Library of Excerpts

Progenesis and Human Puberty: Pubertal Timing as a Heterochronic Variable

An abbrviation of the prepubertal growth period by some 4 years might have had a parallel effect on brain development. ... There is a relation between age at puberty and body build. Early maturers tend to be broad-built pyknic (most "feminine" or "masculine"), while late maturers are of a more linear leptosomic (androgynous) build (Marchall & Tanner 1986). There is also a relation between body build and mental illness. Pyknic body build predominates (90%) in classical manic-depressive psychosis (MDP) and leptosomic-dysplastic body build (80%) in schizophrenia (S) (Kretschmer 1921, 1961). In comparison, only around 20% of the general population were of true pyknic or leptosomic build. It is suggested that MDP is a disorder affecting very maturers (early puberty) and S affects extremely late maturing individuals (late puberty). From the secular trends of 4 years' decline in mean pubertal age, we would expect an increase in MDP and a decline in S. The National Norwegian Case Register comprises all first admissions to psychiatric hospitals and clinics by diagnosis since 1916 (Odegard 1971, Saugstad & Odegard 1980, 1983, 1985, 1986). Between 1926 and 1965, there was a more than 50% increase in first admissions classified as MDP or reactive depression psychosis (ICD 298.0). A majority of the latter is diagnosed as MDP on readmission. Practically all the increase occured after 1955, when in addition as increasing proportion of MDP was being classified as non-psychotic. Non-psychotic depressions (300.4) increased from less than 5% before 1040 to above 10% in the sixties, and to over 20% by 1978. Many of these patients are certified, being considered psychotic. We seem therefore justified in stating that there has been a marked rise in MDP during the last 30 years in Norway." (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 157)

"Under colonization, I link two phenomena often considered separately: the exploitation of renewed abundant resources by the survivors of an in situ population crash, and the chance dispersal of a few colonizing immigrants to new areas with no competitors. Both possess the common feature of presenting to a few individuals a superabundant regime of resources; r strategists should prevail in such a circumstance, since rapid increase in numbers will be so strongly favored. Progenesis represents one of the easiest and most rapid pathways to high r; it should be very common among colonizers." (Gould, S.J. (1977) Ontegeny and Phylogeny. Cambridge: Belknap Press. p. 326)

"McNaughton writes: 'We expect an r-K continuum, the former occuring in a perfect ecological vaccum with no density effects and no competition, the latter occurring in a completely saturated ecosystem where density is high and competition for resources is intense. In the ecological void the optimal adaptive strategy channels all possible resources into progeny, thereby maximizing the rate at which resources are colonized. At ecological saturation, the optimal strategy channels all possible resources into survival and production of a few offspring of extremely high competitive ability. (1975, p. 251)' In simplist tems, r selection will predominate when the density-independent component of natural selection is in control -- when populations can expand with no negative feedback on growth rate by dwindling resources. K selection will prevail when the density-dependent component dominates -- when increase in one genotype must be at the expense of another. Situations favoring r selection might include large, frequent, and unpredictable environmental fluctuations; frequent catastrophic mortality; superabundant resources; and lack of "crowding." K environments tend to be crowded, stable, and benign. Important r environments include those available for colonization (superabundant resources) and those subject to large an unpredictable fluctuations imposing catastrophic, density-independent mortality on the few species able to survive in them. We expect, therefore, to encounter r selection during early stages of colonization and periods of increase in fluctuating populations." (Gould, S.J. (1977) Ontegeny and Phylogeny. Cambridge: Belknap Press. p. 291) [Note: contempory times with the flood of fats, carbs, and proteins create a 'r' environment compelling human puberty to drop to increase the number of progeny]

“We traced spatial, verbal and musical abilities through a seven-year period of adolescence. When we started our study, 60 boys had reached a mean age of 11.72, 60 girls were 11.52 on average. Menarche and mutation served as markers for maturation. We found that early, mid, and late maturers differed on spatial orientation and on tactile-visual discrimination as measured with the Witelson task. No differences between the maturational groups emerged on verbal fluency and on Wing's Standardized Tests of Musical Intelligence. At some stages, sex differences on spatial, verbal, and musical tests emerged, and disappeared at others. The sex differences in performance levels were not associated with a sex-specific relationship between maturation rate and performance levels. We found indications of the usefulness of sex hormone measurement in relation to cognitive and musical development in adolescence.” (Hassler M (1991) Maturation rate and spatial, verbal, and musical abilities: a seven-year-longitudinal study. Int J Neurosci 58 (3-4): 183)

"The pervalence of S [schizophrenia] is persistently high in regions with little improvement in living conditions or with a subsistence economy." (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 158)

"If MDP affects early maturers and S affects late maturers, we would expect MDP to be common in females and S to be common in males. There is a markedly higher life-time risk of MDP in the female sex (1.5-2.0 times) in most investigations (Stromgren 1976, Odegard 1972a, Rawnley 1982). Female onset on MDP is about 10 years earlier, with maximum age-specific rates at 30-40 years as against 40-50 years in the male sex (Lundquist 1945). There is a higher incidence of S in males than females when sought. This has been observed in the USA (Babigan 1980, Norway (Odegard 1971), Denmark (Stromgren 1987) and in the Third World (Sartorius et al. 1986). Onset is earlier, and maximum age-specific rates are observed about 10 years earlier in males than in females (Noreik & Odegard 1967): onset is also more insidious and the course less favourable (Saugstad & Odegard 1980, 1986, Watt et al. 1983, Stromgren 1987, Hafner 1987). (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 158)

"The mean menarcheal age is from a few months to 2 years earlier in the upper than in the lowest social classes (Marchall & Tanner 1986), so we would expect the highest incidence of S in the lowest socioeconomic categories (SEC) and the highest risk of MDP in the upper classes. An excess of S in the lowest strata of society is one of the most consistent findings in psychiatric epidemiology" (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 159)

"Among female high school graduates, MDP was 2.3 times more common than in the general population; among the males 1.7 times higher." (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 159)

