Strength is Functional Because Weakness Impedes Function Absolutely (2017)

*This is a truncated re-post from a final year physiotherapy speech.

Without question, physiotherapy is a revered profession that has become increasingly difficult to enter. The physiotherapy degree attracts the top echelon of students, whom possess the aptitude necessary to solve complex problems that pertain to human function and movement. The curriculum is accordingly intricate but, though stimulating, omits the teaching of certain concepts that are so simple yet intrinsically linked with physical performance; that is, the fundamentals of strength training and exercise prescription. Perhaps the tendency for the typically astute thinker within our field to overcomplicate things is what obscures the necessity to apply basic strength training principles. An emphasis on ‘evidence-based practice (EBP)’ permeates the physiotherapy coursework, and yet what is arguably the most scientifically-backed means of rehabilitation, not to mention injury prevention, is essentially neglected (Hautala, Richards, Takahashi, Tulppo & Hills, 2016; Morley, Anker & von Haehling, 2014). If the physiotherapy curriculum is to truly fulfil its reputation as being grounded in up-to-date scientific science, a greater proportion of the credit units should be dedicated to progressive resistance training (PRT). 

In order to eliminate bias one would perceive from a proposal of this nature, the current physiotherapy cohort of 2017 was surveyed privately to gauge consensus; of the forty-eight responders 98% concurred with the demand for a subject predicated on PRT and exercise prescription. Exercise for Health & Well-being (PTY3EHW) was a second-year subject run for the last time with the current cohort before its abolition. As its name suggests, this subject aimed to explore the role of exercise in improving quality of life in addition to exercise selection for various musculoskeletal and chronic disease populations, both in a theoretical and practical sense. For a subject that boasted great potential, it was ultimately made redundant because it lacked structure and stimulation. Although PTY3EHW provided access to the health sciences faculty gym which is replete with state of the art strength training equipment, time was squandered with students wandering around purposelessly. The abolition of PTY3EHW was unwarranted since exercise, particularly PRT, is so crucial across the entire rehabilitation continuum for any disease state (Gentil, Steele & Fisher, 2017; Kraschnewski et al., 2016). Despite the indisputable benefits linked to PRT, a meagre 10% of Australians perform a sufficient muscle-strengthening activity levels (Bennie et al., 2016).

Having been a strength coach for over two years now, developed an advanced standard of strength, and immersed myself in the scientific literature, it must be said that my conception of strength diverges considerably from the way it is implicitly defined throughout the physiotherapy degree. ‘Strength training’, as used by the vast majority of physiotherapists I have come in contact with, appears to erroneously confuse true strength training with muscular endurance exercise. Training and exercise are distinctly different. This dichotomy lies in the fact that ‘training’ honours a pivotal concept that too often gets overlooked amidst the fixation with ‘functional’ exercise: that is progressive overload. This principle carries substantial weight because it underpins our primary aim with patients’ rehabilitation. This aim is, of course, to promote more robust musculoskeletal structures.

Progressive overload comprises three cornerstones: a stressor, recovery period, and an adaptation (see appendix A; Rippetoe, Kilgore & Bradford, 2006). The first year subjects of human biosciences, that thoroughly explore homeostasis, provide context through which the progressive overload model may be conceptualised. The applied stress must be sufficient to suppress basic cellular processes, and thus stabilise cellular structure and metabolism until the withdrawal of the stressor. Noticeable musculoskeletal discomfort may accompany this stage, indicating the disruption of homeostasis and concomitant events that trigger structural and functional changes. Subsequently, the body responds to this imposed stress via an upregulation of hormones, altered gene activity, increases in metabolic proteins; these processes constitute what is otherwise known as recovery. Rate of adaptation is highly individual, based on previous exposure to specific stressors, but inevitably elapses with adequate recovery. As a result, the threshold at which stress disrupts homeostasis in the individual has increased by virtue of systemic adaptation. Perpetually imposed stress is a crucial element in the progressive overload cycle, but care must be taken as to avoid excessive stress that may negate one’s adaptive capacity. Essentially, an appropriate amount of stress disrupts an organism’s state without overwhelming the capacity to adapt, thus allowing progress to be made in the form of enhanced function or physiological resilience. This understanding is crucial to differentiate between exercise and training and provides insight into effective rehabilitation.

