How to Live Longer And Exercise Shorter?

Let's face it, if exercise was really that much fun, everybody would do it and we wouldn't be fat, diabetic or die of heart disease. So when your doctor tells you that you better start exercising, your immediate question might be: how much do I have to do? The answer is, it depends. It depends on whether you want to hear the polite version or the truth.  [tweet this].

The polite version goes something like this:  As long as you do some exercise, you will see some health benefits. When your doctor gives you this advice, he probably has studies in mind like the one performed by Hamer and colleagues [1]. They show us that as few as 1-2 exercise sessions per week protect against heart disease. I don't really buy it, and neither should you. Here is why:

The researchers took data from 23,747 people of the English and Scottish health surveys and grouped them into one of two groups, depending on the status of their metabolic health. The latter was defined along the risk markers of high blood pressure, low good cholesterol, diabetes status, high waist circumference and inflammatory status. People who had less than 2 of those risk factors made it into the metabolically healthy group, the rest into the unhealthy group. 

Since these surveys had also asked people to self-report their physical activity levels, the researchers were able to investigate, how exercise volume correlates with health outcome. And, lo and behold, over the average follow-up period of 7 years those among the metabolically unhealthy people, who reported exercising just once or twice a week, had the same risk of developing heart disease as the metabolically healthy people. I'm not trying to discredit this study. It is a valid method to look at associations between exercise and health. But we have to keep in mind that it only answers the question whether PA, at this low volume of 1-2 times per week, is associated with heart health. What the study doesn't tell us is, whether this association is of a causal nature. In other words, it really does not tell us whether low-volume PA "...is protective in men and women with clustered metabolic abnormalities" as the authors suggest.

If studies like the one of Hamer and colleagues are used to entice the couch potatoes to pick up exercise, even if it is only once or twice a week, then, by all means, that's a good start. In public health we love this type of message for a simple reason:  We can throw it at the media in the hope of encouraging sedentary people to take up exercise. If the message is effective, there will be fewer heart attacks and early deaths. What we deliberately do not tell you, though, is how effective this exercise is for YOU. We have a number for that. It is called the 'number needed to expose' (NNE). It tells you how many couch potatoes need "to be exposed" to a change in exercise habits in order to prevent one single case of heart attack or death. In the case of Hamer's study that number stands at more than 40. Meaning, for every 40 people, which we convince, we can prevent 1 death from any cause. Good for us. But probably not good enough for you. If you take up our advice, the 1 in 40 simply means a 2.5% chance that this avoided death would have been yours. Not very motivating. Which is why you don't read so much about these numbers.

Now, if you were my client, I would ask you, whether you were interested in getting the best out of the limited time you are willing to invest in exercise. Which brings us to the second version of the answer, which I promised you in the beginning of this post: the truth.

Evidence is accumulating that the intensity at which you exercise is far more important for your health than the total volume of exercise. In an earlier post (Shortcut to Longevity) I introduced the results of the Copenhagen City Heart Study, which showed an association between heart disease mortality and the intensity, but not the volume, of habitual cycling. Of course, what applies to the Hamer study, applies to this study too. An association is not necessarily of a causative nature. But if we take it as an indication that exercise intensity is so important, isn't that bad news and bad news for the couch potato? Not only does he have to exercise, he also has to exercise hard? No, this is where the good news are: There is method of milking this high-intensity effect to the point where it saves you oodles of time.

It is called high intensity interval training, or HIT for short. This acronym should get you excited, because it super-charges the benefit:time ratio of exercising. In fact, if done correctly, you can expect to improve your fitness and endurance to the same extent as you would with traditional continuous endurance exercise while spending 90% less time on exercise [2]! But let's take it a step at a time.

What is HIT? As the name implies, HIT sessions consist of alternating intervals of vigorous and moderate intensity exercise. One-minute intervals of sprinting, interspersed with 3 minutes of jogging at a moderate pace, would be one of a virtually infinite number of variations of HIT. Do this for 16 or 20 minutes thrice a week and I promise you, within 2 weeks, you'll be excited about the noticeable progress you make. That's 60 minutes a week! Should be possible for the tightest of time budgets. After all, time is the most often cited obstacle to taking up exercise. Understandably, because there are only 24 hours in a day, of which statistically, every German spends 4 hours in front of the TV and every American 6 hours. Which really leaves us so little time to do something meaningful, aside from working and sleeping. If that comes across as sarcastic, I'm guilty as charged.

