Obesity – Primary vs. Secondary prevention

I will never forget the very first patient history I ever took. Part of medical school training is they send you onto the wards to gather patient histories and physicals so you learn to gather information effectively as a clinician. My first patient history was on a woman about 35 years old on the orthopedics ward, who was a triple-amputee. She had her legs removed below the thigh, and one arm amputated below the elbow. The cause was imminently preventable. She had type II diabetes that was poorly controlled. She was obese, weighing about 180 lbs despite the removal of large parts of her body. A common problem with diabetics is that they are susceptible to infection in their bones. Diabetics have have poor pain perception from diabetic neuropathy and poor blood supply, the result is that cuts on their extremities go unnoticed, heal poorly, and ultimately result in infection that frequently goes into the bone. The result, osteomyelitis, is persistent infection of the bones from these infections, and, if antibiotics are ineffective, the only treatment is to surgery to remove the infected tissue and often amputation. Such was the case with my patient. She was poor, from Appalachia, had inadequate control of her diabetes, and as a result lost multiple limbs from infection (she was hospitalized for yet another infected bone).

The major reason for the increase in Type II diabetes rates is obesity and lack of exercise. Disturbingly, younger and younger people are presenting with diseases often only seen with age, like type II diabetes and gout. This is unquestionably due to increasing rates of obesity in the US population. Thus, it is with dismay, that I read Sandy Szwarc’s blog Junkfood science, that seems to exist for the sole purpose of denying the health risks of obesity and of being overweight. Sandy, who is on CEI’s staff, routinely writes about obesity as a health-scare, that is not harmful as doctors and health scientists suggest.

To illustrate the problems with her analysis, let’s go through one of her more recent posts on the Obesity Paradox – the apparent decrease in mortality in studies of the obese.

Sandy starts with the startling assertion that fat does not cause heart disease or premature death.

What is most amazing is how long it has been known that body fat doesn’t cause heart disease or premature death, yet how vehemently people hold onto this belief. “The notion that body fat is a toxic substance is now firmly a part of folk wisdom: many people perversely consider eating to be a suicidal act,” wrote Dr. William Bennett, M.D., former editor of The Harvard Medical School Health Letter and author of The Dieter’s Dilemma. “Indeed, the modern belief that body fat is a mortal threat to its owner is mainly due to the fact that, for many decades, the insurance companies had the sole evidence, and if it was wrong they would presumably have had to close their doors.” That can still be said today, although the obesity interests have since grown considerably larger.

One already notes the intimation of a conspiracy in “obesity interests”, but let’s leave that aside for now. But what is this evidence that fat is harmful? For one, obesity is known to be a risk factor for hypertension and other morbidity in children (1,2,3,4,5,6) and increases the risk of diabetes (1,2,3,4,5,6) In adults obesity increases a number of cardiovascular and other morbidities (1,2,3,4) and the health burden of obesity is recognized as a critical public health problem (JAMA free full text) as well as a cause of decreased quality of life (1). Further the statement that obesity does not increase morbidity or mortality based on the book Bennet wrote in 1982 simply can no longer be sustained (1,2,3,4,5,6)

Let us continue.

Ancel Keys and colleagues, for example, examined 16 prospective population studies in seven countries, as well as actual angiographic and autopsy examinations of 23,000 sets of coronary arteries which found no relationship between body fatness and the degree or progression of atherosclerotic build-up. And the most careful studies ever since have continued to support these findings.

This is may be entirely true, but one of the lessons of cardiovascular medicine over the last few decades is that the issue isn’t size of atherosclerotic plaques but rather their stability. Heart attacks and strokes aren’t caused by gradual narrowing and then closure of vessels. Rather, atherosclerotic plaques which form in reaction to inflammatory reactions in the vessel wall suddenly rupture, exposing the the necrotic cores of these plaques to the bloodstream, resulting in pathological activation of the clotting cascade, and then infarction. Size of lesions is largely meaningless with regard to acute coronary and cerebrovascular events. Either way, the evidence is in from epidemiologic studies, obesity, discounting other risk factors, greatly increases risk of cardiovascular disease, some cancers, diabetes, dyslipidemia, joint problems, etc. Continuing:

“Before we delve too far into the possible connections between overweight and heart disease, we should look at the evidence to see whether they are as closely linked as they are conventionally assumed to be,” cautioned Dr. Bennett. “Again, we can use major statistical trends to reassure ourselves that fatness cannot be a very important cause of cardiovascular death….”

He wrote that back in 1982, pointing out how the age-adjusted rate of deaths from heart attacks and strokes since the early 1950s had dropped while weights had increased. Biological truths cannot be reversed. These very same findings continue today. As was reported just last month, the health of Americans continues to improve, and heart disease and cancer rates are dropping as weights increase; and the CDC now estimates that today’s children will live longer than ever in our country’s history.

Again, we’re assessing irrelevant information. Heart disease and cancer rates decrease because of screening, smoking prevention, and better drugs, but the evidence is clear of a link between obesity and morbidity/mortality. This is assessed independently of innovations in medical care, and is an independent factor for increased death rates.

“Detailed epidemiological studies, too, show no impressive connection between obesity and cardiovascular disease,” Dr. Bennett wrote. By that he meant credible, carefully done studies. Junkfood Science readers regularly see how such studies can be manipulated to give the false impression of correlations seeming to show causation by, for example, ignoring confounding factors (like stress, social-economic factors, dieting, and prescription drugs) or using false surrogate endpoints rather than actual clinical disease or deaths. Also, he emphasized, “it cannot be said that fatness in itself causes hypertension…[and] being fat does not, in itself cause diabetes.” Again, those findings continue to hold true today.

