Foods that cause gout, the “disease of kings,” were historically available only to the wealthy. Today, however, nearly everyone can overindulge in rich, unhealthy food and alcohol. As a result, some two million Americans are suffering from gout – just like King Henry VIII.

Gout’s joint inflammation is caused by the crystallization of excessive uric acid in the blood (hyperuricemia). Uric acid is a waste product formed by the breakdown of purines, natural substances found mainly in fatty meats, particularly red meat, and in some fish, grain and vegetable foods.

The latest, most exhaustive and definitive research of 47,150 men over a twelve year period, published in The New England Journal of Medicine, clarifies which purine containing foods may or may not cause gout and which foods may actually help prevent flare-ups in those prone to the disease.

Lead investigator Hyon Choi, MD, DrPH, of Harvard Medical School, found that each daily serving of beef, lamb or pork increased gout risk by 21%. Seafood increased the risk by 7% with each serving per week. Chicken, grains and vegetables, on the other hand, were found to have no risk, whereas two daily servings of low fat dairy were linked to a 50% decrease in gout.

However, recognizing the valuable anti-inflammatory benefits of fish oil, Dr. Choi recommends that you “get the protective components of omega fatty acids that are in fish. “So, if you have gout,” he suggests, “fish oil capsules, rather than eating a lot of seafood”

To be free of gout pain without harmful medication, it only makes sense to achieve and maintain a healthy weight, eat less meat, drink more water and less alcohol and take omega 3 fish oil capsules to naturally prevent and reduce painful inflammation and swelling.

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Gout is a disease common in men but much less so in women. However, menopausal women seem predisposed to gout according to some studies. First signs of the disease are usually big toe pain, but other joints can be affected.

Gout disease is treated via drugs and gout diet – depending on the individual. For some, diets seem to help a lot, others less so. So, it seems, it’s down to the individual work out what works best for them.

Comment:

Your site looks professionally designed. The pain is worst in my legs, but often spreads to my thigh. It’s an emotional rollercoaster during gout attack, pain killers work, but not that well. Health-wise, I feel great, but genetic predisposition to gout disease seems to me to explain a lot in my family. I think it’s a learning process about gout, and gout diets – I read as much as possible. Thanks for putting together a great site! Mr E. R. Gray

Experimentation may be key to finding what works to reduce your gout symptoms.

I think, like with many common ailments, your readers should try different things and if necessary drugs to alleviate their symptoms. Personally, cutting back on alcohol and large meals helped tremendously.

It tried several drug therapies but their side-effects were unacceptable.

Anonymous

After studying many leading gout websites, and trawling through hundreds of gout study abstracts, you may think you could pin-down the main cases of gout - not so! Like many diseases and disorders, there doesn’t seem a single cause, but a multitude of factors that may play a role in the development of this disease.

So here’s what some ‘experts’ think the cause or common causes of gout are:

• Although excess uric acid in the blood is a factor, it does not inevitably lead to gout!
• There is strong correlation between the disorder and diet – the conclusions of 12 year-long study.
• Obesity increases the threat of developing gouty arthritis.
• Some moderately common diseases and disorders, as well as lymphoma, leukemia and psoriasis, may lead to gout.
• It’s known that inherited genetic disorders can cause hyperuricemia which may result in the development of gout in children.
• Menopause may play a role, because pre-menopausal women have a significantly lower risk of developing gout than similar aged men.
• Excessive consumption of certain foods may increase the body's production of uric acid and therefore lead to the disease.
• A defect in specific enzyme metabolism may alter the way the body assimilates and processes purines in some gout suffers.
• Interestingly, it’s been speculated that greater than normal exposure to lead can may lead gout.
• High blood pressure, also known as hypertension, is fairly common among patients with gout, but whether it’s a cause or symptom is unknown.
• Abnormal or unusual metabolism of certain compounds in foods (purines) can result in too much uric acid in a person’s blood stream.
• Gout may follow the development of a different disease.
• Even though diet and excessive alcohol consumption may contribute to the disease, they are not believed to be the main causes of the condition.
• Certain medications may affect kidney function or purine metabolism and therefore influence gout development.
• Heart attack and strokes may predispose an individual to gout.
• Overall, gout may be considered primary or secondary dependent on factors that contribute to high uric acid levels in the bloodstream.
• Dramatic variations in diet or significant weight-gain or weight-loss may cause gout attacks or even contribute to the disease.

Indeed, from all the studies, the causes of gout are mult-factorial! There's no single factor that has been proven to cause the disease.

Gout is caused by excess uric acid in the blood. But what causes high uric acid in the body?

Uric acid, a nucleic acid degradation product, down-regulates dsRNA-triggered arthritis.

Authors: Zare F, Magnusson M, Bergstrom T, Brisslert M, Josefsson E, Karlsson A, Tarkowski A.

Institution: Departments of *Rheumatology and Inflammation Research and Virology, University of Goteborg, Sweden.

Uric acid, the naturally occurring degradation product of purine metabolism, is a danger signal, driving maturation of dendritic cells. It is well known that uric acid crystals display potent proinflammatory properties--the cause of gout--whereas the biological properties of soluble uric acid are less well documented. We have demonstrated previously that nucleic acids of endogenous and exogenous origin display proinflammatory properties. The aim of the present study was to assess the impact of soluble uric acid on in vivo inflammatory responses.

Mice were administered with uric acid suspension in saline or saline alone prior to induction of neutrophil-mediated inflammation, delayed-type hypersensitivity, histamin-induced edema (measure of vasodilation capacity), as well as double-stranded (ds)RNA-triggered arthritis. Frequency and severity of arthritis were decreased significantly in mice exposed to dsRNA and simultaneously treated with uric acid as compared with saline-treated controls. Also, granulocyte-mediated inflammatory response and vasodilation capacity were reduced significantly in mice treated with uric acid as compared with their control group.

The data suggest that down-regulation of inflammation was mediated by skewing the inflammatory response from the peripheral sites to the peritoneal cavity and down-regulating vasodilatatory capacity and thereby affecting leukocyte migration. In contrast, the T cell-mediated delayed-type hypersensitivity reaction was not affected significantly in mice exposed to uric acid. These findings demonstrate that uric acid displays a potent, distant anti-inflammatory effect in vivo. This property seems to be mediated by down-regulation of neutrophil influx to the site of inflammatory insult.

Study link: Gout, uric acid and inflammation.