Why Men Die Younger

It has become a well-known fact that men universally die younger than women. Less common knowledge, however, is the complexity underlying this gendered life-expectancy difference (GLED).

Though men are physically stronger than women, by virtue of significantly greater endogenous levels of testosterone, the GLED estimates tend to range from 5-7 years in favour of females. Females can thus be considered ‘biologically stronger’ than males.

However, it would be reductionistic to solely blame biological differences. Male-female behavioural disparities also account for the non-trivial GLED that transcends the world.

From a social standpoint, men consistently demonstrate greater risk-taking behaviours during adolescence and emerging adulthood. While higher relative levels of testosterone is associated with these social determinants, and can be explained in part for the higher incidence of preventable deaths in males, conformity to hegemonic expressions of masculinity may also pose a contributing factor.

In other words, even in men that may have low-normal levels of testosterone, perceived social pressure to intimate hegemonic forms of masculinity may alter male behaviour to the detriment of lifespan. Further, hegemonic masculinities are attributable to toxic degrees of stoicism, delayed help-seeking and suicide risk. Overall, a dynamic interplay exists between individual and social determinants of male life expectancy.

The research pertaining to testosterone levels and male healthspan is equivocal. An inverted U curve is an appropriate visual representation of this relationship, in that too little and too much testosterone appears inimical to healthspan.

It is important to distinguish healthspan from lifespan. Healthspan is a more recent term that denotes expected quality years of life, whereas lifespan is merely the chronological extent to which someone lives (which could be an existence host to severe and various co-morbidities).

Healthy levels of testosterone confer many benefits, including but not limited to lean body mass, physical strength, protection against mental health disease. On the other hand, male sex hormones may suppress the immune system and be a factor in cardiovascular disease (CVD) representing the primary cause of male deaths worldwide.

Previous research that has investigated the effects of castration suggests that the relative absence of testosterone confers extended lifespan. A 2012 Korean paper specifically looked at eunuchs, males that were castrated at a young age, and observed an increase in life expectancy of 14.4-19.1 years when compared with uncastrated men of homogenous socioeconomic status. In this instance, ‘lifespan’ would seem more apt than ‘healthspan’ given male sex hormones enhance the overall quality of a man’s life.

Given the complexity and equivocality of testosterone, it may not directly be culpable for the higher incidence of CVD and associated GELD. Oestrogen, which women possess to a considerably higher degree than men (especially during reproductive years), does exert protective effects against CVD.  CVD is nevertheless the leading cause of female deaths too, albeit at a reduced absolute incidence.

In short, science and expert analyses has not yet struck an unwavering consensus as to the reasons underpinning men’s shorter life expectancy. We can be confident in saying that social determinants related to male behaviour, and the relatively greater oestrogen levels in women, are notable factors in the entrenched GELD.

The World’s #1 Power Food

If you are like 99.99% of non-Japanese people you either cannot stomach the fermented soybean that is natto, or you’re yet to try it because you’ve only heard how unpalatable it is.

Well, this is a great shame because this traditional Japanese staple is truly the healthiest food in the world. Particularly for foreigners living in Japan where its accessibility is high, you are missing out if you’re not eating natto on the daily.

When considering the criteria of foods that can deservedly be touted ‘super’ or ‘power’ foods, as I prefer to call them, we need to take into account several things. 

Firstly, the nutrient density of a food. This can be considered the micronutrients divided by calories. Micronutrients are vitamins and minerals crucial for hormonal functioning and prevention of disease, and can be esteemed as the smaller cousins of macronutrients that most people erroneously place more importance on.

While natto is more calorific and thus less nutrient-dense than certain vegetables like kale (to use a classic example), it is still abundant in many super important micronutrients and outweighs these other vegetables in other notable criteria.

