Maybe it’s the gout pain in my wrist that’s making me tetchy.
Or maybe it’s the amount of BS I’m seeing today.
New gout research means hope for new gout therapies?
More like new gout research reaches new heights of BS.
Actually, the research I have seen, is probably of massive interest to those who need to understand how gout pain works. It’s just not relevant to us poor gout sufferers. We need better treatment using the therapies already available rather than wasting time and money on inflicting gout on mice.
Let me explain
I’ve seen an editorial in Arthritis Research and Therapy that summarizes recent research. The research basically looks at how pain signals work in the body (of a mouse), particularly where the pain is a reaction to uric acid crystals. You do not really need to understand the summary, but I’ll include it so you see what we’re up against:
It is well known that urate crystals stimulate monocytes and macrophages to elaborate inflammatory cytokines, but the tissue response of the synovium is less well understood. Microarray analysis of mRNA expression by these lining cells may help to delineate the genes that are modulated. Employing a murine air-pouch model, a number of genes expressed by innate immune cells were found to be rapidly upregulated by monosodium urate crystals.
Some will excuse this bafflegab as cutting edge research that is so advanced that jargon is essential. I don’t. I believe that the researchers know full well that messing around with a bunch of mice is no way to solve current gout problems. But that is where the drug companies are pushing their money.
A new gout pain angle.
A new gout pain therapy.
A new medical income stream.
Cynical? You bet.
The whole medical profession and associated drug company funded research is obsessed with finding new ways to combat gout pain.
Am I overreacting? No way.
The editorial summary I mentioned starts with:
Understanding how uric acid crystals provoke inflammation is crucial to improving our management of acute gout.
No it isn’t. What is crucial, is improving the management of existing urate lowering therapies. If allopurinol and other uric acid reducing treatments were planned and monitored properly, gout pain would be virtually eliminated.
Consider a similar situation, comparing your gout with your car. You have an annoying noise from your engine, often so severe that it affects your ability to drive. The mechanic gives you ear muffs. You’re still not happy, so the mechanic inspects the engine, tells you what’s wrong, then sells you updated in-car entertainment with extra volume boosters so you can’t hear the faulty engine noise. You’re still not happy, and friends offer all sorts of advice from extra carpets to adapting loft insulation. And all the time, the fault is wearing away at your engine. It becomes crippled and you can’t use it – just like your gouty old bones.
Fix the fault.
Lower uric acid to the point at which uric acid crystals dissolve. Easy for most gout patients, but even where there are complications, there is a range of options. Nothing will happen if you do not try. Actually, worse than nothing, because uric acid crystals are dangerous.
The summary ends with:
These findings provide new research avenues to investigate the physiopathology of gouty inflammation, and may eventually lead to new therapeutic targets in acute gout.
More gobbledygook saying “Hey lads, just look at all the money we can spend finding new ways to muffle the fault”
I’ve added a new page to my main gout website today, highlighting the dangers of bone erosion in advanced gout. Crumbling joints are a real threat to all gout sufferers. Each year your uric acid stays high, urate deposits are slowly eating away at your bones. No amount of pain relief will change this – you are simply masking the problem until the fateful day the doctor says “Sorry, there’s nothing more we can do.”
And you join your car in the junk yard.