Walking on sunshine

I’ve been using a wheelchair for the most recent fifteen years of my life. But curiously I’m always walking in my dreams!
 
In them I’m usually not at home. I’m usually walking around a building, a shopping center, a store. Even outside.
 
And it is only recently that I’ve started to occasionally notice that I’m holding a cane or crutch in my dreams. But I am still walking. 
 
When They Were Young
 
In my dreamscape, the wheelchair does not ever appear. It seems my brain knows it does not belong.(I wonder if someone who has been confined to a chair since birth appears moving that way in their dreams.)
 
I used to be proud of my long legs; now they get in the way a lot of the time. Still, I would not like to have them removed, so that’s something. Even as inconvenient as they can be, there’s always the chance that I’ll need them someday.
 
But I also used to consider my legs to be fat. I was ashamed that their was no space showing between my thighs, for example. Now that I’ve lost so much muscle, they’re definitely skinny, but not in a good way.  Be careful what you wish for!
 
Is Dreaming Visualization?
 
I’ve been reading about sports visualization. And I wonder if I can take advantage of the finding that your body experiences muscle movement whether it’s real or imagined. To rehearse what it would be like to walk again.
 
Since the brain does not distinguish between real and imagined actions (see here), does it count when I’m sleeping? Am I getting the experience of walking in my dreams? 
 
There are also new products that potentially would allow me to be more mobile, like using a lifeglider, for example.  Yes, I definitely would need legs for this!
 
Now
 
These days I spend most of my time indoors in a wheelchair.  I am reluctant to get overheated, to spend a lot of time outside in the sun, so I stay inside like a housebound vampire.
 
It is not really a hardship for me because I like to spend time alone, to think and read and learn. I enjoy research and I don’t miss hiking or yoga or Tai Chi outside. I don’t miss it but I wish I had the choice to go outside at a moments notice if I wanted to.
 
At this point I understand that I may never walk again. Unless a cure is found, or even a way to reverse the damage done to my myelin. 
 
But then again I see no harm in adding guided visualization about walking to my daily routine. 🙂
 
What I’ve learned this week 
  • Objects, as coins, tools, etc., used by a teacher to illustrate everyday living are called Realia plural noun [ree-ey-lee-uh, -al-ee-uh, rey-ah-lee-uh] 
  • Muscle memory is real
  • Get free online classes from prestigious schools like Yale 
  • One recommended place to get your prescription eyeglasses online for $15ish

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MS and Turmeric

After the assault on my liver, I realized that it now needed my protection. So I have embarked on a mission to consciously try to support it.
 
Like limiting my use of non-prescription drugs and my alcohol intake, moving more (exercise: isn’t that always the case?), staying hydrated, and eating healthier.
 
And I started adding Turmeric to my diet.
 
What is it?
 
You’ve likely heard about this: the new big thing in the long line of big things. It’s an herb that has been shown to affect inflammation as well as protect against heart disease among other things.  Since inflammation is such a problem with MS I paid attention.
 
It turns out that not only is consuming turmeric one way to combat chronic inflammation, it also has been used in traditional medicine to tone the liver and may even have a “protective effect” on it.
 
Yay, two for one! So I’m trying to drink turmeric tea regularly and use the spice in cooking, for example. 
 
Where to get
 
It is used in Indian cooking like yellow curries and is often found in mustards (Some food producers use curcumin, derived from turmeric, as a golden-yellow coloring additive for butter, cheese, canned beverages and other products. When looking for it on the nutrition label under ingredients, look for the name of E100.)
 
It can be found in the spice aisle of your local grocery store or ordered online from Amazon, for example.
 
We’ve been growing turmeric now for a couple of years. I can use it as tea by grating it into a tea ball and soaking in hot water with honey.
 
Food ideas
 
Experts suggest that where there’s turmeric, there should be black pepper. It increases the bioavailability of turmeric by 2000 percent! 
 
Others have added a “good fat” like coconut oil to activate it.
 
