Purpose: To inform development of a culturally sensitive hereditary breast and ovarian cancer communication initiative and related clinical genetic services. Methods: Five focus groups were conducted with 51 female and male Latinos. Educational materials were designed to communicate information about hereditary breast or ovarian cancer and availability of relevant clinical services or prevention strategies. Focus groups explored participants' knowledge, attitudes, and beliefs about hereditary breast and ovarian cancer, BRCA1/2 testing, and communication preferences for hereditary breast and ovarian cancer health messages. Results: Overall, awareness of familial breast and ovarian cancer and availability of genetic risk assessment was low. Once informed, participants held favorable attitudes toward risk assessment and counseling services. Critical themes of the research highlighted the need to provide bilingual media products and use of a variety of strategies to increase awareness about hereditary cancer risk and availability of clinical genetic services. Important barriers were identified regarding family cancer history communication and cancer prevention services. Strategies were suggested for communicating cancer genetic information to increase awareness and overcome these barriers; these included both targeted and tailored approaches. Conclusion: This research suggests that cancer genetic communication efforts should consider community and cultural perspectives as well as health care access issues before widespread implementation. Genet Med 2010:12(2):105-115.

Women and female great apes both continue giving birth into their forties, but not beyond. However humans live much longer than other apes do. Even in hunting and gathering societies, where the mortality rate is high, adult life spans average twice those of chimpanzees, which become decrepit during their fertile years and rarely survive them. Since women usually remain healthy through and beyond childbearing age, human communities include substantial proportions of economically productive postmenopausal women. A grandmother hypothesis(8-12) may explain why greater longevity evolved in our lineage while female fertility still ends at ancestral ages. This hypothesis has implications for the evolution of a wide array of human features. Here we review some history of the hypothesis, recent findings, and questions for ongoing research.

Postmenopausal longevity may have evolved in our lineage when ancestral grandmothers subsidized their daughters' fertility by provisioning grandchildren, but the verbal hypothesis has lacked mathematical support until now. Here, we present a formal simulation in which life spans similar to those of modern chimpanzees lengthen into the modern human range as a consequence of grandmother effects. Greater longevity raises the chance of living through the fertile years but is opposed by costs that differ for the sexes. Our grandmother assumptions are restrictive. Only females who are no longer fertile themselves are eligible, and female fertility extends to age 45 years. Initially, there are very few eligible grandmothers and effects are small. Grandmothers can support only one dependent at a time and do not care selectively for their daughters' offspring. They must take the oldest juveniles still relying on mothers; and infants under the age of 2 years are never eligible for subsidy. Our model includes no assumptions about brains, learning or pair bonds. Grandmother effects alone are sufficient to propel the doubling of life spans in less than sixty thousand years.

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The evolution of distinctively human life history and social organization is generally attributed to paternal provisioning based on pair bonds. Here we develop an alternative argument that connects the evolution of human pair bonds to the male-biased mating sex ratios that accompanied the evolution of human life history. We simulate an agent-based model of the grandmother hypothesis, compare simulated sex ratios to data on great apes and human hunter-gatherers, and note associations between a preponderance of males and mate guarding across taxa. Then we explore a recent model that highlights the importance of mating sex ratios for differences between birds and mammals and conclude that lessons for human evolution cannot ignore mammalian reproductive constraints. In contradiction to our claim that male-biased sex ratios are characteristically human, female-biased ratios are reported in some populations. We consider the likelihood that fertile men are undercounted and conclude that the mate-guarding hypothesis for human pair bonds gains strength from explicit links with our grandmothering life history.grandmother hypothesis | human life history | human evolution | mate guarding | mating sex ratios W e call attention to evidence that connects the evolution of human pair bonds to the male-biased sex ratios in fertile ages that characterize human populations. As in mammals generally, age-specific mortality is higher in males than in females (e.g., refs. 1-3). However, this difference is overshadowed by a distinctive feature of human life history: Oldest ages at parturition are about the same in humans as in other living hominids, the great apes (4, 5), whereas longevity is substantially greater and male fertility continues to older ages (6). Exceptional longevity with a distinctive postmenopausal life stage (7-9) may have evolved in our lineage when grandmothers' subsidies for weaned dependents allowed mothers to have next babies sooner. According to this grandmother hypothesis (10-16), longevity increased as longer-lived grandmothers could help more and so left more longer-lived descendants of both sexes. Women's postfertile life stage (7) produces a bias in the sex ratio of fertile adults with repercussions for male strategies. As longevity increased, olderaged males expanded the pool of competitors for the still-fertile females. With more competitors for each paternity, males' average success in finding new mates inevitably declined until defending a current mate became the better option. Our distinctive life history thus supplies previously unrecognized support for a mate-guarding hypothesis for the evolution of human pair bonds.Here we simulate hominid mating sex ratios with an agent-based model of the evolution of human longevity via grandmothering (13, 15). We then compare simulated sex ratios to demographic data from both great apes and human hunter-gatherers. Having identified the human bias, we connect it to increased male payoffs for mate guarding, noting some broad patterns in humans, the tradeoffs observ...

