The relationship between purines, uric acid and gout: Before discussing the relationship between the three, I would like to add two terms: nucleic acid and nucleotide.
Nucleic acids are responsible for carrying and transmitting genetic information, such as DNA, and are made up of nucleotides.
The nucleotides that are related to purines are guanine nucleotides and adenine nucleotides.
Purine nucleotides are broken down to produce purine bases, which are simply called purines. It can be reused to re-synthesize purine nucleotides.
In primates and birds, uric acid is the end product of purine nucleotide metabolism and is excreted through the kidneys and intestines, maintaining a relative balance in the body, averaging 300 umol /l and not exceeding 420 umol/l. If there is excessive synthesis or reduced excretion, exceeding 420 umol/l, it is called hyperuricemia.
Gout attacks are closely related to hyperuricemia. Gout occurs in about 10-20% of patients with hyperuricemia, and the higher the uric acid level the more likely it is to occur as well, with frequent recurrences. The involvement of the immune system on the basis of hyperuricemia leads to gout attacks.
1. The effect of purines in food on human purine metabolism.
Generally speaking, animal foods contain higher purines than plant foods, considering the high frequency of cellular metabolism in animals, which has more purine nucleotides involved in the decomposition process, resulting in high purine content.
In contrast, the effect of plant foods on uric acid in humans is largely disregarded. Even if the consumption of high purine vegetables does not increase the risk of gout. (Vegetables are all low purine foods)
And purine is easily soluble in water, so when reprocessing or digestion, purine in food will dissolve in water or digestive juices, resulting in increased exogenous intake of purine, so it is not recommended to drink meat soup, hot pot soup to reduce purine intake.
2.Hyperuricemia and gout
To be precise, hyperuricemia and gout are not a concept. Hyperuricemia is caused by increased synthesis or reduced excretion of uric acid or both. The ability of a normal person to maintain a stable level of uric acid means that a balance between synthesis and excretion is achieved.
The pathways of uric acid synthesis and excretion are the same in both normal people and those with hyperuricemia or gout, so it is impossible not to produce uric acid, only that some people show differences due to the interaction of genetic and environmental factors that cause excessive synthesis or reduced excretion of uric acid.
Reduced uric acid excretion leads to hyperuricemia in 80-90% of cases. The main cause is a genetic defect that prevents normal excretion of uric acid due to abnormalities in the urate transport protein, resulting in a hyperuricemic state. Other conditions such as hypertension, insulin resistance, chronic kidney disease and many medications can also lead to abnormal uric acid excretion.
To add, during an acute attack of gout, the excretion of uric acid is increased. This is why the blood uric acid level is lower when it hurts than when it does not.
3. Is gout hereditary?
The occurrence of gout is also divided into sequential factors, i.e. genetic factors and environmental factors interact and work together. 60% of primary gout is related to genetic factors.
Environmental factors are divided into the internal environment and external environment. The internal environment includes obesity, hypertension, lipid metabolism disorders, hyperglycemia, atherosclerosis, drugs and food. The external environment includes altitude, temperature, social pressure, etc. And normal people do not have gout. It has to be on top of hyperuricemia with an immune response involved for gout to occur. And like the presence of high purine diet, strain, cold, drinking alcohol will induce the occurrence of gout, but it is not inevitable.
4, the effect of beer on gout.
Beer has the strongest correlation with gout attacks, compared to white wine and red wine. There are three reasons for this, one is itself rich in guanine, which can synthesize uric acid; secondly, it contains alcohol, which leads to both increased synthesis of uric acid and reduced excretion; thirdly, comrades who drink beer are often paired with seafood and barbecue, which are all high purine foods.
5, the impact of lifestyle changes on hyperuricemia and gout.
Diet and other lifestyle changes are an important part of lowering uric acid. Comrades with good diet alone can lower uric acid by 60-90umol/l, or even a little higher.
But some comrades even if they do very strict, uric acid still does not meet the standard, then you need to cooperate with uric acid-lowering drugs, mainly divided into drugs that inhibit synthesis and drugs that promote excretion, their ability to reduce uric acid is better, but it is still recommended to do a 24-hour uric acid excretion measurement to determine whether the synthesis is increased or excretion is reduced, more targeted in terms of drug use.
6.Commonly used uric acid-lowering drugs.
Inhibiting synthesis mainly includes allopurinol tablets and febuxostat, with the latter having small side effects and large uric acid-lowering strength. The main side effects are liver damage, leukopenia, diarrhea, skin rash, hypersensitivity reactions, gout attacks.
The main drug used in China to promote excretion is benzbromarone, with side effects of abnormal liver function, rash, gastrointestinal symptoms, the appearance of stones, gout attacks, mostly in combination with drugs to alkalize urine (baking soda or sodium potassium hydrogen citrate).
All drugs have side effects, but not everyone happens, but the dangers of hyperuricemia and gout occur in everyone, so the drugs must be used rationally under the guidance of a doctor, without knowing to stare at the side effects and fear of disobeying medical advice, which eventually leads to irreversible lesions.
If you have obesity, hyperlipidemia, hypertension, diabetes, kidney disease, etc., you also need to be actively treated so as to facilitate uric acid control.