"He [Kretschmer] also observed that body build was more leptosomic in non-paranoid S (dementia simplex, hebephrenia and catatonia), than in paranoid S, and that male patients were more pronouncedly leptosomic than female patients. Moreover, when MDP occured in non-pyknic individuals, the course and prognosis were atypical." (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 159)

"The relation between maturational rate and subgroup of S [schizophrenia] is also illustrated from Asia and Africa. These ethnic groups are more mature throughout growth, with greater weight for height than white populations, and an earlier puberty (Marchall & Tanner 1986). There is a greater predominance of paranoid S at the expense of the less treatable non-paranoid categories. Onset is more acute and the course of the disease is more favourable (Sartorius et al. 1986, 1987)." (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 160)

"The final event consists of systematic elimination of redundancy of neuronal synapses (some 40%), perhaps to increase the efficiency of communication between the billions of neurons (Ribchester 1986). Those synapses which are labile or uspecific in terms of their function are hit and they regress. Those cells, axons and synapses that die are dispersed among those that survive (Huttenlocher 1984, Goldman-Rakic et al. 1983, Goldman-Rakic & Rakic 1984, Rakic 1988). The phylogenetically older structures are the first reach concurrence of synaptogenesis, and the anterior and superior frontal cortical regions the last (Goldman-Rakic 1988, Phelps et al. 1988). Any maturational irregularity at this stage is of decisive importance, and is most likely to occur at the extreme rates of maturation. A reduction in this last stage of brain reorganisation could result in insufficient regressive events (persistent redundancy) and MDP. Attenuation of synaptic density beyond the optimal could occur in those with delayed and prolonged puberty and lead to S." (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 161)

"In these non-industrialized populations, visuo-spatial ability as measured by Performance IQ scores predominates over verbal ability (Verbal IQ scores), and there is no sex difference (Berry 1966, 1976). More particularly, Kaerine (1981) studying an Australian aboriginal population with a semi-nomadic hunter and gathering life-style found that the aboriginal children performed at a significantly higher level than the Australian white children from high school she used as controls, when their spatial competence was compared. They used a visual (non-verbal) strategy, and their unusual spatial competence was combined with self-reliance and there was no obvious sex-difference. In contrast, there is a sexual dimorphism in cognitive ability in Western industrialized countries today. Females are reported to excel at tests of fluency, articulation, coding and perceptual speed (Verbal IQ scores) and males at tests of spatial visualization (Performance IQ scores). Male visuo-spatial ability is consistent, whereas the female verbal superiority varies. It seems therefore as if the decline in mean pubertal age by some 4 years (raised maturational rate) has reduced visuo-spatial ability, and may ask: what evidence do we have that there is a relation between rate of maturation and cognitive profile? There is an inverse relation between rate of maturation and spatial ability, whereas verbal ability is unaffected by maturational rate (Waber 1976, 1977). Late-maturing girls and boys (pubertal age 14 1/2 years & 16 1/2 years, respectively = mean + 1 SD according to Marchall & Tanner 1969,1970) invariably scored higher on spatial than on verbal tasks, regardless of sex. They also performed better than early-maturers 12 1/2 years & 14 1/2 years respectively = mean -1 SD) on tests of spatial ability, also regardless of sex. Maturational rate had no particular influence on verbal scores.' (Saugstad, L.F. (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clinical Genetics 36 (3): pp. 163) [note: how closely connected is visuo-spatial abilities to the final stage of cognitive development, abstract thinking?]

"Waber's (1976) study of early and late maturing adolescents was directly addressed to this issue. She found that adolescents with late puberty onset, regardless of phenotypic sex, had better spatial abilities than those with early pubertal onset. Spatial abilities were better than verbal ones among slow maturers, whereas verbal ones were better than spatial ones among early maturers. A subsequent replication revealed that these effects were more dramatic among middle-than lower-class subjects (Waber, Bauermeister, Cohen, Ferber, & Wolff, 1981). In her original paper, Waber (1976) also reported laterality differences between groups as indicated by a dichotic listening procedure. She found that late maturers demonstrated stonger left hemisphere biases for verbal materials than did early maturers and so attributed their ability differences in rates of maturation on hemispheric organization. Specifically, she proposed that a slower maturation rate might allow for the stronger interhemispheric differentiation necessary for good spatial skills (Levy, 1969) and typical of boys (McGlone & Davidson, 1978) to occur. Thus she concluded that maturation rate might be the mechanism responsible for sex-related differences in cognitive functioning (Maccaby & Jacklin, 1974), given that girls typically mature faster than boys. Other investigators have subsequently attempted to replicate Waber's findings, but with only partial success. In Herbst and Petersen's study (Note 1), subjects with better spatial ability were found to mature later than subjects with poorer spatial ability, but they did not differ in hemispheric lateralization. ... It was predicted that, if the Waber hypothesis is correct, children with precocious puberty will display significantly better verbal than spatial skills and individuals with delayed puberty will display significantly better spatial than verbal skills. Moreover, it is also expected that, on a task of cerebral lateral asymmetry, delayed puberty adolescents will be more lateralized than normal, whereas precocious subjects will be less lateralized than normal. ....Studies of the intellectual consequences of precocious puberty indicate that such children tend to have above-average ability, frequently in verbal skills..." (Rovet, J. (1983) Cognitive and neuropsychological test performance of persons with abnormalities of adolescent development: A test of Waber’s hypothesis. Child Development 54: pp. 941-2)

"This decline in the most severe subgroups such as the non-paranoid (hebephrenia, catatonia, dementia simplex) has often been accepted as due to drug treatement. The drugs cannot affect age at onset. The non-paranoid, with their most pronounced leptosomic (dysplastic) body build and particularly early and insidious onset, probably belong to the most extreme categories of late maturers. The marked reduction in these cases is therefore more likely a result of their significant reduction in the population. This is illustrated by the fact that Kretschmer's observation of leptosomic-dysplastic body build (acromegaloidism, eunuchoidism, infantilism, virilism in females, feminity in males, etc.) in 17.5% of schizophrenics (as against 0.4% in MDP) has received no attention lately. In might be due to a reduction in the numbers of these cases. The relation between maturational rate and subgroup of schizophrenia is also illustrated from Asia and Africa, where ethnic groups are more mature throughout growth, with more weight for height than whites, and mature earlier (earlier age at puberty) (Marchall & Tanner, 1986). A greater predominance of paranoid over non-paranoid schizophrenia is observed, and onset is more acute and the course of the disease more favourable, with less chronic defects, than in the European countries included in the WHO study (Sartorius et al, 1986, 1987). (Saugstad LF (1989) Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses. Br J Psychiatry 155: 538)