Anyway, I haven't answered the next logical question, whether HIT also translates into real health benefits. You bet it does. In fact those benefits are so profound, that even heart attack and heart failure patients are now being put on HIT routines. Wisloff and colleagues randomized 27 heart failure patients into 3 training groups [3]: a HIT group which walked three times a week four 4-minute intervals at close to maximal heart rate, with 3-minute intervals of walking at 50% to 70% of maximal heart rate between the high intensity intervals; a moderate-intensity exercise group which walked thrice weekly continuously for 47 minutes at 70% to 75% of maximal heart rate; and a control group which met every 3 weeks for a 47-minute walk. After 12 weeks, the control group showed no improvement in fitness, measured as maximal oxygen uptake. The moderate-intensity group had improved fitness by 14%, whereas the HIT group, which had spent 50% less time on exercise, had an improvement of 54%. Moreover HIT improved arterial function, cholesterol and heart function, significantly better than the continuous moderate-intensity exercise protocol.

In another study, diabetics were put on a HIT protocol consisting ten 60-s sprints interspersed with 60-s moderate-intensity cycling. After only 6 sessions, participants' glucose metabolism had improved substantially and so had their muscles' oxidative capacity [4]. Unfortunately, this study was not controlled, meaning there was no control group to compare the relative benefits of HIT vs. continuous moderate intensity exercise. Which shows, we are still in the early days of finding our ways to optimal protocols for different people with different health issues.

In my lab, we wanted to know whether the high benefit:time ratio of HIT, together with its quickly noticeable results, would entice couch potatoes to do more than a prescribed weekly minimum of three 20-minute hit sessions. After 6 months 76% of our 120 study participants had acquired the habit of exercising more than 150 minutes per week. When they started on our program they had all been sedentary and mostly overweight, but they were otherwise healthy. Over the 6 months they not only improved their fitness substantially but also reduced their weight and improved their risk factors for heart diseases and diabetes [5].

I prefer telling a couch potato that, to gain a health benefit,  (a) he or she has to do exercise, that (b) the exercise has to be of sufficient intensity, and that (c) this benefit can be his or hers at a modicum of time spent on exercise. I prefer that to making polite noises about the benefits of very little exercise, no matter what intensity and volume, because the benefit I would be talking about wouldn't be the benefit she or he is thinking of. 

In the next post I will show you how to design your own HIT routine, how to find the optimal intensities and what to keep in mind when you bring such a routine into a hitherto sedentary life.

Seeing you again coming Monday.

1.    Hamer, M. and E. Stamatakis, Low-Dose Physical Activity Attenuates Cardiovascular Disease Mortality in Men and Women With Clustered Metabolic Risk Factors. Circulation: Cardiovascular Quality and Outcomes, 2012.

2.    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.

3.    Wisloff, U., et al., Superior cardiovascular effect of aerobic interval training versus moderate continuous training in heart failure patients: a randomized study. Circulation, 2007. 115(24): p. 3086-94.

4.    Little, J.P., et al., Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. Journal of Applied Physiology, 2011. 111(6): p. 1554-1560.

5.    Kraushaar, L., Improving the Efficiency of Lifestyle Change Interventions for the Prevention of Cardiometabolic Disease, in School of Public Health Medicine2010, University of Bielefeld: Bielefeld. p. 239.

Hamer, M., & Stamatakis, E. (2012). Low-Dose Physical Activity Attenuates Cardiovascular Disease Mortality in Men and Women With Clustered Metabolic Risk Factors Circulation: Cardiovascular Quality and Outcomes DOI: 10.1161/CIRCOUTCOMES.112.965434

Kent, W. (2011). The effects of sprint interval training on aerobic fitness in untrained individuals: a systematic review British Journal of Sports Medicine, 45 (15) DOI: 10.1136/bjsports-2011-090606.26

