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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:

OVERWEIGHT AND OBESITY: INCIDENCE AND PREVALENCE

  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)

WHY OVERWEIGHT-OBESITY IS A PROBLEM

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).

MY TAKE ON BODY-SHAMING

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!

quotes_my_quotes_body_shaming.jpg

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

TAKE HOME MESSAGE

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

REFERENCES

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.

 

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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.

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cafe_neroGet off the Tube – straight into the nearest Cafe Nero  – pick up your favorite coffee and then off to work – isn’t that what most of us do?! Don’t we all love having our coffees, especially first thing in the morning? Yes, we do! – The reason being?! Well, for sure one of the reasons has got to be that coffee really ‘gets you going’ first thing in the morning. But, have you ever wondered how your innocuous looking cup of coffee manages to do that? Read on to find out more.

CAFFEINE

Let’s face it, we have to drink coffee every single morning coz somewhere along the line, we’ve got addicted to caffeine present in our coffee. It is this caffeine that is responsible for the ‘gets me going’ phenomenon!

It shouldn’t come as a surprise then that caffeine is the most ingested psychoactive drug (stimulant) in the world. It is a of major contents of almost all ‘stimulant’ beverages like tea, coffee, cola and energy drinks (not to mention thermogenic fat loss supplements).

According to Starbucks information on beverages, a tall latte’ contains 150mg of caffeine (filter coffee ‘venti’ – meaning twenty in Italian – is low in calories but contain a whopping 400mg per serving). Taking in that amount of the drug can have profound effects on your physiology.

What exactly are these effects and how does caffeine in your tall, skinny latte’ help you to get ‘switched on’, you might want to ask? Well, read on to find out more.

CHEMICAL STRUCTURE AND PHARMACOKINETICS OF CAFFEINE

But before we get into the intricacies of what makes caffeine tick, let us have a closer look at what caffeine really is. Chemically, caffeine is 1,3,7-trimethylxanthine.

Derived from the purine xanthine, methylxanthines have numerous medicinal applications, especially in lung disease. Apart from caffeine, other methylxanthines of note are theophylline, aminophylline (both of which are used as bronchodilators – in asthma), paraxanthine and theobromine. As you may have guessed, methylxanthines are  cardiac and CNS stimulants and bronchodilators (with individual variations, of course).

On ingestion, caffeine is expeditiously absorbed through the lining of the gastrointestinal tract. Within 15 minutes of consumption of coffee, trace levels of caffeine appear in blood; peak concentrations are reached within an hour 1.

Caffeine is highly lipid soluble (dissolves rapidly and completely in fat). Thus, it can cross cell membranes (of muscle and nerve cells), especially, the blood-brain barrier (a partition which allows only certain chemicals to enter the brain matter).

Caffeine exerts its action (as given below) on various systems through a number of proposed mechanisms.

After exerting its action, caffeine is broken down by the liver and kidneys – metabolites (break down products) that are formed are paraxanthine, theobromin and theophylline1. Incidentally, these metabolites have actions similar to caffeine as well – theophylline is considered even more potent!

ACTIONS OF CAFFEINE 

As mentioned previously, caffeine is the most often used stimulant in the world with prominent actions on the central nervous system as well as metabolism. As opposed to caffeine present in drinks, anhydrous form of caffeine (in the form of capsule/tablet/powder) is more potent.

Pharmacologically, caffeine is a competitive adenosine-receptor agonist, i.e. it serves as a competition for adenosine at its receptor. This receptor is responsible for suppressing neurotransmitters like adrenaline, nor-adrenaline, acetylcholine, dopamine and serotonin. Thus, ingestion of caffeine increases the production of these neurotransmitters.

However, since these neurotransmitters have complex and sometimes conflicting actions, effects of caffeine in endurance, strength and explosive sports (enhancement of performance, recovery and hydration) can be conflicting as well.

However, the main actions of caffeine can be described as under:

  • COGNITIVE EFFECTS

Caffeine improves wakefulness and vigilance. It may be also responsible for improved skill levels, especially those acquired through repeated training 2.

Foskett et. al. demonstrated in their study, improved cognitive parameters in athletes due to caffeine ingestion with enhanced sprint abilities as well as ball passing, ball control and accuracy associated with acute ingestion of caffeine3.

Because caffeine in low to moderate doses (3-6 mg/kg of body weight) has been shown to cause improved concentration during sleep-deprived spells, it may find application in services like the Special Forces 2.

  • THERMOGENIC EFFECTS

Consumption of caffeine causes stimulation of metabolism and a significant increase in the production of energy 4 – thermogenic action of caffeine has been shown to last for almost 3 hours after ingestion 4. Caffeine causes mobilization of free fatty acids and fat oxidation to produce energy during exercise 5-7. Additionally, it causes extra-muscular fat oxidation as well. Thus, caffeine seems to be definitely associated with causing fat loss 7.

These metabolic-stimulatory and fat-burning effects make caffeine a crucial ingredient of most fat-loss supplements (thermogenics).

