Summary

A 12-year study shows that the intake of sugar-sweetened sodas and fructose (from juices and fruits) are clearly linked, in a dose-dependent fashion, with the occurrence of new cases of gout in men.

Introduction

Gout, which is becoming more frequent, is the most common type of inflammatory arthritis in men. The classical picture of an overweight red-faced old man, sitting with his foot up on a stool, was inevitably completed by the glass of port wine in his hand. Overindulgence by the wealthy was regarded as the prime cause. In fact, there has always been a connection between food and drink consumption and gout, which has persisted today and is generally accepted as cause-and-effect. Greater consumption of meat and seafood - high purine-containing foods - has been established as the main cause, probably set against a genetic background of defective purine metabolism. However, factors thought to play a role in the rising frequency of gout today include increases in longevity, the use of diuretics and low-dose aspirin, obesity, kidney disease, high blood pressure, and the metabolic syndrome.

Now one must add another contributing factor to the list: sugar-sweetened soft drinks or sodas. A 12-year study published in the British Medical Journal provides the data that strongly support such a connection.

What was done

The subjects in the study were health professionals - male dentists, optometrists, podiatrists, pharmacists, and veterinarians. There were over 51,500 of them; they were 91% white, and aged 40 to 76 in 1986, the time of recruiting. A questionnaire at enrollment provided information on diet, medical history, and drugs. All those with a history of gout on this questionnaire (2,770-odd) were excluded from the rest of the study.

There were 46,393 men who had no gout at the outset and provided valid questionnaires. The latter included specific questions on how often the subject had consumed sugar-sweetened soft drinks and diet soft drinks; there were nine frequency choices for responses ranging from 'never' to 'over 6 times a day'.

Free fructose intake was calculated as the total fructose intake from the diet plus half the intake of sucrose (the monosaccharide fructose is one component of the disaccharide sucrose).

Every two years repeat questionnaires were sent, which also covered information on weight, medications, and medical conditions. Cases of gout were confirmed using the 11 criteria established by the American College of Rheumatology.

What was found

There were 755 new cases of gout during the 12-year follow-up period. Increasing consumption of sugar-sweetened soft drinks was linked to an increasing risk of gout. The relative risks (RR) for different intakes are given below:

Less than 1 serving a week	1.0 (reference standard)
5 - 6 servings a week	1.29
1 serving a day	1.45
2 or more servings a day	1.85

These RRs were calculated after adjustments had been made for different values in the various groups for these factors: age, calorie intake, BMI, diuretic use, history of high blood pressure, kidney failure, alcohol use, meats, seafood, purine rich vegetables, vitamin C, and diary intake.

There was no apparent relationship between diet sodas and the risk of developing gout.

To calculate the influence of fructose, the subjects were categorized into five classes, or quintiles, according to increasing amounts of fructose. The RRs for different levels of fructose intake are given below:

Lowest quintile of intake	1.0 (reference standard)
Next quintile	1.29
Next quintile	1.41
Next quintile	1.84
Highest quintile	2.02

Further analyses showed that other contributors to fructose intake, such as total fruit juice or fructose-rich fruit (apples or oranges) were also linked to a higher risk of developing gout.

What this study means

The findings show that sugar-sweetened sodas and fructose are clearly linked, in a dose-dependent fashion, with the occurrence of new cases of gout. Further, a principal role for fructose is revealed.

How does this monosaccharide sugar affect the development of gout? Previous work has shown that oral or intravenous fructose administration causes accelerated degradation of some purines and increased purine synthesis, producing a rapid increase in serum uric acid. The uric acid-raising effect of fructose is exaggerated in people with existing elevated uric acid levels or those with a history of gout. Glucose and other simple sugars don't have this effect on serum uric acid levels.

The study authors suggest that the risk for precipitating a gout attack from free fructose intake could be at least as great as that from purine-rich foods, such as a totally meat diet. Thus the conventional low purine diet approach while allowing fructose ad libitum could be a worse option, overall. Of course, sugar-sweetened soft drinks are bad for you for other reasons, too . . .