Wisloff, U., Stoylen, A., Loennechen, J., Bruvold, M., Rognmo, O., Haram, P., Tjonna, A., Helgerud, J., Slordahl, S., Lee, S., Videm, V., Bye, A., Smith, G., Najjar, S., Ellingsen, O., & Skjaerpe, T. (2007). Superior Cardiovascular Effect of Aerobic Interval Training Versus Moderate Continuous Training in Heart Failure Patients: A Randomized Study Circulation, 115 (24), 3086-3094 DOI: 10.1161/CIRCULATIONAHA.106.675041

Little, J., Gillen, J., Percival, M., Safdar, A., Tarnopolsky, M., Punthakee, Z., Jung, M., & Gibala, M. (2011). Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes Journal of Applied Physiology, 111 (6), 1554-1560 DOI: 10.1152/japplphysiol.00921.2011

The one way to make you slim, fit and healthy?

That your fattening lifestyle drives health insurance costs up is nothing but a fat lie. That much I have told you in the previous post. With Marlboro Man and Ronald McDonald doing better for your health insurer's balance sheet than Healthy Living, you might think that public health should look beyond economics as an argument for health.  In this post I will tell you why they shouldn't. 

 And why economics may well turn out to be the one and only way to getting you to exercise and reduce your weight. And, no, with economics I don't mean punishing you with penalty premiums on your health insurance and punitive taxes on your fast food. Let's leave such uninspired nonsense to the politicians. We can do better than that. Before I get to that point, let's pick up the thread from where we left it in the previous post. 

There I introduced you to the fact that the amazing arithmetic of sicker-equals-cheaper has been introduced by economists working in the employment of public health agencies. They are interested in the financial health of their government, not of a health insurance company. From that point of view, convincing smokers to quit and obese people to slim down doesn't seem to make much sense either. Here is why:

When smokers quit, their near-term health care costs may go down, but in the long run they will be offset by higher medical bills for causes unrelated to smoking but related to a longer life [1]. This longer life hurts the government twice. First, when smokers stop lighting up they also stop paying tobacco taxes to the government. Second, with longer lives come longer pension payments. In fact, if all smokers would quit today, we would have very unhappy finance ministers. Ours, here in Germany, would have his tax revenues reduced by € 14.5 Billion per annum. 

What goes for smoking goes for obesity, too. So, how sincere are our politicians with their professed concerns for our health? Is this a pretext for soon taxing your consumption of sugar and fast food? Well, they certainly have the backing of the World Health Organization. The WHO recommended the introduction of punitive taxes in their 2010 Global status report on noncommunicable diseases. What our politicians apparently don't have is the ingenuity to come up with a more innovative solution, for once. Which is why we have to find it. By looking a little closer at the economics of health.  

So, I'm asking you: aside from you personally, who benefits from your health so much, that promoting it makes economic sense? Your employer, for instance. Not only is a healthy employee less often absent from work, he is also more productive while he is at work. The costs related to work absence have been appropriately termed absenteeism, which makes you immediately understand what is meant with its twin, presenteeism. It describes the costs of being less productive while at work. 

As it turns out, presenteeism clobbers companies' profits much more than absenteeism. In fact, for cardiovascular disease and diabetes, the costs of reduced productivity, while at work, exceed those of absenteeism by a factor of 10 [2]. Admittedly, the calculation of presenteeism is not an exact science. But all available evidence points to a substantial return on employers' investments into preventing those chronic diseases, which produce chronically less productive workers. Across companies and nations, the overall cost:benefit ratio has been found to be in the region of 1:2.2 [3]. Which means, for every dollar spent on corporate health promotion, 2.2 dollars are gained. Not bad. But it could be a lot better if you really did prevent those chronic diseases.

Only, you don't. How do I know? By looking at the trends for the 7 metrics used by the American Heart Association (AHA) as the Strategic Impact Goals for improving cardiovascular health. By 2020 cardiovascular health shall be improved by 20%. That doesn't sound very ambitious. But in all likelihood it is way too ambitious. Here is why: Let's look at obesity, which the IOM has just branded a "catastrophic" problem in the U.S.
Instead of falling, the percentage of obese people has been on the rise, again, over the past 10 years, with now 34% of women and 32% of men being obese [4]. Physical activity levels have not improved significantly, neither did dietary habits. Blood sugar control has actually worsened, and blood pressure control has only slightly improved in men. Based on these data the improvements of cardiovascular health in 2020 will be around 6%, not 20%.

