Body-shaming – or fat-shaming – is a relatively new term; it means ‘the action or practice of humiliating someone by making mocking or critical comments about their body shape or size’ (Oxford Dictionaries).

Before we get into the nitty-gritty of what my opinion on the subject is, let have a look at some figures:


  1. In 2014, more than 1.9 billion adults, 18 years and older, were overweight. Of these, over 600 million were obese (WHO Obesity Fact Sheet, Updated Oct., 2017)
  2. Going by current trends, by 2025, 2.7 billion adults will be obese (World Obesity Day, 2017)
  3. At the end of the same year, 41 million children under the age of 5, were overweight or obese (WHO Obesity Fact Sheet, Update Oct., 2017)
  4. According to projections, 70 million kids in the pre-school age will be overweight by obese by the year 2025 (Commission on Ending Childhood Obesity (ECHO), WHO, 2017)
  5. ‘The annual global medical bill for treating the consequences of obesity is expected to reach US$1.2 trillion per year by 2025’ (World Obesity Day, 2017)


Compared with adults with normal weight, overweight-obesity are significantly associated with diabetes, high blood pressure, high cholesterol, asthma, arthritis, and poor health status. (Mokdad et al. 2003). Almost all modern non-communicable disease (NCDs), otherwise known as metabolic disorders (including cancer) are either associated with or show a strong causal relationship with obesity or overweight (Lumeng and Saltiel 2011).

Overweight-obese children and adolescents exhibit an earlier onset and raised risk of metabolic diseases such as type 2 diabetes, throughout life (Abarca-Gómez et al. 2017).


Having gotten all the technicalities out of the way; my point is that those who have worked in the field of obesity prevention and reversal will tell you that living a better and wholesome life involves being healthy and feeling good about oneself. Sorry to break your heart, but all of these things are connected. And, no matter what people say, you can’t feel good with a big belly. And for good reason – because obesity is a disease with all manner of inflammation (chronic, systemic) going on inside of you.

Given that being fat is sure to impact your life in a negative manner, I find it amusing that bloggers these days, instead of inspiring people to raise the proverbial bar (in effect, ‘body-shame’ themselves), tell people to ‘get comfortable in their own skin’. Statements like ‘you look great, the way you are’ or ‘it’s OK to be a plus size’ or ‘its OK to have a belly’, in support of people who have overweight-obesity-metabolic disease problems is like effectively supporting lifestyle diseases. Why would you do that? After all, you don’t support people having addictions or a criminal mindset, do you? You’d want them to change, wouldn’t you?

In my years of experience in the field of obesity, I’ve noticed that overweight-obese people tend to relax the moment they get some support from somewhere. And, that’s why I have a big problem with these ‘anti-body-shaming’ and ‘pro-plus-size model’ crusaders. Fair enough, it is wrong to body-shame others; I wouldn’t want people to body shame others. But I do believe, everyone should be incessantly body-shaming themselves (without being depressed about it, though). Not being happy with your own self, is the surest way to keep improving!


More often, we are not critical enough of our own problems. Hell, if you look at the different stages of change, 80% of us rarely ever do anything about the problems we face in life – a whopping 40% of us don’t even realise there’s a problem, let alone institute changes!

Stages of Change


Being overweight or obese is not healthy. Don’t let anyone convince you otherwise, don’t let anyone tell you that it is OK to be a ‘plus size’ and never let anyone convince you it is OK to have a belly. Because, no it isn’t.

Weight, health-fitness, looks, being happy and excited about your own self and a productive, wholesome life are inherently interconnected.  Don’t wait till someone body-shames you (and even, if they do, take the criticism constructively); you should be body-shaming yourself. You should raise the bar high, and want the best for you.

PS: I wish, people – especially, the ones having a large fan-following – stopped spreading utter nonsense like ‘it’s OK to have a belly’. If you aren’t well-versed with the subject, please refrain from writing about it.

For enquiries on how to effectively treat-reverse or reduce the risk of overweight-obesity-metabolic diseases, please feel free to get in touch with me.

Women's Health Services

Men's Health Services


Abarca-Gómez, Leandra, Ziad A Abdeen, Zargar Abdul Hamid, Niveen M Abu-Rmeileh, Benjamin Acosta-Cazares, Cecilia Acuin, Robert J Adams, et al. 2017. “Worldwide Trends in Body-Mass Index, Underweight, Overweight, and Obesity from 1975 to 2016: A Pooled Analysis of 2416 Population-Based Measurement Studies in 128·9 Million Children, Adolescents, and Adults.” The Lancet 0 (0): 1–16. doi:10.1016/S0140-6736(17)32129-3.

Lumeng, Carey N., and Alan R. Saltiel. 2011. “Inflammatory Links between Obesity and Metabolic Disease.” Journal of Clinical Investigation. doi:10.1172/JCI57132.

Mokdad, Ali H, Earl S Ford, Barbara A Bowman, William H Dietz, Frank Vinicor, Virginia S Bales, and James S Marks. 2003. “Prevalence of Obesity, Diabetes, and Obesity-Related Health Risk Factors, 2001.” JAMA : The Journal of the American Medical Association 289 (1): 76–79. doi:10.1001/jama.289.1.76.

WHO. 2011. “WHO Fact Sheet, Updated Oct., 2017.” WHO Fact Sheet, Updated October, 2017.

WHO. 2016. “Report of the Commission on Ending Childhood Obesity.” WHO. doi:ISBN 978 92 4 151006 6.




‘When the dust settles, you will have known that it was always about ageing well, not just about how fit and strong you were when young… Step back, have a look and never lose sight of the bigger picture!’

– Dr. Deepak S. Hiwale
For more quotes from me, connect with me on ‘Good Reads’ here: https://www.goodreads.com/user/show/47384828-dr-deepak-hiwale

cal_supps_blog1Owing to the incessant advertising from calcium supplements-manufacturing companies, the elderly are often encouraged and coaxed into self-prescribing calcium supplements, in the belief that calcium supplements are good for their health. Traditionally, supplemental calcium has been claimed to be effective for the prevention and management of osteoporosis and fractures. Over the last couple of decades, the prescription and use of calcium supplementation has risen sharply (Tankeu et al. 2017). But is there any proof that calcium supplements work? And, is this exponential rise in the use of calcium pills warranted?

Let us dig a little deeper to know the truth.


A cursory look at the literature immediately throws up the lack of conclusive evidence for the effectiveness of calcium supplements. As if that weren’t enough, use of calcium supplements seem to be strongly associated with cardiovascular events and the risk of death due to cardiovascular or other causes.

The rationale of prescribing calcium supplements, for whatever purpose, especially in the elderly population (already at risk of cardiovascular disease), therefore seems to be quite questionable.


Although there is consensus that calcium intake is crucial for bone health and other physiological functions, the source of calcium intake and quantity remains controversial. While increasing calcium intake through food is both beneficial and safe, acquiring calcium through supplements and pills seems to be neither beneficial nor safe!

cal_supps_blog2It is a popular belief, amongst doctors and lay people, that calcium supplementation is crucial for prevention of osteoporosis – especially, in the elderly in the absence of adequate dietary intake. However, scientific evidence in support of such a ‘belief’ is flimsy, to say the least.

The NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis and Therapy said in 2001 that ‘adequate calcium and vitamin D intake is crucial to develop optimal peak bone mass and to preserve bone mass throughout life, supplementation (with these 2 nutrients) may be NECESSARY in persons not achieving dietary intake’ (NIH 2001). However, this was later challenged by meta-analysis studies which reported results to the contrary – calcium supplementation did not provide any benefit for hip or lumbar bone mineral density and therefore, did not translate into reduced lumbar or hip fracture risk (Bolland et al. 2008; Anderson et al. 2016).

The authors of a meta-analysis study of prospective cohort studies and randomized-controlled trials concluded quite emphatically that calcium supplementation was not beneficial for reduction of fracture risk (Bischoff-ferrari et al. 2007).


A major health concern of calcium supplementation is the associated cardiovascular disease (CVD) risks; ‘a rising body of evidence’ seems to suggest just such a strong association (Tankeu et al. 2017). Calcium supplementation induced progression of atherosclerosis is often suspected as underlying the association between calcium intake and CVD risk (Anderson et al. 2016).

