The role of exercise in weight loss

Regular exercise can help lower the risk of cardiovascular disease, improve bone density and muscle tone, maintain a healthy weight, improve hemoglobin A1c levels, work wonders against psychological stress and anxiety, lessen arthritis pain and lower the risk of Alzheimer’s disease (1,2,3,4).  It will not, however, make you lose weight (5).


You shouldn’t be.  Think about it:  you can consume 500 calories (a slice of cheesecake or a 10 oz Margarita) in just a few minutes, but it takes an adult of 150 lbs over two hours of fast paced walking, or over one hour of vigorous running, to burn the same amount (1).  If you wish to burn more than 500 calories, to lose weight (as opposed to simply burning off the added calories), it will take an additional hour or so to create the desired negative balance. If the Margarita and the cheesecake slice were both a part of your after dinner indulgence, you’re looking at over 1,000 calories (making up half the daily caloric requirement for most healthy adults) that you must make disappear just to maintain your current weight.

In other words, you can’t outrun your mouth.  Or, to be fair, you can’t outrun your mouth if you have a life which includes a job, commute to work, a household to maintain, child care or other such activities as part of your daily routine.  There simply isn’t enough time in the day to compensate (with exercise) for added calories.  Maybe you can pull it off once in a while but most of the time, it’s a bit of a stretch.

If you have a reasonably healthy body mass index (BMI), regular exercise, which includes endurance as well as weight bearing activities, will go a long way toward keeping all your bits and parts in tip-top shape and your weight in a healthy range.  You will also run a significantly lower risk of gaining unwanted pounds.

You may be wondering:  if regular exercise can have such a positive effect on the body, why even mention that it falls short in terms of weight loss?


When you operate under the assumption that working hard at the gym is going to yield equally impressive results on the bathroom scale, you may be deeply disappointed with the outcome, which, in turn, may translate into disillusionment and very likely, a defeatist attitude.   “Nothing I try works” is a phrase I hear frequently from people who busted their butts at the gym for months, five days a week or more, only to see trivial changes in weight, sometimes, almost against all reason, on the plus side.  That all this work has improved their overall endurance is of little comfort when their pant/dress size has not changed for the better.

It’s not a matter of not having worked out hard enough, or long enough, or regularly enough.  It’s a matter of focusing on the wrong approach then feeling helpless when, after all the time and effort invested in it, the approach fails.

In a trial published in the Journal of American Medical Association in 2003, researchers monitored the weight fluctuations of 184 overweight women participating in various levels of physical activities over the course of 12 months (2).  The women were divided into four groups:

  • vigorous intensity / high duration exercise
  • moderate intensity / high duration exercise
  • moderate intensity / moderate duration exercise, and
  • vigorous intensity / moderate duration exercise.

All the participants benefited from varying levels of improvement in cardiovascular fitness by the end of the trial.   There was no significant difference in terms of weight loss between women at the high end of the intensity/duration exercise spectrum and those at the low end.  High intensity workouts lasting longer periods of time did not yield an advantage, in terms of weight loss, over moderate intensity and moderate duration regimens.

Similarly, the authors of a 2007 study looking at the effects of exercise on cardiovascular fitness divided 464 previously sedentary overweight and obese women participants into four groups: a no-exercise control group or one of three groups in which they expended 4, 8 or 12 calories per kilogram of weight, per week, for a period of six months by engaging in various intensities and durations of physical activity (5). Upon completion of the study, the authors found graded dose response changes in heart fitness across all levels of exercise, but no significant changes in weight.  Exercise alone, regardless of intensity or duration, did not amount to a hill of beans in terms of weight loss, even when routines were maintained for as long as six months.

Several factors account for these somewhat counterintuitive outcomes including increased hunger (and, thus, food consumption) as a result of vigorous exercise, a tendency for people to relax their calorie counting on the days they work out (or they think they can indulge today because they are going to work out tomorrow), the notion that they deserve a reward (read: chocolate lava cake) for all the hard work they’ve completed, and a host of other physiological and psychological factors.  These studies are mere drops in a virtual ocean of evidence that weight loss occurs in the wake of dietary changes, rather than as a result of vigorous exercise routines (6).  “Ah, but muscle weighs more than fat!” you might say, “so, no change in weight doesn’t necessarily mean no change in body size!”  True, but the overwhelming evidence suggests the lack of improvement is not specific to weight, but to overall measurements as well, whenever exercise routines are the only intervention. If study participants ended the trials several dress sizes smaller but weighing the same, there would be no point to having this discussion.

That being said, regular physical activity not only helps keep the weight off, but helps protect against a great number of diseases of affluence (cardiovascular disease, diabetes).  As such, it is an important part of any healthy lifestyle (7,8).

If you are trying to lose weight, it is important to focus on making permanent changes  to your dietary habits.  Popular fad diets don’t work in the long run and exercise alone is not going to help you reach your goals.  There is a sense of helplessness that accompanies the generally disappointing outcomes of making uninformed weight loss regimen choices.  You  may end up feeling as though nothing you try works, therefore, there’s no sense in trying.

