Sex Differences in Mate Preferences: a Replication Study, 20 Years Later

Evolutionary psychologists have argued for evolved sex differences in human mate preferences (e.g., (Buss and Barnes Journal of Personality and Social Psychology 50,559–570, 1986; Buss American Scientist 73,47–51, 1985, Behavioral and Brain Sciences 12, 1–49, 1989, 1994). Specifically, they have suggested that men and women place different values on physical appearance, fertility, and economic stability when they choose a long-term partner (e.g., Miller 2000; Buss and Schmitt Psychological Review 100, 204–232, 1993; Fisman et al. 2006; Sprecher et al. Journal of Personality and Social Psychology 66, 1074–1080, 1994). In this short report, we replicated a seminal study that investigated preferences for potential marriage partners (Sprecher et al. Journal of Personality and Social Psychology 66, 1074–1080, 1994) to assess if sex differences in mate preferences may have converged over time due to social change via a crowd-sourced sample (n = 522). The replication was largely successful and, thus, suggests stable sex differences in long-term mate preferences in line with an evolutionary framework. However, we also found evidence for narrowed sex differences for preferences with regard to ethnicity and education. Interestingly, while the original study found no sex difference in the preference for marrying the previously married, the current study showed that women were slightly more inclined than men to prefer a previously married partner. Therefore, these findings also suggest that social change and societal norms could make long-term mate preferences flexible and influence how they develop over time

Combined methylmalonic acidemia and homocystinuria, cblC type. I. Clinical presentations, diagnosis and management

Combined methylmalonic acidemia and homocystinuria, cblC type, is an inborn error of intracellular cobalamin metabolism with a wide spectrum of clinical manifestations that is stated to be the most common inherited disorder of cobalamin metabolism. This metabolic disease is caused by mutations in the MMACHC gene and results in impaired intracellular synthesis of adenosylcobalamin and methylcobalamin, cofactors for the methylmalonyl-CoA mutase and methionine synthase enzymes. Elevated methylmalonic acid and homocysteine with decreased methionine production are the biochemical hallmarks of this disorder. Awareness of the diverse clinical presentations associated with cblC disease is necessary to provide a timely diagnosis, to guide management of affected individuals and to establish a framework for the future treatment of individuals detected through expanded newborn screening. This article reviews the biochemistry, clinical presentations, genotype-phenotype correlations, diagnosis and management of cblC disease