Calcium supplementation – especially in high doses – may increase the risk of non-skeletal adverse effects: cardiovascular and other (Bolland et al. 2013; Anderson et al. 2016; Favus 2011):

  1. Atherosclerosis (formation of atheromatous plagues within arteries),
  2. Myocardial infarction (heart attack),
  3. Stroke (paralysis), and
  4. Non-cardiovascular adverse effects like development of renal calculi (kidney stones)

Calcium supplementation also increases the risk of all-cause mortality (early death due to any reason) (Anderson et al. 2016; Bolland et al. 2013; Michaelsson et al. 2013)! A Swedish study concluded that ‘high intake of calcium is women are associated with higher death rates from all causes and cardiovascular disease’(Michaelsson et al. 2013). Calcium supplements increased heart attack risk by 31%, risk of stroke by 20% and all cause-mortality by 9%, reported a large meta-analysis study of 12,000 patients (Bolland et al. 2010)!

There is ‘consistent evidence from 13 randomised placebo controlled trials involving about 29,000 participants and about 14,000 incident cases of myocardial infractions and strokes’ that calcium supplements (either take alone or in combination with vitamin D) do increase the risk of cardiovascular risks (Bolland et al. 2011).


Several studies have demonstrated a direct – almost causal relationship – between calcium intake and BP reduction (Dickinson et al. 2006; Cormick et al. 2015). Calcium supplementation has also been shown to be of benefit in pregnancy-induced hypertension (PIH), especially pre-eclampsia (Higgins & Green S 2011).

No one knows why and how calcium intake reduces blood pressure (BP). However, almost everyone agrees that since calcium intake affects vitamin D and parathyroid hormones levels. Low levels of calcium intake may lead to increased compensatory release of vitamin D and parathyroid hormone. Increased vitamin D and parathyroid hormone, in turn, increase reactivity of vascular smooth muscle (muscle of the arteries) which raises peripheral resistance and therefore, BP (Cormick et al. 2015; Paziana & Pazianas 2015; Webb 2003).

Raised BP, therefore, seems to be an indirect effect of low calcium levels (owing to low intake) in an individual (Tankeu et al. 2017; Heaney 2006).

Having said that, the above remains a hypothesis and has not been proven conclusively (Tankeu et al. 2017).


Although much of the literature agrees that calcium intake is crucial for bone health and other physiological functions, the source of calcium intake and quantity remains controversial. While calcium supplementation increases the risk of cardiovascular and other adverse effects, dietary calcium intake (through foods) seems to be safe (Xiao et al. 2013; Bolland et al. 2013).

Researchers are of the opinion that people who partake higher doses of calcium supplements to make up for the daily requirement of calcium, are at the greatest risk of coronary atherosclerosis than the ones that get much of their calcium from food sources. On the other hand, those who increase calcium intake through ingestion of calcium-rich foods exhibit a decreased risk of atherosclerosis and therefore, heart attacks or strokes (Anderson et al. 2016).


As opposed to calcium-rich foods, calcium supplements increase the risk of incident CAC (coronary artery calcification, a measure of calcium content in the coronary arteries – higher the CAC score, higher the risk of a heart attack). Also, it is often suggested that calcium supplementation causes a more rapid rise in serum calcium levels, which causes a hypercoagulable state (blood thickens and is more likely to coagulate and contribute to plague formation) (Leifsson & Ahren 1996). This hypercoagulable state increases the risk of cardiovascular mortality (Reid et al. 2011).


As if calcium supplementation itself wasn’t bad enough, many people resort to taking high doses of calcium supplements. A tablet of calcium typically contains 500 to 650mg of calcium. Typically, users resort to popping in a couple of pills or more, thinking ‘more is better’. This is not only wrong but harmful because higher doses increase the health risks.

In a large study of 60,000 plus Swedish women, who were followed up for a median 19 years, it was found that women who took higher doses (1400mg/day and above) – compared to those who stuck to 600-1000 mg/day  were associated with higher rates of cardiovascular diseases and death from all causes (Michaelsson et al. 2013). Another group of researchers reported increased risk of cardiovascular events with a dose of more than 800mg/day (Bolland et al. 2010). Chung et al. have also challenged the ‘more is better’ strategy of calcium supplementation; their study found that a dose of more than 1000 mg/day did elevate the risk for CVD and CVD mortality. The equivalent risk-elevating dose for men was found to be 1500mg/day (Chung et al. 2016).

Taking such grave cardiovascular and mortality risks into consideration, Bolland et al. were of the opinion that any benefits of low-dose calcium supplements for bone health are far outweighed by the high cardiovascular risks (Bolland et al. 2008).



Currently, there’s very little evidence that calcium supplementation, especially over and above the daily recommended allowances, is beneficial for osteoporosis or fracture risk. Given that calcium supplementation does not do what it is supposed to be doing but, on the contrary, increases health risks, the argument in favour of taking calcium pills, at this point in time – for whatever reason – is not a very strong one.

Blanket prescribing (by doctors) of calcium supplements for prevention and treatment of osteoporosis and reduction of fracture risks, especially in the elderly (already) at risk of cardiovascular events, should therefore be STRONGLY DISCOURAGED.

If you indulge in self-prescription of calcium supplements, you need to be wary of the adverse effects.

Calcium-rich foods are an effective and a safe way to increase calcium intake and should always be preferred over calcium supplements.


  1. Calcium supplements are both useless and harmful, especially in high doses
  2. Any benefits of low-dose calcium supplements for bone health are far outweighed by the high cardiovascular risks
  3. Calcium from food sources is both beneficial and harmless





Anderson, J.J.B. et al., 2016. Calcium intake from diet and supplements and the risk of coronary artery calcification and its progression among older adults: 10-year follow-up of the multi-ethnic study of atherosclerosis (MESA). Journal of the American Heart Association, 5(10), pp.1–14.

Bischoff-ferrari, H.A. et al., 2007. Calcium intake and hip fracture risk in men and women : a meta- analysis of prospective cohort studies and randomized controlled. , pp.1780–1790.

Bolland, M.J., Grey, A. & Reid, I.R., 2013. Calcium supplements and cardiovascular risk: 5 years on. Therapeutic Advances in Drug Safety, 4(5), pp.199–210. Available at: http://journals.sagepub.com/doi/10.1177/2042098613499790.

Bolland, M.J. et al., 2010. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. Bmj, 341(jul29 1), pp.c3691–c3691. Available at: http://www.bmj.com/cgi/doi/10.1136/bmj.c3691.

Bolland, M.J. et al., 2008. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Bmj, 336(7638), pp.262–266. Available at: http://www.bmj.com/cgi/doi/10.1136/bmj.39440.525752.BE.

Bolland, M.J. et al., 2011. Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis. Bmj, 342(apr19 1), pp.d2040–d2040. Available at: http://www.bmj.com/cgi/doi/10.1136/bmj.d2040.

Chung, M. et al., 2016. Calcium intake and cardiovascular disease risk: An updated systematic review and meta-analysis. Annals of Internal Medicine, 165(12), pp.856–866.

Collaboration, T.C., Cochrane Database of Systematic Reviews: Protocols. In Chichester, UK: John Wiley & Sons, Ltd.

Cormick, G. et al., 2015. Calcium supplementation for prevention of primary hypertension. Cochrane Database of Systematic Reviews, (6). Available at: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD010037.pub2/abstract.

Dickinson, H.O. et al., 2006. Calcium supplementation for the management of primary hypertension in adults. Cochrane Database Syst Rev, (1469–493X (Electronic)), p.CD004639.

Favus, M.J., 2011. The risk of kidney stone formation : the form of calcium matters 1 – 3. Am J Clin Nutr, 94, pp.5–6.

Heaney, R.P., 2006. Calcium intake and disease prevention TT  – Ingesta de cálcio e prevenção de doença. Arq Bras Endocrinol Metabol, 50(4), pp.685–693. Available at: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302006000400014.

Higgins, J. & Green S, (editors), 2011. Cochrane Handbook for Systematic Reviews of Interventions, Available at: http://www.cochrane-handbook.org.