A healthy diet that focuses on plant based foods goes a long way toward normalizing caloric intake, body weight and metabolic markers with or without the help of an exercise regimen (9,10).  Talk to a dietitian and/or qualified nutrition counsellor and get the help you need to make permanent lifestyle changes.  Some gyms have dietitians on staff whose services are included in your gym membership.  Work on your dietary habits/choices, and the rest will follow.  It is easier and healthier to watch your caloric intake than to fight an uphill battle while trying to  compensate for added calories by working out.


  1. Centers for Disease Control and Prevention, Division of physical activity and obesity.  Why is physical activity important? 2012. Available at:  Accessed June 2, 2012.
  2. Jakicic JM, Marcus BH, Gallagher KI, Napolitano M, Lang W.  Effect of exercise duration and intensity on weight loss in overweight, sedentary women – a randomized trial.  JAMA 2003; 290(10): 1323-1330.
  3. Church TS, et al. Effects of aerobic and resistance training on hemoglobin A1c levels in patients with type 2 diabetes.  JAMA 2010; 304(20): 2253-2262.
  4. Scarmeas N, et al. Physical activity, diet, and risk of Alzheimer’s disease.  JAMA 2009; 302(6): 627-637.
  5. Church TS, Earnest CP, Skinner JS, Blair SN. Effects of different doses of physical activity on cardiorespiratory fitness among sedentary overweight or obese postmenopausal women with elevated blood pressure. JAMA 2007; 297(19):2081-2091.
  6. Rock CL, Flatt SW, Sherwood NE, Karanja N, Pakis B, Thomson CA.  Effect of a free prepared meal and incentivized weight loss program on weight loss and weight loss maintenance in obese and overweight women.  JAMA 2010; 304(16): 1803-1811.
  7. Hankinson AL, et al.  Maintaining a high physical activity level over 20 years and weight gain. JAMA 2010; 304(23): 2603-2610.
  8. Lee I, Djousse L, Sesso HD, Wang L, Buring JE.  Physical activity and weight gain prevention.  JAMA 2010; 303(12): 1173-1179.
  9. Newby PK, Tucker KL, Wolk A. Risk of overweight and obesity among semivegetarian, lactovegetarian, and vegan women. AJCN, 2005; 81: 1267-74.
  10. Vergnaud A, et al.  Meat consumption and prospective weight change in participants of the EPIC-PANACEA study.  AJCN 2010; 92: 398-407.

Protein powders and shakes

A few decades ago, protein powders used to lurk in gyms and so-called “health” food stores. They were stacked neatly on shelves amidst colourful ads that lured would-be buyers with images of famous bodybuilders and athletes whose physiques few of them would ever match. In those days, their primary targets were body builders. Claims varied, but most brands promised increased muscle gain that, according to the ads, run of the mill, food derived protein could not possibly provide.

Today, protein powders have escaped the confines of gyms and health food stores and have become ubiquitous on food market shelves, in pharmacies, and virtually anyplace else food, supplements, or pharmaceuticals are sold. Their user base has changed dramatically to include athletes (professional sports people who are not bodybuilders), recreational athletes (sport hobbyists and/or fitness enthusiasts), and lifestyle users (consumers who think protein powders are healthy snacks and/or will help them lose weight)(1). Vegetarian and vegan consumers of protein powders tend to fall in the last two categories and are likely to believe the powders, or other similar supplements, are necessary to meet their daily protein needs. Some users claim they “feel better” and have more energy when they consume protein powders, while others simply believe that without their daily dosage, their muscles would vanish into thin air.


“The extra protein gives me energy!” is a claim I hear surprisingly often. It is surprising because protein is a lousy source of energy. It is a last resort the body will tap when it runs out of its preferred fuel (particularly during exercise): glycogen (aka stored carbohydrate)(2). You may have heard of athletes engaging in something called “carb-loading” before events. This consists of consuming a higher ratio of carbohydrates to help the body handle the energy requirements of extended activity, particularly if the event involves increasing pace and effort to beat the competition (3). The more intense the exercise, the more carbohydrate the body burns. Consuming carbs before and during exercise helps athletes keep up the pace. In fact, a high carbohydrate diet increases endurance time three-fold when compared to a high protein diet (3). Once glycogen runs out, so does your energy and ability to keep going. Similarly, failing to replenish your glycogen stores after exercise, will impair your ability to recover and achieve your training goals.

During periods of extended low intensity exercise, such as walking, fat becomes an important source of energy, more so if you engage in regular exercise. The more you train, the more your body uses fat for energy when you are resting or performing less strenuous activities. As you pick up the pace, your body switches back to using glycogen.

Image source:  McArdle et al. – Sports and Exercise Nutrition, 3rd Ed., Chapter 5, Macronutrient Metabolism in Exercise and Training, page 157 (3).

