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    Home > Active Ingredient News > Immunology News > Gout after a light diet? This risk factor is overlooked

    Gout after a light diet? This risk factor is overlooked

    • Last Update: 2022-10-26
    • Source: Internet
    • Author: User
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    Standardized drug treatment is the key to treating gout



    Many people know that a high-purine diet is easy to cause hyperuricemia and gout, if you choose a light diet, is uric acid reduced to normal, gout can also heal itself? Sorry, the result may have disappointed
    you.

    A light diet certainly occupies a very important position
    in the treatment of gout.
    However, hyperuricemia and gout themselves are a group of diseases
    of purine metabolism caused by the combination of genetic factors, lifestyle and environment.

    The reason why a disease can become a disease is like the textbook "success can be achieved", and more effort is an important factor in success, but it does not mean that success can be achieved
    by this factor alone.
    Dietary modification is an element of getting rid of diseases, not that they can be cured
    .

    -01-Why do I get gout if I don't eat seafood or meat?

    Patients at high risk of gout are always called upon to reduce purine intake, but often ignore the fact that in addition to purines, gout patients should also pay attention to fructose
    .

    Epidemiological surveys have found that the incidence of gout in developed countries represented by the United States has increased significantly in the past few decades, which is significantly related
    to the widespread use of industrial fructose and excessive intake of fructose.
    A large number of studies have shown that fructose has the potential to induce an increase in uric acid levels in humans
    .

    Fructose is not purine, why can fructose induce an increase in uric acid levels?
    And listen to me seriously: fructose is a simple sugar, its dexterous body can be quickly absorbed by the intestinal mucosa into human
    cells.
    As the "privileged class" of the sugar family, fructose is not subject to the rules of sugar metabolism of the "glucose effect", it can quickly deplete ATP
    (adenosine triphosphate) in the body and deplete phosphate in large quantities
    .
    The depletion of phosphate limits the regeneration of ADP
    (adenosine diphosphate) to ATP, resulting in an increase in
    the substrate AMP (adenosine monophosphate) produced by uric acid.

    A large amount of rapidly absorbed fructose → induce metabolic abnormalities → cause hyperuricemia;
    Large quantities of rapidly absorbed fructose/sucrose → stimulate long-chain fatty acid synthesis→ leading to hypertriacylglycerolemia→ causing insulin resistance → hyperuricemia
    .

    Nowadays, a variety of processed side foods - sweet drinks (including fruit juice, cola and other sugary drinks), candy, pastries, etc.
    are the richest sources of fructose, which means that eating seafood with sweet drinks is no less
    harmful to gout patients than drinking beer.

    In addition, although honey has high nutritional value, its fructose content is as high as 70%; Fruits are rich in nutrients, but they also contain fructose
    .
    Normal consumption of the above foods is good for health, if it is too "hungry", a large intake of fruits and honey with high fructose content at one time is also easy to cause gout
    .

    Therefore, even if the intake of hyperpurine is controlled, but the intake of fructose is not controlled, it is easy to lead to gout
    .

    -02-How does obesity cause gout?

    In the impression of clinicians, typical gout patients often have the following two characteristics at the first visit: one is accompanied by bad lifestyle habits such as drinking and overeating, and the other is that there are different degrees of obesity
    .
    Many studies at home and abroad have shown that
    the higher the body mass index (BMI), the greater
    the possibility of hyperuricemia.

    Excessive fat in the body of obese people can affect purine and uric acid metabolism
    in the body in many ways.

    For example:
    • The accumulation of belly fat can increase the total amount of nucleic acids in metabolism, resulting in increased uric acid synthesis;
    • Fat will be decomposed into fatty acids, promote the synthesis of uric acid and triglycerides by the liver, and increase blood uric acid and blood lipids;
    • Substances such as ketone bodies produced by fatty acid metabolism also reduce the excretion
      of uric acid by the kidneys.
    Some patients may wonder: they don't look fat, their body mass index is normal, why is blood uric acid still high, and even gout? In fact, this kind of looking not fat, not really not fat, they often have a small belly, that is, "abdominal obesity"
    .
    It seems that the weight is not large, but there is a lot of visceral fat, which is also to be taken seriously!