"The non-paranoid schizophrenics with their extreme body build are probably those with the most delayed puberty, whereas puberty is possibly less delayed in paranoid schizophrenia and in subgroups with a favourable prognosis." (Saugstad LF (1989) Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses." Br J Psychiatry 155: 540)

"Early maturers (early puberty) tend to be pyknic (stocky), and late maturers tend to be leptosomic (slender) (Marshall & Tanner, 1986). According to Kretschmer (1921), pyknic body build predominated in MDP (90% of cases) at a time when only around 20% of the general population was of true pyknic or leptosomic build and mean age at menarche was around 15 years. Age at puberty is only partly geneticall determined. The decline in mean age at menarche from just below 17 years 100 years ago to around 13 years today in Western industrialized countries (Marshall & Tanner, 1986) is usually considered a phenotypic response to improved living condidtions. Late maturers (mean +2 s.d.) now experience menarche at about the same age (15 years) as early maturers (mean minus 2 s.d.) a century ago. Concomitantly, there has been a shift from a predominance of leptosomic-athletic and true leptosomic build to pyknic-athletic and true pyknic build. Following this decline in pubertal age, a significant rise in MDP is expected concomitant with a decline in schizophrenia, if MDP dies indeed affect very early maturers and schizphrenia extremely late maturing individuals." (Saugstad LF (1989) Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses. Br J Psychiatry 155:536)

"In Iceland, Helgason (1979) in his follow-up study observed a lifetime risk of MDP of 3.34% as against 2.72% in 1947, and there was also a marked increase in depressive psychosis (298.0) and in non-psychotic depression (300.4). In the Lundby study from Sweden (Hagnell el al, 1982) of in-patients, out-patients, and untreated cases, the probability of suffering a depression increased significantly in both sexes over the period 1947-72, and the risk was highest among those aged 20-30 years. Similar observations have been made in the USA (Klerman, 1978), where there is an alarming increase of depression. ... In contrast, the prevalence of schizophenia is persistently high in poorer populations (e.g. in the Istrian region of Yugoslavia, in certain parts of rural Ireland, the Australian aborigines, the Cree Indians and the Salteaux of Northern Saskatchewan (Crocetti et al, 1964, 1971; Roy et al, 1971; Warner, 1985)). An excessive prevalence of schizophrenia (and extremely lwo prevalence of MDP) has repeatedly been observed in an isolated region of northern Sweden, where according to Book (1953), as late as 1949, poverty was widespread and death rates were high. Moreover, Book commented upon the uniformity of the clinical picture (a particular type of catatonia). Similar harsh conditions prevailed in the neighbouring regions of Finland, where the prevalence rates of schizophrenia are similarly elevated (Vaisanen, 1975; Lehtinen & Vaisanen, 1981)." (Saugstad LF (1989) Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses. Br J Psychiatry 155:537)

"There is a markedly higher lifetime risk of MDP in women than men in most investigations (by 1.5 -2.0 times) (Odegard, 1972a; Stromgren, 1976; Rawnsley, 1982), in agreement with expectation form the hypothesis. Onset of MDP in women is also earlier than in men (maximum age-specific rates 30-40 years v. 40-50 years) (Lundquist, 1945). .... It is usually believed that there is no sex difference in the incidence of schizophrenia, but a higher male incidence has been observed. In the USA, Babigan (1980) found higher male rates, and in Norway over 1926-65, Odegard (1971) found 19% to 36% higher male admission rates. Higher male admission rates have been recorded in Denmark (Stromgren, 1987), and in the Third World (Sartorius et al, 1986, 1987). (Saugstad LF (1989) Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses. Br J Psychiatry 155:537)

"Onset of schizophrenia in men is, as expected, earlier than in women, with a difference in maximum age-specific rates of about ten years (Noreik & Odegard, 1967; Odegard, 1971). Earlier onset in men is distinguished by being more insidious, with greater chronic defects, and on the whole a less favorable course (Saugstad & Odegard, 1980, 1986; Watt et al. 1983; Stromgren, 1987; Hafner, 1987)." (Saugstad LF (1989) Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses. Br J Psychiatry 155: 538)

"Idiopathic or constitutionally delayed puberty is among the less frequent kinds of delayed sexual development, particularly for girls (Reindollar, Bynd, & McDonough, 1981). Idiopathic delay is a matter of an error in the timing of puberty and is not associated with an imbalance or physical disorder. It is usually defined statistically as the appearance of the first signs of puberty 2-3 years (2.4 SD's) beyond the median age, that is, after 14 years of age for girls and 16 for boys (Brook, 1981; Ehrhardt & Meyer-Bahlburg, 1975). Idiopathic delayed puberty, which can run in families (Brook, 1981), is more common in boys than girls and usually co-occurs with short stature (below third percentile) and delayed somatic development throughtout childhood. Unlike precocious puberty, delayed puberty is not associated with a difference in IQ level or any advantage or disadvantage in specific abilities (Money, Drash, & Lewis, 1967); Pollit & Money, 1964). As with precocious puberty, there are no reported studies of hemispheric lateralization in constitutionally delayed children and adolescents." (Rovet, J. (1983) Cognitive and neuropsychological test performance of persons with abnormalities of adolescent development: A test of Waber’s hypothesis. Child Development 54: pp. 943)

