从调查设计研究内容的角度对这篇文章进行评价。The Framingham Heart Study is a long-term, ongoing cardiovascular study on residents of the town of Framingham, Massachusetts. The study began in 1948 with 5,209 adult subjects from Framingham, and is now on its third generation of participants.[1] Prior to it almost nothing was known about the “epidemiology of hypertensive or arteriosclerotic cardiovascular disease”.[2] Much of the now-common knowledge concerning heart disease, such as the effects of diet, exercise, and common medications such as aspirin, is based on this longitudinal study. It is a project of the National Heart, Lung, and Blood Institute, in collaboration with (since 1971) Boston University. [1] Various health professionals from the hospitals and universities of Greater Boston staff the project. History Thomas Royle Dawber was Director of the study from 1949 to 1966. He was appointed as chief epidemiologist shortly after the start of the project, when it was not progressing well.[3] The study had been intended to last 20 years, but at that time Dawber moved to Boston and became chairman of preventive medicine, raising funds to continue the project and taking it with him. By 1968, a fight was underway to keep the Framingham Study going in an era marked by protests, assassinations, the struggle for civil rights, and controversy surrounding America’s military involvement with the Vietnam War. A committee gathered and considered that, after 20 years of research, the Framingham study should come to an end, since their hypothesis had been tested and extensive information concerning heart diseases had been gathered. Despite this conclusion, the study continued, and in 1971, it enrolled a second generation of participants.[1] In 1994, a more diverse sampling of Framingham residents was enrolled as the “Omni cohort.” In April 2002, a third generation was enrolled in the core study, and a second generation of Omni participants was enrolled in the following
year. 2 Strong and weak points 
Over 1000 medical papers have been published related to the Framingham Heart Study. It is generally accepted that the work is outstanding in its scope and duration, and overall is considered very useful. The initial population was 5,209 healthy men and women aged 30 to 62, not the whole of the town population, as is sometimes assumed. It was rightly assumed from the start of the Framingham Heart Study that cardiac health can be influenced by lifestyle and environmental factors, and by inheritance. The Framingham Heart Study is the origin of the term risk factor. Before the Framingham Heart Study, doctors had little sense of prevention. In the 1950s, it was believed that clogging of arteries and narrowing of arteries (atherosclerosis, arteriosclerosis) was a normal part of aging and occurred universally as people became older. High blood pressure (hypertension) and elevated serum cholesterol (hypercholesterolemia) were also seen as normal consequences of aging in the 1950s, and no treatment was initiated. These and further risk factors, e.g., homocysteine, were gradually discovered over the years.[4][5][6][7][8] The Framingham Heart Study, along with other important large studies, e.g., the Seven Countries Study, Nurses’ Health Study, Women’s Health Initiative, also showed the importance of healthy diet, not being overweight or obese, and regular exercise in maintaining good health, and that there are differences in cardiovascular risk between men and women.[9][10] It also confirmed that cigarette smoking is a highly significant factor in the development of heart disease, leading to angina pectoris, myocardial infarction (MI), and coronary death, along with other important studies about smoking, e.g., the British Doctors Study. Recently the Framingham studies have become regarded as overestimating risk, particularly in the lower risk groups, e.g., for UK populations.[13] One question in evidence-based medicine is how closely the people in a study resemble the patient with which the healthcare professional is dealing.[14] There has been discussion of the study in this regard. Researchers recently used contact information given by subjects over the last 30 years to map the social network of friends and family in the study.[15] 3 Framingham Risk Score The 10-year cardiovascular risk of an individual can be estimated with the easy to use Framingham Risk Score, including individuals without known cardiovascular disease. The Framingham Risk Score is based on findings of the Framingham Heart Study.4 Major findings Major findings from the Framingham Heart Study, according to the researchers themselves:[16] 1960s Cigarette smoking increases risk of heart disease. Increased cholesterol and elevated blood pressure increase risk of heart disease. Exercise decreases risk of heart disease, and obesity increases it. 1970s Elevated blood pressure increases risk of stroke. In women who are postmenopausal, risk of heart disease is increased, compared with women who are premenopausal. Psychosocial factors affect risk of heart disease. 1980s High levels of HDL cholesterol reduce risk of heart disease. 1990s Having an enlarged left ventricle of the heart (left ventricular hypertrophy) increases risk of stroke. Elevated blood pressure can progress to heart failure. Framingham Risk Score is published, and correctly predicts 10-year risk of future coronary heart disease (CHD) events. At 40 years of age, the lifetime risk for CHD is 50% for men and 33% for women. 2000s So called “high normal blood pressure” increases risk of cardiovascular disease (high normal blood pressure is called prehypertension in medicine; it is defined as a systolic pressure of 120–139 mm Hg and/or a diastolic pressure of 80–89 mm Hg). Lifetime risk of developing elevated blood pressure is 90%. Obesity is a risk factor for heart failure. Serum aldosterone levels predict risk of elevated blood pressure. Lifetime risk for obesity is approximately 50%. The “SHARe” project is announced, a genome wide association study within the Framingham Heart Study. Social contacts of individuals are relevant to whether a person is obese, and whether cigarette smokers decide to quit smoking. Four risk factors for a precursor of heart failure are discovered. 30-year risk for serious cardiac events can be calculated. American Heart Association considers certain genomic findings of the Framingham Heart Study one of the top research achievements in cardiology. Some genes increase risk of atrial fibrillation. Risk of poor memory is increased in middle aged men and women if the parents had suffered from dementia. 5 To what the study participants consented The Framingham Heart Study participants, and their children and grandchildren, voluntarily consented to undergo a detailed medical history, physical examination, and medical tests every two years,[17] creating a wealth of data about physical and mental health, especially about cardiovascular disease. 6 Genetic research In recent years, scientists have been carrying out genetic research within the Framingham Heart Study. Inheritance patterns in families,[18] heritability and genetic correlations,[19] molecular markers,[20] and associations have been studied. The association studies include traditional genetic association studies, i.e., looking for associations of cardiovascular risk with gene polymorphisms (single-nucleotide polymorphisms, SNPs) in candidate genes, and genome wide association studies (GWAS).[8] For example, one genome wide study, called the 100 K Study, included almost 1400 participants of the Framingham Heart Study (from the original cohort, and the offspring cohort), and revealed a genetic variant associated with obesity. The researchers were able to replicate this particular result in four other populations.[21] Further, the SHARe Study (SNP Health Association Resource Study) uncovered new candidate genes, and confirmed already known candidate genes (for homocysteine and vitamin B12 levels) in participants of the Framingham Heart Study.[22] Because of these exciting genomic results, the Framingham Heart Study has been described as “on its way to becoming the gold standard for cardiovascular genetic epidemiology”. However, clinically, despite these (and other) efforts, the aggregate effect of genes on cardiovascular disease risk beyond that of traditional cardiovascular risk factors has not been established until now