That's how I know that you aren't following your employer's corporate health program. Why would you when you don't follow public health's promotions and recommendations in the first place? Unless, of course, your employer makes you an offer you can't refuse. What would you do if your employer rewarded your participation in his health promotion program with hard cash, additional leave, or a tangible good you desire? What if he tied those benefits to your effort (e.g. your participation rate), or your measurable outcome (e.g. kgs of weight lost, or weight maintenance), or any mixture of effort and result? Would that entice you to pick up healthier habits?

As I have pointed out before, the argument that people who live healthy generate less health care costs than their unhealthily living peers is unsubstantiated. But that should not make us eliminate economics as a metric when it comes to promoting health. On the contrary. By making health an economic good we bring to the table what motivates people most: tangible rewards. The question is, would it get you to pick up exercise, if you didn't do it already, and would it get you to lose weight, if you needed to?

The reason why I'm asking you is, because as a public health scientist, I'm utterly disillusioned with the success rate of our preventive efforts. On one hand, we have this wonderfully simple and enormously effective preventive tool called exercise and weight loss. And on the other hand we have 4 out of 5 people not using this tool. On one hand, we have the new guidelines for the treatment of diabetes [5] and for the prevention of cardiovascular disease  [6], both of which have been released over the past few weeks. Both guidelines acknowledge lifestyle change as the first line of defense against those diseases. But on the other hand we have less than 2% of the population achieving the 7 simple health metrics of the AHA. Guidelines won't change that. So, how can we make the remaining 98% of the population achieve the 7 metrics? Obviously not with the same song and dance that didn't get the job done in the past.

Which is why we need to explore new ways. Taxing your consumption of the foods you enjoy isn't new. Making health an investment good, that's new. But without attracting those people who we haven't reached in the past, it won't work either. Now what do you think?

Will tangible rewards make employees exercise and lose weight?

1.          Temple, N.J., Why prevention can increase health-care spending. The European Journal of Public Health, 2011.

2.          Collins, J.J., et al., The assessment of chronic health conditions on work performance, absence, and total economic impact for employers. J Occup Environ Med, 2005. 47(6): p. 547-57.

3.          Dietmar Bräunig and T. Kohstall, The return on prevention: Calculating the costs and benefits of investments in occupational safety and health in companies, 2012, ISSA: Geneva, Switzerland.

4.          Huffman, M.D., et al., Cardiovascular Health Behavior and Health Factor Changes (1988-2008) and Projections to 2020: Results from the National Health and Nutrition Examination Surveys (NHANES).Circulation, 2012.

5.           Inzucchi, S.E., et al., Management of hyperglycaemia in type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diab tologia, 2012.

6.           Perk, J., et al., European Guidelines on cardiovascular disease prevention in clinical practice (version 2012): The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts) * Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR). European Heart Journal, 2012.

Temple, N. (2011). Why prevention can increase health-care spending The European Journal of Public Health DOI: 10.1093/eurpub/ckr139
 
Collins, J., Baase, C., Sharda, C., Ozminkowski, R., Nicholson, S., Billotti, G., Turpin, R., Olson, M., & Berger, M. (2005). The Assessment of Chronic Health Conditions on Work Performance, Absence, and Total Economic Impact for Employers Journal of Occupational and Environmental Medicine, 47 (6), 547-557 DOI: 10.1097/01.jom.0000166864.58664.29
 
Huffman MD, Capewell S, Ning H, Shay CM, Ford ES, & Lloyd-Jones DM (2012). Cardiovascular Health Behavior and Health Factor Changes (1988-2008) and Projections to 2020: Results from the National Health and Nutrition Examination Surveys (NHANES). Circulation PMID: 22547667
Inzucchi SE, Bergenstal RM, Buse JB, Diamant M, Ferrannini E, Nauck M, Peters AL, Tsapas A, Wender R, & Matthews DR (2012). Management of hyperglycaemia in type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetologia, 55 (6), 1577-96 PMID: 22526604
 
