Chronic Stress, Adverse Health Effects by Jeffrey Dach MD
Mary is a 76 year old retired school teacher who has doing well on her thyroid medication for many years. During her last office visit lab review, her serum cortisol was elevated, 23.5 mcg/dl. This is much higher than the last three lab panels where it was normal, in the 15-16 mcg/dl range. Elevated cortisol suggests increased chronic stress, and Mary admitted she was experiencing more stress in her life. The effects of chronic stress can be devastating to our health, and can be understood by reviewing animal models of chronic stress.
Header Image: A stress ball to reduce stress and muscle tension or to train the muscles of the hand. Author: Andreas Schikora. Link to photo on wikimedia commons.
Animal Models of Chronic Stress
Animal models of chronic stress using Cold Water-Immersion Restraint (CWIR) are useful to study the effects of stress. The poor little mouse is immobilized in a plastic tube, and then immersed in cold water for about an hour. See the image below:
Left image: Fig 9. Schematic Showing Mouse retrained in narrow tube and then immersed in cold water. This is restraint stress. The tube is Patented in China. Courtesy of Zhang et al. “Restraint Stress Causes Acute Gastric Injury In Mice: ” Scientific reports 6 (2016).
This above mouse model of restraint stress induces psychological terror, depression and gastrointestinal injury, similar to humans with high-pressure jobs, trauma, or chronic illness or PTSD (post traumatic stress syndrome).
The Devastating Effects on the Gut: “Leaky Gut”
In 2021, Dr. Zhang reported that stressed mice exhibit severe damage to the gastrointestinal tract, even with acute, single-session exposure. Dr. Zhang found small bowel mucosal damage in the duodenum, jejunum, and ileum. The intestinal villi are dramatically shortened, the villus-to-crypt ratio drops, and goblet cells (which produce protective mucus) decrease. The stressed mice exhibit increased intestinal permeability, also called “Leaky Gut”, with FITC-dextran tracer studies showing more leakage of gut bacteria (LPS) into the blood stream causing low level endotoxemia. (2-3)
Increased Inflammation:
Chronic stress causes disruption and dysbiosis of the gut microbiome, the friendly bacteria in our gut shifts towards aerobic and gram-negative bacteria. Chronic stress causes disruption of the intestinal barier, also called Leaky gut with leakage of gram negative bacteria (LPS) into the blood stream causing endotoxemia. This is highly inflammatory and increases pro-inflammatory cytokines such as TNF-alpha and IL-6. Systemic inflammation and gastric ulceration are commonly seen in animal models. Note: LPS is LipoPolySaccharide, also called endotoxin, the outer membrane of gram negative bacteria which is one of the most toxic substances known to mankind. Circulation of LPS in the blood stream from leaky gut is called endotoxemia. For more on how endotoxemia causes coronary artery disease, see:
Low Level Endotoxemia and Coronary Artery Disease
Stress-related Gastritis and Peptic Ulcer Disease.
In 2020, Dr. Yisireyili studied daily restraint stress for two weeks in mice. The experimental mice developed significant gastric mucosal inflammation, gastric erosions, ulcers, enhanced oxidative stress with markedly increased lipid peroxidation, and elevated 8-OHdG, a market for DNA oxidative damage. This same mechanisms can be seen in human stress-related gastritis and peptic ulcer disease. Note: 8-OHdG is 8-hydroxy-2′-deoxyguanosine. (5)
In 2022, Zhang et al. further showed that IL-6 knockout mice experience significant reduced intestinal damage, underscoring inflammation’s central role. Note: Note: IL-6 is a major inflammatory cytokine. IL-6 knockout mice are genetically modified so they cannot mount an inflammatory reaction, thus preventing stress induced gut barrier dysruption. (2-3)
Human Studies of Chronic Stress
Patients suffering from chronic stress may have irritable Bowel Syndrome (IBS), leaky gut, and flare-ups of inflammatory bowel disease. Interventions to protecting the intestinal barrier disruption are useful here, such as Berberine and Lactoferrin.
