It took 20 years to defeat the host, and bad habits are actually its "accomplices"
For decades, health experts have emphasized that many bad habits can induce heart disease, Alzheimer's disease, type 2 diabetes, and certain cancers, which cause 70% of deaths worldwide.
Excessive intake of red meat, insufficient intake of fruits and vegetables, smoking, drinking, obesity, lack of exercise... They will greatly increase the incidence of these diseases, and once one of these diseases is contracted, the risk of other diseases will also increase accordingly.
People always think that these diseases are "old age" and will cause inflammation.
Originally, inflammation is the immune system's defense mechanism against foreign pathogens, but for the elderly, inflammation itself has become an "invader"—because they are not caused by bacterial infections, they are not contagious, but are caused by bad habits and Caused by genes.
However, is this true?
After investigating various diseases, scientists discovered that the hidden "killers" behind these diseases may be bacteria-some bacteria are very confusing, they tend to hide in cells for a long time, "colluding" the immune system, and gradually invade organs. Then slowly defeat the host.
With the continuous advancement of human research methods, scientists' understanding of the relationship between bacteria and diseases is also constantly improving.
They found that the inflammation induced by some bacteria is beyond traditional cognition and is in line with the pathogenesis of many "senile diseases".
Over the years, scientists have been struggling to find the root cause and treatment of "senile diseases", but they have been frustrated repeatedly.
These new discoveries may mean that the spring of heart disease and Alzheimer's disease patients is coming soon.
■Cold Wave/Compilation
Inflammation "protracted war"
Remnants of phagocytes strengthen themselves
There are many types of "senile diseases", the most common of which is gum disease.
Maricio Toniti of the University of Hong Kong directly classified gum disease as "the most common human disease."
In the United States, 42% of people aged 30 and over suffer from gum disease; among people 65 years of age and over, the rate of gum disease is as high as 60%.
In Germany, 88% of people aged 65 and over suffer from gum disease.
It is worth mentioning that once gum problems occur, the probability of suffering from other senile diseases such as rheumatoid arthritis and Parkinson's syndrome will also increase significantly.
There are two possible explanations for this phenomenon: First, external factors simultaneously induce gum disease and other senile diseases; second, there is a direct causal relationship between gum disease and other senile diseases, that is, gum disease causes other diseases.
At present, more and more evidence points to the latter.
Some circumstantial evidence is very convincing.
Some state governments in the United States use federal medical assistance funds to subsidize residents to prevent and treat gum disease.
Statistics show that the subsidies used by these states to treat diseases such as heart disease, diabetes, stroke, and cancer are reduced by 31% to 67% compared with other states.
Many private insurance companies in the United States have similar findings.
So, how do gum disease bacteria cause other diseases?
The response of the immune system is key.
There are more than 1,000 kinds of bacteria in everyone's mouth, and mild bacteria often envelop malignant bacteria to form a relatively stable community.
In other parts of the body, such as the skin or the lining of the intestine, bacterial communities grow on sheets of epidermal cells.
Tonity pointed out that the skin of these parts often peels off, and the invading bacteria are also removed.
But the tooth cannot peel off the skin, and the bacteria will survive on the hard surface and gradually penetrate the cells and enter the body.
When the bacteria on the teeth multiply, dental plaque begins to harden and penetrate into the gums, causing inflammation.
At this time, human immune cells will swarm in, destroying bacteria and infected human cells at the same time.
In this process, an anaerobic area will be formed between the gums and teeth, where some anaerobic bacteria will multiply wildly.
Among them, Porphyromonas gingivalis is particularly sinister.
Caroline Genke of Tufts University in Massachusetts pointed out that Porphyromonas gingivalis produces certain molecules that block part of the inflammatory process, thereby allowing inflammation to continue.
The result of this situation is that the inflammatory response with a sharply reduced lethality has been trying to kill the bacteria, but it will never be "powerful", and ultimately kills the human cells-Porphyromonas gingivalis will take this opportunity. The wind swallows these protein remains, which is an ability that most bacteria do not possess.
At the same time, human cells "killed" by Porphyromonas gingivalis will release iron, which is used by the bacteria to "expand" itself.
Long-term hidden cells
Stealth migration waiting for the opportunity to make waves
Over time, the bacteria-infected teeth began to loosen, and Porphyromonas gingivalis had already escaped into the blood.
