Who says being fat is bad?

Would you have guessed that, one fine day, health insurers will regret the demise of big tobacco and its contribution to health care costs? Would you have guessed that, when that day arrives, health insurers would also learn to love other frowned-upon-vices of their policy holders, such as getting fat and lazy? Your answer is probably "no, I wouldn't have guessed that in my dreams.". 

And also very probably this answer is based on what you typically read in the media, such as this piece of news titled "Obesity Adds More to Health Care Costs Than Smoking, Study Suggests." released on April 3, 2012, on sciencenews.com. The article text wraps the title message into a substantially larger amount of unsubstantial words, before it concludes what you would probably subscribe to blindfolded: the  "...study [1] provides new insights into the long-term costs of obesity and smoking, showing that both risk factors lead to persistently higher health costs throughout a seven-year follow-up period.". Dah, what else is news?

Well, for one, that the Joe Camels and the lardbuckets, with all their vices, cost their health insurers actually LESS money than Mr. and Mrs Healthy. For one simple reason: the "vice guys" die earlier.

But let's hold that thought for a moment and let's look at the figures. In a Dutch study performed by Pieter van Baal and colleagues, the authors compared the annual and lifetime health care costs of three cohorts, namely the obese, the smokers, and the healthy living people [2]. As the basis of their calculations they used the Dutch National Institute's of Public Health and the Environment (RIVM) chronic disease model, which, the authors assure us, has been widely used and validated in disease and cost projection analyses.

To make their results more comparable internationally, they ran their analyses with altogether 7 different scenarios, to account for different health care systems and for different mortality risk estimates. The latter had been drawn from observations in the U.S. published by Flegal and colleagues [3] who had found declining mortality risks in the obese cohorts. I mention this because I don't want you to suspect that the Dutch authors had based their calculations on an unrealistically high keeling-over rate for the obese. Now, fast forward to the astonishing results.

In all 7 models, as well as in the unadjusted base case scenario, the financially most attractive "villains" to health insurers are the smokers. The most expensive are always the goody-two-shoes healthy-living people. Somewhere in-between are the fat ones. In the model which assumed a yearly 1% increase in health care costs, the lifetime costs for an obese person amounted to € 399,000, compared to which the smoker comes at a 14% discount of € 341,000, but the healthy living person with a 17% premium at € 468,000.

How can that be? The answer is not where you and I would have looked first: The diseases which directly associate with smoking and obesity (heart disease, cancer, diabetes, pulmonary diseases, musculoskeletal disorders). They account only for 20% of total disease costs. The remaining 80% are for ailments and conditions, which come with age. But when that age doesn't come, because you die earlier, then those costs don't come either. And Joe Camel and Ronald McDonald are rather effective in cutting years out of your life, and thereby costs out of your health insurers balance sheet. For 7 and 5 years respectively, to be precise.   

So, where are the premium discounts for the obese and the smoking policy holders? Why are the healthy living people permanently miffed about not getting premium discounts, when they actually cost more? I have to admit, I belong to the latter, too. But recently, after having listened to one of my talks at a conference, a friend of mine, the CEO of a German health insurer, took me aside and told me, that my indignation about the healthy people having to share the cost burden of their willfully negligent peers, was unfounded.

As much as I wanted to disbelieve, I also knew that these insurance guys do one thing very well: calculating risk and premiums. So I had to give him the benefit of the doubt. Which is why I began to check. And by checking, I came to know about quite a number of studies confirming my friend's argument. One of those studies was van Baal's, which I chose to quote from because he is actually working for the Dutch National Institute of Public Health and the Environment. Not that I'm biased in favor of the Dutch. I'm biased in favor of anyone who articulates a viewpoint which is in stark contrast to what I would expect merely on the basis of his association. I mean, here you have someone telling you to NOT confuse health with health care cost savings, when his employer is actually trying to make everyone with a cigarette or a burger in his mouth feel guilty about sending health care costs sky high.  

So what now? Shall we promote the vices and lower our health care costs in a decade-long smoking and feeding frenzy? Well, it's your choice, but I'm not convinced that we have got the reasoning or the arguments right just yet. We need to do a little more detective work to solve this case.

Now, you know how the French, at least in their novels, dish out that piece of advice to the detective: Cherchez la femme (look for the woman)? Maybe it works in the French universe. In mine, I have always found this one to work better: "Cherchez l'argent" (look for the money).

Which will lead us to another few surprising discoveries in the next post. And, of course, a couple more reasons to believe that there are quite some powerful players around who yearn for the good old times when Marlboro Man and Ronald McDonald delivered us from the risk of a costly long life.

PS: To meaningfully pass the time until the next post, watch this video on the calorie cartel

1.           Moriarty, J.P., et al., The effects of incremental costs of smoking and obesity on health care costs among adults: a 7-year longitudinal study. Journal of Occupational and Environmental Medicine, 2012. 54(3): p. 286-91.

2.           van Baal, P.H.M., et al., Lifetime Medical Costs of Obesity: Prevention No Cure for Increasing Health Expenditure.PLoS Med, 2008. 5(2): p. e29.