[abstract] "The hypothesis of a neurodevelopmental aetiology of manic-depressive psychosis and schizophrenia is based on the relation between onset of puberty and the final regressive events in the central nervous system (elimination of 40% of neuronal synapses), and the discrepancy in body build in the two disorders which is similar to that between early- and late-maturing individuals. The marked rise in manic-depressive psychoses and decline in schizophrenia, particularly the non-paranoid categories, accompanying the decline in mean pubertal age by some four years during the past hundred years are taken as evidence that manic-depressive psychosis affects early maturers and schizophrenia particularly affects late maturers. Gender differences and social differentials accord with this theory. Redundancy of neuronal synapses characterises manic-depressive psychosis, and reduced density of synapses is a characteristic of schizophrenia, whereas 'normality', with optimal synaptic density, is in between." (Saugstad LF (1989) Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses. Br J Psychiatry 155:536-44)

"20 children with idiopathic precocious puberty, 27 adolescents with clinically delayed puberty, and an equivalent number of controls matched for age, sex, and IQ were given a battery of tests. These included measures of verbal and spatial abilities and a task assessing hemispheric lateralization using a dichotic listening procedure. Comparisons with matched controls revealed poorer verbal and spatial abilities for precocious males and poorer verbal, but better spatial, abilities for precocious females. Delayed developing males demonstrated superior verbal skills compared with controls, whereas delayed developing females did more poorly than controls in both verbal and spatial areas. On the dichotic task, the only group differing from controls was the delayed developing males, who demonstrated stronger lateral asymmetries. It was suggested that the present findings, which are not consistent with those of former investigations, may reflect methodological differences between studies and the disruptive influence of atypical pubertal onset on normal patterns of sex difference in cognitive functioning." (Rovet, J. (1983) Cognitive and neuropsychological test performance of persons with abnormalities of adolescent development: A test of Waber’s hypothesis. Child Development 54: pp. 941)

"Onset of puberty is usually considered to coincide with the last major step in brain development: the
elimination of some 40% of neuronal synapses. Mean pubertal age has declined by some 4 years during the last 100 years. There is a relation between age at puberty and body build, and between body build and mental illness. The difference in body build between schizophrenia (S) and manic-depressive psychosis (MDP) is similar to that between late and early maturers. It is suggested that S affects late-maturing individuals and MDP very early maturers. The observed marked rise in MDP and decline in the most malignant forms of S (non-paranoid) are in agreement with MDP and S as neurodevelopmental disorders occurring at the extremes of maturation. Maturational irregularities are most likely to occur at the extremes, and it is suggested that abbreviation of the regressive process may have led to persistent redundancy of neuronal synapses in MDP and that prolongation of the process past the optimal has yielded an inadequate synaptic density in S. The lack of cerebral abnormality in the majority of MDP and the presence of only subtle structural deficits in S, are in agreement with this. The two disorders are probably as old as mankind, and early puberty is the necessary factor for the development of MDP and late puberty is the necessary factor for that of S. There is an inverse relation between spatial ability and rate of maturation, whereas verbal ability is unaffected by maturational rate. From a previous predominance in both sexes, spatial ability (Performance IQ scores) has been reduced to below verbal ability (Verbal IQ scores) in the female sex and in early maturing males." (Saugstad LF (1989) Mental illness and cognition in relation to age at puberty: a hypothesis. Clin Genet 36(3):156)

"Dr. Singh....found that menarche is experienced later, on the average, by girls from large families than by those from small families. ... The results are those of Roberts and Dant who suggested that girls born later in sibships mature earlier than those born earlier in the same sibships." (James, W.H. (1973) Age of menarche, family size, and birth order. American Journal Obstetrics Gynecology 116 (2): 292)

"The ethnographic record {e.g., A French Army Surgeon (1898/1972), a 30-year specialist in genitourinary diseases} makes reference to numerous anatomical distinctions which show a similar pattern of whites being between blacks and Orientals. These include the placement of female genitals (Orientals front and high; blacks back and low); angle and texture of erection (Orientals parallel to body and stiff, blacks at right angles to body and flexible); salient buttocks, breasts, and muscularity (Orientals least, blacks most); and size of genitalia (Orientals smallest, blacks largest). We averaged the ethnographic data on erect penis and found the means to approximate: Orientals, 4 to 5.5 in. in length and 1.25 in. in diameter; Caucasions, 5.5 to 6 in. in length and 1.5 in. in diameter; blacks, 6.25 to 8 in. in length and 2 in. in diameter. Women were proportionate to men, with Orientals having smaller vaginas and blacks larger ones, relative to Caucasians. Clitoral size differed in length: in European women, 1.2 in.; in African women, 2 in. variations were noted; in French West Indies, the size of the penis and vagina covaried with amount of black admixture; Arab men, who were often mixed with black, had larger penises than Europeans. Recent data show similar patterns. Measurements taken from living subjects as well as those at autopsy, show the size of testes is twofold lower in Asian men than Europeans (9 g vs 21 g), a difference too large to be accounted for entirely in terms of body size (Diamond, 1986; Short, 1984). Concomitantly, as mentioned, Asian women have lower ovulation rates than Caucasian women, as indexed by dizotic twin frequency, with the frequency per 1000 across several Asian populations being < 4, while for Caucasians it is 8, and for blacks 16 per 1000 (Bulmer, 1970; Diamond, 1986). Contrary to the general trend, Freeman (1934) observed that, at autopsy, American blacks had less heavy testes than American whites (13g vs 15g). Freeman (1934), however, did find that black women had heavier ovaries than white women. Subsequently Daniel, Fienstein, Howard-Peebles, and Baxley (1982) found no black-white difference in testicular volume among American adolescents, while Ajmani, Jain, and Saxena (1985) found larger scrotal circumference in Nigerians than Europeans (212.6 mm vs 195.1 mm or 8.37 in. vs 7.68 in.). A French Army Surgeon (1988/1972) also provided early observations that, in speed of sexual maturation, Orientals < whites< blacks. Several subsequent studies are confirmatory. In the United States, blacks are more precoscious than whites as indexed by age at menarche, first sexual experience, and first pregnancy (Malina, 1979). A national probability sample of American youth found that by age 12, 19% of black girls had reached the highest stages of breast and pubic hair development, compared to 5% of white girls (Harlan, Harlan, & Grillo, 1980), although the same survey found white and black boys to be similar (Harlan, Grillo, Coroni-Huntley, & Leaverton, 1979). Subsequently, Westney, Jenkins, Butts, and Williams (1984) found that 60% of 11-year-old black boys had reached the stage of acelerated penis growth in contrast to the white norm of 50% of 12 1/2-year-olds. This genital stage significantly predicted onset of sexual interest, with 2.2% of the black boys experiencing intercourse by age 11. While some surveys found that Oriental girls enter puberty as early as whites (Eveleth & Tanner, 1976), others suggest that in both physical development and onset of interest in sex, the Japanese, on the average, lag 1.5 to 2 years behind white Americans (Asayama, 1975). (Rushton, J.P. & Bogaert, A.F. (1987) Race differences in sexual behavior: Testing an evolutionary hypothesis. Journal Research in Personality 21(4): pp. 536-7)