At this time, the human immune system begins to secrete antibodies to fight these "invaders."
However, for Porphyromonas gingivalis, the antibody that wants to eliminate it is not only the human body's umbrella, but its own passport.
Once such antibodies begin to secrete, the probability of patients suffering from rheumatoid arthritis, heart disease, and stroke will increase significantly in the next ten years.
Root explained that this is probably because once Porphyromonas gingivalis enters the blood, its epidermal proteins are changed so that it hides in the white blood cells of the immune system.
At the same time, Porphyromonas gingivalis will invade the arterial intima cells and hide in the cells, only occasionally invading new cells.
In this way, Porphyromonas gingivalis escaped the hunting of antibiotics and the immune system.
However, even if it "lives" inside the cell, Porphyromonas gingivalis will silently trigger or block various immune signals, and even change the gene expression of blood cells so that it can migrate to other inflammation sites and make trouble again. .
So, how exactly does Porphyromonas gingivalis link gum disease with diabetes, Alzheimer's disease and other diseases?
There is a possibility that it increases the overall "inflammation load", but it is also possible that Porphyromonas gingivalis is directly "strengthening".
Because in the mouse experiment, the brain, aorta, liver, spleen and kidney, joints, pancreas and other parts of the mouse were detected with this bacteria, and many human tests have similar findings.
The role of Porphyromonas gingivalis is particularly prominent in the study of Alzheimer's disease.
Currently, two-thirds of dementia symptoms are caused by Alzheimer's disease, which is also the fifth leading cause of death in the world.
Scientists have long believed that the cause of Alzheimer's disease is the accumulation of amyloid and tau protein in the brain.
However, the accumulation of these two proteins may not exist in the brains of many dementia patients, and many people who meet the conditions for accumulation of these two proteins may not have dementia.
The most important thing is that any therapy that targets these two proteins cannot effectively relieve symptoms.
Earlier this year, research teams from eight American universities and the San Francisco-based company Connerstone Medical found that 99% of patients who died of Alzheimer's disease contained gingivalase in their brains, and the amount was positively correlated with the severity of the disease.
This protein digestive enzyme can only be produced by Porphyromonas gingivalis.
In addition, the researchers also found Porphyromonas gingivalis in the spinal fluid of these patients.
In people who have never suffered from Alzheimer's disease, about 50% of people have gingival protease and amyloid in their brains, but the content is low.
In mouse experiments, mice in the Porphyromonas gingivalis test group showed symptoms of Alzheimer's disease, and curbing the production of gingival protease can effectively repair brain damage.
This study is enough to make people suspect that Porphyromonas gingivalis causes Alzheimer's disease, because it can take 20 years from brain damage to symptoms.
Casey Lynch of Connerstone Medical pointed out that the symptoms of Alzheimer's disease may be due to the brain damage caused by gingival protease to a certain extent.
Quietly affecting genes
Trigger molecular changes cause disease
Researchers still have a question: How can bacteria affect genes to trigger molecular changes that cause disease?
Swedish scientists discovered that bacteria do have this ability.
People at the highest risk of Alzheimer's disease produce the immune protein ApoE, which is destroyed during an outbreak, and gingival protease is particularly good at destroying ApoE.
More than that, Porphyromonas gingivalis can also invade the heart.
More and more evidence shows that it has a causal relationship with atherosclerosis.
Researchers have found Porphyromonas gingivalis in the fat deposits on the inner walls of the arteries-fat deposits can produce blood clots, which block the cardiovascular and cerebrovascular blood vessels, and eventually induce heart disease or stroke.
Roots pointed out that in the arterial intima, Porphyromonas gingivalis can trigger molecular changes unique to atherosclerosis.
In addition, Porphyromonas gingivalis can also produce lipoproteins that induce atherosclerosis.
In animal experiments on pigs, the way the arteries are damaged is very similar to the effect of a high-fat diet.
Lakshmia Kesavaru of the University of Florida in the United States cultivated active Porphyromonas gingivalis in the aorta of atherosclerotic white mice.
The American Heart Association recognizes that gum disease is an independent cause of cardiovascular disease, but it does not characterize it as a "causal relationship."
The association believes that although the treatment of gum disease can help soften the arteries, there is no research showing that it can reduce the probability of heart disease or stroke.
