Published by
Stanford Medicine

Category

Autoimmune Disease

Autoimmune Disease, Chronic Disease, Health and Fitness, Research, Technology

Video game accessory may help multiple sclerosis patients reduce falls, boost brain connections

Wii_balance_boardNintendo’s Wii Balance Board has helped get people off the couch and moving as they play aerobic video games like Super Hula Hoop or Dance Dance Revolution. Now a study published this week in Radiology shows that the video game console’s balance board may help reduce multiple sclerosis (MS) patients’ risk of falls by rewiring their brains.

In a small study, researchers used an MRI technique called diffusion tensor imaging to analyze changes in the brain of MS patients that used the Wii Balance Board while playing video games for 30-40 minutes a day five days a week.

According to a recent Forbes post:

MRI scans in the MS patients in the study demonstrated significant growth of nerve tracts which are integral in movement as well as balance. It turns out that the changes seen on MRI correlated with improvements in balance as measured by an assessment technique called posturography.

These brain changes in MS patients are likely a manifestation of neural plasticity, or the ability of the brain to adapt and form new connections throughout life, said lead author Luca Prosperini, M.D., Ph.D., from Sapienza University in Rome, Italy.

”The most important finding in this study is that a task-oriented and repetitive training aimed at managing a specific symptom is highly effective and induces brain plasticity.”

“More specifically, the improvements promoted by the Wii balance board can reduce the risk of accidental falls in patients with MS, thereby reducing the risk of fall-related comorbidities like trauma and fractures,”

 added Prosperini.

Researchers cautioned that the improvements in balance did not persist after patients stopped playing the video games, suggesting that patients will need to continue their training in order benefit from the intervention.

Previously: Study analyzes video game-related injuries and Comparing the Wii Fit board to a clinical force platform
Photo by Joachim S. Müller

Aging, Autoimmune Disease, Immunology, Infectious Disease, Research, Stanford News

Our aging immune systems are still in business, but increasingly thrown out of balance

Our aging immune systems are still in business, but increasingly thrown out of balance

business as usual

Stanford immunologist Jorg Goronzy, MD, told me a few years ago that a person’s immune response declines slowly but surely starting at around age 40. “While 90 percent of young adults respond to most vaccines, after age 60 that response rate is down to around 40-45 percent,” he said. “With some vaccines, it’s as low as 20 percent.”

A shaky vaccine response isn’t the only immune-system slip-up. With advancing age, we grow increasingly vulnerable to infection (whether or not we’ve been vaccinated), autoimmune disease (an immune attack on our own tissues) and cancer (when a once well-behaved cell metamorphoses into a ceaselessly dividing one).

A new study led by Goronzy and published in Proceedings of the National Academy of Sciences, suggests why that may come about. The culprit he and his colleagues have fingered turns out not to be the most likely suspect: the thymus.

This all-important organ’s job is to nurture an army of specialized  immune cells called T cells. (The “T” is for “Thymus.”) T cells are capable of recognizing and mounting an immune response to an unbelievably large number of different molecular shapes, including ones found only on invading pathogens or on our own cells when they morph into incipient tumor cells.

Exactly which feature a given T cell recognizes depends on the structure of a receptor molecule carried in abundance on that T cell’s surface.  Although each T cell sports just one receptor type, in the aggregate the number of different shapes T-cells recognize is gigantic, due to a high rate of reshuffling and mutation in the genes dictating their receptors’ makeup. (Stanford immunologist Mark Davis, PhD, perhaps more than any other single individual,  figured out in the early 1980s how this all works.)

T cells don’t live forever, and their generation from scratch completely depends on the thymus. Yet by our early teens the organ,  situated  in front of the lungs at the midpoint of our chest, starts shriveling up and replaced by (sigh – you knew this was coming)  fat tissue.

After the thymus melts away,  new T-cells come into being only when already-existing ones undergo cell division, for example to compensate for the attrition of their neighbors in one or another immune-system dormitory (such as bone marrow, spleen or a lymph node).

