Framingham Heart Study

The Framingham Heart Study is a long-term, ongoing cardiovascular cohort study of residents of the city 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 the study 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

In 1948, the study was commissioned by Congress, with a choice made between Framingham, Massachusetts and Paintsville, Kentucky. Framingham was chosen when residents showed more general interest in heart research than Paintsville. 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; however, interest grew in part due to Dr. Dawber's efforts to promote the study and engage in fundraising after he had been transferred to Boston to accept a chairmanship of preventive medicine. By 1968, it was debated whether the original study had served its purpose and should be terminated as scheduled. 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, Congress failed to accept the recommendation, instead voting to continue the study. The study has been split into different segments, or "cohorts".

  • The Original Cohort, founded in 1948, consisted of 5,209 men and women. Requirements for entry were an age between 30 and 62 years at the time of first examination, with no history of heart attack or stroke. Due to lukewarm interest at first, doctors, nurses and healthcare workers volunteered for the study to set an example for patients.
  • The Offspring Cohort, founded in 1971, was a second generation study for which children of the Original Cohort were eligible. Spouses were also eligible if they had become pregnant with or sired two or more children by a participant in the Offspring Cohort.
  • The Omni One Cohort, founded in 1994, looked at the possible influence of race and heritage as heart risk factors, as well as the changing racial background of Framingham.
  • The Generation Three Cohort, founded in 2002, was a third generation study consisting of children of the Offspring Cohort and grandchildren of the Original Cohort participants. Minimum age for acceptance was 20 years.
  • The Omni Two Cohort, founded in 2003, was a second generation study involving children of Omni Cohort participants. While the Original Cohort had been spaced over decades, the Omni Cohort had a much shorter generational window. On account of this, participants as young as 13 years of age were eligible for the Omni Two Cohort.

Strengths & weaknesses

Over 3,000 peer-reviewed scientific 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.

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 source of the term risk factor. Before the Framingham Heart Study, doctors had little sense of heart disease prevention. In the 1950s, it was believed that clogging of arteries and narrowing of arteries (atherosclerosis, arteriosclerosis) were normal parts of aging, and that they 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 available. These and further risk factors, such as homocysteine, were gradually discovered over the years.[4][5][6][7][8]

The Framingham Heart Study, along with other important large studies, such as the Seven Countries Study and the Nurses' Health Study, also showed that healthy diet, not being overweight or obese, and regular exercise are all important in maintaining good health, and that there are differences in cardiovascular risk between men and women.[9][10] Along with other important studies about smoking, such as the British Doctors Study, it also confirmed that cigarette smoking is a highly significant factor in the development of heart disease, leading in many cases to angina pectoris, myocardial infarction (MI), and coronary death.[11][12]

Recently the Framingham studies have come to be regarded as overestimating risk, particularly in the lower risk groups, such as for UK populations.[13]

One question in evidence-based medicine is how closely the people in a study resemble the patient with whom the health care professional is dealing.[14]

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]

Framingham Risk Score

The 10-year cardiovascular risk of an individual can be estimated with the Framingham Risk Score, including for individuals without known cardiovascular disease. The Framingham Risk Score is based on findings of the Framingham Heart Study.

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. No empirical evidence found to confirm the rumor that filtered cigarettes lower risk of heart disease as opposed to non-filters.
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. By providing contact information, the Framingham Heart Study establishes a network of personal relationships, connecting participants through their relationships—friends, colleagues, relatives and neighbors.[17] 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 had dementia.

Study design

The Framingham Heart Study participants, and their children and grandchildren, voluntarily consented to undergo a detailed medical history, physical examination, and medical tests every three to five years,[18] creating a wealth of data about physical and mental health, especially about cardiovascular disease. A nonprofit charity, called Friends of the Framingham Heart Study, was founded to help defray study costs and spread awareness of heart issues. Membership is limited to participants.

Genetic research

In recent years, scientists have been carrying out genetic research within the Framingham Heart Study.

Inheritance patterns in families,[19] heritability and genetic correlations,[20] molecular markers,[21] 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.[22] 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.[23]

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".[24]

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.[25]

Similar studies
  • The Busselton Health Study has been carried out since 1966 in a high proportion of the residents of Busselton, a town in Western Australia, over a period of many years.[26] A database has been compiled and is managed by the School of Population Health at the University of Western Australia. Although the results of the Busselton Health Study and the Framingham Heart Study are similar in many aspects, the Busselton Health Study also investigated the influence of some factors that had not been investigated in the Framingham Heart Study, e.g., sleep apnea.[27][28]
  • The Caerphilly Heart Disease Study, also known as the Caerphilly Prospective Study (CaPS), is an epidemiological prospective cohort, set up in 1979 in a representative population sample drawn from a typical small town in South Wales, UK.[29] The study has collected wide-ranging data and has led to over 400 publications in the medical press, notably on vascular disease, cognitive function and healthy living.[30][31]
  • The China-Cornell-Oxford Project, also known as the "China-Oxford-Cornell Study on dietary, lifestyle and disease mortality characteristics in 65 rural Chinese counties". This study was later referred to as "China Study I". The successor study is named "China Study II".[32]
  • The Strong Heart Study is an ongoing cohort study of cardiovascular disease and its risk factors among American Indian men and women. The original cohort began in 1984 with 4,549 participants ages 35–74 from 13 tribal nations and communities in Arizona, Oklahoma, North Dakota, and South Dakota.[33]