3.           Flegal, K.M., et al., Excess deaths associated with underweight, overweight, and obesity. Jama, 2005. 293(15): p. 1861-7.

Moriarty, J., Branda, M., Olsen, K., Shah, N., Borah, B., Wagie, A., Egginton, J., & Naessens, J. (2012). The Effects of Incremental Costs of Smoking and Obesity on Health Care Costs Among Adults Journal of Occupational and Environmental Medicine, 54 (3), 286-291 DOI: 10.1097/JOM.0b013e318246f1f4
van Baal PH, Polder JJ, de Wit GA, Hoogenveen RT, Feenstra TL, Boshuizen HC, Engelfriet PM, & Brouwer WB (2008). Lifetime medical costs of obesity: prevention no cure for increasing health expenditure. PLoS medicine, 5 (2) PMID: 18254654
Flegal, K. (2005). Excess Deaths Associated With Underweight, Overweight, and Obesity JAMA: The Journal of the American Medical Association, 293 (15), 1861-1867 DOI: 10.1001/jama.293.15.1861

Guess who is hiding the magic pill to longevity?

Imagine a medicine which protects you against cardiovascular disease, cancers, diabetes, depression and dementia. A medicine which works best when taken regularly and long before any symptoms of any of those diseases appear. A medicine which is cheaper than any supplement or aspirin. Would you take it?

Then why don't you? The name of that medicine is exercise, and ...

...OK, OK, I hear you saying "not again, I have heard that mantra before. Tell me something I don't know!" Which is exactly what I want to do: To tell you something you AND I don't know, because nobody seems to have the answer to the sixty-four-thousand dollar question: Why don't we take this medicine?

Now here is this hot item called swarm intelligence, the phenomenon which, we are being told, makes a horde of blooming idiots come up with solutions worthy of an Einstein's. That should work just fine for us. So, let's put it to the test. I'll tell you first a few facts and my thoughts, after which it is your turn, and then we can look at the results over the next few days, or so.

Now, just so that we all start form the same page, let me recap the effects of exercise. 

Exercise & Heart Disease

Exercise, done right, has been found to reduce the risk of dying from any cause by at least one third with a 9% reduction for every one hour of vigorous exercise performed per week [1]. To be fair, studies which calculate such risks are inherently flawed. They assess exercise through questionnaires, which makes it difficult to reliably judge the amount and intensity of exercise, and whether people stick with a given exercise level and for how long. That's why I like to look at the exercise-health correlation using fitness as the marker. Because fitness is a direct consequence of exercise, and it is something we can objectively measure in the lab.

A fit 45 years old man has only one quarter the lifetime risk of dying from cardiovascular causes compared to his unfit peer [2]. And 20 years later, at the age of 65, being fit means having only half the risk of an unfit 65-year old. So much about exercise and the number one killer of men and women alike, cardiovascular disease. How about the runner-up: cancer?

Exercise & Cancer

The association of fitness with cancer is not as well researched as with cardiovascular disease. But the available data clearly point to a substantial effect. In a study performed in 1300 Finnish men who were followed for 11 years, the physically fit ones, when compared to their least fit peers, had a 60% reduced risk of dying from non-cardiovascular causes, which means mostly cancer [3]. An almost identical value of risk reduction for cancer death had been found in a 16-year study of 9000 Japanese men aged 19-59 [4]. The ones in the highest quartile of physical fitness had a risk of dying from cancer that was 60% lower than the risk of their peers in the lowest quartile.

The fact that fitness correlates so strongly with the risk of dying from cancer might tell us that the intensity of exercise plays a large role. In a study, which followed 2560 men for close to 17 years, the intensity of physical activity was clearly related to cancer mortality. But only in those who were physically active for at least 30 minutes per day did the higher intensity of exercise lower the cancer death risk by close to 50%. Do less than those 30 minutes, and high intensity might not get you away from cancer death. Obviously, low-intensity exercise does neither increase your fitness level nor does it decrease your risk of dying from cancer. The message to all those who play 18 holes on a daily basis: Get a (sports-)life!

Exercise & Dementia

Even less well examined than the exercise-cancer association is the exercise-dementia association. But also here we begin to see a remarkable effect. Results from the first relatively small trials show that physically active elderly have substantially reduced risk of Alzheimer and other forms of dementia, possibly in the range of a 50% risk reduction [5]. 

Why Don't We Exercise?

Ok, so here we are. Obviously, man is made to move. And whether you call exercise medicine or whether you call the lack of exercise a pathogen - which is clinician speak for something nasty that makes you sick - we already know a lot about how exercise does its work biochemically. That's beyond the scope of this post.

What interests me here is the question which I have asked at the beginning of this story: Why do we not take this "medicine" which is free-of-charge and which has a stronger effect than any of those pills for lowering cholesterol or blood sugar or blood pressure?

As researchers we have made no progress at all in answering this question.

The psychologists outdo each other with the creation of behavioral models, which give their inventors a lot of stature, but which have failed to get us one inch closer to the answer. Just to give you an impression, there is the Health Belief Model, the Theory of Reasoned Action, the Theory of Planned Behavior, the Transtheoretical Model of Behavioral Change, the Social Cognitive Theory, the Protection Motivation Theory, the Health Action Process Approach, and probably a few new ones in the making. Their common denominator: no reliable answer to our question.

