View on 23rd December 2017
In only ever had the kind of gout pain caused by the needle-like crystals forming from blood in the foot muscles due to hyperuricemia caused by dehydration. When I had an attack that lasted longer than 3 days — in fact more like 3 weeks — in 2014, I made up my mind to drink plenty of water all the time and not just long enough to end each attack. This hydration level affected the development of other health issues in 2015..2017, as described in this page. But I never had an attack of gout after September 2014.
View on 7th January 2010
My first gout attack was, as far as I remember, in the spring of 2007. I woke up with my left foot feeling as though (as I often say) a steam roller had crushed it to pulp, after which I’d had a painkiller from paramedics but that was now wearing off. This sounds slightly complicated or contrived but that’s the sort of feeling: it can be as bad as I can imagine localized pain ever being, but can fade while the foot is at rest, that is, with no forces acting on it any direction. This last means nothing from its position including gravity — it must be supported but at the ideal level and angle, I must put no weight on it (so cannot stand on it or walk). On days when a foot is this bad, the extreme level of pain returns when I tried to stand or walk on it.
At onset of that first attack, I could not get out for a day or two but I went to doctor (but a locum, not my own doctor, as it happened that time) and got a diagnosis.
Naturally, I had heard of gout with the traditional, widespread but inaccurate connotations attached to it in my memory. I had never had any interest in it or read what caused it. Now, I read in Wikipedia that gout “is caused by elevated levels of uric acid in the blood that crystallizes and deposits in joints, tendons, and surrounding tissues. It affects 1% of Western populations at some point in their life. It is marked by recurrent attacks or acute inflammatory arthritis (red, tender, hot, swollen joint).”
Wikipedia went on: “Treatment with NSAIDs [non-steroidal anti-inflammatory drugs], steroids, or colchicine improves symptoms. Once the acute attack has subsided, levels of uric acid are usually lowered via lifestyle changes and long term prevention with allopurinal.” I also discovered that gout is a listed side effect of my medication taken back then to reduce high blood pressure. The prescription I had been on was for co-tenidone, in which is a combination of the beta blocker atenolol with the diuretic chlortalidone, but my GP had not told me to drink lots of water to make sure I did not get dehydration and thus hyperuricemia. There was thus a snag associated with any attempt to treat my gout pro-actively with medication: medication for gout could fight against the high blood pressure medication.
Evidently the treatments are mostly just for the symptoms. I was having attacks that lasted a few days and I hd no intention of taking a lot of drugs just to improve symptoms. I wanted a strategy that would prevent these levels of uric acid rising in my bloodstream, prevent the crystals ever forming, and thus prevent these sometimes extremely painful attacks even occurring. However, we are told that for the prevention of future attacks of gout, the medication is something called allopurinal; so what is that?
Once again, we turn to Wikipedia, which says: “The primary use of allopurinol is to treat hyperuricemia (excess uric acid in blood plasma) and its complications. Allopurinol does not alleviate acute attacks of gout, but is useful in chronic gout to prevent future attacks.”
So far, so good; but it also says: “Because allopurinol is not a uricosuric, it can be used in patients who have poor kidney function. However, allopurinol has two important disadvantages: its dosing is complex, and some patients will be hypersensitive to it. Therefore, use of this drug requires careful monitoring.” This means that if I were put onto it as a preventative for long term gout, not only would I have three medications instead of the two (which is bad enough in my view) but I would probably have to keep going to the surgery and getting blood taken for testing of uric acid levels or even allopurinol levels. I could risk becoming even more of a chronic occupational invalid (of sorts).
So the other long term treatment is obviously the best policy, and that was the making of those “lifestyle changes”. So, what am I doing? What I have tried to do consistently since my first attack: drinking plenty of water (including some as fruit drink/juice). After all, I have never drunk tea or coffee (regardless of whether or not they can be counted in the amount of anti-dehydration liquid drunk daily, and also regardless of whether or not they in any way increase or reduce the amount of uric acid in the bloodstream); and I have never drunk beer. After a couple of years in Paris (1976..8) when I did occasionally have a glass of wine with friends I haven’t drunk wine of any sort more than once (one glass) in several years because I now dislike its taste almost as much as I hate the taste of beer, though not quite as much. (I could still sip a glasss of wine now if friends were going to be terribly upset if I didn’t; but all beer is just horrible.) So since almost three years ago I should not have had gout again. Having just got past my sixth attack, I think it is (today as I write, on 7th January 2010, it is my first day free of aching feet since the latest attack began in the week between Christmas 2009 and New Year). So I should explain how long these lasted.
