PTSD, Neurotransmitters, and the Adrenals

Post-traumatic stress disorder, or PTSD, is an increasingly common psychological malady with strong connections to the neurotransmitters and adrenal hormones of the HPA axis.¹ PTSD is often manifested in individuals who have experienced physically or psychologically disturbing events, such as combat, natural disasters, gang violence, sexual molestation, witnessing a death, and even childbirth.² People with PTSD commonly suffer from vivid nightmares, unexpected flashbacks, social stress, irritability, anxiety, and/or depression.³

Although PTSD has been experienced by people throughout the millennia, it has become more common in the past 30 years with the uptick in natural disasters and terrorist attacks occurring across the globe. In the US, PTSD has become one of the most common psychiatric disorders as listed by the Diagnostic and Statistical Manual for Psychiatric Disorders (DSM ).⁴ Although PTSD is becoming more prevalent, it is a complex disorder that afflicts individuals differently and is not always easy to understand or treat.⁵ Assessing the HPA axis may provide valuable insight into the symptoms and underlying mechanisms of this complex disorder.

Neurotransmitters and Adrenal Hormones

PTSD is the injury from intense psychological and/or physical stress. In response to stress, the body will increase cortisol and catecholamine (excitatory neurotransmitters: dopamine, norepinephrine, and epinephrine) secretion to prepare for fighting or fleeing from the stressor. Initially, this will spike cortisol and excitatory neurotransmitters, which is observed in people who recently experienced trauma.⁶

However, if this occurs repeatedly over a long period of time, the HPA axis will become dysregulated and imbalances will occur between the excitatory neurotransmitters, inhibitory neurotransmitters, and adrenal hormones. PTSD patients, especially those who have endured repeated interpersonal trauma (e.g. abuse, torture, combat), usually exhibit low levels of cortisol and serotonin, with high levels of dopamine, norepinephrine, epinephrine, and DHEA-S.⁷

Serotonin is an inhibitory neurotransmitter important for mood and exerts inhibition on norepinephrine. It is suppressed by excess cortisol and low levels contribute to the anxiety, irritability, and depression experienced by PTSD patients.⁸ DHEA-S is an adrenal hormone, like cortisol, and usually increases along with cortisol. However, the high DHEA-S observed in PTSD sufferers may be a compensatory effect of depleted cortisol and possibly serve a neuroprotective role and modulate recovery from severe stress.⁹

Dopamine, norepinephrine and epinephrine are catecholamine neurotransmitters. They have an influence on forming and processing memories, a process often impaired in PTSD. Excess norepinephrine and cortisol can damage the hippocampus, the part of the brain responsible for memory. So, it’s not only difficult to focus and remember with imbalanced catecholamines, but hippocampal damage makes it nearly impossible to deal with traumatic memories.

The resulting effect is intense nightmares and flashbacks that are hallmarks of PTSD.¹⁰ Fortunately, evidence suggests that the brain can repair itself once the person is removed from the threatening situation and their catecholamine levels are returned to normal. Repairing the hippocampus and any other damage caused by stress will allow painful memories to be processed so that nightmares and flashbacks can come to an end.¹¹

PTSD Intervention

Since excitatory and inhibitory neurotransmitters along with the adrenal hormones are so closely tied and become significantly imbalanced in PTSD, it seems almost vital to evaluate a patient’s HPA axis as part of their treatment protocol. One group of researchers claimed that if the stressor is removed and norepinephrine and epinephrine levels were returned to normal, then PTSD patients might see their symptoms go away and their mental state improve. This research group found that saffron, a common food spice and folk remedy, has effects comparable to fluoxetine (SSRI) for blocking serotonin reuptake and stimulating GABA receptors.¹² This is worth considering as a non-pharmaceutical treatment since SSRIs and other anti-anxiety/depression medications, which are typical in the treatment of PTSD, can have significant side effects that saffron and other alternative treatments don’t produce.¹³

Sanesco’s Targeted Nutritional Therapy (TNT) formulas Prolent, Lentra, and Tranquilent, have similar effects and may also be useful in PTSD treatment protocols to replenish serotonin, support GABA receptors, and alleviate mood disorders common in PTSD. Other treatments include cognitive behavior therapy (CBT) and eye movement desensitization and reprocessing (EMDR). The goal of CBT is to help patients change how they think about the traumatic event they have experienced via relaxation and positive thinking exercises.

By recording eye movements, EMDR works to aid memory processing in the brain, which is often blunted due to hippocampal damage.¹⁴ Like many psychiatric disorders, PTSD is manifested differently from person to person and treatment is often multidimensional.¹⁵ However, with HPA testing, we are given a window into the neuroendocrine system which may serve as a useful tool in improving the quality of life of people living with PTSD.

References:

1. Wessa, M., Rohleder, N. (2007). Endocrine and inflammatory alterations in post-traumatic stress disorder. Expert Review of Endocrinology & Metabolism, 2(1), 91-122.
2. Asalgoo, S., Jahromi, G. P., Meftahi, G. H., & Sahraei, H. (2015). Posttraumatic stress disorder (PTSD): Mechanisms and possible treatments. Neurophysiology, 47(6), 482-489; Shaban, Z., Dolatian, M., Shams, J., Alavi-Majd, H., Mahmoodi, Z., & Sajjadi, H. (2013). Post-traumatic stress disorder (PTSD) following childbirth: Prevalence and contributing factors. Iranian Red Crescent Medical Journal, 15(3), 177-182.
3. Op. cit. Wessa et al. (2007).
4. Op. cit. Asalgoo et al. (2015); Op. cit. Wessa et al. (2007).
5. Meltzer, E. C., Averbuch, T., Samet, J. H., Saitz, R., Jabbar, K., Lloyd-travaglini, C., & Liebschutz, J. M. (2012). Discrepancy in diagnosis and treatment of post-traumatic stress disorder (PTSD): Treatment for the wrong reason. The Journal of Behavioral Health Services & Research, 39(2), 190-201.
6. Op. cit. Asalgoo et al. (2015); Op. cit. Wessa et al. (2007).
7. Op. cit. Asalgoo et al. (2015); Op. cit. Wessa et al. (2007); Op. cit. Wessa et al. (2007); Spivak B, Vered Y, Graff E et al. (1999) Low platelet-poor plasma concentrations of serotonin in patients with combat-related post-traumatic stress disorder. Biol. Psychiatry 45, 840–845; Yehuda R, Brand SR, Golier JA, Yang RK. (2006). Clinical correlates of DHEA associated with post-traumatic stress disorder. Acta Psychiatr. Scand. 114, 187–193.
8. Op. cit. Spivak et al. (1999); Op. cit. Asalgoo et al. (2015).
9. Op. cit. Yehuda et al. (2007).
10. Op. cit. Asalgoo et al. (2015); Op. cit. Spivak et al. (1999).
11. Op. cit. Asalgoo et al. (2015).
12. Op. cit. Asalgoo et al. (2015).
13. Op. cit. Spivak et al. (1999).
14. Op. cit. Asalgoo et al. (2015).
15. Yehuda, R. (2002). Neuroendocrine alterations in posttraumatic stress disorder. Primary Psychiatry, 9(2), 30-36; Op. cit. Asalgoo et al. (2015).