Stress and autoimmune diseases: What you should know
People generally react to stress in various ways. Chronic stress will manifest itself in ways that leave many people scratching their heads, but most doctors will understand the telltale signs. These can include: Insomnia in people who have never had a problem with sleep, difficulty in controlling blood sugar levels that were previously manageable, sudden bloating upon eating in individuals who have had no previous intolerance to certain foods and many others. Research indicates that CBD can be used to manage stress – as it is used to fight against several autoimmune disorders. However we’d like to dedicate this article to all our friends around the world who suffer from these related illnesses – and welcome them to the Terravida community.
A recent study, in Iceland, linked autoimmune disorders to stress, and more specifically they found that severe stress will increase the likelihood of these diseases.
The study involved the records of more than 100,000 Swedish adults who had been diagnosed with stress-related psychiatric disorders. They also included the medical records of 126,652 siblings of these patients and those of 1.1 million unrelated individuals. The two second groups had no stress-related disorders. The average age of those with stress related psychiatric disorders was 41 and 40% of them were male.
The study was conducted over a ten year period, and showed that a larger number of those with stress-related psychiatric disorder were diagnosed with an autoimmune disease when compared to the other groups observed.
The autoimmune diseases included Addison’s disease, rheumatoid arthritis, psoriasis, multiple sclerosis, Crohn’s and celiac disease. The risk of developing any particular autoimmune disease differed and there was a higher risk for celiac disease than rheumatoid arthritis.
For those worried that a stressful period at work could offset an autoimmune disease, the answer is, NO. The research does not refer to simple stress but to a diagnosed psychiatric disorder. The list of stress disorders that were associated with increased risk included post -traumatic stress disorder, acute stress reaction, and adjustment disorders.
However, they hastened to point out that the differences between the various groups studied were not so significant as to warrant special monitoring of those people who have been diagnosed with a stress disorder. One of the encouraging findings of the report was that treating Post Traumatic Stress Disorder (PTSD) with an antidepressant reduced the risk.
Autoimmune diseases are debilitating and life changing. These include conditions such as multiple sclerosis (M.S.) rheumatoid arthritis, psoriasis (a condition of the skin) and celiac disease (intestinal reaction to gluten), Grave’s disease (overactive thyroid) and anemia.
Even if there is only a weak connection between PSTD and one of the autoimmune diseases, we still need to know why. Scientists are working hard at trying to figure out if changes in cortisol levels or pro –inflammatory cytokine levels could be responsible. There is also the possibility of an over active inflammatory immune system.
Moreover, what makes the study results more concerning is that those who already have to deal with a stress related disorder, which already affects their lives significantly might then have to endure an autoimmune disease which could greatly diminish their quality of life. However, the research found that by treating the depression the risk for contacting an autoimmune disease was greatly reduced. Therefore, treating one lifelong disorder may be the answer to preventing another one from developing.
NNAI and Psychosis are Linked
Research conducted on data from between 1981-1998, in Denmark had uncovered a link between schizophrenia and certain autoimmune disorders. Eaton and his colleagues concluded on reviewing the data presented to them by the Danish Psychiatric Register (which included information on people diagnosed with schizophrenia) that people with a history of autoimmune disease had a 45% increased risk for schizophrenia.
There were also some autoimmune diseases that were more prevalent in schizophrenia sufferers: Acquired hemolytic anemia (a rare blood disease), alopecia areata (causes spot baldness), chronic active hepatitis, intestinal mal-absorption, interstitial cystitis, myositis (muscle inflammation), polymyalgia rheumatic (muscle pain and stiffness caused by inflammation), and Sjögren’s syndrome (a dry eyes / mouth condition), and thyotoxicosis (excess thyroid hormones).
In another study of Danish registers it was found that autoimmune disease increased the risk for schizophrenia by 30% and a history of hospitalization with an infection increased the risk by 60%. This is based on a study by Benros et al, (2011) and was published in the American Journal of Psychiatry, 168, 1303-1310.
Chen and his associates also published a paper in The British Journal of Psychiatry in 2012 in which their observations of 11,000 in-patients with schizophrenia showed increased risks for Celiac disease (causing abnormal intestinal reaction to gluten), Grave’s disease (causes overproduction of thyroid hormone), hypersensitivity vasculitis (inflammation of the blood vessels), pernicious anemia (causes vitamin B12 deficiency) and psoriasis (a condition of the skin).
