Feeds:
Posts
Comments

Posts Tagged ‘Obesity’


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.

LACK OF EVIDENCE FOR EFFECTIVENESS OF CALCIUM PILLS

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.

CALCIUM FOR OSTEOPOROSIS AND REDUCED BONE MINERAL DENSITY

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).

ADVERSE EFFECTS OF CALCIUM SUPPLEMENTATION

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).

CALCIUM AND BLOOD PRESSURE REDUCTION

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).

CALCIUM FROM FOODS IS ‘CARDIO-PROTECTIVE’

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).

cal_supps_blog3

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).

MORE IS NOT BETTER, IT IS WORSE

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).

cal_supps_blog5

TAKE HOME MESSAGE

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.

IN A NUTSHELL

  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

cal_supps_blog4

PLEASE FEEL FREE TO DISCUSS WITH YOUR DOCTOR, THE CARDIOVASCULAR RISKS, IF YOU ARE PRESCRIBED CALCIUM SUPPLEMENTS!

DISCLAIMER

REFERENCES

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.

 

Advertisements

Read Full Post »


SONY DSC


The whole town and his wife seems to be using whey protein.

Whey protein isolate – everybody knows – works; you know it works. It is the best protein for improving body composition (reducing fat while improving lean mass)! Or is it really?!

Whey protein isolate may be the best protein for you in most instances, that may not be the case always! Depending on your fitness goal, whey protein concentrate (and, even casein!) can sometime give whey isolate a run for its money. How is that?!

Well, read on to find out!

However, before we get into the nitty-gritty of which type of whey will best serve your purpose, let us get to know a bit more about why you should supplement with whey, in the first place.


Why should I take whey supplements?

Resistance training causes increase in muscle mass. This is due to increased muscle protein synthesis (MPS) that resistance training induces (Hulmi et al., 2009; Hakkinen et al., 2001; Hulmi et al., 2007). However, intense workouts alone are not enough to keep packing on lean muscle mass; you have to ‘stay anabolic’ most of the time to be able to keep that MPS working for you.

Without complicating matters, here’s a look at how resistance training increases lean muscle mass: a resistance training session causes muscle protein breakdown. This is then followed by repair of the damaged muscle tissue so that the muscles come out stronger the next time you hit the weights. For the muscles to get stronger, however, proteins ingestion (over and above normal needs) is crucial. Needless to say, the process of repair will suffer if you aren’t loading up on proteins.

That resistance training combined with protein supplementation causes muscle hypertrophy is well-documented (Moore et al., 2009; Hulmi et al., 2009; Cribb, Williams, Carey, & Hayes, 2006).  Ingestion of a whey protein supplement either immediately before or after a training session is – considered by some – to be the best for this purpose; also whey increases muscle protein turnover like no other protein. Furthermore, whey protein seems to work equally well in women as well (Josse, Tang, Tarnopolsky, & Phillips, 2010).

Another benefit of supplementing with whey is, improved post-workout recovery  This is likely due to the ‘anti-catabolic’ action of essential amino acids (Bird, Tarpenning, & Marino, 2006; Hoffman et al., 2010; Etheridge, Philp, & Watt, 2008).


What is Whey Protein?

You most likely know that whey is one of the 2 milk proteins – the other being casein. Casein is the more abundant of the two and it is casein that gives milk that white colour. In commercially available cow’s milk, 20% of protein is whey while the rest of it is casein (Hulmi, Lockwood, & Stout, 2010; Ha & Zemel, 2003; Etzel, 2004; Krissansen, 2007).

Whey is produced in large amounts as a by-product in the cheese industry. However, this whey has loads of fat, milk sugar (lactose) and salts in it and is not suitable for improving body composition.

During the process of whey purification, whey concentrate and isolate are produced sequentially. During the initial steps, larger molecules are separated out resulting in formation of whey concentrate. These larger molecules are proteins, lactose, immunoglobulins, amongst other less important ones. To produce whey isolate, cheese whey is passed through an ultrafiltration process (ion exchange or other methods). The ultra membrane filters fat, milk sugar (lactose), salts and other unwanted ingredients leaving behind a pure form of whey (Barile et al., 2009).

Hydrolysates, on the other hand, are formulations where large protein molecules are broken down into smaller fragments. The hypothesis is that this might further increase the rate of absorption of whey. However, this might not be totally true and hydrolysates may not offer much of an advantage over isolates or concentrates.


Types of Whey Protein

Whey is available commercially as either isolate or concentrate. ‘So, what’s the difference between them and which one should I be using’, you might want to ask?

The main difference between the two is the quality and the amount of protein content – isolate is purer and thus will contain almost 100% protein (well, 90-94% to be precise) while whey concentrate will contain protein ranging from 70-85%.

‘Well, that settles it – I am going with whey isolate!’, you might say. Hang on, not so fast! There is more to it than just protein content.


Comparing Whey Isolate and Whey Concentrate

Since whey isolate is higher in protein content, has a better amino acid ratio and thus bioavailability, it is absorbed into your system way quicker than whey concentrate (or any other protein, for that matter). That makes whey isolate the ideal post-exercise anabolic drink (Hulmi et al., 2009). Some researchers have suggested taking whey protein isolate before workouts as well in addition to your routine post-workout shake for maximum benefits (Esmark et al., 2001; Cribb & Hayes, 2006). Quicker absorption will mean almost instantaneous rise in blood amino acids which are then taken up by ‘hungry muscles’.

Having said that, the need for immediate post-workout protein supplementation in now being increasingly questioned (more below).

High protein content and higher quality of protein, however, that does not clinch the deal in favour of whey isolate. Concentrate has something up its sleeve that will make sit up and take notice!

