The Japanese White Rice Paradox Is Dead – Or Did It Even Exist?

The phrase ‘Japanese Paradox’ has been used frequently in recent decades. It is a label that denotes the fascinating ability of Japanese persons to maintain slender builds despite substantial volumes of white rice consumption.

Most often this phrase is uttered by health-conscious westerners who appreciate the concept of glycemic response to food while possessing an awareness of its repercussions in the picture of health.

Ethnicities other than Japanese lack this enviable genetic endowment to withstand the harmful effects that one would expect from LOTS of simple carbohydrates. Right?

Wrong. The Japanese paradox is actually fallacious. Or, at least, a misnomer that is only partially paradoxical.

While Japan boasts impressively low levels of obesity compared to other developed countries (5% vs. 35% in the USA), the prevalence of Type II Diabetes Mellitus (T2DM) only differs marginally by a few percentage points. This underlines how metabolic disease as seen with T2DM is preceded by risk factors independent of BMI.

Instead, recent research emerging from Japanese scientists has magnified lifestyle and diet composition as even more influential in the development of these preventable diseases.

Approximately 30% of daily  energy intake is derived from white rice for the average Japanese person and it remains a fixture at most meals. Bread and pasta consumption is on the rise, in parallel with other westernised convenience foods, but traditional diet staples aren’t usurped easily nor quickly – white rice will continue to constitute the base of most Japanese dishes.

A systematic review conducted by Nanri et al. (2010) demonstrated that, paradoxically, higher quartiles of white rice consumers had significantly lower BMIs, were more physically active, and worked more strenuous exercise throughout the week. But this same portion of participants were at significantly greater risk of T2DM, despite being superficially healthy.

Body habitus is not an accurate predictor of health markers. Japanese persons are typically slight in build with little subcutaneous fat because of a lifestyle that gives rise to an imbalance between energy intake and energy expenditure; large volumes of incidental activity, smaller portion sizes when eating, and pre-occupation with work.

Visceral fat accumulation, on the other hand, is sensitive to other factors that include psychological stress, sleep duration and quality, and the quality (more so than quantity) of food intake.

The females who consumed 3 or more servings of rice in this large study were susceptible to T2DM irrespective of physical activity level, while physically active males meeting exercise guidelines appeared to negate the detrimental metabolic repercussions of frequent white rice consumption.

As such, the connection between white rice intake and Japanese males’ incidence of T2DM is somewhat equivocal, though regular exercise seems instrumental in preserving insulin sensitivity and thus staving off metabolic disease.

A Chinese study corroborates the above findings to a large extent; women who consumed ≥300 g rice/d had a 1.8-fold greater risk of developing T2DM than women who consumed <200 g rice/d.

What about brown rice?

This grain is unanimously considered the healthier alternative to its white counterpart, but most would agree that it lacks the same palatability polished white rice is renowned for. ‘Genmai’ (brown rice in Japanese) is thus an unpopular choice.

It follows that adherence to a research study in which Japanese participants are subject to extended periods of eating conventional brown rice would pose an issue. So Nakayama et al. (2017) instead administered glutinous brown rice (GBR), a variety similar in texture to sushi rice but dissimilar in glycemic effect, to a Japanese group with T2DM for 8 weeks.

Though GBR isn’t as complex a carbohydrate as long-grain basmati brown rice, the diabetic biomarkers of glycated haemoglobin (HbA1c) and post-prandial blood glucose levels were significantly better in this group when compared to the white rice group.

Terashima et al. (2016) even discovered that a single day of GBR consumption in place of white rice noticeably improved blood markers related to diabetes. GBR may stimulate GLP-1 secretion secondary to an increase of short-chain fatty acids produced from dietary fibre by the gut microbial flora. Magnesium, γ-oryzanol (sourced from the bran of GBR) and insoluble fibre are stripped in the process of transforming brown rice to white rice, and all of these compounds exert positive effects on our glycemic stability.

In light of these findings, and with adherence to any dietary intervention being the linchpin in its success, GBR may be a tastier yet still effective alternative to grainier brown rice.