The most recent study, a meta-analysis of 31 previously published studies, was completed in April 2018 and was conducted by Cullen and his colleagues on data collected from over 25 million people. The results showed that there was an association between psychosis and non-neurological autoimmune disorders (NNAI). These are autoimmune disorders that do not affect the brain but the peripheral systems (blood, skin etc.).
There was a positive association between psychosis and celiac disease, Grave’s disease, pernicious anemia, pemphigoid (a rare skin disease) and psoriasis.
The meta-analysis showed a negative association between psychosis and rheumatoid arthritis which affects mostly the joints and ankylosing spondylitis, which is a form of arthritis affecting the spine.
Even though the effect size was rather small with an odds ratio of 1.26, its results were consistent across all research designs.
A temporal analysis showed that there was a co-occurrence of psychosis and autoimmune diseases. It also showed that the presence of psychosis increases the risk of NNAI disorder, and that NNAI disorders also increased the risk of psychosis.
Since different pathways have been implicated, there is still no single explanation for the association of NNAI and psychosis.
One of the explanations for this is that infectious agents might affect the neurons and the brain and directly be causing psychosis; or that they could indirectly be activating the immune system.
Another explanation offered is that through autoimmune mechanisms, immune system proteins are produced, which then attacks various body organs causing inflammation e.g. the blood.
A third possibility seems to indicate two varying but complex developments. In the first, someone who has a genetic predilection and is exposed to stress or infection, this will result in brain irregularities or vulnerabilities. The second one refers to environmental or internal changes. These could be triggered by puberty, bacteria or stress which later results in neuronal circuits which could cause psychosis.
None of these links are new thoughts, many researchers have supported the idea that schizophrenia and autoimmune disorders are connected. Despite these shared views by scientist, Cullen et al are still reluctant to offer recommendations on treatments. However, they do suggest the careful monitoring of people with autoimmune diseases for early signs of psychotic disorders.
Narcolepsy, stress and the autoimmune system
The sleep disorder, narcolepsy, is not as rare as many believe. In the US alone it is estimated that 1.3 million people suffer from it, with symptoms often beginning in childhood or early adulthood. The condition is often not recognized immediately.
The effects of narcolepsy are debilitating, because of sleep disruptions and sufferers experience extreme daytime tiredness and sudden “sleep attacks”. Other symptoms include poor nighttime sleep with frequent awakenings, hallucinations, intense dreams and episodes of paralysis just before sleeping or waking. Cataplexy is another symptom that causes muscle weakness making it impossible for sufferers to move.
The causes of narcolepsy are relatively unknown. However, most people with the condition have decreased levels of hypocretin, a brain protein which regulates sleep-wake cycles. Scientists have identified several factors which can cause low hypocretin levels: a gene mutation, hereditary deficiency, an immune system attack on healthy cells, exposure to toxins, infections and stress also seems to play a significant role.
Recent breakthroughs, through two independent studies, have provided strong evidence that narcolepsy is an autoimmune disorder and is caused by a variation of an immune-system gene that triggers the body’s defense system in a mistaken response.
A team of researchers at Stanford University, concentrated their study on T-cell activity and how they respond to hypocretin. Their subjects included people with narcolepsy and volunteers who showed a genetic predisposition to narcolepsy.
A number of important discoveries were made: The group of patients with narcolepsy had hypocretin-producing neurons stimulating T-cell immune response, whereas, this did not occur in the patients without narcolepsy. In this study, the immune system of the patients with narcolepsy reacted to the hypocretin-producing neurons as if they were a threat instead of recognizing them as the producers of essential neurotransmitters.
The researchers also found that a portion of the hypocretin protein is similar to a protein found in the H1N1 strain of influenza (swine flu) which was widespread in 2009. The vaccinations, used to immunize people in Europe against H1N1, were later associated with a spike in cases of narcolepsy. The vaccine was never used in the US and Europe also stopped its use after the 2009-2010 influenza season.