As stated earlier, in comparison to isolate, whey protein concentrate will contain lesser amount of protein (in the range of 70-85%). However, somewhat similar to casein, whey protein concentrate will get absorbed slowly – this helps you stay anabolic for longer! Slower absorption also helps with absorption of other important nutrients from food like calcium. Not a lot of people know this but calcium plays an important role in causing fat loss (in addition to keeping your bones healthy)! Add to that the added benefit of appetite suppression for longer and casein suddenly become an important tool for your fat-loss goals or intermittent-fasting health journey…

Furthermore, whey protein concentrate is loaded with immunoglobulins – this helps boost your immune system and therefore may be beneficial in dealing with the intense stresses of training (especially if you happen to overtrain!).


Whey Isolate

Pros

    • pure; contains 90-94% protein!
    • purity means that it is great for gaining / maintaining lean mass while getting ripped (ideal when nearing competition or a photo shoot)
    • contains all essential amino acids in the best possible ratios
    • bioavailability for humans is best amongst all proteins – meaning, of the amount ingested, more is likely to be absorbed. For instance, in a scoop containing 25 g of whey isolate, almost all of the protein in there, will be going into your muscle
    • lightening fast absorption; ideal post-exercise drink – helps you get into the anabolic mode almost immediately

Cons

    • pricier than whey protein concentrate – to ensure purity, the commercial production of whey necessitates use of complex filtration procedure, hence the price
    • although whey isolate will help recovery after workouts, it loses out to whey concentrate in some respects. This is so because immune boosting constituents of milk protein like alpha – lactoglobulins and lactoferrins are removed during the purification process

Whey Concentrate

Pros:

    • lot cheaper than whey isolate
    • has a slower absorption rate than whey protein isolates; thus ensures a steady state of elevated amino acids in the blood and helps you stay anabolic for longer. This also reduces the need for frequent dosing
    • slower absorption helps with absorption of other important minerals like calcium and reducing blood glucose and lipid levels
    • induces appetite suppression which may help longer fasting interval, thereby improving body composition and metabolic disease parameters
    • contains immune boosting complexes (alpha – lactoglobulins and lactoferrins) which help post-exercise muscle recovery
    • helps fight diseases – for instance, chronic hepatitis C (Elattar et al., 2010)

Cons:

    • some amount of fat will be present so not ideally suited during times when keeping body fat% down is desirable
    • if you have any degree of intolerance to milk and dairy products, you might want to forget using whey concentrate on account of its lactose content – which is missing from the more purer whey isolate

TAKE HOME MESSAGE

In conclusion, isolate and concentrate are equally good – however, your circumstances – price, training goals and lactose intolerance – should tip the scales in favour of one or the other.


Recent developments

  1. More recently, the presence of a post-workout anabolic window (of opportunity) is being increasing questioned. ‘Not only is nutrient timing research open to question in terms of applicability, but recent evidence has directly challenged the classical view of the relevance of post-exercise nutritional intake with respect to anabolism’ (Aragon and Schoenfeld, 2013). The amount and quality of protein that you consume throughout the day is, now, thought to be more important than immediate post-workout whey ingestion.
  2. BCAAs (branched-chain amino acids – leucine, isoleucine and valine) may be overrated and ‘data do not seem to support a benefit to BCCA supplementation during periods of caloric restriction’ (Dieter BP, Schoenfeld BJ and Aragon AA, 2016).

Reference List

Aragon AA, Schoenfeld BJ (2013). Nutrient timing revisited: is there a post-exercise anabolic window? Journal of the International Society of Sports Nutrition. 2013;10:5 /1550-2783-10-5.

Barile, D., Tao, N., Lebrilla, C. B., Coisson, J. D., Arlorio, M., & German, J. B. (2009). Permeate from cheese whey ultrafiltration is a source of milk oligosaccharides. Int Dairy J, 19, 524-530.

Bird, S. P., Tarpenning, K. M., & Marino, F. E. (2006). Liquid carbohydrate/essential amino acid ingestion during a short-term bout of resistance exercise suppresses myofibrillar protein degradation. Metabolism, 55, 570-577.

Cribb, P. J. & Hayes, A. (2006). Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci.Sports Exerc., 38, 1918-1925.

Cribb, P. J., Williams, A. D., Carey, M. F., & Hayes, A. (2006). The effect of whey isolate and resistance training on strength, body composition, and plasma glutamine. Int J Sport Nutr.Exerc.Metab, 16, 494-509.

Dieter BP, Schoenfeld BJ, Aragon AA.(2016). The data do not seem to support a benefit to BCAA supplementation during periods of caloric restriction. Journal of the International Society of Sports Nutrition;13:21. doi:10.1186/s12970-016-0128-9.

Elattar, G., Saleh, Z., El-Shebini, S., Farrag, A., Zoheiry, M., Hassanein, A. et al. (2010). The use of whey protein concentrate in management of chronic hepatitis C virus – a pilot study. Arch.Med Sci., 6, 748-755.

Esmarck, B., Andersen, J. L., Olsen, S., Richter, E. A., Mizuno, M., & Kjaer, M. (2001). Timing of postexercise protein intake is important for muscle hypertrophy with resistance training in elderly humans. J Physiol, 535, 301-311.

Etheridge, T., Philp, A., & Watt, P. W. (2008). A single protein meal increases recovery of muscle function following an acute eccentric exercise bout. Appl.Physiol Nutr.Metab, 33, 483-488.

Etzel, M. R. (2004). Manufacture and use of dairy protein fractions. J Nutr., 134, 996S-1002S.

Ha, E. & Zemel, M. B. (2003). Functional properties of whey, whey components, and essential amino acids: mechanisms underlying health benefits for active people (review). J Nutr.Biochem., 14, 251-258.

Hakkinen, K., Pakarinen, A., Kraemer, W. J., Hakkinen, A., Valkeinen, H., & Alen, M. (2001). Selective muscle hypertrophy, changes in EMG and force, and serum hormones during strength training in older women. J Appl.Physiol, 91, 569-580.

Hoffman, J. R., Ratamess, N. A., Tranchina, C. P., Rashti, S. L., Kang, J., & Faigenbaum, A. D. (2010). Effect of a proprietary protein supplement on recovery indices following resistance exercise in strength/power athletes. Amino.Acids, 38, 771-778.

