These crystals then lodge in the soft tissues and in the joints of the extremities – classically, the big toe - and cause inflammation, swelling and an excruciating pain that was described memorably by the 18th century bon vivant Sydney Smith as like walking on one’s eyeballs.(3) Because uric acid itself is a breakdown product of protein compounds known as purines – the building blocks of amino acids – and because purines are at their highest concentration in meat, it has been assumed for the past 130-odd years that the primary dietary means of elevating uric acid levels in the blood, and so causing first hyperuricemia and then gout, is an excess of meat consumption. And the pathology of gout has been understood since the British physician Alfred Garrod, in the mid-19th century, identified uric acid as the causative agent the idea being that uric acid accumulates in the circulation to the point that it falls out of solution, as a chemist would put it, and so crystallizes into needle-sharp urate crystals. This made gout the original example of a disease linked to diet and over-consumption, and so, in effect, the original disease of civilization.īut once gout became easily treatable, in the early 1960s, with the discovery of the drug allopuranol, clinical investigators and researchers began to lose interest. Until the late 17th century, when the spread of gout reached almost epidemic proportions in Britain, the disease afflicted almost exclusively the nobility, the rich and the educated, and so those who could afford to indulge an excessive appetite for food and alcohol. The proportion of women afflicted is considerably less at younger ages but still rises over 3 percent by age 60.(1) Moreover, the prevalence of gout seems to have doubled over the last quarter century, coincident (perhaps not coincidentally) with the reported increase in obesity, and it may have increased five- or even six-fold since the 1950s, although a large portion of that increase may be due to the aging of the population.(2) Recent surveys suggest that nearly 6 percent of all American men in their fifties suffer from gout, and over ten percent in their seventies. Gout itself is an interesting example because it is a disease that has gone out of fashion in the last century and yet the latest reports suggest it is not only as prevalent as ever, but becoming more so. Gout and the condition known technically as hyperuricemia, or elevated levels of uric acid, are the most recent examples of this kind of institutional neglect of the potential health effects of fructose, and how pervasive it can be. Either stick to it religiously for at least 2 months and adapt properly, or don’t bother and save yourself some possible flare-ups. The worst thing you can do is go back and forth between keto/carbs whilst you are still adapting. This is explained in the literature later in this thread, basically what happens is ketones compete for excretion with uric acid, but as you keto-adapt this is no longer a problem. If you are newish to low carb/keto and wondering about the dangers, then uric acid levels can rise substantially in the first 2-4 weeks, but they level out after 6-8 weeks. Ash SimmondsĪs usual the conventional wisdom is arse-about with cause/effect, gout etc isn’t primarily caused by purine rich or high protein foods upping uric acid, it’s the inability to effectively clear out uric acid which eventually form crystals in the joints and stones in the kidneys - which is from a feedback loop of inflammation, and usually there’s a catalyst feature which induces it. These crystals then lodge in the soft tissues and in the joints of the extremities –- classically, the big toe - and cause inflammation, swelling and an excruciating pain that was described memorably by the 18th century bon vivant Sydney Smith as like walking on one’s eyeballs. Not everyone who has hyperuricemia goes on to develop gout - individual differences in the formation of crystals and/or in inflammatory responses to those crystals may play a role in whether a person with hyperuricemia will develop the disease.īritish physician Alfred Garrod, in the mid-19th century, identified uric acid as the causative agent the idea being that uric acid accumulates in the circulation crystallizes into needle-sharp urate crystals.
Uric acid then reacts with physiologic sodium to form MSU which can crystallise in painful places. Hyperuricemia (having high uric acid levels in the blood) is a necessary predisposing factor for gout. Gout refers to disease that occurs in response to the presence of monosodium urate (MSU) crystals in joints, bones, and soft tissues.
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