User:Alteripse/pubertal acceleration

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Social aspects of age of menarche

Ellis BJ. Timing of pubertal maturation in girls: an integrated life history approach. Psych Bull 2004, 130:920-58. Review. List of later adverse consequences of early maturation: wt gain, breast & other reprod 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:

• Energetics
• Stress-suppression
• Psychosocial acceleration: family stress accelerates maturation
• Paternal investment: fathers and other men play special role in regulating girls’ development
• Child development (his new synthesis) “reconceptualizes pubertal timing as the endpoint of a developmental strategy that conditionally alters the length of childhood in response to the compositions and quality of family environments to capitalize on benefits of high quality families and mitigate costs of low quality ones.”

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:

• Age at weaning
• Age of sexual maturity or puberty
• Adult body size
• Time to first sexual activity or mating
• Time to first reproduction
• Duration of gestation
• Litter size
• Interbirth interval

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. Chldren 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 psychosocial 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

1. energy scarcity or unreliability, or physical stress (illness, extreme exercise)

2. socioemotional stressors (harsh, neglecting family, absence of warmth and support)

3. father absence

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 downregulates the responsiveness and low stress early in life upregulates 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.

1. Is a stepfather an indicator the mate relationships will be unstable? A series of boyfriends would be especially associated with earlier puberty. No data.

2. Is a stepfather an indicator of a “degraded” family environment? Data is conflicting and probably moderated by quality of stepfather-daughter relationship.

3. Does a genetically unrelated male trigger earlier mammalian maturation? “Male effect” is well-demonstrated in other mammals, including primates, presumably pheromone mediated.

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 pairbonds, 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 psychosoc accel 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 phys abuse (OR about 1.5-6). Probs: no wts, no maternal menarche, no distinction of biol vs non-biol “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 NZ. In both countries, girls with absent fathers from early childhood were twice as likely to be sexually active before age 16 (and 3-5x 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.

additional Miscellaneous items 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.

[edit] Comment

How detailed do I need to be in my criticism of biases and unscientific design in theses article?

I am not planning on any large scale insertions of the above material, so don't devote effort to editing the above in detail.alteripse 14:29, 4 February 2006 (UTC)

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. The design of article is too weak to make any bold statements. Multiple geographic sites, with random phone calls to community to ID subjects should be the minimum standard for research to make bold, broad claims. Interesting that no big urban US cities or rural population. Also, the study doesn't have the mother or daughters collect data in real time. Instead uses their memory of past events. No bio-data to confirm early puberty or menarche.

Starts with a troubling bias that the nuclear family unit, with mother, father, and children living in an indepentant household is the best family structure. In some cultures this doesn't exisist at all.

Could they be actually researching- Do families with biological father present in the home discuss the sexuality of their minor daughter less than those with biological father absent? A sexually active minor daughter and out-of-wedlock pregnancy reflects poorly on the biological father in many communities. Would have greater motivation to hide it. There is much dishonesty about sexuality and reproduction.

Seems to classify the father as present or absent based on whether he lives in the home. Am I right that no attempt to determine the amount of actual contact with biological father. My experience is that ex-wives might not be the best person to discuss the status of of their ex-husband. Made no attempt to contact fathers. Also did not count other males present in home, even if constant from birth. Many family the grandparents are present in household and have large influence. How can this be ignored?

Ellis starts out by saying that early sexual activity and teen age pregnancy is a societal problem. This isn't (for certain historically wasn't) the univeral pov. Today some argue that pregnancy during teen years is desirable in situations where women live hard lives and show signs of aging by mid-twenties. University of Michigan population researchers have written about this. I can find if you want it.

Also in US the age of first pregnancy rose over the course of 20th century despite the rise in divorce. This started before birth control pills and elective abortion were in common use. This makes findings questionable.

When in doubt blame the mother! I have textbook called Bad Mothers: The politics of blame in 20th century America (1998). It spells out the various ways that societies blame mothers for societal ills. (Also my pediatric nursing textbook from 1970's that still mentioned poor mothering as cause for autisim!) Religion, legal, and medicine are used to classify women as bad mothers. Mother's dating practices!!

