 6.5 hours. Yes, objectively measured sleep of more than 6.5 hours was associated with higher death rates. The common folk wisdom of 8 hours of sleep isn’t healthy. The risks found in this study were large, with sleep of more than 6.5 hours associated with about a 3-fold increase in risk, and about a 6-fold increase for greater than 8 hours of sleep.

Keep in mind that these results are for objectively measured sleep, not time spent in bed.

Of interest, self-reported insomnia is not associated with increased health risks.

Although these studies show only association and not causation, one of the authors, Dr. Daniel Kripke, argues elsewhere that “the magnitude and consistency of evidence makes a strong case for causality.” Restricting the amount of sleep may be beneficial, analogous to restricting food.

Short-term sleep restriction has dramatic antidepressant effects.

Sleeping pills kill

Sleeping pills are associated with greatly increased death risks.

Sleeping pills increase risks of overdose, cancer, infections, accidents, and depression. The increased risks of infections were found in a randomized controlled trial, so causation is proven. They produce an excess of deaths at night, probably through affecting breathing, i.e. stopping it, or slowing it enough, such that death ensues.

Furthermore, sleeping pills show little or no benefit, either for sleep or health. They may even increase insomnia.

Many doctors prescribe sleeping pills even when they’re not indicated.

The question arises, how much of the association of sleeping pills with increased health risks arises from side effects of the drugs, or from merely increasing sleep time? Many different types of sleeping pills (“hypnotics”) are associated with increased risks, so it seems likely that merely the fact that they may cause harm in part because they make you sleep more.


The folk wisdom that we need 8 hours of sleep, reinforced by mainstream commentary, appears incorrect.

Health problems may be caused or exacerbated by too much sleep.

People who suffer from insomnia or depression who sleep more than 8 hours may benefit by sleeping less.

Sleeping pills kill. Don’t take them.

PS: For how to live a long, healthy life, see my book, Stop the Clock.

PPS: Check out my Supplements Buying Guide for Men.

Guest Post: The Dangers of Estrogen Dominance in Men

The Dangers of Estrogen Dominance in Men

by Sean Ward

Males are biologically made to produce testosterone at a higher level than women. However, thanks to our modern society, and our tendency to adopt new trends without doing scientific research on them, the balance of hormones in the body has been affected.

We’ve written this article to help people like you understand why estrogen is important, but also to understand why too much of it is bad for your health. Hopefully, you’ll learn enough by the time you’re done reading this to make a good decision for your health.

The Importance of Estrogen in The Male Body

Just because estrogen is the ‘female hormone’ doesn’t mean that men don’t need a healthy supply of it. It regulates the growth of our bones and the way we process cholesterol.

It’s important that you maintain a fine balance of estrogen, because both too much and too little of it can cause a heck of a lot of problems for men.

Problems That Arise From High Estrogen:

  • Estrogen increases the body’s stress hormone, also known as cortisol. Cortisol can lead to blood sugar problems, ultimately leading to diabetes, or other weight-related problems like obesity. Too much cortisol can also increase your desire for high carb, high calorie foods that can all contribute to these problems.
  • Unhealthy levels of estrogen can have negative impacts on the sex drives of both males and females. It becomes much harder for men to achieve and maintain erections if their estrogen levels are too high, which can vastly impact their sex lives.
  • Other side effects of too much estrogen include excessive weight gain, chronic fatigue and headaches, as well as urinary tract infections and loss of muscle mass.

So, what should I do if I have too much estrogen?

If you’re experiencing the symptoms above, don’t rush to assume that you have problems with your estrogen levels. There may be other causes of your symptoms.

However, if you’ve tried other alternatives with no success, or have noted a huge number of these symptoms present at the same time, it might be a good idea to consider trying to balance your estrogen levels.

There are several ways you can attempt to balance your estrogen levels. 

The first thing you should do is consider the reason your estrogen levels are imbalanced. The most common cause of estrogen imbalance is natural: as men age, their bodies produce much higher levels of aromatase. 

This enzyme is responsible for converting testosterone into estrogen – a perfectly normal process.

However, as men age, the levels of which testosterone is converted into estrogen often become higher than is necessary.

While it’s a good idea for men to consume healthy amounts of dietary fats to ensure their body can produce testosterone, body fat is another matter. Excess body fat results in the production of more aromatase, leading to higher estrogens – estradiol and estrone.

Too much of it will provide you with too much testosterone conversion and too much space to store your estrogen.

There are some nutritional options that you can opt for if you seek to reduce the levels of estrogen in your body. The two main nutrients are calcium-d-glucarate and diindolylmethane.

  • Calcium-d-glucarate is a nutrient with many powerful benefits that include lowering the chances of getting cancer, helping your body process protein, and most importantly for us, removing excess estrogen from the body.
  • Diindolylmethane (DIM) is a substance that’s naturally produced by the body when it consumes indole-3-carbinol which is a nutrient found in many vegetables, particularly in those of the cruciferous family.
  • It is possible to directly supplement DIM through supplements you can purchase at your health food store or local pharmacy, but the most effective route is allowing your body to produce its own DIM by eating a healthy diet full of cruciferous vegetables.

DIM works wonders for maintaining the balances of estrogen and testosterone both.

Another great alternative for balancing estrogen levels is to supplement with a hormone known as progesterone. Progesterone helps the human body balance its estrogen levels and ensures that you don’t have either too much or too little.

It’s important to seek your doctor’s advice before starting any supplemental regime, but it’s particularly vital for you to consult a physician before starting to supplement any hormones.

Hormones have direct and powerful functions on many of your body’s systems and they can have plenty of effects, interactions, or conflicts with other supplements or conditions you may be taking.

It’s also vital to let your doctor know if you’re taking any other supplements, medicines, and even vitamins. These can all interact with new hormonal or other supplements.

In conclusion

Estrogen is a necessary hormone for both men and women. However, it’s important to make sure that you strike a fine balance of estrogen. This problem becomes very apparent in men who have too much estrogen, developing a condition known as estrogen dominance.

Estrogen dominance is a serious problem for both genders but the effects can be debilitating for men. The symptoms are diverse and severe and can impact every area of a man’s life – particularly his sex life.

There are various solutions available for balancing estrogen levels in the male body. Most of these solutions are simple cases of supplementing with the right nutrients or eliminating the wrong nutrients.  However, it’s important to remember that consulting your doctor should take precedence over any supplementation.

Estrogen dominance is a serious problem that shouldn’t be taken lightly, and we hope we have helped you learn something today.

By Sean Ward, Founder of Naturally Boost Testosterone, a men’s health blog dedicated to providing natural ways for men to boost hormone levels. Check out to learn more about Sean and his work. You can also find him on Twitter, Pinterest and Facebook.

PS (from P.D. Mangan): For more on aromatase, see my latest book, Best Supplements for Men.

PPS: Check out my Supplements Buying Guide for Men.

Chew Your Own Food

Could there be a connection between having to chew food and health? Is “chew your own food” a dictum that will improve your health and life expectancy? Let’s take a look.

The concept that fruit juice is not as healthy as whole fruit, or even not healthy at all, is not a new one, but the more general notion that you should “chew your own food” was suggested to me over on Twitter by Allan Folz, a frequent commenter on this site.

Fruit juice is associated with the metabolic syndrome

It’s well-known that sodas and other sugar-sweetened beverages – SSBs, the term of art used in nutritional science – lead to weight gain and disruption of metabolism. Frequent consumption of fruit juice is also: consumption of more than 5 servings a week of fruit juice, whether natural or bottled, is, along with other SSBs, associated with increased risk of the metabolic syndrome.

The authors of the study speculate that lesser amounts of fruit juice, at less than 5 servings a week, may not be as harmful because of polyphenols in the fruit that may counteract harmful effects of sugar.

Since this study is observational, it can’t show causation. But we know that sugar and SSBs spike blood sugar and insulin, so there’s reason to think that the association could be causal, at least in part.