Natto satisfies almost the entire spectrum of micronutrients that we need to function optimally, but the hallmark micronutrient in natto is vitamin K2, a nutrient scarce amongst food sources. Vitamin K2 is strongly implicated in the prevention of heart disease and reduced bone mineral density. This is mostly because K2 works synergistically with calcium to promote osteogenesis while averting calcium plaque accumulation in our blood vessels.

Another salient criterion is satiety and this is where natto, believe it or not for the natto-naysayers, easily conquers its competitor foods. Satiety is largely dictated by micronutrient content, protein quantity, and dietary fibre. Countless studies also demonstrate higher post-meal satiety with how savoury a food is, in contrast to foods on the sweet end of the taste spectrum.

Natto’s distinct umami flavour constitutes savoury and it has a solid balance of all the macronutrients. Perhaps more noteworthy is the impeccable quality of these macronutrients; complex carbohydrates to attenuate any rapid blood glucose excursion, a generous omega 3 and 6 essential fatty acid profile, and a protein milieu that boasts the full array of amino acids. 

A superfood isn’t very practical or accessible to everyone if it costs the average weekly grocery budget, and most ‘superfoods’ are ridiculously expensive. This is where natto triumphs again, costing just 39 yen at a local Japanese supermarket for a 3 pack (or 135g). 39 yen is a mere 50 Australian cents.

In Australia, a 4x45g pack will cost you ~$2. And so it is fair to say that the affordability of natto compared to other esteemed superfoods is unparalleled – though it should be a fixture even on the grocery list of those not looking to maximise their health on a budget!

Natto is of course a plant-based food and thus keeps the ethically-mindful crowd happy. I’m not a vegan but if I were this would hands-down be my number one staple. It still is my number 1 powerhouse food as an omnivore. The only other plant-based food that comes close to natto from a protein quality perspective is quinoa.

Protein quality is a huge factor in muscle protein synthesis and this can be a notable shortcoming when eschewing meat and dairy. More specifically, vegan sources of protein lack adequate amounts of the amino acid leucine, which is the most potent stimulator of muscle protein synthesis but only when a threshold of around 3g has been consumed. Natto contains about 2.5g per 1 cup which is quite impressive and sufficient given it will generally be consumed with other food.

Let’s not forget that natto is produced by means of fermentation, similar to sauerkraut and kefir, and so offers the further benefit of gut-friendly probiotics. It is prudent to consume some form of probiotics at least once daily as this good bacteria aids in digestibility of a meal, strengthens the gut’s integrity and thus enhances our ability to assimilate nutrients from food.

How to consume it: I would advise for first-timers to eat it how most Japanese people eat it for breakfast; that is, with rice and an egg or multiple eggs. Crack a raw egg into just cooked rice, then add the natto on top. You can be generous with soy sauce, mustard and any other seasoning if you hold the preconception that natto isn’t tasty.

After you acquire the taste you may find yourself enhancing every meal with a topping of natto…Or at least that’s what I do anyway!

Give this special Japanese staple a go and let me know how you like it.

Time Restricted Eating (TRE) – Where Are We Now?

TRE or intermittent fasting (IF) has gained substantial ground in both the fitness and health spheres since the turn of the 21st century, with purported benefits initially drawing much scepticism. Fitness aficionados scoffed at the idea of skipping but one bi-hourly scheduled meal for fear of hindering muscular growth potential and stalling the metabolism. However, lower meal frequency appears to have a noticeably superior effect on diet-induced thermogenesis (i.e. what most people think of when they claim to “speed up metabolism” with smaller, more frequent meals).

Scientific research continues to cast an overwhelmingly positive light on this practice. In fact, I would go as far as deeming TRE the finest anti-ageing doctor that exists. Usually use of the word ‘panacea’ by health professionals would elicit a due sense of dubiety in me, but periodic abstinence from food is one exception I will allow. Until the research contradicts that line of thought anyway, which won’t happen but must be said given this is a body of research whose surface has barely been probed.

It is extraordinary how something as inherently passive as food abstinence can be an elixir of health.

