Seasonal rhythms and secondary sex ratios.
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Biomedical subjects
Publications and source records attributed to P H Jongbloet.
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Current hypotheses do not explain the concerns about sex ratio modulation at conception, birth or during life, and particularly about sex ratio reversal, e.g. at very young or advanced maternal age, during 'anovulatory seasons', among those of low socio-economic status, or induced by specific lifestyles, etc. These modulations are explained by the introduction of the ovopathy concept and inherent preferential fertilization of non-optimally matured oocytes by Y-bearing sperm. Non-optimal development and implantation of male-biased fetuses results in perennial loss of non-optimal, male-biased fetuses before and after birth. Accumulation of conceptopathology in extreme conditions entrains an increasing male to female ratio and ultimately a decreasing one, i.e. an 'inverted dose-response gradient' or 'dose-response fallacy'.
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The cause of the 'borderline personality disorder' of Vincent van Gogh has been discussed in social-psychiatric terms related to so-called 'substitute children', born after the loss of a previous child. A biological-organic genesis, i.e. the very short birth interval of precisely one year between Van Gogh and his older brother appears to be a more plausible explanation. Personality disorders, which are part of the spectrum of schizophrenic disorders, seem to belong to the very broad 'continuum of reproductive casualties' and to be caused by non-optimal maturation of the oocyte during the postpartum restoration of the ovulatory pattern. This continuum occurs during each of the transitional stages of reproductive life in which the maturation of the oocyte is constrained and consists of chromosomal aberrations, (discordant) monozygotic twins, early and late foetal death, preterm births, intrauterine growth retardation, congenital abnormalities, perinatal and neonatal mortality, cot death, growth and mental defects, and finally, chronic or 'constitutional' diseases. Non-optimal maturation of the oocyte appears to be a risk factor for the reproductive casualties stated.
BACKGROUND: Several studies have reported associations between season of birth and reproductive characteristics such as menarcheal age, fecundability, and twinning, but the results are inconsistent with respect to the location of high- and low-risk seasons. To assess whether this disagreement could be due to the use of populations from different geographic areas and time frames instead of different etiologic pathways, we investigated the season-of-birth dependency of a variety of reproductive outcomes within one time- and area-limited population. METHODS: In a historic follow-up study, the reconstituted families of 800 women born between 1873 and 1887 in or near Rotterdam, The Netherlands, were used to determine eight types of reproductive outcome: childlessness, interval to first pregnancy, pregnancy interval, stillbirth, neonatal death, postneonatal death, multiple birth, and gender of offspring. The relation of these outcomes with season of birth was modeled using cosinor functions with periods of 1 year or a half year. Data were analyzed by use of logistic regression or general estimation equations (GEE), dependent on whether outcomes could occur more than once per woman. RESULTS: Peaks in the model-based risks of reproductive failure were found within two small temporal ranges, January 1 to February 11 and July 1 to August 11 for all outcomes except gender. The picture did not change after controlling for known and possible risk factors, including age, offspring's birth cohort, and some social variables. CONCLUSIONS: This study reconfirms the idea that seasonal factors around conception or birth influence later reproductive characteristics. Observing the consistency of the location of high-risk seasons across a variety of outcomes, the explanation of season-of-birth dependency of different reproductive outcomes need not involve multiple etiological pathways.
Finnish investigators [Vartiainen et al. Environmental Chemicals and Changes in Sex Ratio: Analysis Over 250 Years in Finland. Environ Health Perspect 107:813-815 (1999)] presented the sex ratio of all newborn babies from 1751 to 1997 in order to evaluate whether Finnish long-term data are compatible with the hypothesis that the decrease in the ratio of male to female births after World War I and World War II in industrial countries is caused by environmental factors. They found an increase in the proportion of males from 1751 to 1920, which was interrupted by peaks in male births during World War I and World War II and followed by a decrease thereafter, similar to the trends in many other countries. The turning point of male proportion, however, preceded the period of industrialization and introduction of pesticides and hormonal drugs. Thus, a causal association between these environmental exposures and this decrease is unlikely. In addition, none of the various family parameters (e.g., paternal age, maternal age, age difference in parents, birth order) could explain the historical time trends. Vartiainen et al. concluded that at present it is unknown how these historical trends could be mediated. The postwar secular decline of the male:female ratio at birth is not an isolated phenomenon and parallels the decline of perinatal morbidity and mortality, congenital anomalies, and various constitutional diseases. This parallelism indicates a common etiology and may be caused by reduction of conceptopathology, as a correlate to increasing socioeconomic development. An inverted dose response or the dose-response fallacy due to vanishing male conceptuses explains the low sex ratios before World War I and World War II in newborns from black parents and from the lowest socioeconomic classes.
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Seasonality of effective fecundability was investigated in a cohort of 402 women born in or near Rotterdam, The Netherlands, between 1873 and 1887, and married before the age of 40 years. Applying a newly developed method allowing simultaneous control for inherent couple fecundability, numbers at risk of pregnancy, and multiple confounders, we found a trend towards higher fecundability during the first half of June and the first half of December (P = 0.06). Seasonality of effective fecundability appeared to be strongest for women who married at <20 years of age. Potentially important implications for the study of seasonality of adverse reproductive outcome are discussed.
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The relationship between fecundability and month of birth was investigated in a cohort of 1526 women who married between 1802 and 1929, using only women whose first marriage occurred before the age of 35 years. On the basis of their time to pregnancy (TTP, calculated as time between wedding and first birth minus gestational length), women were categorized into two groups: fecunds (TTP up to 12 months or prenuptial conceptions, n = 1348) and subfecunds (TTP >18 months, n = 118). By use of logistic regression, cosinor functions with a period of 1 year or 6 months and variable shift and amplitude were fitted through the monthly odds of subfecunds versus fecunds. The best fitting curve was unimodal, with a zenith in September (P = 0.13 for H0: no differences). Exclusion of childless women (n = 36, minimum follow-up 5 years) from the subfecunds led to a similar curve (P < 0.01), while childless women, as compared with fecunds, showed a birth distribution that was best represented with a bimodal curve with zeniths in January and July (P = 0.06). This study provides evidence for the existence of differences in fecundability by month of birth. The cause of this relationship is unclear, but may lie in a melatonin-dependent circannual variability of the quality of the oocyte.
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