In order to test the connection between H1N1 and narcolepsy, the scientists wanted to examine whether the immune systems of people with the disorder would attack and destroy the neurons that produce hypocretin, because of its similarity to the H1N1 virus. T-cells from the patients were exposed to H1N1 and the scientists found that there was indeed a spike in T-cell attacks which targeted the hypocretin- producing neurons. Evidence was also found that people who are predisposed could have other similar viruses lead an immune system attack to the source of hypocretin in the body.
Genetic predisposition was also recently studied by scientists at the Center for Integrative Genomics at Switzerland’s University of Lausanne. The link between narcolepsy and a gene variation that is involved in immune system function was investigated.
The human leukocyte antigen system (HLA) is where the genetic variant is located. This system is responsible for targeting potentially dangerous antigens and is supposed to leave living, normal and healthy tissue alone.
This study incorporated a group of 1,261 patients with narcolepsy and a control group of 1,422 people without the disorder. Genotyping was used to identify and map each participant’s individual genetic variations. There are several already known genetic variants within the HLA system. Subjects with one particular variant were found to be 251 times more likely to have narcolepsy and 100% of the participants with narcolepsy had the gene variation.
Another four types of gene variations were discovered that appeared to have a protective effect against the disorder. The scientists agree that the gene variant responsible for narcolepsy is not so rare and they estimate that 20% of the population of Europe has it. Not everyone who has the gene variation will get narcolepsy, but everyone who develops narcolepsy has the variant. This puts those with the gene variation in the high risk category and at-risk individuals are easier to identify and diagnosed correctly.
What are autoimmune disorders?
Autoimmune disorders result from an attack on healthy tissue by the body’s own immune system. This is caused by a mistaken misinterpretation of healthy tissue as potentially harmful and the body’s immune system reacts as it would in the event of a real threat from a virus, bacteria or any other toxins and attacks it.
What happens when we are stressed?
Acute stress begins with a rise in sympathetic arousal, followed by and HPA-axis response. There are seven known processes which take place during acute stress. When someone has chronic stress these two processes can become excessive, muted or irregular, causing cortisol levels to take longer to return to normal. Between two episodes of acute stress these levels may have not returned to normal at all.
Similarly, other activities can go awry during periods of acute or chronic stress in any of the other processes taking place in the body and include: a temporary rise in inflammation; reduced cortical control over emotional reactivity, heightened motivation, an increase in flexibility in the hippocampus and prefrontal cortex, temporary insulin resistance and vulnerabilities within the body clock.
The brain responds to chronic stress by temporarily adapting to change, but it may also structurally change, something called allostasis. Recent research in Sweden showed a possible correlation between chronic stress and a “thinning” in certain areas of the human brain, including the prefrontal cortex.
Does acute stress lead to chronic stress?
Frequent or intense acute stress often leads to chronic stress, but emerging research is showing that chronic stress may emerge even without any obvious or previous source of acute stress.
Contributing factors to chronic stress include: circadian disruption from reduced sunlight or darkness hours, loneliness, not eating well and dissatisfaction within the work environment. Once again we see that any of the pathways that can be affected by chronic stress can then become aggravated.
A body clock mal-function will affect the circadian rhythm, in a sympathetic and parasympathetic tone, and in the cortisol awakening response. This in turn will alter sympathetic reactivity to stress and the HPA-Axis response, moving the brain toward chronic stress.
Chronic psychological stress can bring about chronic inflammation, while inflammation from another source can also trigger stress by increasing sympathetic activity.
Can chronic stress be recognized by any anyone?
Conditions such as diabetes, heart disease, obesity, depression, the common cold and autoimmune disorders carry a risk factor for developing chronic stress. Chronic stress often leads to an opioid addiction, currently a concerning problem in the US.
With the ever rising numbers of diabetics, heart disease sufferers, problems with obesity and depression in the US, it follows that chronic stress needs to be identified within individuals in a timely manner. The symptoms of chronic stress vary, but generally speaking doctors know that disruptions in the circadian rhythm, irritable bowel syndromes and the inability to control blood glucose levels are some of the tell tale signs it.
Since chronic stress is allostatic it can be managed with lifestyle interventions during its early stages. Vigilance is needed in spotting the signs of stress because they are not always as obvious as we are led to believe.
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