Authors/Task Force Members:, Perk J, De Backer G, Gohlke H, Graham I, Reiner Z, Verschuren M, Albus C, Benlian P, Boysen G, Cifkova R, Deaton C, Ebrahim S, Fisher M, Germano G, Hobbs R, Hoes A, Karadeniz S, Mezzani A, Prescott E, Ryden L, Scherer M, Syvänne M, Scholte Op Reimer WJ, Vrints C, Wood D, Zamorano JL, Zannad F, Other experts who contributed to parts of the guidelines:, Cooney MT, ESC Committee for Practice Guidelines (CPG):, Bax J, Baumgartner H, Ceconi C, Dean V, Deaton C, Fagard R, Funck-Brentano C, Hasdai D, Hoes A, Kirchhof P, Knuuti J, Kolh P, McDonagh T, Moulin C, Popescu BA, Reiner Z, Sechtem U, Sirnes PA, Tendera M, Torbicki A, Vahanian A, Windecker S, Document Reviewers:, Funck-Brentano C, Sirnes PA, Aboyans V, Ezquerra EA, Baigent C, Brotons C, Burell G, Ceriello A, De Sutter J, Deckers J, Del Prato S, Diener HC, Fitzsimons D, Fras Z, Hambrecht R, Jankowski P, Keil U, Kirby M, Larsen ML, Mancia G, Manolis AJ, McMurray J, Pajak A, Parkhomenko A, Rallidis L, Rigo F, Rocha E, Ruilope LM, van der Velde E, Vanuzzo D, Viigimaa M, Volpe M, Wiklund O, & Wolpert C (2012). European Guidelines on cardiovascular disease prevention in clinical practice (version 2012): The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by re European heart journal PMID: 22555213

Pass me the salt. And shut up about stroke risk.

They say, statistics lie.

That's a bad rep for a science, which has no other aspiration than that of making sense from data, of discovering an association between salt intake and stroke, of proving that the former causes the latter. Statistics is above lies. Those who interpret it are not. 

Which is why you should be a skeptic when someone is giving you the creeps about your food habits. For instance, by saying that "high sodium intake is associated with an increased risk of stroke", as the researchers of one recently published study do [1].
To be a skeptic isn't about habitually disbelieving. It is about asking the right questions. And there is a method behind this questioning. Unsurprisingly it is called statistics. The good news is, you don't need to be a statistician to become a methodical skeptic. You only need a little help on how to ask those questions and, more importantly, on how to find the answers for yourself. Which is what we are going to do.

On April 12 this year, Hannah Gardener and her colleagues published their findings about the associations between salt intake and risk of stroke in a community of people residing in northern Manhattan [1]. This appropriately named Northern Manhattan Study, or NOMAS, enrolled 2657 residents with a mean age of 69 years, roughly two thirds of whom were aged between 59 and 79 years. Participants completed a food frequency questionnaire with which the researchers attempted to assess the participants' dietary patterns over the one-year period, which preceded this investigation. I'm not going into discussing the potential pitfalls of using a 12-months recall to calculate how many grams of salt you consume every day. Let's just take those numbers as if they were accurate reflections of participants' salt intake. The researchers categorized participants into four groups according to how much sodium they had in their food:    

1.     1.5 grams/day or less

2.     > 1.5 grams - 2.3 grams per day

3.     > 2.3 grams - less than 4 grams per day

4.     4 - 10 grams per day

These categories didn't just occur to them from a close look at the tea leaves. The American Heart Association (AHA) recommends not to take more than 1.5 grams of sodium per day. Before 1.5 grams became the order of the day, it was 2.3 grams in the previous recommendation . Which is why the researchers used group number 1 as the reference, to which they compared the remaining 3 groups. By the way, only 12% of the study participants were in group 1.  

The researchers then checked how many stroke "events" occurred in each group over an average period of 10 years. And they also checked whether there was a significant difference when comparing the groups of higher salt intake with the reference group.

When you do this type of comparison, it pays to keep in mind that salt is not the only potential cause of stroke. Age is too, because the older you are the more likely it is that you'll suffer a stroke within the next ten years. So the researchers had to adjust for age. That's a statistician's way of asking "what would the rate of stroke events be if all participants were equal in age?". They did this adjustment thing not only for age but also for sex, ethnicity and education. Simply, because we know that these factors have an influence on stroke risk, too. This demographic adjustment was the researchers' first model of adjustment. They went a step further with a second and a third model, in which they additionally adjusted for behavioral and then, on top of that, for biological risk factors. In other words, they were very thorough in isolating the stroke risk that associates with eating salt, irrespectively of what else you do to your health. That's good statistics work. Now let's look at the results.

