Don't Give Up on 'High Uric Acid Levels'—The Latest Research on Hyperuricemia and the Scientific Basis of Kansho-ho for Kidney Function and the Autonomic Nervous System
To those who have been told, 'Your uric acid levels are high' during a health checkup
Have you been ignoring the fact that your health checkup results indicated 'high uric acid levels' or that you are 'pre-gout,' simply because you aren't feeling any pain or symptoms yet?
Alternatively, perhaps you have seen family or friends suddenly unable to move due to the excruciating pain of a 'gout attack' at the base of their big toe, and you feel that this might not be someone else's problem after all.
Hyperuricemia refers to a state where the uric acid level in the blood exceeds the standard value (generally 7.0 mg/dL).
It is estimated that approximately 20% or more of Japanese adults are affected, and it is widely known as a lifestyle-related disease.
The problem is that it often progresses for many years with almost no subjective symptoms, only to suddenly erupt one day as a 'gout attack'.
Furthermore, recent research has revealed that hyperuricemia is not just a problem of gout, but is deeply associated with chronic kidney disease, urinary stones, cardiovascular disease, fatty liver, and metabolic syndrome.
If you underestimate 'slightly high uric acid levels,' you may end up paying a heavy price later.
And in recent years, interesting new approaches have been studied in the treatment of hyperuricemia and gout.
The potential for 'uric acid reduction through food-derived components' as shown by the latest research
In 2026, an important study was published in the international nutrition journal 'Nutrients' that verified the combined effects of d-limonene (a natural terpene compound found abundantly in citrus peels) and low-dose allopurinol (a uric acid-lowering drug) in a dual rat model of hyperuricemia and gouty arthritis.
Paper Title: Dose-Sparing Efficacy of d-Limonene with Low-Dose Allopurinol in a Dual Model of Hyperuricemia and Gouty Arthritis in Rats
https://www.mdpi.com/2072-6643/18/1/72
This study (Chidambaram, 2026) investigated whether combining d-limonene, which has antioxidant and anti-inflammatory properties, with allopurinol, the standard drug for gout treatment, could achieve sufficient effects even with a low dose of allopurinol.
Allopurinol is a drug that lowers uric acid levels by inhibiting xanthine oxidase (the enzyme that produces uric acid), but because high doses carry a risk of side effects, methods to reduce the dosage while maintaining effectiveness are being explored.
As a result, the group treated with the combination of d-limonene and low-dose allopurinol showed significant improvements in paw swelling, serum uric acid levels, liver function enzymes (AST/ALT), and kidney function indicators compared to each treatment alone. Furthermore, inflammatory cytokines (IL-1β, TNF-α, IL-6) were markedly reduced, the expression of the NLRP3 inflammasome was minimized, and the oxidative stress balance shifted toward homeostasis (Chidambaram, 2026).
The message of this study is highly significant.
Hyperuricemia and gout are not just problems of 'uric acid levels alone,' but are systemic issues where 'inflammation, oxidative stress, and kidney function' are intricately intertwined, and a multi-faceted approach to these is effective.
Why does hyperuricemia occur?—The triangular relationship of production, excretion, and inflammation
Understanding the fundamental mechanism of hyperuricemia is important for considering effective countermeasures.
Uric acid is a waste product created when a substance called purine is metabolized.
Purines are constantly synthesized and broken down in our bodies, and are also ingested from food (meats, fish roe, beer, etc.).
In healthy individuals, about two-thirds of the produced uric acid is excreted by the kidneys and the rest by the intestines, keeping blood concentrations constant.
Hyperuricemia is classified into three types: 'overproduction type,' 'underexcretion type,' and 'mixed type.'
In Japan, it is estimated that about 60% are 'underexcretion type,' 30% are 'mixed type,' and 10% are 'overproduction type,' meaning that for most, the cause is that 'uric acid excretion from the kidneys is not working well.'
That is precisely why maintaining kidney function is a key pillar of hyperuricemia management.
In addition, as the Chidambaram (2026) study emphasized, a gout attack is not caused solely by high uric acid, but is triggered by an 'inflammatory response to uric acid crystals.'
When the core mechanism of the inflammatory response, called the NLRP3 inflammasome, is activated, large amounts of inflammatory cytokines such as IL-1β are released, causing intense joint inflammation.
Therefore, 'suppressing inflammation and oxidative stress' while lowering uric acid levels is the key to preventing gout and reducing attacks.
The mechanism by which stress and the autonomic nervous system worsen uric acid
In the management of hyperuricemia, the influence of 'chronic stress and the autonomic nervous system' is often overlooked but is actually important.
Chronic stress causes over-tension of the sympathetic nervous system, which fluctuates blood flow to the kidneys and affects uric acid excretion function.
At the same time, chronically high levels of cortisol increase insulin resistance, which acts in a direction that reduces uric acid excretion.
The close association between insulin resistance and hyperuricemia has been shown in many studies.
Stress also affects eating habits.
When stress continues, excessive alcohol consumption, overeating, and lack of exercise are likely to occur, all of which contribute to an increase in uric acid levels.
The experience of 'my uric acid levels worsened during a busy period' or 'I had a gout attack after a series of drinking parties' has this kind of background.
