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Social aspects of age of menarche
Ellis BJ. "Timing of pubertal maturation in girls: an integrated life history approach". Psychological Bulletin 2004, 130:920–58.
Review.
List of later adverse consequences of early maturation: weight gain, breast & other reproductive cancers, teen pregnancy, miscarriages, LBW babies, body image disorders, depression, anxiety, aggressive behavior, substance abuse. Life history theory is a set of widely held evolutionary-developmental basic assumptions applied to explain evolved strategies for distributing metabolic resources between the competing demands of growth, maintenance, and reproduction. E.g., animals in K-selected species in response to stress and chronic food shortage delay pubertal development and reproduction.
He reviews 5 theories about pubertal maturation:
All of these theories are more relevant to girls than boys because the links between environment and reproduction are stronger in girls because females need more resources for reproduction than males. Also more and better research has been performed on girls because of a good marker of puberty (menarche).
Summary of life history theory Life history theory is a method of analysis in animal and human biology, psychology, and especially evolutionary sociobiology which postulates that many of the physiological traits and behaviors of individuals may be best understood in relation to the key maturational and reproductive characteristics that define the life course.
Examples of these characteristics include:
Variations of these characteristics reflect differing allocations of an individual's resources (i.e., time, effort, and energy expenditure) to competing life functions, especially growth, body maintenance, and reproduction.
For an individual, the resources in a particular environment are finite. Time, effort, and energy used for one purpose diminishes the time effort, and energy available for another. For example resources spent growing to a larger body size cannot be spent increasing the number of offspring. Thus allocation of resources involves trade-offs. These trade-offs and strategies can be compared between species. One of the most well-known of these trade-offs is between producing a large number of offspring or a small number of fitter offspring with better reproductive prospects.
A second one is early or late reproduction. Early maturation is favored by nonzero mortality chance in near future, by longer fertility period before menopause (since there is small relationship between ages of menarche and menopause), and greater total reproductive output with shorter generation cycles. Later reproduction is favored by larger body size, lower adult mortality rates, greater energy production and stores with which to support reproduction, and greater success in sexual competition. In humans, early reproduction is penalized by smaller pelvis, earlier growth cessation, lower energy available for fetal development, with consequent higher rates of fetal loss, IUGR, prematurity, birth defects, and retardation. Later human reproduction allows better cognitive and parenting skills, better mate selection, lower mortality from risky behavior, higher educational and economic attainment. Children of adult mothers tend to have better behavioral, social, and survival outcomes.
Ellis argues that genotypic selection should favor neither approach but the plasticity of being able to shift phenotype to use either strategy depending on the environment. The important question then becomes when should individuals stop converting excess energy into growth and begin converting it into reproduction? What the relevant environmental cues that bias individuals toward relatively early or late reproductive development?
Energetics theory of pubertal timing. Chronically low or erratic energy sources in early childhood should result in delay of maturation. Abundant energy sources in early childhood should result in acceleration of maturation. This theory has been supported by many demographic studies in countries with significant differences in diets of high SES vs low SES or urban vs rural girls. The effect has generally not been seen in societies where the lower SES or rural girls are generally adequately nourished. Covarying with high SES are artificial lighting, healthcare exposure, dietary composition, hygiene, family function, divorce & remarriage rates, and physical activity so the energetics-supporting surveys may have other potential explanations as well.
Within a generally well-nourished population, dietary composition has not been shown to be related to timing of puberty except with respect to dietary plant fiber intake (e.g., vegetarian), which is associated with later puberty. It has been hypothesized that high fiber is an indicator of lower protein content and that this is the key variable.
A minor corollary is that late childhood energy abundance following early childhood energy scarcity should result in acceleration of maturation to take advantage of the newly (perhaps transiently) available resources for reproduction.
Energetics theory also predicts higher energy availability results not just in earlier maturation but greater lifetime fertility and reduced fetal wastage. Earlier maturing girls have higher ovarian hormone levels and a shorter interval to ovulation. In late adolescence there are a higher percentage of ovulatory cycles in earlier maturing girls. However, several American and European studies have not supported this prediction of shorter interval to ovulation, and have clearly rejected the prediction of reduced fetal wastage. American studies suggest that highest fertility occurs in women closest to average in age of onset of puberty, with higher infertility in very early and very late maturers. Ellis says this prediction of greater fertility should be clearly rejected.
Stress-suppression theory. Adverse social and physical stressors, including energy scarcity, can delay puberty or disrupt adult reproductive function. Two systems mediate stress: hypothalamic-adrenal, and locus-caeruleus-norepi. Stress can disrupt GnRH and ovarian function in adult women. Some primate studies show that low social rank is associated with delayed puberty, but the mechanism remains uncertain (glucocorticoid vs pheromones etc). Some European studies have found later menarche during wartime. Relation to psycho-social dwarfism is suggested.
