Lightbulb. Skin is an organ

 
I have never really taken care of my skin. I never got acne, just the occasional pimple. I washed my face at least once a day with Phisoderm or Cetaphil, gentle cleansers.
 
I didn’t moisturize regularly, and applied sunscreen only when I planned to spend the day out doing some activity, like skiing or going to the beach. 
 
But this article made me think about my skin as an organ. According to researchers, it is our largest organ, roughly 8 pounds (3.6 kilograms) and 22 square feet (2 square meters).
 
Could it be affecting or partially responsible for my MS? How could it not?
 
Medline
 
I poked around in the National Library of Medicine’s  PubMed* search: [(skin[Text Word]) AND multiple sclerosis[MeSH Terms]], but didn’t see anything relevant. Mind you, I’m not a scientist or expert in medicine. Caveat Emptor! 
 
*PubMed comprises more than 29 million citations for biomedical literature from MEDLINE, life science journals, and online books.
 
 
I did see at lot of discussion about MS and sympathetic skin response (SSR) as diagnostic test. The SSR test measures whether the sympathetic nerves of the skin are working.
 
Apparently in a lot of MSers, the response is absent in one or both limbs, for example. In healthy subjects the response is always there. This is interesting, but not something I think I could fix!
 
Google search
 
Next I tried an internet search. Again I found nothing MS specific, although there are some warnings on various drugs about possible skin cancer. Meaning that some subjects began showing skin cancer during or after the trial.
 
There is no way to tell if the skin cancer was already “on board” before the trial started. Or if the drug made them more sensitive to the sun.
 
 
So there is some involvement there!
 
Ergo
 
Yet again I find interesting (to me) information, but nothing conclusive. Just a vague hypothesis: I think I should be taking care of my skin better.  But who knows what that means?
 
For now, I will just accept prevailing theory until proven otherwise. So I resolve to craft a regular, daily, non-negotiable skin care routine, something like this:
  1. Wash my face once a day, every night. Don’t over wash and risk drying out the skin, causing it to produce more oil.
  2. Shower, wash hair at least once a week. Gross I know, I used to shower daily but it’s hard now. Plus I read this and this
  3. Wash my feet every night before bed, slather with lotion
  4. Slather body lotion daily – moisturize, moisturize, moisturize
  5. Use sunscreen daily or at least before venturing outside anywhere
  6. Ask your GP to include a regular skin cancer check in your annual, or see a dermatologist. Some doctors recommend every year!
  7. Drink lots of water
All this is based on my gut feeling about the right thing to do for me. Your results may vary! 🙂
 
Other stuff
Tagged : / / / / /

Genial Gilenya

I am now taking the oral medication Gilenya (fingolimod). It was first synthesized in Japan in 1992 by chemical manipulation of a naturally occurring antibiotic, and finally approved by the FDA in 2010 as “the world’s first oral MS drug“. 
 
I call it genial because compared to giving myself daily shots, it is just a daily pill I swallow. But “genial” by no means suggests benign. This drug is as toxic as everything else I have tried. Incidences of PML occurring in people taking Gilenya do happen.
 
This Method
 
Everyone’s immune system contains lymph nodes, which are tiny glands containing immune cells (AKA white blood cells) called lymphocytes. Lymphocytes are usually helpful, but in MS they get confused and attack the central nervous system (CNS), and permanently damage the myelin sheath.
 
Gilenya activates sensors on your lymph nodes to restrain some white blood cells. That way, these blood cells aren’t released into the bloodstream, where they can attack. (Other lymphocytes are still circulating and available to do their job, watching out for intruders like viruses and bacteria.)
 
It also activates sensors on your heart, which can cause your heart rate to temporarily slow down. So it is recommended that all users be monitored by a medical professional for at least six hours after the first dose.
 
My Experience
 
I have been taking Gilenya since April 2012. This is from an earlier blog post:
 
…I packed my backpack with items to stave off the boredom of sitting around that long: two books I am currently reading [one fiction and one non-fiction], a book of Sudoku puzzles [I’m addicted!], lip balm…
 
We also brought a cooler with yogurt, granola bars, and sandwiches.  [My husband] brought a fingertip pulse oximeter so I could check my pulse regularly on my own.
 
In the end, the whole experience was pretty anti-climactic, which is probably the best-case scenario, really.  I read one book the entire time, and they let us leave before the rush hour started.
 
It was a record heat in SF, which lent the whole outing a surreal feel, and now that I’m onto Day Five, it is like it never happened…
 
It’s now been 6 years and I have tolerated it fine, but it has not made any amazing difference, as I had secretly wished. 
 
Things I’ve Learned
 
Gilenya might increase your risk of skin cancer. It can render a “live” vaccine inert while using it. And it can interact with a multitude of drugs, including vitamins, and herbal products.
 
