Alcohol and cortisol

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Alcohol and cortisol have a complex relationship. While cortisol is a stress hormone, alcoholism can lead to increased cortisol levels in the body over time. This can be problematic because cortisol can temporarily shut down other bodily functions, potentially causing physical damage.

Contents

Cortisol

Cortisol is a stress hormone secreted by the adrenal gland, which makes up part of the hypothalamic-pituitary-adrenal (HPA) axis. It is typically released at periods of high stress designed to help the individual cope with stressful situations. [1] Cortisol secretion results in increased heart rate and blood pressure and the temporary shut down of metabolic processes such as digestion, reproduction, growth, and immunity as a means of conserving energy for the stress response. Chronic release of cortisol over extended periods of time caused by long-term high stress can result in:

Alcohol and cortisol interactions

High cortisol levels have largely been associated with high alcohol consumption, which is likely due to the disregulation (impaired inhibitory control) of the HPA axis. [1]

History

Research on alcohol's effects on cortisol dates back to the 1950s. Many studies showed a relation between the two; however, they were limited to short-term alcohol ingestion. The first human study to assess the long-term effects of alcohol ingestion on cortisol was conducted in 1966 (Mendelson et al.). They found heightened cortisol levels in both alcoholics and non-alcoholics while actively drinking. Cortisol was overall higher in alcoholics than non-alcoholics, indicating that alcohol has long-term effects on the endocrine system. Also, alcoholics had the highest cortisol levels after drinking stopped, demonstrating symptoms of withdrawal (a hormonal marker of alcohol addiction). [3]

Recent findings

Recent research supports this strong association between high alcohol use and heightened cortisol levels. In one study, overnight urinary cortisol levels were taken from people who regularly drank a large amount of alcohol versus a small amount of alcohol. People who drank more alcohol had higher cortisol levels and lower heart rate variability (which is controlled by the autonomic nervous system, ANS), suggesting a connection between the HPA axis and the ANS. People who drank more alcohol had higher blood pressure and difficulty sleeping, indicative of heightened cortisol levels. [4]

Recent technology has allowed researchers to measure cortisol levels in human hair (showing cumulative cortisol exposure over extended periods of time). This method of measurement has been used to compare long-term cortisol levels in alcoholics, abstinent alcoholics, and non-alcoholics. One recent study revealed that alcoholics had three to four times higher hair cortisol concentrations than abstinent alcoholics or non-alcoholics (consistent with previous research showing periods of alcohol consumption are associated with heightened cortisol levels). Abstinent alcoholics and non-alcoholics had the same low levels of cortisol, suggesting that cortisol levels eventually return to normal after extended cessation. [5]

Related Research Articles

<span class="mw-page-title-main">Adrenal gland</span> Endocrine gland

The adrenal glands are endocrine glands that produce a variety of hormones including adrenaline and the steroids aldosterone and cortisol. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The adrenal cortex itself is divided into three main zones: the zona glomerulosa, the zona fasciculata and the zona reticularis.

<span class="mw-page-title-main">Stress (biology)</span> Organisms response to a stressor such as an environmental condition or a stimulus

Stress, whether physiological, biological or psychological, is an organism's response to a stressor such as an environmental condition. When stressed by stimuli that alter an organism's environment, multiple systems respond across the body. In humans and most mammals, the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis are the two major systems that respond to stress. Two well-known hormones that humans produce during stressful situations are adrenaline and cortisol.

<span class="mw-page-title-main">Corticotropin-releasing hormone</span> Mammalian protein found in humans

Corticotropin-releasing hormone (CRH) is a peptide hormone involved in stress responses. It is a releasing hormone that belongs to corticotropin-releasing factor family. In humans, it is encoded by the CRH gene. Its main function is the stimulation of the pituitary synthesis of adrenocorticotropic hormone (ACTH), as part of the hypothalamic–pituitary–adrenal axis.

<span class="mw-page-title-main">Hypothalamic–pituitary–adrenal axis</span> Set of physiological feedback interactions

The hypothalamic–pituitary–adrenal axis is a complex set of direct influences and feedback interactions among three components: the hypothalamus, the pituitary gland, and the adrenal glands. These organs and their interactions constitute the HPA axis.

<span class="mw-page-title-main">Anterior pituitary</span> Anterior lobe of the pituitary gland

A major organ of the endocrine system, the anterior pituitary is the glandular, anterior lobe that together with the posterior lobe makes up the pituitary gland (hypophysis) which, in humans, is located at the base of the brain, protruding off the bottom of the hypothalamus.

<span class="mw-page-title-main">Cortisol</span> Human natural glucocorticoid hormone

Cortisol is a steroid hormone, in the glucocorticoid class of hormones and a stress hormone. When used as a medication, it is known as hydrocortisone.

<span class="mw-page-title-main">Adrenal insufficiency</span> Medical condition

Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones. The adrenal glands—also referred to as the adrenal cortex—normally secrete glucocorticoids, mineralocorticoids, and androgens. These hormones are important in regulating blood pressure, electrolytes, and metabolism as a whole. Deficiency of these hormones leads to symptoms ranging from abdominal pain, vomiting, muscle weakness and fatigue, low blood pressure, depression, mood and personality changes to organ failure and shock. Adrenal crisis may occur if a person having adrenal insufficiency experiences stresses, such as an accident, injury, surgery, or severe infection; this is a life-threatening medical condition resulting from severe deficiency of cortisol in the body. Death may quickly follow.

