What is Gout?

Gout is one of the most painful forms of arthritis. Gout attack can strike without warning with intense pain usually in the joint of the big toe. But, it may also include the ankles, heels, instep, knees, elbows, hips, thumbs, or fingers.

Gout develops when too much uric acid builds up in your body. Sharp needle-like urate crystals form around your joints beginning in your big toe. Gout does not happen overnight. It is the result of a build-up process that may take months or years. When it reaches a critical level, you get a painful gout attack.

History of Gout

The first written description of gout dates from 2,600 BC, when Egyptians noted gouty arthritis of the big toe. Around 400 BC, the Greekphysician Hippocrates also commented on gout. Writing ca. 30 AD, Aulus Cornelius Celsus appeared to recognize many of the features of gout, including its link with a urinary solute, late onset in women, linkage with alcohol, and perhaps even prevention by dairy products:

“Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera. … Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed. Upon the commencement of pain blood should be let; for when this is carried out at once in the first stages it ensures health, often for a year, sometimes for always. Some also, when they have washed themselves out by drinking asses’ milk, evade this disease in perpetuity; some have obtained lifelong security by refraining from wine, mead and venery for a whole year; indeed this course should be adopted especially after the primary attack, even although it has subsided.^“

Colchicum was described for treatment of rheumatism and swelling in the Ebers Papyrus, ca. 1500 B.C. The use of Colchicum corm for gout probably traces back to ca. 550 A.D., as the “hermodactyl” recommended by Alexander of Tralles. Colchicum corm was used by Ibn Sina and other Islamic physicians, was recommended by Ambroise PAre in the sixteenth century, and appeared in the London. In 1833 P.L. Geiger purified an active ingredient, which he named Colchicine. Colchicum was brought to America by Benjamin Franklin; Franklin suffered from gout himself and had written humorous doggerel about the disease during his stint as Envoy to France. As a drug predating the FDA, colchicine was sold as a generic in the United States for many years. In 2009 the FDA approved colchicine for gout flares, awarding Colcrys a three year term of market exclusivity, prohibiting generic sales, and increasing the price of the drug from $9 to $485 per bottle.

Around 200 AD, the Roman gladiatorial surgeon Galen described gout as a discharge of the four humors of the body in unbalanced amounts into the joints. The word “gout” was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin word “gutta”, meaning “a drop” (of liquid)^.

Historical treatments for gout include gin and numerous medications that have since been found to be not effective. Sodium Bicarbonate (baking soda) is a traditional remedy, thought to work by raising blood pH (lowering blood acidity). However, the added sodium may be inappropriate for some people.

What Causes Gout?

Gout is caused by too much uric acid in the blood (hyperuricemia). Hyperuricemia is caused by a combination of several factors. You are more likely to get hyperuricemia and gout if you:

• Have family members with the disease
• Are a male over 30 years
• Are overweight
• Drink 2 or more alcoholic drinks (especially beer) a day
• Drink 2 or more sweetened soft drinks per day
• Eat excessive amounts of red meats, internal organs, yeast, poultry or seafood
• Smoke 2 or more cigarettes per day
• Regularly use some medicines such as diuretics, aspirin, cyclosporine, or levodopa.

Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons including dietary, genetic, or underexcretion of urate^. About 10% of people with hyperuricemia develop gout.

Gout Treatments

The first thing a doctor gives you is a strong pain killer. This provides only short term relief of pain, and it does not really solve the problem. Various prescription drugs are available for treating gout. These are harsh synthetic chemicals that may have harmful side effects if taken for long periods.

Highly toxic Colchicine is sometimes prescribed for gout. Colchicine is natural poison that may cause vomiting, diarhea, abdominal cramps, kidney failure and in high concentration even death.

Because of the harmful side effects of drugs, many people are choosing an alternative natural cures.

Sign And Symptoms

Gout usually presents as recurrent attacks of acute inflammatory arthritis (a red, tender, hot, swollen joint). The joint that is most commonly affected is the first metatarsalphalangeal joint at the base of the big toe (approximately 75 percent of first attacks) and when this occurs it is known as podagra. The reason gout usually presents in the feet is in part due to the lower temperature^.

People with long-standing hyperuricemia can form tophi (uric acid crystal deposits) in tissues. These are usually hard, non-painful deposits. Extensive tophi that invade bone are associated with arthritis due to bone erosion.

Elevated levels of urine uric acid can lead to uric-acid crystals precipitating in the kidneys which may form kidney stones and lead to urate nephropathy^.

Lifestyle

About 12% of gout is attributed to dietary causes. This includes a strong association with the consumption of alcohol, sugar, and meat and seafood. The intake of dairy products, vegetables, and the total protein intake do not affect the occurrence of gout.

A sedentary lifestyle also increases the risk of developing the disease.

Medical Condition

Gout may present as a complication of other medical conditions.

• Metabolic Syndrome(the combination of hypertension, diabetes, dyslipidemia, truncal obesity, increased cardiovascular disease risk)
• Leukemia

Gout also can develop as a co-morbidity of other diseases, including polycythemia, intake of cytotoxics,obesity, diabetes, hypertension, renal disorders, and hemolytic anemia. Gout is an important complication in a minority of solid organ transplants^.

Gout may occur as a result of renal failure^.

Some studies have established a statistical connection between gout and lead poisoning, and a significant correlation between levels of lead in the body, urate excretion and gout. It is known that lead sugar was formerly used to sweeten wine. This condition is then known as saturnine gout, as saturnus is the alchemical term for metallic lead.

Gout occurs when crystals of uric acid, in the form of monosodium urate, precipitate on the articular cartilage of joints, on tendons, and in the surrounding tissues. Uric acid is a normal component of  blood serum. Uric acid is more likely to form into crystals when there is hyperuricemia, although hyperuricemia is 10 times more common without clinical gout than with it. Gout can also occur when serum uric acid is normal, and when it is abnormally low (hypouricemia). Paradoxically, acute attacks of gout can occur together with a sudden decrease in serum uric acid, such as due to use of drugs (uricosurics, xanthine oxidase inhibitors), or total parental nutrition. However, the sudden decrease may be a consequence of abrupt formation of crystals (removing uric acid from the serum), rather than a cause.Regardless of the serum concentration of uric acid, precipitation of uric acid is markedly enhanced when the blood pH is low (acidosis). A similar pH-sensitive effect occurs in urine, contributing to uric acid nephrolithiasis (kidney stones).

Uric acid is a product of purine metabolism, and in humans is normally excreted in the urine. Purines are generated by the body via breakdown of cells in normal cellular turnover, and also are ingested as part of a normal diet. The kidneys are responsible for approximately two-thirds of uric acid excretion, with the liver responsible for the rest.

Prevention

Both lifestyle modifications and medication can decrease uric acid levels. Medications however are not usually started until one to two weeks after an acute attack has resolved due to theoretical concerns of worsening the attack. They are often not recommended until after a second attack of gout has occurred, unless destructive joint changes, tophi, or urate nephropathy exists^. It is not until this point that medications have been found to be cost effective. Urate lowering measures should be titrated to decrease serum uric acid levels below 360 µmol/L (6 mg/dL)^.