Mental Health: A Report by the Surgeon General

Any discussion of the etiology of mental health and mental illness needs to distinguish three key terms: correlation, causation, and consequences. These terms are often confused. All too frequently a biological change in the brain (a lesion) is purported to be the“cause” of a mental disorder, based on finding an association between the lesion and a mental disorder. The fact is that any simple association—or correlation—cannot and does not, by itself, mean causation. The lesion could be a correlate, a cause of, or an effect of the mental disorder.

When researchers begin to tease apart etiology, they usually start by noticing correlations. A correlation is an association or linkage of two (or more) events. A correlation simply means that the events are linked in some way. Finding a correlation between stressful life events and depression would prompt more research on causation. Does stress cause depression? Does depression cause stress? Or are they both caused by an unidentified factor? These would be the questions guiding research. But, with correlational research, several steps are needed before causation can be established.

If a correlational study shows that a stressful event is associated with an increased probability for depression and that the stress usually precedes depression’s onset, then stress is called a “risk factor” for depression.5 Risk factors are biological, psychological, or sociocultural variables that increase the probability for developing a disorder and antedate its onset (Garmezy, 1983; Werner & Smith, 1992; Institute of Medicine [IOM], 1994a). For each mental disorder, there are likely to be multiple risk factors, which are woven together in a complex chain of causation (IOM, 1994a). Some risk factors may carry more weight than others, and the interaction of risk factors may be additive or synergistic.

Establishing causation of mental health and mental illness is extremely difficult, as explained in Chapter 1. Studies in the form of randomized, controlled experiments provide the strongest evidence of causation. The problem is that experimental research in humans may be logistically, ethically, or financially impossible. Correlational research in humans has thus provided much of what is known about the etiology of mental disorders. Yet correlational research is not as strong as experimental research in permitting inferences about causality. The establishment of a cause and effect relationship requires multiple studies and requires judgment about the weight of all the evidence. Multiple correlational studies can be used to support causality, when, for example, evaluating the effectiveness of clinical treatments (Chambless et al., 1996). But, when studying etiology, correlational studies are, if possible, best combined with evidence of biological plausibility (IOM, 1994b).6 This means that correlational findings should fit with biological, chemical, and physical findings about mechanisms of action relating to cause and effect.

Biological plausibility is often established in animal models of disease. That is why researchers seek animal models in which to study causation. In mental health research, there are some animal models—such as for anxiety and hyperactivity—but a major problem is the difficulty of finding animal models that simulate what is often uniquely human functioning. The search for animal models, however, is imperative.

Consequences are defined as the later outcomes of a disorder. For example, the most serious consequence of depression in older people is increased mortality from either suicide or medical illness (Frasure-Smith et al., 1993, 1995; Conwell, 1996; Penninx et al., 1998). The basis for this relationship is not fully known. The relationship between depression and suicide in adolescents is presented in Chapter 3.

Putting this all together, the biopsychosocial model holds that biological, psychological, or social factors may be causes, correlates, and/or consequences in relation to mental health and mental illness. A stressful life event, such as receiving the news of a diagnosis of cancer, offers a graphic example of a psychological event that causes immediate biological changes and later has psychological, biological, and social consequences. When a patient receives news of the cancer diagnosis, the brain’s sensory cortex simultaneously registers the information (a correlate) and sets in motion biological changes that cause the heart to pound faster. The patient may experience an almost immediate fear of death that may later escalate to anxiety or depression. This certainly has been established for breast cancer patients (Farragher, 1998). Anxiety and depression are, in this case, consequences of the cancer diagnosis,7 although the exact mechanisms are not understood. Being anxious or depressed may prompt further changes in behavior, such as social withdrawal. So there may be social consequences to the diagnosis as well. This example is designed to lay out some of the complexity of the biopsychosocial model applied to mental health and mental illness.

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