See also
  • Long-term experiment

Footnotes
  1. Mahmood, Levy; Vasan, Wang (2013). "The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective" (fee required). Lancet. 383 (9921): 999–1008. doi:10.1016/S0140-6736(13)61752-3. PMC 4159698. PMID 24084292.
  2. Thomas R. Dawber, M.D., Gilcin F. Meadors, M.D., M.P.H., and Felix E. Moore Jr., National Heart Institute, National Institutes of Health, Public Health Service, Federal Security Agency, Washington, D. C., Epidemiological Approaches to Heart Disease: The Framingham Study Presented at a Joint Session of the Epidemiology, Health Officers, Medical Care, and Statistics Sections of the American Public Health Association, at the Seventy-eighth Annual Meeting in St. Louis, Mo., November 3, 1950.
  3. Richmond (2006). "Obituary: Thomas Royle Dawber". BMJ. 332 (7533): 122. doi:10.1136/bmj.332.7533.122. PMC 1326951.
  4. Kannel WB (Feb 1976). "Some lessons in cardiovascular epidemiology from Framingham". Am J Cardiol. 37 (2): 269–82. doi:10.1016/0002-9149(76)90323-4. PMID 1246956.
  5. Lloyd-Jones DM, O'Donnell CJ, D'Agostino RB, Massaro J, Silbershatz H, Wilson PW (Apr 2001). "Applicability of cholesterol-lowering primary prevention trials to a general population: the Framingham Heart Study". Arch Intern Med. 161 (7): 949–54. doi:10.1001/archinte.161.7.949. PMID 11295957.
  6. Sundström J, Vasan RS (2005). "Homocysteine and heart failure: a review of investigations from the Framingham Heart Study". Clin Chem Lab Med. 43 (10): 987–92. doi:10.1515/cclm.2005.173. PMID 16197286. S2CID 23794032.
  7. O'Donnell CJ, Elosua R (Mar 2008). "Cardiovascular risk factors. Insights from Framingham Heart Study". Rev Esp Cardiol. 61 (3): 299–310. doi:10.1016/s1885-5857(08)60118-8. PMID 18361904. S2CID 1854513.
  8. Govindaraju DR; Cupples LA; Kannel WB; O'Donnell CJ; Atwood LD; D'Agostino RB Sr; Fox CS; Larson M; Levy D; Murabito J; Vasan RS; Splansky GL; Wolf PA; Benjamin EJ (2008). Genetics of the Framingham Heart Study population. Adv Genet. Advances in Genetics. Vol. 62. pp. 33–65. doi:10.1016/S0065-2660(08)00602-0. ISBN 9780123744432. PMC 3014216. PMID 19010253.
  9. Nutritional research within the Framingham Heart Study. Millen BE, Quatromoni PA. J Nutr Health Aging. 2001;5(3):139-43.
  10. Women and cardiovascular disease: contributions from the Framingham Heart Study. Murabito JM. J Am Med Womens Assoc. 1995 Mar-Apr;50(2):35-9.
  11. The health risks of smoking. The Framingham Study: 34 years of follow-up. Freund KM, Belanger AJ, D'Agostino RB, Kannel WB. Ann Epidemiol. 1993 Jul;3(4):417-24.
  12. Mortality in relation to smoking: 50 years' observations on male British doctors. Doll R, Peto R, Boreham J, Sutherland I. BMJ. 2004 Jun 26;328(7455):1519.
  13. Brindle P, Emberson J, Lampe F, et al. (2003). "Predictive accuracy of the Framingham coronary risk score in British men: prospective cohort study". BMJ. 327 (7426): 1267. doi:10.1136/bmj.327.7426.1267. PMC 286248. PMID 14644971.
  14. David Hadden (7 September 2002). "Holidays in Framingham?". BMJ. 325 (7363): 544. doi:10.1136/bmj.325.7363.544. PMC 1124063.
  15. Christakis Nicholas A.; Fowler James H. (2007). "The Spread of Obesity in a Large Social Network Over 32 Years". New England Journal of Medicine. 357 (4): 370–379. CiteSeerX 10.1.1.581.4893. doi:10.1056/NEJMsa066082. PMID 17652652.
  16. "Research Milestones". Framingham Heart Study. Archived from the original on 31 July 2017. Retrieved 2 May 2015.
  17. Christakis, Nicholas A.; Fowler, James H. (2008-05-22). "The Collective Dynamics of Smoking in a Large Social Network". New England Journal of Medicine. 358 (21): 2249–2258. doi:10.1056/NEJMsa0706154. ISSN 0028-4793. PMC 2822344. PMID 18499567.
  18. "About the Boston University School of Medicine". Archived from the original on 2010-04-14. Retrieved 2010-05-06.