It would be remiss not to mention several confounding factors that may compound the negative effects of eating white rice. Individuals consuming significantly high amounts of white rice also tend to eat less fat, protein and fibre at the same meal; all of which are known to slow gastric emptying rate and blunt the post-prandial blood glucose spike that we see when sugar is consumed in isolation.

Additional confounders noted in this field of Japanese research include:

• Extensive smoking in Japan, a habit that can impair βcell function and thus glucose metabolism
• 10 hours per day of work appears to be the threshold beyond which metabolic syndrome risk is increased significantly (Kobayashi, 2012)
• Eating speed is positively correlated with greater waist circumference, lower HDL cholesterol, poorer fasting blood glucose levels, hypertension, and ultimately metabolic syndrome (Yamaji, 2018; Nagahama et al., 2014). Observationally, the speed of eating in Tokyo amongst ‘salary men’ is rapid. I have acculturated effortlessly in this regard.

Wrapping things up, white rice isn’t inherently unhealthy but its consumption does necessitate several considerations. Besides serving as a dense source of tasty and simple carbohydrates, it doesn’t provide us with any micronutrients, nor fibre, nor protein. It is therefore a food that doesn’t readily satiate but rather predisposes to overeating while eliciting a hefty blood glucose spike.

The research elucidated in this article has more than likely encouraged a number of readers to exercise some restraint with white rice where possible, but be aware of the confounding factors mentioned above.

Of particular salience is that the Japanese persons in the higher quartiles of white rice consumption ultimately ate little else with their rice to dampen its metabolic impact, and their overall diet lacked an adequate proportion of both protein and fat.

I enjoy white rice as much as the rest of you and, well, living in Japan makes for a difficult time if one is to completely eschew it. Not to mention foregoing sushi trains – no thanks. In saying this, the health-conscious individual understands that white rice probably shouldn’t be consumed at every meal.

Mitigating the metabolic damage chronic white rice intake may induce involves:

• Eating it with generous doses of protein, fat and fibre
• Preceding or succeeding its consumption with somewhat intense physical activity where possible
• Consciously chewing your food (rather than inhaling it like Kobayashi)
• Food sequence

By this last point I mean it is sensible to consume the other macronutrients (protein, fibre, fat) prior to the carbohydrates. In Japan, a set meal typically involves eating foods separate from one another as opposed to one big bolus. I prefer the latter, though, so will usually serve myself the more satiating foods first before topping with white rice.

Discounting that “occasional” (in other words, daily) rice ball, or acquiescing to that rice-heavy dish your friends are eating can be too easy, especially when there appears to be no superficial or immediate health consequences. *I’m still in my 20s with a great metabolism, and I’m not overweight so I can afford it!*

But the surge in preventable metabolic disease in Japan and other developed countries is very real, and living with T2DM is not easy. These morbidities often develop insidiously without obvious notice, making them even more dangerous. They are preventable though, so abandoning a reactive mentality in favour of proactivity is crucial. Be conscientious with your food choices.

References:

Kobayashi, T., Suzuki, E., Takao, S., & Doi, H. (2012). Long working hours and metabolic syndrome among Japanese men: a cross-sectional study. BMC Public Health, 12(1), 395. doi:10.1186/1471-2458-12-395

Mizoue, T., Yamaji, T., Tabata, S., Yamaguchi, K., Ogawa, S., Mineshita, M., & Kono, S. (2006). Dietary patterns and glucose tolerance abnormalities in Japanese men. The Journal of nutrition, 136(5), 1352-1358.

Morimoto, N., Kasuga, C., Tanaka, A., Kamachi, K., Ai, M., Urayama, K. Y., & Tanaka, A. (2018). Association between dietary fibre: carbohydrate intake ratio and insulin resistance in Japanese adults without type 2 diabetes. British Journal of Nutrition, 119(6), 620-628.

Nakayama, T., Nagai, Y., Uehara, Y., Nakamura, Y., Ishii, S., Kato, H., & Tanaka, Y. (2017). Eating glutinous brown rice twice a day for 8 weeks improves glycemic control in Japanese patients with diabetes mellitus. Nutrition & diabetes, 7(5), e273.

Nanri, A., Mizoue, T., Kurotani, K., Goto, A., Oba, S., Noda, M., . . . Group, J. P. H. C.-B. P. S. (2015). Low-carbohydrate diet and type 2 diabetes risk in Japanese men and women: the Japan Public Health Center-Based Prospective Study. PLoS One, 10(2), e0118377.

