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===== Psychological stress and immune function ===== | ===== Psychological stress and immune function ===== | ||
- | Researchers have shown that stress has certain detrimental effects on immune function, including reduced natural kill cell activity, lymphocyte populations, | + | Researchers have shown that stress has certain detrimental effects on immune function, including reduced natural kill cell activity, lymphocyte populations, |
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===== Psychological stress and disease ===== | ===== Psychological stress and disease ===== | ||
- | Some researchers have concluded that stressors may trigger disease in susceptible individuals. These researchers point to retrospective studies, which have found that a high proportion of certain kinds of patients reported uncommon emotional stress before disease onset.(({{pubmed> | + | Some researchers have concluded that stressors may trigger disease in susceptible individuals. These researchers point to retrospective studies, which have found that a high proportion of certain kinds of patients reported uncommon emotional stress before disease onset.(({{pmid> |
- | * periodontal disease (({{pubmed> | + | * periodontal disease (({{pmid> |
- | * Graves' | + | * Graves' |
- | * cardiovascular disease, diabetes, gastrointestinal disease, fibromyalgia, | + | * cardiovascular disease, diabetes, gastrointestinal disease, fibromyalgia, |
- | * many of the common autoimmune diseases including rheumatoid arthritis, psoriasis, insulin-dependent diabetes, and thyroid disease.(({{pubmed> | + | * many of the common autoimmune diseases including rheumatoid arthritis, psoriasis, insulin-dependent diabetes, and thyroid disease.(({{pmid> |
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- | Some bacterial pathogens directly respond to stress-induced neuroendocrine hormones, reacting to stress in parallel to host immune cells. For example, when catecholaminergic nerves within the gut release norepinephrine, | + | Some bacterial pathogens directly respond to stress-induced neuroendocrine hormones, reacting to stress in parallel to host immune cells. For example, when catecholaminergic nerves within the gut release norepinephrine, |
==== Stress hormones promote iron availability ==== | ==== Stress hormones promote iron availability ==== | ||
- | According to Sandrini //et al.//, stress hormones form complexes with iron-sequestering proteins such as transferrin and lactoferrin, | + | According to Sandrini //et al.//, stress hormones form complexes with iron-sequestering proteins such as transferrin and lactoferrin, |
- | A second mechanism is independent of host iron and, instead, involves synthesis of a novel growth stimulator among many different species of bacteria. This autoinducer restores active growth for several pathogens, including //E. coli// O157:H7 and // | + | A second mechanism is independent of host iron and, instead, involves synthesis of a novel growth stimulator among many different species of bacteria. This autoinducer restores active growth for several pathogens, including //E. coli// O157:H7 and // |
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==== Epinephrine as a quorum sensing molecule ==== | ==== Epinephrine as a quorum sensing molecule ==== | ||
- | Epinephrine, | + | Epinephrine, |
- | // | + | // |
- | However, the stress response by the host does not appear to be detrimental in all respects. In // | + | However, the stress response by the host does not appear to be detrimental in all respects. In // |
===== Physical stress and disease ===== | ===== Physical stress and disease ===== | ||
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In susceptible individuals, | In susceptible individuals, | ||
- | * psoriasis and vitiligo (({{pubmed> | + | * psoriasis and vitiligo (({{pmid> |
- | * fibromyalgia (({{pubmed> | + | * fibromyalgia (({{pmid> |
< | < | ||
Motor vehicle collision trauma appears capable of triggering FM, but generally not through direct biomechanical injury. Instead, the evidence suggests that MVC trauma can act as a " | Motor vehicle collision trauma appears capable of triggering FM, but generally not through direct biomechanical injury. Instead, the evidence suggests that MVC trauma can act as a " | ||
- | // | + | // |
- | Microbes in combination with physical stress have been shown to induce memory dysfunction in mice. Mice were infected with the non-invasive intestinal pathogen, // | + | Microbes in combination with physical stress have been shown to induce memory dysfunction in mice. Mice were infected with the non-invasive intestinal pathogen, // |
===== War – a crucible for chronic disease===== | ===== War – a crucible for chronic disease===== | ||
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There are a number of circumstances inherent to war which appear to drive the prevalence of chronic disease. | There are a number of circumstances inherent to war which appear to drive the prevalence of chronic disease. | ||
- | * **Acquisition of new pathogens** – As discussed in a [[http:// | + | * **Acquisition of new pathogens** – As discussed in a [[https:// |
- | * **Physical trauma and stress** – Fibromyalgia patients are more likely to report significant physical trauma prior to disease onset.(({{pubmed> | + | * **Physical trauma and stress** – Fibromyalgia patients are more likely to report significant physical trauma prior to disease onset.(({{pmid> |
- | * **Psychological stress** – Studies have linked traumatic stress exposures to a wide variety of conditions.(({{pubmed> | + | * **Psychological stress** – Studies have linked traumatic stress exposures to a wide variety of conditions.(({{pmid> |
* **Use of vaccines** | * **Use of vaccines** | ||
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Epidemiological evidence that war predisposes combatants, their families, and other noncombatants to increased rates of certain chronic diseases. These conditions include: | Epidemiological evidence that war predisposes combatants, their families, and other noncombatants to increased rates of certain chronic diseases. These conditions include: | ||
- | * **Hypertension and obesity** – Among, displaced Croatians who survived the Croatian War of Independence, | + | * **Hypertension and obesity** – Among, displaced Croatians who survived the Croatian War of Independence, |
- | * **Cancer** – Another study also looking at Croatians found that those who got breast cancer during the war, as opposed to the time before and after the war, were significantly more likely to get it earlier in life and to survive for less time.(({{pubmed> | + | * **Cancer** – Another study also looking at Croatians found that those who got breast cancer during the war, as opposed to the time before and after the war, were significantly more likely to get it earlier in life and to survive for less time.(({{pmid> |
- | * **Chronic Fatigue Syndrome** – Fourteen years after deployment, 1991 Gulf War veterans continue to report a higher prevalence of many adverse health outcomes, compared with Gulf Era veterans including unexplained multi-symptom illness, chronic fatigue syndrome-like illness, posttraumatic stress disorder, and functional impairment.(({{pubmed> | + | * **Chronic Fatigue Syndrome** – Fourteen years after deployment, 1991 Gulf War veterans continue to report a higher prevalence of many adverse health outcomes, compared with Gulf Era veterans including unexplained multi-symptom illness, chronic fatigue syndrome-like illness, posttraumatic stress disorder, and functional impairment.(({{pmid> |
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===== Read more ===== | ===== Read more ===== | ||
- | Mast cell activation plays an important role in stress-mediated disease pathogenesis. | + | Mast cell activation plays an important role in stress-mediated disease pathogenesis. |
- | * [[http:// | + | * [[https:// |
{{tag> | {{tag> | ||
+ | < | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
*Legacy content | *Legacy content | ||
- | * http:// | + | * https:// |
* explain car accidents, etc. as disease triggers1 2 Blaney: “I have observed in many patients that an important precipitator of increased Th1 disease is physical injury. My speculation is that the physical trauma further activated AT1 due to the wound response, suppressing the immune system further and allowing increased bacterial growth.” | * explain car accidents, etc. as disease triggers1 2 Blaney: “I have observed in many patients that an important precipitator of increased Th1 disease is physical injury. My speculation is that the physical trauma further activated AT1 due to the wound response, suppressing the immune system further and allowing increased bacterial growth.” | ||
- | =====References===== | + | =====References=====</ |