Generally, physiotherapists are renowned for having an expansive arsenal of exercises. This gives rise to an unnecessary tendency to vary exercise selection with patients. While the naïve patient may be more than content when administered a wide variety of low-level exercises, or paying for regular physiotherapist-led personal training sessions, the physiotherapist must recognise that this approach to rehabilitation and injury prevention is sub-optimal. In other words, the approach many physiotherapists appear to take (and what we are taught at university) with rehabilitation sparks an initial stress that is not overloaded by a subsequent, specific stress of requisite greater magnitude to elicit ongoing adaptations. Exercise is fantastic in its own right, but it educes health benefits rather than enhanced strength and functional performance that should be at the crux of our professional practice.

Irrespective of whether the patient is provided with low-level exercises, injured tissue will almost invariably normalise when the natural healing course is respected. While caution is necessary to circumvent further injury during the acute phase of healing, the subconsciously held philosophy that optimal rehabilitation can occur in the absence of progressive overload exemplifies a failure to comprehend the basic tenets of human physiology and biomechanics.

‘Functional training’ is undoubtedly a trending theme in the physiotherapy world, representing a practice predicated on closely simulating given task(s) a client is endeavouring to improve in. This movement carries a certain degree of credence in that it upholds the law of specificity which is necessary to advance in any relevant skill. However, ‘functional training’ as it is portrayed by physiotherapists conflates the principles of strength training with task-specific practice. This begets inferior results when compared to dichotomising the two entities, strength training and skill acquisition. Strength is a very generally acquired and expressed characteristic, accumulated through the process of lifting increasingly heavier weights over time. Yes, physiotherapists frequently utilise basic thera-band and bodyweight exercises such as the famous glute bridge and its many variations, but these have their respective shortcomings; they are self-limiting and, quite frankly, inefficient. It is neither necessary nor productive to completely mimic either a sport’s movement pattern or its exact metabolic pathways in the gym. In the extensively common attempt to be sports or function-specific with strength training, many practitioners have gotten so specific with regard to both the metabolic pathway and movement pattern that an increase in strength is severely impeded or impossible. Fundamental barbell exercises like deadlifts, squats and the overhead press are the most ergonomically efficient means of acquiring strength; they are non-specific but develop useful power and strength that can be applied in any context of both athletes and the general populace. With strength training gaining increasing attention, as it deserves, physiotherapy as a profession must recalibrate its standard and understanding of strength. This change starts with amended university curricula, in a manner that serves to revolutionise the way forthcoming generations of physiotherapists think and apply exercise intervention with patients.

Staying within our scope of practice as physiotherapists is a seemingly plausible counter-argument to this proposition. Nonetheless, budding physiotherapists require a firm grasp of strength training and coaching fundamentals if we are to truly consider ourselves ‘movement experts’, and to endorse the indisputable science. In breeding physiotherapists whom appreciate the essence of progressive overload, that underpins effective strength and conditioning, our profession will only be enhanced in a way that sets ourselves apart from other similar fields. Just as clinical Pilates is a commonly attained accreditation by post-graduate physiotherapists, so too should the competency to strength coach be at the very least espoused. The argument for strength coaching aptitude to fall within our expertise outweighs its absence, and its use should by no means be confined to private practice physiotherapy. In fact, correct application of the progressive overload principle is perhaps even more pertinent in the hospital setting.  

