After respiratory infection, the recruiter may suffer from fever, soreness, exhaustion and other one or more uncomfortable symptoms, especially for children, as well as themselves or their families often feel that "sick is too pitiful, have to eat some delicious supplements, even if you don't want to eat more food, increase nutrition and resistance to get better faster", so patients are often compensated during infection and eat fried chicken elbow ice cream and other high-calorie foods. There are also people who hold completely opposite views, thinking that it is faster to be hungry, and if they are recruited, they will not eat anything.
So, which approach is more scientific?
1. Catch up vs. starve
In the earlier
Saving the immune system of face blindness (2): reducing burden
, food and heart introduction, the human immune system and metabolic system have a lot of shared resources, eating too much will cause the metabolic system to seize resources, reduce immunity.
For the average person, eating food is not only delicious, but also contains various nutrients; But for the human immune system, substances that enter the digestive tract (various foods and water) may be nutrients or carry a large number of disease-causing molecules (pathogens or foreign substances), which can be absorbed only if they are harmless.
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A summary of the latest scientific research on the new coronavirus – what daily life factors can help us fight the virus
It has also been introduced that eating too much will reduce the ability of stomach acid to kill the new crown virus, and indirectly promote virus survival and infection.
Speaking of which, readers and friends may already understand. When infected with the flu or new coronavirus, many people will have symptoms such as nausea and do not want to eat, so there is no need to worry at all. This means that in your gut, which determines 70-80% of immune function, and the immune system is focused on fighting the virus, eating less for a few days will not affect your health. But by drinking enough water, your immune system can initiate a process to eliminate the virus.
So, why does eating a large meal after a cold reduce anti-virus ability?
The immune damage caused by excessive diet mainly involves two conditions - postprandial inflammation and metabolic inflammation.
2. Postprandial inflammation
Postprandial inflammation, as the name suggests, refers to the increase in the level of inflammation caused by eating.
Even healthy people, after a high-fat meal, the content of endotoxin in the blood will increase significantly, and even postprandial endotoxemia will appear.
There are 5 main causes of postprandial inflammation:
After high-fat eating, the permeability of the intestinal epithelium increases, and with nutrient absorption, some harmful components of intestinal bacteria metabolism such as endotoxins (also called LPS, lipopolysaccharides) will rub the fat ticket "sneak in".
Taste receptors on human intestinal epithelial cells and airway epithelial cells also recognize microbial signals, and eating more can cause these receptors to be too busy recognizing nutrients to take into account the immune information induced by microorganisms.
Immune receptors on the surface of epithelial cells, such as TLRs (there are 10 in the human body) and NF-κB, also recognize nutritional signals, such as saturated fatty acids, which activate TLR-2 and TLR-4, thereby causing an inflammatory response.
In addition to epithelial cells, another important place for TLRs to be expressed is in immune cells, such as dendritic cells and macrophages. TLR-4 on the surface of immune cells mainly recognizes signals such as bacteria, while TLR-7 in immune cells mainly recognizes nucleic acid signals, such as mitochondrial DNA and viral RNA, which is an important link in the antiviral type I interferon response. Nutrients such as saturated fatty acids and bacterial components such as endotoxins occupy these important receptors and hinder the immune system's antiviral response.
Chylomicrons (formed by fat absorption, mainly triglycerides in food) stimulate fat cells to release complement C3, which not only promotes triglyceride absorption, but also increases inflammation.
This condition of increased inflammation caused by fat is also called dietary fat toxicity, in fact, in addition to high-fat diet, high-sugar diet and emulsifier-containing foods (bread, snacks, etc.) can also cause short-term increased intestinal barrier permeability, as well as endotoxin infiltration. This in turn causes an immune response in organs and tissues that metabolize fats and sugars, such as inflammatory changes in the liver, adipose tissue, and pancreas.
Most people think of acute postprandial inflammation as a normal physiological phenomenon closely related to changes in the gut microbiome caused by eating, and as immune cells engulf and remove incoming pathogenic substances, immune homeostasis is restored. However, for individuals whose bodies are usually weak or have immune deficiencies, this kind of eating is not necessarily an optimistic thing.
After a full meal with high calorie/high fat/additive/low fiber characteristics, the intestinal nutrient density is greatly improved, the barrier permeability will increase, and intestinal gram-negative bacteria and some conditional pathogenic bacteria will take the opportunity to proliferate or "smuggling", and return to normal after a period of time under the monitoring and processing of the immune system.
Eating a nutritious and whole-hearted meal rich in vegetables, whole grains is associated with much lower levels of inflammation, and a cup of probiotic-rich yogurt before a meal can help reduce postprandial inflammation levels, which is beneficial for both normal-weight and obese people.
In addition, changes in human organs (such as the brain, trachea such as digestion and endocrine) and intestinal flora form coordinated rhythms over the long term. Eating at regular times allows these organs to be adequately prepared for nutrient breakdown and absorption, and the postprandial inflammation caused by this time is relatively mild.
