Using data from digitized weekly surveillance reports of notifiable diseases for U.S. cities and states for 1888 through 2011, the authors derived a quantitative history of disease reduction in the United States, focusing particularly on the effects of vaccination programs.

Although the major risk factors for liver cancer have been established, preventive factors for liver cancer have not been fully explored. We evaluated the association between raw garlic consumption and liver cancer in a large population-based case-control study in Eastern China. The study was conducted in Jiangsu, China, from 2003 to 2010. A total of 2011 incident liver cancer cases and 7933 randomly selected population-controls were interviewed. Epidemiological data including raw garlic intake and other exposures were collected, and serum markers of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection were assayed. Overall, eating raw garlic twice or more per week was inversely associated with liver cancer, with an adjusted odds ratio (aOR) of 0.77 (95% confidence interval (CI): 0.62–0.96) compared to those ingesting no raw garlic or less than twice per week. In stratified analyses, high intake of raw garlic was inversely associated with liver cancer among Hepatitis B surface antigen (HBsAg) negative individuals, frequent alcohol drinkers, those having history of eating mold-contaminated food or drinking raw water, and those without family history of liver cancer. Marginal interactions on an additive scale were observed between low raw garlic intake and HBsAg positivity (attributable proportion due to interaction (AP) = 0.31, 95% CI: -0.01–0.62) and heavy alcohol drinking (AP = 0.28, 95% CI: 0.00–0.57). Raw garlic consumption is inversely associated with liver cancer. Such an association shed some light on the potential etiologic role of garlic intake on liver cancer, which in turn might provide a possible dietary intervention to reduce liver cancer in Chinese population.

Obesity–insulin connections have been considered potential risk factors for postmenopausal breast cancer, and the association between insulin resistance (IR) genotypes and phenotypes can be modified by obesity-lifestyle factors, affecting breast cancer risk. In this study, we explored the role of IR in those pathways at the genome-wide level. We identified IR-genetic factors and selected lifestyles to generate risk profiles for postmenopausal breast cancer. Using large-scale cohort data from postmenopausal women in the Women9s Health Initiative Database for Genotypes and Phenotypes Study, our previous genome-wide association gene–behavior interaction study identified 58 loci for associations with IR phenotypes (homeostatic model assessment–IR, hyperglycemia, and hyperinsulinemia). We evaluated those single-nucleotide polymorphisms (SNP) and additional 31 lifestyles in relation to breast cancer risk by conducting a two-stage multimodal random survival forest analysis. We identified the most predictive genetic and lifestyle variables in overall and subgroup analyses [stratified by body mass index (BMI), exercise, and dietary fat intake]. Two SNPs (LINC00460 rs17254590 and MKLN1 rs117911989), exogenous factors related to lifetime cumulative exposure to estrogen, BMI, and dietary alcohol consumption were the most common influential factors across the analyses. Individual SNPs did not have significant associations with breast cancer, but SNPs and lifestyles combined synergistically increased the risk of breast cancer in a gene–behavior, dose-dependent manner. These findings may contribute to more accurate predictions of breast cancer and suggest potential intervention strategies for women with specific genetic and lifestyle factors to reduce their breast cancer risk. Significance: These findings identify insulin resistance SNPs in combination with lifestyle as synergistic factors for breast cancer risk, suggesting lifestyle changes can prevent breast cancer in women who carry the risk genotypes.

The presence of comorbidity becomes increasingly important for its prognostic effect on survival in breast cancer patients with advancing age. This study aimed to evaluate the role of comorbidities including hypertension as a mediator of disparity in survival after metastasis diagnosis between younger (≤51 years) and older (>51 years) patients. A total of 553 patients 26–88 years of age with breast cancer metastasis diagnosis from 1 large urban practice were followed between January 1, 1999, and June 30, 2008. Comorbidity variables and survival were analyzed using Cox regression model. To assess comorbidity variables as a mediator of age-survival relationship, 2 approaches have been applied: (1) Baron Kenny approach and (2) alternative assessment to compute the percentage change in the hazard ratios (HRs). The median survival was 40 months, with 265 (47.9%) alive and 288 (52.1%) dead. Older patients had worse survival than younger patients (HR, 1.43; 95% confidence interval [CI], 1.11–1.84). Hypertension was related to survival (HR, 1.45; 95% CI, 1.12–1.89) when age and other covariates were controlled. The effect of age on survival was no longer significant after adjustment for hypertension (HR, 1.26; 95%, CI 0.97–1.65) or hypertension-augmented Charlson comorbidity score (HR, 1.24; 95% CI, 0.95–1.63). Hypertension-augmented Charlson comorbidity score or hypertension was a strong mediator of age-survival relationship among metastatic breast cancer patients, explaining survival disparity between younger and older patients by 44% and 40%, respectively. The study findings suggest that hypertension should be included in the comorbidity information for decision-making support programs.