It is rare but macular edema (a correctable eye condition causing swelling and blurry vision) may occur within the first 3-4 months of starting. It may be confused with an MS exacerbation, so check with your doctor, and consider annual ophthalmology appointments.
 
Finally, I have started to see reports about a “rebound relapse” phenomenon when users go off it. Obviously, once you go off, you should expect that the “door” of all lymph nodes is no longer being guarded so you most likely will resume MS where you left off.
 
But in about 25% of patients, there is an even more aggressive worsening of MS after stopping and these patients “do not return to the level of function that they had before or during treatment“. This worsening most often happens within 12 weeks of stopping. It is definitely something to consider before you start if you think you will want to go off it to get pregnant, for example.
 
Other stuff

Tagged : / / / / / / /

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.
 
Other stuff

Tagged : / / / / / /

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.
 
Other stuff

Tagged : / / / / / / /

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.
 
Other stuff

Tagged : / / / / /

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.
 
Other stuff
Tagged : / / / / /

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.
 
Other stuff
Tagged : / / / /

How to thank a caregiver

Family caregivers give a lot and don’t always get much in return. As much as they love the people they care for, the work involved in family caregiving can be exhausting. 
 
It is estimated that over 40 million people in the United States are unpaid caregivers to an adult family member or friend. That’s like 21% of the population! 
 
According to the National Alliance For Caregiving, “care delivered by informal and family caregivers add up to $257 billion each year.”
 
Since the count of MSers is now recognized as close to 1M, it would be interesting to see what the numbers are for those caring for someone with MS or another chronic illness.
 
And although the majority of family caregivers are women, more and more men are becoming caregivers too.
 
Imagine How They Feel
 
If you live in the same house as your caregiver, be aware that they may often feel invisible. Everyone’s attention can seem to always go to the MSer, causing them to feel that no one cares about them. Many say, “no one even asks.”
 
Also research shows that the “emotional stress of caring has little to do with the physical condition of the person with MS or the length of time the person has been ill. Emotional stress seems more related to how “trapped” caregivers feel in their situation.”
 
Just know that caregivers give a lot and don’t always get much in return. As much as they love the people they care for, the work involved in family caregiving can be exhausting. 
 
“The most successful carepartners welcome and appreciate the practical and emotional support of other people,” says the NMSS. Also, they “don’t give up the activities or hobbies they enjoy.”
 
What can I give
 
How can you show appreciation to your caregiver? Simply asking them is a great place to start.
 
Other ideas
  • Express your gratitude out loud and often. Brag to others about your caretaker.
  • Write out a note or card. Taking time to hand-write why you appreciate your caregiver can be very meaningful plus it gives them something with kind words they can reread in the future.
  • Suggest a coffee-break or cup of tea. In fact, encourage your caregiver to take breaks. Make sure they are taking time to fill their own tanks so they have the energy to take care of you.
  • Celebrate National Caregiver’s Month (November in the U.S.). It’s an opportunity to draw attention to the needs of all caregivers.
  • Show interest in the things that your caregiver is interested in. It shouldn’t only be about you.
  • Share jokes with each other. There is power in a good laugh. Try to do it at least once a day.
  • Find support services or even classes that might be right for them, or figure out a service they can use to outsource one of their regular chores.
  • Offer to help them with a task you know you can take on. Or, when visitors come, make the most of your time: be prepared with a short list of to-do items you need help with.
  • Try to temper your emotions, maybe make a conscious effort to be cheerful.  Facing perpetual crankiness can be draining.  Remember that your caregiver is not your therapist.
  • For paid help, you can give a bonus, a day off, or a quick call to their supervisor to report what a good job they do.
Look for ways to make your caregiver’s life easier. Even small gestures can make a big difference to someone worn out.
 
Other stuff

Tagged : / / / / /

1M U.S. MSers

I had never heard of it when I first got told of my probable-diagnosis, but once I was told it was probably MS and I mentioned it to other people, almost everybody replied that someone else they knew also had it.
 
So I wondered how many others in the country were also dealing with this disease? How big was my tribe?
 
I called the National MS Society (at that time the WWW was still in its infancy) and got the same answer that they had been giving for years: that there were approx. 400,000 people in the US living with it.
 
I knew that wasn’t correct since everybody seemed to know at least someone afflicted with this disease.
 
I demanded to know what benefit the Society had in keeping the number reported so low? Did it mean the disease was considered an ‘orphan disease,’ eligible for money and tax breaks? No answer.
 
Why it matters
 
Turns out, according to the MS Society today, this 400,000 number was just an estimation based on population growth. In fact, “(i)n the United States, there has not been a scientifically sound, national study of prevalence since 1975.
 