3. Viral infection and postprandial inflammation
Although influenza viruses mainly infect respiratory epithelial cells, which will disturb the airway flora and increase the permeability of the airway barrier, when the pro-inflammatory immune cells and cytokines activated by viral infection circulate to the intestine, they will also "help the abuse" and increase the level of intestinal inflammation, thereby making those harmful pathogenic bacteria eager to move, resulting in abnormal intestinal flora. If you come to a high-fat or high-sugar meal at this time, harmful bacteria or their toxins may rub the fast train of nutrient absorption to invade the human body.
The new coronavirus can infect not only respiratory epithelial cells, but also intestinal epithelial cells. Therefore, the new coronavirus infection will not only disturb the airway flora and increase the airway barrier permeability, but also disturb the intestinal flora and increase the intestinal barrier permeability. At this time, the number of harmful bacteria in the airway and intestines will increase, and they are waiting for the opportunity to invade the human body. At this time, a high-fat or high-sugar meal is equivalent to further increasing the permeability of the intestinal barrier, and using nutrition to open the way for pathogenic bacteria to help pathogenic bacteria enter the body.
Therefore, poor appetite during influenza A or new crown infection is not a pathology, but a signal that the body decides to concentrate on fighting the virus, and almost any animal in the world will instinctively rest, sleep and drink at this moment. Of course, the best choice for human beings at this time is to eat less, drink more water and rest more, which is the most cooperative approach to autoimmune rehabilitation. For example, a cup of probiotic-rich yogurt, sour soy milk, sour cereal milk, or simple foods with high fiber, sugar, sugar and low fat (such as oatmeal, multigrain mixed bean paste, etc.) can promote recovery and help the body clear the virus faster.
Compensating for the damaged body with a large meal after infection actually does more harm than good, and the damage is more than good. Although there may be some psychological compensation, it increases the burden on the immune system, backfires and helps harmful bacteria to invade, so that harmful bacteria can enter the body through the "ticket" of postprandial inflammation, resulting in the immune system having to divide "troops" to deal with harmful bacteria while fighting viruses, thereby delaying the speed of self-removal of viruses.
4. Antiviral ability of adipose tissue and complement system
The effects of short-term excess diet are easy to repair, and long-term damage to the function of adipose tissue. Although people generally regard adipose tissue as a metabolic tissue dedicated to storing energy, in fact, people ignore that adipose tissue also plays important endocrine and immune duties.
Women may have a better understanding of the endocrine effects of fat, just the right fat to maintain normal hormone balance, too little fat will cause menstrual disorders or even menopause, too much fat may induce polycystic ovary syndrome and even breast cancer.
In fact, in addition to sex hormones and metabolic hormones such as leptin, adipose tissue is also the site for the synthesis of a variety of complement molecules such as complement C3, D factor (FD) and factor B (FB) and cytokines.
The complement system (Complement system) is one of the main components of the human immune system, which is very important for innate immunity and specific immunity, and Chinese English name can be understood and is a patch specially for the human immune system.
If immune cells are fully armed warriors, the mucosal barrier is a solid wall with a progressive and complex structure, and the complement system is a very well-designed AI monitoring system.
The complement system is a precisely regulated automated reaction system consisting of about 50 soluble or membrane-bound proteins. Complement molecules are widely distributed on the surface of blood, interstitial fluids and cell membranes, constantly patrolling, and once a bad foreign body is found, it will be labeled as a dangerous product (complement molecules can be deposited on the surface of any cell, debris, microorganism or artificial material), and activate other complement molecules through cascade (a step-by-step amplification method) to initiate an attack. The principle of attack of complement is: all unlabeled "do not attack" (mainly complement regulatory molecules, which can be synthesized on their own or obtained from plasma) are uniformly attacked.
In antiviral immunity, the role of the complement system is mainly manifested in the following 6 points:
In the case that C3b can be deposited on the surface of the virus, the detected virus is directly neutralized, and the membrane perforation complex (MAC) is formed through a signaling cascade reaction to lyse the virus;
When C3b cannot be deposited on the surface of the virus, assist in assisting antibodies to neutralize the virus and lyse the virus;
Labeling the virus, which promotes the phagocytosis of immune cells;
Induce differentiation of endemic B cells and produce specific antibodies, and promote the formation of memory B cells;
Promote differentiation, proliferation and migration of virus-specific T cells.
Label virus-infected cells and promote lysis of these cells.
The health of adipose tissue affects the function of the complement system, too little will reduce the effectiveness of the complement system, too much may reduce the accuracy of the complement system.
4. Adipose tissue and metabolic inflammation
If the inflammatory response after eating does not have enough time to subside, such as starting the next meal when the postprandial inflammation has not subsided, endotoxin will never be completely cleared, which will cause chronic inflammation in the long run. At this time, it may only be overweight or obese on the outside, but physiologically it is adipose tissue dysfunction, metabolic endotoxemia and metabolic inflammation (metaflammation).
