Health Psychology. Michael Murray
mechanism called the circadian clock’ (Gamble et al., 2014: 466). Recent studies suggest that the circadian clock has been a feature of evolution for at least 2.5 billion years. Disruption of the clock through genetic or environmental means can precipitate disorders, including cardio- metabolic diseases and cancer. Realigning circadian rhythms can be beneficial in the treatment of endocrine-related disorders.
Gender, sexual dimorphism and identity
The biological basis for gender identity, if there is one, is unknown. The basis of biological sex is better understood. A single factor – the steroid hormone testosterone – accounts for most, and perhaps all, of the known sex differences in neural structure (Morris et al., 2004). Testosterone is said to ‘sculpt’ the developing NS by inhibiting or exacerbating cell death and/or by modulating the formation and elimination of synapses. Testosterone masculinizes both the brain and the body, yet experience can interact with testosterone to enhance or diminish its effects on the CNS.
The steps leading to masculinization of the body appear to be consistent across mammals. The Y chromosome contains the sex-determining region of the Y (Sry) gene and induces the undifferentiated gonads to form as testes (rather than as ovaries). The testes secrete hormones to masculinize the rest of the body. Two masculinizing testicular hormones are antimullerian hormone, a protein that suppresses female reproductive tract development, and testosterone, a steroid that promotes the development of the male reproductive tract and masculine external genitalia (Morris et al., 2004). In masculinizing the body, testosterone binds to the androgen receptor protein and then this steroid-receptor complex binds to DNA, promoting differentiation as a male. If the Sry gene is absent (as in females, who receive an X chromosome from the father), the gonad develops as an ovary, and the body, unexposed to testicular hormones, forms a feminine configuration. The genitalia will only respond to testicular hormones during a particular time in development, which constitutes a sensitive period for hormone action: hormonal treatment of females in adulthood is claimed to have negligible effects on genital morphology (Morris et al., 2004).
Contrary to the mainstream hormonal accounts of gender identity, the concept of sexual neutrality at birth, after which infants differentiate as masculine or feminine as a result of social experiences, was proposed by John Money and colleagues (Money and Erhardt, 1972). In the human brain, structural differences have been described that seem to be related to gender identity and sexual orientation (Swaab, 2004). However, the evidence is highly equivocal. Solid evidence for the importance of postnatal social factors in gender identity is lacking. The truth is we simply do not know.
Vitamin D and its deficiency
The importance of the molecule vitamin D has been recognized since its discovery by Edward Mellanby in 1920. The chemical structure of vitamin D was determined in 1932, and it was only then found to be a steroid hormone, more specifically, a secosteroid. Vitamin D normally arises in the skin from sunlight or it can come from food, such as oily fish, or from supplements. It is metabolized in the liver and kidney. Vitamin D metabolites appear to be involved in a host of cellular processes, including calcium homeostasis, immunology, cell differentiation and regulation of gene transcription (Bouillon et al., 1995). Vitamin D is the main hormone regulating calcium phosphate homeostasis and mineral bone metabolism. A variety of tissues can express vitamin D receptor (VDR) and vitamin D is implicated in the regulation of the IS, the cardiovascular system, oncogenesis and cognitive functions (Halfon et al., 2015).
Hormones can act as immunomodulators, altering the sensitivity of the IS. T cells have a symbiotic relationship with vitamin D, by binding to the steroid hormone version of vitamin D, calcitriol, but T cells express the gene CYP27B1, the gene responsible for converting the pre-hormone version of vitamin D, calcidiol, into the steroid hormone version, calcitriol. The decline in hormone levels with age is partially responsible for the weakened immune responses in older people. Conversely, some hormones are regulated by the IS, notably thyroid hormone activity. The age-related decline in immune function is also related to decreasing vitamin D levels in the elderly. As people age, two things happen that negatively affect their vitamin D levels. First, they stay indoors more due to decreased activity levels. This means that they get less sun and therefore produce less vitamin D via solar radiation. Second, as a person ages the skin produces less vitamin D.
Hypovitaminosis D is associated with decreased muscle function and performance and an increase in disability. On the other hand, vitamin D supplementation improves muscle strength and gait, especially in elderly patients. A reduced risk of falls has been attributed to vitamin D supplementation due to direct effects on muscle cells. Finally, a low vitamin D status is associated with a frail phenotype. Many authorities recommend vitamin D supplementation for frail patients.
Vitamin D deficiency is a factor in a variety of illnesses. Pereira-Santos et al. (2015) found that the prevalence of vitamin D deficiency was 35% higher in obese people and 24% higher in overweight people. Vitamin D deficiency was associated with obesity irrespective of age, latitude, cut-offs to define vitamin D deficiency and the Human Development Index of the study location. Altered vitamin D and calcium homeostasis are also associated with the development of Type 2 diabetes mellitus. Pittas et al. (2007) reviewed observational studies and clinical trials in adults with outcomes related to glucose homeostasis. Observational studies showed an association between low vitamin D status, calcium or dairy intake and prevalent Type 2 diabetes mellitus or metabolic syndrome. There are inverse associations with the incidence of Type 2 diabetes mellitus or metabolic syndrome. Trials with vitamin D and/or calcium supplementation suggest that combined vitamin D and calcium supplementation may have a preventive role for Type 2 diabetes mellitus only in populations at high risk (i.e., those with glucose intolerance).
Microbiome research
The new field of microbiome research studies the microbes within the gut and the effects of these microbes on the host’s well-being. Microbes influence metabolism, immunity and behaviour. One mechanism appears to involve hormones because specific changes in hormone levels correlate with the presence of the gut microbiota. The microbiota produce and secrete hormones, respond to host hormones and regulate expression levels of host hormones (Neuman et al., 2015). Increasing evidence links both hormones and the microbiome to immune responses under both healthy conditions and autoimmune disease. There are many interconnections and the microbiome and hormones may work through shared pathways to affect the immune response (Neuman et al., 2015).
Organisms within the gut play a role in the early programming and later responsivity of the stress system. The gut is inhabited by 1013–1014 micro-organisms, which is ten times the number of cells in the human body, and contains 150 times as many genes as our genome (Dinan and Cryan, 2012) or, according to Verdino (2017), 360 times. When pathogens such as Escherichia coli enter the gut, the HPA can be activated. Stress can induce an increased permeability of the gut, allowing bacteria and bacterial antigens to cross the epithelial barrier and activate a mucosal immune response, which in turn alters the composition of the microbiome and leads to an enhanced HPA drive. Research indicates that patients with irritable bowel syndrome and major depression show alterations of the HPA which are induced by increased gut permeability. In the case of irritable bowel syndrome, the increased permeability can respond to probiotic therapy. The gut microbiota play a role in regulating the HPA. In a double-blind, placebo-controlled trial, participants were given a fruit bar that contained either the probiotic formula or a similarly tasting placebo bar for 30 days (Messaoudi et al., 2011). The experimental fruit bar group reported significantly lower levels of anxiety, anger, depression and somatization, on a number of self-report measures. Lower levels of cortisol were also evident in the fruit bar condition compared to the control group. Verdino (2017) cautiously concludes his review of the growing connection between gut health and emotional well-being as follows: “… it is crucial not to oversimplify the idea that nutritional intervention and a healthy gut will be the panacea for profound psychological difficulties. Severe mood and paralyzing anxiety disorders are not going to be cured with probiotic yogurt and prebiotic fiber, alone” (Verdino, 2017: 4).
The immune and neuroendocrine