In a nutshell, if you’re looking for extra energy, put away the protein powder and have some healthy carbs instead.


Muscle growth occurs as the result of training, not from the overconsumption of protein. There is only so much protein the body will use before it stores the excess away. Protein powders are digested faster than food derived protein, making protein available for muscle repair in a more expedited manner. “Aha!” you might say, “so, they ARE good for something!” Well, not really. In the long run, the end result is about the same – except, perhaps, for your wallet.

Studies looking at the effects of supplementation and strength training combined show insignificant or no difference between placebo and control groups (2,4).  In their 2009 joint position paper on nutrition and athletic performance, the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine concluded the following (5):

“Current evidence indicates that protein and amino acid supplements are no more or no less effective than food when energy is adequate for gaining lean body mass. Although widely used, protein powders and amino acid supplements are a potential source for illegal substances such as nandrolone, which may not be listed on the ingredient label.”

In other words, as long as you meet your body’s protein requirements, it doesn’t make much difference if you’re getting the protein fast, from a powder, or slower, from food. What matters most is timing (6). Consumption of protein and carbohydrate containing foods immediately after training is far more important if you want to see results. The sooner you eat, the better. Letting as little as two hours pass after a workout without eating will lead to a lot of disappointment on your part if you’re looking to build muscle mass (7).


For best results in terms of performance and overall health (the latter is sometimes overlooked when people consider a plan of action in the short term), remember that supplements are not a replacement for healthy food choices.

Eat breakfast, consume the appropriate amount of calories for your body (don’t forget to eat healthy fats), stay hydrated and be sure to eat before and after exercise. If you like coffee or tea, you may be surprised to know that caffeine is an effective ergogenic aid, particularly in racing events, but also in short term, high intensity events, if consumed one hour before exercise (8,9). If you’ve given up coffee and tea because you think it will hinder your performance, dehydrate you, or interfere with electrolyte balance, you may want to reconsider your choice (8,9,10).

While studies on the effects of protein restriction on performance have yielded inconclusive results, the same is not true when it comes to carbohydrate restriction which has been shown to be detrimental (11,12). The importance of carbohydrate consumption after workouts can not be overemphasized. The aforementioned position paper on nutrition and athletic performance provides the following guidelines for performance athletes (5):

  • Carbohydrate recommendations for athletes range from 6-10 g/kg (2.7-4.5 g/lb) body weight per day depending on extent and duration of exertion (5).
  • Protein recommendations for endurance and strength trained athletes range from 1.2-1.7 g/kg (0.5-0.8 g/lb) body weight per day. The authors stress that food sources can easily meet requirements and supplementation is not necessary (5).
  • Fat intake should range from 20%-35% of total energy intake. Note that consuming less than this will not improve performance (5).
  • Before exercise, a meal or snack “should provide sufficient fluid to maintain hydration, be relatively low in fat and fiber to facilitate gastric emptying and minimize gastrointestinal distress, be relatively high in carbohydrate to maximize maintenance of blood glucose, be moderate in protein, be composed of familiar foods, and be well tolerated by the athlete.”(5)
  • During exercise, it is important to replace fluid losses and “provide carbohydrates (approximately 30-60 g per hour) for maintenance of blood glucose levels.”(5)
  • After exercise, “a carbohydrate intake of ~1.0-1.5 g/kg (0.5-0.7 g/lb) body weight during the first 30 minutes and again every 2 hours for 4 to 6 hours will be adequate to replace glycogen stores. Protein consumed after exercise will provide amino acids for building and repair of muscle tissue.”(5)

To put things in perspective, let’s consider the nutritional requirements of a 160 pound male professional soccer player:

Calories: approx. 4,000 per day
Protein: approx. 110 grams per day, or 11% of daily calories
Carbs: approx. 640 grams per day, or 64% of daily calories
Healthy Fats: approx. 111 grams per day, or 25% of daily calories

Notice that although 110 grams of protein per day represents quite a bit more than the amount of protein recommended for weekend athletes or sedentary persons, this amount does not represent a higher percentage of daily calories. In other words, it is not added (or supplemented) protein.


If the only way you are meeting your protein requirements is by supplementing with protein powders, there is something wrong with your diet. It should not be difficult to meet the recommended 10% to 15% of your daily calories in the form of protein. In fact, I would be very surprised if this is the case, given the abundance of food varieties available in North America. In the unlikely event you are not getting enough protein or the necessary ratios of essential amino acids, tweaking your diet will be better for your health (and for your wallet) in the long run than starting a protein supplementation habit.


