Parity and total, ischemic heart disease and stroke mortality. The Adventist Health Study, 1976–1988

In a prospective study with information about life style and reproductive factors, we assessed the relationship between parity and total, ischemic heart disease, and stroke mortality. The large majority of the 19,688 California Seventh-day Adventist women included did not smoke or drink alcohol, 31 percent never ate meat and physical activity was relatively high. Cox proportional hazard analysis was conducted with parity as the main independent variable and with adjustment for a number of other possible confounders. During follow-up from 1976 through 1988, there were 3,122 deaths; 782 deaths from ischemic heart disease and 367 deaths due to stroke. There were no relationships between parity and total mortality (P-value for overall effect of parity = 0.32). Grand multiparous women (>4 children) had somewhat increased ischemic heart disease mortality (MRR = 1.45, 95% CI: 1.15, 1.84) before adjustment for educational level. After adjustment for educational level and marital status, there were no relationship with mortality from ischemic heart disease (P = 0.29) or stroke (P = 0.72). In parous women, there were, after adjustment for age at first delivery, some suggestions of an increased total mortality in women with one child. For ischemic heart disease and stroke mortality, no associations were found. Stratified and adjusted analyses confirmed these results. Thus, we found no consistent relationships between parity and total, ischemic heart disease or stroke mortality. However, a longer follow-up would have been helpful and the conclusions may be somewhat influenced by the lifestyle of the women included

Ocean Acidification-Induced Food Quality Deterioration Constrains Trophic Transfer

Our present understanding of ocean acidification (OA) impacts on marine organisms caused by rapidly rising atmospheric carbon dioxide (CO2) concentration is almost entirely limited to single species responses. OA consequences for food web interactions are, however, still unknown. Indirect OA effects can be expected for consumers by changing the nutritional quality of their prey. We used a laboratory experiment to test potential OA effects on algal fatty acid (FA) composition and resulting copepod growth. We show that elevated CO2 significantly changed the FA concentration and composition of the diatom Thalassiosira pseudonana, which constrained growth and reproduction of the copepod Acartia tonsa. A significant decline in both total FAs (28.1 to 17.4 fg cell−1) and the ratio of long-chain polyunsaturated to saturated fatty acids (PUFA:SFA) of food algae cultured under elevated (750 µatm) compared to present day (380 µatm) pCO2 was directly translated to copepods. The proportion of total essential FAs declined almost tenfold in copepods and the contribution of saturated fatty acids (SFAs) tripled at high CO2. This rapid and reversible CO2-dependent shift in FA concentration and composition caused a decrease in both copepod somatic growth and egg production from 34 to 5 eggs female−1 day−1. Because the diatom-copepod link supports some of the most productive ecosystems in the world, our study demonstrates that OA can have far-reaching consequences for ocean food webs by changing the nutritional quality of essential macromolecules in primary producers that cascade up the food web

Maternal age and offspring adult health: evidence from the health and retirement study

Advanced maternal age is associated with negative offspring health outcomes. This interpretation often relies on physiological processes related to aging, such as decreasing oocyte quality. We use a large, population-based sample of American adults to analyze how selection and lifespan overlap between generations influence the maternal age–offspring adult health association. We find that offspring born to mothers younger than age 25 or older than 35 have worse outcomes with respect to mortality, self-rated health, height, obesity, and the number of diagnosed conditions than those born to mothers aged 25–34. Controls for maternal education and age at which the child lost the mother eliminate the effect for advanced maternal age up to age 45. The association between young maternal age and negative offspring outcomes is robust to these controls. Our findings suggest that the advanced maternal age–offspring adult health association reflects selection and factors related to lifespan overlap. These may include shared frailty or parental investment but are not directly related to the physiological health of the mother during conception, fetal development, or birth. The results for young maternal age add to the evidence suggesting that children born to young mothers might be better off if the parents waited a few years