Ironically, I first implemented fasting in 2013 for a rationale perhaps least supported by the science to date, which was to directly increase my testosterone levels. I employed a flexible 16/8 hour fasting/eating window religiously for 3 years during which time I gained ~25kg of lean weight. My testosterone improved too, but this was because I replaced daily running with progressive resistance training 3-4 days a week while eating a calorie surplus.

The science mostly demonstrates small but insignificant reductions in testosterone levels amongst male participants, but a definitive answer to IF’s effects on testosterone won’t be elucidated for some time. This question needs to be investigated in the context of strength training participants over at least a medium to longer term study method. There is a dearth of the latter at present.

Indirectly, however, my provisional understanding is that habitual TRE does improve the androgen profile of males over time by virtue of other improved markers which will be explored below.

Awareness of IF as a tool to promote diet adherence is widespread in the fitness community, pioneered by Ori Hofmekler (The Warrior Diet) and Martin Berkhan (The Leangains Method) originally. Of course, it makes sense that limiting oneself to a certain timeframe in which food can be consumed should translate to less daily calories when compared with ad-libitum feeding. In other words, a calorie deficit and thus weight loss becomes more achievable.

I don’t need to necessarily lose more weight, though. So what compels me to fast 18+ hours most days?

8 weeks into resumption of daily fasting, albeit this time for longer bouts and with a few fundamental changes, both physical and non-physical benefits have already manifested. My skin has improved, waist circumference has lessened by 2 inches, greater perceived clarity of thought and working memory, improved digestion and satiety… and most profoundly, a deep sense of Zen that grows in accordance with extent of time in the fasting state.

“Yeah, that’s great, but N = 1”.

Let’s synthesise the main findings from recent scientific literature.

Cognition and Brain-Derived Neutrophic Factor (BDNF)

Brain-derived neurotrophic factor (BDNF) is a secretory growth factor that supports the survival of existing neurons and promotes synaptogenesis and differentiation of new neurons (Park and Poo, 2013).

BDNF is crucial in the context of our mental capacity and cognition and dysregulation of BDNF is associated with the onset of several neurodegenerative diseases, including Alzheimer’s Disease. It is something we can never have too much of.

Mammalian food deprivation and fasting consistently demonstrates reduction in size of most organs, except the brain and the testes. Quite to the contrary, IF enhances brain function via upregulation of BDNF and its associated increase in neurogenesis (growth of new brain tissue, pathways).

Exercise has this effect too, but fasting appears to be even more powerful as a driver of BDNF. Short and intense bouts of exercise during the fasting phase appears to be highest yield.

Ad-libitum eating downregulates BDNF which is known to accelerate brain dysfunction as we age.

Other pros of elevating BDNF include:

  • Neuronal resistance to brain injury and tissue damage (an area pertinent to TBI victims especially)
  • May modulate depressive symptoms like anti-depressant medication (successful intervention with the latter increasing blood levels of BDNF)
  • Regulation of appetite and circadian rhythm, crucial to counter overeating
  • Helps with re-myelination of nerves after nerve-related injuries
  • Aids in glucose metabolism
  • Helps with control of the cardiovascular and gastrointestinal systems

Visceral Fat and Metabolic Disease

As mentioned above, IF can shrink fatty organ tissue. This phenomenon can even take place when subjects consume the same calories (‘iso-caloric’) as the control subjects and maintain overall body weight.

Visceral fat, the fat that suffuses our vital organs, is far more dangerous to our health than subcutaneous fat (beneath the skin). An individual with who is moderately overweight with the latter can be healthy, but visceral fat is never absolutely benign.

Metabolic disease such as Type II Diabetes Mellitus (T2DM) is at an unprecedented high in developed countries and we know that adiposity of the liver, both alcohol-induced and non-alcoholic fatty liver (NAFLD), is a significant predisposing risk factor to such.

At this point in time there is a far greater volume of studies looking at fasting’s effect on mice with fatty liver, though human studies of this nature are still continuing to grow in number. Regardless, fasting windows of 18+ hours promote glycogenolysis and subsequent lipolysis of the diseased liver in NALFD patients.