Mother blaming in itself is a great topic. I think the peak of mother-blaming by doctors for many childhood diseases was the mid-20th century, when not only autism but chronic physical diseases like inflammatory bowel disease and asthma were often explicitly blamed on mothers by experts. Currently the medical condition I see most often that is frequently associated with mother (or family) blame and guilt is childhood obesity and it is difficult to disentangle all the social factors that have contributed to it. Sometimes it is more family-blaming, but mothers still get the brunt of it. I do note with some surprise that you interpret these father-effect-on-puberty papers as "anti-mother" when they arguably indict abandonment by fathers even more. It is clear from your post, from the apparent purposes of the guy who originally posted the reference, and from some of the published responses, that people have a powerful urge to immediately interpret this type of stuff as either attacking or supporting their own sociopolitical pov about families. As an endocrinologist I think the putative "father effect" a fascinating research topic but I find it discouraging that some people would assume that even considering it worthy of research is somehow a political transgression.

There are also issues of medicalization of society and using medicine for social control.

Wow. This topic obviously presses your button. To date I have not heard any doctors weighing in on either side of this one, so wait until we actually do something before invoking that one. I am the kind of doctor who "owns" early puberty as a medical problem and I see children with this daily. It has always surprised me how distressed parents get over mild degrees of earliness. Part of the reason pediatric endocrinologists have shown little interest in this "father effect" is because we deal with children who are early by several years, so we don't find a factor that affects puberty by a few months very impressive. We think the weight aspect of early puberty of far more social concern.alteripse 14:29, 4 February 2006 (UTC)

All that said, I have no problem with mentioning the research. But, it needs to be short and state its bias too. --FloNight 01:33, 4 February 2006 (UTC)

I am slowly working up to it in the puberty article, but let me finish the addition before you attack it, please. alteripse 14:29, 4 February 2006 (UTC)

[edit] holding area for social effects section for menarche

Some of the least understood environmental influences on timing of puberty are social and psychological. In comparison with the effects of genetics, nutrition, and general health, social influences are small, shifting timing by a few months rather than years. The most important part of a child's psychosocial environment is the family.

Some of the aspects of family structure and function reported to be independently associated with earlier female puberty:

• Absence of father from the home frome early childhood
• Presence of stepfather or other genetically unrelated males in the home from early childhood
• Prolonged childhood sexual abuse
• High conflict famly relationships
• Being adopted from an underdeveloped country into a affluent home

Some of the aspects of family structure and function reported to be independently associated with later puberty:

• Larger family size
• Warmer, closer or more positive relationship with biological father
• Warmer, more supportive, low stress family environmnent

Other research has focused on the effect of childhood stress on timing of puberty, especially female. Stress is a vague term and studies have examined conditions ranging from family tensions or conflict to wartime refugee status with threat to physical survival. The more dire social conditions have been found to be associated with delay of maturation, an effect that may be compounded by dietary inadequacy. There is more uncertainty and mixed evidence as to whether milder degrees of stress or early-life undernutrition can accelerate puberty in girls as would be predicted by life history theory and demonstrated in many other mammals.

Our understanding of these environmental effects is incomplete and the following observations and cautions are relevant:

• Mechanisms of these social effects are unknown, though a variety of physiological processes, including pheromones, have been suggested based on animal research.
• Most of these "effects" are statistical associations revealed by epidemiologic surveys. Statistical associations are not necessarily causal, and a variety of covariables and alternative explanations can be imagined. Effects of such small size can never be confirmed or refuted for any individual child.
• Nearly all of the research on these effects has concerned girls, partly because female puberty requires greater physiologic resources and partly because it involves a unique event (menarche) that makes survey research into female puberty much simpler than male.
• Despite the small magnitude of effect, interpretations of the data are politically controversial because of the ease with which this type of research can be used for political advocacy. Accusations of bias based on political agenda sometimes accompany scientific criticism.