Hospital-associated deconditioning (HAD) is an increasingly prevalent concern, with rehospitalisation rates post-discharge comprising a substantial percentage of all admissions (Berry et al., 2013; Dharmarajan et al., 2013; Vashi et al., 2013). Hospital-bound patients undergo extended periods of immobility which often engenders declines in muscle protein synthesis (MPS), muscular strength, and independence with activities of daily living (ADLs) to name but a few constituents of HAD. These commonly observed deficits in acutely unwell patients may be noteworthy contributors to the above mentioned hospital readmission rates. The decline in function seen in acute hospitalisations may be avoidable with appropriately dosed physiotherapy intervention; indeed, Lafont, Gerard, Voisin, Pahor & Vellas (2011) go as far as labelling it iatrogenic disability. Physiotherapists play pivotal roles in the hospital environment and post-acute care (PAC) setting as to restore patients to their pre-admission level of function (LOF), and thus ultimately improve the unlikelihood of rehospitalisation. Considering the alarming hospital readmission statistics, however, exhorts us to identify potential physiotherapeutic deficiencies that may be at fault.

Physiotherapists are described in the literature as administering low-intensity exercises, that do not meaningfully improve functional reserve or maximise physical function, to patients with HAD because they perceive these intensities as safer (Kortebein, 2009). Higher injury incidence in strength training athletes is a pervasive misconception held not only by antiquated physiotherapists but so too the general public. To dispel this concern, it is important to acknowledge the drastically lower prevalence of injuries across the weightlifting sports when compared to team sports (Keogh & Winwood, 2017). ‘Functional reserve’ denotes the capacity for older adults to tolerate additional stressors or illnesses without loss of independence, so it is a crucial biomarker that needs to be improved upon. It appears that physiotherapy in this population is almost entirely based on historical tradition rather than scientific rigour, with a lot of strength training coming only as an afterthought to gait and transfer re-training. The importance of PRT in this setting cannot be overstated to improve functional outcomes and ultimately reduce rehospitalisation rates.

Traditionally, physiotherapists have used general conditioning as treatment for older adults with HAD, which may encompass basic ambulation down the ward corridor, group exercise classes that do not satisfy training principles, or haphazard active range of motion (AROM) exercises. According to Seynnes et al. (2004), this approach does not adequately address impairments in physical function that are strong predictors of adverse events, and should henceforth be reconsidered. Endorsing a rehabilitation hierarchy that instead emphasises high-intensity PRT carries the most scientific merit and may significantly improve long-term outcomes in acute hospital patients (Falvey, Mangione & Stevens-Lapsley, 2015). The latter authors juxtapose the traditional paradigm with their proposed paradigm shift and a convincing premise that appropriately dosed PRT is more feasible than aerobic conditioning in this population (see appendix B). Strikingly, it is the older adult with HAD that has a dose-dependent response to strength training, carrying the implication for higher intensities to foster sustainable gains (Koopman & van Loon, 2009).

Further, Theou et al. (2011) allay the misconception that higher intensity PRT is inherently more injurious than conservative exercise prescription in this demographic of vulnerable patients. Advancing supine bed exercises and relatively unfruitful AROM drills to weight-bearing movements with external loads, up to 70-80% of 1RM, is required to truly stimulate physiological adaptations. The American College of Sports Medicine concurs with the notion that PRT be endorsed as a first-line intervention in frail elderly patients (Chodzko-Zajko et al., 2009). Again, the distinguishing factor between the antiquated paradigm and this proffered paradigm is that of progressive overload.

Undeniably, my background lends itself to some degree of bias in light of the fact I have both witnessed and experienced significant benefits from strength training. In saying this, the science does not lie and only continues to mount in favour of getting stronger. Quite profoundly, a recent systematic review discovered a statistically significant correlation between grip strength and prolonged lifespan (Leong et al., 2015). Assayed from a sizeable cohort of 139,691 35-70 year-old subjects, it was found that grip strength predicts not only all-cause mortality but also cardiovascular (CVD) mortality, non-CVD mortality and CVD disease occurrence. In fact, magnitude of subjects’ grip strength was considered more telling than the more frequently implicated systolic blood pressure. These findings are nothing short of remarkable but alas, sit-to-stands and 1kg dumbbell curls will not elicit meaningful adaptations in grip strength.