In 2015, Dr. Kelly reviewed human studies showing psychological stress increases intestinal permeability (Leaky Gut), alters the gut microbiome, and promotes translocation of bacterial products from the gut to the bloodstream (endotoxemia), driving systemic inflammation and stress-related depression and other neuro-psychiatric disorders via the microbiota-gut-brain axis. See Dr. Maes article on Leaky Gut and Chronic Depression: Depression and Leaky Gut. (11)
In 2017, Dr. Yaribeygi highlighted how chronic stress makes our intestinal barrier more permeable (Leaky Gut), contributing to gastrointestinal and systemic inflammatory effects. (10)
Depression-Like Behaviors and Sleep Disruption
In 2019, Dr. Yasugaki showed that Cold Water-Immersion Restraint Stress (CWIRS) daily for three weeks in mice is a reliable model for depression. Mice develop despair-like behavior, anhedonia (loss of pleasure), and other signs of depression, reversed by antidepressant drugs. Dr. Yasugaki also showed chronic stress disturbs sleep: Non-REM sleep (non-rapid eye movement sleep) increases and time awake decreases over weeks,often correlating with a drop in body weight. This is all indicative of poor quality sleep. In addition, many animal studies show anxiety-like behaviors, reduced exploration activity, and decreased cognitive ability. (1)
Depression and Behavioral Despair
In 2016, Dr. Chu et al. showed that even a single 24-hour session of restraint stress in mice simulates entrapment and induces long-lasting depression. The mice exhibit anhedonia, the inability to experience pleasure, or profound loss of interest in activities previously enjoyable. The mice also exhibit behavioral despair, meaning the mice are immobilized and fail to swim during the forced swim test. After 35 days of chronic stress, mice also exhibited reduced brain glucose uptake on FDG-PET scans, especially in hippocampus, cortex, and striatum. The mice exhibit decreased adult hippocampal neurogenesis and gene expression in prefrontal cortex and hippocampus linked to depression. These long-term changes were reversible with the SSRI drug, fluoxetine (Prozac), showing how a single severe restraint event can trigger prolonged mood disruptions, impaired neurogenesis, and metabolic shifts similar to human depression and PTSD. (4)
These findings align closely with human depression, where sleep fragmentation, altered REM sleep, and Hypothalamic Pituitary Axis (HPA) activation are commonly seen with chronic stress.
In 2015, Dr. Kelly et al. further connected stress-induced gut barrier dysfunction and microbiota shifts to human depression and anxiety through inflammatory signaling. (11)
Hormonal, Oxidative, and Systemic Stress Responses
In 2016, Dr. Jiang et al. demonstrated that restraint stress powerfully activates the HPA axis in mice, with robust corticosterone elevation. Note: HPA is Hypothalamic Pituitary Axis. (6)
Stress Elevates Serum Cortisol
As expected, stress strongly activates the HPA axis, with elevated corticosterone, the rodent version of cortisol in humans. Very early after stress induction, mice lose weight and stop eating. Oxidative stress ramps up with increased lipid peroxidation, altered antioxidant enzymes, along with immune suppression. Some studies note increased susceptibility to infection, adrenal changes, neurobiological shifts in mood-regulating brain areas like the hippocampus and prefrontal cortex, and even pain hypersensitivity in some longstanding stress studies.
Acute (1-hour) cold water restraint stress in mice (CWIR) effects the gastrointestinal tract permeability and microbiome. Chronic stress over weeks builds on the behavioral and sleep cumulative damage.
Human Relevance: Broader Health Consequences of Chronic Stress
Animal models of stress align give insights to explain clinical observations in human studies linking severe chronic stress to GI disorders, mood issues, and systemic inflammation and cardiovascular disease in humans.