I have only had half a dozen attacks, for maybe a week each, over almost 3 years. That first time the attack came on a Wednesday (out of the blue: I just woke up with it) and disappered by the Sunday. Six weeks later, as far as I can recall, it came again, also on Wednesday, and this time went by Friday! After that 2nd attack I only had another one more than a year later, which lasted a couple of weeks; then one last March, which lasted almost three weeks — the longest ever, but mild for most of that time Then I had an attack in December 2009 from 5th to 15th inclusive; and again from the last week that month to 6th January 2010. It has gone completely today, 7th January 2010. So, the attacks have been widely spaced, seemingly random, and I have a strategy that should work (well, most of the time) without complicating the already significant permanent medication regime I am on.
My first reaction to discovering the side effect situation, my though process went as follows. We all know that if we took too much to heart all the small print on those little pages that come inside boxes of pills we would never take any medication ever again; and yet the long list of possible side effects of the high blood pressure medication does include gout. I reckon that once we are in the territory of dealing with an illness that is the side effect of a medication which I am taking daily for life (apparently) for another illness, if we have a rational strategy to minimize that does not imply yet another medication to add to the daily cocktail, this is better than resorting to yet another medication. That I don’t always manage to ensure that I get through the 2 to 4 litres I don’t doubt; whether it is this that brings (or, allows) it back, or whether certain foods (of which I might by chance eat more during one period of a few weeks than during another such period) provoke an attack, or whether it is just that the water drinking regime is not an absolute guarantee the attacks will stay away, I don’t know. My sister and a few solicitous friends have asked whether I have tried eating cherries or drinking cherry juice; and I have. There are a great many web pages of advice and opinion about gout — understandably, since high blood pressure and heart disease are so common in our population, and since gout can be so extremely painful and disabling when it attacks — and many different theories about what causes the crystals to form so quickly at certan times, making the attack onset. To those who suggest particular supplements I have had to say that I won’t be experimenting with taking things including particular foods in significantly increased quantities, or supplements of particular substances, without discussing with my doctor because of the complexity of the interactions between clusters of medications that one is taking all at the same time over long periods — many years — for chronic and (in the medical profession’s judgement) even more serious conditions.
The next time I saw my own doctor after the second attack, he had seen the writeup that I had had gout, and as this was just a regular review of long term prescriptions, I said I’d read up the cause (sharp crystals forming) and had decided that increasing my drinking — at least 2 litres, and in summer up to 4 litres, of water or fruit juice per day — as a continual measure against dehydration (the reason the high blood pressure medication is a cause of gout) was the best way to deal with the problem, rather than taking another medication daily for the rest of my life, which is what the standard medical and pharmaceutical advice pages say will happen if one starts on specific medications against gout. He agreed. Anything up to 4 litres, especially in summer, is not too much water for the kidneys in a normal otherwise healthy large adult, and gives the body plenty of scope to eliminate the solutes that come out of solution and form the crystals that produce the pain that is gout.
So I have just been doing that. I discussed it again with the GP since; he has this review of my 2 main medications (high blood pressure & anti-depressant/anti-anxiety) twice a year and is aware that the former has the side effect of provoking gout. The response/reaction to that fact is to reinforce the drinking policy. We are both still of the same opinion that further medication is best avoided which I take as meaning, provided I can put up with the occasional attack (even though they are a nuisance and even rather depressing, in the sense downheartening, at the time) and keep well enough hydrated at all times.
The reason that medication to reduce high blood pressure can provoke gout by leading to dehydration is that it has two components of which one is a diuretic, and the reason for that is that the body also has to get rid of some other solutes that can cause blood pressure to remain high. Water retention is actually a sign that one is not drinking enough and not giving the liver and kidneys enough water to work with when trying to dissolve away and get rid of certain solutes that are the products (you might say bi-products, as they are of no use) of normal metabolism. They are just the chemical trash left over, if you like, from the process of converting food into stuff we do need, but the way the human species has evolved to deal with that trash is to dissolve it in water and wash it away. Some animal species have radically different metabolisms from ours; all that is the detailed stuff of biochemistry and zoology. All I can do with the resources I have is make sure I drink enough.
Now I must just go and have another glass of water....