Framingham Heart Study

Framingham Heart Study -
Celebrating 75 Years of Discoveries

The year was 1944.  President Franklin Delano Roosevelt was planning for the Allied landing at Normandy.  Around the same time, out of concern from his daughter, the President admitted himself to Bethesda Naval Hospital in March of 1945 for a second opinion. Leaders who had met with him as well as family members were concerned about Roosevelt’s well being. He was out of breath when he exerted himself, experienced excessive sweating, had abdominal distention, and bluish skin color.  Tests revealed the president had blood pressure of 186/108 and an “increase in size of the cardiac shadow.” This is when the president received his first diagnosis of hypertension, hypertensive heart disease, and cardiac failure.¹”  There was little the cardiologist could do.  He ordered FDR to reduce alcohol and smoking and ordered digitalis therapy, a low salt diet, and bed rest. Two weeks later the president’s blood pressure had risen to 240/130 after unsuccessful phenobarbital treatment. 

In 1945 the president’s physician wrote “the President appears to be a very sick man.” A few weeks later President Franklin D. Roosevelt died of a cerebral hemorrhage with blood pressure of 300/190. Cardiovascular disease was a leading cause of death at the time, but not much was known about it to be able to prevent or treat it.

In 1948 President Harry Truman signed the “National Heart Act.”  It was the impetus of the Framingham Heart Study.

The Framingham Heart Study began in 1948. The study is still ongoing today.  It recently celebrated its 75th anniversary and is in its third generation of cohorts. The original 5,209 cohorts consisted of people between the ages of 28 to 62 years old living in Framingham, Massachusetts. Framingham was chosen because it was a factory town of 28,000 middle class residents and there were many cardiologists at nearby Harvard University.  Unlike many previous studies, nearly half the participants were women.  The framers were also intentional about recruiting families which they hoped would keep people in the study and continue within families for generations to come. Soon afterwards, the study was moved to Boston, where 6,000 of the 10,000 Boston residents were recruited into the study. The study was turned over to the National Heart Institute, and upon receiving additional funding, robust studies began.

Population cohorts for the heart study:

CohortFirst YearSize% FemaleSalient Features
Offspring1971512452%Children of the Original Cohort, and their spouses
Third Generation2002409553%Children of the Offspring Cohort
New Offspring Spouse200310354%Spouses of Offspring Cohort who were not initially enrolled in FHS, and whose 2 children are in Third Generation Cohort. Added to improve statistical power
Omni 1199450658%To reflect the increasing ethnical diversity of the community. African-American, Hispanic, Asian, Indian, Pacific Islander and Native American
Omni 2200341057%Recruited in order to achieve 10% of Third Generation Cohort size

Data entry form for the Original Cohort c1947. Courtesy: NHLBI archives.

Framingham investigators were concerned about the viability of study continuing when the threat of the 20 year funding commitment was coming to an end.  They went nationwide to get private funds to continue the study.  In 1971, federal funding for the study resumed. Children of the original participants were recruited as well as their spouses.

Thomas Dawber became the second director of the study in 1949 and noted physicians were caring for patients who were already ill. He believed changing the way medicine was practiced was “essential for advances.” He knew from past experience this would be difficult to do and thought the root of this difficulty was from the education and training physicians received.  Medical textbooks taught diastolic blood pressure was a more important number than systolic blood pressure in determining high blood pressure. The study investigators were ready to engage in “epidemiological activism.”

With 14 years of data under their belt, the Framingham investigators challenged what was believed to be true at the time that diastolic pressure was an accurate indicator of high blood pressure, and were able to demonstrate a strong link that indeed, systolic pressure was a stronger predictor of cardiovascular events.

The Report of the Joint National Committee on Detection in 1977 (47 years into the study) still recommended diastolic pressure be used to diagnose and treat high blood pressure. However, over the next 10 years and several randomized controlled trials concluded systolic blood pressure was a better indicator, and the use of diastolic pressure as an indicator was eliminated.

The Framingham Heart Study data also changed the emphasis to preventing cardiovascular disease of those at risk rather than only treating people who already had cardiovascular disease. The term “risk factors” which is commonly used today was made popular by Framingham Heart Study director William Kennel in 1961. This lead to clinical risk scores using the following factors: age, total cholesterol, weight, ECG abnormality, hemoglobin, cigarettes smoking, and systolic blood pressure. The Framingham Risk Score made it easier for physicians to classify people at low, intermediate, or high risk for coronary heart disease.

It is hard to imagine, but it has only been since 1971 that data has shown high blood pressure as a leading risk factor for heart failure. The study demonstrated high blood pressure proceeded heart failure three-quarters of the time vs coronary artery disease in less than 40% of the cases.²

As a result of the Framingham Heart Study establishing a single set of criteria for diagnosing the risk of heart failure, data showed the 5 year mortality rate after being diagnosed went from 70% in 1950 to 59% in 1999 for men and from 57% to 45% for women.³  The previous report published in 1971 concluded 2 in 5 men were alive five years after heart failure diagnoses and women had a similar numbers.⁴ The improvement was partly due to the uniform criteria that had been established, and part was due to the use of beta-blockers and ACE inhibitor medications.

