In the long history of evolution, life sprouted from a hot, boiling pot of primordial soup to the emergence of humans and their journey to where we are today, perhaps from just a series of coincidences. The growth of all things and the survival of species depend on the precise transmission of genetic information. However, in every transmission of information, there is a certain probability of genetic mutations. Although the vast majority of mutations are ineffective and do not have any consequences, in very rare cases, mutations may occur in key genes, causing disease and death. In some rarer cases, mutations may even become the key to evolution. The X-Men film series is a science fiction interpretation of the principle of genetic mutation, which is the driving force of evolution. In mammals, purines are gradually metabolized into uric acid, which is then broken down into allantoin and excreted in the urine under the action of liver urate oxidase. About 20 million years ago, the common ancestor of humans and gorillas, —- archaeopteryx, experienced a far-reaching genetic mutation. The immediate effect of this mutation was the inactivation of the enzyme urate oxidase. This also meant that uric acid could not be broken down further and became an end product of purine metabolism, which could only be gradually removed with the help of physical pathways such as the kidneys, bile ducts and intestines. The mutations that occur in the field of nutrient metabolism are often catastrophic. For example, a mutation in the gene for glucose dehydrogenase 6 phosphate leads to an enzyme deficiency that triggers acute hemolytic anemia (fava bean disease) in patients who consume foods such as fava beans; another example is that infants with a congenital lactase gene defect suffer from vomiting and diarrhea after consuming breast milk or cow’s milk, and are barely able to grow. But this mutation was different, it fell from the sky and gave a great gift to the evolution of archaic apes: due to the loss of function of urate oxidase, uric acid excretion was slowed down and the organism acquired a stable and long-lasting uric acid concentration. The result of the genetic mutation was solidified by the law of genetic center, and to this day, humans and gorillas still have much higher levels of uric acid than other mammals. Today we already know that uric acid is a natural antioxidant in the body, scavenging toxic free radicals produced during physiological and pathological processes, and plays an important role in anti-oxidative stress, neuroprotection, and anti-inflammation. It has even been suggested that the reason humans have a longer lifespan than most mammals is inextricably linked to the elevated uric acid brought about by this genetic mutation. Health killer In today’s society, uric acid does not make a good impression, and gout sufferers see it as a nightmare. The reason is that high uric acid, together with high blood pressure, high blood sugar and high blood cholesterol, has become one of the four major killers that seriously threaten people’s health. Long-term high uric acid can cause gouty arthritis, kidney damage, atherosclerosis, aggravate high blood sugar and many other hazards. From evolutionary pushers to health killers, what is this all about? The answer is not complicated, similar to the other “three highs”, human survival is also inseparable from the necessary blood pressure, blood sugar, blood lipid levels. However, once the concentration of uric acid is too high and exceeds its solubility, it will form tiny precipitates and precipitate out of the blood and deposit in the joints and kidneys, etc. High uric acid will also directly stimulate the target organs and cause various damages. Therefore, we need to limit the level of uric acid in the blood to a safe range, just as we control blood pressure, blood sugar and blood lipids. It is now believed that uric acid should not exceed 420 μmol/L in men and 360 μmol/L in women, and for patients with hyperuricemia, it is necessary to make lifestyle adjustments or initiate medication. Do not overdo it Doctors have long noted an interesting phenomenon: patients with gout have a lower incidence of Parkinson’s disease (a common degenerative disease of the nervous system). Even in patients with Parkinson’s disease, those with higher uric acid levels progress more slowly than those with lower uric acid levels. A similar phenomenon can be seen in studies of the relationship between uric acid and cardiovascular disease: the incidence of cardiovascular disease is lowest when uric acid levels are at moderate levels, while cardiovascular disease increases when uric acid levels are either too low or too high. There are many other similar evidences, which confirm the two sides of uric acid from different perspectives: physiological protection at normal concentrations and pathological damage at abnormal concentrations. Therefore, it is important to prevent overkill during uric acid-lowering therapy. Ignoring the physiological function of uric acid, thinking that “the lower the better” and even asking for “eliminating the evil” are the major taboos of uric acid reduction therapy. Clinically, when the uric acid level reaches the standard consistently and there is no acute attack of gout, you can try to reduce the dosage or stop the medication under the guidance of the doctor, but of course, you should continue to keep regular testing of the uric acid level.