Insulin resistance is a hallmark of NAFLD and T2DM, so improving the state of our liver with TRE may restore the efficiency with which we metabolise glucose and even reverse these diseases over time.

With the exception of a true ketogenic diet, eating ad-libitum or ‘around the clock’ as we are so socially conditioned to do induces chronically elevated blood glucose levels. This is a key mechanism in the development of insulin receptor resistance that eventually manifests as T2DM.

Anti-ageing

Many advocates of IF label it the bona fide fountain of youth for its cellular cleansing mechanism known as ‘autophagy’. Autophagy is essentially the degradation of old cells and proliferation of new cells. By preventing the toxic accumulation of damaged protein and organelles, particularly mitochondria, autophagy limits oxidative stress, chronic tissue damage, and oncogenic signaling, which suppresses cancer initiation.

Protein oxidation, on the other hand, appears to accelerate the ageing process by nullifying the autophagic compounds responsible for its life extension benefits. But we should all be acutely aware of how important protein intake AND quality is from the viewpoint of performance, anti-fragility, and muscular development.

Perhaps it is the fact that the traditional Okinawan diet comprised a mere 10% of protein that this blue zone boasts such a lofty life expectancy. Similarly, vegetarianism and veganism may be correlated with longer lifespan not by virtue of less saturated fat and cholesterol; rather, it is likely the naturally lower intake of protein.

What’s the fun in living longer if you’re skinny, weak and lack sex drive?

My advice is not to eschew protein, or consciously limit it, but to incorporate generous amount of high quality protein (in the vicinity of 2-3x bodyweight in kg) in your daily fasting regime.

In doing so, muscle retention is at least encouraged and consideration for longevity is exercised.

Improved Heart Rate Variability (HRV)

I mentioned to my friend recently how I have come to identify a perceptible state of zen the deeper I go into a fast, which at first didn’t make sense to me given cortisol (the major stress hormone) expectedly rises during this time.

So I dived into the science.

Periodic fasting reduces systolic blood pressure, heart rate; and increases HRV. HRV is a less commonly known biomarker that denotes the variation of timespan from one heart beat to the next one, i.e. from R- to R-wave in the electrocardiogram (ECG) of “normal to normal beats”. A healthy amount of HRV helps us transition between parasympathetic (‘rest and digest’) and sympathetic (‘fight or flight’) nervous states.

Patients with major depressive disorder (MDD) and anxiety demonstrate remarkably lower levels of HRV. Conversely, we see rises in HRV with laughter and meditative exercise like yoga.

In short, IF seems to have a powerful influence on our mood and perception of stress.

TRE > Caloric Restriction Alone

Given the limited time window one has to eat when employing an IF protocol, caloric restriction (CR) and thus weight loss is almost inevitable. However, the studies that do examine pure CR compared with IF alone suggest comparable improvements in health biomarkers.

When the  IF group isn’t in a calorie deficit, the time-contingent abstinence elicits notable gains in insulin sensitivity, cellular processing and beiging of white adipose tissue. These positive changes can elapse despite nil to minimal subcutaneous fat loss.

So even if you’re not concerned with body weight or physique changes, in which calorie counting is necessary to quantify and monitor progress, simply abbreviating your eating window will bolster your health.

Practical Application

There are many iterations of TRE and, though the 5:2 method in which only 2 days of the week sees drastic calorie reduction has gained traction in recent years, I prefer a more consistent and substantial fast.

My first implementation of IF closely resembled the 16:8 Leangains Method formulated by Berkhan, and during this time I would tend to push the eating window far into the PM.

My more recent regime differs in a few ways with the most notable changes being a shorter and earlier eating window. However, some flexibility is always necessary to foster sustainability so it is in this regard that I will simply try to eat the bulk of calories in the middle of the day.

