Gout is an inflammatory disease caused by uric acid crystals, not liver dysfunction

Gout is the most common chronic inflammatory joint disease, affecting more than 50 million people worldwide by counts measured in 2020. Current trends suggest that its prevalence will increase by more than 70% by 2050^[1].

Gout is caused by the accumulation of uric acid crystals in the body, leading to sudden flares of severe and incapacitating joint pain. Gout flares usually spontaneously resolve after a week or two, but can cause complications, including damage to kidneys and joints.

In August 2024, Anthony William, who calls himself the “Medical Medium”, made claims regarding the causes of gout and possible treatments for this condition. Yet, William holds no relevant medical degrees. According to his website, William’s health knowledge comes from “the unique ability to converse with the Spirit of Compassion, who provides him with extraordinarily advanced healing medical information that’s far ahead of its time”.

William published a disclaimer on his website acknowledging that he is not and never has been a licensed medical doctor, nutritionist, or healthcare professional of any kind. The disclaimer also states that William “does not render medical, psychological, or other professional advice or treatment, nor does it provide or prescribe any medical diagnosis, treatment, medication, or remedy”.

Yet in direct contradiction with this disclaimer, William published an Instagram post in August 2024 claiming that uric acid crystals “aren’t the cause of gout or the cause of gout’s pain”. Instead, William described gout as a “liver condition” caused by a “sluggish, stagnant liver overburdened from toxins”. To resolve gout, William recommended “reducing protein and fat” in the diet to alleviate pain associated with gout flares.

However, these claims are inaccurate. We explain why below.

Uric acid crystals are indeed responsible for gout flare

Contrary to the claim, it’s the accumulation of uric acid crystals in the joints that causes inflammation and pain during gout flares.

The first step towards gout is a buildup of uric acid in the body. Uric acid occurs naturally in our body as a byproduct of purine breakdown—a component of DNA.

Once synthesized in the body’s cells, uric acid enters the bloodstream, is filtered by the kidneys, and eventually excreted through urine. When uric acid regulation imbalances occur, such as too much production or too little excretion, the concentration of uric acid increases. This is called hyperuricemia.

Hyperuricemia can sometimes, but not always, cause the uric acid to crystalize instead of remaining diluted in the blood. Those uric acid crystals then accumulate in joints, mostly in the feet.

White blood cells then detect those crystals and trigger an inflammatory response^[2,3]. Other white blood cells then infiltrate the joint, further amplifying the inflammation^[4]. This infiltration of white blood cells, as well as the release of pro-inflammatory molecules, cause the joint swelling and pain that people experience during a gout flare^[2,3].

However, the mechanism of gout is complex due to the intricacies of how our body works. For instance, hyperuricemia doesn’t always lead to gout. Some people may have elevated uric acid levels yet never experience a gout flare. Others might even have uric acid crystals accumulate in their joints without any symptoms. These cases might cause some to question the role of uric acid in gout, as suggested by William’s claim.

However, these observations don’t disprove the central role of uric acid crystals in gout. They can be explained by the fact that uric acid crystallization is influenced by several factors beyond its concentration, such as temperature and pH levels^[3,5,6].

Additionally, the body has anti-inflammatory mechanisms that can sometimes counteract the inflammation triggered by uric acid crystals^[3].

In other words, while high uric acid is a risk factor for gout and uric acid crystals in the joints are direct causes of gout flares, certain other conditions must be in place for these flares to occur.

While uric acid is produced in the liver, gout isn’t a liver condition

William’s claim that gout is a liver condition tied to toxins or a “sluggish” liver is unsupported and seems to allude to the popular yet scientifically unsubstantiated trend of detox cures.

The liver is one of the main sites of uric acid production in the body^[7,8]. Thus, a liver producing an abnormally high amount of uric acid could contribute to hyperuricemia, which increases the risk of gout. However, this doesn’t mean that liver dysfunction or toxin accumulation is the primary cause of gout.

First, uric acid levels are influenced by many factors. For example, a purine-rich diet increases the amount of purine to be degraded and, in turn, increases the amount of uric acid. Alternatively, kidney diseases can lead to insufficient excretion of uric acid in the urine, resulting in increased uric acid blood levels. Other risk factors also contribute to uric acid buildup and gout, such as age, family history, obesity, and conditions like heart disease. Thus, someone can have high uric acid levels while still maintaining a healthy liver.