  1. Overview of the Sports Nutrition Market—Food, Beverages and Supplements, 2010; ISSN 1920-6593 Market Analysis Report, AAFC No. 10745E.
  2. Maughan RJ. Nutrition in Sport – Volume VII of the Encyclopedia of Sports Medicine. MA: Blackwell Science, Inc.; 2000.
  3. McArdle WD, Katch FI, Katch VL. Sports and Exercise Nutrition, 3rd Ed. MD: Lippincott Williams & Wilkins; 2009.
  4. Williams AG, van den Oord M, Sharma A, Jones DA. Is glucose/amino acid supplementation after exercise an aid to strength training? Br J Sports Med, 2001;35:109-113.
  5. Nutrition and athletic performance. Journal of the American Dietetic Association, 2009; 109(3):509-527.
  6. Poole C, Wilborn C, Taylor L, Kerksick C. The role of post-exercise nutrient administration on muscle protein synthesis and glycogen synthesis. Journal of Sports Science and Medicine, 2010;9:354-363.
  7. van Essen M, Gibala MJ. Failure of protein to improve time trial performance when added to a sports drink. Med Sci Sports Exerc. 2006;38:1476-1483.
  8. Cox GR, Desbrow B, Montgomery PG, Anderson ME, Bruce CR, Macrides TA, Martin DT, Moquin A, Roberts A, Hawley JA, Burke LM. Effect of different protocols of caffeine intake on metabolism and endurance performance. Journal of Applied Physiology, 2002:93:990-999.
  9. Paluska SA. Caffeine and exercise. Current Sports Medicine Reports, 2003;2:213-219.
  10. Bell DG, McLellan TM. Effect of repeated caffeine ingestion on repeated exhaustive exercise endurance.  Medicine & Science in Sports & Exercise, 2003; DOI: 10.1249/01.MSS.0000079071.92647.F2
  11. Knechtle B, Knechtle P, Mrazek C, Senn O, Rosemann T, Imoberdorf R, Ballmer P. No effect of short-term amino acid supplementation on variables related to skeletal muscle damage in 100 km ultra-runners – a randomized controlled trial. Journal of the International Society of Sports Nutrition, 2011;8:6.
  12. Ivy JL, Res PT, Sprague RC, Widzer MO. Effect of a carbohydrate-protein supple- ment on endurance performance during ex- ercise of varying intensity. Int J Sport Nutr Exerc Metab. 2003;13:382-395.

Lab meat – a healthier alternative?

Over the last decade, news stories featuring the advent of lab meat technology and its pink and pasty results have been peppering the virtual landscape, showing up in places like NBC, Forbes and a number of other news outlets.  It seems the lab grown burger is now ready for production, and, at some point in the future, for sale in your local stores and restaurants.  It has been touted as a way to improve diets in emerging economies by introducing cheaply produced meat on their markets, but is it any healthier than its traditionally produced counterpart?


Lab grown meat is cultivated from animal cells, so, in the case of hamburger, the cells come from a cow.  Unlike conventional meat, lab meat can be produced with far less fat, but not without the use of growth hormones, seeing how it has to grow quickly in order to be profitable (1).  Since lab meat is real animal flesh, haem iron is present, as is the increased risk for cardiovascular disease and bowel cancer it represents (see my earlier post on iron).  Producers are going out of their way to make sure this type of iron is included in the final product since they see any deviation from the real thing as a downside in terms of marketing (1).

No mention has been made regarding the presence of neu5gc in non-human mammals, nor of any possibility that lab meat can be produced without it (2). This is unfortunate given this molecule’s effects on the human body include a chronic state of low grade inflammation (for as long as meat and dairy are consumed),   involvement in arteriosclerosis, cancer progression, and the facilitation of hemolytic ureic syndrome, among other things (3,4,5). “Neu5Gc is present both in endothelium overlying plaques and in subendothelial regions, providing multiple pathways for accelerating inflammation” in arteriosclerosis (3).

Neu5gc is a sialic acid present on cell surfaces of all mammals with the exception of humans. We do not produce it, but we have antibodies which, to the surprise of its discoverers, are unable to fight it off completely (4).  When found setting up camp in our bodies it is there because we ingested it (5).  It is the only known non-human dietary molecule that becomes incorporated onto human cell surfaces  even after the immune system responds against it.  The immune response to the ever-present molecule sets off a repeating cycle wherein the resulting chronic inflammation helps tumours grow even as antibody response is boosted.  But it isn’t all bad news. All this research into what is now known as the “meat eater’s molecule” has yielded one surprising result:  aggressively boosting antibody response against it may help fight the tumours it helps produce in the first place (4).  Of course, staying away from eating the meat of four legged creatures, natural or lab made, would be the easiest way to avoid this whole cycle.

Lastly, animal protein is animal protein regardless of whether it comes from a slaughtered animal or artificially maintained animal cells.  Recent evidence suggests animal protein may increase cardiovascular disease risk in healthy men after controlling for confounders such as saturated fat (7).  Potential manufacturers have considered introducing plant protein into their final product but canned the idea as fears this may raise allergy issues for consumers prevailed (1).


Lab meat will give the environment and farm animals a break, to be sure, but, aside from containing less fat than conventional animal products, daily consumption will yield many of the same risk factors as conventional, organic, or wild caught meats.


