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Gout: The Missing Chapter from Good Calories, Bad Calories
For many of us Gout sufferers, it seems that doing Atkins if a bit of a trade-off. You lose weight, but pay for it by suffering from worsening gout attacks.
Well, it seems that there is some evidence that meat and protein aren't to blame for gout, but fructose...
For many of us Gout sufferers, it seems that doing Atkins if a bit of a trade-off. You lose weight, but pay for it by suffering from worsening gout attacks.
Well, it seems that there is some evidence that meat and protein aren't to blame for gout, but fructose...
The actual evidence, however, has always been less-than-compelling: Just as low cholesterol diets have only a trivial effect on serum cholesterol levels, for instance, and low-salt diets have a clinically insignificant effect on blood pressure, low-purine diets have a negligible effect on uric acid levels. A nearly vegetarian diet, for instance, is likely to drop serum uric acid levels by 10 to 15% percent compared to a typical American diet, but that’s rarely sufficient to return high uric acid levels to normality, and there is little evidence that such diets reliably reduce the incidence of gouty attacks in those afflicted.
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The evidence arguing for sugar or fructose as the primary cause of gout is two-fold. First, the distribution of gout in western populations has paralleled the availability of sugar for centuries, and not all refined carbohydrates in this case. It was in the mid-17th century, that gout went from being exclusively a disease of the rich and the nobility to spread downward and outward through British society, reaching near epidemic proportions by the 18th century. Historians refer to this as the “gout wave,” and it coincides precisely with the birth and explosive growth of the British sugar industry and the transformation of sugar, in the words of the anthropologist Sydney Mintz, from “a luxury of kings into the kingly luxury of commoners.” British per capita sugar consumption in the 17th century was remarkably low by modern standards, a few pounds per capita per year at the turn of the century, but the change in consumption over the next century and a half was unprecedented: between 1650 and 1800, following the British acquisition of Barbados, Jamaica and other “sugar islands”, total sugar consumption in England and Wales increased 20- to 25-fold.
The second piece of evidence is much less circumstantial: simply put, fructose increases serum levels of uric acid. The “striking increase” in uric acid levels with an infusion of fructose was first reported in the Lancet in the late 1960s by clinicians from Helsinki, Finland, who referred to it as fructose-induced hyperuricemia. This was followed by a series of studies through the late 1980s confirming the existence of the effect and reporting on the variety of mechanisms by which it came about. Fructose, for instance, accelerates the breakdown of a molecule known as ATP, which is the primary source of energy for cellular reactions and is loaded with purines. (ATP stands for adenosine triphosphate; adenosine is a form of adenine, and adenine is a purine.) And so this in turn increases formation of uric acid. Alcohol apparently raises uric acid levels through the same mechanism, although beer also has purines in it. Fructose also stimulates the synthesis of purines directly, and the metabolism of fructose leads to the production of lactic acid, which in turn reduces the excretion of uric acid by the kidney and so raises uric acid concentrations indirectly by that mechanism.
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The evidence arguing for sugar or fructose as the primary cause of gout is two-fold. First, the distribution of gout in western populations has paralleled the availability of sugar for centuries, and not all refined carbohydrates in this case. It was in the mid-17th century, that gout went from being exclusively a disease of the rich and the nobility to spread downward and outward through British society, reaching near epidemic proportions by the 18th century. Historians refer to this as the “gout wave,” and it coincides precisely with the birth and explosive growth of the British sugar industry and the transformation of sugar, in the words of the anthropologist Sydney Mintz, from “a luxury of kings into the kingly luxury of commoners.” British per capita sugar consumption in the 17th century was remarkably low by modern standards, a few pounds per capita per year at the turn of the century, but the change in consumption over the next century and a half was unprecedented: between 1650 and 1800, following the British acquisition of Barbados, Jamaica and other “sugar islands”, total sugar consumption in England and Wales increased 20- to 25-fold.
The second piece of evidence is much less circumstantial: simply put, fructose increases serum levels of uric acid. The “striking increase” in uric acid levels with an infusion of fructose was first reported in the Lancet in the late 1960s by clinicians from Helsinki, Finland, who referred to it as fructose-induced hyperuricemia. This was followed by a series of studies through the late 1980s confirming the existence of the effect and reporting on the variety of mechanisms by which it came about. Fructose, for instance, accelerates the breakdown of a molecule known as ATP, which is the primary source of energy for cellular reactions and is loaded with purines. (ATP stands for adenosine triphosphate; adenosine is a form of adenine, and adenine is a purine.) And so this in turn increases formation of uric acid. Alcohol apparently raises uric acid levels through the same mechanism, although beer also has purines in it. Fructose also stimulates the synthesis of purines directly, and the metabolism of fructose leads to the production of lactic acid, which in turn reduces the excretion of uric acid by the kidney and so raises uric acid concentrations indirectly by that mechanism.
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