Sugar-Sweetened Beverages and Cancer Risk: A Narrative Review.

Cancer continues to be a major public health challenge worldwide, not only for being one of the leading causes of death but also because the number of incident cases is projected to grow in the next decades. Meanwhile, sugar-sweetened beverages (SSB) consumption has risen since the past century and constitutes a considerable fraction of added sugars in daily diet. Several studies have analyzed the relationship between SSB intake and health and found substantial evidence for effects on obesity, type 2 diabetes and metabolic syndrome. However, there is little knowledge about the relationship of SSB with cancer risk. It may be speculated that there is an indirect relationship between SSB and cancer through obesity and metabolic syndrome, but obesity-independent associations through hormonal imbalances or chronic inflammation could also exist. In this review, we describe the epidemiological evidence of the association of SSB and the risk of cancer in adults. Although the epidemiological evidence linking SSB consumption and cancer risk is still limited, prospective studies suggest that high SSB intake may increase the risk of obesity-related cancers, breast and prostate cancer.

Explaining the increment in coronary heart disease mortality in Mexico between 2000 and 2012.

BACKGROUND: Mexico is still in the growing phase of the epidemic of coronary heart disease (CHD), with mortality increasing by 48% since 1980. However, no studies have analyzed the drivers of these trends. We aimed to model CHD deaths between 2000 and 2012 in Mexico and to quantify the proportion of the mortality change attributable to advances in medical treatments and to changes in population-wide cardiovascular risk factors. METHODS: We performed a retrospective analysis using the previously validated IMPACT model to explain observed changes in CHD mortality in Mexican adults. The model integrates nationwide data at two-time points (2000 and 2012) to quantify the effects on CHD mortality attributable to changes in risk factors and therapeutic trends. RESULTS: From 2000 to 2012, CHD mortality rates increased by 33.8% in men and by 22.8% in women. The IMPACT model explained 71% of the CHD mortality increase. Most of the mortality increases could be attributed to increases in population risk factors, such as diabetes (43%), physical inactivity (28%) and total cholesterol (24%). Improvements in medical and surgical treatments together prevented or postponed 40.3% of deaths; 10% was attributable to improvements in secondary prevention treatments following MI, while 5.3% to community heart failure treatments. CONCLUSIONS: CHD mortality in Mexico is increasing due to adverse trends in major risk factors and suboptimal use of CHD treatments. Population-level interventions to reduce CHD risk factors are urgently needed, along with increased access and equitable distribution of therapies.

Factors associated with healthy aging in septuagenarian and nonagenarian Mexican adults.

OBJECTIVE: To examine the factors associated with healthy aging in a cohort of Mexican adults after a follow-up of 14 years. STUDY DESIGN: Participants were part of a prospective cohort of the Mexican Healthy Aging Study (MHAS), from which we included 5142 individuals aged 63 years or more. MAIN OUTCOME: Healthy aging, defined as reaching age 77 or 90 without major chronic conditions or physical limitations. MEASURES: Information on age, education, marital status, smoking, alcohol consumption, physical activity, self-perceived depression, health conditions and history of age-related diseases was collected at baseline and follow-up. RESULTS: Among the overall cohort, 57.8% experienced healthy survival to age 77 and 42.2% had died before age 77 or were undergoing normal aging. Participants with long-lived parents and who exercised had a lower risk of being non-healthy agers. Being overweight, obese or a smoker increased the risk of being a non-healthy ager. Physically active participants had increased odds of healthy aging at age 77 (OR: 1.17; 95% CI: 1.01-1.46) and at age 90 (OR: 1.5; 95% CI: 1.01-2.24). Depression had a negative relationship with healthy aging at age 90 (OR: 0.66; 95% CI: 0.45- 0.97). Maternal longevity was associated with healthy aging only at age 77 (OR = 1.34; 95% CI: 1.04-1.72). CONCLUSIONS: Our findings support the view that a combination of genetic and behavioral factors is associated with healthy aging. In accordance with findings in Caucasian populations, our data suggest for the first time that there might also be a genetic determinant for healthy ageing in Latin Americans.

Longitudinal associations between blood lead concentrations lower than 10 microg/dL and neurobehavioral development in environmentally exposed children in Mexico City.

OBJECTIVE: Increasing evidence suggests that 10 microg/dL, the current Centers for Disease Control and Prevention screening guideline for children's blood lead level, should not be interpreted as a level at which adverse effects do not occur. Using data from a prospective study conducted in Mexico City, Mexico, we evaluated the dose-effect relationship between blood lead levels and neurodevelopment at 12 and 24 months of age. METHODS: The study population consisted of 294 children whose blood lead levels at both 12 and 24 months of age were < 10 microg/dL; blood lead levels were measured by graphite furnace atomic absorption spectroscopy; Bayley Scales of Infant Development II were administered at these ages. The outcomes of interest were the Mental Development Index and the Psychomotor Development Index. RESULTS: Adjusting for covariates, children's blood lead levels at 24 months were significantly associated, in an inverse direction, with both Mental Development Index and Psychomotor Development Index scores at 24 months. Blood lead level at 12 months of age was not associated with concurrent Mental Development Index or Psychomotor Development Index scores or with Mental Development Index at 24 months of age but was significantly associated with Psychomotor Development Index score at 24 months. The relationships were not altered by adjustment for cord blood lead level or, in the analyses of 24-month Mental Development Index and Psychomotor Development Index scores, for the 12-month Mental Development Index and Psychomotor Development Index scores. For both Mental Development Index and Psychomotor Development Index at 24 months of age, the coefficients that were associated with concurrent blood lead level were significantly larger among children with blood lead levels < 10 microg/dL than it was among children with levels > 10 microg/dL. CONCLUSIONS: These analyses indicate that children's neurodevelopment is inversely related to their blood lead levels even in the range of < 10 microg/dL. Our findings were consistent with a supralinear relationship between blood lead levels and neurobehavioral outcomes.