Hulmi, J. J., Ahtiainen, J. P., Kaasalainen, T., Pollanen, E., Hakkinen, K., Alen, M. et al. (2007). Postexercise myostatin and activin IIb mRNA levels: effects of strength training. Med Sci.Sports Exerc., 39, 289-297.

Hulmi, J. J., Kovanen, V., Selanne, H., Kraemer, W. J., Hakkinen, K., & Mero, A. A. (2009). Acute and long-term effects of resistance exercise with or without protein ingestion on muscle hypertrophy and gene expression. Amino.Acids, 37, 297-308.

Hulmi, J. J., Lockwood, C. M., & Stout, J. R. (2010). Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein. Nutr.Metab (Lond), 7, 51.

Josse, A. R., Tang, J. E., Tarnopolsky, M. A., & Phillips, S. M. (2010). Body composition and strength changes in women with milk and resistance exercise. Med Sci.Sports Exerc., 42, 1122-1130.

Krissansen, G. W. (2007). Emerging health properties of whey proteins and their clinical implications. J Am Coll.Nutr., 26, 713S-723S.

Moore, D. R., Tang, J. E., Burd, N. A., Rerecich, T., Tarnopolsky, M. A., & Phillips, S. M. (2009). Differential stimulation of myofibrillar and sarcoplasmic protein synthesis with protein ingestion at rest and after resistance exercise. J Physiol, 587, 897-904.

Read Full Post »


You’d probably find this hard to believe but empirical physicians like Galen and Hippocrates, many millennia ago, predicted the ‘epidemic’ of  human obesity and the problems that it would cause (1)! Despite such warnings, most cultures of the world, even to this day, have tended to look upon obesity as a sign of good health (2).

More often than not, you are made to believe that lack of physical activity (PA) combined with overeating leads to (overweight and) obesity. However, that is now being questioned. Notwithstanding the reasons for overweight and obese, being overweight or obese puts you at a greater risk of metabolic disorders like diabetes, cardiovascular diseases, arthritis and cancer, to name a few (1-7).

According to NHANES, up until the end of 2010, of the adult US population (older than 20 years), 33% were overweight, 35.7% obese and 6.3% were classified as extremely obese (8) – that makes for a staggering 75% of adults with ‘weight problems’! While those figures are from 2010, one can only imagine what the picture must be like now!

In other parts of the world, prevalence of obesity and overweight is quite similar to (if not more extreme than) that in the US. According to Jacob C. Seidell, obesity is as common in the UK as in the US (9). Countries undergoing rapid economic growth – notably in Latin America and Asia – reflect similar figures as well (10).

As if these figures aren’t frightening enough, get a load of this – in 2010, medical bills for treating obesity and overweight individuals in the US alone was $270 billion (11;12)! Add to that, the costs for treating the associated ill-effects – cardiovascular disease, diabetes and others – and you’d understand why humanity can no longer afford to be overweight anymore.

3-Meal-a-Day? Really?!

Owing to the current ‘epidemic proportions’ (I have tended to call it a pandemic – and rightly so!) of obesity and its ill-effects – our dietary patterns have come into sharp focus. Although, ‘3-meals a day’ is the norm in most geographical areas of the world, there is no scientific basis for this being the best strategy for achieving optimal human health. In recent times, therefore, researchers have begun to question the rationale of the traditional ‘3-meals a day’ diet and have wondered if reduction in the number of meals (less than 3) may prove to be beneficial in fighting obesity.

6-Meals-a-Day?! Get out of ‘ere!

Most dietitians, fitness and weight-loss gurus are likely to recommend ‘6-meals-a-day’ type of diet (snacking) for weight-loss. The general perception is that smaller, frequent meals during the course of the day increase metabolic rate and are generally better for maintaining a healthier weight. However, contrary to popular belief, there is no scientific proof – none whatsoever – that ‘snacking’ bumps up your metabolism and will help you lose weight! There is some evidence that increasing the frequency of meals (snacks) – while keeping calories constant – may affect physiological parameters favorably – lower serum glucose, insulin and lipid levels (13;14). However, the proof in favor of reduced meal frequency (as compared to snacking) in preventing metabolic diseases as well as obesity is much stronger.

In addition to the lack of evidence for its effectiveness, there are several downsides of frequent snacking. Reducing meal frequency, on the other hand, may prove to be a win-win situation for you!

Downsides of frequent snacking

    • A snack when eaten in a non-hungry state, may cause weight gain – this is likely due to the calorie-dense nature and high sugar content of the snack; such snacks, by default will be poor in nutrients; these lead to decreased satiety and subsequently, increased hunger (15)
    • Even if your snack was high in protein (a protein shake, for instance), it wouldn’t amount to much suppression of hunger. Consequently, the energy intake during the next meal would still be higher than after a ‘no-snack’ (or skipped meal) period  (16)
    • Furthermore,  frequent  snacking  has  been  shown  to  increase  the  risk  of developing type-2 diabetes (17)

Positives of reduced meal frequency (and intermittent fasting)

(13;17-21)
    • reduced body weight,
    • arrested development of metabolic diseases,
    • improved quality of health, and
    • longevity

Interestingly enough, the benefits derived from reduced food intake work independent of the number of calories consumed (18;20).

Based on these observations, recent dietary trends (although not by ‘mainstream nutritionists’) have tended to recommended reduced meal frequency (and intermittent fasting) over frequent snacking.

So, what exactly are the health benefits that you can expect by reducing the number of times you eat in a day? In addition to the obvious benefits on body weight and body composition, there are other benefits to be had as well. Here are some (18;22;23):

    • decreased blood insulin levels
    • decreased blood glucose levels
    • decreased blood pressure
    • decreased heart rate
    • decreased predisposition to cardiac or brain cell injury
    • enhanced immunity

Improvement in the above mentioned physiological parameters will help you prevent or reduce the severity of disorders like obesity, diabetes – type 2 and cardiovascular diseases. In case, you are wondering why reducing meal frequency would work for you, have a look through some of the theories that have been proposed by researchers for the alleged benefits of reduced meal frequency.