  19. Lloyd-Jones DM; Nam BH; D'Agostino RB Sr; Levy D; Murabito JM; Wang TJ; Wilson PW; O'Donnell CJ (May 2004). "Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring". JAMA. 291 (18): 2204–11. doi:10.1001/jama.291.18.2204. PMID 15138242.
  20. Atwood LD, Wolf PA, Heard-Costa NL, Massaro JM, Beiser A, D'Agostino RB, DeCarli C (Jul 2004). "Genetic variation in white matter hyperintensity volume in the Framingham Study". Stroke. 35 (7): 1609–13. doi:10.1161/01.str.0000129643.77045.10. PMID 15143299.
  21. Elias MF, Sullivan LM, D'Agostino RB, Elias PK, Jacques PF, Selhub J, Seshadri S, Au R, Beiser A, et al. (Oct 2005). "Homocysteine and cognitive performance in the Framingham offspring study: age is important". Am J Epidemiol. 162 (7): 644–53. doi:10.1093/aje/kwi259. PMID 16107567.
  22. Herbert A, Gerry NP, McQueen MB, Heid IM, Pfeufer A, Illig T, Wichmann HE, Meitinger T, Hunter D, et al. (Apr 2006). "A common genetic variant is associated with adult and childhood obesity". Science. 312 (5771): 279–83. Bibcode:2006Sci...312..279H. doi:10.1126/science.1124779. PMID 16614226. S2CID 23455470.
  23. Hazra A, Kraft P, Lazarus R, Chen C, Chanock SJ, Jacques P, Selhub J, Hunter DJ (Dec 2009). "Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway". Hum Mol Genet. 18 (23): 4677–87. doi:10.1093/hmg/ddp428. PMC 2773275. PMID 19744961.
  24. Jaquish CE (Oct 2007). "The Framingham Heart Study, on its way to becoming the gold standard for Cardiovascular Genetic Epidemiology?". BMC Med Genet. 8 (1): 63. doi:10.1186/1471-2350-8-63. PMC 2151937. PMID 17916250.
  25. Overview of the risk factors for cardiovascular disease. Wilson PWF. In: UpToDate [Textbook of Medicine]. Basow DS (Ed). Massachusetts Medical Society, and Wolters Kluwer publishers. 2010.
  26. A list of publications from the Busselton study
  27. Knuiman MW, Vu HT (Oct 1997). "Prediction of coronary heart disease mortality in Busselton, Western Australia: an evaluation of the Framingham, national health epidemiologic follow up study, and WHO ERICA risk scores". J Epidemiol Community Health. 51 (5): 515–9. doi:10.1136/jech.51.5.515. PMC 1060537. PMID 9425461.
  28. Marshall NS, Wong KK, Phillips CL, Liu PY, Knuiman MW, Grunstein RR (Feb 2009). "Is sleep apnea an independent risk factor for prevalent and incident diabetes in the Busselton Health Study?". J. Clin. Sleep Med. 5 (1): 15–20. doi:10.5664/jcsm.27387. PMC 2637161. PMID 19317376.
  29. The Caerphilly; Speedwell Collaborative Group. (September 1984). "Caerphilly and Speedwell collaborative heart disease studies". Journal of Epidemiology and Public Health. 38 (3): 259–262. doi:10.1136/jech.38.3.259. PMC 1052363. PMID 6332166.
  30. Elwood P, Galante J, Pickering J, et al. (2013). "Healthy Lifestyles Reduce the Incidence of Chronic Diseases and Dementia: Evidence from the Caerphilly Cohort Study". PLOS ONE. 8 (12): e81877. Bibcode:2013PLoSO...881877E. doi:10.1371/journal.pone.0081877. PMC 3857242. PMID 24349147.
  31. Elwood PC, Longley M (2010). "My Health – Whose Responsibility – a jury decides". J Epidemiol Community Health. 64 (9): 761–4. doi:10.1136/jech.2009.087767. PMID 19897471. S2CID 21137383.
  32. China Study II, Cornell University.
  33. "Strongheart Study - Center for American Indian Health Research - College of Public Health". strongheartstudy.org. Retrieved 2021-06-01.

Works cited

  • Daniel Levy and Susan Brink. (2005). A Change of Heart: How the People of Framingham, Massachusetts, Helped Unravel the Mysteries of Cardiovascular Disease. Knopf. ISBN 0-375-41275-1.

Further reading
  • Giroux Élodie (2012). "The Framingham Study and the Constitution of a Restrictive Concept of Risk Factor". Social History of Medicine. 26 (1): 94–112. doi:10.1093/shm/hks051.
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