Nanri, A., Mizoue, T., Noda, M., Takahashi, Y., Kato, M., Inoue, M., . . . Group, J. P. H. C. b. P. S. (2010). Rice intake and type 2 diabetes in Japanese men and women: the Japan Public Health Center–based Prospective Study–. The American journal of clinical nutrition, 92(6), 1468-1477.

Oba, S., Nagata, C., Nakamura, K., Fujii, K., Kawachi, T., Takatsuka, N., & Shimizu, H. (2010). Dietary glycemic index, glycemic load, and intake of carbohydrate and rice in relation to risk of mortality from stroke and its subtypes in Japanese men and women. Metabolism, 59(11), 1574-1582.

Sawada, K., Takemi, Y., Murayama, N., & Ishida, H. (2018). Relationship between rice consumption and body weight gain in Japanese workers: white versus brown rice/multigrain rice. Applied Physiology, Nutrition, and Metabolism(ja).

Shimabukuro, M., Higa, M., Kinjo, R., Yamakawa, K., Tanaka, H., Kozuka, C., . . . Masuzaki, H. (2013). Effects of the brown rice diet on visceral obesity and endothelial function: the BRAVO study. British Journal of Nutrition, 111(2), 310-320. doi:10.1017/S0007114513002432

Sugiyama, M., Tang, A., Wakaki, Y., & Koyama, W. (2003). Glycemic index of single and mixed meal foods among common Japanese foods with white rice as a reference food. European journal of clinical nutrition, 57(6), 743.

Tajima, R., Kimura, T., Enomoto, A., Yanoshita, K., Saito, A., Kobayashi, S., . . . Iida, K. (2017). Association between rice, bread, and noodle intake and the prevalence of non-alcoholic fatty liver disease in Japanese middle-aged men and women. Clinical Nutrition, 36(6), 1601-1608.

Terashima, Y., Nagai, Y., Kato, H., Ohta, A., & Tanaka, Y. (2016). Eating glutinous brown rice for one day improves glycemic control in Japanese patients with type 2 diabetes assessed by continuous glucose monitoring. Asia Pacific journal of clinical nutrition.

Watanabe, S., Mizuno, S., & Hirakawa, A. (2018). Obesity and Chronic Diseases. Journal of Obesity and Chronic Diseases| Volume, 2(1), 13.

Yamaji, T., Mikami, T., Kobatake, K., Kobayashi, K., Tanaka, H., & Tanaka, K. (2018). Gobbling your food is the risk factor of obesity and metabolic syndrome. European Heart Journal, 39(suppl_1), ehy565.

Zhang, G., Pan, A., Zong, G., Yu, Z., Wu, H., Chen, X., . . . Chen, X. (2011). Substituting White Rice with Brown Rice for 16 Weeks Does Not Substantially Affect Metabolic Risk Factors in Middle-Aged Chinese Men and Women with Diabetes or a High Risk for Diabetes–4. The Journal of nutrition, 141(9), 1685-1690.

Disconnecting From Tech To Reconnect With Life

It was last year that I was on the end of a crucial reaffirmation. My brother had just introduced me to a captivating interview in which Simon Sinek, a leadership guru, was passionately illuminating the detriment of modern technology addiction. The talk was specifically delivered in the context of millennials, a cohort to which I belong.

It was my first acquaintance with Sinek and an impactful first impression it was; Sinek has this unique ability to make one feel as though he is speaking in one’s very direction and thus naturally engages the individual within a larger audience. He is the expert on leadership and behavioural psychology, after all.

I had read and listened to Eckhart Tolle’s work for many years prior and so was aware of the concepts that modern technology is generally inimical to; enlightenment, presence, state of consciousness and so on. Despite this knowledge, and a fascination with the growing research pertaining to mindfulness, I was perpetually denying a personal battle with mild addiction to modern technology.

As a small business owner operating on various social media platforms I was succumbing to the black hole that social media can very easily become and it was unquestionably retarding my productivity, mental health and ultimate sense of fulfilment.

