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LETTERS TO THE EDITOR |
Department of Psychiatry; Washington University School of Medicine; St. Louis, Missouri (Freedland)
Department of Psychology; University of British Columbia; Vancouver, Canada (Miller)
Department of Medicine; Division of Cardiovascular Medicine; University of Florida; Malcom Randall VA Medical Center; Gainesville, Florida (Sheps)
We thank Drs. Schneiderman and Williams for their thoughtful critique of our editorial on the Great Debate. In light of their negative reaction to it, we want to make it clear that we were not criticizing them. If we had said more about their performance in the debate, it would have been to praise the command of the literature, the insight into the issues, and the rhetorical skill they exhibited. It exemplified their long dedication and many contributions to our field.
The problem was not with the debaters but with the material they had to work with. As Schneiderman and Williams point out in their critique, the negative side insisted that the debate exclude trials aimed at improving clinical outcomes in serious organic diseases by modifying health-related behaviors such as diet, exercise, or adherence to medications. Consequently, the affirmative side essentially had to fight with their hands tied behind their backs. Health behavior interventions such as the Diabetes Complications and Control Trial (1) have yielded some impressive findings. Instead of being allowed to highlight such findings, they had to make the much more difficult case that treatment of various forms of emotional dysregulation such as depression or excessive anger improves medical outcomes in conditions such as heart disease, cancer, and HIV/AIDS. We focused on this issue rather than on health-behavior interventions because that was what the debate was about. As they also point out, there had been very few large, randomized clinical trials (RCTs) to support the affirmative side’s case. Although 5 years have passed since then, and although considerable progress has been made in the interim, we still have few large RCTs to support this proposition, and we still need more of them.
Schneiderman and Williams dispute our contention that the debate was an important event that raised some profound questions about biobehavioral research. Their humility about the debate is admirable, and we acknowledge having used some dramatic language to make our point. However, we still consider the debate to have been an important event.
The audience was not systematically polled, and we do not claim to know what everyone in attendance thought about the session. Some were indeed disappointed in the outcome, but we agree with Schneiderman and Williams that neither the debate nor any subsequent developments have thrown the scientific community into despair. Those who were disappointed were not let down by the studies that were discussed, the researchers who conducted them, the quality of the debate, or the deftness of the debaters. The debate simply confronted us with an unpleasant reality: Despite all of the progress that had been made in our field, the evidence in support of the proposition was still far from convincing, at least from the perspectives of three eminent medical journal editors. That was disappointing but not a reason for despair. To the contrary, it was a reason to rededicate ourselves to the goals of our research and to redouble our efforts to achieve them. In this sense, we have something in common with medical scientists who have been struggling for decades to find cures for various forms of cancer. They have made tremendous progress in some areas but little in others, and their patients are still dying of cancer in large numbers. We cannot afford the luxury of despair any more than they can.
Among the diseases addressed in the debate, heart disease stands out as the one with the strongest evidence supporting the emotional dysregulation hypothesis. The current strength of the evidence in this area nevertheless pales in comparison to the indisputable proof that dyslipidemia is a causal risk factor for coronary disease and that treatment of hypercholesterolemia improves medical outcomes in coronary disease. The evidence is so overwhelming that it is hard to believe that there was ever any doubt about it, yet as discussed in a fascinating series of articles by Daniel Steinberg (2–6), the dyslipidemia hypothesis was extremely controversial for decades. The long journey from the first studies of cholesterol to the widespread acceptance of aggressive treatment of hypercholesterolemia spanned most of the 20th century. The link between hypercholesterolemia and coronary heart disease (CHD) morbidity and mortality was not established until 1984, with the publication of the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT) (7,8). Since then, numerous studies, including the CARE, MIRACL, LIPID, LIPS, WOSCOPS, and IDEAL trials (9–14) and others, have shown that modification of cholesterol levels directly affects CHD morbidity and mortality. If a debate about cholesterol were held today, it would not be about whether it is a causal risk factor in coronary disease; lipidology has progressed far beyond that point. It would not even be about whether treating hypercholesterolemia improves medical outcomes in coronary heart disease. It would probably be about which specific dietary modifications and which specific statins, at which dosages, for which patients, improve which medical outcomes.
Our own journey only started in earnest around the same time that the LRC-CPPT outcomes were published. The Great Debate examined the evidence for the emotional dysregulation hypothesis only about a decade later. We had a long way to go at the time, much longer than cholesterol researchers had left to go. We’re unquestionably closer now than we were then. But have we proven yet, to the contemporary standards of evidence-based medicine, that treatment of depression, excessive anger, stress, anxiety, type D personality, or any other form of emotional dysregulation improves hard medical outcomes in heart disease, cancer, or AIDS? In plain English, the answer is no, not yet.
We still have a long way to go. We need to build a much larger database of rigorous epidemiologic, mechanistic, and interventional studies in order to accrue evidence that is strong enough to convince not only those of us who do this kind of research but also the broader medical community. We completely agree with Schneiderman and Williams that the best way to move the field forward is to conduct more of these kinds of studies and that large RCTs are going to play a particularly important role.
DOI:10.1097/01.psy.0000228011.36347.f2
REFERENCES
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  S. M. Saravay Presidential Address: Academy of Psychosomatic Medicine Tucson, AZ November 2006 Psychosomatics, February 1, 2008; 49(1): 3 - 7. [Full Text] [PDF]
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