Steve Dominy of Connerstone Medical believes that even if the risk of heart disease or stroke cannot be effectively reduced, it is because the treatment of gum disease can only relieve the inflammatory load of the arteries, but cannot eliminate the already existing gingival porphyrosis in the blood vessels. Phromomonas.
To demonstrate whether there is a causal relationship between Porphyromonas gingivalis and heart disease, more clinical trials are needed, but the practical problem is that the trial is expensive and difficult, and the "bacteria theory" is still in the early stage of research.
Dental disease related to the whole body
Find a new solution to illness caused by lifestyle habits
The association between Porphyromonas gingivalis and type 2 diabetes is even clearer.
Diabetes patients lose insulin sensitivity and cannot regulate blood sugar autonomously.
At present, cases of type 2 diabetes are spread all over the world, and lifestyle habits are generally considered as its potential pathogenic factors.
However, the truth may not stop there.
Because high blood sugar can damage immune cells, diabetes can exacerbate gum disease.
Conversely, gum disease can also exacerbate diabetes.
The American Academy of Periodontology pointed out that in addition to changing lifestyle habits, diabetic patients can also treat gum disease to alleviate the condition.
Many diabetes research associations also recommend this method, but no organization has clearly listed gum disease as a causative factor of diabetes.
However, there is evidence that the effect of Porphyromonas gingivalis on diabetes is not only reflected in increasing the inflammatory load in the body, but also directly acting on the liver and pancreas, thereby reducing insulin sensitivity.
Genke believes that for a complex disease, causality is difficult to prove.
The current known situation is: if mice are infected with a large number of Porphyromonas gingivalis, they will not only suffer from gum disease, but also diabetes, rheumatoid arthritis, atherosclerosis, fatty liver, and similar Alz Symptoms of Haimer's disease.
In the human body, gum disease can also greatly increase the risk of other diseases.
Porphyromonas gingivalis lurks in the damaged tissues and imperceptibly transforms the cells to induce specific diseases.
If there are indeed directly related causes of these senile diseases, then the treatment methods will be ready.
Moreover, once these assumptions are established, many empirical talks about living habits will have a scientific basis.
For example, alcoholics are more likely to be infected with Porphyromonas gingivalis and suffer from gum disease; smoking helps Porphyromonas gingivalis invade gum cells; as for Alzheimer’s disease, it can only be done through exercise. To reduce the risk of disease, this may be because fitness can inhibit inflammation, and Porphyromonas gingivalis can be taken advantage of.
Let's look at eating habits again.
Douglas Kyle of the University of Manchester pointed out that human blood contains a large number of latent bacteria, and they just need trace amounts of iron to stimulate activity and ultimately cause disease.
This explains why excessive intake of red meat, sugar, or insufficient intake of fruits and vegetables can lead to senile disease-all these conditions increase blood iron.
Break through traditional concepts
Flossing can make the brain healthier
Dominy pointed out that the academic community should have a clearer understanding of the role of periodontal disease and clearly list it as a causative factor of senile disease.
But at least so far, no official medical institution recommends that patients “see the dentist” to treat geriatric diseases.
Although the relationship between gum disease and Alzheimer's disease is the most obvious, the World Health Organization's Alzheimer's disease prevention guidelines published last May did not mention the prevention and treatment of gum disease.
WHO official Benoit Varena said: “There is not enough evidence that treating gum disease can reduce the risk of dementia.”
Margaret Gatz of the University of Southern California said that flossing can make the brain healthier, but many people scoff at this suggestion.
It is this kind of ridicule from "common sense" that has prevented the "germ theory" from becoming a mainstream topic in the medical community.
Thomas Kocher of Greifswald University in Germany pointed out that “Dentistry and other medical disciplines have always been distinct and never cooperated.” This has led to a deep-rooted idea: diseases such as heart disease are mainly caused by lifestyle problems. It has nothing to do with bacteria.
Such medical conclusions generally take decades to be subverted.
For example, scientists have proven that gastric ulcers are not caused by life stress or gastric acid, but by Helicobacter pylori.
Maybe in a few decades, many experts will have to admit that amyloid may have nothing to do with Alzheimer's disease, and high cholesterol will not cause heart disease.
As the average age of the global population continues to rise, perhaps as long as a few decades later, we will face a crisis of a full-scale outbreak of senile diseases. By then, the health systems and even social systems of various countries will be under tremendous pressure.
Mankind is in urgent need of some new medical theories for senile diseases, and we must face up to the role of bacteria.