Psychosocial acceleration theory. Perhaps extreme stress delays puberty and moderate stress accelerates it. Many other human studies have found that stress accelerates puberty. This life history model is credited to Belsky (Belsky, J., Steinberg, L., & Draper, P. (1991). "Childhood experience, interpersonal development, and reproductive strategy: An evolutionary theory of socialization". Child Development, 62, 647–670.) As expressed by Chisholm, "When young mammals encounter conditions that are not favorable for survival—i.e., the conditions of environmental risk and uncertainty indexed by emotional stress during development—it will generally be adaptive for them to reproduce early."
Ellis distinguishes 3 types of childhood stress
Many studies show pubertal acceleration associated with family stress (e.g., Hulanicka: father absence, parental alcoholism, prolonged parental illness).
Bidirectionality of influence of puberty on parent-child relationship. Early maturation may result in changes in the child or signals from the child that affect family relationships. Other than a single paper (Dorn, L. D., Hitt, S. F., & Rotenstein, D. (1999). "Biopsychological and cognitive differences in children with premature vs. on-time adrenarche". Archives of Pediatrics and Adolescent Medicine, 153, 137–146.) demonstrating association of behavioral adjustment problems with premature adrenarche, no data.
Family environmental stress is not a unitary dimension. Ellis suggests separately analyzing "family warmth and positivity" from "family conflict and coercion".
Studies show family warmth correlates with later menarche. (Ellis, B. J., McFadyen-Ketchum, S., Dodge, K. A., Pettit, G. S., & Bates, J. E. (1999). "Quality of early family relationships and individual differences in the timing of pubertal maturation in girls: A longitudinal test of an evolutionary model". Journal of Personality and Social Psychology, 77, 387–401.) "suggests that parent child closeness may decelerate pubertal maturation". However two studies suggest the effect may be frequency of parent child interaction, whether positive or negative (i.e., even frequent parent-child arguing was associated with delayed maturation). Although many studies found association of "warm" family relationships with later puberty, most are concurrent or retrospective and thus do not settle which direction is important and what is causal. Prospective studies have better potential for that but have been less consistent.
Less consistent results have been obtained regarding relationship of parent-child conflict and coercion and earlier puberty.
Ellis proposes U-shaped stress relationship, where earliest maturation occurs in moderate stress environments, and the CRH and LC-norepi systems are most reactive. This may be mediated by early plasticity of the CRH and LC-norepi systems. High stress early in life down-regulates the responsiveness and low stress early in life up-regulates responsiveness of the systems but some children with extreme stress may upregulate (PTSD). Ellis says that most western family environments rated as stressful would actually fall short of the extreme stress environments of war and psychosocial deprivation models.
He also says that evidence about hormonal stress mechanisms is mixed, with some evidence that the suppressive effects of CRH and AVP on GnRH generator are not mediated by glucocorticoids but by intra-CNS mechanisms.
Potentially relevant animal studies. In prepubertal female pigs, exposure to boars raises cortisol and accelerates maturation, but this effect can be abolished by dex or adrenalectomy.
Paternal investment theory. Draper and Harpending proposed that the developmental pathways underlying variation in daughters' reproductive strategies are especially sensitivie to the father's role in the family and mothers's sexual attitudes and behvairo in early childhood. [Draper, P., & Harpending, H. (1982). "Father absence and reproductive strategy: An evolutionary perspective". Journal of Anthropological Research, 38, 255–273. Draper, P., & Harpending, H. (1988). "A sociobiological perspective on the development of human reproductive strategies". In K. B. MacDonald (Ed.), Sociobiological perspectives on human development (pp. 340–372). New York: Springer-Verlag.]
Ellis et al have sharpened this to "a unique and central role for quality of paternal investment in regulation of daughters' sexual development, separate from the effects of other dimensions of psychosocial stress and support in the child's environment". He notes that humans are the only great ape in which fathers participate in feeding and care of offspring, so human paternal investment must be a recent evolutionary strategy. Paternal investment theory "posits that girls detect and internally encode information specifically about the quality of paternal investment during approximately the first 5 years of life as a basis for calibrating the development of (a) neurophysiologic systems involved in timing of pubertal maturation and (b) related motivational systems, which make certain types of sexual behavior more or less likely in adolescence". Important cues include presence or absence of fathers, frequency & quality of father daughter interaction, quality of father-mother interaction, mother's attitude toward men, mother's sexual and repartnering behavior, daughter's exposure to mother's boyfriends and stepfathers.