Stress Increases Cardiovascular Disease
As mentioned above, one of the earliest events induced by chronic stress is intestinal barrier dysfunction, also called Leaky Gut, leading to translocation of gram negative bacteria into the circulation (also called low level endotoxemia), systemic inflammation and cardiovasacular disease. In 2020, Dr. Caitlin Lewis studied intestinal barrier dysfunction and its association with cardiovascular disease, even suggesting that preventing or treating intestinal barrier dysfunction is a valid therapy for preventing and treating cardiovascular disease. writing:
The gut microbiome and intestinal dysfunction have emerged as potential contributors to the development of cardiovascular disease (CVD). Alterations in gut microbiome are well documented in hypertension, atherosclerosis, and heart failure and have been investigated as a therapeutic target…Increased intestinal permeability is observed in patients and mouse models of CVD. This increased intestinal permeability can enhance systemic inflammation, alter gut immune function, and has been demonstrated as predictive of adverse cardiovascular outcomes… We outline key studies that have investigated intestinal permeability in hypertension, coronary artery disease, atherosclerosis, heart failure, and myocardial infarction. We highlight the central mechanisms involved in the breakdown of barrier function and look at emerging evidence for restored barrier function as a contributor to promising treatment strategies such as short chain fatty acid, probiotic, and renin angiotensin system-targeted therapeutics. (16)
In 2008, Dr. Dimsdale reviewed the evidence that psychological stress promotes coronary artery disease through sympathetic nervous system activation, endothelial dysfunction, increased inflammation, increasing atherosclerosis and myocardial infarction. Dr. Dimsdale writes:
There is an enormous amount of literature on psychological stress and cardiovascular disease…Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors’ contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress “causes” the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients’ suffering and enhance their quality of life. (12)
In 2017, Dr. Yaribeygi found chronic stress in humans contributes to cardiovascular disease (coronary artery disease), type 2 diabetes, disruption of the gastrointestinal barrier, depression and other neuropsychiatric disorders. (10)
In 2021, Dr. Levine detailed the mind-heart-body connection, showing that chronic stress and depression significantly elevate risks of coronary heart disease, stroke, and recurrent cardiovascular events via shared inflammatory and autonomic nervous system mechanisms. (13)
In 2007, Dr. Golden showed how stress and depression, via HPA axis hyperactivity and cortisol elevation, promote insulin resistance and type 2 diabetes in humans. (15)
In 2015, Dr. Mariotti provided insights into the molecular biology of brain-body communication under chronic stress, linking chronic stress to cardiovascular disease, diabetes, and depression through persistent systemic inflammation. (14)
Chronic Stress and Nervous Breakdown and Catatonia
The classic 1949 war movie, “Twelve O’Clock High” with Gregory Peck reveals the effect of chronic stress on B-17 pilots during the World War Two. I was impressed with the movie in how it accurately depicts the effects of chronic stress in bomber pilots in wartime, especially the effect of learned behavioral despair. After many weeks of stressful daylight bombing raids, the bomber pilot, Gregory Peck suffers a nervous breakdown and is carried away in a catatonic state. This behavior is similar to the learned behavioral despair in the restraint stress experiments in mice discussed above.
Immune Dysfunction
In 2005, Drs. Glaser and Kiecolt-Glaser reviewed how chronic stress induces immune dysfunction, showing how psychological stress disrupts the immune response, including reduced natural killer cell activity, impaired T-cell function, and altered cytokine profiles, leading to increased susceptibility to infections, delayed wound healing, and heightened risk of inflammatory and immune-related diseases. (8)
Increased Cancer Risk
In 2004, Dr. Reiche examined the connections between stress, depression, immune dysfunction and increased cancer risk. Dr. Reiche found chronic stress and chronic depression suppresses immune surveillance with decreased cytotoxic T-cell and natural killer cell activity, while promoting persistent HPA axis activation. These effects contributes to cancer development and progression. (9)
Massive Catecholamine Release
Chronic stress is causes the release of massive adrenal hormones called catecholamines. This is extremely deleterious to our immune system, increases susceptibility to viral infection, and delays wound healing. Chronic stress has been implicated in cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, gastric ulcer, as well as cancer. Note catecholamines are epinephine (adrenalin), norepinephrine (noradrenaline) and dopamine.
Can Chronic Stress Cause Cancer?
This leads us to an important question: Can chronic stress cause or accelerate cancer? Let’s examine an animal model of chronic stress to answer this question. As mentioned above, the animal model of chronic stress involves restraining mice in narrow tubes for a few hours every day. To make matters worse, the mice are immersed in cold water.
Fig 3B. Beta-adrenergic signaling in stress-enhanced Acute Lymphoblastic Leukemia (ALL) progression. Mice were injected with cancer cells tagged with fluorescent marker (blue areas tagged with Blue flourecent dye). The Green Ellipse shows control mice NO STRESS, injected with (ALL) cancer cells. Red Ellipse shows STRESSED mice with increased cancer growth compared to controls. Propranolol treated mice (Beta Blocker) had actual regression of cancer compared to controls. Figure is Courtesy of Lamkin, Donald M., et al. (7)
Lymphoblastic Leukemia Xenograft Model in Mice
In 2012, Dr. Lamkin used acute lymphoblastic leukemia (ALL) xenograft model in mice undergoing restraint stress. Human acute lymphoblastic leukemia (ALL) cells were tagged with a BLUE flourescent marker and then injected into SCID mice. Seethe above images of this mouse experiment. The propranolol treated mice has smaller blue flourescent tracer deposits compared to controls indicating less cancer growth. Note: SCID is Severe Combined Immune Deficient mice. Two weeks of daily restraint stress significantly enhanced ALL tumor burden and dissemination compared to non-stressed controls. This acceleration of cancer growth was induced by Beta-adrenergic signaling and was completely blocked by the beta-blocker drug, propranolol. Propranolol-treated mice showed reduced cancer progression, and in some cases regression, compared to controls. These findings demonstrate that chronic stress can causally accelerate cancer progression through sympathetic nervous system activation. A valid anti-cancer strategy is to block sympathetic nervous system activation using a beta-blocker drug such as propranolol. (7)
How Does Stress produce Beta-Adrenergic Nervous System Stimulation?