"Compared to whites the black respondents in this sample entered puberty at a later age, but did tend to leave home earlier." (Rushton, J.P. & Bogaert, A.F. (1987) Race differences in sexual behavior: Testing an evolutionary hypothesis. Journal Research in Personality 21(4): pp. 539)

"Also of interest is the phylogenetic information found in Irwin's ontogenetic comparisons. As shown in Fig. 7-2, song development is characterized by a definite sequence of changes. By comparing the ontogenies of certain species to such a sequence, she found, for example, some groups that are clearly paedomorphic, in singing continuous songs and other traits (ratain memicry and have many syllable types). Eventhe type of heterochrony leading to the paedomorphosis was discernable in some cases. The mimids are apparently neotenic for song development. They never reach the adult stage of crystallized song. Instead the song develops slowly throughout life, ever-changing until they die. They are like perpetual juveniles for song development, continually learning new syllables and dropping old one. In contrast, the reed warblers appear to be progenitic. Their songs crystallize at a relatively earlier stage than most and no new one are learned thereafter." (McKinney, M.L. & McNamara, K.J (1990) Heterochrony: The Evolution of Ontegeny: Plenum Press, New York p. 281-2)

"Experimental work has shown that removal of the corpora allata (the endocrine glands that secrete juvenile hormones) of immature male desert locusts, which prevents them from reaching maturity, not only inhibits production of the accelerting pheromone, and thus the potential for induction of maturity in other males, but seems also to result in a pronounced delay in the onset of normal maturity in others (Norris and Pener, 1965). It has been suggested (Butler, 1967) that similar accelerating pheromones may also be present in ladybirds (Coccinellidae), coming into effect when immature adults congregate. The pheromone induces synchronous sexual maturity, allowing mating followed by dispersal." (McKinney, M.L. & McNamara, K.J (1990) Heterochrony: The Evolution of Ontegeny: Plenum Press, New York p. 110)

"The groups with the earliest median age for menarche (first mentrual period) are the well-off in Istanbul (age 12.3), Singapore (12.4) and Hong Kong (12.5), and Afro-Americans (12.5). Those with the latest menarche are in New Guinea and East Africa (15.5 to 18.0)." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 275)

"The growth of Africans in Africa is limited in most populations by undernutrition and disease, especially in the first few years after birth, to which period special attention in given. Well-off groups of Africans (e.g. Yoruba in Nigeria belonging to the upper classes) grow in height and weight very much as do Europeans, and in the United States recent surveys have established that children of predominantly African descent are taller and heavier at all ages than children of European descent, even at somewhat lower economic levels. This is chiefly because the Afro-American children mature faster from birth onwards, alike in dental development, skeletal maturity, pubertal development (mean menarche age 12.5 years compared with 12.8 years) and percentage of adult height attained at successive ages. There is little reason to suppose that groups of Africans in Africa would not grow similarly if their environmental conditions were better." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 274)

"Asiatics, even those who are growing up under the best circumstances, are less tall at all ages than well-off Europeans and Africans. Chinese and Japanese mature as early or earlier than well-off Africans and considerably earlier than populations in Northwest Europe.....At puberty Asiatics have a different pattern of skeletal maturation from Europeans and Africans, increasing their rate of maturing more swiftly and reaching full skeletal maturity earlier." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 274)

"Recent recall data [Eskimos] indicate an earlier menarche (13.8 years; Milan, 1970) than was reported formerly (14.2 years; Levine, 1953). Skeletal development is similar to that of European children (Pawson, 1974a)." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 269)

"The frequent improvement [epilepsy] at puberty suggests that even at this relatively late age hormones affect the areas of abnormal cortex that are the postulated cause of this form of epilepsy." (Geschwind & Galaburda 1987: 204, Cerebral Lateralization)

"Sexually immature, prepubescent boys enjoy a range of sexual response similar to that of adult women. Kinsey and his coworkers reported, "The most remarkable aspect of the preadolescent population is its capacity to achieve repeated orgasm in limited periods of time. This capacity definitely exceeds in the ability of teen-age boys who, in turn, are much more capable than older males." The response of young boys, including mulitiple climax without losing an erection, "is," according to biologist Donald Symons, "perhaps similar to orgasmic women." Neither prepubescent orgasmic boys nor women ejaculate sperm, and thus the "ability of females to experience multiple orgasms may be an incidental effect of their inability to ejaculate."" (Margulis, L & Sagan, D. (1991) Mystery Dance, On the Evolution of Human Sexuality: Summit Books, New York pp. 86)

"Consider, as an example, a female prepubescent mouse left on her own. Eventually, of course, she will reach puberty. But put an adult male into the cage with her and she will reach puberty earlier. This intriguing phenomenon, known as the Vandenbergh effect, is produced by pheromones, odors in the male's urine that cause a behavioral or psysiological response in other animals. These pheromones, when smelled by the female, crank up her ovulatory machinery. The male's urine does this trick even when the male isn't present---just dab a smidgen of male urine on females and, voila, earlier puberty. Moreover, the more male sexual hormones the mouse has in his bloodstream, the more effective he is at accelerating the onset of puberty. Conversely, when a prepubescent female mouse is exposed to a large number of adult females, puberty is delayed---why bother if there are no guys around? Once again the signal is a pheromone, found in the urine of the adult females. Block the young female's sense of smell, and the puberty delay no longer occurs." (Sapolsky 1997: 47, TheTrouble With Testosterone)