  • ENHANCED EXERCISE ABILITY 

It is believed that caffeine enhances exercise performance. This is owing to its ‘glycogen-sparing effect’ – decreased utilization of muscle glycogen for energy during exercise – fats are used instead. Thus, owing to muscles glycogen lasting longer, the setting in of fatigue is prolonged.

Also, caffeine supports formation of new glycogen (glycogenesis) and thus aids in recovery after an intense exercise session.

Enhanced secretion of endorphins induced by caffeine is also a presumed mechanism in enhancing exercise performance 8 – the resultant decrease in pain perception leading to ‘feel good factor’ of beta-endorphins is well-documented 9.

In addition to the above findings, research also suggests that caffeine can improve neuromuscular transmission and muscle contraction 10;11 – both isometric and muscle endurance components are improved 10.

 To conclude, research overwhelmingly supports the view that caffeine enhances performance in endurance events 5;12, sports involving muscle power-strength components 13;14 as well as high intensity team sports 14;15.

TAKE HOME MESSAGE

So, the next time you are sipping that favourite coffee of yours, you know exactly what it is doing to you!

To sum up, caffeine has the following effects:

  • is more potent when ingested in the anhydrous state (as a tab/capsule/powder supplement rather than as coffee)
  • aids in sports performance
  • improves skills acquisition in sports – like ball control and passing
  • supports new glycogen formation (glycogenesis) and thus helps quicker recovery from an exercise session
  • prolongs exercise induced fatigue – by their ‘glycogen-sparing’ effect so you can keep going for a longer
  • improves neuromuscular transmission and muscle contraction
  • has thermogenic effects – stimulates metabolism causing burning of calories
  • induces fat loss – mobilizes fatty acids from fat stores and uses these as substrate (instead of glycogen) for producing energy
  • improves concentration – especially during sleep-deprived states
  • secretes beta-endorphins – makes you feel good

 References

  1.  Harland BF. Caffeine and nutrition. Nutrition 2000; 16(7-8):522-526.
  2. Lieberman HR, Tharion WJ, Shukitt-Hale B, Speckman KL, Tulley R. Effects of caffeine, sleep loss, and stress on cognitive performance and mood during U.S. Navy SEAL training. Sea-Air-Land. Psychopharmacology (Berl) 2002; 164(3):250-261.
  3. Foskett A, Ali A, Gant N. Caffeine enhances cognitive function and skill performance during simulated soccer activity. Int J Sport Nutr Exerc Metab 2009; 19(4):410-423.
  4. Astrup A, Toubro S, Cannon S, Hein P, Breum L, Madsen J. Caffeine: a double-blind, placebo-controlled study of its thermogenic, metabolic, and cardiovascular effects in healthy volunteers. Am J Clin Nutr 1990; 51(5):759-767.
  5. Ivy JL, Costill DL, Fink WJ, Lower RW. Influence of caffeine and carbohydrate feedings on endurance performance. Med Sci Sports 1979; 11(1):6-11.
  6. Erickson MA, Schwarzkopf RJ, McKenzie RD. Effects of caffeine, fructose, and glucose ingestion on muscle glycogen utilization during exercise. Med Sci Sports Exerc 1987; 19(6):579-583.
  7. Spriet LL, MacLean DA, Dyck DJ, Hultman E, Cederblad G, Graham TE. Caffeine ingestion and muscle metabolism during prolonged exercise in humans. Am J Physiol 1992; 262(6 Pt 1):E891-E898.
  8. Laurent D, Schneider KE, Prusaczyk WK, Franklin C, Vogel SM, Krssak M et al. Effects of caffeine on muscle glycogen utilization and the neuroendocrine axis during exercise. J Clin Endocrinol Metab 2000; 85(6):2170-2175.
  9. Grossman A, Sutton JR. Endorphins: what are they? How are they measured? What is their role in exercise? Med Sci Sports Exerc 1985; 17(1):74-81.
  10. Kalmar JM, Cafarelli E. Effects of caffeine on neuromuscular function. J Appl Physiol 1999; 87(2):801-808.
  11. Lopes JM, Aubier M, Jardim J, Aranda JV, Macklem PT. Effect of caffeine on skeletal muscle function before and after fatigue. J Appl Physiol 1983; 54(5):1303-1305.
  12. Hogervorst E, Bandelow S, Schmitt J, Jentjens R, Oliveira M, Allgrove J et al. Caffeine improves physical and cognitive performance during exhaustive exercise. Med Sci Sports Exerc 2008; 40(10):1841-1851.
  13. Woolf K, Bidwell WK, Carlson AG. The effect of caffeine as an ergogenic aid in anaerobic exercise. Int J Sport Nutr Exerc Metab 2008; 18(4):412-429.
  14. Beck TW, Housh TJ, Schmidt RJ, Johnson GO, Housh DJ, Coburn JW et al. The acute effects of a caffeine-containing supplement on strength, muscular endurance, and anaerobic capabilities. J Strength Cond Res 2006; 20(3):506-510.
  15. Schneiker KT, Bishop D, Dawson B, Hackett LP. Effects of caffeine on prolonged intermittent-sprint ability in team-sport athletes. Med Sci Sports Exerc 2006; 38(3):578-585.

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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.

 

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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.

 

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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.

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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.

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