In 1997 I came across a tidbit that I thought was funny. It turns out that MS and gout are mutually exclusive, meaning that if you get one you likely don’t get the other and vice versa.
I’d love to know what researchers were looking for when they found that out! But there it is. We are lucky I guess. Although I suppose if I was able to choose I would choose gout.
I understand the pain is excruciating, but it can be treated with medication. Even without treatment you could recover within 1 to 2 weeks.
Also it affects men more than women. Interesting because according to NMSS, MS affects at least two to three times more women than men.
What Cases It?
Gout is caused by an overabundance of uric acid (UA) in the blood. This may be brought on by genetic factors, or by “what was once characterized as a “rich man’s diet” (high amounts of meat, seafood, alcohol and sweetened drinks)”.
It is produced by the body and is the main component of urine in both humans and primates. Normally, it is excreted from the body via the kidneys in the urine. But when UA backs up, causing high levels in the blood, it forms crystals in the joints which results in gout.
But these same high UA levels also appear to prevent the development of MS leading to my question: which came first? Does MS prevent us from getting gout? Or does getting gout prevent a person from getting MS?
How Can Knowing This Help Us?
Researchers now know that UA acts as a “free radical” scavenger in the body. For example, as part of basic daily processing, any body produces “highly reactive” molecules that create inflammation and damage nerve fibers. UA acts as an antioxidant and just “mops them up”.
It also has been shown in animal models of MS to reduce inflammatory flare-ups in the brain and slow the passage of inflammatory cells into the central nervous system. It even prevented paralysis in mice. Unfortunately not in humans.
Another recent study found that lower UA was associated with disability progression, as well as cognitive decline.
Even more recently, another study found that “UA levels declined during the course of MS, which suggested that the periodic flare-ups of inflammation that occur in MS may ultimately exhaust the body’s antioxidant reserves.”
So I assume then that keeping UA levels up is a good thing for MSers as well as supporting my antioxidant levels. I will add the forbidden-for-gout foods to my diet to increase my levels of UA. See list here.
Where To Next?
As researchers point out, “There are many things that have worked in [the mouse model] that haven’t worked in MS, or have only modest effects.”
That leads to another question I have: since animals generally don’t produce UA because they have an enzyme that breaks it down, we have to artificially induce it in them. So doesn’t this enzyme skew the test results?
Also would UA protect you from getting worse if you already had it? Because right now there is very little that can be done for those of us that have transitioned to secondary-progressive (SPMS).
Obviously I’m not a scientist. But clearly, I think the relationship between UA and brain inflammation should continue to interest scientists.
I pledge to bring it up at my next neurologist appt. at least.