Matthew Dalby has looked at the science on the metabolic reactions to whole fruit as opposed to fruit juice. Orange juice caused a greater rise in insulin than whole oranges, and the juice caused a reactive hypoglycemia. Results were similar when comparing apples to apple juice.

So, eating whole fruit doesn’t appear to cause the same glucose and insulin responses as does consuming fruit juice.

Dense, acellular carbohydrates

Many people believe that carbohydrates cause obesity, or that they’re a large contributing factor, but a few facts get in the way of that thesis.

Notably, many populations have eaten high amounts of carbohydrates throughout history, and in the present, without suffering high rates of obesity. For example, the Kitavans, so often held up as an example of excellent health, eat a diet that contains about 75% of calories as carbohydrates, and they have no cardiovascular disease, cancer, or obesity.

Mass obesity is a recent phenomenon.

The answer to this question could be that it’s not carbohydrates that cause obesity, but a particular type: dense, acellular carbohydrates.

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity

The author, Ian Spreadbury, writes that neither glycemic index, fat, or carbohydrates can be causes of obesity, but that flour, sugar, and refined fats alter the gut microbiota, causing inflammation and obesity. Similar to the effects of sugar on dental health, the dense, acellular carbohydrates – flour, sugar, and processed food – cause inflammatory reactions and changes in the gut microbiome that tubers, leaves, and fruit do not.

Processed grains and sugar offer a greater density of food and affect the body differently from whole, unprocessed foods. Adding fat to the mix, especially in the form of seed oils, produces a “double hit”, with the result being mass obesity.

Mechanical disruption of food

It seems likely that mechanically disrupting food, and especially when fiber is removed, changes the way the body handles it. Mechanical disruption, such as grinding of flour and juicing of fruit, creates a calorie-dense food that humans are not adapted to by evolution. Our genes are not meant to handle it.

Nut butters are another example of mechanically disrupted food. I’ve read, but can’t currently find the answer, that nut butters provide more calories than the nuts themselves, simply because the butters have more surface area and the gut therefore digests it more, whereas a good proportion of actual nuts pass through the digestive tract without being digested.

Don’t drink your calories

The adage “don’t drink your calories” comes from a study that found that drinking caloric beverages with a meal, whether the beverage was milk, cola, or orange juice, led to the consumption of more calories while the subjects reported no difference in satiety.

There’s something about liquid calories that doesn’t register with the normal appetite control system, so if you drink calories, that could put you on the road to weight gain, or stall weight loss.

The same principle might apply to seed oils or even olive oil. Or milk or cream.

In fact, using this principle, we may not even need to invoke the ideas above about how the gut microbiome is affected by process foods. It could be that they merely provide more calories with less satiety.

Don’t eat processed food

The big lesson here is: don’t eat processed food.

Almost by definition, it’s been refined and mechanically disrupted. Processed food is likely a big factor in obesity, either because of its refining, including added refined sugar, or because most of it contains seed oils.

Whole, unprocessed foods are not mechanically refined, and don’t appear to upset appetite regulatory systems or the gut microbiome, and do not cause inflammation.

Another point is that carbohydrates may not be so bad as long as they’re in a more natural state, such as vegetables, tubers, fruits, and greens. Although if I were overweight I would certainly be careful even with those. Physically active people may, however, have little problem with them.

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

PPS: Check out my Supplements Buying Guide for Men.

Vegetable Oils Cause Insulin Resistance

In some recent articles, we’ve seen that vegetable oils cause obesity, heart disease, promote male infertility and aging, and are just generally bad news. In this article we’ll look at the evidence that vegetable oils cause insulin resistance.

Corn oil causes insulin resistance in mice

In a study (full paper), mice were placed on a high-fat diet, with fat at 40% of calories, which is not terribly high for humans but is for mice. One group got their fat as corn oil, the other as olive oil.The group on corn oil developed hyperinsulinemia (high blood insulin) and insulin resistance. See charts below.The corn oil diet also spontaneously decreased locomotor activity, and by a great deal. See charts below.Could increasing consumption of seed oils like corn oil be partly responsible for an increase in couch potato lifestyle? Maybe people who consume a lot of this stuff don’t feel like moving around much, and therefore increased seed oil consumption contributes to obesity by decreasing the amount of exercise.Excess omega-6 consumption in mice is associated with negative metabolic and cardiovascular outcomes. Seed oils are loaded with omega-6 fatty acids.

Decreasing seed oil consumption in humans

That’s all very well for mice, but what about in humans? Does decreasing consumption of seed oils do anything for metabolism or obesity?Turns out, it does.A group of 93 men with non-alcoholic fatty liver disease, which is a consequence of obesity as well as sugar and seed oil consumption, were randomized to use either olive oil, canola oil, or soybean oil for cooking, at no more than 20 g a day. The study took place in India, where there’s a high consumption of seed oils in cooking – just like there is here in the U.S.The olive oil group lost weight, and compared to canola oil, decreased insulin resistance and fasting blood sugar, and increased HDL. The canola oil group improved in some measures, but not as much as the olive oil group. (Canola is a “less bad” seed oil.) No changes were seen in the soybean oil group.This study shows that a relatively small dietary change, using olive oil instead of soybean oil for cooking, can result in significant improvments in metabolism, and lends more evidence to the concept that seed (vegetable) oils cause obesity.

The health establishment recommends seed oils

The American Heart Association recommends “heart-healthy” seed oils. Here’s their list of “healthy” oils:

  • Canola
  • Corn
  • Olive
  • Peanut
  • Safflower
  • Soybean
  • Sunflower

The only one on that list that’s truly healthy is olive oil. The others will make you fat, diabetic, and give you heart disease.Other establishment health organizations make the same claims.Their advice is perverse. You’re much better off doing the opposite.Their counsels have also fueled the obesity epidemic.The evidence they’ve used for their recommendations is wrong. Re-analysis of studies that randomized people to polyunsaturated fats as are found in seed oils found that benefits occurred only when omega-3 fatty acids were more or less accidentally increased. When omega-6 alone was increased, death rates increased.The evidence they’ve used is hopelessly biased.Vegetable oils are better termed industrial seed oils both for their source, which is not vegetables but seeds, and for their mode of production, an industrial process that uses high heat and organic, gasoline-like solvents.If you want to preserve or attain good health, don’t use them.If you need fat for cooking, use butter, ghee, lard, tallow, or coconut oil. For cold uses, olive oil.

PS: For more on how to live longer, see my book Stop the Clock.

PPS: Check out my Supplements Buying Guide for Men.


Guest Post: How Lifting Weights Transformed My Life

A reader in Sweden asked me, unsolicited, if I would like to publish his story about what lifting weights has done for him. I’m glad I said yes, it’s a great article that shows how getting into shape via weightlifting changes many other aspects of your life for the better.

How Lifting Weights Transformed My Life

by a Rogue Heath and Fitness reader in Sweden

(I have to preface that throughout this I didn’t go on a certain diet or took any kind of steroid. I’ve always eaten pretty well, no junk food and very little in the way of sugar and alcohol. The only thing I did was to add daily protein shakes to my normal diet.)

It’s been almost exactly one year since I first joined a gym and started lifting weights, and with that I find it fitting to look back and evaluate.

I’m a man in my late twenties, married, and have two kids; aged 1 and 3 years respectively. I work as a middle school teacher which includes long working weeks, bringing work home, and being mentally exhausted at the end of each day. When I get home I eat dinner, play with the kids for a bit and by 7:30 P.M. they’re both often asleep.

Here’s where I have around three hours of free time before I have to go to bed if I want something that even resembles sleep, and one year ago, I decided to spend some of those hours in the gym three days per week.

It’s been one of the hardest things I’ve ever done, but as it happens, it’s also one of the best things I’ve done.

I know that many people, especially young, tired fathers like myself, have a hard time getting started. So did I. Before this I had looked into bodyweight fitness, sporadically did a routine or two just so I could fool myself that I was actually doing something. One day however, I was lucky enough to be struck by reality. I went to pick up my wife (who was pregnant at the time) and our daughter. Daughter wanted to be carried home and my wife was unable to, “no problemo; dad will handle this”, right? After all, it’s just a couple of hundred meters. About half way home, I started to struggle. I remember thinking “Damn, this is heavy.” and then it all hit me at once.