Corticotropes are basophilic cells in the anterior pituitary that produce pro-opiomelanocortin (POMC) which undergoes cleavage to adrenocorticotropin (ACTH), β-lipotropin (β-LPH), and melanocyte-stimulating hormone (MSH). These cells are stimulated by corticotropin releasing hormone (CRH) and make up 15–20% of the cells in the anterior pituitary. The release of ACTH from the corticotropic cells is controlled by CRH, which is formed in the cell bodies of parvocellular neurosecretory cells within the paraventricular nucleus of the hypothalamus and passes to the corticotropes in the anterior pituitary via the hypophyseal portal system. Adrenocorticotropin hormone stimulates the adrenal cortex to release glucocorticoids and plays an important role in the stress response.

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A Corticotropin-releasing hormone antagonist is a specific type of receptor antagonist that blocks the receptor sites for corticotropin-releasing hormone, also known as corticotropin-releasing factor (CRF), which synchronizes the behavioral, endocrine, autonomic, and immune responses to stress by controlling the hypothalamic-pituitary-adrenal axis. CRH antagonists thereby block the consequent secretions of ACTH and cortisol due to stress, among other effects.

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<span class="mw-page-title-main">Cortisol awakening response</span> Physiological response

The cortisol awakening response (CAR) is an increase between 38% and 75% in cortisol levels peaking 30–45 minutes after awakening in the morning in some people. This rise is superimposed upon the late-night rise in cortisol which occurs before awakening. While its purpose is uncertain, it may be linked to the hippocampus' preparation of the hypothalamic-pituitary-adrenal axis (HPA) in order to face anticipated stress.

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Glucocorticoid deficiency is a condition where the body doesn’t produce enough glucocorticoid hormones.

Maternal fetal stress transfer is a physiological phenomenon in which psychosocial stress experienced by a mother during her pregnancy can be transferred to the fetus. Psychosocial stress describes the brain's physiological response to perceived social threat. Because of a link in blood supply between a mother and fetus, it has been found that stress can leave lasting effects on a developing fetus, even before a child is born. According to recent studies, these effects are mainly the result of two particular stress biomarkers circulating in the maternal blood supply: cortisol and catecholamines.

Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These changes can lead to transgenerational stress inheritance.

Fetal programming, also known as prenatal programming, is the theory that environmental cues experienced during fetal development play a seminal role in determining health trajectories across the lifespan.

Opioid-induced endocrinopathy (OIE) is a complication of chronic opioid treatment. It is a common name for all hypothalamo-pituitary axis disorders, which can be observed mostly after long term use of opioids, both as a treatment and as a substance of abuse.

In social psychology, social buffering is a phenomenon where social connections can alleviate negative consequences of stressful events.

References

  1. 1 2 Dai, Xing; Thavundayil, Joseph; Santella, Sandra; Gianoulakis, Christina (2007). "Response of the HPA-axis to alcohol and stress as a function of alcohol dependence and family history of alcoholism". Psychoneuroendocrinology. 32 (3): 293–305. doi:10.1016/j.psyneuen.2007.01.004. PMID   17349749. S2CID   39315868.
  2. ↑ Lupien, Sonia J.; McEwen, Bruce S.; Gunnar, Megan R.; Heim, Christine (2009). "Effects of stress throughout the lifespan on the brain, behaviour and cognition". Nature Reviews Neuroscience. 10 (6): 434–45. doi:10.1038/nrn2639. PMID   19401723. S2CID   205504945.
  3. ↑ Mendelson, Jack; Stein, Stefan (1966). "Serum Cortisol Levels in Alcoholic and Nonalcoholic Subjects During Experimentally Induced Ethanol Intoxication". Psychosomatic Medicine. 28 (4): 616–26. CiteSeerX   10.1.1.503.1374 . doi:10.1097/00006842-196607000-00037. S2CID   147372625 . Retrieved 2014-01-07.
  4. ↑ Thayer, Julian F.; Hall, Martica; Sollers, John J.; Fischer, Joachim E. (2006). "Alcohol use, urinary cortisol, and heart rate variability in apparently healthy men: Evidence for impaired inhibitory control of the HPA axis in heavy drinkers". International Journal of Psychophysiology. 59 (3): 244–50. doi:10.1016/j.ijpsycho.2005.10.013. PMID   16325293.
  5. ↑ Stalder, Tobias; Kirschbaum, Clemens; Heinze, Kareen; Steudte, Susann; Foley, Paul; Tietze, Antje; Dettenborn, Lucia (2010). "Use of hair cortisol analysis to detect hypercortisolism during active drinking phases in alcohol-dependent individuals". Biological Psychology. 85 (3): 357–60. doi:10.1016/j.biopsycho.2010.08.005. PMID   20727937. S2CID   14554271.
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