    -03-Wasting vegetarians: genetic factors/genetic defects can also cause goutSome
    gout patients with a light diet and emaciated body shape tend to be more confused: I am very self-disciplined in my diet and living habits, and my body is not fat, why am I still "shot"?
    Because genetic factors/genetic defects are also one of the
    important factors that cause gout.
    It should be noted that there are two main causes of gout related to genetic defects: one is inheritance, and such patients often have a family history of
    gout.
    Another genetic defect is difficult to find a basis for family history, and the presence of a genetic mutation
    needs to be considered.

    At present, research has found some genetic defects that affect purine metabolism and all aspects of uric acid excretion, eventually leading to hyperuricemia and gout
    .

    From the perspective of uric acid excretion, mutations in the human SLC22A12, SLC2A9 and ABCG2 genes will promote the decrease
    of uric acid excretion.
    Mutations in MTHFR
    (methylenetetrahydrofolate reductase) and RGPRT (hypoxanthine guanine phosphoribosyltransferase) genes will increase
    the production of uric acid in the human body.


    If the patient has gout susceptibility genes BCAS3, RFX3, KCNQ1, they may promote the deposition of uric acid in the joints by participating in different mechanisms such as inflammatory pathways and regulating the immune system, thereby promoting the attack
    of gout.


    -04-Gout
    can not rely on diet control alone, standardized treatment is indispensable
    in the human uric acid pool, the main source of uric acid is endogenous, accounting for about 80% of the total uric acid, and uric acid from food sources accounts for only 20%.

    In addition to a small part of the purines in food absorbed by cells, most of them are further decomposed into purines in the intestinal mucosal cells, and these purines are mainly degraded into uric acid and excreted
    .

    More than 90% of hyperuricemia has different degrees of uric acid excretion disorders, any hereditary diseases, drugs, metabolic disorders that affect glomerular filtration or reduce renal blood flow, damage renal tubular excretory function will lead to reduced
    uric acid excretion.

    Does diet control lower uric acid? The answer is yes
    .
    Can diet alone cure gout? The answer is often not
    .
    The basal uric acid value of the vast majority of gout patients is 500μmo/L ~ 800μmo/L or even higher
    .
    But what is the target upper limit for uric acid control in adults with gout? 360 μmo/L or less
    (guidelines recommend less than 300 μmo/L for patients with tophi).


    So, how much uric acid can be lowered with a strict low-purine diet?
    Yang Cong et al.
    conducted a 2-year follow-up study on 186 patients with hyperuricemia/gout in plateau areas showed that regular exercise control diet reduced blood uric acid by an average of 120 μmol/L after 1 year, and blood uric acid by 220 μmol/L
    after 2 years.
    At present, there is still no systematic study on this in the world, and in the real world, the vast majority of patients are far from
    the recommended continuous uric acid compliance requirements even if they strictly control their diet.

    In fact, even with an extremely strict low-purine diet, the body will still produce purines and metabolize them into uric acid
    .
    In patients with uric acid excretion disorders and endogenous metabolic disorders, uric acid after a light diet is still overwhelmed
    .
    Excessive diet control, for many young patients, will lead to imbalance of nutrients and imbalance of social and family activities
    .

    Standardized drug treatment is the key to the treatment of gout, and diet, weight control and good living habits are important links in the prevention and treatment of
    gout.
    During the treatment process, patients should actively cooperate with the attending physician to formulate an adjustment plan
    .
    Standardize medication on time and in sufficient amounts, control uric acid values at ideal levels, maintain an optimistic and relaxed positive attitude, and review regularly to control the condition
    more comprehensively.







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