Some recommendations I found online:
 
I just stirred up a tsp of tumeric and a tsp of coconut oil.  Put a thick layer between two gingersnaps.   Delicious!
 
I use in my coffee in the monrning. A pinch of turmeric, a pinch of cinnamon and little of black pepper. It tastes good and I have had no pains and no infections. I am going on 81 years old.
 
I use in coffee with spices, too, with some almond milk and stevia, Sometimes organic cocoa.
 
You can also add turmeric to sour cream or your favorite dips and serve it with fresh vegetables 
 
Turmeric is especially complementary to egg dishes, such as egg salad, frittatas and omelets.
 
 
Finally,  I found a few other things that turmeric Can be good for:  teeth whitening and arthritis pain 
 
I’m really curious to know if turmeric and chocolate milk would go good together. I’ll keep you posted on that.
 
What I learned this week

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Stress and my “clutter threshold”

“Accept the limitations of the space you have, and declutter enough that your stuff fits comfortably in that space.”
–Dana White, Decluttering At The Speed Of Life
 
I imagine most people have already figured this out by adulthood. And I wouldn’t consider myself slow. But as a kid, I never paid attention to how things stayed clean.
 
I adjust too easily to an imperfect situation: “…grabbing a coffee cup from the top rack of the dishwasher or a pair of socks from the pile on the couch doesn’t feel the least bit awkward, so the visible pile doesn’t register as a problem.”
 
Where did all this stuff come from
 
I figured out laundry in college as I needed clean clothes and bedding, for example. And I learned to keep the floor clean because, like Dana White points out, “if your floors are clean, everyone thinks your house is clean.
 
I pretty much always lived alone and kept my home clean enough for visitors. But when I got married suddenly we had two households of stuff in one house. And I never realized how to be disciplined about decluttering. Everything seemed useful!
 
Now that we both have mobility issues, it’s become obvious that we can’t move freely around this much stuff anymore. The aforementioned Dana White has written extensively about this. Luckily, she speaks to me.
 
Clutter threshold<
 
Dana talks about how we all have our own “clutter threshold,” the point at which all the stuff we own has become overwhelming. That if we live above it, our space is out of control and hard to keep clean, but if we can declutter down below it, our space at least stays manageable.
 
That’s where I’m aiming now. Decluttering is getting rid of things we don’t need. But the point of decluttering is to keep stuff. It isn’t to get rid of things we want to keep; it’s to identify those things and then to make space to enjoy those things.
 
Clutter is one of my triggers 
 
It’s also about the stress I feel living in an out-of-control environment.
 
A 2013 study showed that while both positive (like a wedding or the birth of a new child) and negative (like living over my clutter threshold) stress can impact the course of our MS, the negative stress can actually trigger disease activity.
 
 
So I’m working on changing my mind-set, my ultimate goal for my home. I aim to have less stress by having less stuff.
 
Other stuff
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Troublesome Tysabri

In 2004, a new MS drug was approved by the FDA. As opposed to an interferon, Tysabri (natalizumab) is “a monoclonal antibody”.  For more explanation, try this.
 
It blocks white blood cells from binding to molecules which want to drag them into the brain where they would cause inflammation.
 
As an aside, at this point, all the MS meds aim to reduce inflammation in the brain. This is a primary goal. Symptom management. Because we STILL don’t know what causes the disease. Ergo we still can’t say any of them “works” beyond their ability to reduce inflammation in some brains.
 
In healthy (read ‘non-treated’) people this process is desired. It happens when the body is fighting an infection. Without this process, those on it are more susceptible to infection. The body is without one of its tools.
 
Just a year after it was approved, my neuro switched me. 
 
My First Infusion
 
When I began Tysabri I was cautiously optimistic. It was a big deal: a new drug administered by monthly infusion as opposed to those icky (to me) daily shots. So I went for my first infusion on Thur., 2/24/2005.
 
At this point, I needed to walk with a cane, I was experiencing some rapid loss of energy daily (fatigue) and had a bout of double vision. But the infusion went fine, and I was hopeful I’d see improvement soon.
 
