In the last couple of years I have suffered from gout. The very first time it was so excruciating that I failed when I tried to walk from my house to the GP surgery, only 500 yards away!
Since then there have been recurrences which were not so bad, but I felt that they were getting more frequent so I asked my nephrologist about gout when I had my annual check up just before Christmas. This seemed like a reasonable thing to ask, considering that gout is caused by uric acid in the blood, and urate level is one of the many things which I have been tested for ever since I became potential living donor.
The common response when I tell someone that I have gout is "Isn't that to do with drinking too much port?" Instantly, you know that they need education!
Gout was once a problem which only affected the well-off so it was associated with what they ate and drank and, yes, one of those things was port. However, the point is that the average person at that time did not have a good enough diet to raise their urate level to the point at which they could be affected by gout. It was just the high consumption of lots of "good food and drink" which caused the gout in the well-off people (and principally the men, I suspect).
By the late 17th C, gout did start to affect the rest of the population and this has continued, generally thought to be due to the improvement in diet of the so-called working class. Research in the 19th C by the British physician Alfred Garrod identified uric acid as the causative agent into the causes of gout; the idea being that uric acid
accumulates in the circulation and crystallizes into needle-sharp
urate crystals. 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"! 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.
It is still generally thought that consuming foods which are high in purines will make you more likely to suffer from gout, and these high purine foods include lots of things which are otherwise good for you such as "oily fish" (omega oils) and "whole grain"! The list even includes Marmite and beer (both due to yeast). In a series of studies in the 1960s, clinical investigators first linked
hyperuricemia to glucose intolerance and high triglycerides, and then
later to high insulin levels and insulin resistance. The gout research effectively ended in the 1960s when the drug allopurinol was discovered which is effective at reducing the amount of urate produced. This cessation of research was understandable as gout is not fatal and so when a cure is found, there is no point in spending further research effort on it. However, the effect of ending research is that the commonly-accepted view is not challenged, althugh some scientists have said that "low-purine diets have a negligible effect on uric acid levels". I have been educating people about purines as the cause (as the bottle of port in my drinks cupboard has been there for about five years and is still not empty) but I have just found an alternative culprit.
That new culprit is that the rise in the incidence of gout in the UK might be linked to the massive increase in the sugar trade in the 18th - 19th C. It has been demonstrated that fructose consumption and uric acid levels are linked. The earlier researchers later admitted that they were unaware that
sucrose is 50% fructose (and the other 50% is glucose, if you were wondering).
The hypothesis is that sugar (sucrose) and high fructose corn syrup (which is used in many foods) would
constitute the worst of all carbohydrates when it comes to uric acid and
gout. The fructose would increase uric acid production and decrease
uric acid excretion, while the glucose, through its effect on insulin,
would also decrease uric acid excretion. Thus, it would be reasonable to
assume or at least to speculate that sugar is a likely cause of gout,
and that the patterns of sugar consumption explain the appearance and
distribution of the disease.
The trouble is that this is still only a unproven hypothesis. However, I offer it as a possibility for anyone who suffers from gout as it might just help them to cure the actual cause rather than simply address the problem with allopurinol for the rest of their lives.
Much of the above comes from the blog of Tim Ferriss (https://tim.blog/2009/10/05/gout/) where he presents it as the missing chapter from Good Calories, Bad Calories by Gary Taubes, a science journalist and author. I don't know if either of them are also medical doctors, but I know I'm not!