You see, until now I had only seen reality, I had never tasted it. And now I was getting force-fed more than I could chew, and every scenario in which I could fail because of my lack of strength flashed through my head. The next day I went down to my local gym and bought a membership.

My first gym session was a nerve-wracking experience, as it is; and has been, for many others. My theory for this is that you’re forced to see yourself as you really are – the true you. At home you can delude yourself, thinking you’re stronger then what you actually are. And at an empty gym, you have no one to measure up against, so you’re still somewhat okay. But in a gym full with people, normal people just like yourself, you get a taste of reality. And it doesn’t always taste very well.

What made it even worse was the fact that my local gym happens to be one of this country’s best gyms, where a lot of those who work out also compete in some form of lifting. It’s extremely rare to see someone “untrained”. And every time I walk through those doors, I become the smallest and weakest person in there. I could have let it scare me away but I chose to stay, and I’m glad I did.

Gradually, I started to change my perspective. I started to see these athletic people as people to emulate instead of being envious of. After a while, I started asking other people questions between their sets. I remember asking a mountain of a man why he did a certain cable exercise because I was genuinely curious, and I got an extremely informative answer. As I started lifting weights I also stopped assuming I knew everything; I mean, if I wasn’t as strong as I thought I was, why would I be as smart as I thought I were? Soon enough, this mind-shift started spilling over into other areas of my life. Like work.

Coincidentally, I also started my first teaching job a year ago, and when I first started, I thought I had everything under control, but pretty soon reality was once again shoved down my throat. A few months in, I was still doing pretty much everything on a day-to-day basis which was extremely stressful. But then I started dropping all pretenses that I knew everything and started asking questions instead, asking colleagues, taking advice, admitting to students that I didn’t know everything and asked them to look something up if I didn’t know it, and had them report back their findings to me. After that it didn’t take long before I was one of the more likable teachers at school. Because as soon as you admit to yourself that you aren’t that all-knowing entity that’s always right, your words and actions start coming from a place of humility and sincerity, and people seem to notice that. But there was something else as well.

Apart from two nasty colds that kept me out of the gym for almost six weeks in total, I had been going three times per week, doing full-body workouts on both machines and with free weights, and the results had started to show. Gradually, shirts started to become tighter and I was walking more upright and with more confidence than before, and as it turns out, people respond well to that too. Getting attention and focus in the classroom became easier as well. Now, you could argue that this change was due to me becoming more confident in my line of work in general and that the students had gotten to know me, but would that have happened this fast without lifting? My answer would be no.

What about home and family life then? I’m more active with the kids, and throwing them around and carrying them, like many kids enjoy, isn’t that hard anymore. The relationship between me and my wife is also a lot better. In fact, just about everything is overall… better. And apart from the examples I gave above that’s about as precise as I can be.

Because our experiences will differ; we are all in different situations and we respond differently to things. Lifting weights did not only bring about an increase in energy and better physical health for me, but also personal insights – for which I’m grateful.

Today I’m comparing myself less and less to others, in all areas of life. And while I’m not a huge guy with big lift numbers (just recently hit 225 on the bench press if that matters to you), and I think it would be nice to get a little bigger, I don’t obsess over it because that isn’t my goal. My goal is to be the best version of me possible, and nothing has helped more with that than weightlifting.

PS (from P.D. Mangan): If you want to learn more about weightlifting, see my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Drop Sets in Resistance Training

High-intensity weight training differs from traditional resistance training in that it involves performing a set to momentary muscular failure, that is, the point at which the weight or resistance can’t be moved for another repetition. Traditional resistance training normally makes use of multiple sets per exercise, each set for a fixed number of reps, and not necessarily to failure. One way to increase the intensity of sets in high-intensity training is through the use of drop sets.

Drop sets – what they are

When performing a set in high-intensity weight training, the goal is to reach momentary muscular failure, at which point all muscle motor units are recruited and the anabolic (muscle-building) stimulus is maximized.

Lifting to failure does not mean lifting until you think it’s too difficult, or to when you feel like stopping, but when you physically cannot complete another single repetition. Reaching failure requires dedication and supreme effort.

Sometimes it’s hard to know whether you have truly reached failure. At the end of the set, you can be wondering whether you stopped too soon, could you have done another rep, did I wimp out and not get to failure?

This is where drop sets come in. Drop sets allow you to ensure that you’ve really lifted until failure.

“Drop” in drop sets means dropping the weight. When you perform a set to failure, you then drop the weight by 10 to 15%, and then immediately perform the same exercise to failure, which might involve only 1 or 2 more reps. You can then drop the weight again, repeat, and do this several times. Doing this with as little time between changing the load is crucial; you don’t want to rest, to give your muscles time to recover.

By the time you get to the end of a drop set, the muscles involved are completely fatigued and you know you’ve gone to failure. You may find that you can’t do another rep using a weight only half as heavy as the one you started with.

Do drop sets work?

The number of variables and techniques in weight training is almost as many as the number of practitioners. Everyone swears by what works for them, but unfortunately many of the traditional practices in weight training have little scientific backing.

Many practitioners of high-intensity weight training, such as Mike Mentzer, have recommended drop sets, but science should have the final word.

One recent study assigned participants to one of three different groups: breakdown (drop) sets, heavy-load breakdown, and traditional (multiple set) training, twice a week for 12 weeks. There were no significant differences in muscular endurance or body composition between groups.

Another study had participants doing only one exercise, dumbbell curls, either 3 sets of low-load curls, 3 sets of high-load, or one drop set, all performed to momentary muscular failure. Muscle cross-sectional area (a proxy for muscle mass), increased similarly in all groups. Muscular endurance improved more in either drop set or low-load. Maximum strength increased only in the high-load and drop set conditions. The drop-set group had the lowest amount of training time per session. The authors concluded that drop sets were as good as multiple sets but with less training time.

In another study, participants performed either a single drop set or 3 sets to failure with 90 seconds rest between sets on a single exercise, the cable triceps push-down. Muscle strength and size increased in both groups, and acute markers of muscle stress were greater in drop set. The authors concluded that “superior muscle gains might be achieved” with a single drop set compared to multiple sets.

What can we conclude about drop sets from these studies?

One study showed no difference, another was mixed, and the last showed possibly better improvement with drop sets.

  1. A single drop set is at least as good as multiple sets. A drop set takes less time yet compares favorably to multiple sets, which means you can spend less time in the gym. Multiple sets aren’t necessary.
  2. Performing a drop set may be better for solo weight trainers. I reach this conclusion because in most weight-training studies, coaches are present at every move to encourage participants to exert all-out effort and to reach muscular failure. Most of us don’t have the luxury of a coach, so performing a drop set may be a good way to absolutely ensure that you reach momentary muscular failure.

I perform drop sets on most of my exercises, and I can now be more confident that they’re an effective way to train. At least in my case, they may be superior, since after performing a single set to failure I often doubt myself as to whether I’ve truly gone to failure, and a drop set practically guarantees that you do so.

Drop sets are more readily done using machine moves, since racking weights from a barbell can take long enough that the muscles involved recover somewhat while you’re getting the barbell ready for the next leg of your drop set. On a machine, it’s usually just a matter of quickly moving a peg. Dumbbells work well with drop sets too, since most gyms have racks of dumbbells with different weights, so you can easily replace a set of dumbbells and then quickly grab the next weight down.

Drop sets are really inconvenient with the deadlift, at least in my gym, since replacing 20 kg (45 lb) plates on a barbell on the floor takes time. So when I do deadlifts, I often use another technique similar to a drop set, rest-pause. Rest-pause involves resting just long enough, perhaps 5 to 10 seconds, after a set until you’re able to perform one more repetition. This can be repeated as many times as you like – I typically do it around 3 times.

PS: For more on the benefits of resistance training, see my book, Muscle Up.

