PTSD is a psychiatric and metabolic disorder that can develop in people who have experienced or witnessed a traumatic event. For more on PTSD and cPTSD click here.
What are metabolic disorders? Metabolic disorders include type 2 diabetes, fatty liver, high cholesterol levels, high triglycerides, high blood sugar and more disorders caused by inflammation in the body.
There is emerging evidence that PTSD influences both the brain and body. PTSD is also a stealth systematic metabolic disorder. It involves most of the body including the central nervous system (CNS) as well as neuroendocrine, metabolic and inflammatory systems (see discussion about this in Krantz et al. 2022).
Basically, this means that the physical disorders currently associated with PTSD; like type 2 diabetes, cardiovascular disease, obesity and heart disease; are actually a direct result of damaged physiological systems (Rosenbaum et al. 2015, Michopoulos et al. 2016).
Having PTSD contributes to developing the physical symptoms of metabolic syndrome (MetS). There is a codependent relationship between developing metabolic disorders, obesity and PTSD. This suggests that some concealed neuroendocrine and metabolic changes are present in PTSD that can either increase the risk for systemic metabolic dysfunction or trigger a fundamental change in metabolism due to experiencing a traumatic experience (Michopoulos et al. 2016).
PTSD is also related to a strong immune response, which includes an increase in inflammatory chemicals and a reduction in anti-inflammatory chemicals (Sun et al. 2021). Mast cell activation is implicated in brain injury, stress, and PTSD (Kempuraj et al. 2017). Mast cells are white blood cells that respond when foreign substances threaten the body.
These can include reducing brain inflammation, anti-inflammation diets and lifestyle, going out in nature, and being kind to yourself.
Deanne J: "I’ve done many different kinds of therapy. I'm always willing to listen and try. But I am still fighting my personal nightmares, flashbacks, chronic hyper vigilance, severe anxiety and so on. I’m so frustrated by all of it. Objectively, I can see that I’ve improved myself somewhat over the years, but I still feel so dysregulated. I feel I am missing a piece I need to heal."
Johann Heinrich Füssli The Nightmare (1790-1791) oil on canvas.
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The changes PTSD causes in the metabolism, sympathetic nervous system (SNS), and neuroendocrine systems are extremely similar to the changes seen in metabolic disorders, such as diabetes and obesity (Michopoulos et al. 2016). Metabolic disorders increase body and brain inflammation, activate glia in the brain to cause chronic pain, and cause weight gain.
It is not just in the brain, it affects the body as well. Trauma and stress changes your brain and your body. PTSD, cPTSD and trauma can cause lasting changes in the amygdala, hippocampus and the prefrontal cortex regions of the brain. The amygdala is involved with fear and aggression responses (Martin et al. 2009).
PTSD messes with your neurotransmitters, hormones and neuromodulators. Neurotransmitters are chemicals that carry messages between neurons while neuromodulators regulate and influence neurons.
★ Serotonin (5-HT) is a neurotransmitter and hormone that regulates mood, memory, reward, sleep, behavior, appetite, and gut (gastrointestinal homeostasis). People with PTSD, produce less serotonin and fewer serotonin transporters (5-HTT). This is significantly associated with higher anxiety and greater depression (Michopoulos et al. 2015).
★ People with PTSD have altered hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) (Michopoulos et al. 2015). As you can guess from the name, the HPA axis is the complex interaction between the hypothalamus, pituitary gland and the adrenal glands. This system is a main neuroendocrine system; which controls interactions between the endocrine system and the nervous system. It influences things like immunity, mood, desire, emotions, digestion, and metabolism.
★ People with PTSD and cPTSD have more norepinephrine (NE). They also produce more NE during stress (discussion Michopoulos et al. 2015). Ne is a neurotransmitter and catecholamine which influences mood regulation, attention, focus, alertness, and blood pressure.