Chronic stress stimulates the adrenal medulla to secrete massive amounts of the catecholamines, epinephrine and norepinephrine. These stress hormones stimulate the Beta Adrenergic receptors in the nervous system, as well as directly on cancer cells in some cases.
Adrenal metastatic disease is quite common in aggressive cancers. Circulating tumor cells will tend to migrate to the adrenal medulla secreting high concentrations of catecholamines, thus causing large adrenal masses.
Conclusion: Chronic stress is unhealthy because it releases catecholamines which activate the sympathetic nervous system. Cancer cells can be sensitive to beta-adrenergic stimulation caused by chronic stress, which stimulates cancer cell growth and progression. Animal models of stress provide valuable mechanistic insights into the gut-brain axis, stress-related mucosal disease, and depression. Clinical observations links chronic stress to gastro-intestinal barrier dysfunction, chronic systemic inflammation, depression,immune dysfunction, accelerated cancer progression, coronary artery disease, type 2 diabetes, and other conditions in humans.
For patients struggling with stress-related conditions, the medical literature suggests a few interventions:
1) Support the HPA axis with adaptogens and lifestyle changes.
2) Heal the gut with diet and probiotics,
3) Optimize sleep
4) Beta-Blockers (propranolol), Bioidentical Hormones, NDT natural desiccated thyroid and cortisone (Cortef) may be helpful in selected cases.
Chronic stress isn’t “just in your head”, it reshapes your biology. If you’re dealing with fatigue, gut issues, mood changes, or sleep problems that won’t quit, this could be the tip-off of the effects of chronic stress. For more on chronic stress and adrenal fatigue, explore other articles on my site. Managing stress proactively is one of the best investments in your long-term health. (1-15)
Supplements for Reducing Elevated Cortisol of Chronic Stress
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Self Help Books On Managing Stress on Amazon
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Articles with Related Interest:
Low Level Endotoxemia and Coronary Artery Disease
Low Level Endotoxemia, Depression, Endocrinopathy and Coronary Artery Disease
Can Chronic Stress Cause Cancer?
Dr. Michael Maes on Depression and Leaky Gut
Adrenal Insufficiency, HPA Dysfunction and Fatigue
If you liked this article, you might like my book, Heart Book (left cover image) at this link on Amazon.
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References
1. Yasugaki, Sawako, et al. “Effects of 3 Weeks of Water Immersion and Restraint Stress on Sleep in Mice.” *Frontiers in Neuroscience*, vol. 13, 2019, article 1072. https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2019.01072/full (PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC6813282/).
2. Zhang, Yuan, et al. “Acute Cold Water-Immersion Restraint Stress Induces Intestinal Injury and Reduces the Diversity of Gut Microbiota in Mice.” *Frontiers in Cellular and Infection Microbiology*, vol. 11, 2021, article 706849. https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2021.706849/full (PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC8551804/).
3. Zhang, Yuan, et al. “Knockout of IL-6 Mitigates Cold Water-Immersion Restraint Stress-Induced Intestinal Epithelial Injury and Apoptosis.” *Frontiers in Immunology*, vol. 13, 2022, article 936689. https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.936689/full (PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC9732082/).
4. Chu, X., et al. “24-hour-restraint stress induces long-term depressive-like phenotypes in mice.” *Scientific Reports*, vol. 6, 2016, article 32935. https://www.nature.com/articles/srep32935.
5. Yisireyili, Maimaiti, et al. “Chronic Restraint Stress Induces Gastric Mucosal Inflammation with Enhanced Oxidative Stress in a Murine Model.” *Psychology Research and Behavior Management*, vol. 13, 2020, pp. 383–393. https://pmc.ncbi.nlm.nih.gov/articles/PMC7210023/ (DOI: 10.2147/PRBM.S250945).
