Paradoxes — Compel us to think
We may know, intellectually, that correlations can never show causation, but when a correlation seems to confirm a reason we believe, it’s very easy to find ourselves falling for the fallacy, anyway, and to not even consider other explanations. We may call our belief “common sense” or what “everyone knows,” without realizing that we’ve come to believe it simply because it’s all we ever hear. It may never even occur to us to question an axiom — especially if we never hear about the evidence which contradicts or disproves it. The obesity paradox wouldn’t be a paradox at all, for example, if the public had been hearing objective reports of medical research all along.
The next four posts will share with you four recently published studies in peer-reviewed medical journals that the media ignored. Like countless other studies that the public never hears about, these articles probably didn’t come with press releases because there was nothing to sell you or to promote. In JFS’s objective to help you get a fuller story and to encourage all of us to think critically and for ourselves*, we’ll share these studies. They could be said to be about the obesity paradox, healthy lifestyle paradox and figure flaw-paradox…
Anymore, epidemiology has become a vehicle to find associations between every aspect of our everyday lives or our physical features and risks for some feared disease. And it’s being misused to convince us that our diets and lifestyles or appearances are the cause of ill-health. Blame, guilt and fear are the bread and butter of health marketing. That’s why carefully controlled epidemiological studies that find no link — those null studies that rarely get reported — are especially valuable. If there’s not even a strong link between two variables, then a variable can’t possibly have a causal role. Null studies tell credible scientists, and should tell us, to move on and stop worrying about that.
It can often be difficult for the public to understand what makes some epidemiological studies stronger than others — such as dredging through data compiled from self-reported questionnaires versus actual measurements from medical exams. Epidemiological studies have reported contradictory correlations between fatness and mortality risk among mature adults and it’s often suggested that it’s because cardiovascular fitness hadn’t been considered and could be an independent confounding factor.
Fat and fitness
Researchers, led by Dr. Paul McAuley with the Department of Human Performance and Sport Sciences at Winston-Salem State University in North Carolina, set to test the hypothesis that high cardiovascular fitness and high BMI were associated with a lower risk for death among healthy older men. As they noted, most studies, and the strongest ones, point to an inverse relationship between BMI among mature adults and mortality, with obesity having a protective role. Obesity’s survival advantage among patients with a wide range of diseases and health problems has also been especially well documented in the medical literature. Could being fat be associated with lower risk for premature death among healthy adults, and is fitness an independent risk factor?
Method. The researchers examined the data of 2,469 men consecutively enrolled in the Veterans Exercise Testing Study who had completed a full physical medical exam and maximal exercise testing** at one of two university-affiliated Veterans Affairs medical centers during 1987-2004. The men were age 65 years and older. Mortality data was gathered from the Social Security Death Index and the California Death Registry. They restricted their study to healthy men to rule-out those who might be underweight or physically inactive because of health problems. Their results were published in the Journal of Gerontology A Biological Sciences and Medical Sciences.
Findings. Among 981 healthy older men, 208 died during 6.9 years of follow-up. Compared to the reference ideal of a “healthy” BMI (20-24.9), men who were overweight were associated with a 34% lower risk for all-cause mortality, while the obese men (regardless of the degree of obesity) were associated with a 44% lower risk. In contrast, men with BMIs under 20 had more than a two-fold higher risk for premature death. When cardiovascular fitness was controlled for (as measured by MET = 3.5 mL/kg/min oxygen uptake on exercise tests), the slim men with BMIs below 20 were associated with an even higher 2.5 fold higher risk for premature death. Meanwhile, the most obese men had the lowest risk for all-cause mortality of all, at less than half (HR= 0.44) the “normal” weight men. As the authors noted, none of these correlations were significant. However, they do help to dispell popular beliefs about the deadliness of being fat as we age.
The researchers attempted to parse out these relationships by looking at obesity and physical fitness as they relate to risks for all-cause mortality. They eliminated all of the underweight men with BMIs below 20. Still, the overweight men had a lower risk for death than the “normal” weight men, and the obese men had the lowest risks of all (about half that of “normal” weight men), at every level of fitness.
In fact, the men who were the most obese and sedentary had a similar risk for all-cause mortality (HR=0.56) as the “normal” weight men who were the most physically fit (HR=0.49). This finding certainly didn’t make the headlines. Beliefs among the general public about both the benefits of exercise and the dangers of obesity as people age appear beyond what the evidence supports.