  1. Datar I, Betti M. Possibilities for an in vitro meat production system.  Innovative Food Science and Emerging Technologies, 2010;11:13-22.
  2. Varki A. Uniquely human evolution of silica acid genetics and biology. PNAS, 2010;107(2):8939-8946.
  3. Pham T, Gregg CJ, Karp F, Chow R, Padler-Karavani V, Cao H, Chen X, Witzum JL, Varki N, Varki A.  Evidence for a novel human-specific xeno-auto-antibody response against vascular endothelium. Blood, 2009;114(25):5225-35.
  4. Hedlund M, Padler-Karavani V, Varki N, Varki A. Evidence for a human-specific mechanism for diet and antibody-mediated inflammation in carcinoma progression.  PNAS, 2008;105(48):18936-41.
  5. Lofling JC, Paton AW, Varki NM, Paton JC, Varki A.  A dietary non-human silica acid may facilitate hemolytic-uremic syndrome.  Kidney Int., 2009;76(2):140-144.
  6. Varki N, Varki A. Diversity in cell surface silica acid presentations: implications for biology and disease.  Laboratory Investigation, 2007;87:851-7.
  7. Preis SR, Stampfer MJ, Spiegelman D, Willett WC, Rimm EB.  Dietary protein and risk of ischemic heart disease in middle-aged men. Am J Clin Nutr, 2010;92:1265-72.

Caloric restriction

In 1935, a study on caloric restriction in mice provided evidence, for the first time, that such an undertaking can promote longevity and disease fighting ability in mammals1.  Until then, only studies on yeast and lower animals had been completed in this area of research.  The novelty of the mouse study soon wore off, however, and the findings were not revisited until some time in the late 1980’s / early 1990’s, when interest in caloric restriction was renewed.  At that time, scientists wondered if the effects would be similar in primates, and, as a result, in humans.

Longitudinal studies using primates were soon underway, and now, nearly three decades later, the results look promising.  The primates of choice, for most undertakings, were (are) Rhesus monkeys.  Rhesus monkeys have a lifespan of approximately 35 to 40 years, making them easier to study, in terms of longevity and disease development, than higher primates such as chimpanzees or humans, whose lifespans are generally twice as long.

Research using mice, and a host of other species, continued alongside primate studies in an effort to accumulate as much comparable data as possible.  Yeast research has also continued, in most part due to striking working mechanism similarities that seem to span across all species studied thus far.

The question on everyone’s mind was “will caloric restriction have the same effect on all species studied?”.   An affirmative answer would strongly suggest the same to be true of humans.  Indeed, this is precisely what research to date has determined:  all species studied thus far have reacted in much the same way to caloric restriction.  Human studies following these findings have also yielded promising results.


Caloric restriction should not be confused with, or lead to, malnutrition.  Two types of caloric restriction have been identified to have an effect on aging and disease:  transient and sustained caloric restrictions.   Moderate and pronounced caloric restrictions have been found to improve health and longevity.

Transient caloric restriction refers to short-term restrictions that occur once, or several times, over the course of the lifespan.   Sustained caloric restriction involves a drop in daily caloric intake from the onset of the study through the end of the subject’s life.  Of these, sustained, pronounced caloric restriction has been found to have the greatest positive impact on disease prevention and longevity.

Moderate caloric restriction entails a reduction of daily caloric intake by 15% to 17%, whereas, pronounced caloric restriction involves a reduction of approximately 30%.  In terms of human caloric needs, 30% less calories would translate into a reduction of approximately 700 calories per day for a healthy adult whose BMI is in the recommended range and who normally consumes 2,500 calories daily, leading to a total caloric intake of 1,800 per day. 


Transient caloric restriction studies are scarce, yet, they are as important as sustained restriction studies because the former is the most likely to be implemented by people over the course of their lives.  While most people have difficulty maintaining sustained caloric restriction for the entirety of their lifespans, many have dieted over the courses of their lives, and some have repeatedly engaged in “yo-yo dieting”, the latter having been shown by recent studies to be most likely to have detrimental effects on overall health.

The Dutch famine of 1944 – 1945 has been the subject of a number of studies on transient caloric restriction and its long term effects, in most part because the subjects were human. The first studies of the Dutch famine had surprising results (which more recent studies have since replicated).  Unlike sustained moderate or pronounced caloric restriction, transient restriction emerged as a risk factor for breast cancer later in life.  In addition, women who were exposed to the famine as children experienced subsequent reproductive difficulties.

This discovery prompted researchers to attempt replicating the findings using animal models.  They were not disappointed.  Studies in mice have repeatedly shown that while sustained caloric restriction works wonders against cancer onset and development, transient restriction has the opposite effect.  A study on the influence of underfeeding during the “critical period”, or thereafter, on carcinogen-induced mammary tumors in rats, concluded that transient restriction followed by ad libitum feeding could lead to increased cancer risk.  Another similar study by Kritchevsky on the promotion phase of cancer development found that not only was the risk of cancer increased in the wake of transient caloric restriction (“yo-yo dieting”), but that the study subjects gained a disproportionate amount of weight, very quickly, once the restriction was lifted3.


