Daily stress can induce fibromyalgia. Fibromyalgia refers to chronic muscle pain all over the body, which may be accompanied by symptoms such as insomnia, anxiety
Daily stress can induce fibromyalgia. Fibromyalgia refers to chronic muscle pain all over the body, which may be accompanied by symptoms such as insomnia, anxiety and depression. The pathogenesis has always been an unsolved mystery. Chen Zhicheng, a researcher and research team from the Institute of Biomedicine of China Academy of Sciences, discovered the possible physiological and psychological pathogenesis of fibromyalgia and the key inhibitory factors. The paper was published in the September 2020 issue of Rheumatology Yearbook.
Fibromyalgia cannot be cured. The most common symptom of fibromyalgia is chronic muscle ache all over the body, accompanied by fatigue, insomnia, anxiety and uneasiness. It is sometimes called "princess disease", and when you are a little tired, you will feel pain all over. At present, the pathogenesis of the disease is not clear in medicine, and patients often can't find a clear cause after continuous referral, so there is no exclusive drug treatment, so they can only relieve the symptoms first, but the effect is quite limited.
Fibromyalgia is a very common but mysterious pain disease. Among adults, about 2 ~ 6% people suffer from this disease, which is characterized by chronic systemic muscle pain, accompanied by fatigue, insomnia, anxiety, depression and other symptoms, which seriously affects the quality of life of patients and even leads to disability. However, IStock found clinically that mental stress in daily life can induce or aggravate the symptoms of fibromyalgia. Behind most patients is a story, which may include family, relatives and friends, economy, work and other issues. Who is the cause and the result of psychological stress and fibromyalgia? What is the pathogenic mechanism behind it? "We must establish an animal model that can respond to fibromyalgia to verify the relationship between psychological stress and fibromyalgia." Chen Zhicheng.
Before that, let's look at how the pain is caused.
In the past, it was thought that tissue acidification would cause pain. 1980, the Germans did human experiments and injected acidic substances directly into the human body. It was found that it did cause pain, and the faster the flow rate, the more painful it was, which preliminarily proved the causal relationship between acid and soreness. However, the molecular mechanism of acid-induced nerve pain has not been determined.
Chen Zhicheng tried to establish an animal model of fibromyalgia. They injected acidic saline into mice first, then pressed muscles or squeezed the soles of mice's feet with fine nylon thread. They found that mice will shrink their feet when they touch * * *, which shows that there is indeed "hyperalgesia", but this hyperalgesia will disappear after 24 hours. However, if you hit in the same position again within five days, it will lead to pain allergy that lasts for about one month, and there will be mirror pain, which successfully conforms to the characteristics of fibromyalgia.
This mouse experimental model provides a platform for Chen Zhicheng to deeply study how tissue acidification induces chronic muscle pain from the molecular mechanism of neurology.
There are nociceptive nerves in all tissues of our body, and there are many ion channels or receptor molecules that can be activated by acid, among which the most important ones include acid-sensitive ion channels (ASICs) and capsaicin receptor protein (TRPV 1). Chen Zhicheng experiment found that if ASICs or TRPV 1 were inhibited by drugs, muscle acidification after five days could not induce chronic pain. However, if muscle acidification occurs again the next day, it will still induce hyperalgesia for 7 ~ 10 days. Therefore, Chen Zhicheng concluded that the first acidification of muscle tissue not only induced short-term pain allergy, but also led to plastic changes of muscle pain nerves. Therefore, it is enough to develop chronic pain through muscle acidification again within five days.
All tissues in our body have nociceptive nerves, and there are many ion channels or receptor molecules corresponding to different pain sources on the nociceptive nerves, among which acid-sensitive ion channels (ASICs) and capsaicin receptor protein (TRPV 1) can be activated by acid. In order to understand the molecular mechanism of ache in neuroscience, the next step is to establish an animal model of ache caused by psychological stress. How? Noise is a good tool! General sources of stress are difficult to quantify, but noise can be converted into decibels and programmed, which is easier to master.
They let the mouse stay in the cage and play sharp ultrasonic noise from time to time, which may not be heard by human ears. Repeat it six times a day, and then repeat it for two days after two days ... As a result, the mice under noise pressure developed pain allergy for about one month. "We found that the key is to have uncertain, intermittent and repeated pressures. If it lasts for a short time, mice will not have chronic pain allergy. 」
In addition, patients with fibromyalgia are often accompanied by diseases, such as anxiety, depression and other emotional problems. They observed the pain-allergic mice, and their anxiety behavior became obvious: generally healthy mice like to explore and play everywhere, and dare to walk to the open and hanging parts on both sides when they are put into the cross maze, while mice with anxiety behavior like to hide in a hidden space and dare not run out.
Stress-> lipid oxidation-> After establishing an animal model of pain signals, he and the research team wanted to know what caused the pain in the body.
They analyzed the lipids in the blood of mice and found that mice metabolized a special group of lipids after being stressed. "We found an oxidized lipid LPC 16:0: 0, which makes people shine!" Chen Zhicheng said. It turns out that a few years ago, French scientists found that this oxidized lipid LPC 16:0: 0 can specifically sense the acid-sensitive ion channels of ASIC3 on * * * sensory neurons. That's right. Everything seems to be connected.
After repeated experiments, the outline of the pathogenic mechanism is gradually clear! External pressure source (noise) will lead to the increase of oxidative stress in mice, which will lead to abnormal lipid metabolism, produce excessive oxidized lipid LPC 16:0: 0, activate ASIC3 acid-sensitive ion channels on muscle sensory neurons, and cause pain allergy, which will last for * * * and turn into chronic pain.
There is something in the study (source | Chen Zhicheng). The treatment of fibromyalgia has begun to take shape.