Menarche Drops again

The following article is a 2008 study in Taiwan on 214 post-adolescent girls from central Taiwan and their birth mothers and grandmothers.

CONCLUSION: The results showed a significant decrease in the onset age of menstruation over three generations, with a positive effect on age at menarche from mothers to daughters and from grandmothers to granddaughters. (This is 10 years after I wrote Buried Alive). This is from the Annals of Human Biology:

Age at menarche of three-generation families in Taiwan. Chang SR, Chen KH

Unique Identifier 18654871
Authors Chang SR. Chen KH.
Authors Full Name Chang, Shiow-Ru. Chen, Kuang-Ho.

Institution School of Nursing, National Taiwan University College of Medicine, Taipei, Taiwan.

Title Age at menarche of three-generation families in Taiwan.

Source Annals of Human Biology. 35(4):394-405, 2008 Jul-Aug.

Abstract BACKGROUND: Menarche is a critical transition and biological event for women. Age at menarche is an important variable for women's health and appears to be decreasing from generation to generation. AIM: This study describes the distributions of recalled age at menarche of women in three-generation families, examines generational differences, and evaluates the effects of birth mothers' and birth grandmothers' recalled age at menarche on their daughters. SUBJECTS AND METHODS: This cross-sectional investigation was performed on 214 post-adolescent girls from central Taiwan and their birth mothers and grandmothers. The descriptive analysis, analyses of mixed effect models, and multiple linear regression analyses were employed to examine the relationships of age at menarche for three generations within families. RESULTS: The distribution of age at menarche moved significantly earlier over the three generations. The mean ages at menarche were 15.16 +/- 1.75, 14.50 +/- 1.50, and 13.00 +/- 1.26 years for grandmothers, mothers, and daughters, respectively. Four factors for the daughters' age at menarche (adjusted for age at the time of the study and geographical location) were identified. The first three were reinforcing effects. These were the product of the mothers' and grandmothers' ages at menarche, the product of the mothers' geographical locations and ages at menarche, and the product of the grandmothers' ethnicity and ages at menarche. The fourth factor was the grandmothers' ethnicity. CONCLUSION: The results showed a significant decrease in the onset age of menstruation over three generations, with a positive effect on age at menarche from mothers to daughters and from grandmothers to granddaughters.

Genetic and environmental influences on pubertal timing assessed by height growth.

Wehkalampi K, Silventoinen K, Kaprio J, Dick DM, Rose RJ, Pulkkinen L, Dunkel L

Unique Identifier 18293372 Status MEDLINE Authors Wehkalampi K. Silventoinen K. Kaprio J. Dick DM. Rose RJ. Pulkkinen L. Dunkel L. Authors Full Name Wehkalampi, Karoliina. Silventoinen, Karri. Kaprio, Jaakko. Dick, Danielle M. Rose, Richard J. Pulkkinen, Lea. Dunkel, Leo. Institution Hospital for Children and Adolescents, Helsinki University Hospital, 00290 Helsinki, Finland.

Title Genetic and environmental influences on pubertal timing assessed by height growth. Source American Journal of Human Biology. 20(4):417-23, 2008 Jul-Aug.

Abstract Secular trends towards earlier puberty, possibly caused by new environmental triggers, provide a basis for periodic evaluation of the influence and interaction of genetic and environmental effects on pubertal timing. In such studies, a practical marker that reflects timing of puberty in both genders needs to be used. We investigated genetic and environmental influences on pubertal timing by using change in the relative height between early and late adolescence (HD:SDS, height difference in standard deviations) as a new marker of pubertal timing. HD:SDS correlated well with age at peak height velocity in a population of men and women with longitudinal growth data. In 2,309 twin girls and 1,828 twin boys, HD:SDS was calculated between height SDs at age 11.5 and 17.5, and 14.0 and 17.5 years, respectively. Quantitative genetic models for twin data were fitted to estimate the genetic contribution to HD:SDS. We also investigated whether the same genetic factors influenced individual differences between HD:SDS and development of secondary sex characteristics prospectively collected by pubertal development scale (PDS). Genetic effects contributed to 86 and 82% of the variance in HD:SDS in girls and boys, respectively, when using the same model including additive genetic and specific environmental factors. In girls, 30% and in boys, 49% of the genetic factors affecting PDS and HD:SDS were the same. Future comparison of the results of periodic evaluations allows estimation of possible changes in the effects of environment on timing of puberty. In such studies, HD:SDS can be used as a practical marker of pubertal timing

Genetic control of pubertal timing.