Only in the group of people with a daily sodium intake above 4 grams per day was the rate of stroke significantly higher than in the group of people who had reported to take no more than 1.5 grams. The take-home point in this case is, that consuming 4 grams or more of sodium per day was associated with a significantly increased risk of stroke in this population. Now here is the first question which you should ask:

What do you mean with "significant"?

To a statistician it does NOT mean what it probably means to you - "substantial". "Significant" is statistician speak for "probably not due to chance". In this case it means, there is some association between eating more than 4 grams of sodium per day and the risk of suffering a stroke within 10 years from now. Now you can shoot the second question:

How large is this "significant" difference in risk?

Let's take the AHA's demarcation line of 1.5 grams of sodium: Of those whose salt consumption was not more than that, 7.5% suffered a stroke. Whereas 9% of the sodium delinquents did. While this is not the correct way of comparison, it puts things into a clearer perspective. So, let's do it the correct way, and look at the risk in terms of event rates, that is in events per thousand person-years. There you have 7 strokes per thousand person-years in the group of low-sodium consumers vs. 8.9 strokes per 1000 person years in the rest. With these figures you can ask one very important question:

How many strokes could have been prevented among the sodium delinquents if they had gone easy on the salt?

The answer is: one in five. That is, 80% of the strokes that did occur in this group would have occurred even if they had consumed salt according to AHA recommendations. The picture is quite a bit different if you look only at the group of highest salt consumers, those who reported consuming more than 4 grams of sodium per day. In that group, "only" 60% of the strokes that did occur would have happened if they had lowered their salt consumption. Now, here comes your (almost) final question:

How relevant are these data to me?

Not at all if you are below the age of 40. That was the threshold for enrollment. Which obviously doesn't mean that you should go on a salt rampage until you hit 40 and then cut back to a daily dose of 1.5 grams of sodium per day. It simply means, the data from this study are not applicable to you, because your profile doesn't match the profile of the study participants.

Now let's assume, you are on the wrong side of 60, and let's also assume, that you measured your sodium intake to be more than 1.5 grams per day (and mind you, to get 1.5 grams of sodium you need to put 3.75 grams of salt on your food). Your next question would be:

What's MY stroke risk for the next 10 years?

About 9%. That is, of 11 guys who have exactly the same profile as you do, one will suffer a stroke over the next 10 years. Whereas, if you had found yourself to consume less than the 1.5 grams of sodium, that ratio would still be 1 out of 14.  That's a 20% reduction. And who says that cutting down on salt will get you this 20% risk reduction? Which amounts to your last question:

Does high salt consumption cause stroke?

Who knows? The study of Hannah Gardener and colleagues CANNOT answer this question. Their study design can only show you that there is an association. It CANNOT show causation. Which is why Dr. Gardener  and colleagues are not correct to conclude that "The new American Heart Association dietary sodium goals will help reduce stroke risk." That's an assumption of causality, which would require a different study design. For example, a study in which one group of participants is given sodium at the AHA recommended level and at least one other group is given sodium in excess of those 1.5 grams. For ten years, mind you. And without the participants or their physicians knowing who gets what. It's called a double blinded, randomized, controlled trial. It's the gold standard to prove causality. Try to do that with salt in a real life setting.

Naturally, Reuters blared out on 25th April "High salt intake linked to higher stroke risk". As usual, the media types gleefully dramatize studies like these. They feed you the bits and pieces which sell print.

But statistics are above the razzle-dazzle. Those who interpret them are obviously not. That's why it pays to be a skeptic and to take those statements literally with a pinch of salt.  

1.           Gardener, H., et al., Dietary sodium and risk of stroke in the northern Manhattan study. Stroke, 2012. 43(5): p. 1200-5.

Gardener, H., Rundek, T., Wright, C., Elkind, M., & Sacco, R. (2012). Dietary Sodium and Risk of Stroke in the Northern Manhattan Study Stroke, 43 (5), 1200-1205 DOI: 10.1161/STROKEAHA.111.641043

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

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