That's why I would like to try swarm intelligence. If the "swarm" of readers of this blog post, that is you and me, is large enough, we might just come up with an answer that is worth pursuing in a more methodical way.

So, I'll go ahead and tell you a few suspicions which I have. And then, at the risk of baring my soul to the point where you might not find me a likable person, I will tell you what motivates me to do an early morning 90-minutes exercise session almost every day of the week.

But first the suspicions which I have why so few people get themselves to do even the bare minimum of exercise:

1.     Is it because we can't see, I mean literally see, the effects? Would some sort of visual feedback about the benefits and effects of exercise inside your body motivate you to exercise?

2.     Is it because we rather react than act? That is, we only do something to cure a disease once it's manifest rather than prevent it? But then, why do we have intelligence and one of its nifty byproducts called foresight in the first place?

3.     Is it because we are so focused on a pill or an operation as the only tools, which work against a disease, that we simply can't appreciate the value of something so simple and cheap as exercise?

4.     Why do we use the lousy excuse "no time" when we have several hours to spend in front of the TV EVERY day? Regardless of how busy we are with our work?

These are just a few questions which come to mind. They amount to asking why we don't exercise. 

But it will be equally helpful to ask the question: what is it, that KEEPS YOU exercising? 

Because from those who do, we can learn, how to motivate those who don't. Provided we get an honest answer. My suspicion is, the answers which we get in research, are mostly edited for "political correctness". The couch potatoes hide behind the time constraints, because being busy is not perceived as a character flaw, being lazy is. And what could possibly be a character flaw of the exerciser?

Well, I give you mine. The instinctive gratification with which my inner brute views the overweight person in front of me at the check-out queue or in the waiting room, the gratification that comes from being reminded of his risk for disease and suffering being a lot greater than mine (in German we have that word "Schadenfreude"), the gratification that comes from telling him, in my mind only, of course, "I have that strength of will that you don't". 

That's a gratifying incentive, to be sure. But it's not the only one. The main reason why I run every morning, no matter what the weather or the size of the hangover from Saturday's evening (yeah, it happens to all of us) is, that I have seen enough people who suffered a stroke or a heart attack. And I have seen their remorse of not having done enough while there was still time. I fear that. That's what keeps me running.

And what is it for you? Honestly. Let's hear it, and let's see whether we find a common thread, which research has overlooked so far. Remember, as a swarm we are supposed to be far more intelligent than as individuals.

1.           Samitz, G., M. Egger, and M. Zwahlen, Domains of physical activity and all-cause mortality: systematic review and dose-response meta-analysis of cohort studies. International Journal of Epidemiology, 2011.

2.           Berry, J.D., et al., Lifetime Risks for Cardiovascular Disease Mortality by Cardiorespiratory Fitness Levels Measured at Ages 45, 55, and 65 Years in Men: The Cooper Center Longitudinal Study.J Am Coll Cardiol, 2011. 57(15): p. 1604-1610.

3.           Laukkanen, J.A., et al., Cardiovascular Fitness as a Predictor of Mortality in Men. Archives of Internal Medicine, 2001. 161(6): p. 825-831.

4.           SAWADA, S.S., et al., Cardiorespiratory Fitness and Cancer Mortality in Japanese Men: A Prospective Study. Medicine and Science in Sports and Exercise, 2003. 35(9): p. 1546-1550.

5.           Buchman, A.S., et al., Total daily physical activity and the risk of AD and cognitive decline in older adults.Neurology, 2012.

Samitz G, Egger M, & Zwahlen M (2011). Domains of physical activity and all-cause mortality: systematic review and dose-response meta-analysis of cohort studies. International journal of epidemiology, 40 (5), 1382-400 PMID: 22039197

Berry JD, Willis B, Gupta S, Barlow CE, Lakoski SG, Khera A, Rohatgi A, de Lemos JA, Haskell W, & Lloyd-Jones DM (2011). Lifetime risks for cardiovascular disease mortality by cardiorespiratory fitness levels measured at ages 45, 55, and 65 years in men. The Cooper Center Longitudinal Study. Journal of the American College of Cardiology, 57 (15), 1604-10 PMID: 21474041

Laukkanen, J. (2001). Cardiovascular Fitness as a Predictor of Mortality in Men Archives of Internal Medicine, 161 (6), 825-831 DOI: 10.1001/archinte.161.6.825

SAWADA, S., MUTO, T., TANAKA, H., LEE, I., PAFFENBARGER, R., SHINDO, M., & BLAIR, S. (2003). Cardiorespiratory Fitness and Cancer Mortality in Japanese Men: A Prospective Study Medicine & Science in Sports & Exercise, 35 (9), 1546-1550 DOI: 10.1249/01.MSS.0000084525.06473.8E

Buchman AS, Boyle PA, Yu L, Shah RC, Wilson RS, & Bennett DA (2012). Total daily physical activity and the risk of AD and cognitive decline in older adults. Neurology, 78 (17), 1323-9 PMID: 22517108

Your shortcut to longevity.