Another 2002 study on the effects of sustained caloric restriction in mice found a 60% reduction in the number of precancerous intestinal polyps in mice at high risk for gastrointestinal cancers4.  The same study found that mice consuming a diet high in fruits and vegetables had 33% fewer polyps that the control mice, suggesting that even moderate caloric restrictions have a positive effect on the reduction of tumor formation.

A longitudinal study on Rhesus monkeys which began in 1989 at the Wisconsin National Primate Research Center (WNPRC) is perhaps one of the most telling in that it documented not only the effects of sustained caloric restriction on cancer, but on longevity and overall health of the subjects.  The photographic account/evidence of physiological changes is most striking1.

The Rhesus monkeys who participated in the WNPRC study generally have a lifespan of about 27 years.  All animals were adults when the study began (the results of which are a testament that it is never too late to impact the outcome of one’s life), ranging in ages from 7 years to 14 years.  Over the course of a six month period, the caloric restriction group (CR group) was slowly acclimated to a 30% decrease in daily caloric intake.  The CR animals maintained this level of caloric intake for the remainder of their lives.

Age related diseases in Rhesus monkeys had been well documented at the WNPRC and are very similar to those of humans’.  They include cancer, cardiovascular disease, and diabetes.  Over the course of the study, the CR animals experienced a decrease in body weight while maintaining a healthy BMI, thus, reducing their risk for obesity, which, in turn, is a risk factor for cancer.  Furthermore, they consistently experienced improved metabolic function, specifically, insulin sensitivity.  The incidence of cancer, which normally increases with age in Rhesus monkeys, was reduced by 50% in the CR group (as was the incidence of cardiovascular disease, also by 50%).  The biological age of the CR group monkeys became significantly younger than that of their cohorts in the control group.  A similar effect has been found in studies of people on long term CR1.


Restriction of calories stresses the organism resulting in a response by DNA repair enzymes and apoptosis (programmed cell death) which protect the body from environmental insults.  “[The] proliferation of cells is reduced with both increased rates of apoptosis together with decreased DNA synthesis and increased DNA repair, limiting the number of preneoplastic lesions. Oxidative stress is reduced, resulting in decreased reactive oxygen species that can damage DNA. Furthermore, of interest to hormone associated tumours, levels of a number of hormones and growth factors are altered during caloric restriction: glucocor- ticoids are increased whereas concentrations of IGF-I (and to a lesser extent IGFBP-3 resulting in decreased bioavailability of IGF-I), insulin, prolactin, estrogens and leptin are decreased.”3.

A DNA transcription factor called heat shock factor 1 (HSF1), which is regulated by the enzyme sirtuin 1 (SIRT1), exists as a monomer in unstressed mammalian cells.  It responds to stresses such as the free radicals that play a role in carcinogenesis by resolving damaged, misfolded, and aggregated proteins.  As we age, the amount of SIRT1 protein decreases and HSF1 concentration increases.  Sustained caloric restrictions has been found to cause overexpression of SIRT1, which, in turn, enhances the ability of cells to survive prolonged exposure to heat shock temperatures.  SIRT1, therefore, functions as a positive cofactor of HSF1 and enhances the heat shock response5.

The discovery that caloric restriction is beneficial has been publicized in the main stream media for many years, albeit not as heavily as it deserves to be. Public reaction has generally been positive, yet, as expected, no sustained efforts to adopt lower calorie lifestyles have been observed in the general population.

In the West, where high calorie foods are stocked in great proportions on supermarket shelves and fast food restaurants pepper the landscape in astronomical numbers, temptation is unavoidable.  It is around every corner, invading our homes, workplaces, and cars via the airways, with corporate advertisements designed to entice and titillate, all of which are backed by significant market research into what people like and what works best to get them pining for the goods on display.  Few people stand a chance, and fewer yet are aware of the impact such advertisements and supermarket food displays have on us. Most of us are convinced that such things do not sway us, yet our collective Western girth seems to indicate otherwise.

Complicating matters is the average person’s upbringing and dietary habits that follow and impact our lives since before we are born.  According to recent studies, an expectant mother’s dietary choices can influence her unborn child’s future eating habits and overall health2.  High fat, high calorie food exposure in the womb can adversely affect the development of normal leptin balance in the fetus and can predispose the child to calorie rich food cravings that eventually result in life long weight and related health problems.  Adding insult to injury, most parents will feed their children the same kind of unhealthy diets that they themselves consume, further ensuring that poor dietary habits become engrained and more difficult to break later on.  Many still believe that being plump and cherub-like are desirable qualities in small children and often insist that children finish everything on their plates.

