When it comes to preventative steps in neurologic illness, understanding how stress affects our bodies and minds is a top priority. We know that many psychiatric disorders such as depression, anxiety, and PTSD (1) are exacerbated by stress and driven by traumas.
Stress plays a role in brain health and cognition, and recent studies tell us there is a likely relationship between emotional trauma and dementia. We are learning more about which underlying factors impact this risk relationship the most, and how an integrative health approach might be the best strategy for prevention and treatment.
Maladaptive or Chronic Stress
The term “stress” refers to our body’s natural response to any challenging situation. There is a difference between adaptive stress — the type of stress that allows us to act productively in a dangerous situation, for example — and maladaptive stress. Maladaptive stress or distress is a physiologic state where the body doesn’t get to recover from the stressful event and remains in the state of nervous system arousal or collapse.
Maladaptive or chronic stress, reflects long-term or unrelenting conditions of physical or mental exertion and time when the body doesn’t get a chance to rest or experience relief or recovery. Rather than just being “stressed”, our bodies are “stressed out.” Since the brain is in continuous communication with the rest of the body through the neuroendocrine, metabolic, and immune systems, chronic stress can cause dysregulation and imbalances throughout the body, brain and affect mood and mind.
The Role of the HPA Axis
While the specific stressors vary, the biological stress response system is a common physiological pathway that deals with environmental stress.
The hypothalamic pituitary adrenal axis (HPA axis) responds to environmental stressors by creating physiological reactions in the central nervous system (CNS) and peripheral nervous system (PNS) to deal with stressors and support homeostasis, allowing our bodies return to calm and safety. One of the most common yet impactful responses of the HPA axis to stress is the production of cortisol, which is a hormone that can regulate your mood, motivation, and metabolism.
In moderation, this hormone works perfectly to restore your body during and after a stressor. But chronic stress exposure (or even the perception of stress) can lead to long-term overproduction of cortisol, which can disrupt your immune system, cardiovascular health, the health of your gut and sleep. Excess cortisol can harm your brain and negatively affect cognition.
Too much cortisol is toxic and can wear down your brain’s ability to function properly and can even impact the hippocampus, a region of the brain that deals with memory consolidation (2).
Chronic Stress and Alzheimer’s Risk
Stress-related disorders, including PTSD, acute stress reaction, adjustment disorder, and other stress reactions, have been shown to increase risk of neurodegenerative diseases (3). Previous chronic depression is associated with a twofold increase in likelihood of developing dementia, according to a cross-sectional study known as the MIRAGE study (4).
One study found a twofold increase in cognitive impairment in 9/11 survivors diagnosed with PTSD and MDD compared to controls (5). This may be the result of a chronically dysregulated stress system that is characteristic of PTSD. Potential pathways explaining the association between PTSD and dementia include the HPA axis’ dysregulation of cortisol, which can impact cognitive ability and memory not only at the time of trauma, but also later into our lifespan (6).
A recent study (7) expanded the research in this area, observing that the relationship between existing genetic factors in the HPA axis and exposure to long-term disruptions such as overproduction of cortisol — which lead to inflammation — can indeed increase the risk of Alzheimer’s. Chronic stress and long-term cognitive function are thus importantly linked.
The integrity of our DNA (8) and the production of the hormone dehydroepiandrosterone (DHEA) (9) are also affected by chronic stress, and disruptions to their function are implicated in cognitive impairment.
Addressing Chronic Stress
From a brain health perspective there are compelling reasons to resolve old traumas. Healing old traumas can relieve us emotionally and spiritually, but it can also rectify the resulting hormonal and chemical imbalances that come along with maladaptive CNS and PNS reactivity. One of the most compelling reasons to release old traumas is to create opportunities for better relationships, as unresolved traumas can interfere with how we connect with others, our ability to love and feel loved.
Fortunately, there are science-driven treatments for trauma, including:
Somatic-based trauma relief techniques
When people are connected to the sensations and perceptions in their bodies during a therapy session, they are able to follow those sensations, track them and release them. Being able to integrate fragmented memories into a coherent narrative about the trauma or life experience is one of the characteristics these trauma therapies share.
With these evidence-based treatments, those suffering from unresolved trauma can take advantage of positive neuroplasticity and strengthen the neurological pathways that correspond with improved emotional regulation, integration of difficult memories and overall behavioral health.
Learn more about integrating positive neuroplasticity into your health plan, read my blog on ilenenaomirusk.com.
With the help of tools trauma specialist, social support and a dedication to healing, trauma release can become an opportunity to increase resilience, develop cognitive reserve and open doors to more meaning and purpose in life. In addition, it may open the doorway to a greater sense of freedom and health, benefit social and emotional wellness and might prove to be one of the many valuable prevention strategies for neurodegenerative disease.
Stress and trauma have been shown to impact the immune system, the gastrointestinal system and brain function, with the latest research suggesting a role in Alzheimer’s risk. To learn more about how an integrative health approach may help you minimize this risk, reach out to us at info@HealthyBrain.clinic.
Gunak, M. M., Billings, J., Carratu, E., and Marchant, N. Favarato G., Ortega V., (2020). Post -Traumatic Stress Disorder as a Risk Factor for Dementia: systematic review and meta-analysis. British Journal of Psychiatry 1-9, doi:10. 1192
Scaer R. (2001) The Body Bears the Burden: Trauma, Dissociation, and Disease. The Haworth Medical Press. New York, New York.
Lupien, S.J., de Leon, M., de Santi, S., Convit, A., Tarshish, C., Nair, N.P., Thakur, M., McEwen, B.S., Hauger, R.L., Meaney, M.J., 1998. Cortisol levels during human aging predict hippocampal atrophy and memory deficits. Nat. Neurosci. 1, 69–73.
Lebedeva, A., Sundström, A., Lindgren, L., Stomby, A., Aarsland, D., Westman, E., Winblad, B., Olsson, T., and Nyberg, L. (2018). Longitudinal relationships among depressive symptoms, cortisol, and brain atrophy in the neocortex and the hippocampus. Acta Psychiatrica Scandinavica 137, 491–502.
Greenberg, M.S., Tanev, K., Marin, M.F., and Pitman, R.K. (2014). Stress, PTSD, and dementia. Alzheimer’s and Dementia 10.
Clouston SA, Kotov R, Pietrzak RH, Luft BJ, Gonzalez A, Richards M et al. (2016) Cognitive impairment among World Trade Center responders: long term implications of re-experiencing the 9/11 terrorist attacks. Alzheimer's & Dementia (Amst) 4, 67–75.
Armstrong, A.M., Porter, T., Quek, H., White, A., Haynes, J., Jackaman, C., Villemagne, V., Munyard, K., Laws, S.M., Verdile, G., Groth, D. (2021). Chronic stress and Alzheimer's disease: the interplay between the hypothalamic–pituitary–adrenal axis, genetics and microglia. Biological Reviews. https://doi.org/10.1111/brv.12750
Yehuda, R., Brand, S.R., Golier, J.A., and Yang, R.K. (2006). Clinical correlates of DHEA associated with post-traumatic stress disorder. Acta Psychiatrica Scandinavica 114, 187–193.
Gill, J., Vythilingam, M., and Page, G.G. (2008). Low cortisol, high DHEA, and high levels of stimulated TNF-α, and IL-6 in women with PTSD. In Journal of Traumatic Stress, pp. 530–539.