As you can imagine, having high amounts of NE can cause fight, freeze or flight responses such as hyperalertness, anxiety, agitation, headaches, dizziness, blurred vision, irregular heartbeat, high blood pressure, diarrhea and loss of appetite. In extreme cases it can cause psychosis and other cognitive changes (memory issues, confusion, trouble with focus).
★ Increased amounts of catecholamines such as NE flooding the body are associated with panic attacks and other fear-related mood and anxiety disorders (Martin et al. 2009).
★ Severe and chronic stress activate inflammation pathways in your body and brain (Lui et al. 2017). This causes body and brain inflammation.
On a practical note, this means treating the metabolic disorder part of PTSD will also help treat the psychological aspects of PTSD. There is research showing that reducing whole body inflammation also reduces brain inflammation. You can start by following a anti-inflammatory diet which will reduce whole body as well as brain inflammation.
Elisabeth Baumann: A Wounded Danish Soldier c1865 oil on canvas.
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PTSD causes persistent activation of microglia, especially in prefrontal cortex and hippocampus (Deri et al. 2021, Yang et al. 2025). For more on why this is a bug problem see What Causes Chronic Pain Loops.
Pro‐inflammatory cytokines are significantly elevated in people with PTSD:
This is significantly associated with PTSD symptoms.
Anti-inflammatory cytokines are significantly lower in people with PTSD:
Being stressed activates central nervous system inflammatory pathways
Discussion Yang et al. 2025
Around 70% of the general population will experience some sort of traumatic event in their lifetime, but only 10-20% of those will eventually develop PTSD symptoms (Michopoulos et al. 2016). Why are some people more susceptible than others?
People with PTSD experience real physical changes to the grey matter of the brain. Changes occur in the hippocampus and prefrontal brain regions such as the anterior cingulate cortex (Bremner et al. 2006). The hippocampus is part of the brain that is involved in learning, memory, and handling of stress. It also works with the medial prefrontal cortex, a part of the brain that regulates the emotional response to stress and fear. The anterior cingulate cortex helps regulate emotions, makes decisions and regulates blood pressure and heart rate.
There is some debate over whether PTSD causes a reduction in prefrontal brain regions or if having a smaller hippocampus and prefrontal brain region is a risk factor for developing PTSD. Research has shown both theories are possible (Butler et al. 2017).
Gilbertson et al. (2002) reported that Vietnam veterans with PTSD and their non-combat exposed co-twins had smaller hippocampal volumes than those of combat exposed non-PTSD veterans and their co-twins. In contrast, Bremner et al. (1995) reported Vietnam veterans with PTSD had an 8% smaller hippocampus than those without PTSD. Kasai et al (2008) also found that veterans with PTSD had smaller reduced gray matter volume than their non-combat exposed co-twins or combat veterans without PTSD.
Interestingly, Butler et al. (2017) found that longer military deployments were associated with smaller regional grey matter brain volumes in combat soldiers without PTSD. There was no correlation between hippocampal volume and length of deployment. People on military deployments are often exposed to stress, traumatic events, loss and ethical dilemmas. Stress exposure reduces hippocampus size (McEwen and Morrison 2013).

Women with PTSD do not adapt to fearful situations. In women with PTSD, low levels of estradiol are associated with impaired fear extinction (which is a risk factor for anxiety disorders). Normal fear extinction is when you learn not to respond to a conditioned fear response after multiple exposures to whatever you are scared of. Women with PTSD and lower levels of estradiol are not less fearful even after exposure.
Women with PTSD can have altered stress responses, immune system reactions and movement responses. Women with PTSD, but not men, have high levels of pituitary adenylate cyclase-activating polypeptide (PACAP). PACAP is involved in stress-related behavior and physiology. It can suppress or modulate immune and inflammation responses, alter psychomotor responses (coordination of sensory or cognitive processes with movement), modulate cortisol levels, and influence cellular death (Xu et al. 2016). PACAP also regulates hippocampal activity (Johnson et al. 2020).