Now that the deficiencies of the common physiotherapy approach to exercise prescription have been comprehensively expounded, the new curriculum should address these needs. I am well aware of the rigorous process implementing a new subject to the course entails. As such, I believe the most feasible course of action is to initially incorporate lectures and corresponding practical classes within second year subjects such as ‘Physiotherapy Practice & Development A (PTY2PDA)’ and ‘Physiotherapy Practice Development B (PTY3PDB)’. Placing this module proximal to the second year anatomy subjects will facilitate a sounder grasp of functional anatomy and physiology. The lectures would explore the fundamentals of progressive overload, powerlifting, gymnastics or bodyweight training, Olympic weightlifting and bodybuilding. Quintessential rehabilitative physiotherapy, namely theraband resistance training and clinical Pilates, may also be unpacked in this series of exercise-based content. To consolidate the theoretical knowledge gleaned from this series of lectures, students will have the opportunity to partake in entry-level practical classes that cover the essential elements of these training modalities. Each of these resistance training methods have relevance in a rehabilitative and physical performance sense, and thus a basic familiarity with them embodies a key objective in this module. Accordingly, students will have an elementary competency to both coach and execute the core lifts. This learning is paramount for several reasons: it will solidify our profession as the true leaders in human performance and movement; new graduates will have the capacity to take patients from early stage to the advanced stage of rehabilitation while ultimately enhancing performance in the given individual’s sport; and our expertise will cater to patients of any athletic or non-athletic disposition. Within the next decade, I envisage strength training becoming the new clinical Pilates – it really is that powerful when done properly.

Recommended reading for this SBP module:

Rippetoe, M. (2013). Starting Strength: Basic Barbell Training (3rd Edition). The Aasgard Company.

Boyle, M. (2011). Advances in Functional Training. On Target Publications.

Wade, P. (2011). Convict Conditioning: How to Bust Free of All Weakness-Using the Lost Secrets of Supreme Survival Strength. Dragon Door Publications.

Everett, G. (2016). Olympic Weightlifting: A Complete Guide For Athletes & Coaches. Catalyst Athletics.

References

Bennie, J. A., Pedisic, Z., Van Uffelen, J. G., Charity, M. J., Harvey, J. T., Banting, L. K., . . . Eime, R. M. (2016). Pumping iron in Australia: prevalence, trends and sociodemographic correlates of muscle strengthening activity participation from a national sample of 195,926 adults. PLoS One, 11(4), e0153225.

Berry, J. G., Toomey, S. L., Zaslavsky, A. M., Jha, A. K., Nakamura, M. M., Klein, D. J., . . . Kaplan, W. (2013). Pediatric readmission prevalence and variability across hospitals. JAMA, 309(4), 372-380.

Chodzko-Zajko, W. J., Proctor, D. N., Singh, M. A. F., Minson, C. T., Nigg, C. R., Salem, G. J., & Skinner, J. S. (2009). Exercise and physical activity for older adults. Medicine & Science in Sports & Exercise, 41(7), 1510-1530.

Dharmarajan, K., Hsieh, A. F., Lin, Z., Bueno, H., Ross, J. S., Horwitz, L. I., . . . Suter, L. G. (2013). Diagnoses and timing of 30-day readmissions after hospitalization for heart failure, acute myocardial infarction, or pneumonia. JAMA, 309(4), 355-363.

Falvey, J. R., Mangione, K. K., & Stevens-Lapsley, J. E. (2015). Rethinking hospital-associated deconditioning: proposed paradigm shift. Physical Therapy, 95(9), 1307-1315.

Gentil, P., Steele, J., & Fisher, J. (2017). Why intensity is not a bad word–Benefits and practical aspects of high effort resistance training to the older. Clinical Nutrition.

Hautala, A., Richards, M., Takahashi, T., Tulppo, M., & Hills, A. (2016). Strength training in physical therapy. Physiotherapy, 102(1), 5-6.

Keogh, J. W., & Winwood, P. W. (2017). The epidemiology of injuries across the weight-training sports. Sports Medicine, 47(3), 479-501.