Leifsson, B.G. & Ahren, B., 1996. Serum calcium and survival in a large health screening program. J Clin Endocrinol Metab, 81(6), pp.2149–2153. Available at: http://www.ncbi.nlm.nih.gov/pubmed/8964843.

Michaelsson, K. et al., 2013. Long term calcium intake and rates of all cause and cardiovascular mortality: community based prospective longitudinal cohort study. Bmj, 346(feb12 4), pp.f228–f228. Available at: http://www.bmj.com/cgi/doi/10.1136/bmj.f228.

NIH, 2001. Osteoporosis prevention, diagnosis, and therapy. JAMA, 285, pp.785–795.

Paziana, K. & Pazianas, M., 2015. Calcium supplements controversy in osteoporosis: a physiological mechanism supporting cardiovascular adverse effects. Endocrine, 48(3), pp.776–778.

Reid, I.R. et al., 2011. Cardiovascular effects of calcium supplementation. Osteoporos Int, 22(6), pp.1649–1658.

Tankeu, A.T., Ndip Agbor, V. & Noubiap, J.J., 2017. Calcium supplementation and cardiovascular risk: A rising concern. Journal of Clinical Hypertension, 19(6), pp.640–646.

Webb, R.C., 2003. Smooth muscle contraction and relaxation. Advances in physiology education, 27(1–4), pp.201–6. Available at: http://www.ncbi.nlm.nih.gov/pubmed/14627618.

Xiao, Q. et al., 2013. Dietary and supplemental calcium intake and cardiovascular disease mortality: the National Institutes of Health-AARP diet and health study. JAMA internal medicine, 173(8), pp.639–46. Available at: /pmc/articles/PMC3756477/?report=abstract.


Each day, Apollo’s fiery chariot makes its way across the sky, bringing life-giving light to the planet. For the ancient Greeks and Romans, Apollo was the god of medicine and healing as well as of sun and light—but Apollo could bring sickness as well as cure. Today’s scientists have come to a similarly dichotomous recognition that exposure to the ultraviolet radiation in sunlight has both beneficial (prevents obesity and metabolic disorders) and deleterious effects (sunburn, skin cancer) on human health

– M. Nathaniel Mead

Sunlight Oct 2017


As way back as the mid-1920s, Windaus et al. suggested that skin, when exposed to sunlight, produced the active form of vitamin D (D3) from a cholesterol precursor – 7-dehydrocholesterol (Holick, 2016).

Synthesis in the skin is the major source (up to 90%) of vitamin D in humans. Lack of appreciation that sun exposure is the major source, is the primary reason why vitamin D deficiency is now a worldwide epidemic! Very few foods contain enough vitamin D; foods fortified with vitamin D aren’t of much use either: often inadequate to satisfy even a child’s (let alone an adult’s) vitamin D requirement!


Vitamin D is a master hormone rather than just a vitamin per se – has multi-system functions. Few of these are:

  1. Calcium-bone metabolism, nerve impulse generation & conduction
  2. Functioning of the muscle, heart, pancreas and endocrine organs
  3. Strengthens immunity, fights infections including TB
  4. Plays a role in cancer prevention – lung, colon, and breast, to name a few


Vitamin D deficiency has a worldwide prevalence; it underpins the etiology of several chronic metabolic-endocrine disorders, including obesity. Experts define deficiency as 25(OH)-vitamin D blood levels of < 20 ng/mL; blood level of 25-hydroxyvitamin D of >75 nmol/L, or 30 ng/ml is required for optimal health.

  • Osteoporosis, and fractures
  • May increase risk of metabolic disease including obesity, diabetes, hypertension, and autoimmune diseases
  • Increases risk of infections – deficiency compromises functioning of immunity
  • Increases risk of cancers – those exposed to more sunlight during their lifetimes are less likely to die of cancers. Also, cancer-related death rates decline as one moves toward the lower latitudes (between 37°N and 37°S)


Obese individuals exhibit 35% greater prevalence of vitamin D deficiency compared to leaner ones. It is suspected obese individuals – owing to the social stigma attached with being obese – are more likely to reduce their exposure to sunlight, perform fewer outdoor activities and / or use clothes that cover much of the  body; this limits the exposure to sun and consequently, hampers cutaneous (skin) vitamin D synthesis.


  • Increased metabolic clearance of vitamin D possibly with enhanced uptake by fat tissue (vit. D is fat-soluble), leaving little in the plasma to do its job
  • Increased differentiation of pre-adipocytes (immature fat cells) into adipocytes (mature fat cells) capable of storing fat
  • Increased inflow of calcium into fat cells, leading to increased fat production
  • Increased secretion of parathyroid hormone, shown to be linked to obesity


80-90% of vitamin D present within the human body originates from skin synthesis where sunlight activation plays a key role; rest is supplied through food or supplementation (these sources pale in comparison to sunlight!).


In most humans, exposure to sunlight remains the major source. The recommendations for the avoidance of all sun exposure due to risk of skin cancer has put the world’s population at risk of vitamin D deficiency. 

coloured_lady_sunlight.jpgDaily solar exposure – to maintain physiologically effective serum levels – 15 minutes in summer and 20 minutes in early fall or late spring is recommended; coloured people require twice as long.

Interestingly, from November to March, in countries north of 37° latitude regions, no amount of solar exposure is sufficient!

In individuals who tend to burn easily / tan poorly, exposure to sun should not exceed 20 minutes per day ; exposure longer than 20 minutes does not further increase vitamin D synthesis but could increase risk of skin cancer!


Few foods contain vitamin D; foods fortified with vitamin D are also an alternative.

  • Fatty Fish: tuna, mackerel, salmon, sardines (and caviar), fish Oils: Cod liver oil
  • Eggs (yolk), milk, cheeses, fortified dairy products and orange juices
  • Mushrooms


Oral Vitamin D3 supplementation rather than solar exposure, should be used by fair-skinned, sun-sensitive individuals.

As mentioned earlier, blood level of 25-hydroxyvitamin D of >75 nmol/L, or 30 ng/ml is required for optimal health. In the absence of adequate sun exposure, supplementation with 800-1000 IU vitamin D/day is needed to achieve the above levels. Pharmaceutical form of vitamin D in the US is vitamin D2; in Canada, Europe, Japan and India, vitamin D3.


  1. Catherine Shore-lorenti et al, Clinical Endocrinology (2014) 81, 799-811
  2. Garland et al., Am J Public Health. 2006 Feb;96(2):252-61
  3. M. Nathaniel Mead, Environmental Health Perspectives. April 2008; 11(4)
  4. M. Pereira-Santos et al., Obesity Reviews. April 2015; 16(4):341–349
  5. Michael M. Holick, Anticancer Res. 2016 Mar;36(3):1345-56
  6. Michael F Holick and Tai C Chen, Am J Clin Nutr  2008;87(suppl): 1080S-6S.






It is generally believed that deep squats and ‘knees beyond toes’ increase the risk of lumbar spine and knee joint injury. ‘Sitting back into a chair’ and avoiding deep knee flexion, thus keeping the knees from moving past the toes in the bottom position, during a barbell squat, is usually recommended to minimize this risk. However, you’d be surprised to know that the opposite, in fact, seems to be true!


Jerry Gamallo,Based on biomechanical calculations, the highest retropatellar compressive forces are seen at 90°. With increasing flexion, the wrapping effect, functional adaptations & soft tissue contact between the back of thigh and calf contributes to an enhanced load distribution and enhanced force transfer with lower retropatellar compressive stresses.

Studies comparing joint kinetics between when forward displacement of the knees was restricted vs. not restricted found that restricting forward movement of the knees minimizes stress on knees, but forces are likely, inappropriately transferred to the hips & lower-back; proper joint loading may necessitate knees moving past your toes!


Squat deep; don’t worry about knees beyond toes.


1. Hartmann et al. Sports Med., 2013.

2. Fry et al. J Strength Cond Res., 2003.


To Jerry Gamallo of Venatõr Athletics, CA for allowing me to use his pictures.


