Why do I still get gout after a light diet? This risk factor is overlooked by many people!

*For medical professionals only

Standardized medication is the key to treating gout

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


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

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

-01- If you don't eat seafood or meat, why do you get gout?

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

Epidemiological investigations 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 application of industrial fructose and the excessive intake of fructose.
A large number of studies have shown that fructose has the potential to induce elevated uric acid levels in
humans.

Fructose is not a purine, why can fructose induce an increase in uric acid levels in humans?
And listen to my serious reasoning: fructose as a simple sugar, its dexterous body can be quickly absorbed by the intestinal mucosa into human cells
.
Fructose, as the "privileged class" of the carbohydrate family, is not bound by the rules of carbohydrate metabolism of the "glucose effect", and it can quickly deplete ATP (adenosine triphosphate) in the body, depleting phosphate in
large quantities.
The consumption of phosphate limits the regeneration of ADP (adenosine diphosphate) to ATP, so that the substrate AMP (adenosine monophosphate) produced by uric acid increases
.

A large amount of rapidly absorbed fructose → induce metabolic abnormalities→ cause hyperuricemia;
A large amount of rapidly absorbed fructose/sucrose → stimulate the synthesis of long-chain fatty acids→ leading to hypertriacylglyceridemia → cause the body's resistance to insulin→ cause hyperuricemia
.

Nowadays, all kinds of processed side foods - sweet drinks (including fruit juices, colas and other sugary drinks), candy, pastries, etc.
are the richest sources of fructose, which means that when eating seafood, sweet drinks are no less
harmful to gout patients than drinking beer.

In addition, although honey has high nutritional value, the fructose content is as high as 70%; Fruits are rich in nutrients, but also contain fructose
.
The normal consumption of the above foods is conducive to health, if too "hungry", a large amount of one-time intake of fruits and honey with high fructose content is also easy to cause gout
.

Therefore, even if the intake of high purines 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 living habits such as drinking alcohol 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 BMI (number of constitutions), the greater the possibility of hyperuricemia
.

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

For example:

• The accumulation of belly fat can increase the total amount of nucleic acids in the metabolism, which leads to an increase in uric acid synthesis;
• Fats are broken down into fatty acids, which 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 will also reduce the excretion of uric acid by the kidneys
  .
  

Perhaps some patients may wonder: they do not look fat, the body mass index is normal, why is the blood uric acid still high, and even gout? In fact, this kind of look is 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 paid attention to!
-03- Wasting vegetarians: Genetic factors/genetic defects can also cause gout
patients with a light diet and emaciated body tend to be more confused: I am very self-disciplined in my diet and living habits, and I am not fat, so 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 associated with genetic defects: one is heredity, 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.

Current research has found that some genetic defects 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 body SLC22A12, SLC2A9, and ABCG2 genes will promote a decrease in
uric acid excretion.
Mutations in MTHFR (methylenetetrahydrofolate reductase) and RGPRT (hypoxanthine guanine phosphate ribotransferase) genes will increase uric acid production in
humans.

If patients have gout susceptibility genes BCAS3, RFX3, and KCNQ1, they may contribute to the deposition of uric acid in the joints by participating in different mechanisms such as inflammatory pathways and regulating the immune system, thereby contributing to the onset
of gout.

-04-
Gout can not rely solely on the control of diet, 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 the uric acid from food sources accounts for only 20%.

In addition to a small part of the purines in food are absorbed by cells, most of them are further broken down into purines in the cells of the intestinal mucosa, which are mainly degraded into uric acid and excreted outside
the body.

More than 90% of hyperuricemia have different degrees of uric acid excretion disorders, and any hereditary, drug, and metabolic disorders that affect glomerular filtration or reduce renal blood flow and impair tubular excretion function will lead to reduced
uric acid excretion.

Can a controlled diet lower uric acid? The answer is yes
.
Can dietary control alone cure gout? The answer is often not
.
The basic uric acid value of most gout patients is 500 μmo/L to 800 μmo/L or even higher
.
But what is the target upper limit for uric acid control in adult gout patients? 360 μmo/L or less (in patients with tophic, guidelines recommend 300 μmo/L or less
).

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

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

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.
In the process of treatment, the patient should actively cooperate with the attending doctor's formulation of the adjustment plan
.
Standardize the medication on time and in sufficient amounts, control the uric acid value at the ideal level, maintain an optimistic and relaxed positive attitude, and regularly review to control the condition more comprehensively
.






Where to look for more endocrine clinical knowledge? Come to the "Doctor's Station" and take a look 👇