PPS: Check out my Supplements Buying Guide for Men.

Magnesium Decreases Death Rates

Magnesium is a mineral (a metal) that the body requires for over 300 different biological reactions, and in fact virtually every living organism requires it. While we ingest magnesium in food, the evolutionarily recent upsurge in processed food consumption means that many people are magnesium deficient, which can have dire consequences. Adequate dietary magnesium lowers death rates.

Magnesium decreases death rates

Many studies have looked at the relation between magnesium and health, so a recent meta-analysis (analysis of other studies) reviewed 40 different studies that used a total of over 1 million people: Dietary magnesium intake and the risk of cardiovascular disease, type 2 diabetes, and all-cause mortality: a dose–response meta-analysis of prospective cohort studies. A prospective cohort study collects various data on a group of people at one point in time, and then follows them for a period of time to see what happens to their health.

The study found no relation between cardiovascular disease and magnesium intake, which the authors felt may be due to a limited number of studies in their analysis.

The study did find a lower incidence of stroke, heart failure, type 2 diabetes, and all-cause mortality.

Specifically, each 100 mg per day increment in magnesium intake was associated with risks of

  • 7% less stroke
  • 22% less heart failure
  • 19% less diabetes
  • 10% lower all-cause mortality, that is, death from any cause.

Graphically illustrated, that looks like this:

Among U.S. adults, 68% consumed less than the recommended daily allowance of magnesium, so the relation of magnesium to health is not a trivial matter.

Note that all of the above is based on association, and causality is not proven. But given the benefits of magnesium supplementation, we have good reason to believe that increasing magnesium intake will benefit health.

How to get more magnesium

If you consume more magnesium, you could save yourself from a number of health problems, not to mention an early grave. The Recommended Daily Allowance (RDA) for magnesium is 420 mg for men and 320 mg for women.

People normally have about 22 to 26 grams of total magnesium in their bodies, which shows its great importance – compare to iron at about 3 to 4 grams.

Magnesium is lost on a daily basis via normal excretion, including sweat and urine. Alcohol consumption can cause greater-than-usual loss of magnesium.

Foods that are high in magnesium include leafy greens such as spinach, as well as cocoa, nuts, and beans. This could be an important reason that chocolate and nuts have been found to have health benefits.

Hard water used to be an important source of magnesium, but is less so now since fewer people drink it. Drinking hard water is associated with lower rates of sudden cardiac death.

Personally, I take 200 mg of magnesium as a supplement daily. Different types of magnesium have widely variant rates of absorption, and it’s been consistently shown that magnesium citrate is most bioavailable. (Here’s the brand I use.)

Bottom line

Be sure you get enough magnesium. If you eat a diet of whole, unprocessed foods and don’t drink alcohol excessively, you’re likely fine. If you eat processed junk and drink soda, you’re likely not fine.

I take a magnesium supplement for insurance. It’s that important.

PS: I discuss magnesium and other important minerals in my most recent book, Best Supplements for Men.

PPS: Check out my Supplements Buying Guide for Men.

Vegetable Oils Cause Obesity

Researchers debate the fundamental causes of the obesity epidemic, and dietary changes are the most likely reasons. But which changes? Experts have pointed their fingers at sugar, refined carbs, excess fat, not enough protein, too little exercise, and many others. But one of the main causes may be hiding in plain sight, since there’s good evidence that vegetable oils cause obesity, alone or in combination with other nutrients.

Vegetable oil consumption has increased

Vegetable oils are better termed industrial seed oils, since they are not made from vegetables but from the seeds of grains via an industrial process. They are not natural foods, since the means of making them in any quantity have only been available for about the past 120 years. Consumption of seed oils has risen dramatically in recent decades. See charts below, showing annual seed oil consumption per person in kilograms. (Source.)

For comparison, the chart below shows other food consumption trends in recent decades. The consumption of dairy, beef, and pork are all down; grains are higher, and sugar about the same. Soy oil is way up, as is chicken, which perhaps not coincidentally also contains large amounts of the omega-6 fats that are also found in seed oils.

Linoleic acid is the main omega-6 fatty acid found in seed oils, and its consumption has greatly increased.

Note a couple of things about this chart. 1) The U.S. has the highest rate of obesity and also the highest linoleic acid consumption. 2) The chart only begins in 1960, so compared to earlier, say 1900, current consumption is way higher.

“The most striking modification of the US food supply during the 20th century was the >1000-fold increase in the estimated per capita consumption of soybean oil from 0.006% to 7.38% of energy.” (Source.) Other estimates put consumption as high as 20% of calories.

Vegetable oils are obesogenic

Suppose we set up a 3-way contest among nutrients to see which one could get mice the fattest. The nutrients are soybean oil, coconut oil, and fructose (of which 50% of table sugar is composed).

The clear winner is soybean oil: Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse.

Soybean oil made mice obese, induced diabetes, and caused fatty liver.

Linoleic acid, the main omega-6 fat, elevates endogenous cannabinoids and induces obesity at a concentration of 8% of calories. When the concentration is only 1%, it does not induce obesity.

Supplementation of the diet with soybean oil increases triglycerides, a sign of insulin resistance. Furthermore, it stimulates macrophage foam cell formation, a crucial step in atherogenesis leading to coronary heart disease.

Blame it on the American Heart Association

Why did the consumption of soybean oil increase so dramatically? In part because the American Heart Association advised Americans to replace saturated fat with vegetable oils.

Americans took that advice, and soybean oil consumption skyrocketed.

The recommendation of the AHA to replace natural foods with an industrial product that humans didn’t evolve to eat – let’s just say that it didn’t turn out well.

Vegetable oils cause obesity

Vegetable oils cause obesity in animals and are likely involved in the obesity epidemic in humans.

These seed oils are ubiquitous; besides obvious sources like bottles of vegetable oil and margarine, virtually all processed food contains them. To stay healthy and lean, or to return to that state, avoid them.

Eat whole, unprocessed foods, and to cut back even more on omega-6 intake, avoid chicken and most nuts.

Avoiding seed oils to maintain leanness and health should be done in conjunction with avoidance of sugar and refined carbohydrates.

PS: Besides avoiding seed oils, a lot more on what you can do for health and long life is in my book, Stop the Clock.

PPS: Check out my Supplements Buying Guide for Men.

Exercise Prevents Cancer

Exercise prevents cancer, an idea which is one of the main themes of my book Muscle Up. How much does it lower the risk? A recent meta-analysis found up to 42% less risk for 10 different cancers, including esophageal, liver, lung, kidney, and many other cancers. An interesting question is how exercise prevents cancer, and some recent research sheds light on this.

It’s often assumed that exercise prevents cancer because those who exercise are in better physical condition, and that seems at least partially correct. For instance, obesity is associated with cancer, and if exercise helps to prevent obesity, then it would prevent cancer too. But science shows that acute bouts of exercise can inhibit the growth of cancer cells.

Blood taken from men after exercise inhibits cancer

A remarkable study looked at how blood serum taken from men post-exercise dramatically inhibited the growth of cancer cells.

The experiment took 23 young men, average age 22, and had them do a bout of high-intensity cycling, 6 1-minute intervals at 90% max, with 1-minute rest intervals in-between. They had blood drawn before the bout, and then at 5 minutes, 1 hour, and 24 hours post exercise. The blood was centrifuged and the serum (liquid part) was placed into media that contained cancer cells, which were different types of non-small cell lung cancer cells. Controls were cells grown in their usual media, without human serum added. The cells were allowed to grow for 7 days, and then counted. Chart below shows the results.


Huge inhibition of cancer growth, up to 75% using serum taken 5 minutes post-exercise.

Why does this happen? One possibility is lack of growth factors. Insulin was not a factor, since they found no difference in insulin between pre- and post-exercise specimens, but IGF-1 (insulin-like growth factor 1) was different, so that may be the answer.

There’s also evidence that can let us speculate that weight lifting might be superior in this regard (as I’ve long maintained), because molecules secreted by exercising muscle, called myokines, may be involved in suppression of cancer growth.