These results are consistent with the largest Aerobic Center Longitudinal Study (ACLS) at the Cooper Clinic in Dallas, Texas, on younger adults which had focused on fitness and reported it attenuates the risks associated with obesity. The ACLS had clinically followed more than 25,000 civilian men for over ten years and the data actually found a small, consistent survival advantage the heavier the men were. The Cooper Institute of Aerobics Research has performed similar studies on more than 113,000 women.
Not surprisingly, the media largely ignored this latest study. While it’s an epidemiological study and not evidence of causation, its value as a null study was lost. The public also didn’t hear another point the authors made: that cardiovascular fitness is influenced by many factors, which includes age and heredity.
Yet the popular condemnation of people without high fitness levels is rarely recognized as a form of discrimination. Fitness and lifestyle preventive medicine have become such big business, and bigger politics, many people have come to believe that everyone must engage in similar types and intensities of activity (i.e. exercise) to live longer and be healthy. Those who don’t follow leisure-time exercise regimens are labeled as having sedentary lifestyles and blamed for putting themselves at risk for premature death, even when they're active all day in their work.
Besides wordsmith plays on definitions, correlations between exercise and lifespan can mislead us when we fail to remember that leisure-time exercise and sports activities are largely markers for youth and socioeconomic status — yet older age, and lower class and poverty, are two of the biggest risk factors for chronic diseases of aging and death. Fitness, body type, physical abilities and strength also have strong hereditary components. Yet a correlation between people who don’t have athletic physiques and their lower participation in sports activities is often mistaken for reverse causation.
Today’s beliefs in exercise can also mean we fail to explore other potential links that are equally, if not more, important to people’s overall health and well being. The most careful exercise intervention studies show that inappropriate conclusions about causes and effects have overlooked more significant social and productive activities.
Beliefs can also mean we fail to weigh the risks for harm of imposing our beliefs that everyone needs to have the same lifestyles and follow one-size-fits-all exercise prescriptions, in order to be healthy. What may be healthful for some 20-year olds, for example, may not be for a growing child or older adult or senior.
Babyboomers, the first generation to grow up exercising, have led to what’s known among medical professionals as boomeritis. Sports and exercise injuries have become the number two reason for doctor’s visits, behind the common cold, according to the CDC’s National Ambulatory Medical Care Surveys. Athletic activities among middle-aged adults were the source of 488 million work day restrictions in 2002, according to the Bureau of Labor Statistics, while the Consumer Product Safety Commission documented that by 1998, sports-related injuries among boomers were responsible for $18.7 Billion in medical costs. The AHRQ's Medical Expenditure Panel Survey (MEPS) found that injury-related medical care accounted for about 57 percent of all payments made by Worker's Compensation programs in 2002. The medical literature continues to bring reports of similar risks for injuries among children.
Scientists understand the importance of testing hypotheses about causes and effects — and balancing overall benefits over risks — using carefully designed randomized, controlled clinical trials and measuring hard clinical outcomes. Yet, every randomized, controlled clinical trial of “healthy lifestyles,” as popularly defined, has failed to significantly reduce premature deaths from all causes or to prevent chronic diseases of old age.
As the recent review in the Journal of the American Medical Association pointed out, this is what separates science from ideology.
© 2009 Sandy Szwarc. All rights reserved.
* Social media marketing is sadly helping to train us not to think. It’s more comfortable to see what everyone else says and what’s popular, such as on online forums, before deciding what we will believe.
** Clinical Evaluation and Exercise Testing
All participants completed a symptom-limited maximal exercise test using an individualized ramp treadmill protocol… Immediately prior to the exercise test, height and weight were measured using standard procedures, and BMI was calculated as weight in kilograms divided by the square of height in meters. A microcomputer automatically increased workload after an individualized walking speed was established and predicted values for maximal exercise capacity were entered. A 12-lead electrocardiogram was recorded each minute, and blood pressure was recorded on alternate minutes throughout the test. Standard clinical criteria for terminating the tests (e.g., fall in systolic blood pressure, STsegment depression >2.0 mm, dangerous arrhythmias) were followed, but no heart rate or time limit was imposed, and a maximal effort was encouraged. Standardized equations were used to determine the calculated peak METs on the basis of treadmill speed and grade . Exercise capacity was expressed as the maximal MET value attained during the exercise test.