If you don't die from an accident, a serious infection or a cancer, you'll live as long as your arteries let you. And how long they let you is all in your hands. I know this sounds over-simplified, but it's biomedical knowledge in a nutshell. Lets look at what happens in and to your arteries and what that means for keeping them in mint condition. 

 You may have thought about your arteries as elastic tubes, which transport blood to where its oxygen and nutrient load is needed. But there is more to it. For example, there is this very thin lining which separates the muscular elastic wall of the arteries from the blood stream. This lining is called the endothelium, and it is where the difference is made between lifestyle and death style.

The endothelium is a one-cell-thin layer which has often been likened to the teflon coating on your non-stick pots and pans. The only true part of that analogy is the non-stick part. It prevents cholesterol and fat from docking on to endothelial cells and gradually growing into atherosclerotic plaques. When they rupture, blood clots form and those clots might cause a heart attack or stroke. I say "might" because not all plaque ruptures turn into such dramatic events, but we will get to this later.

Many people think that a chronic overdose of cholesterol or fat, or simply aging, are the causes of atherosclerosis. That was the working hypothesis of scientists 50 years ago. But it doesn't jibe with the observation that half of all patients with confirmed atherosclerotic lesions, have cholesterol values within the normal range [1]. That's because plaques grow WITH cholesterol, any amount of cholesterol, but they start growing ON inflammation. Chronic inflammation, to be precise. And chronic inflammation grows on your physical activity habits. Or rather the lack thereof.

Inflammation in itself is nothing bad. It's a process by which cells rid themselves of invaders. Only when inflammation becomes chronic do we have a problem. To avoid chronicity, endothelial cells have a mechanical switch. Or, as we call it in biomedicine: a mechanoreceptor. Those receptors respond to pulsatile blood flow. That is, if those receptors are being hit often, long and strong enough by blood waves gushing through the artery, they trigger an anti-inflammatory cascade of hormonal reactions. If we don't keep hitting those receptors, the cascade turns pro-inflammatory and the career of the atherosclerotic plaque begins. The extremely complex biochemical happenings do not concern us here. What concerns us is that this pounding of the endothelial cell receptors doesn't come from sitting around, or from playing golf or from walking through the park. It only comes from vigorous physical activity.  Which explains the growing evidence for the relative benefits of more intensive vs. less intensive physical activity.

One example is a recent study by researchers who had followed close to 20000 adults aged 20-90 for almost 20 years, monitoring their cycling habits and their health [2]. The study took place in the Danish city of Copenhagen where 5 Million people own 4 Million bicycles. Male study participants who reported habitual cycling at the highest of three intensity levels lived on average 5.3 years longer than their peers in the lowest intensity group, independent of the duration of cycling. Of course, this was a prospective cohort study, which only allows us to talk association but not causality. But its findings match nicely with the expectations we have from our knowledge about the anti-inflammatory effects of higher-intensity exercise. Specifically, that high-intensity exercise inhibits the oxidative processes which precede and coincide with inflammation in the endothelial cells [3]. These effects were either absent or negligible in exercise of moderate intensity. By the way, this second study had been performed in women. I point that out, just so that you don't think what applies to male Danes may not apply to women. 

Now, what's the good news in all this for those devotees of the minimalistic physical activity lifestyle, otherwise known as couch potatoes?

The good news is, that you don't have to spend hours in endurance exercise. In my lab we have seen significant improvements in fitness and health with thrice weekly 20-minutes high-intensity interval training (HIT). In our HIT routine our participants spent those 20 minutes with 4 consecutive intervals, in each of which they ran or cycled for 4 minutes at moderate intensity, followed by a 1-minute all-out sprint, with no break between intervals. A recent review confirmed the benefits of HIT [4], which accumulate with a significantly smaller time commitment to exercise, than what is required for conventional endurance exercise.

There is more good news. Remember that I mentioned that the rupture of an atherosclerotic plaque "may" cause a heart attack or stroke. That's because we know a couple of interesting and encouraging things about such plaques. First, plaques may be of a "vulnerable" or of a "stable" type. The stable ones don't rupture easily but the vulnerable ones do. Secondly, not all those plaque ruptures end in a heart attack or stroke. Most ruptures actually don't. And we can't predict exactly which ones will cause problems, and when. So there is a large element of chance in all this. Third, plaques can change their status from vulnerable to stable or vice versa within weeks or months.

The good news in all this is that it is in your hands, or rather in your exercise, whether your existing plaques become more stable, and whether you decrease or increase the chance of a heart attack or stroke. All it takes is the intensity of your exercise.

The bad news, those insights take away your excuse of lack of time. Think about it, what are 60 minutes a week for HIT, when the average German spends 4 hours PER DAY watching TV, and the average American tops that with another 2 hours a day.

So, when you want to know whether your physical activity habits qualify as a lifestyle or a death style, keep the simple reasoning in mind: exercise determines the health of your arteries, and the health of your arteries determines your longevity. And the shortcut to the latter goes via HIT.   

1.           Braunwald, E., Shattuck lecture--cardiovascular medicine at the turn of the millennium: triumphs, concerns, and opportunities.N Engl J Med, 1997. 337(19): p. 1360-9.