For a manmade construct that purports to enhance life modern technology appears to paradoxically diminish it in endemic proportions. Sinek parallels modern technology addiction with other forms that include alcoholism and gambling.

The commonality in addiction is a self-cultivated dependency on a powerful hormone that we know as ‘dopamine’. This stress-numbing hormone is produced every time we imbibe ethanol; every time we trigger a pokies machine; and every time we check our phones for fresh notifications.

It is scary when considering the statistics: approximately 80% of millennials sleep in close proximity to their smartphones, more than half check for notifications at least once during the night, and one third periodically interact with it over the course of a night (Julie Albright, PhD in digital sociology).

The research supports the concern that social media addiction inhibits development of the interpersonal skills that relationships survive, let alone thrive, on. And even though our awareness of its perils is gaining ground, consumerism continues to parallel the swelling prevalence of mental health illness.

This isn’t at all surprising when we consider that identities conveyed through social media are usually beset with disparities between others’ perceptions of us and our reality. In the same vein, addiction to modern tech is distinctly associated with low self-esteem, anxiety, narcissism, envy and general life satisfaction; all of which are antagonistic to constructing authentic relationships. Indeed, a fading art amongst many a millennial and one that may very realistically be extinguished by Gen Z and Gen ‘Alpha’.

Outside of the interpersonal sphere, is our obsession with modern technology not making us less efficient in our everyday work? The ‘privilege’ of convenience that it portrays ironically masquerades as our biggest source of disruption to deep work. It isn’t necessarily our fault, either. Immersion in a society that is unconditionally one with their tech infects us with an unhealthy behaviour that is incredibly difficult to shake.

Aldous Huxley opined that “Technological progress has merely provided us with a more efficient means of going backwards”. Quite an extreme perspective but in a lot of ways it really has.

So how does one go about dissipating this pronounced addiction with modern tech and its incorporeal offspring, social media?

The reason we persistently fall prey to the bane of our own invention is that our willpower simply cannot single-handedly defeat such addiction. We set ourselves up for failure by equipping the temptation wherever we go. Having the internet readily available with the smartphone always within arm’s reach composes the perfect storm.

Removal of temptations that predispose us to perpetual negative habits is the fundamental first step in annihilating addiction. “But I need my smartphone!?” Yes, we occasionally do need to use data for practical necessities… though if one is well organised, then the ‘need’ to message or check on work-related notifications during the day drastically diminishes.

As such, outside of practical means, quarantine the smartphone wherever possible so that the temptation to mindlessly check it is nullified. Every time this seemingly insignificant act is carried out, the willpower passively strengthens and the obsessive compulsive behaviour disintegrates.

None of us are impervious to unhealthy habits and this is something I still struggle with, but have undoubtedly improved in this year. More recently, I saw my move to a new country (Japan) as a terrific opportunity to further this practice of temptation elimination. I have deliberately avoided arranging a phone plan, instead opting to utilise Wi-Fi only when practically necessary.

Yes, it may not be permanent but until that time comes (or doesn’t) it is a lifestyle decision propitious to greater fulfilment.  

I have learnt to love being disconnected from the interweb, allowing me to invest more time into the things that matter; studying a second language, building relationships with fascinating people in person, offering more value and writing. In other words, I am better extracting the essence of life that can so easily be sabotaged by our feckless use of technology.

*Of course, this technique is applicable to food choices and other habits antithetical to our health. Give the willpower an assist.

References:

Blackwell, D., Leaman, C., Tramposch, R., Osborne, C., & Liss, M. (2017). Extraversion, neuroticism, attachment style and fear of missing out as predictors of social media use and addiction. Personality and Individual Differences, 116, 69-72.

Hawi, N., & Samaha, M. (2018). Identifying commonalities and differences in personality characteristics of Internet and social media addiction profiles: traits, self-esteem, and self-construal. Behaviour & Information Technology, 1-10.

Liu, C., & Ma, J. (2018). Social media addiction and burnout: The mediating roles of envy and social media use anxiety. Current Psychology, 1-9.

Turel, O., He, Q., Brevers, D., & Bechara, A. (2018). Delay discounting mediates the association between posterior insular cortex volume and social media addiction symptoms. Cognitive, Affective, & Behavioral Neuroscience, 1-11.

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.