Basically, every bout of intense exercise floods your bloodstream with anti-cancer molecules, and/or it removes pro-cancer molecules.

This isn’t the only study that has found such an effect.

Exercise serum inhibits prostate cancer cell growth. Researchers believe that the exercise serum increases expression of the p53 gene, which arrests cell growth.

Exercise abolishes cancer-promoting effect of fat tissue

Animals fed a high-fat diet – which we know usually consists of large amounts of seed oils and sugar – become obese, with large amounts of adipose (fat) tissue, and extracts of this tissue placed in a medium growing cancer cells increases the proliferation of those cancer cells.

Physical activity can completely abolish this effect of high-fat diets on cancer proliferation.

We hypothesized that voluntary physical activity (PA) would counteract the deleterious adipose-dependent growth microenvironment to which a breast cancer is exposed. We show that PA altered the adipokine secretion profile of adipose in a volume-dependent manner. This alteration resulted in growth inhibition of estrogen receptor positive breast cancer cells in culture. Furthermore, stabilizing adiponectin receptor 1 expression in the cancer cells made them resistant to the cell cycle entry effects that accompany obesity.

Fat tissue generates cytokines that promote the proliferation of cancer cells, and physical activity diminishes or abolishes the effect, which is dose-dependent, i.e. more exercise means less cancer promoting cytokines.

In another study, blood serum from breast cancer survivors was used in media to see its effect on cancer cell growth. Six months of exercise training in these women increased VO2max and muscle strength, and reduced cytokines. Yet serum from these exercise-trained women had no effect on cancer cell growth.

Serum taken after a 2-hour exercise session did reduce cancer cell viability.

Systemic changes to a 2 h exercise session reduced breast cancer viability, while adaptations to 6 months of training had no impact. Our data question the prevailing dogma that training-dependent baseline reductions in risk factors mediate the protective effect of exercise on breast cancer. Instead, we propose that the cancer protection is driven by accumulative effects of repeated acute exercise responses.

So cancer prevention is not (entirely) a matter of your level of physical fitness, but a matter of how intensely and often you exercise.

In animals (mice) that were implanted with tumor cells, voluntary running reduced tumor growth by over 60%. The researchers believe that exercise mobilized natural killer (NK) cells, which attack cancer.

Together, these results link exercise, epinephrine, and IL-6 to NK cell mobilization and redistribution, and ultimately to control of tumor growth.

This result suggests that exercise might actually attack cancer cells in people who already have cancer.

For anti-cancer therapy, exercise

Every time you do a bout of high-intensity exercise, you flood your bloodstream with anti-cancer molecules, or remove molecules that promote cancer growth.

One substance that’s been overlooked by researchers doing these experiments is iron, and cancer feeds on iron. Exercise that is intense enough and protracted enough can cause iron deficiency. If someone exercises intensely and regularly, he would likely be depriving any incipient cancer cells of the iron they need to grow.

There’s a widespread belief that cancer just happens, and that, except for not smoking, there’s not a lot you can do about it. Nothing could be further from the truth; there are many ways to prevent cancer.

You can add exercise to the list of cancer prevention interventions.

PS: For more on exercise and cancer, see my books Stop the Clock and Dumping Iron.


PPS: Check out my Supplements Buying Guide for Men.

Health Screening Is Ineffective and May Cause Harm

Health screening is the practice of checking someone for health conditions he or she may not know about. In other words, health screening means medically examining an apparently healthy person, instead of the normal practice in which a person seeks out a doctor to diagnose an illness or treat symptoms of a disease. Examples include screening for prostate, breast, lung, and cervical cancer, as well as cardiovascular disease. Contrary to what most people think, health screening is ineffective and may cause harm. That’s what the evidence says.

Why health screening may cause harm

The aim of health screening is to detect a disease that doesn’t currently have any symptoms.

Unfortunately, health screening can generate two different kinds of errors: false negatives and false positives.

If the screening test(s) or exam generates a false negative result, then the disease goes undetected, and the screen has failed to do what it was meant to do.

If the screen generates a false positive, then the patient can get treated for a disease that doesn’t exist, and that can result in serious harm. Chemotherapy or a mastectomy for non-existent cancer would almost certainly result in avoidable harm to a patient, as would unnecessary invasive coronary artery procedures.

How prevalent are the problems of false positive tests and unneeded treatment? They appear to be large enough to turn the process of health screening into one that causes more harm than benefit, as we’ll see.

Why health screening may be ineffective

In the case of cancer, which is perhaps the most common reason for health screening, the burden on patients is measured in terms of survival, usually 5-year survival. If a cancer patient is treated and survives for 5 years, that is usually deemed a cure, even if the patient dies at 5 years and 1 day after diagnosis.

This aspect of measuring the consequences of cancer or its treatment when using a health screen results in lead-time bias.

The point of health screening for cancer is to catch the cancer early, on the grounds that the earlier the cancer is found and treated, the better the prognosis. However, survival time, by which treatment results are measured, may be extended by finding the cancer early, even if the patient dies on the same day that he would have otherwise. That’s lead-time bias. See chart below. (Source.)

In this example, the patient has received no benefit from cancer screening, even though the case would be touted as showing a much longer survival.

Another way that health screening leads to spurious results is overdiagnosis bias. See chart below. (Same source.)

In this (hypothetical) case, no patients have been helped but many have been harmed.

The evidence

Now that we’ve seen how health screening may be ineffective and cause harm, let’s look at the actual evidence.

Lung cancer: In the Mayo Lung Project Randomized Trial, patients who were screened for lung cancer via chest x-ray had more cancers detected and were more likely to be in an early stage of lung cancer; they had almost double the 10-year survival rate. Yet the mortality in both groups, screened and non-screened, was the same. Therefore increased survival was the result of lead time and overdiagnosis.

Breast cancer: In breast cancer screening by mammography, a meta-analysis found no difference in 10-year survival between screened and non-screened. However, the screened group had up to 20% more lumpectomies and mastectomies as well as radiation treatment. The authors state:

If we assume that screening reduces breast cancer mortality by 15% and that overdiagnosis and overtreatment is at 30%, it means that for every 2000 women invited for screening throughout 10 years, one will avoid dying of breast cancer and 10 healthy women, who would not have been diagnosed if there had not been screening, will be treated unnecessarily. Furthermore, more than 200 women will experience important psychological distress including anxiety and uncertainty for years because of false positive findings.

The authors believe that women should be fully informed of both potential benefits and harms before they enroll in screening. In an older article (from 2000), one of the same authors (with a different co-author) states:

Screening for breast cancer with mammography is unjustified. If the Swedish trials are judged to be unbiased, the data show that for every 1000 women screened biennially throughout 12 years, one breast-cancer death is avoided whereas the total number of deaths is increased by six. If the Swedish trials (apart from the Malmö trial) are judged to be blased, there is no reliable evidence that screening decreases breast-cancer mortality.

Even breast self-examination in women younger than about 35 years old may cause more harm than good:

It is argued that women who find asymptomatic benign breast lesions by breast self-examination (BSE) are exposed to unnecessary anxiety, unnecessary medical investigations (including invasive procedures), and potential risks of false reassurance. “False positives” so greatly outnumber patient-detected cancers below age 30 to 35 that the potential for net benefit from BSE in this age group is remote. BSE in younger women, by encouraging invasive and costly medical investigation of many asymptomatic benign breast lumps needing no treatment, could well do more harm than good.

Prostate cancer: A Cochrane meta-analysis of prostate cancer screening trials found no decrease in mortality from prostate cancer or all causes.

General health screening: What happens when you merely see a doctor for a check-up, without any symptoms of illness? No decrease in mortality, and the confidence interval included a possible increase in mortality, that is, a confidence interval of the risk ratio for total mortality of 0.95 – 1.03.

One exception in health screening that may be beneficial is geriatric interventions, which significantly reduce the odds of falls and hospital admissions and increased the odds of living at home.

