Many of my patients share stories where they have suffered years and years of trauma, abuse, and emotional neglect. The courage to share their stories is incredible. What some people have gone through is indescribable. I am often reacting the same way when I hear stories like these. My reaction is to say something like this: “Thank you for trusting me with your story. I can’t imagine having to live with the memories you have to live with daily.” Words do not convey the experience of sharing one’s story of their trauma, in many instances.
One way I can help support these patients is by providing information to them that is necessary for them to move forward to begin a life that is “worth living” again, as Marsha Linehan, prolific researcher, Psychotherapist, and creator of DBT. One major question I like to try to answer for people is the effects of long-term stress due to trauma on your body. Long-term stress impacts different parts of your brain, ultimately creating problems for other areas of your body. I want to shed some light on the connection between two main components of your body that are triggered by long-term stress. The two components are aldosterone and Andrenocotrophic, both are types of stress hormones.
One major component of the brain that is triggered by long-term stress is called the hypothalamus. The main function of the hypothalamus is to release hormones, regulate body temperature, maintain daily physiological cycles, control appetite, manage sexual behavior, and regulate emotional responses. Long-term stress triggers the hypothalamus to release the corticotropin-releasing hormone. These hormones will target cells in the anterior pituitary gland.
The pituitary gland will then release a different hormone called the Andrenocotrophic hormone (ACTH). ACTH alerts the adrenal gland, more specifically the adrenal cortex; the adrenal cortex begins to produce aldosterone. Aldosterone is a steroid hormone and is lipid-soluble; this means that it can enter a cell and access a cell’s nucleus easily. Aldosterone is often produced to maintain or regulate blood pressure. Aldosterone is created from cholesterol in the adrenal cortex by a series of enzyme reactions. Enzymes are the “gas” that create important reactions in the body so that certain cells are produced to maintain the body’s overall health. Briefly, cholesterol moves across the outer mitochondrial membrane towards the inner membrane where the first enzyme in the steroidogenic pathway is located. Several other enzyme reactions occur before cholesterol is converted to aldosterone. One major reaction that occurs that helps convert cholesterol to aldosterone is done by dehydrogenases and mixed-function oxidases, many of which belong to the cytochrome P450 superfamily of haem-containing enzymes. This enzyme reaction requires a coupled coenzyme system (adrenodoxin/adrenodoxin reductase) which transfers electrons to the P450 enzyme, acting as a reducing equivalent for the hydroxylation reaction. In short, maintaining a well-balanced production of enzymes helps convert cholesterol to aldosterone.
Long-term stress may trigger increased levels of aldosterone which can lead to hypertension and cardiovascular damage. In the vascular system, aldosterone is known to balance vascular tone, possibly by increasing the pressor response to catecholamines and impairing the vasodilatory response to acetylcholine or by upregulating Ang II receptors. Access aldosterone also promotes collagen deposition in blood vessels, enhancing vascular remodeling at the expense of compliance. This remodeling was originally intended to act as an adaptation of arterial hypertension caused by aldosterone excess. However, research shows that chronic aldosterone administration in the presence of NaCl (sodium) has been shown to stimulate perivascular and interstitial cardiac fibrosis and cardiac hypertrophy independently of changes in blood pressure.
Lastly, the mechanism of aldosterone-induced fibrosis is unclear. Researchers are sure today that an excess of aldosterone will increase collagen I synthesis in cardiac fibroblasts. Histological features of aldosterone-induced cardiac fibrosis include an increase of cardiac myocytes and fibroblasts and intense perivascular inflammation.
In summary, long-term stress, often dues to trauma, can produce aldosterone in excess which leads to:
- Hypertension and cardiovascular impairments.
- Negatively impact the central nervous system.
- Gene expression is negatively impacted due to an excess of aldosterone.
Stress causes psychological suffering, and we can see from a molecular perspective that stress, especially long-term, have significant effects on our biological systems.
 Connell, J. M. C., & Davies, E. (2005). The new biology of aldosterone. The Journal of Endocrinology, 186(1), 1-20.
Ramon Diaz, Jr. M.A., LPC, NCC, CCTS, CDBT
Clinical Complex Trauma Specialist (CCTS-1),
Certified Dialectical Behavioral Therapist (C-DBT),
in progress, Certified Alcohol & Drug Abuse Counseling (CADC),
Clinical Therapist – Sprout Family Clinics
Adolescent and Family Therapist – Bridgeview Clinical Services