2.           Schnohr, P., et al., Intensity versus duration of cycling, impact on all-cause and coronary heart disease mortality: the Copenhagen City Heart Study. European Journal of Cardiovascular Prevention & Rehabilitation, 2011.

3.           Ciolac, E.G., et al., Effects of high-intensity aerobic interval training vs. moderate exercise on hemodynamic, metabolic and neuro-humoral abnormalities of young normotensive women at high familial risk for hypertension. Hypertension Research, 2010. 33(8): p. 836-843.

4.           Kent, W., The effects of sprint interval training on aerobic fitness in untrained individuals: a systematic review.British Journal of Sports Medicine, 2011. 45(15): p. A8.

Schnohr, P., Marott, J., Jensen, J., & Jensen, G. (2011). Intensity versus duration of cycling, impact on all-cause and coronary heart disease mortality: the Copenhagen City Heart Study European Journal of Cardiovascular Prevention & Rehabilitation, 19 (1), 73-80 DOI: 10.1177/1741826710393196

It's not your genes, stupid.

Imagine traveling back in time and meeting your caveman ancestor of 10,000 years ago. Imagine telling him about what life is like today: that, with the tap of a finger you turn darkness into light, a cold room into a warm one and a tube in the wall of your cave into a spring of hot and cold water. You tell him...

you can fly from one place to another, and watch any place on this Earth without ever leaving your cave. You tell him you never have to run after your food, or fear that you run out of it. Your ancestor will have a hard time believing you. In his world only his gods can do all that.

Then you tell him how some of your friends think his way of life is preferable for health, which is why you are visiting him because you want to see for yourself. Before I get to your ancestor's most likely answer, let's get on the same page with those friends of ours first.

You have probably heard them talk about the past 10,000 years having done nothing to our genetic make-up. In other words, your ancestor's DNA blueprint was the same as yours. Today this blueprint collides  with a space age environment in which we don't expend any energy to get our food, and the food we acquire delivers far more energy and far less nutrients than what had been the case during 99.9% of human evolution. 

According to this view, today's epidemics of obesity, diabetes, cardiovascular diseases and cancer are simply the collateral damage of this collision. This explanation is so persuasive that it is being parroted by every media type and talking head who can spell the word  'genetics'. I'm afraid it is not that simple. Here is why:

Remember when the 3 billion letters, or base-pairs, of the human genome had first been decoded at the beginning of this century. This decryption had been delivered with the promise of revolutionizing medicine. Aside from new therapies, the hottest items were prognostic and diagnostic tools, which, we were made to believe, would lay in front of each individual his biomedical future. And with this ability to predict would come the ability to prevent, specifically all those diseases which result from an unfavorable interaction between genes and environment.

Almost ten years later we are nowhere near this goal. OK, we have identified some associations between some genetic variants and the propensity to become obese or get a heart attack or diabetes. But these associations are far from strong and they hardly help us to improve risk prediction. Just this year, Vaarhorst and colleagues had investigated the ability of a genetic risk score to improve the risk prediction of conventional risk scores which are based on biomarkers, such as the ones used in the Framingham score. Less than 3% of the study participants would have been reclassified based on the genetic risk score [1].

In a study which was released just yesterday, genetic markers for the development of diabetes in asymptomatic people at high risk, did not improve conventional biomarker risk scoring at all [2]. 

Obviously we are not simply our genes. This is because genes do not make us sick or healthy. Genes make proteins. And on the way from gene to protein a lot of things happen on which genes do not have any influence. To express a gene, as biologists call it, that gene must first be transcribed on RNA and then translated from RNA into the final protein. Whether a gene is transcribed in the first place depends on whether it is being made accessible for this transcription process. Today we know at least two processes which can "silence" the expression of a gene, even though it is present in your DNA. These processes are called DNA methylation and histone modification. Simply imagine them as Mother Nature's way of keeping a gene under wraps.

That's a good thing if the protein product of the silenced gene would be detrimental to your health. It could well be the other way round, too. Anyway, these happenings have been called epigenetics. Epigenetic mechanisms enable cells to quickly match their protein production with changing environmental conditions. No need to wait for modifications of the genetic blueprint which takes many generations and a fair element of chance to materialize. The most astonishing discovery is that these epigenetic changes may become heritable, too. Which means, there is really no need to change the genetic code. 

I believe you get the picture now. While it is true that your ancestor's genetic code is indistinguishable from yours 10,000 years later, the way your body expresses this code in the form of proteins and hormones can differ in many ways. Which is why researchers are now as much excited about epigenetics as they used to be about genetics 10 years ago.

I don't want to be the party pooper, but whenever I see such excitement I'm reminded of how it has often evaporated after some further discoveries. Here I'm skeptical because of the picture, which we are beginning to see. Insulin, for example, is known to regulate the expression of many genes. At least in rats it has been shown that insulin's suppressive effect on gene expression in the liver, can be altered by short term fasting [3]. That means, relatively minor behavioral changes may affect the way our organism expresses its genetic code.   