This is more of a ‘stump article’; I have tried to keep it short and interesting. However, for those of you want more evidence, hold on to your horses – I will addressing this issue in more detail in the near future.



In recent years, in comparison to conventional aerobic endurance training (AET), resistance training (RT) is being touted as a superior method of weight loss. And most fitness experts seem to agree wholeheartedly. But, is this really true?

Delve a bit deeper into science and you realise that evidence for RT being a better weight-loss tool, is not all that strong and AET (and in some individuals, high-intensity, interval training – HIIT) may be better! This is especially true in women.

Interesting to note here that while RT has its own set of metabolic benefits, AET may still be better than RT at reducing risks of metabolic disorders too.


Resistance Training and Fat LossIt is a common (and, somewhat dogmatic) belief amongst exercisers, exercise-fitness professionals and clinicians that resistance or strength training (ST), in addition to improving your lean body mass (LBM), is the best way to burn more calories and therefore, lose weight as well.

And, this is how – they’ll tell ya – it (apparently) works:

  • RT or ST has the potential to increase your LBM, also called fat-free mass (FFM), including muscle mass – there is enough evidence to support this 1–4
  • Skeletal muscle is the most metabolically active tissue in the body – well, no! Its more complicated than that (see below)
  • Increase in muscle mass translates into more calories burned throughout the day, even when resting – evidence equivocal (see below)
  • Therefore, more muscle you carry, more is your resting metabolic rate (RMR) and more calories you burn throughout the day (increase in total daily energy expenditure (TDEE)
  • Increase in TDEE (with or without a nutritional calorific deficit) leads to weight loss


While all of the above sound good in theory, everything isn’t as cut and dry as they make it out to be.

Metabolic Rates of Organs and Tissues


  1. Skeletal muscle IS NOT the most metabolically active of the tissues in the body – your heart and the kidneys are! These organs have the highest metabolic rates, 2x those of the liver and the brain and a whopping 35x that of the skeletal muscle! 5 Having said that though, of all the tissues, skeletal muscle may indeed contribute significantly towards energy expended during the day. This is so because skeletal muscle wins on account of sheer mass – it weighs much more than all these other organs mentioned.
  2. Increased muscle mass does not bump up your metabolism to the point that it will burn additional calories which will translate into weight loss:
  • Previous studies examining the effects of RT on RMR have reported mixed results – both in men and women 2,3,6–15
  • Only older men (and not older women or younger men and women) show an elevated RMR in response to RT; most studies support this finding 2,3,6,10,11,13
  • In younger men & women and in older women, there seems to be a consistent lack of change in RMR in response to RT; the association between RT and rise in RMR all but disappears 7,8,12,14,15
  • Recent studies have shown mixed results too – with some showing an increase in RMR in response to RT; 16,17 others, a no change. 18,19 Interestingly, one study showed a fall in RMR in response to ‘dieting’, which could not be stopped by resistance training 20
  • A rare study that compared the effects of RT on RMR across various age groups, reported no changes in RMR in either young or older individuals! 12
  • A study by Lemmer et al. 17 reported some curious findings: RMR in response to RT is more affected by gender than age; men are more likely to benefit from RT than women, when younger and older men were pooled together, a significant increase in RMR with RT was shown, and younger and older women showed no effect on RMR in response to RT

In a nutshell, RT does not alter energy expenditure significantly outside of the exercise session and especially in younger men or in women across all age groups.


Misinterpretation of current ACSM and other guidelines 21–23 have led to the dogmatic belief amongst exercise-fitness professionals that RT has conclusively been proven to reduce body weight. In reality, a closer look at existing literature suggests that the evidence for RT as an effective tool for weight-loss remains equivocal, at best. 24–29

  • The ACSM guidelines on ‘strategies for weight loss and prevention of weight regain in adults’ states that, ‘research evidence does not support RT as effective for weight loss’ and points out that ‘the effects of RT for prevention of weight gain (after initial weight loss) are largely unknown’ 21
  • While few studies have observed some reduction in body fat with RT,30–32 others have found no effect on body fat % even when the intervention was continued for 12-52 weeks 33–35
  • Interestingly, one study found a gender-based differential effect of RT on body fat – reduction in body fat was observed in the group containing younger and older men pooled together but not in women. 17 This finding is not dissimilar to the findings from other studies that RT enhances RMR only in older men 7,8,12,14,15

There is, however, a need to mention here that although RT does not seem to contribute significantly to calorie expenditure outside of the exercise session or fat loss, it is associated with numerous health benefits – increased lean mass, improved work capacity and decreased chronic disease risk factors (sarcopenia), to name a few. 36,37


HIIT_blogHIIT, they will tell you, will not only burn calories during the workout but also increase your calorie expenditure through the rest of the day (through increased excess post-exercise oxygen consumption – EPOC). And, that will translate into weight loss.

EPOC or oxygen debt, as it used to be called previously, is the mechanism by which the body makes up for the oxygen deficit created during an exercise session by increasing oxygen consumption well after cessation of exercise – breathlessness you experience for a few minutes after you’ve climbed to the top of the stairs, is an example.

In reality, increase in EPOC after an HIIT session is modest (only 6-15% of your total energy expenditure). EPOC alone, therefore, may be insignificant for causing weight / fat loss. 38

Having said that, a study published in 2002 in the European Journal of Applied Physiology utilising circuit type of resistance training with relatively heavy weights and short rest periods generated EPOC which increased resting metabolic rate by 21% and 19% for 24 and 48 hours post- workout. As the authors content, if these numbers are applied to a typical 180-pound individual, it would amount to 773 calories expended over 2 days after cessation of the exercise session! 39 So, prima facie, it appears that HIIT does have benefits.

However, there are practical problems when implementing HIIT workout programs in overweight-obese / untrained individuals. It is difficult to achieve the high-intensity for a long enough duration required to elicit a high enough EPOC to be of any consequence for  increased calorie expenditure and therefore induce fat / weight loss. Furthermore, prescription of such complex methods of training – needing highly skilled movements – is likely to reduce exercise enjoyment and long-term adherence in novice and out-of-shape individuals.

In seasoned exercisers, however, HIIT and EPOC may be an effective way to bump up calorie burning and improve body composition.


Also known as ‘low-intensity, steady state’ (LISS) cardio or ‘long, slow distance’ (LSD) training, aerobic endurance training (AET) may just be the best tool out there, for most people when it comes to losing fat.

Researchers from the University of Pittsburgh, Pennsylvania, conducted a study comparing RT with AET in young women 40. The results will come as a surprise (for most)! Apparently, not only is AET better than RT at reducing body fat % but it also wins hands down when it comes to:

  • Improving cardiorespiratory fitness
  • Improving insulin sensitivity
  • Reducing visceral adipose tissue (fat surrounding organs)
  • Reducing abdominal fat, and
  • Reducing inter-muscular (within muscle) fat

Other studies have also supported the idea that AET may be better at reducing visceral and abdominal fat, not to mention, the overall body fat%.

  • A study published in Dec, 2012 reported that while AET and combined AET/RT exercise programs caused more weight loss than RT alone, AET/RT and RT resulted in increased lean mass. However, although requiring a double time commitment over AET alone, a combined AET/RT exercise program did not result in ‘significantly more weight loss over AET alone41
  • Another study published in the American Journal of Physiology – Endocrinology and Metabolism concluded that AET caused significant reductions in:
    1. Whole body fat including subcutaneous abdominal fat, visceral adipose tissue (VAT – fat around the organs, responsible for metabolic disorders) and liver fat content
    2. plasma liver enzymes, esp. alanine aminotransferase (enzyme reflecting the amount of liver damage), and
    3. HOMA (Homeostasis Model Assessment – a measure of the level of your steady state pancreatic beta cell function (%B) and insulin sensitivity (%S)

Resistance training, on the other hand, failed to significantly affect these variable 42

  • Owing to results like these, it shouldn’t come as a surprise that AET is recommended to be central to exercise programs for reducing body fat, especially VAT and its metabolic adverse effects – obesity and other metabolic disorders 43
  • Even in the absence of significant weight loss, AET may improve metabolic disease parameters, esp. in patients of type 2 diabetes 44


aerobic training in womenWhy do women prefer conventional AET?