Theories for Benefits of Reduced Meal Frequency

Oxidative Stress Theory

The processes of ageing and development of ‘ageing-related diseases’ are due to oxidative stresses that our bodies are exposed to on a daily basis; the dreaded free oxygen radical (otherwise known as reactive oxygen) is responsible for these stresses. Reduced meal frequency and intermittent fasting tends to slow down and reduce the production of these oxygen radicals and thereby, the oxidative processes (17;19;24); hence, the reported benefits.

Energy Metabolism Theory

The Energy Metabolism Theory suggests that dietary restriction – either as reduced meal frequency or intermittent fasting – has a positive influence on calorie equation. Furthermore, it increases sensitivity to key hormones, especially, insulin (25). And, since insulin resistance plays a major role in the development of obesity and other metabolic diseases, increased insulin sensitivity as a result of reduced meal frequency is more than likely to be of benefit.

Cellular Stress Response Theory

The Cellular Stress Response Theory is quite an interesting theory; it proposes that decreasing your meal frequency induces a stress response from cells. The stress response involves up-regulation of receptors and genes – this makes cells stronger so they can cope with all kinds of physiological or pathological stresses (24). The end result – a healthier you with better chances of fighting metabolic disease.

Data obtained from animal studies has supported the fact that reducing meal frequency can be beneficial to general health and well-being (18;26-28). Additionally, human clinical studies have also reported the benefits of reduced meal frequency (26). Also, regular consumption of breakfast (although, I am not a big proponent of the ‘healthy breakfast’ idea, a story for another day) while reducing the frequency of meals through the rest of the day seems to have an even bigger effect – both on obesity and disease prevention (27-29).

TAKE HOME MESSAGE

Six-meals-a-day diet is history! Reducing meal frequency is the ‘in-thing’. Regular breakfast consumption while reducing the frequency of meals through the rest of the day has several positive benefits on human health such as:

    • improvements in body composition,
    • reduction of risk for cardiovascular-metabolic diseases, and
    • an anti-aging effect

A WORD OF CAUTION THOUGH – don’t go overboard and eat tons of calories at one go, suddenly; you’d have build up gradually if were to, let’s say eat a 1500 calorie meal of nutrient-dense foods and then fast for 20 hours!

Another thing you need to be wary of is that this kind of diet would work best if you added some amount of exercise training to it – short and brutal workouts like high-intensity interval training, sprint intervals or Olympic lifting would work wonders!

I don’t know about you, but with an impressive ‘benefits profile’ like that, I’d be certainly tempted to give reduced meal frequency a try.

PS: This article is more relevant for those looking to lose weight and improve general well-being and health; sports-specific nutrition is a totally different ball game!

 

References

(1) Belkina AC, Denis GV. Obesity genes and insulin resistance. Curr Opin Endocrinol Diabetes Obes 2010; 17(5):472-477.

(2) Haslam D. Obesity: a medical history. Obes Rev 2007; 8 Suppl 1:31-36.

(3) Bastard JP, Maachi M, Lagathu C, Kim MJ, Caron M, Vidal H et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw 2006; 17(1):4-12.

(4) Grossman SP. The role of glucose, insulin and glucagon in the regulation of food intake and body weight. Neurosci Biobehav Rev 1986; 10(3):295-315.

(5) Guyenet  SJ,  Schwartz  MW.  Clinical  review:  Regulation  of food  intake, energy balance, and body fat mass: implications for the pathogenesis and treatment of obesity. J Clin Endocrinol Metab 2012; 97(3):745-755.

(6) Mayer J. Glucostatic mechanism of regulation of food intake. 1953. Obes Res 1996; 4(5):493-496.

(7) Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008; 359(3):229-241.

(8) Fryar CD, Carroll MD, Ogden CL. Prevalence of Overweight, Obesity and Extreme  Obesity Amongst  adults:  United  States,  Trends  1960-1962  Through  2009-2010.

(9) Seidell JC. Obesity, insulin resistance and diabetes–a worldwide epidemic. Br J Nutr 2000; 83 Suppl 1:S5-S8.

(10) Seidell JC, Rissanen A. Time trends in the worldwide prevalence of obesity. In: Bray GA, Bouchard C, James WPT, editors. Handbook of Obesity. New York: Marcel Dekker; 1998. 79-91.

(11) Behan DF, Cox SH, Lin Y, Pai J, Pedersen HW, Yi M. Obesity and its Relation to Mortality and Morbidity Costs. 2010. Obesity and its Relation         to         Mortality         and         Morbidity         Costs. http://www.soa.org/research/research-projects/life-insurance/research- obesity-relation-mortality.aspx

(12) Xia Q, Grant SF. The genetics of human obesity. Ann N Y Acad Sci 2013; 1281:178-190.

(13) Jenkins DJ, Wolever TM, Vuksan V, Brighenti F, Cunnane SC, Rao AV et al. Nibbling  versus  gorging:  metabolic  advantages  of  increased  meal frequency. N Engl J Med 1989; 321(14):929-934.

(14) Timlin MT, Pereira MA. Breakfast frequency and quality in the etiology of adult obesity and chronic diseases. Nutr Rev 2007; 65(6 Pt 1):268-281.

(15) Arnold  L,  Mann  JI,  Ball  MJ.  Metabolic  effects  of  alterations  in  meal frequency in type 2 diabetes. Diabetes Care 1997; 20(11):1651-1654.

(16) Marmonier  C,  Chapelot  D,  Louis-Sylvestre  J.  Effects  of  macronutrient content and energy density of snacks consumed in a satiety state on the onset of the next meal. Appetite 2000; 34(2):161-168.

(17) Mekary RA, Giovannucci E, Willett WC, van Dam RM, Hu FB. Eating patterns and type 2 diabetes risk in men: breakfast omission, eating frequency, and snacking. Am J Clin Nutr 2012; 95(5):1182-1189.