"And what were the physiological consequences for these baboons in Utopia? [African boboons eating westerners garbage] First the good news: Young baboons grew faster, reaching developmental landmarks such as puberty at earlier ages. These beneficial changes were exactly what one would expect of humans switching from a lean subsistence diet to a more affluent Westernized fare. In the countries of the West the age of first menstruation has declined from an estimated fifteen years during the 1800's to our current average of about twelve and a half, and diet is thought to have much to do with that. The trend in baboons has been particularly well documented by Jeanne Altmann of the University of Chicago, a biologist studying both foraging and garbage-eating troops in another part in Kenya. Among her animals, eating garbage had led to the onset of puberty at age three and a half instead of age five. Females now typically give birth for the first time at age five, a year and a half earlier than before. (Sapolsky 1997: 130, TheTrouble With Testosterone)

"It could be the case that although growth of the left hemisphere is slowed to a greater extent in lefthanders than in righthanders, it may attain a greater final size in lefthanders. This could occur with the growth period is prolonged---for instance, when pregnancy is longer than average or when puberty is late, which would allow for further development in childhood." (Geschwind & Galaburda 1987: 98, Cerebral Lateralization)

"The primary reason for the lack of size change in the skull and face of the pygmies is probably related to a combination of early growth priority of these structures (especially reflected in those measurements incorporating the skull base: basion-nasion and basion-prosthion), plus the fact that in humans overall skull size is negatively allometric to body size and weight. This is even true of the facial skeleton in humans, so that a marked change in body weight may result in little or no alteration in facial size. Evidence to this effect can be seen in the pubertal growth spurt, during which males become signifacantly larger than females in height and weight, but metric aspects of facial size are still largely indistinguishable (Keen, 1950)" (Shea, B.T. & Gomez, A.M. (1988) Tooth scaling and evolutionary dwarfism: an investigation of allometry in human pygmies. American Journal of Physical Anthropology 77 (1): pp. 129)

From chart in Shea extracted from Eveleth and Tanner. Age of Menarche: Europe 13.3 yrs, Descendants of Europeans abroad 12.9 years, Africa 14.9 years, Descendants of Africans abroad 13.2 years, Near East and India 13.6 years, Asiatics 13.1 years, Pacific Islanders 16.2 years. (Shea, B.T. (1989) Heterochrony in human evolution: the case for neoteny reconsidered. Yearbook of Physical Anthropology 32: pp. 84)

"Although the growth rates of girls and boys are almost identical in infancy and childhood, a noticeable difference occurs at about age ten, when girls start to grow faster than boys, achieving the maximum rate by age twelve and completing their growth by age fifteen. Boys, by contast, do not start their growth spurt until two years later than girls and do not acheive full growth until approximately seventeen to eighteen. Four-fifths of the mean height difference of 10 cm between adult men and women is accounted for by the delayed onset of the growth spurt in boys, which allows them a longer growing time, and only one-fifth by the increased magnitude of that growth. (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 146)

Since maternal investment in the developing fetus is principally in the form of nutrients, it is not surprising that recent research has shown that it is the level of such nutrients stored in the mother's body - fat, in other words - which is critical to fertility. This finding explains why the age of menarche (the point at which a young women begins to menstuate) has dropped progressively with rises in living standards in general and nutrition in particular, from an average of 15.5 years a century ago in the USA to one of 12.6 years today. It also explains why body weight, rather than other indicators such as height, appears to be the critical factor. Body fat increases prior to menarche by a factor of 120 percent and in so doing reaches a critical level of 24 percent by weight at the onset of sexual cycling. However, early sexual cycles tend to be infertile and irregular, and a further increase in body fat proportion to a typical 28 percent is achieved by age eighteen, at which point full fertility is normally achieved. So sensitive is the female body to body weight variations that some women athletes can turn their sexual cycles on and off at will with just a three-pound change in weight. " (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 161)

[from abstract]"The physical and hormonal changes of puberty are presented and the wide range of ages at which the pubertal process may begin is emphasized. The great variability in the timing of onset of adolescence, its rate of progression, and the age of completion are detailed. The causes of delayed adolescence in males and females are considered. The most common form of delayed adolescent development is termed constitutional delay in growth and development, which may occur sporadically, or may be the familial pattern of growth and development or may reflect a suboptimal nutritional environment. The evaluation of such children, including appropriate historical review, physical examination, and laboratory assessment, is outlined. In most patients with constitutional delay in growth and development, strong reassurance is sufficient therapy. In other subjects, treatment with androgens (boys) or estrogens (girls) may be indicated. In patients with primary systemic diseases accociated with delayed maturation, specific treatment which eradicates the illness will often be followed by resumption of growth and development. In subjects with primary disorders of the hypothalamus, pituitary, or gonads, replacement therapy with androgens or estrogens is indicated. If gonadal function is intact, these patients may eventually become fertile with appropriate use of hypothalamic and/or pituitary hormones." (Root AW, Reiter EO (1976) Evaluation and management of the child with delayed pubertal development. Fertil Steril 1976 27(7):745-755)

"Skeletal maturation of Tibetans and Sherpas is similarly retarded and is considerably and consistently behind Quechua bone age, being on average delayed by about 5 ' years' on Greulich-Pyle standards in 13-year-old boys and 11-year-old girls. Moreover, Sherpas and Tibetans have a smaller total bone area, less cortical bone, and more medullary area than European Americans or Quechuas. An admittedly only approximate figure for menarche gives an average 18.1 years, one of the latest in the world." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 266)

"In every urban-rural comparison so far reported urban girls have an earlier menarche than rural girls (Fig 197). In Australia (Jones et al., 1973) and the USA (MacMahon, 1973) the differences are very small. As with growth in body size, age at menarche is closely related to the health and nutritional level of an individual or a population." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 256)