Chronic stress further increases systemic chronic inflammation and oxidative stress.
From the perspective of 'addressing inflammation and oxidative stress' as shown in the study by Chidambaram (2026), stress management becomes an important viewpoint in the management of hyperuricemia and gout.
Addressing what 'medication and diet' alone cannot reach
Standard treatment for hyperuricemia and gout centers on uric acid production inhibitors (such as allopurinol and febuxostat), uricosuric agents (such as benzbromarone), anti-inflammatory drugs for gout attacks (NSAIDs, colchicine, steroids), dietary therapy (restriction of purines, alcohol, sugar, and fructose), and lifestyle improvements (moderate exercise, fluid intake, and weight management).
As shown in the study by Chidambaram (2026), complementary approaches to reduce medication dosage are also being researched.
These are absolutely essential, and continuous management by an internal medicine or rheumatology specialist is the key to preventing complications.
Furthermore, in parallel with pharmacotherapy and dietary therapy, approaches from within the body—such as 'managing chronic stress,' 'restoring autonomic nervous system balance,' 'maintaining kidney function,' 'reducing systemic chronic inflammation and oxidative stress,' and 'improving insulin resistance'—play an important role in the fundamental improvement of hyperuricemia and the prevention of gout attacks.
Scientific data on Kanshoho showing its 'effect on the internal environment surrounding hyperuricemia'
For the multiple issues involved in the progression of hyperuricemia—chronic stress, autonomic nervous system over-tension, decreased kidney function, chronic inflammation, and oxidative stress—the scientific data for 'Kanshoho,' a treatment method developed in 2007, indicates a direction for conditioning the internal environment that supports the prevention and improvement of hyperuricemia.
Of particular note is the confirmed increase in homoarginine after treatment.
Homoarginine is an amino acid involved in nitric oxide (NO) synthesis, and its increase is organized as a direction that supports the improvement of kidney function from the perspective of vasodilation and improved renal blood flow.
Since approximately two-thirds of uric acid is excreted by the kidneys, the direction of supporting kidney function has direct significance in hyperuricemia management.
As an effect on metabolites, a decrease in N2-Phenylacetylglutamine has been confirmed, which is an important change suggesting a reduction in metabolic load on the liver and kidneys.
Furthermore, a decrease in Taurolithocholic acid 3-sulfate (TLCS), which is involved in the induction of inflammatory cytokines, and a decrease in 5β-tetrahydrocortisol (5β-THF), a stress hormone metabolite, have been confirmed, showing a direction common to 'addressing inflammation and oxidative stress,' which was important in the study by Chidambaram (2026).
As an effect on the autonomic nervous system, an increase in blood serotonin and a downward trend in the LF/HF ratio after treatment have also been confirmed, which is significant data as a way to alleviate stress-induced metabolic deterioration and address factors that worsen hyperuricemia.
Now, while you have 'no symptoms,' is the chance to take serious action
If a health checkup points out high uric acid levels, the first step is to visit an internal medicine or rheumatology department to accurately evaluate your current state (whether it is an overproduction type or an underexcretion type) and the presence of complications (kidney function, cardiovascular risk, fatty liver, etc.).
Depending on the diagnosed condition, the basis is to continue pharmacotherapy, dietary therapy, and lifestyle improvements under a doctor's guidance.
As daily self-care, it is important to restrict foods high in purines (liver, fish roe, beer, etc.), moderate alcohol consumption, especially beer, restrict fructose (soft drinks, etc.), ensure sufficient fluid intake (2L/day or more), engage in moderate exercise, and maintain a healthy weight.
Foods such as citrus fruits rich in d-limonene, as shown by Chidambaram (2026), are also interesting options from a complementary perspective.
On top of that, combining approaches from within the body—managing chronic stress, restoring autonomic nervous system balance, maintaining kidney function, and reducing systemic chronic inflammation and oxidative stress—is a scientifically rational strategy for fundamentally improving hyperuricemia.
Kanshoho is worth incorporating as one of the options for those working on the prevention and improvement of hyperuricemia, as it is an approach that involves multiple biological indicators—autonomic nervous system, microcirculation, and anti-inflammatory response—while working on muscle tension with ultra-low load.
Now, while you have 'no symptoms,' is the greatest chance to prevent gout attacks and complications.
Your body will surely respond to correct, multifaceted care.
References
Chidambaram K. Dose-Sparing Efficacy of d-Limonene with Low-Dose Allopurinol in a Dual Model of Hyperuricemia and Gouty Arthritis in Rats. Nutrients. 2026;18(1):72. https://www.mdpi.com/2072-6643/18/1/72
Kanshoho Official Website (Treatment Overview and Development Background) https://www.471203.com/
Kanshoho/Biochemical Hormone Data https://www.kanshoho.com/jp/biochemistry-hormones-kanshohokanshoho.html/
Kanshoho/Metabolite Data https://www.kanshoho.com/jp/metabolites-kanshoho.html/
Kanshoho/Autonomic Nervous System Data https://www.kanshoho.com/jp/ans-kanshoho.html/
List of Kanshoho Academic Presentations and Papers https://www.kanshoho.com/jp/Papers-conference.html/
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