208 Autism and Exposure to Environmental Chemicals
involved in the occurrence of gender differences in anxiety. Estrogen replace
ment has repeatedly been shown to increase mood and decrease anxiety in
postmenopausal women. Other studies indicate that testosterone also plays
a critical role in the regulation of anxiety in humans. Chemical castration
through androgen blockade therapy in men with prostate cancer was corre
lated with an increase in anxiety. When treatment ceased, anxiety levels
decreased.
Androgens play a critical role in the regulation of the hypothalamic–
pituitary–adrenal (HPA) axis, with administration of testosterone reducing
the rise of stress hormones [adrenocorticotropic hormone (ACTH) and corti
costerone] following exposure to a stressful situation (Figures 7.7–7.9).
Increased HPA axis activation is often correlated with increased anxiety, which
suggests that androgens may regulate the display of anxiety‐related behavior
by depressing HPA axis activation.Play Fighting and Aggression
Play fighting includes two major components (playful attack and playful
defense) and is a common juvenile behavior in many mammalian species
that appears to be regulated by sex hormones. In rodents, play fighting peaks
30–40 days after birth, and occurs more frequently in males than females. Play
fighting is decreased in male rodents castrated at birth and its frequency begins
to decline at the onset of puberty.
In summary, it is reasonable to conclude that testosterone and its receptors,
ARs, normally contribute to masculinization and engineering of male brain
morphology and behavior.Adverse Effects of EDCs and Their Mechanisms of Action
It will require many books to provide analyses of the adverse effects of EDCs.
However, in Figure 7.13 we have summarized some of the adverse effects of
EDCs. In Table 7.1 we have further depicted the known mode of action of EDCs.
The effects are varied and not entirely clear. Recent research indicates that cer
tain EDCs may cause epigenetic changes (heritable changes in gene expression
that are not due to mutations in the genes); we have already discussed (Chapter 6)
the definition and the mechanisms of epigenetic changes that may last for gen
erations (transgenerational effects) across numerous organ systems [121–125].
Studies consistently show that some EDCs impair key processes in ovarian
development in animal models, adversely affect the structure and function of
the postnatal ovary by inhibiting follicle growth and/or increasing programmed
cell death (apoptosis) in animal models, and disrupt steroid hormone levels in
animals and women.