It’s been thought that the immune-system’s capacity to recognize and mount a response to pathogens (or incipient tumors) fades away because with age-related T-cell loss comes a corresponding erosion of diversity:  We just run out of T-cells with the appropriate receptors.

The new study found otherwise.  “Our study shows that the diversity of the human T-cell receptor repertoire is much higher than previously assumed, somewhere in the range of one billion different receptor types,” Goronzy says. “Any age-associated loss in diversity is trivial.” But the study also showed an increasing imbalance, with some subgroups of T cells (characterized by genetically identical  receptors)  hogging the show and other subgroups becoming vanishingly scarce.

The good news is that the players in an immune response are all still there, even in old age. How to restore that lost balance is the question.

Previously: How to amp up an aging immune response, Age-related drop in immune responsiveness may be reversible and Deja vu: Adults’ immune systems “remember” microscopic monsters they’ve never seen before
Photo by Lars Plougmann

Autoimmune Disease, Evolution, Immunology, Microbiology, Nutrition, Public Health, Stanford News

Civilization and its dietary (dis)contents: Do modern diets starve our gut-microbial community?

Civilization and its dietary (dis)contents: Do modern diets starve our gut-microbial community?

hunter-gatherer cafe

Our genes have evolved a bit over the last 50,000 years of human evolution, but our diets have evolved a lot. That’s because civilization has transitioned from a hunter-gatherer lifestyle to an agrarian and, more recently and incompletely, to an industrialized one. These days, many of us are living in an information-intensive, symbol-analyzing, button-pushing, fast-food-munching society. This transformation has been accompanied by consequential twists and turns regarding what we eat, and how and when we eat it.

Toss in antibiotics, sedentary lifestyles, and massive improvements in public sanitation and personal hygiene, and now you’re talking about serious shake-ups in how many and which microbes we get exposed to – and how many of which ones wind up inhabiting our gut.

In a review published in Cell Metabolism, Stanford married-microbiologist couple Justin Sonnenburg, PhD, and Erica Sonnenburg, PhD, warn that modern civilization and its dietary contents may be putting our microbial gut communities, and our health, at risk.

[S]tudies in recent years have implicated [dysfunctional gut-bug communities] in a growing list of Western diseases, such as metabolic syndrome, inflammatory bowel disease, and cancer. … The major dietary shifts occurring between the hunter-gatherer lifestyle, early Neolithic farming, and more recently during the Industrial Revolution are reflected in changes in microbial membership within dental tartar of European skeletons throughout these periods. … Traditional societies typically have much lower rates of Western diseases.

Every healthy human harbors an interactive internal ecosystem consisting of something like 1,000 species of intestinal microbes.  As individuals, these resident Lilliputians may be tiny, but what they lack in size they make up in number. Down in the lower part of your large intestine dwell tens of trillions of  single-celled creatures – a good 10 of them for every one of yours. If you could put them all on a scale, they would cumulatively weigh about four pounds. (Your brain weighs three.)

Together they do great things. In a Stanford Medicine article I wrote a few years back, “Caution: Do Not Debug,” I wrote:

The communities of micro-organisms lining or swimming around in our body cavities … work hard for their living. They synthesize biomolecules that manipulate us in ways that are helpful to both them and us. They produce vitamins, repel pathogens, trigger key aspects of our physiological development, educate our immune system, help us digest our food and for the most part get along so well with us and with one other that we forget they’re there.

But when our internal microbes don’t get enough of the right complex carbohydrates (ones we can’t digest and so pass along to our neighbors downstairs), they may be forced to subsist on the fleece of long carbohydrate chains (some call it “mucus”)  lining and guarding the intestinal wall. Weakening that barrier could encourage inflammation.

The Sonnenburgs note that certain types of fatty substances are overwhelmingly the product of carbohydrate fermentation by gut microbes. These substances have been shown to exert numerous anti-inflammatory effects in the body, possibly protecting against asthma and eczema: two allergic conditions whose incidence has soared in developed countries and seems oddly correlated with the degree to which the environment a child grows up in is spotlessly hygienic.