Kaminski BA, Palmert MR

Unique Identifier 18622205 Status MEDLINE

Authors Kaminski BA. Palmert MR. Authors Full Name Kaminski, Beth A. Palmert, Mark R. Institution Division of Pediatric Endocrinology, Rainbow Babies and Children's Hospital, Case Western Reserve University, Cleveland, Ohio, USA. Title Genetic control of pubertal timing. [Review] [85 refs] Source Current Opinion in Pediatrics. 20(4):458-64, 2008 Aug.

Local Messages MMH 4,6- Abstract PURPOSE OF REVIEW: Puberty is an important developmental and life stage that leads to sexual maturation and reproductive capability. Although the physiology of puberty is similar among individuals, the timing of puberty is quite variable and affected by environmental and genetic influences. Identification of the responsible genetic factors will greatly enhance the understanding of the key components and the modulation of the hypothalamic-pituitary-gonadal axis. RECENT FINDINGS: Genetic analyses are increasingly elucidating the genetic basis of pathological abnormalities in pubertal timing, including causes of idiopathic hypogonadotropic hypogonadism and Kallmann syndrome. Ongoing studies are also investigating the genetic control of puberty in the general population, although no definitive association between genetic variants and variations in pubertal timing has been discovered so far. SUMMARY: This review summarizes recent advances regarding the genetic control of pubertal timing and presents areas for future investigation. [References: 85]

Endocrinology and metabolism.

Root AW

Unique Identifier 18622202 Status MEDLINE Authors Root AW. Authors Full Name Root, Allen W. Title Endocrinology and metabolism. Source Current Opinion in Pediatrics. 20(4):446-7, 2008 Aug. Local Messages MMH 4,6- Publication Type Editorial. Introductory Journal Article.

Pubertal development and menarche.

DiVall SA, Radovick S

Unique Identifier 18574204 Status MEDLINE Authors DiVall SA. Radovick S. Authors Full Name DiVall, Sara A. Radovick, Sally. Institution Division of Endocrinology, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.

Title Pubertal development and menarche. [Review] [88 refs]

Source Annals of the New York Academy of Sciences. 1135:19-28, 2008.

Abstract Puberty is the developmental process that culminates in reproductive capability and is the result of a complex series of molecular and physiological events. The release of gonadotropin-releasing hormone from specialized neurons of the hypothalamus begins the hormonal cascade that causes gonadal activation and the physical changes of puberty. Several factors have been proposed to influence the activation of the hypothalamus to trigger puberty, but the involved pathways have not been fully elucidated. The recent observations that the age of pubertal onset may be lowering in American girls calls attention to the lack of knowledge of modulating factors that affect the pubertal process. Genes necessary for puberty have been found by studying persons who do not achieve puberty; such studies have provided insights into the pathways necessary for pubertal development. A multidisciplinary focus is required to elucidate the complex mechanisms involved in the initiation and progression of puberty. [References: 88]

Multifactorial inheritance, rates of maturation and psychiatry's taxonomic dilemma: on Saugstad's "radical proposition" for two extremes of brain function and structure.