Koopman, R., & van Loon, L. J. (2009). Aging, exercise, and muscle protein metabolism. Journal of Applied Physiology, 106(6), 2040-2048.

Kortebein, P. (2009). Rehabilitation for hospital-associated deconditioning. American journal of physical medicine & rehabilitation, 88(1), 66-77.

Kraschnewski, J. L., Sciamanna, C. N., Poger, J. M., Rovniak, L. S., Lehman, E. B., Cooper, A. B., . . . Ciccolo, J. T. (2016). Is strength training associated with mortality benefits? A 15year cohort study of US older adults. Preventive medicine, 87, 121-127.

Lafont, C., Gérard, S., Voisin, T., Pahor, M., & Vellas, B. (2011). Reducing “iatrogenic disability” in the hospitalized frail elderly. The journal of nutrition, health & aging, 15(8), 645-660.

Leong, D. P., Teo, K. K., Rangarajan, S., Lopez-Jaramillo, P., Avezum, A., Orlandini, A., . . . Kelishadi, R. (2015). Prognostic value of grip strength: findings from the Prospective Urban Rural Epidemiology (PURE) study. The Lancet, 386(9990), 266-273.

Morley, J. E., Anker, S. D., & von Haehling, S. (2014). Prevalence, incidence, and clinical impact of sarcopenia: facts, numbers, and epidemiology—update 2014. Journal of cachexia, sarcopenia and muscle, 5(4), 253-259.

Rippetoe, M., Kilgore, L., & Bradford, S. E. (2006). Practical Programming for Strength Training (Vol. 222): Aasgaard Company.

Seynnes, O., Fiatarone Singh, M. A., Hue, O., Pras, P., Legros, P., & Bernard, P. L. (2004). Physiological and functional responses to low-moderate versus high-intensity progressive resistance training in frail elders. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 59(5), M503-M509.

Theou, O., Stathokostas, L., Roland, K. P., Jakobi, J. M., Patterson, C., Vandervoort, A. A., & Jones, G. R. (2011). The effectiveness of exercise interventions for the management of frailty: a systematic review. Journal of aging research, 2011.

Vashi, A. A., Fox, J. P., Carr, B. G., D’Onofrio, G., Pines, J. M., Ross, J. S., & Gross, C. P. (2013). Use of hospital-based acute care among patients recently discharged from the hospital. JAMA, 309(4), 364-371.

Circumventing biceps rupture in the deadlift

Though a relatively rare injury, there appears to be a non-trivial number of social media videos showcasing distal biceps brachii tendon ruptures (DBBTR).

No injury is absolutely ‘preventable’ but the likelihood of incurring something as unfortunate as a DBBTR can be reduced significantly with programming and biomechanical considerations.

Pre-disposing factors to DBBTR:

-Conventional deadlift

-Mixed grip (with most tears occurring in the left bicep)

-Eccentrically loaded elbow extension

DBBTR almost exclusively occurs when a mixed grip is employed. The supinated bicep must brook a greater internal moment than the contralateral, pronated arm, and there is higher margin for eccentric bicep loading; especially when the deadlift is initiated with an excessive degree of elbow flexion. 

Given the mechanism of injury, reducing its incidence altogether may be achieved with a hook grip and/or a double overhand grip. These have their own limitations though, with hook grip imposing a huge amount of stress and often pain on the thumb (not to mention its susceptibility to osteoarthritis), and double overhand typically not allowing a strength trainee to lift maximal loads. The mixed grip is slightly more risky with regard to DBBTR, but the documented incidence is still a mere 3% of all biceps injuries. *For the sake of this short article, deadlifting with straps will not be expounded.