(18) Anson RM, Guo Z, de CR, Iyun T, Rios M, Hagepanos A et al. Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. Proc Natl Acad Sci U S A 2003; 100(10):6216-6220.

(19) Guo Z, Ersoz A, Butterfield DA, Mattson MP. Beneficial effects of dietary restriction on cerebral cortical synaptic terminals: preservation of glucose and glutamate transport and mitochondrial function after exposure to amyloid beta-peptide, iron, and 3-nitropropionic acid. J Neurochem 2000; 75(1):314-320.

(20) Wang ZQ, Bell-Farrow AD, Sonntag W, Cefalu WT. Effect of age and caloric restriction on insulin receptor binding and glucose transporter levels in aging rats. Exp Gerontol 1997; 32(6):671-684.

(21) Wing RR, Blair EH, Bononi P, Marcus MD, Watanabe R, Bergman RN. Caloric restriction per se is a significant factor in improvements in glycemic control and insulin sensitivity during weight loss in obese NIDDM patients. Diabetes Care 1994; 17(1):30-36.

(22) Lane MA, Mattison J, Ingram DK, Roth GS. Caloric restriction and aging in primates: Relevance to humans and possible CR mimetics. Microsc Res Tech 2002; 59(4):335-338.

(23) Wan R, Camandola S, Mattson MP. Intermittent fasting and dietary supplementation with 2-deoxy-D-glucose improve functional and metabolic cardiovascular risk factors in rats. FASEB J 2003; 17(9):1133-1134.

(24) Sohal RS, Weindruch R. Oxidative stress, caloric restriction, and aging. Science 1996; 273(5271):59-63.

(25) Speakman JR, Selman C, McLaren JS, Harper EJ. Living fast, dying when? The  link  between  aging  and  energetics.  J  Nutr  2002;  132 (6  Suppl 2):1583S-1597S.

(26) Stote KS, Baer DJ, Spears K, Paul DR, Harris GK, Rumpler WV et al. A controlled trial of reduced meal frequency without caloric restriction in healthy,  normal-weight,  middle-aged  adults.  Am  J  Clin  Nutr  2007; 85(4):981-988.

(27) Farshchi HR, Taylor MA, Macdonald IA. Deleterious effects of omitting breakfast on insulin sensitivity and fasting lipid profiles in healthy lean women. Am J Clin Nutr 2005; 81(2):388-396.

(28)  Smith  KJ,  Gall  SL,  McNaughton  SA,  Blizzard  L,  Dwyer  T,  Venn  AJ. Skipping breakfast: longitudinal associations with cardiometabolic risk factors in the Childhood Determinants of Adult Health Study. Am J Clin Nutr 2010; 92(6):1316-1325.

(29) Yamamoto R, Kawamura T, Wakai K, Ichihara Y, Anno T, Mizuno Y et al. Favorable life-style modification and attenuation of cardiovascular risk factors. Jpn Circ J 1999; 63(3):184-188.

 

Read Full Post »


Health and fitness professionals and researchers (me included!) have always cried hoarse about the downsides of obesity. For decades, obesity has been reported to impair health and reduce longevity (Allison et al., 2008). So much so, that research community has branded obesity as a disease (2008) which increases mortality and decreases longevity (Fontaine, Redden, Wang, Westfall, & Allison, 2003). There is, also, strong proof for causal effect of obesity in increasing mortality (4, 5). Conversely, calorie restriction (I don’t totally agree to calorie deficit plans – they aren’t for everyone!) to lower body weight has been shown to prolong life (Weindruch & Walford, 1988).

Notwithstanding the strong evidence for obesity being a curse, there are some curious findings about obesity in humans – those that will make you wonder if being fat is really that bad for you! There seems to be a reason why we gain weight as we age – well, in that case, does obesity afford some protective effect on human existence? Research into the so-called ‘obesity paradox’ certainly points in that direction.

Obesity Paradox

Obesity seems to have a protective effect in people suffering from a major injury or illness; this is called obesity paradox – in such individuals, being fat helps in that it increases survival time.

‘Among persons who already have heart failure, outcomes seem to be better in obese persons as compared to lean persons’ (Niedziela et al., 2014).  The direct causal relationship of obesity in this curious phenomenon is, however, a matter of intense debate (Habbu, Lakkis, & Dokainish, 2006).

Another equally curious observation reported by academicians is that lower body mass indices (underweight or those just under normal) are associated with an elevated mortality rate.  While individuals who are mildly overweight reflect the lowest mortality rates (Childers & Allison, 2010 and Niedziela et al., 2014). Mind you, the extremely obese are worse off though!

Take home message

Although ‘leaner is better’ may be true in most people – especially, in those who are disease-free and injury-free – obesity does seem to provide benefits in the diseased or injured, particularly in middle-aged individuals. This may be part of the reason why we put on weight as we age (Heo et al., 2003).

However, before you jump the gun and start advising middle-aged people to forget about getting lean, do keep in mind that there is, as yet, no conclusive evidence for the protection offered by being overweight or downright obese. Further research providing concrete proof needs to be conducted before we change our views on obesity.

Until that time, I’m afraid, its back to Olympic lifting platforms and HIIT and your nutrient-dense meals! Go people…!

 References 

Obesity as a disease: The Obesity Society Council resolution (2008). Obesity (Silver.Spring), 16, 1151.

Allison, D. B., Downey, M., Atkinson, R. L., Billington, C. J., Bray, G. A., Eckel, R. H. et al. (2008). Obesity as a disease: a white paper on evidence and arguments commissioned by the Council of the Obesity Society. Obesity (Silver.Spring), 16, 1161-1177.

Childers, D. K. & Allison, D. B. (2010). The ‘obesity paradox’: a parsimonious explanation for relations among obesity, mortality rate and aging? Int J Obes (Lond), 34, 1231-1238.

Fontaine, K. R., Redden, D. T., Wang, C., Westfall, A. O., & Allison, D. B. (2003). Years of life lost due to obesity. JAMA, 289, 187-193.