This information is so patently false as to be offensive. There is no question of a link between obesity and diabetes, and obesity and hypertension. I have no doubt, that if my first patient had not been morbidly obese, she wouldn’t be losing limbs to type II diabetes before age 40. I know of no responsible physician that would deny these links. But let’s go onto the latest study showing the harmlessness of obesity in Sandy’s eyes.

Which brings us to a study in the current issue of the American Journal of Medicine, led by cardiologist Dr. Seth Uretsky, M.D., at St. Luke’s-Roosevelt Hospital in New York. By now, we should not be surprised that the media is not reporting on this study, like all the others that go against popular groupthink. These researchers set out to see if the “obesity paradox” of lower morbidity and mortality with increasing body mass index exists with heart disease patients.

The patients were from the INVEST trial, a prospective, randomized international study of 22,576 patients age 50 and older who had hypertension and coronary artery disease. Their heart disease was confirmed and defined as having had a documented heart attack, coronary angiogram with more than 50% stenosis in at least 1 major coronary artery, angina pectoris, or evidence of ischemia on at least 2 different modalities of stress tests (electrocardiogram, echocardiogram, radionuclide scan) that were consistent. The patients received extensive cardiovascular workups in the clinical setting including BMI calculations, and were followed for an average of 2.7 years. The primary outcomes for this study were all-cause mortality, heart attacks and strokes.

Their findings? Compared to ‘normal’ weight patients, the thin patients had 74% higher risk of both death and having a heart attack or stroke, whereas the ‘overweight’ patients had 29% lower risk. But the obese had the lowest risks of all, nearly half that of ‘normal’ weight patients. Only at the very highest BMIs did the risks begin to creep up but they were still less than the overweight and most notably less than the ‘normal’ weight patients. The reverse “J” curve of their graph was amazing similar to that shown earlier this year in a Stanford University-led study of women. The most significant endpoint, all cause mortality, is where the lower risks with fatness were especially striking.

In contrast with these epidemiologic studies, our analysis…among patients with a history of hypertension and coronary artery disease, overweight and class I to III obesity were associated with a decreased risk of morbidity and mortality compared with normal-weight patients, despite less blood pressure control. This finding is consistent with the notion of an “obesity paradox” that has been described in patients with documented cardiac disease (eg, heart failure), patients undergoing percutaneous coronary intervention, and patients with coronary artery disease referred for single photon emission computed tomography.

Now this study actually is very interesting, even if it does conflict with others that failed to show such an effect. The thinner patients, who had an average age about 10 years higher than any of the other groups, also had a higher mortality after adjusting for co-morbidities.

This is where the issue of primary prevention comes in. It is clear that obesity causes a host of morbidities and mortality, but in older populations in these studies the relationship is less clear, and things like weight loss are associated with a higher risk of mortality. There are many reasons for this. For one, in study groups for evaluating drugs, as in this case, investigators strive to make sure patients get quality care as part of an ethical investigation. The high BMI cohort in this case, even if not perfectly controlled, did have treatment for all the co-morbidities of obesity that the doctors could address. Further, in older patients, you expect a weight gain of about 1lb a year. When weight starts decreasing in an elderly patient, this is what’s known as a bad sign. It is likely the “protective effect” that is observed is from the fact that healthy patients maintain weight, while losing weight is often associated with worsening health in an elderly cohort.

Losing weight therefore appears to be a risk for death, and it is also possible that dieting in an older population simply isn’t a safe proposition anyway. The message you should take home from all these studies of obesity and weight loss or gain is simple. It is very difficult to improve health through making people lose weight, and diets rarely have long lasting effects. Exercise, even in the overweight, is the most likely intervention to improve markers of cardiovascular health. In the overweight, appropriate management of symptoms like hypertension, diabetes etc., is effective in decreasing mortality. And finally, the best way to prevent the diseases of obesity is to avoid obesity in the first place. It’s called primary prevention.

Once people are overweight, it is very difficult for them to return to a normal weight, especially as they age. Clinicians, before diet, should probably stress management of the co-morbidities of high-blood pressure, high cholesterol, and insulin resistance, while encouraging exercise first and foremost. Treatment should not be delayed while expecting weight-loss, which rarely takes.

Especially in children, avoiding obesity is becoming increasingly critical. Diabetes is a serious disease that, if poorly controlled as it is in so many cases, results in terrible outcomes like I saw in my first patient. The best thing we can do for children’s health is emphasize exercise, outdoor activity, and get the damn purified and processed sugars out of their diet, which cause obesity and may independently affect insulin sensitivity. While studies may show that obese patients may experience similar or even better morbidity and mortality to normal weight people, one has to remember these are people who are experiencing control of their blood-pressure, blood sugar, cholesterol etc. Many patients, like my first patient, aren’t so lucky as to have good insurance, regular doctor’s visits, good discipline, or to be enrolled in a clinical trial. The best thing that can be done for them is to prevent obesity and their disease from occurring in the first place.

This constant denial of any negative consequence of obesity is irrational, contrary to the clinical evidence, and is, quite simply, just crankery. While some of Sandy’s skeptical writings do hit the mark (the social-networking study of obesity on the Framingham study being a good example), I have to say she’s more of a skeptic like Steven Milloy of Junkscience (who she links – there’s a bad sign), also a CEI fellow, and noted global warming crank. While they have some capacity to recognize real nonsense, the central message is one denying the rational interpretation of the literature.