Medications for MS Are Up, Age at Diagnosis Is Down
Why are these two studies strumming a common chord on my myelin-compromised axons? Well, it’s like this …
As an old-timer with the disease now, I have seen many changes in the treatment of MS over the years. Going from just a couple of disease-modifying therapies (DMTs) when I was diagnosed — and I know some of our readers remember when there were none — to nearly two dozen DMTs is a perfect example of both how long I’ve lived with MS and how much progress has been made.
I was 35 when I heard the words, “You have multiple sclerosis.” At the time, that was smack-dab in the middle of the average age of diagnosis. Now far more people are diagnosed in their twenties than in their fifties and pediatric MS is a thing.
Early Diagnosis Makes a Difference in Outcome
Linking these two aspects of MS is the understanding that early diagnosis and treatment (using those DMTs) has a profound effect on improving what a person’s MS looks like 20 and 30 years down the road post-diagnosis.
The earlier you know you have MS, the earlier you can begin treatment, and the earlier you can begin to make other modifications to your lifestyle to improve your chance at a better life.
Recent MS studies show that shedding a few pounds can be good for long-term prognosis — or at least that putting on extra weight can be bad for progression. That means the second paper I mentioned gives us another early intervention that may be helpful.
Lifestyle Makes a Difference, Too
If UPFs are bad for long-term outcomes in cognitive function for people who don’t have MS, then they must be for us as well. And let’s remember that cognitive decline (sometimes called cog fog) is an accepted symptom of MS.
Early diagnosis — which, according to the Neurology study, occurs four years earlier than it did before 1982, with 80 percent of people being diagnosed within one year of symptom onset — allows patients and doctors to treat the disease earlier in the disease’s progression.
Knowing of other health course corrections — like reducing the amount of ultra-processed foods in our diets — that reduce some MS-similar symptoms in non-MS patients can only be helpful as well.
Now, it must be said that there is no proof that the mechanism of UPF-related cognitive decline is the same as MS-related decline. But if we know that MS can cause this decline, and UPFs can cause it, too, why would we risk layering the two?
So two studies that may not be related to one another in their origins or methodology seem to make sense to put in the same chapter as I file away more things about MS that as our old pal Rusty used to say in her comments, “Make you go, ‘Hmmmmm.’”
Wishing you and your family the best of health.
Cheers,
Trevis