Trauma-exposed women (69 total) but not trauma-exposed men (20 total) had significantly higher PACAP levels. This was associated with increased functional connectivity in the central amygdala (Clancy et al. 2023). The PACAP increase combined with increased functional connectivity may show how the PACAP system modulates amygdala activity to influence threat reactivity in stress/trauma-related disorders.
The Comfort of the Fog by Wilhelm Kotarbiński (1848-1921) oil on canvas.
*Names and some minor identifying details in all stories in this website are changed to protect people's privacy.
This information is for informational purposes only and does not constitute medical advice, diagnosis, or treatment.
People with PTSD can show physiological changes and disorders in many different body systems. Some organ systems that are influenced are the neuroendocrine and metabolic systems (diabetes, metabolic disorders, hypertension),central nervous system (dementia, sleep disorders), autoimmune and inflammatory systems (asthma, rheumatoid arthritis) and cardiovascular disorders like heart disease (discussion of this in Krantz et al. 2022). Pietrzak et al. 2012 reported that people with PTSD (9,463 adults over 60 years old) were more likely to have hypertension, heart disease, angina pectoris (severe heart pain), tachycardia (racing heart), stomach ulcer, gastritis, arthritis and poorer physical functioning than people without PTSD.
PTSD is a significant risk factor for the development and progression of cardiovascular disease (Krantz et al. 2022). Compared with matched people in the general population, people with PTSD had an almost double the risk for developing MetS. This was a large study with 9,673 people suffering from PTSD and 6852 people who were controls (Rosenbaum et al. 2015). This included a higher incidence of abdominal obesity, high blood pressure, insulin resistance and abnormal blood lipids. PTSD also often occurs with other disorders such as depression, sleep disorders and substance abuse.
Bellis MA, Hughes K, Ford K, Quigg Z, Butler N, Wilson C. Comparative relationships between physical and verbal abuse of children, life course mental well-being and trends in exposure: a multi-study secondary analysis of cross-sectional surveys in England and Wales. BMJ Open. 2025 Aug 5;15(8):e098412. doi: 10.1136/bmjopen-2024-098412. Full article.
Blais RK, Tirone V, Orlowska D, Lofgreen A, Klassen B, Held P, Stevens N, Zalta AK. Self-reported PTSD symptoms and social support in U.S. military service members and veterans: a meta-analysis. Eur J Psychotraumatol. 2021 Feb 4;12(1):1851078. doi: 10.1080/20008198.2020.1851078. Full article.
Boehler J. The Efficacy of Cognitive Processing Therapy for PTSD Related to Military Sexual Trauma in Veterans: A Review. J Evid Based Soc Work (2019). 2019 Nov-Dec;16(6):595-614. doi: 10.1080/26408066.2019.1666767. Summary.
Bremner JD, Randall PR, Scott TM, Bronen RA, Seibyl JP, Southwick SM, Delaney RC, McCarthy G, Charney DS, Innis RB. MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress disorder. Am J Psychiatry. 1995;152:973–981. Full article.
Bremner JD. Neuroimaging in posttraumatic stress disorder and other stress-related disorders. Neuroimaging Clin N Am. 2007 Nov;17(4):523-38, ix. doi: 10.1016/j.nic.2007.07.003. Full article.
Bremner JD. Traumatic stress: effects on the brain. Dialogues Clin Neurosci. 2006;8(4):445-61. doi: 10.31887/DCNS.2006.8.4/jbremner. PMID: 17290802; PMCID: PMC3181836. Full article.
Boe HJ, Holgersen KH, Holen A. Reactivation of posttraumatic stress in male disaster survivors: the role of residual symptoms. J Anxiety Disord. 2010 May; 24:397-402. Article summary.
Butler O, Adolf J, Gleich T, Willmund G, Zimmermann P, Lindenberger U, Gallinat J, Kühn S. Military deployment correlates with smaller prefrontal gray matter volume and psychological symptoms in a subclinical population. Translational Psychiatry. 2017;7:e1031-. Full article.