In addition to being involved in the complement system, adipose tissue is also an important immune cell pool. In addition to fat cells, there are also pre-adipocytes (which can differentiate into fat cells and macrophages), mast cells (which can secrete various cytokines) and macrophages, T cells, B cells, NK cells, neutrophils and eosinophils.
Adipose tissue can secrete more than 50 adipokines, which not only regulate metabolism, but also produce cytokines-like effects and regulate immunity. Adipokines such as leptin, resistin, and angiopoietin-like protein 2 promote inflammation, while cytokines such as adiponectin and lipase (homologs of complement factor D) fight inflammation.
For example, leptin can promote the activation and proliferation of monocytes, macrophages, granulocytes, NK cells and dendritic cells, promote T cell activation and secretion of pro-inflammatory cytokines. Adiponectin inhibits the activation of NF-κB pro-inflammatory pathway, inhibits the release of pro-inflammatory cytokines by macrophages, and promotes the secretion of anti-inflammatory cytokine IL-10.
Nutritional status can affect not only the metabolism and endocrine function of adipose tissue, but also the function of immune cells. With proper nutrition, adipose tissue-resident macrophages express anti-inflammatory genes and maintain the anti-inflammatory microenvironment of adipose tissue.
But on a long-term high-fat, high-calorie diet:
Intestinal flora harmful bacteria and their harmful products such as endotoxin increase, intestinal barrier permeability increases, low-dose endotoxin continues to penetrate into the body, after a large meal, a larger dose of endotoxin rubbing the ticket of chyme particles into the body, some smaller harmful bacteria will also be mixed in;
In order to prevent the invasion of harmful bacteria, various pro-inflammatory immune cells in the intestine increase, anti-inflammatory immune cells decrease, and the intestine is in a low-level chronic inflammatory state;
With the influx of a large amount of nutrients into adipose tissue, the volume of adipocytes increases, and under stress conditions such as hypoxia and endoplasmic reticulum stress, NF-κB and other signaling pathways are activated, and granulocytes are recruited to come to adipose tissue, and people's weight gradually exceeds the standard or even obesity;
Adipocytes express stress-related signals (such as NKp46) on the cell surface under stress conditions, promoting the activation and proliferation of NK cells in adipose tissues.
The pro-inflammatory cytokines released by neutrophils and NK cells, as well as the pro-inflammatory adipokines released by adipocytes, recruit macrophages from other sites and stimulate the proliferation of original macrophages in adipose tissue;
CD8T+ cells proliferate, NK cells secrete IFN-γ, promote macrophages from anti-inflammatory M2 type to pro-inflammatory M1 type;
Anti-inflammatory immune cells such as regulatory T cells, IL2 and eosinophils gradually decrease or even disappear, M1 macrophages cause low-level inflammation, and the intestine and adipose tissue are in a pro-inflammatory state;
Pro-inflammatory immunity affects the function of the liver and pancreas, insulin sensitivity decreases, fat synthesis in the liver increases;
The spread of the pro-inflammatory state throughout the body is called systemic inflammation, inducing diseases such as diabetes and nonalcoholic fatty liver disease.
In obesity, a low-level pro-inflammatory state (i.e., metabolic inflammation), the risk of chronic diseases such as diabetes increases, and the ability to fight infection decreases. The anti-virus combat power in the body seems to be very sufficient, but the immune cells are often in a state of exhaustion and even enter a tense state of wind and noise, and the "accuracy" of the complement system is reduced, not only attacking pathogen signals, but also attacking the suspected pathogen's own substance, which is often said to be the kind of fire and innocent. Once the new crown or influenza A virus is infected, the risk of severe disease is also higher.
However, the ability to fight infection in excess of nutrition is slightly stronger than in the starvation state. When starved or deficient in nutrients, the energy supply of immune cells in the body is also limited, immune cells have insufficient raw materials and energy to synthesize antibacterial substances, immune cells such as neutrophils and macrophages move slowly, and the number of progenitor cells of B cells and T cells decreases. At this time, the immune system is in a state of insufficient combat power, and the ability to fight infection is significantly reduced.
Food & Heart Warm Summary:
Loss of appetite when catching a cold is an instinct of animals, and it is also a signal that the body decides to concentrate on fighting the virus, at this time, eat some active yogurt or a simple diet, drink plenty of water, and ensure adequate sleep not only to do the logistics for the immune system, but also to educate the immune system to accurately recognize the target of attack. At this time, eating and drinking will cause postprandial inflammation, which not only increases the chance of pathogenic bacteria invasion, increases the work burden of the immune system, but also delays the speed of virus clearance. Do not make up for colds or respiratory infections, when the result of "making up" will often backfire and the gains outweigh the losses.
Of course, not eating or drinking after a cold is not conducive to recovery, meals can be eaten less, but sufficient water is essential, the human body can use the original reserves of the liver, adipose tissue and muscle sugar and fat to provide energy, but must obtain a lot of water from the outside world. So eating less when you have a cold, a little hunger can help clear the virus, but the water can't stop, eat yogurt foods rich in live probiotics, or simple high-fiber foods can help recovery.