Observations like these support the idea that we are not our genes, but what we make of them. In plain words: let's not hide behind the "it's-our-stone-age-genes" excuse, to explain why we are fat and lazy and ultimately chronically sick.

Now, back to your ancestor and his response to your friends' suggestions that his way of life is preferable for health. When you also tell him you live a lot longer than the 40 years he has on average, he'll tell you: You have got some nutcase friends over there. Let me live like a god first and then I'll worry about health later.

Maybe, we are not so different from our stone age ancestors after all. 

1.           Lu, Y., et al., Exploring genetic determinants of plasma total cholesterol levels and their predictive value in a longitudinal study. Atherosclerosis, 2010. 213(1): p. 200-205.

2.           Schmid, R., et al., Current Genetic Data Do Not Improve the Prediction of Type 2 Diabetes Mellitus: The CoLaus Study.Journal of Clinical Endocrinology and Metabolism, 2012.

3.           Zhang, Y., et al., Insulin-Regulated Srebp-1c and Pck1 mRNA Expression in Primary Hepatocytes from Zucker Fatty but Not Lean Rats Is Affected by Feeding Conditions. PLoS ONE, 2011. 6(6): p. e21342.

Lu, Y., Feskens, E., Boer, J., Imholz, S., Verschuren, W., Wijmenga, C., Vaarhorst, A., Slagboom, E., Müller, M., & Dollé, M. (2010). Exploring genetic determinants of plasma total cholesterol levels and their predictive value in a longitudinal study Atherosclerosis, 213 (1), 200-205 DOI: 10.1016/j.atherosclerosis.2010.08.053 

Zhang Y, Chen W, Li R, Li Y, Ge Y, & Chen G (2011). Insulin-regulated Srebp-1c and Pck1 mRNA expression in primary hepatocytes from zucker fatty but not lean rats is affected by feeding conditions. PloS one, 6 (6) PMID: 21731709

To hell with exercise

Who says that exercise is medicine? For one, the American College of Sports Medicine (ACSM) of which I'm a professional member. Then, how can I say it isn't?

Let's look first at the conventional view of the benefits of exercise. There is a large and increasing amount of evidence which clearly tells us that exercise prevents today's number 1 killer: cardiovascular disease. That is, heart attack, stroke and peripheral vascular disease. Mind you, what is common knowledge today emerged only some 50 years ago when Morris and colleagues discovered that UK bus conductors, the guys climbing up and down the double-decker London buses, had better fitness and fewer heart attacks than their all-day-seated driver colleagues [1].

In the years since then our knowledge about the effects of physical activity on cardiovascular, metabolic and mental health has virtually exploded. From this evidence the U.S. Dept. of Health and Human Services (HHS) concluded in 2008 that the most active people of the population have a 35% reduced risk of dying from cardiovascular disease compared to the least active people [2]. The WHO lists insufficient physical activity (PA) as the 4th leading cause of death world wide after high blood pressure, tobacco use and high blood glucose. What's wrong with this picture? High blood pressure and high blood glucose are known consequences of a sedentary lifestyle. So is obesity, which ranks 5th place on the WHO killer list. Which is why physical inactivity deserves top spot on that list.

What most people don't know is the way lack of physical activity causes all those diseases, from insulin resistance and diabetes to arterial dysfunction and atherosclerosis, and from there to heart attack, stroke, kidney failure. The mechanisms are extremely complex, and, while we have untangled quite some of them, there are probably a lot more to discover. I'll try to make this the subject of one of the next blog posts. 

Now you are probably asking yourself, how the hell, with all this evidence, will I ever be able to make my point that physical activity is not a medicine. Ok, here it comes: it's a matter of viewpoint. The one I'm taking is the one of evolutionary biology. Let me play its advocate and present as evidence a couple of insights.

First, our human ancestors, who had roamed this Earth as hunter/gatherers for the most part of human existence, had, by necessity, a much more physically active lifestyle. A lifestyle which required at least 1.7 to 2 times the normal resting energy expenditure [3]. [To get an idea about resting energy expenditure and physical activity levels and how they are calculated, simply follow the links to the videos.] Those ancestors' genes are what we have inherited. And these genes are exposed to a lifestyle which is vastly different from the ones under which these genes evolved. Specifically with a view to physical activity, which brings me to evidence no 2:

What we typically observe today are physical activity levels with factors of somewhere between 1.2 and 1.4 of our resting energy expenditure. That's true for most people.

Even if you were to follow the ACSM's recommendation of 30 minutes of moderate to vigorous exercise on at least 5 days per week, would you NOT reach the level of 1.7 if you are working in a typical office job or doing house work. Which means, the physical activity levels which we recommend today, do not add a behavioral type of medicine into our lives, they merely reduce the extent of a "poisonous" behavior called sedentism. It's like cutting down from 2 packs of cigarettes per day to 1 pack. Would you call this a "medicine"? Would the ACSM call that a medicine? With respect to exercise they do.