Paternal investment theory does not equate father absence with stress. Quality of father investment and variation of environmental stressors are separate environmental influences on pubertal timing. Not all cross-cultural studies have supported this.
The effect of father absence is partly mediated by presence of stepfathers and other males because it degrades the genetic benefits of cooperation and fitness sharing. "From a life history perspective, it is to the child's advantage to make the pubertal transition earlier in adverse home environments."
Many studies have demonstrated that father absence is associated with earlier puberty in girls. Magnitude of effect is 1.3 to 9 months. Notably, this effect has not been shown in African-American populations (Ellis wonders if they are already "maximally accelerated").
Other studies have shown that greater paternal involvement in daughter's care is associated with later pubertal maturation. More positive father-mother relationships are also associated with later daughter puberty.
The theoretical effect of stepfather presence is potentially complex.
Can the absent father effect be distinguished from the stepfather effect? Not consistently. Can absent father effect be distinguished from a stress effect? Ellis says yes: "In total, the present data suggest that the quality of fathers' investment in the family is the most important feature of the proximal family environment relative to daughter's pubertal timing."
The combination of factors suggest that earliest social acceleration would occur when a stepfather sexually abuses a stepdaughter. Earlier maturation has been reported by Herman-Giddens, M. E., Sandler, A. D., & Friedman, N. E. (1988). "Sexual precocity in girls. An association with sexual abuse?" American Journal of Diseases of Children, 142, 431–433.
Larger community studies suggest the magnitude of the effect may be 6 months. None of the studies distinguished prepubertal sexual abuse from pubertal sexual abuse so that direction of causation remains an open question.
Criticisms of psychosocial accelerator and paternal investment theories. Most important one is that genetic factors shared by mothers and daughters cause earlier puberty, earlier sexual behavior, earlier pregnancy, and higher likelihood of divorce and this effect is not dependent on family environment.
X-linked androgen receptor theory. A specific variant of X-linked androgen receptor gene results in aggression, impulsivity, promiscuity, marital conflict and dissolution and is transmissible from fathers to daughters so they appear associated with father absence, earlier menarche, and precocious sexuality. Two studies contradict each other about this.
It has also been proposed that there are wide variations of magnitude of genetic susceptibility to these environmental influences, and that these mechanisms may only apply to subsets of the population. There is some evidence of genetic variation in susceptibility to and response to other environmental factors such as parenting styles.
A critique based on evolutionary theory ("dads and cads") also suggests the paternal investment theory may have flaws. The core issue is whether fathers' and mothers' reproductive strategies provide children with reliable information about reproductive opportunities and constraints that they are likely to encounter during adulthood. Chisholm and Ellis say yes.
Both psychosocial acceleration theory and paternal investment theory see puberty as part of an integrated reproductive strategy that (a) responds to the circumstances of early childhood and (b) feeds forward to sociosexual and parental behavior in adulthood. These theories link earlier maturation with earlier sexual behavior, more partners, unstable pair bonds, less parental investment in children. Conversely, later maturation is linked to later sexual behavior, and all the converses.
Child development theory. This is Ellis' own formulation in response to above. He contrasts it with psychosocial acceleration and paternal invest theories because it conceptualizes timing of puberty as part of an integrated strategy that alters the length of childhood in response to early environment, extending it in high quality and shortening it in lower quality situations. It resembles the other two in its view of pubertal timing but not in the assumed linkage with later pairbonding and parenting behaviors. Higher social quality environments reduce the cost of delaying reproduction. Ellis says the evidence is weak that earlier puberty changes the quality of later sexual behavior, mating, and parenting.
Prior to life history theory, timing of puberty was said to be 50% genetic, with the environmental variables being weight (BMI), nutrition, exercise, physical illness, number of siblings, and altitude. Social experience prior to 1991 was not thought to have much of an effect.
Romans SE, Martin JM, Gendall K, Herbison GP. "Age of menarche: the role of some psychosocial factors". Psychosocial Medicine 2003, 33:933–9.
Research study and review of topic. Research study: questionnaire to random selection of 2225 NZ women (response rate 73%); those reporting childhood sexual abuse (apparently about 31) and matched nonCSA controls were invited to interviews (response rate 80%): 251 CSA, 224 nonCSA were interviewed. The two groups were divided by whether menarche occurred before (20%) or after (80%) 12y. Odds ratios for menarche before 12y were associated with about 14 social experience variables, including lower SES, lacking a father, changes of home, family conflict, "low control" and "low care" fathering and mothering styles, prolonged or frequent CSA, physical abuse, reported being loner, all at 95% CI of about 1.1 to 2.5–6.4. Highest OR was for prolonged CSA and physical abuse (OR about 1.5–6). Problems: no weights, no maternal menarche, no distinction of biological vs non-biological "fathers". Conclusion: "We wonder if CSA during this time accelerates menarche."