Habbu, A., Lakkis, N. M., & Dokainish, H. (2006). The obesity paradox: fact or fiction? Am J Cardiol, 98, 944-948.

Heo, M., Faith, M. S., Mott, J. W., Gorman, B. S., Redden, D. T., & Allison, D. B. (2003). Hierarchical linear models for the development of growth curves: an example with body mass index in overweight/obese adults. Stat.Med, 22, 1911-1942.

Niedziela J, Hudzik B, Niedziela N, Gasior M, Gierlotka M, Wasilewski J et al. The obesity paradox in acute coronary syndrome: a meta-analysis. Eur J Epidemiol 2014; 29(11):801-812

Weindruch, R. & Walford, R. (1988). The Retardation of Aging and Disease by Dietary Restriction. Springfield, IL: C.C. Thomas Publisher.

 

Read Full Post »


00000SusThe worldwide prevalence of obesity has reached epic proportions. So much so, that calling obesity a pandemic wouldn’t amount to exaggeration! In addition to putting individual lives on the line, obesity has the ability to severely increase health care costs, negatively impacting on most economies of the world 1;2.

So, what is it that causes obesity – you might want to ask!


What causes obesity?

Well. traditionally, we have been told that ‘excess intake of calories coupled with decreased expenditure’ is the immediate cause of obesity. Excess calories are treated as reserve food material (read: fats) and deposited as triglycerides (TGs) inside adipose tissue (fat stores). However, having said that,it does not seem to be as simple as that.

Recently, it is increasingly being suggested (and, I am one of those who believes in this) that obesity may be a metabolic disorder where your nutrient metabolism goes for a toss. Also, rather than how many calories you consume, what kind of food you eat (and where the calories are coming from) will define if you stay lean or pack on weight; ingestion of nutrient-dense food is likely to make you leaner and healthier than foods that are only rich in calorie and poor in nutrients.

Also, a number of (as yet poorly understood) factors play a causative role: hormones, metabolic enzymes, metabolic rate, nutrient partitioning and calorie partitioning abilities of the individual. It must be emphasized here that the kind of food you eat will have a massive influence all of the aforementioned factors.

Anthropometric tell-tale signs of obesity are:

  • Increased waist circumference
  • Increased waist-hip ratio
  • Increased body mass index (BMI)

Adverse-effects of being Obese?

In addition to the much publicized ill-effects of obesity (given below), not many people are aware that obesity causes testosterone deficiency (TD) as well. Testosterone has a prominent effect on metabolism; deficiency can add to the problems. In addition, low levels of T can have a detrimental effect on a person’s psyche, making it hard to stick to a prescribed regimen of healthy food and exercise to counter obesity. Thus a ‘vicious cycle’ connection exists between obesity and low testosterone levels.

Well-known adverse-effects of obesity are:

  • Metabolic syndrome
  • Cardiovascular disease (CVD)
  • Diabetes Mellitus (Type 2 DM)
  • Hypertension (rise in blood pressure)

Testosterone deficiency and Obesity in Men

Testosterone (as the major male sexual hormone) is responsible for the male sexual and reproductive functions. However, not many people are aware that it plays a significant role in calorie utilization and metabolism as well. The exact mechanisms by which testosterone levels are affected in / contribute to obesity remain a mystery 3.

However, here are some interesting facts connecting testosterone to obesity are: testosterone:

  • causes nitrogen retention (read: increasing muscle mass, as part of the anabolic process) 3;4, low levels in obesity therefore cause loss of lean muscle
  • affects body composition in a positive way by reducing fat mass and increasing lean muscle mass 5, low levels therefore, reverse these effects
  • stimulates hormone sensitive lipase (enzyme responsible for fat breakdown), inhibits triglyceride uptake and mobilises fat from fat stores 6, low levels in obesity therefore, lead to increased fat deposition
  • an inverse relationship exists between parameters of obesity (WC, WHR and BMI) and plasma testosterone levels in an individual 3
  • an inverse relationship also exists between the ill-effects of obesity like metabolic syndrome, hypertension, type 2 diabetes and plasma levels of testosterone 7
  • number of studies report the irrefutable proof that low testosterone levels are connected with diabetes and cardiovascular disease 8;9
  • low levels of testosterone definitely connected with all-cause mortality 10

Thus, it can safely be said that testosterone is responsible for maintaining and increasing muscle while burning fat; low levels are responsible for fat deposition resulting in obesity, diabetes, cardiovascular disease, metabolic syndrome and increased mortality 3-5;7-10.


How can obesity be treated?

A number of strategies have been proposed by researchers, physicians and fitness professional to fight obesity. Some of these are:

  1. Calorie Deficit: This involves ‘dieting’, using liquid diets, etc. However, this causes loss of lean mass in addition to fat loss
  2. Calorie Deficit combined with Exercise: This maintains lean mass whilst causing weight loss, however a number of people have found this pretty hard to stick to
  3. Surgery (gastric binding or bariatric): effective but reserved only for the morbidly obese

A novel, effective method proposed for treating obesity is combining exercise and healthy diet with testosterone replacement therapy (TRT) – especially if accompanying signs and symptoms suggestive of hypogonadism are present. Additionally, as opposed to other modes of treatment, testosterone has the potential to elevate mood and energy and reduce fatigue 11.


Future research

Although TRT sounds like an exciting treatment option for tackling obesity, the plasma levels of testosterone at which therapy should be initiated remain undefined. Currently, it is recommended only in individuals diagnosed with testosterone deficiency (hypogonadism / erectile dysfunction).

A sad fact is that most doctors treating obese patients with diabetes or cardiovascular disease are not aware of the connection of testosterone with obesity and the potential benefits of testosterone therapy. Furthermore, the misconception that testosterone increases cardiovascular risk 12 and chances of pancreatic cancer prevents clinicians from prescribing testosterone 13.

There is a definite and realistic need to further explore this option for treating obesity in men. Also, an effort should be initiated to educate both doctors as well as members of the general population (who are struggling with obesity and its ill-effects) regarding the benefits of testosterone replacement therapy.


