Reproductive biology

Humans have diverse mating systems. There is no consensus about which, if any, mating system is the oldest, and the triggers initiating human pair-bonding remain obscure. Many ideas are not testable. Species-specific mating systems occur in many mammals, and are often affected by the degree of sexual dimorphism. However, unlike other mammals, there appears to be no relationship between the degree of sexual dimorphism and a particular mating system in humans. Formal social rules often govern the choice of mate, and elaborate marriage customs can exist. Incest taboos forbidding the mating of relatives are widespread. These taboos are most effective in maintaining genetic diversity when group size is small. Human partners may travel significant distances after marriage to live with the spouse's family. This activity promotes gene flow, while increasing inter-group contacts and the dispersal of ideas. Both sexes can leave their natal group. Some genetic analysis tracking male (Y chromosome) versus female (mitochondrial DNA) dispersion indicates that females may disperse more.

Humans have no breeding season, and human females experience no estrous cycling. Singleton births are the norm, but some families and populations have an elevated frequency of dizygotic twinning, because more than one egg can be re leased and fertilized. The human sex ratio is usually skewed at conception and birth to favor males. The neonatal sex ratio is highly responsive to a variety of local influences. Male mortality exceeds that of females, and so the sex ratio gradually declines with age. The sex ratio is approximately equal at reproductive maturity; after this, females tend to outnumber males. Male mortality caused by violence and accident exceeds that of females. Male mortality caused by infectious diseases is also higher than that of females, and parasite load is higher in males. Higher male mortality caused by violence and the increased male parasite susceptibility appear to be the evolutionary consequences of sexual selection.

In comparison to other catarrhine primates, where males may be more than twice the size of females, humans have only a small degree of sexual dimorphism. Depending upon the population, humans have 4-7% statural dimorphism. Statural dimorphism differences are higher in populations with tall stature, and lower in populations with small stature. Human body weight dimorphism averages about 11%. Much human sexual dimorphism involves soft-tissue characters. Subcutaneous fat patterning, seen especially in breast, thigh, and buttock fat depots, is markedly different in human males and females. Females also carry a larger percentage of subcutaneous fat than males do. Even in hunter-gather groups, where humans are very active and lean, subcutaneous body fat as measured by skinfold thickness is 5-15% in males and 20-25% in females.

Humans mature slowly, so that the onset of puberty is delayed relative to pongids and other catarrhines. In females, the onset of puberty is signaled by menarche, or first menstruation. This is triggered by a critical amount of body fat. The hormone leptin, released by fat, appears to trigger menarche. Reduction of body fat in a cycling female suppresses menstruation.

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