Familial adenomatous polyposis (FAP) is the second most common hereditary colorectal cancer syndrome and confers a nearly 100% lifetime risk of developing colorectal cancer. Understanding factors that facilitate and inhibit genetic testing and cancer surveillance in children who are members of families affected by FAP will better equip clinicians to clarify misunderstandings and facilitate appropriate care. The aims of this study were to examine parental attitudes and beliefs regarding endoscopic surveillance and genetic testing in minors at risk for developing FAP. This cross-sectional study includes analyses of qualitative and quantitative interview data collected from parents of children with or at risk for FAP. This report includes data from 28 parents with a total of 51 biological children between 10–17 years of age. The parents had a clinical and/or genetic diagnosis of FAP. Most commonly reported facilitators included provider recommendation (surveillance) and personalized medical management (genetic testing). Most commonly reported barriers included lack of provider recommendation (surveillance) and cost (genetic testing).

Although the power model published by Hansen et al. (2008) fit the human data best, Faddy and Gosden's (1996) differential equation model may be a more useful characterization of human follicular atresia. However, these models leave a great deal of variation unexplained. Mouse strain comparisons show that follicle loss in genetically distinct subpopulations can differ substantially from the pattern in the aggregate population. This indicates that differences in follicular stock size between and within populations depend upon more than a single predictor (i.e. age or follicle stocks at previous time points). Our reliance upon data from Western populations represents this study's most important limitation. Expanding data collection to include likely covariates and a wider range of human populations would improve the basis for predicting individual trajectories of follicle loss as more women worldwide opt to delay childbearing and risk aging beyond their own windows of fertility.

Objectives Slower rates of aging distinguish humans from our nearest living cousins. Chimpanzees rarely survive their forties while large fractions of women are postmenopausal even in high-mortality hunter–gatherer populations. Cellular and molecular mechanisms for these somatic aging differences remain to be identified, though telomeres might play a role. To find out, we compared telomere lengths across age-matched samples of female chimpanzees and women. Methods We used a monochrome multiplex quantitative polymerase chain reaction to assay canonical telomere repeats in blood cells from captive female chimpanzees (65 individuals; age: 6.2–56.7 years) and compared them to the same measure in human females (43 individuals; age: 7.4–57.3 years). Results Our samples showed little difference in attrition rates between the species (~0.022 T/S per year for chimpanzees and ~0.012 T/S per year for humans with overlapping 95% confidence intervals), but telomeres were twice as long in chimpanzees as in humans (T/S ratios = 2.70 and 1.26, respectively). Conclusions Based on the longevity differences, we initially hypothesized that telomere shortening rates would be faster in chimpanzees than in humans. Instead, it is shorter telomere length that appears to be the derived state in humans. This comparison indicates that better characterization of physiological aging in our closest living relatives will be indispensable for understanding the evolution of distinctive human longevity.