References

(1) Kypreos KE. Mechanisms of obesity and related pathologies. FEBS J 2009; 276(20):5719.

(2) Freedman DH. How to fix the obesity crisis. Sci Am 2011; 304(2):40-47.

(3) Traish AM, Feeley RJ, Guay A. Mechanisms of obesity and related pathologies: androgen deficiency and endothelial dysfunction may be the link between obesity and erectile dysfunction. FEBS J 2009; 276(20):5755-5767.

(4) Singh R, Artaza JN, Taylor WE, Braga M, Yuan X, Gonzalez-Cadavid NF et al. Testosterone inhibits adipogenic differentiation in 3T3-L1 cells: nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors. Endocrinology 2006; 147(1):141-154.

(5) Emmelot-Vonk MH, Verhaar HJ, Nakhai Pour HR, Aleman A, Lock TM, Bosch JL et al. Effect of testosterone supplementation on functional mobility, cognition, and other parameters in older men: a randomized controlled trial. JAMA 2008; 299(1):39-52.

(6) Traish AM, Abdou R, Kypreos KE. Androgen deficiency and atherosclerosis: The lipid link. Vascul Pharmacol 2009; 51(5-6):303-313.

(7) Dhindsa S, Miller MG, McWhirter CL, Mager DE, Ghanim H, Chaudhuri A et al. Testosterone concentrations in diabetic and nondiabetic obese men. Diabetes Care 2010; 33(6):1186-1192.

(8) Aversa A. Drugs targeted to improve endothelial function: clinical correlates between sexual and internal medicine. Curr Pharm Des 2008; 14(35):3698-3699.

(9) Cattabiani C, Basaria S, Ceda GP, Luci M, Vignali A, Lauretani F et al. Relationship between testosterone deficiency and cardiovascular risk and mortality in adult men. J Endocrinol Invest 2012; 35(1):104-120.

(10) Araujo AB, Dixon JM, Suarez EA, Murad MH, Guey LT, Wittert GA. Clinical review: Endogenous testosterone and mortality in men: a systematic review and meta-analysis. J Clin Endocrinol Metab 2011; 96(10):3007-3019.

(11) Saad F, Aversa A, Isidori AM, Gooren LJ. Testosterone as potential effective therapy in treatment of obesity in men with testosterone deficiency: a review. Curr Diabetes Rev 2012; 8(2):131-143.

(12) Traish AM, Kypreos KE. Testosterone and cardiovascular disease: an old idea with modern clinical implications. Atherosclerosis 2011; 214(2):244-248.

(13) Morgentaler A. Testosterone replacement therapy and prostate cancer. Urol Clin North Am 2007; 34(4):555-63, vii.

Read Full Post »


For many-a-years, ‘treadmill-users’ in gyms – especially women – have been subjected to immense ridicule by those that swear by the resistance training method as the only way of training – there’s been an ever increasing tendency to criticise people using the treadmill or indulging in aerobic activities. The advent of CrossFit (and the Concept 2 Rower) hasn’t helped matter since CrossFitters have also jumped into the fray as the ‘treadmill bashers’.

The basis of the criticism springs from the thinking that lifting weights is far better than aerobic training when it comes to losing fat. Although much of the evidence for such thinking is anecdotal, the proof for the idea that ‘weight-training’ is far better than aerobic training – like treadmill runs – is flimsy to say the least. Yet, all ‘knowledgeable fitness experts’ seems to agree unanimously that weight training is far better than treadmill running for fat loss! Read my blog here on why I think resistance training may not be a great fat loss as is usually made out.

Notwithstanding what bodybuilders of CrossFitters might suggest, runners have always maintained that running (as in long-distance running) continues to be the best darn way to lose fat! Having said that, I have always maintained that running does come at a risk (of injuries); this is how I feel about long-distance running! However, this blog post is more about the fact that treadmill running seems to be a great fat loss strategy and yet, it seems to have copped a lot of unwarranted heat.

Argument(s) for Resistance Training

Lifting weights – also called resistance training (RT) – increases muscle mass and tone. This increase in muscle mass – since muscle is the most metabolically active tissue in the body – translates into more calories burned throughout the course of the day, even when resting, they say.

In short, resistance training bumps up your metabolic rate. This, they believe, is in contrast to aerobic training (AT) where you’d burn calories only when you exercise but nothing much after!

Not surprisingly, most ‘knowledgeable’ fitness experts – thinking along these lines – suggest RT over AT for burning fat.

Well, it just may be that  fitness gurus may have been wrong and those’ women on treadmills’ may have been right all along – if a new study, published in the American Journal of Physiology – Endocrinology and Metabolism is to be believed (Lee et al., 2013).

Evidence in Favour of Aerobic Training 

Researchers from the University of Pittsburgh, Pennsylvania, conducted a study comparing resistance training with aerobic training in young women (Lee et al., 2013). The results were astonishing (for most!) – to say the least! Apparently, not only is AT 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 fat (fat within muscle)

Other studies have also supported the idea that aerobic training 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 AT and combined AT/RT exercise programs caused more fat loss than RT alone, AT/RT and RT resulted in increased lean mass. However, although requiring a double time commitment over AT alone, a combined AT/RT exercise program, the authors observed, did not result in ‘significantly more fat loss over AT alone’ (Willis et al., 2012)
    • Another study published in the American Journal of Physiology – Endocrinology and Metabolism concluded that aerobic training caused significant reductions in body fat (including subcutaneous abdominal fat), visceral and liver fat, plasma liver enzymes, alanine aminotransferase (enzyme reflecting the amount of liver damage) and HOMA (Homeostasis Model Assessment – a measure of the level of your steady state beta cell function (%B) and insulin sensitivity (%S)). Resistance training, on the other hand, failed to significantly affect these variable. Also, AT was found to be more effective that RT at reducing abdominal as well as body fat (Slentz et al., 2011)

Aerobic Training and Metabolic Disease

An interesting observation is that aerobic training seems to be better than resistance training in reducing the risk of metabolic syndrome (obesity, diabetes, cardiovascular conditions and what-have-yous). Researchers from the Duke University Medical Center showed that the results of a combination of AT and RT exercise regimen – although more effective at reducing the risk of metabolic disease than RT alone – were not significantly different from AT alone (Bateman et al., 2011). This effectively suggests  that the RT component may be contributing very little to the disease prevention effect of an AT-RT exercise program

Why Women prefer Treadmills?