I had just moved in with my boyfriend. So the next morning we watched the news together in horror: scrolling across the bottom of the screen was a notice that Tysabri had been taken off the market because several subjects of its latest study had died!
 
The fallen test subjects had developed a severe brain infection, called Progressive Multifocal Leukoencephalopathy (PML). 
 
PML
 
It is described as “a viral disease characterized by progressive damage (-pathy) or inflammation of the white matter (leuko-) of the brain (-encephalo-) at multiple locations (multifocal).”
 
We now know that PML is caused by the JC virus, something we all already carry, but is usually kept in check by a healthy immune system, something we MSers don’t have. 
 
Other risk factors include duration of therapy and presence of the anti-JC virus antibodies. 
 
If they aren’t already triggered, these antibodies might appear after time on Tysabri, for example. This is what doctors are looking for every six months; it’s a “marker”–not that the individual definitively has PML, but that they are more likely to get it.
 
My Second Infusion
 
Eventually the drug was brought back to market, based on the reasoning that its benefits were greater than the risk. And in 2011, my neuro tried me on it again.
 
And again, the first infusion went fine. I had regressed to using a wheelchair to get around and I was tele-commuting full-time from home. Again I felt cautiously optimistic.
 
The next month I was sitting next to another MSer and she was saying how great she was doing on the drug. I nodded and smiled, hoping for the same.  
 
Suddenly she looked at me oddly and said “You’re starting to break out in hives. I can see it on your face! Aren’t you itchy?”
 
The nurse rushed over and discontinued the infusion right away. As she pumped me full of Benadryl and Solumedrol, she told me that I was now hypersensitive to Tysabri. That ruled it out for me ever again.
 
I admit I was disappointed. 
 
This is on the 2019 Safety Information: “Patients who receive TYSABRI for a short exposure (1 to 2 infusions) followed by an extended period without treatment are at higher risk of developing anti-natalizumab antibodies and/or hypersensitivity reactions on re-exposure”
 
Helpful tip: Know the medicines you take. Keep a list of them to show your healthcare provider and pharmacist whenever you get a new medicine.
 
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Caustic Copaxone

My liver toxicity from Avonex meant that I couldn’t take anything else with interferon, ruling out all other MS drugs at the time, except for one: Copaxone.
 
Copolymer-1, as the chemical was originally called, was discovered by scientists in the 1960s in Israel. Again, I don’t know what they were looking for, but they discovered that it suppressed MS-like disease in mouse models.
 
[As an aside, this is called Experimental Autoimmune Encephalomyelitis (EAE), still accepted today as a murine model for this disease. Interesting because MS doesn’t seem to appear in the animal kingdom, or maybe their lives are just too short to foster development of a slow-progressing disease like this. So scientists needed an animal model to study and use in tests. But we still don’t know what causes human MS, so the thing researchers use to induce it in animals may sometimes cause unintended consequences hard to tease out (i.e., was our result due to the mechanism of the disease itself or a reaction to the variable, which is not found in human subjects?) Something to make you go “hmmm”. ]
 
Drug development continued and it was finally approved for the Relapsing-Remitting form of MS (RRMS) in 1996.
 
How It May Work
 
Now known as glatiramer acetate (brand name Copaxone), it is a synthetic (man-made) protein that mimics a component of the myelin sheath and seems to block damaging cells, though the process is still not understood.
 
Some researchers believe that it acts as faux material to lure and distract the attacking cells away from their real target, but others believe it actually alters the body’s immune function itself.  Concerns about this persist but there is no evidence yet to prove it.
 
Anyway, my neuro switched me to this. I administered myself sub-cutaneous shots of 20mg daily for 7 years, from June 2003 until July 2010.
 
More recently the FDA has approved a newer 40mg dose injected only 3 times a week, and there are some reports that those taking the higher dose less often have fewer side effects. But the lower dose and schedule are still used as well.  
 
