Stress & Infertility
Stress is commonly defined as a state of real or perceived threat to homeostasis (self-regulation) that may challenge an organisms well-being. In order to restore homeostatic conditions, we activate a complex range of responses involving the endocrine, nervous and immune system, collectively know as the stress response. Hans Selye developed valuable insights into the role of stress in disease. According to Seyle, stress in itself should not be viewed in a negative context, we all need stress to stimulate and develop ourselves. It is not the stressor that determines the response, instead it is the individual’s internal reaction, which then triggers the response. This internal reaction is highly individualised. What one person may experience as stress, the next person may view entirely differently. Stress arises as a maladaptation response to stressors.
So how does stress affect fertility?
The hypothalamic-pituitary-adrenal (HPA) axis, comprised of the hypothalamus, pituitary gland, and adrenal glands, regulates the body’s adaptive response to stress. Activation of the HPA axis, put very simply, causes the anterior pituitary gland (an organ in the body that starts our hormone cascade) to produce and secrete cortisol (our stress hormone) from the adrenals. Secretion of ACTH (a stress hormone) from our adrenal glands is a classic response to stress. This reallocation of resources during the stress response suppresses the reproductive axis, which gives priority to survival rather than reproduction. In addition, high levels of cortisol inhibit our HPA axis from mediating the function of the hypothalamic-adrenal-gonadal (HPG) axis, which is responsible for the maturation of the reproductive organs and our reproductive competence, shutting down the one system that allows us to reproduce. Various stressors include but are not limited to infection, malnutrition, anxiety and depression.
Stress hormones act directly at the level of the testis or ovaries through inhibition of steroid hormone production (the hormones we need to start the reproductive process. Studies have also found that stress hormones can block oestrogen induced uterine growth and differentiation, as well as embryo implantation in rats. A 2013 study found that ‘stress provokes an elevation in glucocorticoid concentration which precedes a decline in testosterone concentration in the male… severe stress is associated with decreased sperm concentration’. Stress affects reproductive function from a male perspective, as well as female.
Additionally, stress will likely exacerbate conditions that likely contribute to an infertile picture. For instance, hypothyroidism, a common but under diagnosed condition that means the thyroid is under-active and making insufficient amounts of thyroid hormones, can be suppressed further. Cortisol production can inhibit secretion of TSH (thyroid stimulating hormone) making it much harder for the body to make sufficient hormones in order to support the HPG axis in initiating conception. Most importantly, during the few months of pregnancy, the foetus relies on the mother for thyroid hormones. Thyroid hormones are important in normal brain development and growth of the foetus. Hypothyroidism in the mother can have long-lasting effects on the foetus.
What about stress in pregnancy?
As a practitioner, I like to work with clients to adapt healthier dietary and lifestyle habits that support not only their fertility journey, but parenthood too. Stress regulation is one of those habits I like to support, especially BEFORE having a newborn baby! But what does stress actually do to a pregnant body and does it have an impact on the foetus? Throughout the second and third trimesters of pregnancy, the placenta secretes substantial amounts of CRH (corticotrophin-releasing hormone = a stress hormone). It is hypothesised that the increasing levels of this stress hormone may serve as a ‘placental clock’ – a mechanism that is responsible for the duration of gestation and the onset of a pro-contraction trait to initiate labour (I know – mental!). Elevated CRH levels in the blood on top of the CRH produced in the placenta can stimulate a pathway in the pituitary gland to increase stress hormones resulting in preterm labour. Preterm labour is the leading cause of infant mortality and morbidity, despite substantial resources devoted to reducing the rate of prematurity. Although preterm birth can be multifactorial, maternal stress has been identified as a potential causal factor. Another study found that ‘Women experiencing high levels of psychosocial stress during pregnancy are at significantly increased risk for shortened gestation and preterm delivery’. Although cortisol levels rise naturally towards the end of pregnancy, stress-induced levels of cortisol may inappropriately stimulate the signalling mechanisms contributing to initiation of labour and therefore result in preterm birth.
Does stress have an impact on your future baby?
A 2017 study found that ‘Maternal stress in pregnancy can shape childhood outcomes in a range of developmental domains including temperament, cognition, language skills, and motor functioning. High levels of maternal pregnancy-specific anxiety was associated with increased negative temperament in children. Exposure to elevated concentrations of cortisol early in gestation has also been associated with a slower rate of development over the first postnatal year…’ Additionally, there have been studies that show prenatal maternal stress can differently affect outcomes for each sex beyond the neonatal period. Females, but not males, exposed to elevated levels of maternal cortisol early in pregnancy had a significantly enlarged amygdala (associated with memory formation and processing of emotions and memories associated with fear) and increased levels of anxiety in childhood, which persisted into preadolescence. Another study found that ‘the foetal environment can also influence susceptibility in offspring to later conditions… aetiology of such symptoms suggests that programming of the HPA axis in utero is linked to development of insulin resistance, diabetes and cardiovascular disease in adulthood.’
Whilst it seems that there are many stressors that can have a negative affect on reproductive function, many of these are modifiable lifestyle factors that can be addressed. Blood sugar balancing and nutritious well balanced meals also play a huge part in the stress and HPA axis response as well as microbiome health (gut, oral, vaginal and seminal)!
References
Joseph, DN & Whirledge, S. (2017). ‘Stress and the HPA Axis: Balancing Homeostasis and Fertility’
Whirledge S. & Cidlowski, JA. (2013). ‘Glucocorticoids, Stress and Fertility’