Clancy KJ, Devignes Q, Kumar P, May V, Hammack SE, Akman E, Casteen EJ, Pernia CD, Jobson SA, Lewis MW, Daskalakis NP, Carlezon WA Jr, Ressler KJ, Rauch SL, Rosso IM. Circulating PACAP levels are associated with increased amygdala-default mode network resting-state connectivity in posttraumatic stress disorder. Neuropsychopharmacology. 2023 Jul;48(8):1245-1254. doi: 10.1038/s41386-023-01593-5. Full article.
Deri Y, Clouston SAP, DeLorenzo C, Gardus JD 3rd, Bartlett EA, Santiago-Michels S, Bangiyev L, Kreisl WC, Kotov R, Huang C, Slifstein M, Parsey RV, Luft BJ. Neuroinflammation in World Trade Center responders at midlife: A pilot study using [18F]-FEPPA PET imaging. Brain Behav Immun Health. 2021 Jun 30;16:100287. doi: 10.1016/j.bbih.2021.100287. Full article.
Gilbertson MW, Shenton ME, Ciszewski A, Kasai K, Lasko NB, Orr SP, Pitman RK. Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nat Neurosci 2002; 5: 1242–1247. Full article.
Iqbal J, Huang GD, Xue YX, Yang M, Jia XJ. The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder. Front Neurosci. 2023 Dec 5;17:1281401. doi: 10.3389/fnins.2023.1281401. Full article.
Johnson GC, Parsons R, May V, Hammack SE. The Role of Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Signaling in the Hippocampal Dentate Gyrus. Front Cell Neurosci. 2020 Apr 30;14:111. doi: 10.3389/fncel.2020.00111. Full article.
Kasai K, Yamasue H, Gilbertson MW, Shenton ME, Rauch SL, Pitman RK. Evidence for acquired pregenual anterior cingulate gray matter loss from a twin study of combat-related posttraumatic stress disorder. Biol Psychiatry. 2008 Mar 15; 63(6):550-6. Full article.
Kempuraj D, Selvakumar GP, Thangavel R, Ahmed ME, Zaheer S, Raikwar SP, Iyer SS, Bhagavan SM, Beladakere-Ramaswamy S, Zaheer A. Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer's Disease Pathogenesis. Front Neurosci. 2017 Dec 12;11:703. doi: 10.3389/fnins.2017.00703. Full article.
Killgore WDS, Vanuk JR, Dailey NS. Treatment with morning blue light increases left amygdala volume and sleep duration among individuals with posttraumatic stress disorder. Front Behav Neurosci. 2022 Sep 12;16:910239. doi: 10.3389/fnbeh.2022.910239. Full article.
Korem N, Duek O, Ben-Zion Z, Spiller TR, Gordon C, Amen S, Levy I, Harpaz-Rotem I. Post-treatment alterations in white matter integrity in PTSD: Effects on symptoms and functional connectivity a secondary analysis of an RCT. Psychiatry Res Neuroimaging. 2024 Sep;343:111864. doi: 10.1016/j.pscychresns.2024.111864. Summary.
Krantz DS, Shank LM, Goodie JL. Post-traumatic stress disorder (PTSD) as a systemic disorder: Pathways to cardiovascular disease. Health Psychol. 2022 Oct;41(10):651-662. doi: 10.1037/hea0001127. Full article.
Liu YZ, Wang YX, Jiang CL. Inflammation: The Common Pathway of Stress-Related Diseases. Front Hum Neurosci. 2017 Jun 20;11:316. doi: 10.3389/fnhum.2017.00316. Full article.
Lussier AA, Zhu Y, Smith BJ, Cerutti J, Fisher J, Melton PE, Wood NM, Cohen-Woods S, Huang RC, Mitchell C, Schneper L, Notterman DA, Simpkin AJ, Smith ADAC, Suderman MJ, Walton E, Relton CL, Ressler KJ, Dunn EC. Association between the timing of childhood adversity and epigenetic patterns across childhood and adolescence: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC) prospective cohort. Lancet Child Adolesc Health. 2023 Aug;7(8):532-543. doi: 10.1016/S2352-4642(23)00127-X. Full article.