As if the results of the studies mentioned above didn’t come as shocking enough for you, here’s something that is even more thought-provoking – something that might answer your question of why women tend to favour treadmills over free-weights!

It appears that AET is more effective in (overweight and obese, both young and older) women than in men 40. Furthermore, there is some evidence to suggest that women enjoy AET more than RT 45; the opposite seems to be true with young men – they seem to enjoy RT more.

My hunch is that women find AET more enjoyable because it is more effective for them! Not surprisingly then – call it nature or subconscious minds at work – there seems to be a very valid reason why you see more women heading to the treadmill rather than the ‘free-weights section’!


Abdominal obesity is a prominent risk factor for metabolic disease (type II diabetes, cardiovascular disease, etc.). 46 Results from the STRRIDE study suggest that AET was associated with significant reductions in VAT, a measure of abdominal obesity. 47,48 

The authors of the STRRIDE study are of the opinion that AET ‘resulted in significant decreases in visceral, subcutaneous, and total abdominal fat without changes in caloric intake’48 

Although in comparison to AET, it does not cause much difference in measures of fat tissue, RT does cause a significant reduction in CRP (C-reactive protein, a parameter, high levels of which, suggests a low-grade, chronic systemic inflammation with the potential to develop into cardiovascular disease and diabetes type II). 49 Interesting to note here that an inverse association seems to exist between aerobic fitness and chronic systemic inflammation.50,51  A sedentary lifestyle increases inflammatory markers. 49

Conflicting data exists over the superiority of AET over RT for the reduction of metabolic disease risk parameters (HbA1c, blood lipids including triglycerides and LDL particle size). Having said that, regular and long-term, moderate intensity exercise seems to increase HDL and lower triglycerides, even in the absence of weight loss. 52

Although RT has benefits of its own, a combination of AET and RT exercise regimen – although more effective at reducing the risk of metabolic disease than RT alone – were not significantly different from AET alone 53. This effectively suggests that the RT component may be contributing precious little (if at all) to the disease prevention effect of an AET-RT exercise program. However, it should not be ruled out that AET and RT may both be working synergistically to reduce the risk of metabolic diseases.


Of all the components of human daily energy expenditure (BMR, thermic energy of food, exercise-related activity thermogenesis (EAT) and non-exercise activity thermogenesis (NEAT)), NEAT is the most modifiable parameter and is capable of significantly pushing up your total daily energy expenditure (TDEE) than exercise sessions (!), even in intense exercisers 54.

Components of energy expenditure

Even very low-level physical activities like mastication (chewing) and fidgeting can increase energy expenditure by 20-40% above your resting metabolic rate!

NEAT includes energy expenditure of walking, talking, going for your job, sitting, toe-tapping, shopping, dancing, etc.


It is likely that AET (treadmill runs) may be more effective than RT – especially in overweight women – for reducing body fat and preventing metabolic diseases. Also,

  • RT seems to contribute very little (directly) towards fat loss
  • RT does not seem to contribute towards (metabolic) disease prevention or management as much as AET does
  • Combination of RT and AET does not seem to afford any more benefits over AET alone when weight loss or metabolic disease management is the prime goal


Looking at much of the evidence, the question that begs to be answered is: ‘what if we were all wrong about our weight-loss exercise strategies and indeed, about our obsession with the fat-burning abilities of resistance training? And, what if those women on treadmills were right all along?!

I reckon, it’s time we stopped ridiculing (or even downright laughing at) those men / women who hit the treadmill every single time they’re at the gym.


  • Resistance training may be contributing precious little towards calorie burning outside of exercise sessions and eventual weight loss!
  • HIIT in overweight – obese and untrained individuals HIIT may not be ideal; in seasoned exercisers, may lead to significant calorie expenditure both in and outside of the exercise sessions
  • Aerobic Endurance training seems to be the best tool for total body weight and fat reduction – needs to a be an integral part of almost every weight-loss program
  • Aerobic Endurance training wins hands down for metabolic disease management
  • Women do not seem to respond as well to resistance training, aerobic endurance training and HIIT may be better options
  • NEAT can contribute significantly to total daily energy expenditure – staying active through the day can really bump your calorific expenditure (probably more so than RT or AET)

PS: much of the above applies to those interested more in fat loss and metabolic disease prevention. If muscle mass accruing or maintenance is of importance, such as in ‘strength-power athletes, RT becomes indispensable. Point to take away is that you need to pay attention to a calorie deficit nutrition plan and indulge in aerobic training more often than not. This article does not ask you to away with resistance training. 