So, OK, if you had been attracted to this post in the hope of finding some excuse for not doing exercise, or some argument to get those exercise evangelists, like myself, off your back, I'm sorry to have disappointed you. No, actually, I'm not sorry. And neither will you be, if you get your physical activity level above those 1.7. Then you may just start calling exercise a medicine. Until then, chances are you will still go to hell with exercise, because you get too little of it. Certainly too little to stay out of that hell of heart disease, stroke, diabetes and many cancers.

1.           Morris, J.N. and P.A. Raffle, Coronary heart disease in transport workers; a progress report. Br J Ind Med, 1954. 11(4): p. 260-4.

2.           Physical Activity Guidelines Advisory Committee, Physical Activity Guidelines Advisory Committee Report, 2008, U.S. Department of Health and Human Services: Washington, D.C.

3.           Eaton, S.B. and S.B. Eaton, An evolutionary perspective on human physical activity: implications for health. Comp Biochem Physiol A Mol Integr Physiol, 2003. 136(1): p. 153-9.

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MORRIS JN, & RAFFLE PA (1954). Coronary heart disease in transport workers; a progress report. British journal of industrial medicine, 11 (4), 260-4 PMID: 13208943
Eaton, S., & Eaton, S. (2003). An evolutionary perspective on human physical activity: implications for health Comparative Biochemistry and Physiology - Part A: Molecular & Integrative Physiology, 136 (1), 153-159 DOI: 10.1016/S1095-6433(03)00208-3

Screw Your Health?!

So, what's your excuse for not exercising enough, for smoking, for not watching your diet, for getting fatter every year, and therefore having high blood pressure, and too much glucose and cholesterol in your blood?

 That's what the American Heart Association has been telling you for so many years NOT to do. How can I be sure that you, dear reader, are one of those people who only pay lip service to health? I can't, but as a numbers guy I go with the statistics. 

And when health is concerned the statistics tell me that there are obviously only two types of people. Those who do enough for their health, and those who merely think they do. The latter make up 98.8% of the population [1]. That is, only one in a hundred meets all 7 health metrics: not smoking, eating a healthy diet, no overweight, sufficiently physically active, normal blood pressure, normal levels of glucose and cholesterol. Four out of every 5 Americans meet 4 or less of those metrics. Actually, only one in four meets 4 metrics. How can that be when having at least 6 of those metrics will cut your risk of dying from cardiovascular disease by 75% compared to those who meet one criterion or none? How much more incentive do you want?

That's the frustrating question I'm asking myself every day. Because whether it is in the US, in Germany or anywhere else in this world, maintaining health and preventing disease is a frustrating service to provide. I used to think this is so, because when you don't feel it, it is health. And what you don't feel, you don't appreciate. But if that was true, the first diagnosis of a chronic condition, such as heart disease or diabetes, should surely be a wake-up call. But it isn't. Only 40% of smokers quit when  being told that they have such a chronic disease, and that smoking will make it worse [2]. That's still a lot compared to the behavior change in exercise: Nil, no change at all.  And for every American who quit smoking in 2011 another American became obese. 

If you have read my earlier blog posts, you'll remember that I'm a strong advocate of recognizing the autonomic neurohormonal mechanisms which certainly drive our eating and exercising behaviors. But we are not exclusively controlled by those. We still have a few brain centers which give us the abilities and skills that make us human: volition, reasoning, intelligence. Of course you can use them to find the most elaborate excuses for your health behaviors, or rather for the lack thereof. But he who is good for making excuses is seldom good for anything else. That's what Benjamin Franklin said. Are you good for something else? Make that something your health. And start today. Here!

1.           Yang, Q., et al., Trends in Cardiovascular Health Metrics and Associations With All-Cause and CVD Mortality Among US Adults. JAMA: The Journal of the American Medical Association, 2012.

2.           Newsom, J.T., et al., Health Behavior Change Following Chronic Illness in Middle and Later Life. The Journals of Gerontology Series B: Psychological Sciences and Social Sciences, 2011.

Yang, Q., Cogswell, M., Flanders, W., Hong, Y., Zhang, Z., Loustalot, F., Gillespie, C., Merritt, R., & Hu, F. (2012). Trends in Cardiovascular Health Metrics and Associations With All-Cause and CVD Mortality Among US Adults JAMA: The Journal of the American Medical Association, 307 (12), 1273-1283 DOI: 10.1001/jama.2012.339 

 Newsom, J., Huguet, N., McCarthy, M., Ramage-Morin, P., Kaplan, M., Bernier, J., McFarland, B., & Oderkirk, J. (2011). Health Behavior Change Following Chronic Illness in Middle and Later Life The Journals of Gerontology Series B: Psychological Sciences and Social Sciences, 67B (3), 279-288 DOI: 10.1093/geronb/gbr103

Do vitamin supplements make you healthier?

The (non-)sense of vitamin supplementation?

Almost one in two American adults is a regular user of vitamin and mineral supplements, either in the form of single- or multivitamin/mineral formulations (MVMS). It all adds up to a market of US$ 9 Billion annually, or one third of the total US supplements market. Does all the pill-popping help their users to achieve better health or longevity? 

That's one question raised by Björn, one of the readers of my blog. Thanks, Björn, I wanted to write on this subject for some time. You just got me going on this a little earlier than I would have otherwise. And also thanks for the second question: Does the latest technology of delivering the drug (not to your house, but within your body to your organism's cells) via "nano-encapsulation" improve that health effect in any way? Let me try to answer these questions one by one.