At present, I aim to consume  1-2 big meals and perhaps a snack within a 4-7 hour window, minimising food intake within a few hours of bed time. The primary reason for the latter is that elevated insulin can interfere with melatonin production and consequently diminish sleep quality. It is still a relatively grey area of research but a plausible hypothesis that has been verified by several papers.

The ‘ideal’ eating window, in light of recent literature, seems to be in the AM but this can be impractical for social reasons. Striving to eat within the middle of the day to early evening strikes a sensible compromise. A few alcoholic drinks prior to bed won’t impact insulin significantly and can actually improve insulin sensitivity in the medium to long term, so this doesn’t pose a concern. Choose alcoholic beverages lower in sugar content (spirits ftw) where possible, of course.

Consider self-experimenting by pushing your usual breakfast back by 2 hours and eating an earlier dinner at, say, 5.30pm. Prolong breakfast by an hour each week as a means to gradually habituate.

References

Aksungar, F. B., Sarikaya, M., Coskun, A., Serteser, M., & Unsal, I. (2017). Comparison of Intermittent Fasting Versus Caloric Restriction in Obese Subjects: A Two Year Follow-Up. J Nutr Health Aging, 21(6), 681-685. doi:10.1007/s12603-016-0786-y

Anton, S. D., Moehl, K., Donahoo, W. T., Marosi, K., Lee, S. A., Mainous III, A. G., . . . Mattson, M. P. (2018). Flipping the metabolic switch: understanding and applying the health benefits of fasting. Obesity, 26(2), 254-268. 

Dolgoff-Kaspar, R., Baldwin, A., Johnson, S., Edling, N., & Sethi, G. K. (2012). Effect of laughter on mood and heart rate variability in patients awaiting organ transplantation: a pilot study. Altern Ther Health Med, 18(4), 53-58. 

Horne, B. D., Muhlestein, J. B., & Anderson, J. L. (2015). Health effects of intermittent fasting: hormesis or harm? A systematic review. The American journal of clinical nutrition, 102(2), 464-470. 

Lee, C., & Longo, V. (2016). Dietary restriction with and without caloric restriction for healthy aging. F1000Research, 5. 

Levine, M. E., Suarez, J. A., Brandhorst, S., Balasubramanian, P., Cheng, C.-W., Madia, F., . . . Wan, J. (2014). Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population. Cell metabolism, 19(3), 407-417. 

Longo, V. D., & Mattson, M. P. (2014). Fasting: molecular mechanisms and clinical applications. Cell metabolism, 19(2), 181-192. 

Marosi, K., & Mattson, M. P. (2014). BDNF mediates adaptive brain and body responses to energetic challenges. Trends in Endocrinology & Metabolism, 25(2), 89-98. 

Mattson, M. P., Longo, V. D., & Harvie, M. (2017). Impact of intermittent fasting on health and disease processes. Ageing Research Reviews, 39, 46-58. 

Nicoll, R., & Henein, M. Y. (2018). Caloric Restriction and Its Effect on Blood Pressure, Heart Rate Variability and Arterial Stiffness and Dilatation: A Review of the Evidence. International journal of molecular sciences, 19(3), 751. 

Schrieks, I. C., Heil, A. L., Hendriks, H. F., Mukamal, K. J., & Beulens, J. W. (2015). The effect of alcohol consumption on insulin sensitivity and glycemic status: a systematic review and meta-analysis of intervention studies. Diabetes Care, 38(4), 723-732. 

Wan, R., Weigand, L. A., Bateman, R., Griffioen, K., Mendelowitz, D., & Mattson, M. P. (2014). Evidence that BDNF regulates heart rate by a mechanism involving increased brainstem parasympathetic neuron excitability. Journal of Neurochemistry, 129(4), 573-580. doi:doi:10.1111/jnc.12656

Young, H. A., & Benton, D. (2018). Heart-rate variability: a biomarker to study the influence of nutrition on physiological and psychological health? Behavioural pharmacology, 29(2-), 140.