Review: Factors prev reported to be associated with earlier menarche: growing up with no father, difficult relations with parents, parental conflict, family stress. These were incorporated into sociobiological theory by Belsky et al in 1991. Early maturing girls come from conflicted families, feel insecure about close relationships, develop internalizing symptoms, and behavior problems. These lead to early sex, unstable pair bonds, and high fertility. This is called a "quantitative reproductive strategy" and a major component is limited investment by parents, especially father. Larger quantity of children makes sense in evolutionary terms when parenting is unreliable or poor quality.
Not all studies have supported the pathway from early childhood behavior problems to early menarche. Other potential explanations: Menarche is inheritable. Mothers of precocious girls had earlier menarche, entered high risk relationships earlier, resulting in association of daughters' early menarche with absent father. Absence of father may be associated with different family emotional life, different parenting competence, poverty, etc. No mention of earlier puberty causing CSA.
Steinberg, L. (1988). "Reciprocal relation between parent-child distance and pubertal maturation". Developmental Psychology, 24, 122–128.
One year observational study showing physical puberty increased autonomy and parent child distance but that these may also accelerate physical progression the "accelerating hypothesis"). Too short an interval to make much of it.
Kim, K., & Smith, P. K. (1998a). "Childhood stress, behavioural symptoms and mother-daughter pubertal development". Journal of Adolescence, 21, 231–240.
Retrospective self-report. More remembered conflict correlated with earlier menarche. Authors acknowledge that genetic mechanisms may underlie both earlier menarche and personality styles.
Ellis, B. J., McFadyen-Ketchum, S., Dodge, K. A., Pettit, G. S., & Bates, J. E. (1999). "Quality of early family relationships and individual differences in the timing of pubertal maturation in girls: A longitudinal test of an evolutionary model". Journal of Personality and Social Psychology, 77, 387–401. Summarized in Ellis 2004. 8 year prospective study of 173 girls. Father's presence, more father-daughter affection, more mother-daughter affection by kindergarten predicted later puberty by 7th grade. Father presence and affection were most important. Why? In all cultures, mothers invest more in child raising and paternal investment varies widely. Young girls are born with the ability to adjust tempo of sexual maturation to the fathering style experienced. Same speculations of cause described in 2004.
Ellis, B. J., & Garber, J. (2000). "Psychosocial antecedents of variation in girls' pubertal timing: Maternal depression, stepfather presence, and marital and family stress". Child Development, 71, 485–501.
Survey of 87 girls confirmed expectation that history of maternal depression, stepfather presence, and marital stress are associated with earlier puberty. Authors suggest stepfather presence and family stress act independently to accelerate puberty.
Comings, D. E., Muhleman, D., Johnson, J. P., & MacMurray, J. P. (2002). "Parent-daughter transmission of the androgen receptor gene as an explanation of the effect of father absence on age of menarche". Child Development, 73, 1046–1051.
Authors propose that a X-linked androgen receptor mutation (the 16 GGC repeat variation of the AR gene) carries higher risk of impulsivity and aggressiveness in males. In females at a weight loss clinic the 16 GGC repeat was associated with earlier menarche, parental divorce, and absent father by seven years of age. However, note that the 16 repeat is the most common AR allele.
Ellis, B. J., Bates, J. E., Dodge, K. A., Fergusson, D. M., Horwood, L. J., Pettit, G. S., & Woodward, L. (2003). "Does father absence place daughters at special risk for early sexual activity and teenage pregnancy?" Child Development, 74, 801–821.
This is first prospective study to see if early father absence predicts early sexual behavior independently of other social variables. This was a pair of longitudinal studies from kindergarten to 12th grade in US and from infancy to 18 in New Zealand. In both countries, girls with absent fathers from early childhood were twice as likely to be sexually active before age 16 (and 3–5 times as likely to get pregnant in teens) as father-present girls. Absence from late childhood was intermediate in both respects. In both samples, father absence constituted a unique and independent path to early sexual activity and adolescent pregnancy. Among the controlled for variables were SES, academic performance, early conduct problems, other familial stressors.
Variation of mean menarchal age ranges from 12.0 to 18.5 Earlier puberty of foreign adoptions; effect is greater when girls are adopted at older age (Proos, 91). Could high vegetarian diet include plant signals that delay fertility? Number of siblings delays puberty, as does altitude.