The mixed grip for maximal deadlift attempts is worthwhile for the reward, and there are notable strategies one can implement to innoculate the distal biceps tendon from rupture:

  1. Awareness of proper latissimus dorsi (lat) engagement from the floor, when initiating the conventional deadlift. The DBBTR is observed when the bicep tendon cannot withstand the eccentric load of a heavy deadlift, so we need to commence the pull with maximal lat engagement  and minimal elbow flexion (cue “long arms”). If commencing the pull with even a few superfluous degrees of elbow flexion, this represents heightened mechanical demand on the bicep. On the other hand, conceptualising the barbell as an extension of both arms (and particularly the supinated arm), the arms will remain securely taut and enable a biomechanically efficient deadlift. The DBBTR tends to occur in the second half of the deadlift, when the lifter is exerting effort to extend the hips and trunk – it is during this portion that a mildly flexed bicep naturally succumbs to fall extended, while the body stands erect and joints stack in alignment

2. Chin-ups and pull-ups with a controlled eccentric phase, employing full range of motion (ROM). Staple movement aside, chin-ups are a terrific prophylactic exercise for DBBTR because they build specific load capacity in the distal biceps tendon. And when one progresses to weighted chin-ups with external load added, while retaining tempo eccentric and full ROM, the biceps tendons acquire kevlar-like tensile strength.

Don’t let the fear of a DBBTR pose a deterrent from either conventional deadlifts or mixed grip, but do pay heed to the above suggestions. After all, a few sets of heavy conventional deadlifts is more effective than the average person’s entire month of training. King of the lifts.

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 ‘Perfect’ Regime – Minimalism Wins

Admittedly, I used to identify with the ‘biohacking’ movement. This was circa 2013/2014 when I was just embarking on a journey to restore my health. After years of over-training, the product of running intensively in a chronically underfed state, I was desperate to discover some promising means to ‘hacking’ my way back to health. Alas, I was engrossed by the minutiae and became somewhat dogmatic when questioned about my unorthodox practices.

‘Biohacking’ is a term formulated by a specific crowd of health and fitness enthusiasts, and denotes the practice of modulating one’s own biology to engender greater longevity, wellness and even performance. It is a movement that has evidently grown in popularity, as seen on social media, and can be lauded for its intention to innovate novel ways of improving health.

However, in an increasingly morbid and fat developed world, the vast majority of us do not benefit from scientifically ambiguous strategies. In fact, I would argue that to succumb to the allure of ‘biohacking’ is to impose on ourselves an additional barrier to sustainable health and wellness. It is merely another distraction, masquerading as a productive pursuit to expedite one’s  goals.

Personally, and empirically, progress is positively correlated with minimalism. In all domains of life but, in the context of this article, health and fitness. Fatiguing our mental-processing and decision-making faculties on trifles consequentially diminishes the time and effort we can devote to the fundamentals. Concerning one’s self with ‘biohacking’ before mastering the basics is like obsessing over which ETF to invest in before earning an income.

We must humble ourselves to the admission that mastering the basics is a lifelong journey, and one that is intrinsically rewarding. As with anything meaningful, ‘hacking’ our way to accelerate its attainment is usually implausible and always unfulfilling.

With diet, minimising the choices of foods and consistently consuming moderate-to-high protein makes the process so much more effortless. The truth is, you don’t need to “eat a rainbow” of colours every day to get in all the micronutrients you need. Most wholefoods already possess a wide spectrum of macro- and micro-nutrients that cover your bases. Think potatoes, spinach, eggs, fatty fish etc.

So while there’s purported advancements in discovering the ‘ultimate’ nutrition regime for long-term healthy bodyweight and composition, there’s little progress made in the way of sustaining human behaviour. Deliberating over an excessive variety of food choices daily weakens our resolve to commit to the habit, consumes precious time, and often insults the hip pocket.

Dopamine is generally considered the ‘pleasure’ hormone, but the reality is that it flourishes on novelty. When we anticipate new experiences, new foods, new sensations – and satisfy them – dopamine is downregulated and requires further novelty. Hence, over-eating is as normal as Covid-19 now.

Variety is not the spice of life. Nor is it an efficient path to success.