A reduction in caloric intake generally requires a significant change in food choices.  A person accustomed to eating a diet heavy in processed foods, meats, and dairy would have a fair amount of difficulty reducing caloric intake while at the same time continuing to enjoy these foods and not be left feeling hungry.  Reduced caloric intake without a life-long struggle against hunger can only be achieved by adopting a Mediterranean, vegetarian, or vegan life style.  Since most people are unfamiliar with these kinds of eating styles, they often assume they would feel hungry or deprived and opt not to try.  Some who attempt to make significant changes are ill prepared to do so and usually revert to their old, familiar ways.


That caloric restriction has a positive effect in the prevention of cancer, degenerative diseases in general, and on the extension of lifespan is difficult to dispute.  The overwhelming evidence suggests it is a plausible tool for prevention and, as is the case for diabetes and heart disease, an effective tool in the treatment of a number of illnesses.  Implementation of sustained, pronounced caloric restriction, however, is difficult because most people do not have the tools (psychological and practical) to make such a lifestyle change a permanent one.  Sustained, moderate caloric restriction stands a better chance of implementation and sustainability, however, it is a viable option only when coupled with education (i.e. cooking methods, shopping habits, family support).

Transient caloric restriction is perhaps the most likely to be adopted by most people, however, there are risks involved in choosing this path that may outweigh the benefits.  Transient caloric restriction followed by a return to “normal” feeding habits has been shown to be detrimental to health and to be a risk factor for cancer.  This kind of dietary restriction, commonly known as “yo-yo dieting” is not recommended, and is particularly dangerous for persons who already have cancer.


  1. Colman RJ, Anderson RM, Johnson SC, Kastman EK, Kosmatka KJ, Beasley TM, Allison DB, Cruzen C, Simmons HA, Kemnitz JW, Weindruch R.  Caloric restriction delays disease onset and mortality in Rhesus monkeys.  Science 2009;  325:201-204.
  2. Wellcome Trust (2008, July 1). Poor Diet During Pregnancy May Have Long Term Impact On Child’s Health, Study Suggests. ScienceDaily. Retrieved November 23, 2009, from­ /releases/2008/06/080630200951.htm
  3. Elias SG, Peeters PHM, Grobbee DE, van Noord PAH.  Transient caloric restriction and cancer risk (The Netherlands).  Cancer Causes Control 2007; 18:1-5.
  4. Federation Of American Societies For Experimental Biology (2002, April 25). Even Moderate Caloric Restriction Lowers Cancer Risk In Mice. ScienceDaily. Retrieved November 24, 2009, from­ /releases/2002/04/020424073022.htm
  5. Saunders L, Verdin E.  Stress response and aging. Science 2009; 323:1021-1022

Coffee may protect against cardiovascular disease


Coffee drinking was first recorded in the Middle East over 500 years ago.  Today, coffee is one of the most popular beverages in the world, with over 70 countries supplying it and nearly every country in the world consuming it.  Thanks to its popularity, it is not surprising that coffee and its components have been the subjects of a wide range of studies that assess the risks and benefits of consumption.

Findings on the association of coffee consumption and cardiovascular disease (CVD) risk have been contradictory, with some studies revealing an increased risk for CVD, others showing no risk, and some finding benefits against it (1,2,3). Gender differences, types and amounts of coffee consumed, genetic factors, a tendency to focus on caffeine alone, lengths of studies, and a host of other confounders can make findings appear contradictory. Yet, in spite of these somewhat conflicting results, recent findings appear to offer some support to the hypothesis that low to moderate consumption of coffee may offer protection against some of the risk factors for CVD over the long term.


Inflammation is a normal response to injury and plays an important role in tissue repair and restoration of tissue function.  However, prolonged inflammation can be too much of a good thing, in no small part due to its involvement in oxidative stress – chronic inflammation is a major contributor to a host of degenerative diseases, including CVD (2,3).  A 2008 study of 459 Japanese women revealed a significant, independent, inverse correlation between coffee consumption and serum C-reactive protein (CRP) levels (2).  This is an important finding because CRP has been recognized as a marker for systemic inflammation and has been shown to have predictive value for CVD, stroke, and death (4). Similarly, the Iowa Women’s Health Study provides additional support through its finding of an inverse association of coffee consumption with death attributed to inflammatory diseases (3).


Oxidized LDL plays a key role in the pathogenesis of atherosclerosis (5).  It has a number of atherogenic properties, so, the body uses a complex defense system to rapidly remove it from circulation.  Dietary and genetic factors can aid or overwhelm this system. The susceptibility of LDL to oxidation is dependent upon serum concentrations of conjugated dienes, lipid hydroperoxides, and antioxidant species (5). Diets high in fruits and vegetables confer protection against this susceptibility, in part, by providing a consistent, dependable source of antioxidants.  Data from a study on the effects of caffeic acid on LDL indicates that the consumption of just one cup of coffee (200 ml) per day significantly improves oxidative resistance in humans (5).