"Recent studies from Austalia (Jones et al., 1973) and the USA (Hamill et al., 1972) both showed no significant differences in height and weight between city and country children. The US study concludes that at the same income level there were no discernable differences in height or weight means between 6 and 11-year old rural farm children and children in twenty-four central cities ranging from New York City to Colombia, South Carolina. These results are substantiated by the earlier report on American adults (Hathaway & Foard, 1960) which showed no consistent differences in height or weight in relation to urbanisation (Fig. 194). It seems likely then that the urban-rural differences in Central, South and East European populations reflect primarily an economic differential between town and country." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 253-4)

"In all populations from which we have data menarche is earlier in chldren from well-off families than in the underprivledged (Fig. 187; see also Table 15). In Newcastle-upon-Tyne (England) median ages of menarche were 13.3 years for girls from professional and managerial families and 13.7 years for girls from unskilled, manual working class families (Miller, Billewicz & Thomson, 1972). Number of children in the family may also affect age of menarche. In Northeast England, at least, the social class influence apparently operates through family size. Girls from larger families had consistently later menarche than those from smaller ones, as in most data, and when this effect was allowed for the differences due to father's occupation disappeared (Roberts, Rozner & Swan, 1971). (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 244-5)

"Chinese in Hong Kong have one of the earliest recorded medians (12.5 for well-off, 12.8 for middle class and 13.3 for poor) and Japanese are relatively early (12.9). New Zealand Maori are earlier (12.7) than New Zealand Europeans (13.0), both figures being derived from a full national survey (Fig. 167). Though Africans in Africa, even those apparently well-off, are relatively late (13.4, Uganda; 14.1, Nigeria), Afro-Americans are early, averaging 12.5 (Fig.167). People largely of European-African mixture in Cuba average 13.0 over the whole island, but about 12.6 in Havana. It seems likely, therefore, that in good environmental conditions Africans may be as early-maturing in this parameter as Asiatics and southern Europeans, and earlier than the peoples of Northern and Central Europe. Girls in the Near East have a relatively late menarche, with the exception of well-off girls in Istambul who at 12.3 have the earliest median of any population studied. Even the poor in Estanbul average 13.2 years. In India the well-off average about 12.8, and the poor up to 14.5. The people with the latest menarche are the Melanesians of New Guinea, having medians ranging from 15.5 to 18.4 years (Fig. 167). Menarche is delayed by chronic undernutrition. In the poor rural area of 'Appalachia' in the southern United Stated thirty undernourished Euro-American girls followed longitudinally had a mean menarcheal age of 14.4 years against 12.4 in the well-nourished controls (Dreizen, Spirakis & Stone, 1967). They were likewise delayed in skeletal maturation and shorter in height during childhood, though they reached the height of the controls at maturity. ... In the nineteenth century menarche occured on average around 15 years in England and in Norway and Finland at nearly 17 years (Tanner, 1966c). The trend shown in Fig. 168 (a) represents about 0.3 years per decade. There is some evidence that this trend is now stopping...." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 213-217)

"Afro-American girls have menarche some 0.3 years earlier than European-descended girls (12.5 compared to 12.8 years) and in both sexes dental and skeletal development is advanced in Afro-Americans (Garn et al., 1972a,b). Thus, part of their greater height is due to earlier maturation. Figs. 173 and 174 show the weight curves. Whereas Washington and London children are quite similar from 1 year until puberty, birth weights appear to be lower in African descendants when US samples adjusted for income, maternal age, parity and smoking and compared (Penchaszadeh et al., 1972). Hong Kong Chinese are lighter at every age. Thus they are lower in weight-for-height than London and Washington children, who are similar. In summary then, Afro-American children growing up under favorable conditions are a little taller and heavier than Europeans and Euro-Americans living in the same cities. This is partly or wholly because they are a little more advanced in maturity. Asiatics, on the other hand, under equally favourable circumstances are smaller despite being still further advanced in maturity." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 229)

"Brook & Lloyd (1973) and others have shown that obese children and adults have more fat cells than the non-obese, and there is evidence to suggest these are caused to appear by overfeeding i early infancy. Once present, they are never lost." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 244)

"In all populations from which we have data menarche is earlier in chldren from well-off families than in the underprivledged (Fig. 187; see also Table 15). In Newcastle-upon-Tyne (England) median ages of menarche were 13.3 years for girls from professional and managerial families and 13.7 years for girls from unskilled, manual working class families (Miller, Billewicz & Thomson, 1972). Number of children in the family may also affect age of menarche. In Northeast England, at least, the social class influence apparently operates through family size. Girls from larger families had consistently later menarche than those from smaller ones, as in most data, and when this effect was allowed for the differences due to father's occupation disappeared (Roberts, Rozner & Swan, 1971). (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 244-5)

"Rate of maturation is influenced both by heredity and environment. Identical twin sisters growing up together is a good environment differ in age at menarche only by 1 or 2 months; sisters by an average of nearly a year (Tanner, 1962). Poorly-off children, on the other hand, have a later menarche than better-off children in all populations studied. Indeed the first effect of under-nutrition is to slow down growth and postpone the ages of appearance of the various criteria of physical maturity. Not all maturational systems are equally affected however. Dental maturity is less influenced by the postnatal environment than is age of sexual maturation, because the teeth are laid down early in growth and require little interaction with the enviroment later. Thus different measures of maturity measure different things; one population might be advanced in dental age but delayed in bone age, a second population, the reverse." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 199)

Within a particular population final adult height is not related to the speed with which it is reached.; on average, early and late developers end up about the same size. "Even in shape there is only a small difference, late-maturers ending usually as more linear people with low weight-for-height." (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 198)