  1. Byrne HK, Wilmore JH. The relationship of mode and intensity of training on resting metabolic rate in women. Int J Sport Nutr Exerc Metab. 2001;11(1):1-14. doi:10.1017/CBO9781107415324.004.
  2. Campbell WW, Crim MC, Young VR, Evans WJ. Increased energy requirements and changes in body composition with resistance training in older adults. Am J Clin Nutr. 1994;60(2):167-175. http://www.ncbi.nlm.nih.gov/pubmed/8030593. Accessed October 12, 2016.
  3. Poehlman ET, Toth MJ, Ades PA, Calles-Escandon J. Gender differences in resting metabolic rate and noradrenaline kinetics in older individuals. Eur J Clin Invest. 1997;27(1):23-28. http://www.ncbi.nlm.nih.gov/pubmed/9041373. Accessed October 11, 2016.
  4. Washburn RA, Donnelly JE, Smith BK, Sullivan DK, Marquis J, Herrmann SD. Resistance training volume, energy balance and weight management: rationale and design of a 9 month trial. Contemp Clin Trials. 2012;33(4):749-758. doi:10.1016/j.cct.2012.03.002.
  5. Wang Z, Ying Z, Bosy-Westphal A, et al. Specific metabolic rates of major organs and tissues across adulthood: evaluation by mechanistic model of resting energy expenditure. Am J Clin Nutr. 2010;92(6):1369-1377. doi:10.3945/ajcn.2010.29885.
  6. Ballor DL, Harvey-Berino JR, Ades PA, Cryan J, Calles-Escandon J. Contrasting effects of resistance and aerobic training on body composition and metabolism after diet-induced weight loss. Metabolism. 1996;45(2):179-183. http://www.ncbi.nlm.nih.gov/pubmed/8596486. Accessed October 12, 2016.
  7. Broeder CE, Burrhus KA, Svanevik LS, Wilmore JH. The effects of either high-intensity resistance or endurance training on resting metabolic rate. Am J Clin Nutr. 1992;55(4):802-810. http://www.ncbi.nlm.nih.gov/pubmed/1550062. Accessed October 12, 2016.
  8. Cullinen K, Caldwell M. Weight training increases fat-free mass and strength in untrained young women. J Am Diet Assoc. 1998;98(4):414-418. doi:10.1016/S0002-8223(98)00094-7.
  9. Pratley R, Nicklas B, Rubin M, et al. Strength training increases resting metabolic rate and norepinephrine levels in healthy 50- to 65-yr-old men. J Appl Physiol. 1994;76(1):133-137. http://www.ncbi.nlm.nih.gov/pubmed/8175496. Accessed October 12, 2016.
  10. Ryan AS, Pratley RE, Elahi D, Goldberg AP. Resistive training increases fat-free mass and maintains RMR despite weight loss in postmenopausal women. J Appl Physiol. 1995;79(3):818-823. http://www.ncbi.nlm.nih.gov/pubmed/8567523. Accessed October 12, 2016.
  11. Taaffe DR, Pruitt L, Reim J, Butterfield G, Marcus R. Effect of sustained resistance training on basal metabolic rate in older women. J Am Geriatr Soc. 1995;43(5):465-471. http://www.ncbi.nlm.nih.gov/pubmed/7730525. Accessed October 12, 2016.
  12. Rall LC, Meydani SN, Kehayias JJ, Dawson-Hughes B, Roubenoff R. The effect of progressive resistance training in rheumatoid arthritis. Increased strength without changes in energy balance or body composition. Arthritis Rheum. 1996;39(3):415-426. http://www.ncbi.nlm.nih.gov/pubmed/8607890. Accessed October 12, 2016.
  13. Treuth MS, Hunter GR, Weinsier RL, Kell SH. Energy expenditure and substrate utilization in older women after strength training: 24-h calorimeter results. J Appl Physiol. 1995;78(6):2140-2146. http://www.ncbi.nlm.nih.gov/pubmed/7665410. Accessed October 12, 2016.
  14. Van Etten LM, Westerterp KR, Verstappen FT. Effect of weight-training on energy expenditure and substrate utilization during sleep. Med Sci Sports Exerc. 1995;27(2):188-193. http://www.ncbi.nlm.nih.gov/pubmed/7723641. Accessed October 12, 2016.
  15. Van Etten LM, Westerterp KR, Verstappen FT, Boon BJ, Saris WH. Effect of an 18-wk weight-training program on energy expenditure and physical activity. J Appl Physiol. 1997;82(1):298-304. http://www.ncbi.nlm.nih.gov/pubmed/9029230. Accessed October 12, 2016.
  16. Kirk EP, Donnelly JE, Smith BK, et al. Minimal resistance training improves daily energy expenditure and fat oxidation. Med Sci Sports Exerc. 2009;41(5):1122-1129. doi:10.1249/MSS.0b013e318193c64e.
  17. Lemmer JT, Ivey FM, Ryan AS, et al. Effect of strength training on resting metabolic rate and physical activity: age and gender comparisons. Med Sci Sports Exerc. 2001;33(4):532-541. http://www.ncbi.nlm.nih.gov/pubmed/11283427. Accessed October 11, 2016.
  18. Hunter GR, Byrne NM, Sirikul B, et al. Resistance training conserves fat-free mass and resting energy expenditure following weight loss. Obesity (Silver Spring). 2008;16(5):1045-1051. doi:10.1038/oby.2008.38.
  19. Meckling KA, Sherfey R. Randomized Trial of Hypocaloric, High-Protein Diet on Body Compo, Resting Metabolic Rate – meckling2007.pdf. Vol 32.; 2007:743-752. doi:10.1139/H07-059.
  20. Geliebter A, Maher MM, Gerace L, Gutin B, Heymsfield SB, Hashim SA. Effects of strength or aerobic training on body composition, resting metabolic rate, and peak oxygen consumption in obese dieting subjects. Am J Clin Nutr. 1997;66(3):557-563. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9280173.
  21. Donnelly JE, Blair SN, Jakicic JM, et al. American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc. 2009;41(2):459-471. doi:10.1249/MSS.0b013e3181949333.
  22. Pollock ML, Franklin BA, Balady GJ, et al. Resistance Exercise in Individuals With and Without Cardiovascular Disease. Circulation. 2000;101(7).
  23. Williams MA, Haskell WL, Ades PA, et al. Resistance Exercise in Individuals With and Without Cardiovascular Disease: 2007 Update. Circulation. 2007;116(5).
  24. Aldana SG, Greenlaw RL, Diehl HA, et al. Effects of an intensive diet and physical activity modification program on the health risks of adults. J Am Diet Assoc. 2005;105(3):371-381. doi:10.1016/j.jada.2004.12.007.
  25. Andersen RE, Wadden TA, Bartlett SJ, Zemel B, Verde TJ, Franckowiak SC. Effects of lifestyle activity vs structured aerobic exercise in obese women: a randomized trial. JAMA. 1999;281(4):335-340. http://www.ncbi.nlm.nih.gov/pubmed/9929086. Accessed October 11, 2016.
  26. Bravata DM, Smith-Spangler C, Sundaram V, et al. Using pedometers to increase physical activity and improve health: a systematic review. JAMA. 2007;298(19):2296-2304. doi:10.1001/jama.298.19.2296.
  27. Curioni CC, Lourenço PM. Long-term weight loss after diet and exercise: a systematic review. Int J Obes (Lond). 2005;29(10):1168-1174. doi:10.1038/sj.ijo.0803015.
  28. Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr. 1992;56(2):320-328. http://www.ncbi.nlm.nih.gov/pubmed/1386186. Accessed October 11, 2016.
  29. Delecluse C, Colman V, Roelants M, et al. Exercise programs for older men: mode and intensity to induce the highest possible health-related benefits. Prev Med (Baltim). 2004;39(4):823-833. doi:10.1016/j.ypmed.2004.03.023.
  30. Ferrara CM, Goldberg AP, Ortmeyer HK, Ryan AS. Effects of aerobic and resistive exercise training on glucose disposal and skeletal muscle metabolism in older men. J Gerontol A Biol Sci Med Sci. 2006;61(5):480-487. http://www.ncbi.nlm.nih.gov/pubmed/16720745. Accessed October 11, 2016.
  31. Olson TP, Dengel DR, Leon AS, Schmitz KH. Changes in inflammatory biomarkers following one-year of moderate resistance training in overweight women. Int J Obes (Lond). 2007;31(6):996-1003. doi:10.1038/sj.ijo.0803534.
  32. Polak J, Moro C, Klimcakova E, et al. Dynamic strength training improves insulin sensitivity and functional balance between adrenergic alpha 2A and beta pathways in subcutaneous adipose tissue of obese subjects. Diabetologia. 2005;48(12):2631-2640. doi:10.1007/s00125-005-0003-8.
  33. Hunter GR, Wetzstein CJ, Fields DA, Brown A, Bamman MM. Resistance training increases total energy expenditure and free-living physical activity in older adults. J Appl Physiol. 2000;89(3):977-984. http://www.ncbi.nlm.nih.gov/pubmed/10956341. Accessed October 11, 2016.
  34. Hunter GR, Bryan DR, Wetzstein CJ, Zuckerman PA, Bamman MM. Resistance training and intra-abdominal adipose tissue in older men and women. Med Sci Sports Exerc. 2002;34(6):1023-1028. http://www.ncbi.nlm.nih.gov/pubmed/12048332. Accessed October 11, 2016.
  35. Schmitz KH, Jensen MD, Kugler KC, Jeffery RW, Leon AS. Strength training for obesity prevention in midlife women. Int J Obes Relat Metab Disord. 2003;27(3):326-333. doi:10.1038/sj.ijo.0802198.
  36. Frontera WR, Meredith CN, O’Reilly KP, Knuttgen HG, Evans WJ. Strength conditioning in older men: skeletal muscle hypertrophy and improved function. J Appl Physiol. 1988;64(3):1038-1044. http://www.ncbi.nlm.nih.gov/pubmed/3366726. Accessed October 11, 2016.
  37. Hurley BF, Redmond RA, Pratley RE, Treuth MS, Rogers MA, Goldberg AP. Effects of strength training on muscle hypertrophy and muscle cell disruption in older men. Int J Sports Med. 1995;16(6):378-384. doi:10.1055/s-2007-973024.
  38. LaForgia J, Withers RT, Gore CJ. Effects of exercise intensity and duration on the excess post-exercise oxygen consumption. J Sports Sci. 2006;24(12):1247-1264. doi:10.1080/02640410600552064.
  39. Schuenke M, Mikat R, McBride J. Effect of an acute period of resistance exercise on excess post-exercise oxygen consumption: implications for body mass management. Eur J Appl Physiol. 2002;86(5):411-417. doi:10.1007/s00421-001-0568-y.
  40. Lee S, Deldin AR, White D, et al. Aerobic exercise but not resistance exercise reduces intrahepatic lipid content and visceral fat and improves insulin sensitivity in obese adolescent girls: a randomized controlled trial. Am J Physiol Endocrinol Metab. 2013;305(10):E1222-9. doi:10.1152/ajpendo.00285.2013.
  41. Willis LH, Slentz CA, Bateman LA, et al. Effects of aerobic and/or resistance training on body mass and fat mass in overweight or obese adults. J Appl Physiol. 2012;113(12):1831-1837. doi:10.1152/japplphysiol.01370.2011.
  42. Slentz CA, Bateman LA, Willis LH, et al. Effects of aerobic vs. resistance training on visceral and liver fat stores, liver enzymes, and insulin resistance by HOMA in overweight adults from STRRIDE AT/RT. Am J Physiol Endocrinol Metab. 2011;301(5):E1033-9. doi:10.1152/ajpendo.00291.2011.
  43. Ismail I, Keating SE, Baker MK, Johnson NA. A systematic review and meta-analysis of the effect of aerobic vs. resistance exercise training on visceral fat. Obes Rev. 2012;13(1):68-91. doi:10.1111/j.1467-789X.2011.00931.x.
  44. Kadoglou NPE, Iliadis F, Angelopoulou N, et al. The anti-inflammatory effects of exercise training in patients with type 2 diabetes mellitus. Eur J Cardiovasc Prev Rehabil. 2007;14(6):837-843. doi:10.1097/HJR.0b013e3282efaf50.
  45. Lee S, Bacha F, Hannon T, Kuk JL, Boesch C, Arslanian S. Effects of aerobic versus resistance exercise without caloric restriction on abdominal fat, intrahepatic lipid, and insulin sensitivity in obese adolescent boys: a randomized, controlled trial. Diabetes. 2012;61(11):2787-2795. doi:10.2337/db12-0214.
  46. Alberti KGMM, Zimmet P, Shaw J. Metabolic syndrome–a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabet Med. 2006;23(5):469-480. doi:10.1111/j.1464-5491.2006.01858.x.
  47. Strasser B. Physical activity in obesity and metabolic syndrome. Ann N Y Acad Sci. 2013;1281:141-159. doi:10.1111/j.1749-6632.2012.06785.x.
  48. Slentz CA, Aiken LB, Houmard JA, et al. Inactivity, exercise, and visceral fat. STRRIDE: a randomized, controlled study of exercise intensity and amount. J Appl Physiol. 2005;99(4).
  49. Donges CE, Duffield R, Drinkwater EJ. Effects of resistance or aerobic exercise training on interleukin-6, C-reactive protein, and body composition. Med Sci Sports Exerc. 2010;42(2):304-313. doi:10.1249/MSS.0b013e3181b117ca.
  50. Aronson D, Sheikh-Ahmad M, Avizohar O, et al. C-Reactive protein is inversely related to physical fitness in middle-aged subjects. Atherosclerosis. 2004;176(1):173-179. doi:10.1016/j.atherosclerosis.2004.04.025.
  51. Panagiotakos DB, Pitsavos C, Chrysohoou C, Kavouras S, Stefanadis C, ATTICA Study. The associations between leisure-time physical activity and inflammatory and coagulation markers related to cardiovascular disease: the ATTICA Study. Prev Med (Baltim). 2005;40(4):432-437. doi:10.1016/j.ypmed.2004.07.010.
  52. Carroll S, Dudfield M. What is the relationship between exercise and metabolic abnormalities? A review of the metabolic syndrome. Sports Med. 2004;34(6):371-418. http://www.ncbi.nlm.nih.gov/pubmed/15157122. Accessed October 18, 2016.
  53. Bateman LA, Slentz CA, Willis LH, et al. Comparison of aerobic versus resistance exercise training effects on metabolic syndrome (from the Studies of a Targeted Risk Reduction Intervention Through Defined Exercise – STRRIDE-AT/RT). Am J Cardiol. 2011;108(6):838-844. doi:10.1016/j.amjcard.2011.04.037.
  54. Levine JA. NEAT – Levine.pdf. Vol 62.; 2004:S82-97. http://www.ncbi.nlm.nih.gov/pubmed/15387473. Accessed October 16, 2016.