Ugh
 
I’m not sure if I would’ve welcomed news of a less frequent dosing option. I hated the shot I took everyday, and I doubt a higher dosage less often would’ve made that much difference. 
 
I rotated injection spots on my body as I was instructed, but no matter where I shot, it felt like I was injecting acid. 
 
For the first few years, I tried to dutifully apply ice packs to the area, both before and after it, as I was told, but it always seemed to make it worse.
 
Finally one day I tried heat instead. Ahhh, the relief!
 
Who’s In Charge Here?
 
Wanting to check that I wasn’t harming things, I called the helpline. But the nurse on the other end told me that she hadn’t received any information ether way. But as far as she understood it, it wasn’t affected by heat.
 
We decided that if a heating pad worked for me, I could continue doing it until I heard otherwise.
 
And as I was looking over new prescribing documents about this drug, I found this: “Before use, allow the solution to warm to room temperature.” Doh! Why didn’t I think of that?
 
Helpful tip: Know the medicines you take. Keep a list of them to show your healthcare provider and pharmacist whenever you get a new medicine.
 
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Anxious Avonex

In December 2000 my doctor and I decided to start me on Avonex.
 
A younger sibling to Betaseron, Avonex was approved by the FDA in May 1996. It is also an interferon – beta 1A versus beta 1b – and it works in a similar way, attempting to tamp down the inflammation in the brain.
 
But again, even today, the way it works in MS is not known.
 
And as far as the availability of a generic, it is a “biologic” drug which means it is made from human or animal materials (complex biotechnological process) rather than through a chemical manufacturing process.
 
Starting Regular Deliveries
 
Most people who take any of the interferons “will have flu-like symptomsearly in the course of therapy (emphasis mine). So the instructions recommended I take it with something like ibuprofen to reduce the expected fever. 
 
These days it comes in other forms, like a prefilled syringe or even an epi-type pen, but back then each dose came as a kit with a vial of powder, a “diluent” (water), a syringe and needle, plus various small packets of rubbing alcohol and bandages.
 
My regular deliveries also included a small sharp’s container for disposal of used syringes and needles.
 
Learning to Inject Myself
 
Avonex would require that I give myself a shot every week.  So naturally I asked my friend and neighbor to join me at the training session so we both could administer it to me.
 
It was kind of eye-opening that sticking a needle into an orange was so similar to giving myself a shot. I was surprised at how easy it slid into the skin. I don’t know why but I expected some resistance! 
 
The nice thing about Avonex is that it is a weekly injection. So I never had to alternate injection spots.
 
But one problem I had at that time was what to do with the full sharp’s containers. There didn’t seem to be a standard procedure for how to dispose of needles, much less a sharp’s container.
 
Now I notice an instruction on the directions: “Check with your healthcare provider about the right way to throw away the container. There may be local or state laws about how to throw away the used syringes and needles. “
 
My First Shot
 
The first time I did my injection I deliberately did not take it with ibuprofen because I wanted to see how severe the fever would get. Lo and behold, it did.
 
Later I was scolded by a doctor friend of mine. She said that since fever is a warning signal to the body, and since I had been warned to take something with the injection for just that, I should’ve just done it to begin with! I always did after that.
 
But I never could learn to inject myself with ease. Every week I sat holding the shot in my hand above my thigh willing myself to just plunge it in.
 
I Develop Jaundice
 
Then one day I couldn’t keep my breakfast down, vomiting. Next I was walking by the mirror and I noticed that my eyeballs were yellow. So I went to an emergency clinic where I was diagnosed with severe liver toxicity. I was told to stop the Avonex immediately.
 
Unfortunately this meant that any interferons were now off-limits to me. That was most everything else on the market for MS at the time. But not everything.
 
Next up, Copaxone.
 
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Before Betaseron

In 1991 I was 26 and working as a waitress in a local pub.
 
I started to get brief moments of what felt like a buzzing in the back of my head that prefaced a loss of all strength; whatever I was carrying I dropped. Eventually it was happening every ten minutes or so and lasted for about 20 seconds.
 