When you talk about vitamins, you talk about essential micronutrients, for which the human organism has either no or only a very limited ability to produce (e.g. Vitamin D) on its own. If you want to group vitamins according to their solubility you'll find that they come in two flavors: water soluble and fat soluble. Of course, you could group them for any other biochemical characteristic, but grouping them according to their solubility makes immediate sense when you keep in mind that the fat soluble ones (A, D, E and K) can accumulate in your body's tissues, whereas the water soluble Vitamins typically can't. Whatever can accumulate, can also accumulate to the point where there is too much of it in a body's tissue. So, yes, too much of a good thing may turn into a not so good thing, as is the case for vitamins A and E for example. Or, too much of a good thing may just be flushed out of the body, as is the case with water-soluble vitamin C.

The supplement industry certainly does a good job convincing the public that supplementing one's diet with additional vitamin formulations is good for one's health. It's certainly good for the industry's bank accounts. In such cases it always pays to ask one simple question: Where is the evidence?  

In a meta-analysis of randomized clinical trials (RCT, the gold standard of clinical research methodology), the authors investigated the effects of vitamins E and A on the risk of cardiovascular disease and death in altogether 220,000 patients [1]. The effects? Zilch. The authors recommendation? The evidence does not support any recommendation for the use of Vitamins E and A. On the contrary, they found a slight increase in all-cause and cardiovascular disease mortality associated with vitamin A supplementation.

In another 2007 review on the subject, published in the American Journal of Clinical Nutrition, its author came to the same conclusion, stating that "Results to date are not compelling concerning a role for MVMs in preventing morbidity or mortality from cancer or CVD." [2] The two largest trials on Vitamin A and E supplementation in smokers, the Finnish Alpha-Tocopherol Beta-Carotene (ATBC Trial) and the US Carotene and Retinol Efficacy Trial (CARET) enrolled 29,000 and 18,000 smokers. In the Finnish trial, supplementation with Vitamin A increased the risk for lung cancers by 18% within a 5 to 8-year observation period [3]. And the US trial was halted after 2 years for the same reason: a 28% increase in lung cancer risk, a 26% increase in risk for dying from cardiovascular disease [4]. In 22,000 healthy men who had been observed for 12 years, supplementation with vitamin A showed neither benefit nor harm [5].  

So where is the evidence for you to believe that buying Vitamin E and A supplements will make you healthier and live longer? Maybe I'm blinded by a perverse distrust of everything a sales man tells me, but I can't see it.

So, how about multi-vitamins? In the group of people with the highest take-up rate of multivitamins: post-menopausal women? Again, the authors of a study which pooled the data from the Women's Health Initiative trial and observational study cohorts, come to the same conclusion "the WHI CT and OS cohorts provide convincing evidence that multivitamin use has little or no influence on the risk of cancer or CVD in postmenopausal women." [6].

Not even for infections is there any evidence that MVMS have any protective effect on those most vulnerable, the elderly [7]. 

Of course, keeping all this in mind, the nagging question remains: would there be an effect if only the delivery of the drug in the human body was improved? After all, if vitamins are essential for survival, and if vitamin supplementation does not improve health, then there are several possible reasons for this observation. For instance, we might get enough vitamins from our food, and adding vitamins has simply no effect. Or, maybe we have vitamin deficiencies but the supplements are ineffective in delivering their vitamin loads.

Which brings us to Björn's second question: "Does nano-encapsulation improve the effect of MVMS?

And may I add my nagging question: Or is "nano-whatever" just a cool gimmick of the industry to push a market, which currently grows only moderately? In the next post (Monday 16. April) I'll try to answer this question. So, stay tuned. 

1.           Vivekananthan, D.P., et al., Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials. Lancet, 2003. 361(9374): p. 2017-23.

2.           Prentice, R.L., Clinical trials and observational studies to assess the chronic disease benefits and risks of multivitamin-multimineral supplements. American Journal of Clinical Nutrition, 2007. 85(1): p. 308S-313S.

3.           The Effect of Vitamin E and Beta Carotene on the Incidence of Lung Cancer and Other Cancers in Male Smokers. New England Journal of Medicine, 1994. 330(15): p. 1029-1035.

4.           Omenn, G.S., et al., Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med, 1996. 334(18): p. 1150-5.

5.           Hennekens, C.H., et al., Lack of Effect of Long-Term Supplementation with Beta Carotene on the Incidence of Malignant Neoplasms and Cardiovascular Disease. New England Journal of Medicine, 1996. 334(18): p. 1145-1149.

6.           Neuhouser, M.L., et al., Multivitamin Use and Risk of Cancer and Cardiovascular Disease in the Women's Health Initiative Cohorts.Archives of Internal Medicine, 2009. 169(3): p. 294-304.

7.           El-Kadiki, A. and A.J. Sutton, Role of multivitamins and mineral supplements in preventing infections in elderly people: systematic review and meta-analysis of randomised controlled trials. BMJ, 2005. 330(7496): p. 871.