Eating Chili "gets angry"
Pepper is the favorite of many people.
But after eating Chili, the oral mucosa will feel burning and even swelling.
Later, it will also lead to acid reflux, stomach pain and anal pain.
Patients with hemorrhoids can also induce hemorrhoids, and even people without hemorrhoids can cause rectal bleeding.
Even intact skin without damage will feel burning when exposed to capsaicin.
These are collectively referred to as "getting angry" caused by eating Chili peppers.
Many people are obsessed with whether these "stimuli" caused by eating peppers are "getting angry". Is getting angry a science?
In fact, this is unnecessary.
As long as the "irritating" symptoms described above are true, what is the difference between calling them "excessive internal heat", "upper inflammation", "upper inflammation" or any other name?
For example, you are called "Li Wei Zheng Guang" on the other side, but your parents call you "Sanwazi". You are still you.
Spicy is not the same taste.
Why are peppers so "irritating"?
It is now known that this intense stimulation of pepper is caused by capsaicin in pepper. In fact, capsaicin was isolated by scientists as early as 1876, and its chemical structure was confirmed by 1920 as a vanillin.
In China, spicy or pungent has always been regarded as one of the five classic tastes, namely, the so-called sweet, sour, bitter, spicy and salty, with mixed flavors.
In foreign countries, spicy is never a taste, but is considered as a feeling of hot pain.
Whether it is a taste or not, the molecular mechanism of capsaicin, a strong stimulus (so-called science), has not been clarified. It was not until 1997 that capsaicin receptor was successfully cloned.
Because capsaicin belongs to vanillin in chemical structure, this receptor was originally named vanillin receptor VR 1, commonly known as capsaicin receptor.
Further research shows that VR 1 receptor is essentially a cation channel, and the cation channel with similar structure is not just VR 1, but a superfamily with many members, which is called transient receptor potential (TRP) receptor family. According to the structural characteristics and discovery order, capsaicin receptor was finally named TRPV 1.
At present, it is known that TRPV 1 is activated by capsaicin, which causes the influx of calcium ions and produces action potential. Electrical signals are transmitted along the nerve and relayed through the thalamus, producing a feeling of heat and pain in the cortex.
So science has proved that spicy is not a taste.
Why does capsaicin cause "excessive internal heat"?
There are many articles on this topic on the Internet, but there seems to be no scientific explanation.
So, what is the real science of eating Chili "getting angry"?
As mentioned above, TRPV 1 is a cation channel. As a receptor, it can be activated by dozens of known substances and factors, including heat (the temperature threshold determined by in vitro experiments is > 42), acid (pH < 5.9), ethanol, trypsin, tryptase, allicin and ginger oil.
In addition, TRPV 1 is widely distributed in the body together with other members of TRP family, and acts as a wide range of receptors, such as temperature sense.
According to the textbooks we studied in the past, our skin and mucous membranes, as well as other parts of the body, are all distributed with receptors dedicated to sensing various stimuli. For example, there are temperature sensors, pain sensors, tension sensors and so on. In fact, in the past, the molecular structure and mechanism of these feelings were not clearly understood. What the book says is just to make up these easy-to-understand things to fool students.
Even today, the exact mechanism of feeling is still unclear.
However, it is known that sensation is produced by some receptors at the axon end of primary sensory neurons (so-called sensory nerve endings), such as TRP superfamily, which receive various stimuli and convert them into neuroelectric signals.
Among them, primary sensory neurons can be divided into two categories: one is to feel nociceptive stimuli, called nociceptive sensory nerves. Nerve fibers are mainly unmyelinated thin type C fibers, which are also called capsaicin-sensitive nerves in the early stage because of their sensitivity to capsaicin. Another feeling is harmless stimulation.
Although TRPV 1 is distributed in various tissues in vivo, immunohistochemical studies have confirmed that it is widely distributed in various nociceptive nerve fibers.
Another feature of these sensory nerves sensitive to capsaicin is that they are also peptidergic nerves. After the receptor is activated, it will not only produce electrical signals to upload feelings, but also secrete a series of neuropeptides.
Now we know that this neuropeptide series is a long list. Several of them have been studied in depth and their functions have been understood. For example, calcitonin gene-related peptide produces vasodilation, leading to congestion. Substance P increases capillary permeability, leading to plasma extravasation and edema. Neurokinin can stimulate pain. These neuropeptides work together to present a typical inflammatory reaction, which is called neurogenic inflammation.