The same can be said for training. From physiotherapists conflating strength training with ‘functional’ activities, to the recreational gym-goer ‘confusing’ their muscles with constant exercise variety. The only confusion lies in what goal they are striving for, because science and logic most certainly don’t consider this best practice.

My purpose isn’t to deride people’s training regimes. Witnessing proactivity when it comes to health is fantastic, and I commend anyone performing exercise.

I do want people to fully reap the rewards of their time and effort, though.  Because unless you’re a health or fitness professional, you don’t want to be spending perverse amounts of time in the gym, scoping research, questioning best practices; that isn’t your job. That is my job.

And one is deluding one’s self if achieving the greatest results with the least amount of time and effort isn’t the ultimate goal.

I want to inculcate to the masses that the basics are indeed sexy, and progress will escalate exponentially the more simplified your regime becomes. Because when there are only a select number of movements to perform, or foods to eat, or meals to consume, or goals in mind (notwithstanding ambitious ones)… We have no choice but to make it count.

Be a minimalist, and strive towards mastery the old-fashioned way.

On Cultivating One’s Own Garden First

18th century philosopher, Voltaire, famously asseverated that “one must cultivate one’s own garden”. I am not a gardener, though I do appreciate the aesthetic of a verdant landscape, but this metaphor is increasingly apt for all of us in modern society.

Largely because of technological advancements we are able to scope the affairs of any location in the world at any given time. We can swiftly gain a thorough sense of what our distant acquaintances are up to via our commonly superfluous social media networks. We can speculate on business rivals’ visions. We can compare our physiques and training regimes to ‘influencers’ on Instagram. And so on and so forth.

In short, and with our smartphones invariably tethered to our hands, we are constantly tending to the gardens of others. While our own backyard burgeons with weeds.

And our plants, perhaps symbolic of the meaningful pillars in our individual lives, wilt from neglect.

Even the most headstrong of us succumb to the ineluctable perils of modern technology. The algorithms that drive traffic to and within social media platforms are constantly being refined, and individualised based on tracked personal activity, to become even more addictive.

With greater addiction to our devices comes greater use, plunging us further into a fearful state of missing out (‘FOMO’)… At the expense of our immediate environments, our direct eco-system, our own garden. Perpetual consumption of extraneous content quickly becomes a black hole that clouds our own sense of self, our unique viewpoint of the world; stymieing the unvarnished individuality we are all born into.

Life satisfaction and fulfilment derived from that with which we engage in, is intrinsically linked to the depth of agency we wield over our lives. In other words, the greater the sense of control we perceive ourselves to have the more likely we are to be happy. We have little to no control over the affairs of others, and yet we spend perverse amounts of time scrolling through such every day.  Distracting ourselves from our own reality, and immediate sphere of influence.

Former American President Theodore Roosevelt averred that “comparison is the thief of joy”. There is profound truth to this quote, and it complements what has already been said above. However, it carries most relevance for the aspiration of success. For authentic success is an inalienable manifestation that is born from intrinsic motives, and attained on one’s own terms. However, It seems that a vast majority of us today are quantifying and qualifying markers of success on extrinsic motives, and arriving at goals that are fuelled by the approbation of others. This pervades the fitness domain, particularly; a domain typified by egocentricity and vanity – traits governed by interpersonal influences.

In this realm, if one isn’t comparing oneself with another’s profile or posts, one is often posting to elicit validation from others more so than to derive fulfilment from the workmanship itself; the process culminating in the ‘art’. When our decisions are governed by the opinions of others, we lose respect for ourselves and become hard-pressed to extract meaning from our pursuits.

Venturing too far and too frequently from one’s own garden can easily degrade one’s otherwise remarkable life, induce anxiety, stir up insanity by way of self-delusions, and rob us of the privilege it is to be a human being. On the other hand, muffling the ubiquitous noise in a distracting world, to cultivate skills and a sense of individuality that we can be proud of, is a healthy means to not only retain sanity, but also to exert a positive influence over the environment and relationships that truly matter to us. Our nuclear sphere. Not the great digital nowhere.

First, you must cultivate your own garden.

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.

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.