Why health screening doesn’t work: medical care may cause harm

There are several reasons why investigators have found that health screening produces little to no effect on mortality.

One reason is that when you see a doctor for any reason, he may check you out for other illnesses. For instance, just about everyone gets a lipid (cholesterol) panel run often; doctors check blood pressure regularly. So seeing a doctor when you have no illness may be superfluous.

A more important reason is that medical care does not entail all benefit and no harm.

If you are screened for cancer and some suspicious sign is found, you may be subject to everything from further exams, to a biopsy, to chemotherapy, and whether you have cancer or not, those are associated with harms ranging from anxiety to death. Obviously, it’s even worse if you have no cancer and are subject to these.

Even for something as simple as a lipid panel, the results could encourage a doctor to prescribe a statin, which could lead to worse health.

Prescription drugs carry risk, maybe even high risk. So if you have some form of health screen, you could end up being prescribed a high-risk drug. Above we noted that breast cancer screening resulted in no decrease in mortality, but those screened has 20% more mastectomies; if some of those patients did not in reality have cancer, they suffered harm from getting checked.

What about ferritin, a test for body iron that most people, especially men, ought to know the results of? In this case, potential for harm is minimal to non-existent, since donating blood or therapeutic phlebotomy are the most common procedures for dealing with a high ferritin, and these have low risk. The same goes for checking testosterone, since interventions involve a low risk of harm. In any case, checking levels of ferritin or testosterone, or other hormones, such as thyroid, do not necessarily entail screening for disease.


The impetus that has led health authorities to recommend health screening may have come with good intentions. On its face, they do make some sort of sense. Unfortunately, risks are inherent to medical treatment, and diagnosis isn’t perfect.

Trade-off between benefit and harm is crucial for health screening:

Thus, health screening should only be recommended when five criteria are satisfied:

(1) the burden of illness should be high,

(2) the tests for screening and confirmation should be accurate,

(3) early treatment (or prevention) must be more effective than late treatment,

(4) the test(s) and treatment(s) must be safe, and

(5) the cost of the screening strategy must be commensurate with potential benefit.

Probably very little health screening satisfies all of those criteria.

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

PPS: Check out my Supplements Buying Guide for Men.

Knowledge and Action Are Needed to Change

Both knowledge and action are needed for change. What does that mean exactly? If you want to change, you must know the right steps to take, but you must also be willing to put that knowledge into action. Both are required.


Suppose you’re overweight or obese, and you decide to lose weight. To change yourself. You go to your doctor and ask him how to do this. Will that help?

Probably not. A study of U.S. physicians found that, in their sample (498 physicians), 53% were overweight or obese.

That means that more than half of doctors either don’t know how to lose weight, or lack the will to do so. Given the intense drive and ambition required of people to become physicians, lack of knowledge seems more likely.

If you check the internet or popular diet books, many of these won’t have the right knowledge either. If they did, one wouldn’t expect a combined overweight/obesity rate of 70%.

The same principle applies to many other areas of life which you might want to change. Generally, the more universal the problem that needs addressing, the more different the opinions you’ll find and the more likely it is that those opinions will be wrong; that is, they’ll have little relation to reality and won’t help you solve the problem.

Some examples of areas where you’re likely to get bad information:

  • dating and sex relations
  • physical fitness
  • healthy food
  • education
  • dressing well.

There are at a couple of reasons that sources may be unreliable: they genuinely don’t know the right answers; or they act out of self-interest, i.e. they’re corrupt.

Many sources genuinely don’t know the right answers. Take the matter of healthy food. For several decades now, medical authorities have told us to eat a low-fat diet for health. It will keep our cholesterol levels low and thus prevent heart disease, they’ve said. But it turns out that low-fat diets are associated with higher death rates. Oops.

Other sources of information are corrupt.

Take the matter of college education. Asking a college counselor if you need more education is like asking a barber if you need a haircut. Counselors and other college officials are simply not going to recommend that you don’t need their expensive product, despite the fact that a a degree in gender studies is unlikely to get you a more exalted job than a Starbucks barista.

Corruption is rampant among health authorities too. Many doctors who recommend statins have lucrative ties to the drug industry. Can you believe their recommendations?

In other areas, self-interest isn’t necessarily financial. For instance, a man taking dating advice from a woman isn’t usually a good idea.

How does one discover whether information is correct or not?

There are a few signs to look for. For example, see whether the person or institution that provides the information benefits from providing it, directly or indirectly. While some will legitimately charge money for good information, if they benefit by telling the population in general to follow their instructions, then be suspicious.

If a source has financial ties to a recommended product, then be careful.

If a source has a bad track record in providing information or in making predictions, or no track record at all, then scrutinize it carefully.


To change oneself, knowledge is not enough. All the knowledge in the world won’t help you if you’re unwilling to take action and use that knowledge.

Take the overweight or obese person. Assuming he obtains the right knowledge, putting it into practice requires effort and willpower. Reading a book doesn’t make fat melt away. When I tell people what I eat, the most common response is “I could never stop eating” whatever it is I tell them I don’t eat.

Likewise in other areas that you want to change.

Inertia is a strong influence in life. Most people prefer to do what they’ve always done. Habits become ingrained and change can be difficult.

Furthermore, you’re influenced by everyone around you. If they all do something one way, for instance if they all eat the same kind of food, dress a certain way, and generally live their lives a certain way, then you’re more likely to do that too.

Taking action to change something often requires going against the grain and thinking for yourself. If you worry about what others will think, you’re unlikely to make the change you want and need. So don’t care about what others think; they’re probably not thinking at all about you anyway. People are concerned about themselves, and the idea that you’ll be shunned is a phantom.

Only you can take responsibility for yourself and to change. No one else can do it.

Maybe life hasn’t been fair to you, although the concept of fairness applied to life is a dubious one. Even so, only you can make the change.


Skepticism is a virtue, but too much skepticism can be a vice. Be judicious in evaluating whether a source of information is reliable or not. Seek out experts, but scrutinize their integrity.

Take personal responsibility for enacting change. Blame others or circumstances all you want, but that won’t help you change.

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

PPS: Check out my Supplements Buying Guide for Men.

Are Antidepressants Placebos?

Antidepressant drugs are now taken by around 11% of Americans over the age of 12, though that could be an underestimate. Women are more likely to take them, and almost one quarter of American women in their 40s and 50s take them. While the number of people taking them is a matter of concern, a larger question is how they work. Are antidepressants placebos? There’s good evidence that they are, and that’s how they work.

Evidence from clinical trials

Drug companies perform clinical trials in order to get their drugs approved by the FDA (and other agencies outside the U.S.), and may also run trials after approval. Clinical trials usually include a group of patients taking a placebo, and then any improvement in health markers of interest (depression, in the case of antidepressants) is compared to improvement, if any, in the placebo group.

Patients in clinical trials are not supposed to know whether they are receiving a placebo or the real drug, and neither are their doctors. This is known as a double-blinded trial.

When patients enter a clinical trial of antidepressants, the researchers tell them that they may receive either the active drug or a placebo, but they won’t know which one. There are a couple of reasons for that.

One is that, if someone knew that he was taking, or going to take, a placebo instead of the real drug, he’d be less likely to enter or remain in the trial.

Another is that the placebo effect may depend largely or entirely on the power of suggestion, so if a patient knows he’s getting a placebo, it may not work.

In clinical trials of antidepressants, the effect of the drug over the placebo has, in most cases, been quite small. In fact, the differences between antidepressants and placebos is so small as to be clinically insignificant.

Different types of antidepressants

Now, there’s something odd about clinical trials of antidepressants.

Antidepressants are of different types; that is, they allegedly affect different aspects of physiology and thus have different mechanisms.

Tricyclic antidepressants are an older type. No one is really sure how they’re supposed to work.

Newer types include selective serotonin uptake inhibitors (SSRIs), selective norepinephrine uptake inhibitors (SNRIs), and even selective serotonin uptake enhancers (SSREs).

In clinical trials, the difference between placebo and drug has been remarkably similar and small, no matter what type of drug was tested. That really doesn’t make much sense.