Historical Perspective

Believe it or not, gout – previously called ‘the disease of the kings’ or arthritis of the rich as opposed to rheumatism – arthritis of the poor! – was first described by the Egyptians (when it was known as podagra) in 2640 BC. It was later recognised by Hippocrates in the 5th century BC, who referred to it as ‘the unwalkable disease’ and went on to describe its presentation and disease course in striking detail – most of his clinical perceptions of the conditions are still as relevant today as they were 2,500 years ago (Nuki & Simkin, 2006; Star & Hochberg, 1993)! Talk about being ‘ahead of time’!

Modern day Prevalence of the Disease

In more recent times, gout and hyperuricemia (raised uric acid levels in blood), have shown a steady rise in prevalence and incidence (doubled), especially in the US (Choi, Atkinson, Karlson, Willett, & Curhan, 2004; Choi & Curhan, 2008; Roubenoff et al., 1991). Population studies have reported the incidence of gout in much of the developed world to range between 1-2% (Richette & Bardin, 2010); incidence of hyperuricemia may be as high as 15-20% (Doherty, 2009; Mikuls et al., 2005). Males are more likely to be affected – 80% of cases of gout in Northern Europe tended to be men (Annemans et al., 2008; Doherty, 2009). It is the commonest inflammatory arthritis in men (Choi et al., 2004; Choi & Curhan, 2008; Richette & Bardin, 2010; Roubenoff et al., 1991) and the most common inflammatory arthritis in older women (Doherty, 2009). Prevalence increases with age, in both sexes (Doherty, 2009; Star & Hochberg, 1993). Age and gender specificity of the condition explains the rarity of the conditioning in young, pre-menopausal women (Doherty, 2009; Wallace, Riedel, Joseph-Ridge, & Wortmann, 2004).

Natural Course of the Disease

Gout / gouty arthritis refers to an acute attack of inflammatory arthritis, provoked by the release of monosodium urate (MSU) crystals into joint spaces. Natural course of the disease (Doherty, 2009; Richette & Bardin, 2010, 2012; Wallace et al., 2004) is characterised by 3 distinct phases:

  1. Asymptomatic hyperuricemia (raised serum uric acid – sUA),
  2. Episodes of acute attacks, and
  3. Asymptomatic, inflammation/pain-free intervals and progression on to chronic gouty arthritis

Characteristic presentation of an acute attack is typically an inflamed base of (usually) the big toe (the first metatarsophalangeal – MTP – joint), with warmth, redness and pain. Rarely, other joints may also be involved.

Pathogenesis: The Conventional View

There is no denying that diet does play a crucial role in prevention and treatment of gout. Traditionally, hyperuricemia – resulting from an increased production of uric acid (due to increased purine breakdown after ingestion of purine-rich, animal-based, proteinaceous foods) has been suggested to be majorly causative of gout. In humans, uric acid is the final metabolite of both dietary and endogenously produced purine metabolism (Richette & Bardin, 2012). Sometime during the Miocene period, it is believed that human beings lost the ability to produce an enzyme called ‘uricase’ , which is normally responsible for converting the insoluble uric acid into highly soluble, allantoin (Doherty, 2009). When the accumulation of uric acid (98% of which is present in ionic form) crosses a saturation point, it combines with Na+ in the extracellular spaces and forms MSU crystals and precipitates into joint spaces leading to gout (Richette & Bardin, 2010, 2012). Not surprising then, that avoiding purine-rich foods – meats, poultry, fish, soy and non-soy legumes – with the aim of reducing sUA, is the standard dietary advice given and followed. Conventional pharmaceutical approach (urate lowering therapy – ULT), through the use of drugs like allopurinol, also aims to reduce sUA (Richette & Bardin, 2012). That said, there seem to be some major problems with this hypothesis at all levels:

