For nearly 60 years, the Framingham Heart Study has examined the natural history, risk factors, and prognosis of cardiovascular, lung, and other diseases. Recruitment of the Original Cohort began in 1948. Twenty-three years later, 3,548 children of the Original Cohort, along with 1,576 of their spouses, enrolled in the Offspring Cohort. Beginning in 2002, 4,095 adults having at least one parent in the Offspring Cohort enrolled in the Third Generation Cohort, along with 103 parents of Third Generation Cohort participants who were not previously enrolled in the Offspring Cohort. The objective of new recruitment was to complement phenotypic and genotypic information obtained from prior generations, with priority assigned to larger families. From a pool of 6,553 eligible individuals, 1,912 men and 2,183 women consented and attended the first examination (mean age: 40 (standard deviation: 9) years; range: 19-72 years). The examination included clinical and laboratory assessments of vascular risk factors and imaging for subclinical atherosclerosis, as well as assessment of cardiac structure and function. The comparison of Third Generation Cohort data with measures previously collected from the first two generations will facilitate investigations of genetic and environmental risk factors for subclinical and overt diseases, with a focus on cardiovascular and lung disorders.

Objectives To relate cancer since entry into the Framingham Heart Study with the risk of incident Alzheimer's disease and to estimate the risk of incident cancer among participants with and without Alzheimer's disease.Design Community based prospective cohort study; nested age and sex matched case-control study.Setting Framingham Heart Study, USA.Participants 1278 participants with and without a history of cancer who were aged 65 or more and free of dementia at baseline . Main outcome measuresHazard ratios and 95% confidence intervals for the risks of Alzheimer's disease and cancer.Results Over a mean follow-up of 10 years, 221 cases of probable Alzheimer's disease were diagnosed. Cancer survivors had a lower risk of probable Alzheimer's disease (hazard ratio 0.67, 95% confidence interval 0.47 to 0.97), adjusted for age, sex, and smoking. The risk was lower among survivors of smoking related cancers (0.26, 0.08 to 0.82) than among survivors of non-smoking related cancers (0.82, 0.57 to 1.19). In contrast with their decreased risk of Alzheimer's disease, survivors of smoking related cancer had a substantially increased risk of stroke (2.18, 1.29 to 3.68). In the nested case-control analysis, participants with probable Alzheimer's disease had a lower risk of subsequent cancer (0.39, 0.26 to 0.58) than reference participants, as did participants with any Alzheimer's disease (0.38) and any dementia (0.44).Conclusions Cancer survivors had a lower risk of Alzheimer's disease than those without cancer, and patients with Alzheimer's disease had a lower risk of incident cancer. The risk of Alzheimer's disease was lowest in survivors of smoking related cancers, and was not primarily explained by survival bias. This pattern for cancer is similar to that seen in Parkinson's disease and suggests an inverse association between cancer and neurodegeneration. IntroductionLimited data suggest that cancer survivors have a decreased risk of Alzheimer's disease and that people with Alzheimer's disease have lower rates of cancer. [1][2][3][4][5][6] Evidence of an inverse relation between Parkinson's disease and most cancers is now convincing. [7][8][9][10][11][12][13] A link between cancer and neurodegeneration is plausible as they share several genes and biological pathways, including inappropriate activation and deregulation of the cell cycle. [14][15][16][17][18][19][20][21][22] Signaling along these pathways results in opposite end points: in the case of cancer, uncontrolled cell proliferation, and in the case of neurodegeneration, apoptotic cell death. Proteins such as p53, a major regulator of apoptosis, and Pin1, which has a dual role in cell cycle control and protein folding, play a key part in the pathophysiology of both Alzheimer's disease and cancer. 15 A better understanding of the biological links between these two families of diseases is already opening new therapeutic horizons.In one population based cohort study, people with prevalent cancer had a 43% lower risk of ever developing Alzheimer's disease, and thos...

BACKGROUND: It is unclear whether the increased risk of colon cancer associated with obesity differs for men and women, by distribution of body fat, or by location of the tumor. The primary goal of this study was to address these questions. METHODS: Eligible subjects from the Framingham Study cohort were classified according to body mass index (BMI) and waist size during two age periods: 30-54 y (n ¼ 3764) and 55-79 y (n ¼ 3802). All eligible men and women were cancer-free at baseline and had complete information on the following potential confounders: age, sex, education, height, activity, smoking, and alcohol. There were 157 incident lifetime cases of colon cancer among those followed beginning at 30-54 y of age and 149 lifetime cases among those whose follow up began at 55-79 y. Subjects were stratified further by gender, activity, and tumor location. The Cox Proportional Hazards Models were used to adjust for possible confounding by the above-described factors. RESULTS: A BMI Z30 led to a 50% increased risk (95% CI: 0.92-2.5) of colon cancer among middle-aged (30-54 y) and a 2.4-fold increased risk (95% CI: 1.5-3.9) among older (55-79 y) adults. The BMI effect was stronger for men than for women and for cases occurring in the proximal colon. These adverse effects generally diminished when waist was added to the multivariable models. A larger waist size (Z99.1 cm (39 in) and 101.6 cm (40 in) for women and men, respectively) was associated with a twofold increased risk of colon cancer; this risk increased linearly with increasing waist size and was evident for both proximal and distal colon cancer. There was no attenuation of these effects when BMI was added to the multivariable models. A larger waist had a particularly adverse effect among sedentary subjects (relative risk (RR) ¼ 4.4 for middle-aged adults; RR ¼ 3.0 for older adults). CONCLUSION: These findings suggest that waist circumference is a stronger predictor of colon cancer risk than is BMI, and that central obesity is responsible for an increased risk of cancer of both the proximal and distal colon.