Several studies have shown a J-shaped association between coffee consumption and CVD risk (5). This is similar to the association seen with wine consumption – drinking a small amount each day improves your odds of avoiding CVD, but overdoing it swiftly swings those odds against you and adds a number of other health and social problems to your tab.

The correlation with lowered CVD risk may be a result of protection conferred by polyphenols, volatile aroma compounds, and eterocyclic compounds found in coffee, all of which contribute to its antioxidant capacity (3).  Since plasma antioxidants increase after its consumption, coffee has been associated with reduced oxidative stress (3).   The consumption of coffee for a period of just seven days has been shown to significantly decrease LDL serum concentrations and LDL susceptibility to oxidation (5).


The above mentioned anti-oxidative effect of coffee consumption on LDL has not been replicated in filtered coffee studies (5).  This may be due, in part, to the ability of paper filters to keep some of coffee’s antioxidants from passing through, and, thus, from being consumed.  However, paper filtered and instant coffee do not raise LDL levels after consumption, whereas, LDL serum concentrations have been shown to increase in the wake of drinking unfiltered coffee (6). Consumption of 6 cups of boiled coffee (i.e. French press, espresso) per day was estimated to increase serum LDL levels by 17.8 mg/dL (6).  Diterpene cafestol is the likely cause of this increase. So, on one hand unfiltered coffee improves LDL oxidative resistance (which is good), but raises LDL levels (which is bad).


Caffeine has been shown to increase blood pressure in people who are not habitual caffeine consumers (6).  The key word here is “habitual”.  Partial tolerance to caffeine’s effects on blood pressure takes place in as little as one week in most people (6).  Thus, it is difficult to extrapolate the findings on increased blood pressure to long term use of coffee.  In addition, trials comparing the effects of caffeine capsules vs. placebo capsules have shown much stronger effects than trials looking at caffeinated coffee vs decaffeinated coffee consumption (6).  This is likely due to the fact that coffee is not comprised of caffeine alone.  Instead, coffee, whether caffeinated or decaffeinated, contains a number of antioxidants and other compounds which confer protection against the detrimental effects of its caffeine component (6).

Perhaps most telling of the importance of these other components in coffee was the finding that caffeinated cola consumption is associated with a higher incidence of hypertension than caffeinated coffee consumption (6).  Something to keep in mind the next time you feel like frowning when you see a teenager, or even a child, sipping a Cafe Misto. Furthermore, chlorogenic acid, a component of coffee, has been shown to reduce blood pressure in hypertensive rats (6).  And, in humans, green coffee bean extracts, which are low in caffeine, were shown to reduce hypertension in a randomized, Japanese trial (6).


Instant coffee and filtered coffee can protect against CVD if consumed in quantities of up to 4 cups (not mugs!) per day.  Unfiltered coffee does not and can have detrimental effects in the long run if it is consumed on a regular basis.  All caffeinated coffee, regardless of how it is prepared, is contraindicated for persons who already have CVD and/or high blood pressure.

So, put away the soda, espresso, and espresso mixed drinks (i.e. latte, cappuccino) and reach for instant or filtered coffee instead.  Your heart will thank you.  I’m not suggesting you must swear off the aforementioned concoctions for the rest of your days. I certainly haven’t.  But if you are drinking unfiltered coffee on a daily basis, you may want to reconsider and train your palate to enjoy the many other varieties of roasts available that are prepared with paper filters.  Or you can rig your espresso machine to brew using paper.

Let me know how that works out.  🙂


1)    Balk L, Hockstra T, Twisk J.  Relationship between long-term coffee consumption and components of the metabolic syndrome:  the Amsterdam Growth and Health Longitudinal Study.  Eur J Epidimiol 2009; 24: 203-209.

2)    Kotani K, Tsuzaki K, Sano Y, Maekawa M, Fujiwara S, Hamada T, Sakane N.   The relationship between usual coffee consumption and serum C-reactive protein level in a Japanese female population.  Clin Chem Lab Med 2008; 46(10): 1434-1437.

3)    Andersen L, Jacobs D, Carlsen M, Blomhoff R.  Consumption of coffee is associated with reduced risk of death attributed to inflammatory and cardiovascular diseases in the Iowa Women’s Health Study.  Am J Clin Nutr 2006; 83: 1039-1046.

4)    American Heart Association.  Inflammation, heart disease and stroke:  the role of C-reactive protein.  2010.  Available at:  Accessed May 9, 2010.

5)    Natella F, Nardini M, Belelli F, Scaccini C.  Coffee drinking induces incorporation of phenolic acids into LDL and increases the resistance of LDL to ex vivo oxidation in humans.  Am J Clin Nutr 2007; 86: 604-609.

6)    Van Dam R M.  Coffee consumption and risk of type 2 diabetes, cardiovascular diseases, and cancer.   Appl Physiol Nutr Metab 2008; 33: 1269-1283.