Framingham Heart Study

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 eects 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 sta the project.

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 inuenced
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]

History

The Framingham Heart Study, along with other important large studies, e.g., the Seven Countries Study, Nurses
Health Study, Womens 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 dierences in cardiovascular risk
between men and women.[9][10] It also conrmed that
cigarette smoking is a highly signicant 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.[11][12]

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 ght was underway to keep the Framingham
Study going in an era marked by protests, assassinations,
the struggle for civil rights, and controversy surrounding
Americas 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.

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

Strong and weak points

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 ndings
of the Framingham Heart Study.

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
1

SIMILAR STUDIES

Major ndings

a detailed medical history, physical examination, and

medical tests every two years,[17] creating a wealth of data
Major ndings from the Framingham Heart Study, ac- about physical and mental health, especially about cardiovascular disease.
cording to the researchers themselves:[16]
1960s Cigarette smoking increases risk of heart disease.
Increased cholesterol and elevated blood pressure 6 Genetic research
increase risk of heart disease. Exercise decreases
risk of heart disease, and obesity increases it.
In recent years, scientists have been carrying out genetic
research within the Framingham Heart Study.
1970s Elevated blood pressure increases risk of stroke.
[18]
heritability and geIn women who are postmenopausal, risk of heart Inheritance patterns in families,
[19]
[20]
netic
correlations,
molecular
markers,
and associdisease is increased, compared with women who are
ations
have
been
studied.
The
association
studies inpremenopausal. Psychosocial factors aect risk of
clude
traditional
genetic
association
studies,
i.e.,
looking
heart disease.
for associations of cardiovascular risk with gene poly1980s High levels of HDL cholesterol reduce risk of morphisms (single-nucleotide polymorphisms, SNPs) in
heart disease.
candidate genes, and genome wide association studies
(GWAS).[8] For example, one genome wide study, called
1990s Having an enlarged left ventricle of the heart (left the 100 K Study, included almost 1400 participants of the
ventricular hypertrophy) increases risk of stroke. Framingham Heart Study (from the original cohort, and
Elevated blood pressure can progress to heart fail- the ospring cohort), and revealed a genetic variant asure. Framingham Risk Score is published, and cor- sociated with obesity. The researchers were able to replirectly predicts 10-year risk of future coronary heart cate this particular result in four other populations.[21]
disease (CHD) events. At 40 years of age, the life- Further, the SHARe Study (SNP Health Association Retime risk for CHD is 50% for men and 33% for source Study) uncovered new candidate genes, and conwomen.
rmed already known candidate genes (for homocysteine
levels) in participants of the Framing2000s So called high normal blood pressure increases and vitamin B12 [22]
ham
Heart
Study.
risk of cardiovascular disease (high normal blood
pressure is called prehypertension in medicine; it
is dened as a systolic pressure of 120139 mm
Hg and/or a diastolic pressure of 8089 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 ndings of the Framingham Heart
Study one of the top research achievements in cardiology. Some genes increase risk of atrial brillation.
Risk of poor memory is increased in middle aged
men and women if the parents had suered from
dementia.

To what the study participants

consented

The Framingham Heart Study participants, and their children and grandchildren, voluntarily consented to undergo

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.[23]
However, clinically, despite these (and other) eorts, the
aggregate eect of genes on cardiovascular disease risk
beyond that of traditional cardiovascular risk factors has
not been established until now.[24]

7 Similar studies
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.[25] 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 investigated also
the inuence of some factors that had not been not
investigated in the Framingham Heart Study, e.g.,
sleep apnea.[26][27]
The Caerphilly Heart Disease Study, also known
as the Caerphilly Prospective Study (CaPS), is an
epidemiological prospective cohort, set up in 1979

3
in a representative population sample drawn from
a typical small town in South Wales, UK.[28] 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.[29][30]
China-Cornell-Oxford Project, also known as
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.[31]

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 27 (9921): 617523.
doi:10.1016/S01406736(13)61752-3. 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 Ofcers, 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 (fee required).
BMJ 332 (7533): 122.
doi:10.1136/bmj.332.7533.122.
[4] Some lessons in cardiovascular epidemiology from Framingham. Kannel WB. Am J Cardiol. 1976 Feb;37(2):26982.
[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): 94954.
doi:10.1001/archinte.161.7.949.
[6] Sundstrm J, Vasan RS (2005). Homocysteine and heart
failure: a review of investigations from the Framingham
Heart Study. Clin Chem Lab Med. 43 (10): 98792.
doi:10.1515/cclm.2005.173.
[7] O'Donnell CJ, Elosua R (Mar 2008). Cardiovascular
risk factors. Insights from Framingham Heart Study.
Rev Esp Cardiol 61 (3): 299310. doi:10.1016/s18855857(08)60118-8.

[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 62: 3365.
[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.
[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. doi:10.1056/NEJMsa066082. PMID 17652652.
[16] http://www.framinghamheartstudy.org/about/
milestones.html
[17] http://www.bumc.bu.edu/busm/BUSM-About.html
[18] 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 ospring. JAMA. 291 (18):
220411. doi:10.1001/jama.291.18.2204.
[19] 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): 160913.
doi:10.1161/01.str.0000129643.77045.10.
[20] 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 ospring study: age is important. Am J Epidemiol 162 (7): 64453. doi:10.1093/aje/kwi259.
[21] 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. doi:10.1126/science.1124779.

11

[22] Hazra A, Kraft P, Lazarus R, Chen C, Chanock SJ,

Jacques P, Selhub J, Hunter DJ (Dec 2009). Genomewide signicant predictors of metabolites in the onecarbon metabolism pathway. Hum Mol Genet 18 (23):
467787. doi:10.1093/hmg/ddp428.
[23] 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.
[24] 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.
[25] A list of publications from the Busselton study
[26] 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): 5159.
doi:10.1136/jech.51.5.515.
[27] 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):
1520.
[28] The Caerphilly and Speedwell Collaborative Group.
(September 1984).
Caerphilly and Speedwell
Journal of
collaborative heart disease studies..
Epidemiology and Public Health 38 (3): 259262.
doi:10.1136/jech.38.3.259. PMC 1052363. PMID
6332166.
[29] 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.
doi:10.1371/journal.pone.0081877.
PMC 3857242.
PMID 24349147.
[30] Elwood PC, Longley M (2010). My Health Whose
Responsibility a jury decides. J Epidemiol Comm Hlth.
64 (9): 7614. doi:10.1136/jech.2009.087767. PMID
19897471.
[31] China Study II, Cornell University.

9.1

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.

10

Further reading

Giroux lodie (2012). The Framingham Study and

the Constitution of a Restrictive Concept of Risk

EXTERNAL LINKS

Factor. Social History of Medicine 26 (1): 94112.

doi:10.1093/shm/hks051.

11 External links
Framingham Heart Study - ocial web site
Heart Center of MetroWest - Cardiology group including William P. Castelli, MD - Former Director
of Framingham Heart Study

12
12.1

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