That is to say, capsaicin can directly cause inflammation in the stimulated part, which is the science behind capsaicin causing excessive internal heat.
Neurogenic inflammation
What? Did I learn a fake textbook? Isn't inflammatory reaction a patent of immune system? How dare anyone go so far as to bypass the immune system and launch an inflammatory war without authorization?
There's no need to make such a fuss. Neuroinflammation is nothing new.
As early as 1 century ago and 190 1 year ago, scientists had stimulated the dorsal root ganglion of the spinal cord to cause skin swelling in the dominant area, and put forward the concept of neurogenic inflammation unrelated to immune response.
However, because there is no way to understand its molecular mechanism, it has been shelved by people.
Neurogenic inflammation has been paid more attention in recent decades, and the determination of related cellular mechanisms and transmitters began in the 1980s, especially after scientists used substance P and calcitonin gene-related peptide to simulate inflammatory reaction in 1995.
What is neurogenic inflammation?
Simply put, any factor identified by primary sensory nerves as possibly causing real or potential harm may directly stimulate neurons to produce neuropeptides, which are released from nerve endings, and directly stimulate local vasodilation, increase vascular permeability and increase plasma exudation without going through the immune system, showing typical "redness, swelling and heat pain" of inflammatory reaction.
Distribution of capsaicin receptor and expression of capsaicin gas
Capsaicin is dehydrogenated and metabolized in vivo, so irritating capsaicin and capsaicin can only contact TRPV 1 receptor, and activate the expression of sensory nerve fibers in skin, digestive tract, airway and conjunctiva.
TRPV 1 exists, and it can also express inflammatory neuropeptides, that is, sensory nerves that can be stimulated by capsaicin to cause neurogenic inflammation, which are widely distributed in oral mucosa, esophagus, stomach, small intestine, colon and rectum mucosa, smooth muscle nerves, and some non-nerve tissues.
In other words, capsaicin can stimulate the whole digestive tract mucosa to produce neurogenic inflammatory reaction, congestion and edema, significantly increase vascular permeability, and even bleeding. Especially in rectum, the distribution density of TRPV 1 is many times that of colon, so it is more sensitive to capsaicin and more prone to bleeding. This is the reason why eating Chili peppers causes hemorrhoids bleeding.
Nerves in oral mucosa and anus belong to somatic sensory nerves, which can directly produce stress heat pain when stimulated by capsaicin.
Although the esophagus, stomach, small intestine, colon and rectum are innervated by visceral nerves, capsaicin stimulation will not directly produce the feeling of hot pain. However, neurogenic inflammation can increase the pain sensitivity of these parts and make visceral pain caused by other stimuli sensitive.
For example, after eating Chili, the stomach and esophageal mucosa are more sensitive to acid damage, which is more likely to cause heartburn, stomachache and other symptoms. Similarly, when there are other inflammatory diseases in the gastrointestinal tract, such as Crohn's disease and ulcerative colitis, eating peppers will aggravate the symptoms of these diseases.
It should be pointed out that because neurogenic inflammation is mild and transient and self-healing, these symptoms after eating Chili do not mean that the original disease is aggravated. That is to say, capsaicin stimulation did not really aggravate the disease.
The activation of TRPV 1 of the intermuscular nerve of gastrointestinal smooth muscle can also increase the smooth muscle movement, which can obviously lead to malabsorption, and substances that are not fully digested and absorbed enter the colon, causing osmotic diarrhea. This is why some people have diarrhea when they eat Chili.
Eating Chili "getting angry" does not require "getting angry" treatment.
Neurogenic inflammation induced by capsaicin and mediated by TRPV 1 is a defense response of the body to substances identified as potentially harmful, and participates in the main defense system of the body together with the inflammatory response mediated by the immune system.
However, unlike infectious inflammation and autoimmune inflammation mediated by immune response, neurogenic inflammation is usually temporary and mild, and it will pass quickly without any treatment.
Besides TRPV 1 antagonist, there are no drugs and methods for treatment at present.
Therefore, any "fire-reducing" drugs and methods that claim to treat "excessive internal heat" caused by eating Chili peppers are deceptive.