Unblinding and active placebos

As mentioned, clinical trials are supposed to be blinded, ideally double-blinded, to get objective results.

It appears that in many or most cases of clinical trials of antidepressants, a large proportion, as much as 85%, of both the subjects and their doctors become unblinded by correctly guessing whether the subjects are taking a drug or a placebo.

How does that happen? Because drugs have side effects. In the case of antidepressants, they may cause dry mouth, sexual dysfunction, insomnia, and many other things. When patients experience side effects, they know that they’re taking the real drug, as do their doctors. When they experience no side effects, they assume that they’re getting a placebo.

Unblinding in clinical trials is an important source of bias.

When trials have both a blinded and non-blinded observer, the non-blinded observer’s estimate of the drug’s effects are 36% greater than the blinded observer’s.

 If we assume that the blinding is broken for all patients in the antidepressant trials, and adjust for the bias the loss of blinding causes, we will find that antidepressants have no effect (odds ratio 1.02).

One way to get around this problem is to use “active placebos”, that is, placebos that have side effects. When trials have done this, they’ve found very little difference between antidepressants and placebos. The difference was so small as to be clinically insignificant.

The conclusion is that antidepressants are “active placebos”. Patients get better because they believe that they’re taking a powerful drug, which in reality is either weak or powerless, beyond its effect as a placebo.

Placebos are powerful

The fact that antidepressants have little to no efficacy over and above that of a placebo doesn’t mean that they don’t work, only that most or all of their efficacy is due to the placebo effect.

Placebos are powerful.

Placebos that are taken twice a day are more effective than those taken once a day.

Injectable placebos are even more effective.

A great deal, or even all, of the effectiveness of arthroscopic surgery for osteoarthritis is due to a placebo effect. In a controlled trial, placebo (sham) surgery was as effective as real surgery. Sham surgery to repair a a meniscus tear in the knee was as effective as real surgery.

Mammary ligation was a surgical procedure used for several decades to treat angina pectoris, until a trial found that it was no better than sham surgery.

These surgical procedures were believed to work, because they did. Patients reported relief, even cures, but that was all due to a placebo effect.

Patients have overdosed on placebos and required emergency treatment.

In conditions with a large psychological component, such as depression and pain, placebo effects can be powerful. On the other hand, placebos don’t lower blood sugar.

What to do about antidepressants

There are no good answers here. Depression is a serious problem that, at least in moderate to severe cases, requires treatment.

One view might be to say that if antidepressants work as placebos, then fine, just keep using them. The problem with that view is that these are drugs, with many adverse side effects, including increased violence and suicide in some cases. It appears to be unethical to give powerful drugs that are no more effective than placebos.

On the other hand, for a doctor to tell a patient that he’s giving him a placebo lowers, though it may not abolish, the effectiveness of the treatment.

And lying to a patient by giving him a placebo and telling him it’s a drug also seems unethical.

My suggested alternative is to give a patient something known to have antidepressant effects, such as magnesium citrate or fish oil capsules. Feel free to poke holes in that idea.

Psychotherapy may be an alternative. It’s at least as effective as second-generation antidepressants in the short term,  and better in the long term, since relapse rates are lower.

Most of the information in this article comes from an excellent book, The Emperor’s New Drugs: Exploding the Antidepressant Myth,  by Irving Kirsch, PhD, a professor at Harvard. I couldn’t put the book down, it was that good.

Relevant to what to do about antidepressants, Kirsch strongly states, “Antidepressant medication should not be discontinued without first discussing it with your doctor.” [Emphasis in the original.]

Some quotes from the book’s preface:

“When we analyzed all of the data – those that had been published and those that had been suppressed – my colleagues and I were led to the inescapable conclusion that antidepressants are little more than active placebos, drugs with very little specific therapeutic benefit, but with serious side effects.”

In response to the knowledge that these drugs were approved by government regulatory agencies: “And yet I remain convinced that antidepressant drugs are not effective treatments and that the idea of depression as a chemical imbalance in the brain is a myth.”

“The chemical effect of antidepressant drugs may be small or even non-existent, but these medications do produce a powerful placebo effect.”

Psychiatric drugs cause harm

Psychiatric drugs, including antidepressants, may cause serious harm, especially in the elderly. Given their potential for harm, it’s open to question whether many of these drugs should have been approved for human use in the first place. As Dr. Peter Gøtzsche has written, psychopharmacology is not evidence-based medicine:

This chapter argues two evidence-based conclusions: not only are psychiatric drugs dramatically overprescribed and overvalued but the harms they unleash completely overwhelm any benefits accrued. While accepting numerous reasons for our current prescribing epidemic, this chapter focuses on the manipulation of most placebo controlled trials, the systematic underreporting of drug harms, the industry-led misrepresentation of drug safety and efficacy and the medical denial of the substantial role withdrawal and abstinence symptoms play in convincing patients to stay on drugs. This chapter concludes that a thorough and independent review of the evidence base reveals that psychiatric drugs, apart from calming some people down when taken short term, “have failed to deliver what patients want, which is to work specifically for specific mental or emotional problems.” Since mental illness is rarely chronic and lifelong, it argues there is no scientific justification for the widespread lifelong use of psychiatric drugs. If we are to restore balance, and reverse these harms, a total reappraisal of what the evidence teaches must be translated into reformed prescribing guidelines.

This is yet another instance in a long series of mainstream medicine getting something very wrong.

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

PPS: Check out my Supplements Buying Guide for Men.

The Current Prospects of Extending Lifespan

I’ve written extensively on anti-aging and life extension, and I’ve put into practice many of the methods I’ve written about. Yet, what are the current prospects of extending lifespan? Will any interventions substantially lengthen our lives, or is all or much of it an exercise in futility?

The current limit to human lifespan

Aubrey de Grey, the well-known life-extension advocate and researcher, recently gave an interesting talk to a group of demographers on the limits to human longevity, as they currently stand. De Grey points out that Jeanne Calment, the world record holder in lifespan, died at age 122 some 20 years ago, and despite there being far more centenarians alive now, no one has come close to her record. The current world’s oldest person is 117 years old.

Why, despite better health care, living conditions, advanced technology, or whatever makes people healthier and longer-lived, has no one breached the world record of 122 years?

We know that mortality rises with aging at an exponential rate. De Grey shows, through demographic analysis, that at about the age of 114, the death rate rises at something like a super-exponential rate, and therefore it’s extremely difficult to get past that mark.

There’s some difficulty in the analysis, as de Grey acknowledges, simply because there are so few people alive at that age. That being said, it looks like the age of around 115 years marks the current upper limit of human lifespan. A few people with the right genes and/or lifestyle, like Calment, may live a few years longer.

Why 115?

What is so critical about the age of 115? It could be the loss of dopamine neurons. The chart below shows the loss of dopamine neurons in aging; the decline occurs at a steady rate in most people, but when they decline and die at a faster rate, so that someone has only 30% of these neurons left, Parkinson’s disease exists. At the level of 10% left, death occurs.

Iron and the brain: iron's crucial role in aging

In normal people, that is, those without Parkinson’s, the loss of dopamine neurons reaches the life-critical 10% threshold at about the age of 115.

The analysis that reached this conclusion comes from the scientist Joseph Knoll, who developed the drug deprenyl. Deprenyl has extended the lifespans of rats dramatically, and while it’s available by prescription, it seems to be under-utilized and, in any case, we don’t know much about its prospects in human life extension.

I’ve suggested that the loss of dopamine neurons could be due to iron, and if – and it may be a big if – the connection of dopamine neurons with the human lifespan limit of 115 years is true, either deprenyl or control of body iron could be ways to get past that limit.

Other interventions

Aspirin may be a cheap, easy way to get significant lifespan extension. Based on a 13% lower mortality rate in aspirin users, Josh Mitteldorf calculated that aspirin might add 2 years to life expectancy. That’s a surprisingly low amount of life extension, but the exponential mathematics of aging make it so. In essence, interventions need to be increasingly effective just to stay up with rising rates of death.