deVries MW

Unique Identifier 18516513 Status MEDLINE Authors deVries MW. Authors Full Name deVries, Marten W. Institution Center for Public Mental Health Dept. Psychiatrie en Neuropsychologie, University of Maastricht, Post Bus 616, 6200 MD, Maastricht, The Netherlands Title Multifactorial inheritance, rates of maturation and psychiatry's taxonomic dilemma: on Saugstad's "radical proposition" for two extremes of brain function and structure. [Review] [9 refs] Source European Archives of Psychiatry & Clinical Neuroscience. 258 Suppl 2:25-8, 2008 Jun. Abstract This paper reviews aspects of Letten F. Saugstad's Maturation Theory in relation to the Kraepelinian dichotomy and psychiatric classification. The maturation theory is based on existing neuroscience, cross-national and mental health case register data and offers an innovative alternative to current etiological formulations. The maturational theory holds (1) that manic depressive illness relates to early maturation and (2) the schizophrenic syndrome relates to late maturation. The foundation of these processes lies in cerebral pruning of excitatory synapses particularly at puberty but also at a number of earlier crucial periods in development. The process of synaptic pruning has by puberty eliminated some 40% of the synapses, leading to the disappearance of glutematergic excitatory synapses without apparently appreciably influencing inhibitory GABAergic neurons. As a consequence, early maturation is related to the manic-depressive syndrome and characterized by increased neural excitability. Conversely, late maturation is related to schizophrenia characterized by diminished neural activity. Saugstad demonstrates using cross-national and neuroscience studies the multifactoral and environmental influences on rates of maturation and thereby mental illness. Using these data Saugstad reasons her agreement with the Kraepelinian dichotomy based on the existence of two extremes in brain structure and function developed through interactions between the person and the environment. [References: 9] Publication Type Journal Article. Research Support, Non-U.S. Gov't. Review

Normal och avvikande pubertet hos pojkar. [Normal and deviating puberty in boys].

Hagenas L

Unique Identifier 18511972 Status MEDLINE Authors Hagenas L. Authors Full Name Hagenas, Lars. Institution Barnendokrinologiska Enheten, Astrid Lindgrens Barnklinik, Karolinska Sjukhuset, S-171 76 Stockholm. Title [Normal and deviating puberty in boys]. [Review] [15 refs] [Norwegian] Source Tidsskrift for Den Norske Laegeforening. 128(11):1284-8, 2008 May 29. Abstract BACKGROUND: Onset of puberty in boys is more complex than in girls, and delayed onset is the most common puberty complication in boys. This article presents the physiology of normal development of male puberty and the background for commonly associated disturbances. MATERIAL AND METHOD: The article builds on clinical experience and relevant publications within pediatric endocrinology. RESULTS AND INTERPRETATION: Mechanisms involved in pubertal development of gonads remain unclear despite intensive research. Height growth as well as the age for onset of puberty are influenced by environmental factors. Genetic factors are however more important determinants within a defined population and one usually inherits the probability for both early and delayed puberty. Gonadotropin releasing hormone (GnRH) neurons in the hypothalamus secrete GnRH in intermittent pulses to the pituitary glands that respond with pulsatile LH and FSH production. These neurons are thus decisive for testicle activity and therefore puberty development. GnRH-neurons are inactive during childhood because many types of hypothalamic neurons suppress them. Puberty starts when this suppression is reduced and kisspeptin-producing neurons stimulate GnRH neuron activity. At a testicle volume of 4 mL the Leydig cells' testosterone production has reached such a level that pubertal changes become apparent. Delayed or incomplete puberty sometimes occurs in certain syndromes, and complete lack of puberty can also be syndrome-related. Klinefelter's syndrome is associated with gonad dysgenesis expressed as gradual reduction of gonadal function starting after puberty. Cancer treatment during childhood; especially radiation therapy of the gonads, may cause hypogonadism and infertility. It is therefore essential to follow gonad function closely in these patients. In conclusion, each doctor treating children should be able to evaluate the degree of puberty development and when needed request adequate laboratory tests. [References: 15] Publication Type English Abstract. Journal Article. Review.

Juvenility in the context of life history theory.

Hochberg Z

Unique Identifier 18337281 Status MEDLINE Authors Hochberg Z. Authors Full Name Hochberg, Z. Institution Meyer Children's Hospital, Rambam Medical Center and Technion-Israel Institute of Technology, Haifa, Israel. Title Juvenility in the context of life history theory. Source Archives of Disease in Childhood. 93(6):534-9, 2008 Jun. Local Messages MMH 55- 1980-, OLH 46-67 Abstract Homo sapiens is unique in having four prolonged and pronounced postnatal pre-adult life history stages: infancy, which lasts for 30-36 months and ends with weaning from breast feeding in traditional societies; childhood, which lasts for an additional 2-4 years and concludes in a degree of independence as regards protection and food provision; a juvenile stage of 3-4 years that terminates with readiness for sexual maturation; and adolescence, which lasts for 3-5 years and culminates in fertility. Juvenility implies two transitional periods which are only experienced by humans: a transition from childhood to juvenility and from juvenility to adolescence. Juvenility, "the age of reason and responsibility" and concrete operation, coincides with elementary school age and offers opportunities to prepare for the social complexity of adolescence. Here I define the transition to juvenility by three variables: adrenarche (the onset of adrenal androgen generation), growth pattern (decelerating from a linear childhood growth velocity) and adiposity rebound acceleration of body mass index. The data presented suggest that this period is endowed with programming/predictive adaptive responses of body composition to the environment. Publication Type Journal Article.