6. Jiang, Sunny Zhihong, and Lee E. Eiden. “Activation of the HPA Axis and Depression of Feeding Behavior Induced by Restraint Stress Are Separately Regulated by PACAPergic Neurotransmission in the Mouse.” *Stress*, vol. 19, no. 4, 2016, pp. 374–382. https://pmc.ncbi.nlm.nih.gov/articles/PMC5564370/ (DOI: 10.1080/10253890.2016.1174851).
7. Lamkin, Donald M., et al. “Chronic stress enhances progression of acute lymphoblastic leukemia via β-adrenergic signaling.” *Brain, Behavior, and Immunity*, vol. 26, no. 4, 2012, pp. 635–641. https://pubmed.ncbi.nlm.nih.gov/22306453/ (PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC3322262/; DOI: 10.1016/j.bbi.2012.01.013).
8. Glaser, Ronald, and Janice K. Kiecolt-Glaser. “Stress-induced immune dysfunction: implications for health.” *Nature Reviews Immunology*, vol. 5, no. 3, 2005, pp. 243–251. https://pubmed.ncbi.nlm.nih.gov/15738954/ (DOI: 10.1038/nri1571).
9. Reiche, Edna Maria Vissoci, et al. “Stress, depression, the immune system, and cancer.” *The Lancet Oncology*, vol. 5, no. 10, 2004, pp. 617–625. https://pubmed.ncbi.nlm.nih.gov/15465465/ (DOI: 10.1016/S1470-2045(04)01597-9).
10. Yaribeygi, Habib, et al. “The Impact of Stress on Body Function: A Review.” *EXCLI Journal*, vol. 16, 2017, pp. 1057–1072. https://pmc.ncbi.nlm.nih.gov/articles/PMC5579396/.
11. Kelly, John R., et al. “Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders.” *Frontiers in Cellular Neuroscience*, vol. 9, 2015, article 392. https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2015.00392/full.
12. Dimsdale, Joel E. “Psychological Stress and Cardiovascular Disease.” *Journal of the American College of Cardiology*, vol. 51, no. 13, 2008, pp. 1237–1246. https://www.sciencedirect.com/science/article/pii/S0735109708002581.
There is an enormous amount of literature on psychological stress and cardiovascular disease…Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors’ contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress “causes” the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients’ suffering and enhance their quality of life.
13. Levine, Glenn N., et al. “Psychological Health, Well-Being, and the Mind-Heart-Body Connection: A Scientific Statement From the American Heart Association.” *Circulation*, vol. 144, no. 9, 2021, pp. e368–e402. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000947.
14. Mariotti, Agnese. “The effects of chronic stress on health: new insights into the molecular mechanisms of brain-body communication.” *Future Science OA*, vol. 1, no. 3, 2015, FSO23. https://pmc.ncbi.nlm.nih.gov/articles/PMC5137920/.
15. Golden, Sherita Hill, et al. “A review of the evidence for a neuroendocrine link between stress, depression and diabetes.” *Current Diabetes Reviews*, vol. 3, no. 4, 2007, pp. 252–259. (Available via PubMed or academic databases).
16. Lewis, Caitlin V., and W. Robert Taylor. “Intestinal barrier dysfunction as a therapeutic target for cardiovascular disease.” American Journal of Physiology-Heart and Circulatory Physiology (2020).
The gut microbiome and intestinal dysfunction have emerged as potential contributors to the development of cardiovascular disease (CVD). Alterations in gut microbiome are well documented in hypertension, atherosclerosis, and heart failure and have been investigated as a therapeutic target…Increased intestinal permeability is observed in patients and mouse models of CVD. This increased intestinal permeability can enhance systemic inflammation, alter gut immune function, and has been demonstrated as predictive of adverse cardiovascular outcomes… We outline key studies that have investigated intestinal permeability in hypertension, coronary artery disease, atherosclerosis, heart failure, and myocardial infarction. We highlight the central mechanisms involved in the breakdown of barrier function and look at emerging evidence for restored barrier function as a contributor to promising treatment strategies such as short chain fatty acid, probiotic, and renin angiotensin system-targeted therapeutics.
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Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
954-792-4663
my web site: https://drjeffreydachmd.com/
my personal blog: www.jeffreydachmd.com
Bioidentical Hormones 101 Second Edition
Menopausal Hormone Replacement, Health Benefits
Natural Thyroid Toolkit by Jeffrey Dach MD
Cracking Cancer Toolkit ebook
Cracking Cancer Toolkit print version
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www.naturalmedicine101.com
www.bioidenticalhormones101.com
www.truemedmd.com
www.drdach.com
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