Unbeknownst to me, the neurologist I had been sent to suspected I had MS. In those days an MSer was usually only given a possible diagnosis on the first visit, then probable based on observation of repeated incidents over time. There wasn’t even a test to definitively diagnose it.
 
The MRI
 
But it just so happened that there was this newfangled machine called a magnetic resonance imaging (or MRI) machine that would work like an x-ray but better. It would show him detailed pictures of what was inside my head. And he wanted me to go get a scan from this machine.
 
It was still so new (and expensive) there was only one in the entire SF bay area. When I got there the tech just told me they would do it twice: once as-is and the second time they would inject me with dye and scan again.
 
I laid in the machine and heard all this banging around me and contemplated what they were seeing and waiting for the injection. But after the first round of scans the tech came back and said they were done and I could go home.
 
The quasi-diagnosis
 
I realized later that they didn’t give me the second scan with the dye because they didn’t need to, that they could see the lesions without it.
 
Anyway, the doctor told me I had probable MS. Even with the confirmation of the MRI, which could show multiple brain lesions in a live person as opposed to autopsy after death, the presence of multiple lesions only mostly confirms it.
 
And at the time there was no treatment, nothing they could do. He told me all he could recommend was that I go home and move to the first floor and prepare for a possible wheelchair future.
 
The new era
 
Then in 1993 just two years after I was diagnosed, the FDA approved the first drug for MS, now known as a disease modifying treatment (DMT): Betaseron. It is produced by Bayer Healthcare Pharmaceuticals but even today they still don’t understand exactly how it works.
 
Researchers do know it is a protein produced naturally by the body in response to viral infections. And that one of the things it does to cells in the nervous system is to direct them to produce less pro-inflammatory and more anti-inflammatory agents.
 
They believe that by reducing inflammation in the brain, we will ease the still unexplained attacks by our own immune system on the myelin sheaths that insulate the fibers that connect our neurons.
 
(phew, I can see I need to back up and do a future post on the nervous system!)
 
What I concluded
 
For this story the point I’m trying to make is that the delivery system of this drug (a sub-cutaneous self injection every other day) seemed too extreme for the 26-year-old me since I had no symptoms. Also it was a brand new drug. I didn’t want to be a guinea pig. I thought it was fine to wait. I was wrong.
 
Next time: Anxious Avonex
 
As always, tell your healthcare provider about all the medicines you take, including prescription and nonprescription medicines, vitamins, and herbal supplements.
 
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MS or gout

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?
 
 
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.
 
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How you think matters

I’ve been reading the book Talk is Not Cheap!: Saving the High Costs of Misunderstandings at Work and Home. The author explains, “Thoughts are not idle.  Make yours work for, not against, you.”
 
What has intrigued me is the discussion of the two halves of the brain and how we can use them. 
 
The Logical Side
 
She explains that when it is awake and alert, the left part of my brain tries to protect me by reminding me of messages I got while growing up and outcomes of previous experiences, for example.  
 
But when the logical part of my brain shuts down at night, the right side, the creative part, is always on. And, as it turns out, is very gullible. 
 
So when the right brain is unrestrained by the left, I can dream.  But also I can trick it!  
 
The Creative Side
 
Since the left-brain is slow to re-engage after turning off–say right before you fall asleep and as you wake up–you can consider this prime time to influence your thinking.
 
It also turns out that the right part of our brains can’t tell the difference between actually performing an action and just imaging it.
 
Put Into Practice
 
Using this information, for example, as part of their training athletes will enter a relaxed state (which turns off the left half) and just imagine that they are playing their sport.
 
And when one of my MS callers admitted that she often wakes up in a panic, I suggested she try repeating affirmations or practice visualizations right before bed and again when she first wakes up.
 
In fact I now consider the 30-minutes before I go to sleep and the 30-minutes after I wake up, to be fragile, sacred, potent!
 
Editor’s note: Originally posted on 08.25.10. Updated re-post. 
 
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