Functional connectivity in the first year of life in infants at-risk for autism: a preliminary near-infrared spectroscopy study Brandon Keehn, Jennifer Wagner, Helen Tager-Flusberg, and Charles A Nelson
Excerpt: Although we are currently unable to determine whether differences in [increased] connectivity at 3- and [statistically insignificant reduced connectivity at] 12-months were driven by infants that will later go on to meet diagnostic criteria for ASD, the results add to a growing body of evidence suggesting that atypical connectivity may be an potential endophenotype for ASD (e.g., Barnea-Goraly et al., 2010).
|Functional and structural connectivity of frontostriatal circuitry in Autism Spectrum Disorder Sonja Delmonte, Louise Gallagher, Erik O’Hanlon, Jane Mc Grath, and Joshua H Balsters|
Excerpt: Frontostriatal circuitry plays an important role in social motivation, which is postulated to underlie deficits in social interaction and communication in Autism Spectrum Disorder (ASD) (Dawson et al., 2005, 2012; Chevallier et al., 2012).
My comment: Functional connectivity is nutrient-dependent and pheromone-controlled via hormone organization and hormone activation linked directly from the sensory environment to behavior. Within minutes of birth, sex differences occur in hormone-dependent functional connectivity, which is primarily influenced by the epigenetic effects of food odors and pheromones on GnRH secretion, and LH, which leads to sex differences in nutrient-dependent pheromone-controlled social behavior throughout life. The link to the sex differences in rates of autism becomes perfectly clear in this excerpt from Exploring the Biological Contributions to Human Health: Does Sex Matter? ( 2001 )
Excerpt: “Within a few minutes after birth, the concentration of LH in serum increases abruptly (about 10-fold) in the peripheral blood of the male newborn but not in that of the female newborn. This short-lived surge in LH release is followed by an increase in the serum testosterone level during the first 3 hours that persists for 12 hours or more. In the female neonate, LH levels do not increase, and FSH levels in both males and females are low in the first few days of neonatal life. After the fall in circulating placental steroid levels, especially estrogens, during the first few days after birth, serum FSH and LH levels increase and exhibit a pulsatile pattern with wide perturbations for several months. The FSH pulse amplitude is greater in female infants, and the FSH response to hypothalamic luteinizing hormone-releasing hormone (LHRH) or gonadotropin-releasing hormone is higher in females than males throughout childhood; LH pulses are higher in males. A sex difference in plasma FSH and LH values is also present in anorchid boys and agonadal girls less than three years old.
The high gonadotropin concentrations in infancy are associated with a transient second wave of differentiation of fetal-type Leydig cells and increased serum testosterone levels in male infants for the first 6 months or so and with elevated estradiol levels intermittently in the first 1 to 2 years of life in females. The mean FSH level is higher in females than males during the first few years of life. By approximately 6 to 8 months of age in the male and 2 to 3 years of age in the female, plasma gonadotropin levels decrease to low values until the onset of puberty.”
In the real world of evolutionary biology the link to sex differences in behavior throughout life would be the obvious sex differences in the response of male infants compared to female infants, since it predicts all other differences in hormone-organized and hormone-activated behavior, which include the differences manifested in the prevalence of autism spectrum disorders (ASDs). If ASDs are considered to be disorders of social interaction and communication, it would make sense to look first for differences in the genetically predisposed innate response that links sensory stimuli to hormone-organized and hormone-activated behaviors associated with attachment. Instead, researchers tend to look at brain imagery associated with visual input and look at oxytocin levels that are so far downstream of their dependence on nutrient-dependent pheromone-controlled GnRH pulse frequency that statistical analyses of results are invariably confounded. Meaningless results are, however, meaningfully interpreted and drug/behavioral interventions are prescribed. You may recall my first question about obvious/ misrepresentations of cause and effect in circumstances such as these. I always ask, “Is there a model for that?” Mutation-driven evolution is not a model of anything!