  1. Although, high intake of purine-containing foods does indeed increase the risk of urate deposition, and increases up to five-fold, the risk of gout attack amongst known patients, how it does so, still remains a query (Zhang et al., 2012)
  2. Meat-eaters will typically have other confounding factors as well – a diet high in sugar, sweetened beverages, refined grains, processed meats and low ingestion of fruits and veggies, not to mention cigarette smoking and ingestion of alcohol (which itself increases uric acid levels – more on this later)
  3. Purine-rich vegetarian foods do not seem to increase the risk – it has been reported that dietary intake of soy and non-soy legumes reduces the risk of gout (Teng, Pan, Yuan, & Koh, 2015)
  4. In rare cases, gouty arthritis can develop in patients with no history of hyperuricemia (McCarty, 1994; Urano et al., 2002)
  5. It is not the sUA per se but the rapid dissolution of already formed urate deposits and precipitation of MSU crystals in the joint spaces is what triggers
    an acute attack of gout (Richette & Bardin, 2012) – attacks during the first few months of initiation of a ULT supports this notion
  6. Although mechanisms vary, other factors or conditions can also lead to an acute attack through lowering of urate levels: systemic inflammation, ingestion of whiskey and post-surgery. Alcohol intake is associated with both increased endogenous urate production (Bleyer & Hart, 2006) and rapid, transient decrease in sUA through its uricosuric (increased renal excretion of uric acid) actions
  7. Release of pro-inflammatory molecules, cytokines and interleukins (IL-6), which are a hallmarks of systemic inflammation, have been shown to stimulate the hypothalamo-pituitary-adrenocortical axis leading to release of cortisol (Dunn, 2000; Wang & Dunn, 1999). It is suggested that cortisol may be secreted through the same mechanism in gouty arthritis too. Cortisol has a uricosuric effect (McCarty, 1994) and thus, may contribute to an acute attack of gout
  8. 20-25% of asymptomatic patients with sUA exhibit MSU crystal deposits in their joints – especially the knees and the first MTP joint (Pineda et al., 2011; Puig et al., 2008; Richette & Bardin, 2012) and yet do not suffer from attacks of gout – suggesting that other factors must be at play
  9. There is ample evidence to suggest that genetic factors, obesity (especially, during early adulthood) and systemic inflammation contribute significantly to gout (Bleyer & Hart, 2006; Roubenoff et al., 1991; Teng et al., 2015; Urano et al., 2002). And, a serious discussion on these factors by the research community is long overdue.
  10. Genetic and other metabolic disorders (suggestive of systemic inflammation) occur concurrently with gout: obesity, diabetes, chronic renal failure, to name a few

The Fructose Connection

Whereas fructose from natural sources seem to be benign, there is some evidence to suggest that higher intake of fructose – especially, through artificial sources (high-fructose corn syrup and excess of table sugar), may produce metabolic anomalies, including hypertriglyceridemia and sUA (Angelopoulos et al., 2009). Fructose does this through both increased endogenous production and reduced renal excretion (Nakagawa et al., 2006).

Take Home Message

  1. Not enough evidence that avoiding meats will reduce uric acid levels or likelihood of an acute attack of gout
  2. Raised uric acid levels, by themselves may not be responsible for an acute attack of gout
  3. If you already have hyperuricemia, beware of factors or conditions that cause sudden reduction in serum uric acid levels – avoid alcohol
  4. Fructose from artificial sources (including but not limited to, sweetened beverages) should be avoided
  5. Reduction of system inflammation (weight loss, paleo / keto diet) may help


Angelopoulos, T. J., Lowndes, J., Zukley, L., Melanson, K. J., Nguyen, V., Huffman, A., & Rippe, J. M. (2009). The effect of high-fructose corn syrup consumption on triglycerides and uric acid. The Journal of Nutrition, 139(6), 1242S–1245S. https://doi.org/10.3945/jn.108.098194

Annemans, L., Spaepen, E., Gaskin, M., Bonnemaire, M., Malier, V., Gilbert, T., & Nuki, G.(2008). Gout in the UK and Germany: prevalence, comorbidities andmanagement in general practice 2000-2005. Annals of the Rheumatic Diseases,67(7), 960–6. https://doi.org/10.1136/ard.2007.076232

Bleyer, A. J., & Hart, T. C. (2006). Genetic factors associated with gout and hyperuricemia. Advances in Chronic Kidney Disease. https://doi.org/10.1053/j.ackd.2006.01.008

Choi, H. K., Atkinson, K., Karlson, E. W., Willett, W., & Curhan, G. (2004). Purine-rich foods, dairy and protein intake, and the risk of gout in men. The New England Journal of Medicine, 350(11), 1093–1103. https://doi.org/10.1056/NEJMoa035700

Choi, H. K., & Curhan, G. (2008). Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ (Clinical Research Ed.), 336(7639), 309–12.https://doi.org/10.1136/bmj.39449.819271.BE

Doherty, M. (2009). New insights into the epidemiology of gout. Rheumatology (Oxford, England), 48 Suppl 2(suppl 2), ii2-ii8. https://doi.org/10.1093/rheumatology/kep086

Dunn, A. J. (2000). Cytokine activation of the HPA axis. Annals of the New York Academy of Sciences, 917, 608–17. Retrieved fromhttp://www.ncbi.nlm.nih.gov/pubmed/11268389

McCarty, D. J. (1994). Gout without hyperuricemia. JAMA, 271(4), 302–3. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8295290

Mikuls, T. R., Farrar, J. T., Bilker, W. B., Fernandes, S., Schumacher, H. R., & Saag, K. G.(2005). Gout epidemiology: results from the UK General Practice ResearchDatabase, 1990-1999. Annals of the Rheumatic Diseases, 64(2), 267–72.https://doi.org/10.1136/ard.2004.024091

Nakagawa, T., Hu, H., Zharikov, S., Tuttle, K. R., Short, R. A., Glushakova, O., … Johnson, R. J. (2006). A causal role for uric acid in fructose-induced metabolic syndrome. American Journal of Physiology – Renal Physiology, 290(3).

Nuki, G., & Simkin, P. A. (2006). A concise history of gout and hyperuricemia and their treatment. Arthritis Research & Therapy, 8 Suppl 1(Suppl 1), S1.

Pineda, C., Amezcua-Guerra, L. M., Solano, C., Rodriguez-Henríquez, P., Hernández-Díaz, C., Vargas, A., … Gutiérrez, M. (2011). Joint and tendon subclinical involvement suggestive of gouty arthritis in asymptomatic hyperuricemia: an ultrasound controlled study. Arthritis Research & Therapy, 13(1), R4. https://doi.org/10.1186/ar3223

Puig, J. G., de Miguel, E., Castillo, M. C., Rocha, A. L., Martínez, M. A., & Torres, R. J. (2008). Asymptomatic hyperuricemia: impact of ultrasonography. Nucleosides, Nucleotides & Nucleic Acids, 27(6), 592–5. https://doi.org/10.1080/15257770802136040

Richette, P., & Bardin, T. (2010). Gout. Lancet (London, England), 375(9711), 318–28. https://doi.org/10.1016/S0140-6736(09)60883-7

Richette, P., & Bardin, T. Purine-rich foods: an innocent bystander of gout attacks?, 71Annals of the Rheumatic Diseases 1435–1436 (2012). BMJ Publishing Group Ltd and European League Against Rheumatism. https://doi.org/10.1136/ard-2011-201215.Pineda

Roubenoff, R., Klag, M. J., Mead, L. A., Liang, K. Y., Seidler, A. J., & Hochberg, M. C. (1991). Incidence and risk factors for gout in white men. JAMA, 266(21), 3004–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1820473

Star, V. L., & Hochberg, M. C. (1993). Prevention and Management of Gout. Drugs, 45(2), 212–222. https://doi.org/10.2165/00003495-199345020-00004

Teng, G. G., Pan, A., Yuan, J. M., & Koh, W. P. (2015). Food sources of protein and risk of incident gout in the Singapore Chinese Health Study. Arthritis and Rheumatology, 67(7), 1933–1942. https://doi.org/10.1002/art.39115

Urano, W., Yamanaka, H., Tsutani, H., Nakajima, H., Matsuda, Y., Taniguchi, A., … Kamatani, N. Inflammatory Process in the Mechanism of Decreased Uric Acid Conc during Acute Gouty Arthritis.pdf, 29The Journal of rheumatology 1950–3 (2002). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12233891

Wallace, K. L., Riedel, A. A., Joseph-Ridge, N., & Wortmann, R. (2004). Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. The Journal of Rheumatology, 31(8), 1582–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15290739

Wang, J., & Dunn, A. J. (1999). The role of interleukin-6 in the activation of the hypothalamo-pituitary-adrenocortical axis and brain indoleamines by endotoxin and interleukin-1 beta. Brain Research, 815(2), 337–48. https://doi.org/10.1016/s0006-8993(98)01091-9

Zhang, Y., Chen, C., Choi, H., Chaisson, C., Hunter, D., Niu, J., & Neogi, T. (2012). Purine-rich foods intake and recurrent gout attacks. Annals of the Rheumatic Diseases, 71(9), 1448–53. https://doi.org/10.1136/annrheumdis-2011-201215