Since the U.S. government never required MS incidence (number of people NEWLY diagnosed) or MS prevalence (number of people currently living with it) be reported or followed, the MS Society and others just estimate.  
 
To be fair, I do recognize the difficulty counting incidence of a disease in which there is no definitive criteria for diagnosis.
 
But it is said that “Society expects epidemiology to accurately document our health.” Difficult or not.
 
Studying MS leads to understanding its impact on people’s lives, their finances, and the healthcare and services people with MS need. Keeping an accurate count of us should underscore the extent of economic burden to our society.
 
It could also help scientists know if MS is spreading, and if there are MS clusters that hint at factors that may trigger MS.
 
New numbers
 
Since the government has shown little interest, the Society finally decided to do it for themselves and launched the MS Prevalence Initiative to determine a better way to determine a “scientifically sound and economically feasible” estimate of the number of MSers in the U.S.
 
They went on to explain that they are now using new and improved measurements because it had been so hard to count before. 
 
And I was both pleased and dismayed when I saw a new notice that a recent study more accurately showed that close to 1 million people in the country have this disease, more than twice the number they had been using.
 
They also noted that “the dramatic jump seen in prevalence has more to do with methodology than an actual rise in the number of MS cases” though they don’t discount that possibility. Sigh.
 
Related stuff
Tagged : / / / / / /

Lorna’s briefest history of the ADA

Curb Cut At Night (Luke Keller ©2019)
Curb Cut At Night (Luke Keller ©2019)
As an MSer, I feel like I’m kinda late to the party with regards to understanding how important the ADA is. I was diagnosed in 1991 but didn’t really experience physical disability until later in my life.
 
Why I care
 
The NMSS says “The ADA covers almost everyone with MS — not only people who use wheelchairs. It covers every person with an impairment that substantially limits one or more major life activities.”
 
How lucky am I to be living in this era? I take my electric wheelchair for coffee, I do all my banking online, I am able to work from home as a reasonable accommodation, and I write my blog with voice-to-text dictation.
 
mini-lift
Mini-Lift (Luke Keller ©2019)
In fact, in his book, Enabling Acts (see full site below), Lennard Davis says “Today we routinely see kneeling buses and buses with wheelchair lifts as a part of the urban landscape. It is an aspect of the success of the ADA that many of its accomplishments are now invisible to us since they are so much a part of our lives.” (Emphasis mine)
 
How it came about
 
For example, one city might mandate a reserved parking space close to the entrance of stores. But it wasn’t a federally mandated law, no comprehensive legislation. It was a catch-as-catch-can basically wherever needed.
Pool Lift (Luke Keller ©2019)
Pool Lift (Luke Keller ©2019)
 
Before the ADA, lawmakers were passing little laws here and there to correct disparate problems that suddenly (to them) popped up.
 
Then in the 1960s, civil rights for disenfranchised groups seemed to culminate in the Civil  Rights Act of 1964. And while in the immediate aftermath, the feeling among lawmakers was that trying for disability civil rights then was way over-reaching, the seed was planted.
 
Then in the 1960s, civil rights for disenfranchised groups seemed to culminate in the Civil  Rights Act of 1964. And while in the immediate aftermath, the feeling among lawmakers was that trying for disability civil rights then was way over-reaching, the seed was planted.
 
According to Davis, the initial idea behind the ADA was sparked by language slipped into what would become the Rehabilitation Act of 1972 for soldiers who were wounded in Vietnam. It said “No otherwise qualified handicapped individual in the United States, as defined in Section 7(6), shall, solely by reason of his handicap, be excluded from the participation in, be denied the benefits of, or be subjected to discrimination under any program or activity receiving federal financial assistance.” After many pushes, it was (reluctantly) signed by Nixon in 1973.
Bus driver lowering ramp (Luke Keller ©2019)
Bus driver lowering ramp (Luke Keller ©2019)
 
Next, after 20 years, and presumably once we had become used to the idea (sigh), the non-partisan National Council on Disability drafted the first version of the Americans with Disabilities Act. There was more political back and forth, but finally it was signed into law by Pres. George H.W. Bush in 1990. Then further amended and signed by Pres. (Bill) Clinton in 2009. Phew!
 
We made this
 
Some people are convinced that programs as monumental as the ADA will never again pass in our divided and hostile government. I hope that is not the case. As a collective, we Americans have shown the we can come up with all manner of clever solutions. 
 
Reading about the ADA made me realize how impactful it can be when the two parties of Congress work together to produce something for our common good. And it’s not perfect, but it makes space to let the creativity of society continue to reinvent how things could be made easier and more useful. 
 
Related stuff

Tagged : / / / / / /