Metformin is another drug advocated for life extension. A recent review and meta-analysis found that metformin was associated with 7% lower all-cause mortality in diabetics vs non-diabetics. That number could vary, since non-diabetics taking metformin might have a lower death rate, but there’s no data on that, or, metformin could have less effect on non-diabetics.

Nonetheless, a 7% lower mortality rate isn’t even as good as aspirin, and would get us less than 2 years of extra life.

Rapamycin is another anti-aging drug, which has had good results in animal experiments. Its most notable proponent, Mikhail Blagosklonny, believes that combinations of rapamycin with metformin, aspirin, and others, could get us past the current limit to human longevity. But even he says that, because modern medicine has already extended human lifespan, we can’t expect the amount of extension seen in animal studies. It would be less.

My point here is that current prospects for lifespan extension don’t seem terribly impressive. They probably won’t get masses of people to 120, and probably won’t get anyone to, say, 150.

Overlapping mechanisms

If some of these anti-aging interventions work through overlapping mechanisms, then we can’t expect simple additive effects.

For example, if metformin and aspirin both work through activating AMPK – and of course they both surely have other mechanisms – then we can’t expect that taking both metformin and aspirin together will simply give us a 20% (13% + 7%) decrease in mortality.

Or, if someone practices calorie restriction, currently the most robust anti-aging intervention known, and he takes metformin (or aspirin), that he will get additional benefit from the drugs.

What about genetics?

I’ll use myself as an example.

My late father lived to be 87 years old, and he did not take care of himself. He smoked until his early 50s, when persistent chest pain from coronary artery disease compelled him to quit. In older age, he became overweight and drank more than he should have, and did no exercise but golf. Yet through modern medicine, he made it to 87, and he seemed to enjoy life doing so. His lifespan was well beyond that of the average male, which is currently around 80, which he achieved by doing precisely nothing in the way of what we would consider life extension.

My mother is still alive at age 95. She’s lived a more sober life, has never been overweight, and used to walk a good deal but no longer does.

I’ve inherited genes from both of them. I’m going to take a wild guess and say that even if I did nothing in the way of anti-aging, I could probably live into my 90s.

Of course, I exercise, eat right, and practice other good health habits. But how much more lifespan will those get me? If I’m already “scheduled” to live into my 90s, other interventions may not do a lot more.

Likewise, if I take both fish oil and aspirin, which I do, maybe one or the other is superfluous. Maybe both. Maybe little can get me past my 90s, since I may already be “programmed” to live that long by my genes.

I don’t know. I’ll continue to practice good health habits along with interventions that hopefully will extend my lifespan, but one needs to be realistic about how effective they may be.

What is needed is a thorough understanding of aging along with the technology to change it. Many discoveries have been made, and technology breakthroughs may be on the horizon, but to my knowledge there isn’t yet any technology that will extend human lifespan.

Life extension is about better health

Anything that improves health and prevents chronic disease, such as heart disease and cancer, should extend lifespan.

Aging massively increases the risk of chronic disease; indeed it could be said that massively increased health risk is the very definition of aging.

So if you can prevent or delay chronic disease, you are delaying aging and extending lifespan.

Yet, if you don’t get one disease, you live long enough to get another. Think about it: if you lower the death rate from heart disease, you’re going to increase the death rate from cancer. (After having heart disease much of his adult life, my father died of cancer.) A true anti-aging intervention will prevent or delay the appearance of all diseases of aging.

For myself, I have to say that the prospect of extending my life beyond what may be my “natural” lifespan, perhaps in the 90s, seems, well, not much to count on.

Yet I don’t want to get the chronic diseases of aging. I’d like to be healthy until the end.

So for me, practicing life extension and remaining healthy (and hopefully happy) are one and the same.

At this moment in history, that’s perhaps all one can ask.

PS: I believe one of the most important ways to delay aging is by controlling body iron, as I discuss in my book, Dumping Iron.

PPS: Check out my Supplements Buying Guide for Men.

Vegetarians Don’t Live Longer

A vegetarian diet is widely thought to be healthy. Bias in favor of it is pervasive, given that for several decades the health establishment has denigrated meat and saturated fat as causing heart disease and even cancer. Unfortunately, the bias appears to be false, since vegetarians don’t live longer, as we’ll see in this article.

Seventh-Day Adventists and vegetarianism

The Seventh-Day Adventists are a Christian religious denomination that advocates vegetarianism. Not all Adventists are vegetarians but the church strongly promotes the practice to its members, and to others as well. They’ve been characterized as having an “anti-meat agenda”.

Some studies done in Seventh-Day Adventists have found lower mortality rates in the vegetarians among them.

However, a recent meta-analysis (analysis of other studies) found “that there is modest cardiovascular benefit, but no clear reduction in overall mortality associated with a vegetarian diet. This evidence of benefit is driven mainly by studies in SDA [Seventh-Day Adventists], whereas the effect of vegetarian diet in other cohorts remains unproven.”

The study found that the only evidence of “modest” benefit was in studies using Adventists.

Adventists also have a high intake of fruits and vegetables, are encouraged to abstain from alcohol and smoking, they have a low divorce rate and of course are religious.

All of these factors could help explain better health among them, with vegetarianism playing little to no role.

Likewise, non-Adventist vegetarians are more likely to have all of these factors also. Less smoking and drinking, more exercise, less likely to be overweight, in general, to be much more health conscious. Studies that have found better health among vegetarians that did not correct for these factors haven’t truly isolated the factor of vegetarianism.

Vegetarianism in a large population

A recent study done in Australia looked at 267,180 men and women age 45 and over, part of the 45 and Up cohort study. Following adjustment for confounding factors – like those mentioned above, such as smoking, body mass index, etc. – they found that vegetarians don’t live longer than others.

Following extensive adjustment for potential confounding factors there was no significant difference in all-cause mortality for vegetarians versus non-vegetarians. There was also no significant difference in mortality risk between pesco-vegetarians or semi-vegetarians versus regular meat eaters. We found no evidence that following a vegetarian diet, semi-vegetarian diet or a pesco-vegetarian diet has an independent protective effect on all-cause mortality.

Whether the subjects never ate meat, or only seldom, or whether they ate only fish, the results were the same. The study did not distinguish between vegans, who eat no animal products at all, and vegetarians, however.

What this means

Several conclusions can be drawn from this study.

One is that other studies that found better health outcomes in vegetarians, but did not adjust for other health factors, are heavily biased, simply because vegetarians and non-vegetarians are not drawn from the same group of people. Vegetarians are more health conscious, probably also higher IQ and socioeconomic status, exercise more, etc., and those factors, not refraining from eating meat, are what drive health differences.

The second conclusion is more important.

We’ve been, and are being, told by multiple health authorities that eating meat is the main factor behind the epidemic of modern diseases, such as heart disease, cancer, diabetes, etc.

Based on this study, that cannot be true. If meat caused heart disease and the rest, we could expect to see large differences in death rates between vegetarians and non-vegetarians. But we don’t.

The hypothesis of meat as the cause of modern disease is a phantom.

Dietary causes of modern diseases are themselves likely to be modern, in which case we should be looking at sugar, refined carbohydrates, and vegetable oil, all of which are either modern or the consumption of which has increased radically and coincided with the onset of modern diseases.

The foods that man has eaten for a couple million years, such as meat and fish, should have killed off the human race if they were harmful. Instead, humans populated the earth while eating them.

Meat is a health food.

Did health authorities get anything right?

Is anything that mainstream health authorities recommend correct?

Smoking is bad, and exercise is good, so they got those right.

But saturated fat and cholesterol bad? Wrong.

Meat is unhealthy? Wrong.

Fortifying food with iron? A mistake.

Statins? Also a mistake.

Low-fat diets for weight loss? Nope.

You should be skeptical of what mainstream health authorities recommend. In many cases, it would be wiser to do the opposite.

Here’s my video I did today on this topic.


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

PPS: Check out my Supplements Buying Guide for Men.