Second, even elevated uric acid levels in the blood don’t always lead to crystal deposition and gout, as previously discussed.

There is evidence suggesting a link between fatty liver disease and gout, as both conditions often appear in the same individuals^[9,10]. However, this is because they share common risk factors and biological pathways, not because one directly causes the other.

In summary, gout isn’t a liver condition, even if the liver produces the molecule involved in gout. Medical institutions also don’t mention the liver as a cause of gout and rather describe the disease as a chronic arthritis influenced by many risk factors.

Controlling one’s diet may reduce the risk of gout flares but diet isn’t the primary factor to treat the disease

William’s claim that reducing fat and protein intake alleviates gout symptoms may contain a grain of truth, but is misleading.

As mentioned in the previous section, a purine-rich diet is a risk factor for gout as it increases the production of uric acid. Purine-rich foods include organ meat like liver or kidney, red meat, corn syrup, and some seafood like scallops and tuna.

Therefore, a low-fat, low-protein diet may involve cutting down on foods like red meat, which would in turn reduce purine intake. Furthermore, excessive weight is also a risk factor for gout. Thus, a healthy diet composed of fewer fats and less red meat could help to lower the risk of gout.

That said, diet isn’t the main gout risk factor nor an effective treatment for gout on its own. Nicola Dalbeth, a rheumatologist and professor of medicine at the University of Auckland, explained:

“It’s not usually because someone is drinking or eating the wrong things. These are old-fashioned views about the disease which are really unhelpful. […] We’ve published data looking at the effects of weight loss and various dietary interventions. None of these interventions led to major reductions in uric acid to an acceptable level. I’m not saying it’s not important to try to live a healthy life, but excessive focus on diet as the major strategy for gout management is wrong.”

Rather, Dalbeth said that gout treatments such as the medication allopurinol can reduce the amount of uric acid and prevent gout complications:

“Allopurinol works by helping the body clear the crystals over time, but it can take a number of years to achieve this clearance. […] Some of our recent trials have demonstrated that getting the uric acid level down and treating those crystals can prevent progression of joint damage.”

Conclusion

Gout is a common condition caused by the buildup of uric acid crystals in the joints, not by liver dysfunction or toxins. While the liver plays a role in uric acid production, gout is influenced by multiple factors, including diet, kidney function, genetics, and overall health. Managing diet may modestly reduce the risk of gout flares. Treatments such as medications like allopurinol can lower uric acid levels and prevent long-term joint damage.

 

REFERENCES

• 1 – Cross et al. (2024) Global, regional, and national burden of gout, 1990–2020, and projections to 2050: a systematic analysis of the Global Burden of Disease Study 2021. The Lancet Rheumatology
• 2 – Ko & Martinon (2017) Inflammation in gout: mechanisms and therapeutic targets. Nature reviews rheumatology.
• 3 – Dalbeth & Haskard (2005) Mechanisms of inflammation in gout. Rheumatology.
• 4 – Jeong et al. (2017) CD14+ Cells with the Phenotype of Infiltrated Monocytes Consist of Distinct Populations Characterized by Anti-inflammatory as well as Pro-inflammatory Activity in Gouty Arthritis. Frontiers in immunology.
• 5 – Zhang WZ. (2021) Why Does Hyperuricemia Not Necessarily Induce Gout? Biomolecules.
• 6 – Rodriguez-Navarro C. (2024) Unraveling the pathological biomineralization of monosodium urate crystals in gout patients. Communications biology.
• 7 – Bobulescu & Moe (2012) Renal Transport of Uric Acid: Evolving Concepts and Uncertainties. Advances in Chronic Kidney Disease.
• 8 – El Ridi & Tallima (2017) Physiological functions and pathogenic potential of uric acid: A review. Journal of Advanced Research.
• 9 – Shih et al. (2015) Association between serum uric acid and nonalcoholic fatty liver disease in the US population. Journal of the Formosan Medical Association.
• 10 – Sun et al. (2023) Association Between Serum Uric Acid and Non-Alcoholic Fatty Liver Disease: An Updated Systematic Review and Meta-Analysis. Clinical Epidemiology.