[from abstract]"The physical and hormonal changes of puberty are presented and the wide range of ages at which the pubertal process may begin is emphasized. The great variability in the timing of onset of adolescence, its rate of progression, and the age of completion are detailed. The causes of delayed adolescence in males and females are considered. The most common form of delayed adolescent development is termed constitutional delay in growth and development, which may occur sporadically, or may be the familial pattern of growth and development or may reflect a suboptimal nutritional environment. The evaluation of such children, including appropriate historical review, physical examination, and laboratory assessment, is outlined. In most patients with constitutional delay in growth and development, strong reassurance is sufficient therapy. In other subjects, treatment with androgens (boys) or estrogens (girls) may be indicated. In patients with primary systemic diseases accociated with delayed maturation, specific treatment which eradicates the illness will often be followed by resumption of growth and development. In subjects with primary disorders of the hypothalamus, pituitary, or gonads, replacement therapy with androgens or estrogens is indicated. If gonadal function is intact, these patients may eventually become fertile with appropriate use of hypothalamic and/or pituitary hormones." (Root AW, Reiter EO (1976) Evaluation and management of the child with delayed pubertal development. Fertil Steril 1976 27(7):745-755)

"The frequent improvement [epilepsy] at puberty suggests that even at this relatively late age hormones affect the areas of abnormal cortex that are the postulated cause of this form of epilepsy." (Geschwind & Galaburda 1987: 204, Cerebral Lateralization)

"Consider, as an example, a female prepubescent mouse left on her own. Eventually, of course, she will reach puberty. But put an adult male into the cage with her and she will reach puberty earlier. This intriguing phenomenon, known as the Vandenbergh effect, is produced by pheromones, odors in the male's urine that cause a behavioral or psysiological response in other animals. These pheromones, when smelled by the female, crank up her ovulatory machinery. The male's urine does this trick even when the male isn't present---just dab a smidgen of male urine on females and, voila, earlier puberty. Moreover, the more male sexual hormones the mouse has in his bloodstream, the more effective he is at accelerating the onset of puberty. Conversely, when a prepubescent female mouse is exposed to a large number of adult females, puberty is delayed---why bother if there are no guys around? Once again the signal is a pheromone, found in the urine of the adult females. Block the young female's sense of smell, and the puberty delay no longer occurs." (Sapolsky 1997: 47, TheTrouble With Testosterone)

"And what were the physiological consequences for these baboons in Utopia? [African boboons eating westerners garbage] First the good news: Young baboons grew faster, reaching developmental landmarks such as puberty at earlier ages. These beneficial changes were exactly what one would expect of humans switching from a lean subsistence diet to a more affluent Westernized fare. In the countries of the West the age of first menstruation has declined from an estimated fifteen years during the 1800's to our current average of about twelve and a half, and diet is thought to have much to do with that. The trend in baboons has been particularly well documented by Jeanne Altmann of the University of Chicago, a biologist studying both foraging and garbage-eating troops in another part in Kenya. Among her animals, eating garbage had led to the onset of puberty at age three and a half instead of age five. Females now typically give birth for the first time at age five, a year and a half earlier than before. (Sapolsky 1997: 130, TheTrouble With Testosterone)

"It could be the case that although growth of the left hemisphere is slowed to a greater extent in lefthanders than in righthanders, it may attain a greater final size in lefthanders. This could occur with the growth period is prolonged---for instance, when pregnancy is longer than average or when puberty is late, which would allow for further development in childhood." (Geschwind & Galaburda 1987: 98, Cerebral Lateralization)

"The primary reason for the lack of size change in the skull and face of the pygmies is probably related to a combination of early growth priority of these structures (especially reflected in those measurements incorporating the skull base: basion-nasion and basion-prosthion), plus the fact that in humans overall skull size is negatively allometric to body size and weight. This is even true of the facial skeleton in humans, so that a marked change in body weight may result in little or no alteration in facial size. Evidence to this effect can be seen in the pubertal growth spurt, during which males become signifacantly larger than females in height and weight, but metric aspects of facial size are still largely indistinguishable (Keen, 1950)" (Shea, B.T. & Gomez, A.M. (1988) Tooth scaling and evolutionary dwarfism: an investigation of allometry in human pygmies. American Journal of Physical Anthropology 77 (1): pp. 129)

From chart in Shea extracted from Eveleth and Tanner. Age of Menarche: Europe 13.3 yrs, Descendants of Europeans abroad 12.9 years, Africa 14.9 years, Descendants of Africans abroad 13.2 years, Near East and India 13.6 years, Asiatics 13.1 years, Pacific Islanders 16.2 years. (Shea, B.T. (1989) Heterochrony in human evolution: the case for neoteny reconsidered. Yearbook of Physical Anthropology 32: pp. 84)

"Although the growth rates of girls and boys are almost identical in infancy and childhood, a noticeable difference occurs at about age ten, when girls start to grow faster than boys, achieving the maximum rate by age twelve and completing their growth by age fifteen. Boys, by contast, do not start their growth spurt until two years later than girls and do not acheive full growth until approximately seventeen to eighteen. Four-fifths of the mean height difference of 10 cm between adult men and women is accounted for by the delayed onset of the growth spurt in boys, which allows them a longer growing time, and only one-fifth by the increased magnitude of that growth. (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 146)

Since maternal investment in the developing fetus is principally in the form of nutrients, it is not surprising that recent research has shown that it is the level of such nutrients stored in the mother's body - fat, in other words - which is critical to fertility. This finding explains why the age of menarche (the point at which a young women begins to menstuate) has dropped progressively with rises in living standards in general and nutrition in particular, from an average of 15.5 years a century ago in the USA to one of 12.6 years today. It also explains why body weight, rather than other indicators such as height, appears to be the critical factor. Body fat increases prior to menarche by a factor of 120 percent and in so doing reaches a critical level of 24 percent by weight at the onset of sexual cycling. However, early sexual cycles tend to be infertile and irregular, and a further increase in body fat proportion to a typical 28 percent is achieved by age eighteen, at which point full fertility is normally achieved. So sensitive is the female body to body weight variations that some women athletes can turn their sexual cycles on and off at will with just a three-pound change in weight. " (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 161)

"In the rural areas of most of these countries the children are smaller and later-maturing than those represented above. (Eveleth, P.B. & Tanner, J.M. (1976) Worldwide Variation in Human Growth: Cambridge Univ. Press, London p. 24)