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

It appears that aerobic training is more effective in (overweight and obese) women than in men (Lee et al., 2013). Furthermore, there is some evidence to suggest that women enjoy AT more than RT (Lee et al., 2012)the opposite seems to be true with young men – they seem to enjoy RT more (now come on, do we even need any proof of that?!).

My hunch is that is that women find aerobic training more enjoyable because it is more effective for them! Not surprisingly then – call it nature or the 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’!

Conclusion

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

    • RT contributes very little (if at all) to fat-loss
    • RT contributes very little towards (metabolic) disease prevention
    • the above seem to be the job of the  good old aerobic training

Furthermore, as opposed to popular belief, a combination of aerobic and resistance training does not seems to afford any more benefits over aerobic training alone when losing body fat is your prime goal. So, out goes the almost ancient ‘fitness program’ of alternate days of weight training and cardio.

I reckon – in light of recent research findings – women are advised to get as much cardio under their belt as they can. After all, Jane Fonda did manage to get into top shape without too much of lifting, didn’t she?! So, if you feel like it, don’t let anyone stop you from jumping on to the treadmill, girls!

TAKE HOME MESSAGE

It appears that for overweight or obese individuals – especially women – aerobic training may still be the best way to go, not only to reduce body fat but also to reduce the risk of metabolic diseases as well.

Although, it can be argued here that studies cited have shortcomings (and a well-qualified researcher will likely, blow the results of these studies to smithereens), it has to be acknowledged these studies do have the potential to make us think twice.The question that begs to be answered is ‘what if we were wrong about our fat-loss strategies and indeed, about our obsession with resistance training and what if those women on treadmill were right all along?!

Until such a time that someone comes up with concrete proof about resistance training being so damn good that we can totally do away with aerobic training, let’s us keep our minds open. AND, let’s also stop ridiculing (or even downright laughing at) those women who hit the treadmill every single time!

References

Bateman, L. A., Slentz, C. A., Willis, L. H., Shields, A. T., Piner, L. W., Bales, C. W. et al. (2011). 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, 108, 838-844.

Lee, S., Bacha, F., Hannon, T., Kuk, J. L., Boesch, C., & Arslanian, S. (2012). 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, 61, 2787-2795.

Lee, S., Deldin, A. R., White, D., Kim, Y., Libman, I., Rivera-Vega, M. et al. (2013). 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, 305, E1222-E1229.

Slentz, C. A., Bateman, L. A., Willis, L. H., Shields, A. T., Tanner, C. J., Piner, L. W. et al. (2011). 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, 301, E1033-E1039.

Willis, L. H., Slentz, C. A., Bateman, L. A., Shields, A. T., Piner, L. W., Bales, C. W. et al. (2012). Effects of aerobic and/or resistance training on body mass and fat mass in overweight or obese adults. J Appl.Physiol (1985.), 113, 1831-1837.

Read Full Post »


adfAlternate day modified fasting (ADMF) is a new and (I believe) an effective tool in the global war against obesity.

Over the past 30 years, the incidence of obesity has increased alarmingly so much so that more than 1 in 3 American adults is now obese (Kruger, Ham, & Prohaska, 2009). The most common method prescribed by most clinicians as well as fitness professionals to fight obesity is daily calorie restriction or fasting every single day (Steyer & Ables, 2009).

However, since fasting every day has been found to be quite impractical since most overweight and obese individuals find this quite difficult to adhere to (8-10), a new method called the alternate day modified fasting has been evolved (Varady & Hellerstein, 2007).

This new methods involves a day of normal eating which is alternated with a day of fasting or modified fasting where the calorie intake is to be reduced to almost 25% of the normal calorie intake. This is done with the aim to increase adherence to fasting and accumulating the advantages of fasting over prolonged period of time. Several studies have found this to be an effective method to cause weight loss (Halberg et al., 2005; Johnson et al., 2007; Heilbronn, Smith, Martin, Anton, & Ravussin, 2005).

However, before you commit to thinking that ADMF is just the ‘magic wand’ you needed and it will alone solve all your problems, you cannot be more wrong! You have to realise that ADMF with high intensity interval training (which causes appetite suppression) when combined with high protein intake (usually in the form of protein supplementation) will make a sea of a difference in helping you lose fat while maintaining lean body mass.

References

Halberg, N., Henriksen, M., Soderhamn, N., Stallknecht, B., Ploug, T., Schjerling, P. et al. (2005). Effect of intermittent fasting and refeeding on insulin action in healthy men. J Appl.Physiol, 99, 2128-2136.

Heilbronn, L. K., Smith, S. R., Martin, C. K., Anton, S. D., & Ravussin, E. (2005). Alternate-day fasting in nonobese subjects: effects on body weight, body composition, and energy metabolism. Am J Clin Nutr., 81, 69-73.

Johnson, J. B., Summer, W., Cutler, R. G., Martin, B., Hyun, D. H., Dixit, V. D. et al. (2007). Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. Free Radic.Biol.Med, 42, 665-674.

Kruger, J., Ham, S. A., & Prohaska, T. R. (2009). Behavioral risk factors associated with overweight and obesity among older adults: the 2005 National Health Interview Survey. Prev.Chronic.Dis., 6, A14.

Steyer, T. E. & Ables, A. (2009). Complementary and alternative therapies for weight loss. Prim.Care, 36, 395-406.

Varady, K. A. & Hellerstein, M. K. (2007). Alternate-day fasting and chronic disease prevention: a review of human and animal trials. Am J Clin Nutr., 86, 7-13.

Read Full Post »

Older Posts »