词条 | Framingham Heart Study |
释义 |
The Framingham Heart Study is a long-term, ongoing cardiovascular cohort study on 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 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. HistoryIn 1948, the study was commissioned by Congress, with a decision made between Framingham, Massachusetts or Paintsville, Kentucky. Framingham was ultimately chosen when it had shown 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 continuing 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 had been split into different segments, or "cohorts".
Strengths and weaknessesOver 1,000 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. 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) 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 initiated. 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] 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] Framingham Risk ScoreThe 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 findingsMajor findings from the Framingham Heart Study, according to the researchers themselves:[16]
Study designThe 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. 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 researchIn 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".[23] 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.[24] Similar studies
See also
Footnotes1. ^1 {{cite journal |author1=Mahmood, Levy |author2=Vasan, Wang | title= The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective | journal=Lancet | year=2013 | volume=383 | pages=999–1008| url=http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2813%2961752-3/fulltext | format=fee required | doi=10.1016/S0140-6736(13)61752-3 | pmid=24084292 | issue=9921 | pmc=4159698}} {{refbegin}}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. ^{{cite journal | author=Richmond | title=Obituary: Thomas Royle Dawber | journal=BMJ | year=2006 | volume=332 | pages=122 | url=http://bmj.bmjjournals.com/cgi/content/full/332/7533/122 | format=fee required | doi=10.1136/bmj.332.7533.122 | issue=7533| pmc=1326951 }} 4. ^{{cite journal | author = Kannel WB | date = Feb 1976 | title = Some lessons in cardiovascular epidemiology from Framingham | url = | journal = Am J Cardiol | volume = 37 | issue = 2| pages = 269–82 | doi=10.1016/0002-9149(76)90323-4| pmid = 1246956 }} 5. ^{{cite journal |vauthors=Lloyd-Jones DM, O'Donnell CJ, D'Agostino RB, Massaro J, Silbershatz H, Wilson PW | date = Apr 2001 | title = Applicability of cholesterol-lowering primary prevention trials to a general population: the Framingham Heart Study | url = | journal = Arch Intern Med | volume = 161 | issue = 7| pages = 949–54 | doi=10.1001/archinte.161.7.949| pmid = 11295957 }} 6. ^{{cite journal |vauthors=Sundström J, Vasan RS | year = 2005 | title = Homocysteine and heart failure: a review of investigations from the Framingham Heart Study | url = | journal = Clin Chem Lab Med | volume = 43 | issue = 10| pages = 987–92 | doi=10.1515/cclm.2005.173| pmid = 16197286 }} 7. ^{{cite journal |vauthors=O'Donnell CJ, Elosua R | date = Mar 2008 | title = Cardiovascular risk factors. Insights from Framingham Heart Study | url = | journal = Rev Esp Cardiol | volume = 61 | issue = 3| pages = 299–310 | doi=10.1016/s1885-5857(08)60118-8| pmid = 18361904 }} 8. ^1 {{cite book |author1=Govindaraju DR |author2=Cupples LA |author3=Kannel WB |author4=O'Donnell CJ |author5=Atwood LD |author6=D'Agostino RB Sr |author7=Fox CS |author8=Larson M |author9=Levy D |author10=Murabito J |author11=Vasan RS |author12=Splansky GL |author13=Wolf PA |author14=Benjamin EJ | year = 2008 | title = Genetics of the Framingham Heart Study population | url = | journal = Adv Genet | volume = 62 | issue = | pages = 33–65 |doi=10.1016/S0065-2660(08)00602-0 |pmid=19010253 |pmc=3014216 |series=Advances in Genetics |isbn=9780123744432 }} 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. ^{{cite journal |author=Brindle P |title=Predictive accuracy of the Framingham coronary risk score in British men: prospective cohort study |journal=BMJ |volume=327 |issue=7426 |pages=1267 |year=2003 |pmid=14644971 |doi=10.1136/bmj.327.7426.1267 |pmc=286248 |name-list-format=vanc|author2=Emberson J |author3=Lampe F |display-authors=3 |last4=Walker |first4=M |last5=Whincup |first5=P |last6=Fahey |first6=T |last7=Ebrahim |first7=S}} 14. ^{{cite journal |author=David Hadden | title=Holidays in Framingham? | journal=BMJ |date=7 September 2002 | volume=325 | pages=544 | url=http://bmj.bmjjournals.com/cgi/content/full/325/7363/544 | doi=10.1136/bmj.325.7363.544 | issue=7363}} 15. ^{{cite journal | author = Christakis Nicholas A. | authorlink = Nicholas A. Christakis | authorlink2 = James H. Fowler | author2= Fowler James H. | year = 2007 | title = The Spread of Obesity in a Large Social Network Over 32 Years | url = | journal = New England Journal of Medicine | volume = 357 | issue = 4| pages = 370–379 | doi = 10.1056/NEJMsa066082 | pmid = 17652652 | citeseerx = 10.1.1.581.4893 }} 16. ^{{cite web|title=Research Milestones|url=https://www.framinghamheartstudy.org/about-fhs/research-milestones.php|website=Framingham Heart Study|accessdate=2 May 2015}} 17. ^{{cite web |url=http://www.bumc.bu.edu/busm/BUSM-About.html |title=Archived copy |accessdate=2010-05-06 |deadurl=yes |archiveurl=https://web.archive.org/web/20100414101335/http://www.bumc.bu.edu/busm/BUSM-About.html |archivedate=2010-04-14 |df= }} 18. ^{{cite journal |author1=Lloyd-Jones DM |author2=Nam BH |author3=D'Agostino RB Sr |author4=Levy D |author5=Murabito JM |author6=Wang TJ |author7=Wilson PW |author8=O'Donnell CJ |date=May 2004 | title = Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring | url = | journal = JAMA | volume = 291 | issue = 18| pages = 2204–11 | doi=10.1001/jama.291.18.2204|pmid=15138242 }} 19. ^{{cite journal |vauthors=Atwood LD, Wolf PA, Heard-Costa NL, Massaro JM, Beiser A, D'Agostino RB, DeCarli C |date=Jul 2004 | title = Genetic variation in white matter hyperintensity volume in the Framingham Study | url = | journal = Stroke | volume = 35 | issue = 7| pages = 1609–13 | doi=10.1161/01.str.0000129643.77045.10|pmid=15143299 }} 20. ^{{cite journal |vauthors=Elias MF, Sullivan LM, D'Agostino RB, Elias PK, Jacques PF, Selhub J, Seshadri S, Au R, Beiser A |date=Oct 2005 | title = Homocysteine and cognitive performance in the Framingham offspring study: age is important | url = | journal = Am J Epidemiol | volume = 162 | issue = 7| pages = 644–53 | doi=10.1093/aje/kwi259|pmid=16107567 |display-authors=etal}} 21. ^{{cite journal |vauthors=Herbert A, Gerry NP, McQueen MB, Heid IM, Pfeufer A, Illig T, Wichmann HE, Meitinger T, Hunter D |date=Apr 2006 | title = A common genetic variant is associated with adult and childhood obesity | url = | journal = Science | volume = 312 | issue = 5771| pages = 279–83 | doi=10.1126/science.1124779|pmid=16614226 |display-authors=etal}} 22. ^{{cite journal |vauthors=Hazra A, Kraft P, Lazarus R, Chen C, Chanock SJ, Jacques P, Selhub J, Hunter DJ |date=Dec 2009 | title = Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway | journal = Hum Mol Genet | volume = 18 | issue = 23| pages = 4677–87 | doi=10.1093/hmg/ddp428 | pmid=19744961 | pmc=2773275}} 23. ^{{cite journal | author = Jaquish CE |date=Oct 2007 | title = The Framingham Heart Study, on its way to becoming the gold standard for Cardiovascular Genetic Epidemiology? | url = | journal = BMC Med Genet | volume = 8 | issue = 1| page = 63 | doi=10.1186/1471-2350-8-63|pmid=17916250 |pmc=2151937 }} 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. ^{{cite journal |vauthors=Knuiman MW, Vu HT |date=Oct 1997 | title = 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 | url = | journal = J Epidemiol Community Health | volume = 51 | issue = 5| pages = 515–9 | doi=10.1136/jech.51.5.515|pmid=9425461 | pmc=1060537}} 27. ^{{cite journal |vauthors=Marshall NS, Wong KK, Phillips CL, Liu PY, Knuiman MW, Grunstein RR |date=Feb 2009 | title = Is sleep apnea an independent risk factor for prevalent and incident diabetes in the Busselton Health Study? | url = | journal = J Clin Sleep Med. | volume = 5 | issue = 1| pages = 15–20 |pmid=19317376 |pmc=2637161 }} 28. ^{{cite journal|author1=The Caerphilly |author2=Speedwell Collaborative Group. |title=Caerphilly and Speedwell collaborative heart disease studies.|journal=Journal of Epidemiology and Public Health|date=September 1984|volume=38|issue=3|pages=259–262|pmid=6332166 |pmc=1052363|doi=10.1136/jech.38.3.259}} 29. ^{{cite journal |vauthors=Elwood P, Galante J, Pickering J, etal | year = 2013 | title = Healthy Lifestyles Reduce the Incidence of Chronic Diseases and Dementia: Evidence from the Caerphilly Cohort Study | url = | journal = PLOS ONE | volume = 8 | issue = 12| page = e81877 | doi = 10.1371/journal.pone.0081877 | pmid=24349147 | pmc=3857242}} 30. ^{{cite journal |vauthors=Elwood PC, Longley M | year = 2010 | title = My Health – Whose Responsibility – a jury decides | url = http://jech.bmj.com/content/64/9/761 | journal = J Epidemiol Comm Hlth. | volume = 64 | issue = 9| pages = 761–4 | doi=10.1136/jech.2009.087767 | pmid=19897471}} 31. ^China Study II, Cornell University. Works cited
Further reading
External links{{Commons category}}
6 : 1948 establishments in Massachusetts|Framingham, Massachusetts|Epidemiological study projects|Heart|Cohort studies|Health research |
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