In the mid 1900’s, clinical data from Framingham and other studies confirmed a link between diabetes and vascular disease. The Framingham Heart Study demonstrated a three-fold increase in cardiovascular mortality for those with diabetes and a higher risk for heart failure.

Studies in the early 1900’s showed a link between cholesterol and cardiovascular disease. In 1977 Framingham investigators showed the lower the HDL, the higher the risk for coronary heart disease.  An indicator already known was the relationship between high LDL and coronary heart disease. 

William Castelli, the fourth director of the Framingham Heart Study, indicated the study revealed a 2 to 3 fold excess risk of heart failure in participants less than 50 years old who where overweight. They found the risk for heart failure attributed to obesity was 14% in women and 11% in men – more so than for heart valve disease, diabetes, or thickening of the heart wall.⁵

The Framingham Heart Study also determined atrial fibrillation was a risk factor for stroke, resulting in the standard of care used today of prescribing anticoagulation medication.

In 2002 the study began recruiting a third generation of cohorts, giving priority to 879 families who already had participants in the study. Minorities were recruited in 1994 and again in 2004, totaling nearly 1,000 minority recruits from Framingham since Framingham had few minorities living in the town when the study began. 

DNA sequencing of participants began in 2006 to study what role genetics plays in cardiovascular disease. Hundreds of genetic variants have since been identified. As a result, this information is used in personalized medicine today, not only to identify, but to personalize treatment of certain diseases.

This historic study began in 1948, knowing nothing about the cause of President Roosevelt’s deadly stroke three years earlier.  It was really the beginning of a grass-roots effort to understand heart disease. Through this study, information commonly known today surrounding heart disease was discovered.  It introduced the phrase “risk factors” for both heart disease and stroke.  Those factors include high blood pressure, obesity, high cholesterol, smoking, and atrial fibrillation. It created the Framingham Risk Score which  is still used today as one measurement to predict the likelihood of a 10 year cardiovascular event occurring which physicians can use to begin preventative measures to slow down or reverse the disease. Some of the other discoveries include physical activity reducing risk of heart disease and obesity increasing the risk. We learned atrial fibrillation is a risk factor for all cause mortality, that lifetime risk of middle age adults developing high blood pressure is 9 out of 10.  Also social networks are influential to help quit smoking as well as a trait of obesity.  We learned high leptin levels can protect against dementia and Alzheimer’s. Because the study includes generations of family members, scientists are able to study what role genes play in diseases including heart disease. It has been discovered that a specific brain structure  contributes to neurodegenerative disease as well as learning genes may play a role in Alzheimer’s and dementia.  Sleep apnea can increase the risk of stroke. The study found vascular stiffness is a precursor and not a result of high blood pressure and that genetic variation of various genes increasing risk of influencing aortic-valve calcification. 

It is truly remarkable the vast scope of information about heart disease that has been learned as a result of this monumental study. It has changed the conversations regarding heart disease going from not having any treatments available to having medications to treat heart disease to identifying modifiable risk factors.  According the to the National Institute of Health, deaths from heart disease were nearly 750,000 in 1968 and dropped to 365,000 in 2014.  Half the decline in deaths were due to reducing the risk factors through lifestyle and diet learned from this study. 

Dr. Dariush Mozaffarian, cardiologist and professor at the Friedman School of Nutrition Science and Policy at Tufts University tells us “lifestyle should be the first thing we should be prescribing in the clinic and it should be the first thing that public health and health care systems are focusing on because you’re only in the doctor’s office 30 minutes a year.”⁶

The research continues. What the future holds in our understanding of heart disease during this ongoing study will be exciting to learn.

¹ Bruenn HG. Clinical Notes on the Illness and Death of President Franklin D. Roosevelt. Annals of Internal Medicine. 1970;72:579-91. [PubMed] [Google Scholar].

² McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham study. N Engl J Med. 1971;285:1441–6. [PubMed] [Google Scholar].

³ Levy D, Kenchaiah S, Larson MG, et al. Long-term trends in the incidence of and survival with heart failure. N Engl J Med. 2002;347:1397–402. [PubMed] [Google Scholar].

⁴ McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham study. N Engl J Med. 1971;285:1441–6. [PubMed] [Google Scholar]

⁵ Kenchaiah S, Evans JC, Levy D, et al. Obesity and the risk of heart failure. N Engl J Med. 2002;347:305–13. [PubMed] [Google Scholar]

⁶ Weinmtraub, K. (2023, Oct. 2). FDR’s Death Led to Pivotal Research. Retrieved from

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