Marmar CR, Schlenger W, Henn-Haase C, Qian M, Purchia E, Li M, Corry N, Williams CS, Ho C, Horesh D, Karstoft K, Shalev A, Kulka RA. Course of Posttraumatic Stress Disorder 40 Years After the Vietnam WarFindings From the National Vietnam Veterans Longitudinal Study. JAMA Psychiatry. 2015;72:875-881. Full article.
Martin EI, Ressler KJ, Binder E, Nemeroff CB. The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. Psychiatr Clin North Am. 2009 Sep;32(3):549-75. doi: 10.1016/j.psc.2009.05.004. Full article.
McEwen BS, Morrison JH. The brain on stress: vulnerability and plasticity of the prefrontal cortex over the life course. Neuron. 2013; 79:16-29. Full article.
McLean CP, Levy HC, Miller ML, Tolin DF. Exposure therapy for PTSD in military populations: A systematic review and meta-analysis of randomized clinical trials. J Anxiety Disord. 2022 Aug;90:102607. doi: 10.1016/j.janxdis.2022.102607. Article summary.
Michopoulos V, Norrholm SD, Jovanovic T. Diagnostic Biomarkers for Posttraumatic Stress Disorder: Promising Horizons from Translational Neuroscience Research. Biol Psychiatry. 2015 Sep 1;78(5):344-53. doi: 10.1016/j.biopsych.2015.01.005. Full article.
Michopoulos V, Vester A, Neigh G. Posttraumatic stress disorder: A metabolic disorder in disguise? Exp Neurol. 2016 Oct;284(Pt B):220-229. doi: 10.1016/j.expneurol.2016.05.038. Full article.
Pietrzak RH, Goldstein RB, Southwick SM, Grant BF. Physical health conditions associated with posttraumatic stress disorder in U.S. older adults: results from wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions. J Am Geriatr Soc. 2012 Feb;60(2):296-303. doi: 10.1111/j.1532-5415.2011.03788.x. Full article.
Rosenbaum S, Stubbs B, Ward PB, Steel Z, Lederman O, Vancampfort D. The prevalence and risk of metabolic syndrome and its components among people with posttraumatic stress disorder: a systematic review and meta-analysis. Metabolism. 2015 Aug;64(8):926-33. doi: 10.1016/j.metabol.2015.04.009. Article summary.
Samuelson KW. Post-traumatic stress disorder and declarative memory functioning: a review. Dialogues in Clinical Neuroscience. 2011;13:346-351. Full article.
Sun Y, Qu Y, Zhu J. The Relationship Between Inflammation and Post-traumatic Stress Disorder. Front Psychiatry. 2021 Aug 11;12:707543. doi: 10.3389/fpsyt.2021.707543. Full article.
Xu Z, Ohtaki H, Watanabe J, Miyamoto K, Murai N, Sasaki S, Matsumoto M, Hashimoto H, Hiraizumi Y, Numazawa S, Shioda S. Pituitary adenylate cyclase-activating polypeptide (PACAP) contributes to the proliferation of hematopoietic progenitor cells in murine bone marrow via PACAP-specific receptor. Sci Rep. 2016 Feb 29;6:22373. doi: 10.1038/srep22373. Full article.
Yang L, Lu J, Zhao Z, Zhang Z, Yang W, Zhang G. Research Progress on Inflammation and Immune Dysregulation in PTSD. Brain Behav. 2025 Jun;15(6):e70633. doi: 10.1002/brb3.70633. Full article.
Zaccari B, Higgins M, Haywood TN, Patel M, Emerson D, Hubbard K, Loftis JM, Kelly UA. Yoga vs Cognitive Processing Therapy for Military Sexual Trauma-Related Posttraumatic Stress Disorder: A Randomized Clinical Trial. JAMA Netw Open. 2023 Dec 1;6(12):e2344862. doi: 10.1001/jamanetworkopen.2023.44862. Full article.