Framingham Heart Study

Framingham Heart Study Contributions to Health Psychology

The Framingham Heart Study (FHS) is one of the leading prospective, longitudinal studies of cardiovascular disease (CVD) in the world. This study was initiated in 1948 with support from the National Heart Institute (now the National Heart, Lung and Blood Institute). The three major objectives were to (1) obtain data on arteriosclerotic and hypertensive CVD, (2) determine prevalence of all forms of CVD, and (3) test the efficiency of various diagnostic procedures. The objectives encompassed the desire to identify risk factors leading to CVD and to understand how to modify and prevent them. The term “risk factors” was coined by Framingham investigators.

Cardiovascular diseases and events included coronary deaths, heart attacks {myocardial infarction), congestive heart failure, heart pain {angina pectoris), coronary artery diseases, and stroke. Common biological CVD risk factors of concern include high blood pressure {hypertension), diabetes, obesity, high cholesterol, family history of CVD, genetic disposition to CVD, smoking, and age. Diseases of the brain (including vascular disease, dementias, and Alzheimer’s disease) became a target of investigation as the study progressed.

The study is in its 55th year. Most persons were free of CVD when they joined the study at the first time (baseline) of data collection. Data collection was repeated approximately every 2 years. For those initially free of CVD, data were collected before CVD developed (prospective data, collection). Thus it was possible to determine the role these risk factors played in the emergence and progression of CVD.

As early as 1978, the Framingham epidemiologists began to describe the role of psychosocial variables as risk factors for CVD. As just an example, Type A (aggressive, overly ambitious, hostile, and cynical) behavior, anxiety, and worry are associated with the development of CVD, even when biological risk factors such as hypertension, diabetes, high cholesterol, and obesity are taken into account.

Cognitive function has been studied in relation to CVD. The cognitively debilitating effects of stroke were described in 1998. A series of studies of the relationships between biological risk factors for CVD and cognitive functioning were initiated in 1990 using data collected between 1954 and 1978. The reasoning was as follows. Biological risk factors for CVD have adverse effects on brain function. They should be associated with lowered performance on neuropsychological tests.

These hypotheses were confirmed. Risk factors present in midlife, high blood pressure, diabetes, obesity, and smoking, were related to modest deficits in cognitive functioning years later. Moreover, modestly lowered cognitive functioning in midlife, particularly on tests of memory, was related to a higher likelihood of developing dementia in old age.

By 2003, two major findings of importance had emerged from studies with cognitive functioning outcomes: (1) biological CVD risk factors are associated with a lowering of cognitive functioning that is proportional to the number of risk factors present, and (2) in some individuals, mild cognitive dysfunction may herald the development of dementia in very old age and many years after it is first detected.

As early as 1971 a new prospective longitudinal study with the children of the FHS participants (the Offspring Cohort) began. The neuropsychological battery was expanded and an important diagnostic tool was added, magnetic resonance imaging (MRI). The brain images resulting from MRI allowed a quantification of specific types of brain injuries related to CVD risk factors. These studies with the Offspring Cohort have already begun to lead to a better understanding of the mechanisms by which CVD risk factors lead to brain injury and, in turn, to lowered cognitive functioning.

Finally, in 2003 prospective longitudinal investigations of the children of the Framingham Offspring Cohort began. Among other contributions, these multigenerational studies with the offspring are expected to lead to a better understanding of the role of genetic factors in the progression from poor cognitive functioning to dementia.


  1. Eaker, E. D., Pinsky, J., & Castelli, W. P. (1992). Myocardial infarction and coronary death among women: Psychosocial predictors from a 20-year follow-up of women in the Framingham Study. American Journal of Epidemiology, 135, 854-864.
  2. Elias, M. E, Elias, P. K., Robbins, M. A., Wolf, P. A., & D’Agostino, R. B. (2001). Cardiovascular risk factors and cognitive functioning: An epidemiological perspective. In S. Waldstein & M. F. Elias (Eds.), Neuropsychology of cardiovascular disease (pp. 83-104). Hillsdale, NJ: Erlbaum.
  3. Haynes, S. G., Feinleib, M., Levine, S., Scotch, N., & Kannel, W. B. (1978). The relationship of psychosocial factors to coronary heart disease in the Framingham Study. American Journal of Epidemiology, 107, 384-402.
  4. Kase, C. S., Wolf, P. A., Kelly-Hayes, M., Kannel, W. B., Beiser, A., & D’Agostino, R. B. (1998). Intellectual decline after stroke. The Framingham Study. Stroke, 29, 805-812.
  5. Markovitz, J. H., Matthews, K. A., Kannel, W. B., Cobb, J. L., & D’Agostino, R. B. (1993). Psychological predictors of hypertension in the Framingham Study: Is there tension in hypertension? Journal of the American Medical Association, 270, 2439-2443.
  6. Seshadri, S., Beiser, A., Selhub, J., Jacques, P. E, Rosenberg, I. H., D’Agostino, R. B., et al. (2002). Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. New England Journal of Medicine, 346, 476-483.

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