A digenic combination of polymorphisms within ESR1 and ESR2 genes are associated with age at menarche in the Spanish population.

Mendoza N, Moron FJ, Quereda F, Vazquez F, Rivero MC, Martinez-Astorquiza T, Real LM, Sanchez-Borrego R, Gonzalez-Perez A, Ruiz A

Unique Identifier 18421025 Status MEDLINE Authors Mendoza N. Moron FJ. Quereda F. Vazquez F. Rivero MC. Martinez-Astorquiza T. Real LM. Sanchez-Borrego R. Gonzalez-Perez A. Ruiz A. Authors Full Name Mendoza, Nicolas. Moron, Francisco Jesus. Quereda, Francisco. Vazquez, Francisco. Rivero, Mari C. Martinez-Astorquiza, Txanton. Real, Luis M. Sanchez-Borrego, Rafael. Gonzalez-Perez, Antonio. Ruiz, Agustin. Institution Servicio de Ginecologia y Obstetricia, Hospital Universitario Virgen de las Nieves, Granada, Spain. Title A digenic combination of polymorphisms within ESR1 and ESR2 genes are associated with age at menarche in the Spanish population. Source Reproductive Sciences. 15(3):305-11, 2008 Apr. Abstract In the present study, the authors look at an association of genetic variants within estrogen synthesis and signaling pathways and age at menarche (AAM) in Spanish women. They analyzed 9 polymorphisms in 6 different genes in 714 well-characterized postmenopausal women from Spain. They performed a quantitative trait locus study of these markers individually or in digenic combinations in relation to AAM. None of the studied markers, with the exception of the follicle-stimulating hormone receptor (P = .013), were significantly associated with AAM in the Spanish population, and no marker demonstrated an association of statistical significance after multiple testing corrections (P > .0055). In contrast, linear regression analysis suggests epistatic interactions including ESR1 and ESR2 loci in relation to AAM in the series (P = .003). The results suggest that epistatic interactions of ESR1 and ESR2 alleles could be associated with advancing AAM among Spanish women. Publication Type Journal Article. Multicenter Study. Research Support, Non-U.S. Gov't

Chromosomal regions 22q13 and 3p25 may harbor quantitative trait loci influencing both age at menarche and bone mineral density.

Pan F, Xiao P, Guo Y, Liu YJ, Deng HY, Recker RR, Deng HW

Unique Identifier 18379822 Status MEDLINE Authors Pan F. Xiao P. Guo Y. Liu YJ. Deng HY. Recker RR. Deng HW. Authors Full Name Pan, Feng. Xiao, Peng. Guo, Yan. Liu, Yong-Jun. Deng, Hong-Yi. Recker, Robert R. Deng, Hong-Wen. Institution The Key Laboratory of Biomedical Information Engineering of Ministry of Education, and Institute of Molecular Genetics, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, People's Republic of China. Title Chromosomal regions 22q13 and 3p25 may harbor quantitative trait loci influencing both age at menarche and bone mineral density. Source Human Genetics. 123(4):419-27, 2008 May. Abstract Late age at menarche (AAM), an important type of endocrinopathy in females, is associated with lower bone mineral density (BMD), a major risk factor for osteoporosis. The correlation is mainly mediated through common genetic factors, which are largely unknown. A bivariate genome-wide linkage scan was conducted on 2,522 females from 414 Caucasian pedigrees to identify quantitative trait loci influencing both AAM and BMD. The strongest linkage signal was detected on chromosome 22q13. Other regions such as the 3q13, 3p25, 7p15, and 15q13 were also suggested. The inferred promising candidate genes in the linkage regions may contribute to our understanding of pathogenesis of endocrinopathy and osteoporosis in females. Publication Type Journal Article. Research Support, N.I.H., Extramural. Research Support, Non-U.S. Gov't. main page