Previously: Joyride: Brief post-antibiotic sugar spike gives pathogens a lift, The future of probiotics and Researchers manipulate microbes in the gut
Photo by geraldbrazell

Autoimmune Disease, Chronic Disease

Empowered is as empowered does: Making a choice about living with lupus

We’ve partnered with Inspire, a company that builds and manages online support communities for patients and caregivers, to launch a patient-focused series here on Scope. Once a month, patients affected by serious and often rare diseases share their unique stories; this month’s bonus column comes from Pattie Brynn Hultquist, C.H

“How do you do it?”

I get it. A mother of five, a wife, a childcare provider, president of the condo board. Chartered herbalist, scrapbook design team member, wool and fiber spinner, avid camper. Yoga enthusiast, a weight-training type-2 diabetic – the list continues.

How, exactly, does one manage living with an autoimmune disease like lupus: the disease of a thousand faces, the epitome of “You don’t look sick”?

When I first received my diagnosis of systemic lupus erythematosus I was devastated not only for myself but for my family, friends and extended personal communities. It wasn’t just me receiving a diagnosis on that brilliantly colored fall day in 2010; it was my entire social network.

Lupus can affect people very differently. Some people have skin issues. Some have joint pains. Some, like myself, also have had a heart attack, pericarditis and kidney issues that makes taking medications a game of pharmaceutical roulette: sometimes, medications makes me feel worse.

That isn’t living. That’s existing.

I joined forum after forum, community after community, group after group, all over the Internet. I had to know how to live with an autoimmune disease. What I found were either the “Whine-1-1” or the “Positive 24/7!” I left them all.

I felt a little like Neo when offered a choice between the red pill and the blue pill.

My choice?

Taking neither and forging my own way through this made-for-TV-movie kind of life living with a chronic disease.

I started a blog. I started sharing how I, a mother of five in the chaos of my reality, was living with lupus. I wrote about the good, the bad, the ugly, and the deliriously exhausted life I live. It struck a chord with many who know chronic illness for its complexity. There were so many people experiencing the very same thing!

I went from blogger to globally recognized health advocate. And one day I told my primary care physician about my writing. I told her about how many people are suffering in silence because they feel “invisible” not just with their health-care teams, but with friends and even family. I even told her about how I felt that way, myself. She told me, in all honesty, that she had never really considered the magnitude of social effects that someone’s diagnosis can engender.

I was stunned. Sure, she had mentioned my husband and children at our appointments, yet she conceded that she had simply not considered event invitations no longer extended (I simply can’t commit to one way or another because lupus can flare up at any given time with pain, exhaustion or sickness), or, of having often to redefine my abilities and seek out new friendships in order to keep proactively engaged in life.

That was the day I illustrated the research, networking and usage benefits of social media as my outlet, and she became empowered to begin treating the socio-emotional impact of health care: how interpersonal communities and social media can be a powerful tool in the health-care toolbox for individual patients.

The result? I was validated by the health-care professional who is most intimately aware of the clinical and physical demands of this disease on my body and how it affects my entire social network. Validation heightens my confidence to be a proactive patient. Proactive behavior advances whole-body health care and awareness.

Choice is a beautiful thing.

Pattie Brynn Hultquist, C.H., is a globally recognized lupus and chronic illness health advocate at her weblog, Lupus Interrupted. A team captain for the Walk for Lupus, held annually, she participates in fundraising efforts at Gold Award levels for Lupus Ontario. She can be found on multiple social media platforms sharing information, resources and the realities of living with chronic conditions, her supportive family always within reach.

Autoimmune Disease, Chronic Disease, Clinical Trials, Patient Care

Two decades with scleroderma: How I find answers to hard-to-solve questions

The day I was diagnosed with scleroderma 21 years ago was devastating for my parents and me, to say the least. I was 15 years old and I remember thinking: I have what? Scleroderma? What is that? Can you spell that?

Not much was known about the disease and, since the Internet was in its infancy, we couldn’t simply Google “scleroderma” to learn more about it or find support groups. There was no one to bounce off ideas with. My father, who was a diligent researcher, consulted medical textbooks. Meanwhile, my mother, who was born with the “gift of gab,” sought information from anyone and everyone who crossed her path. But ultimately we were forced to rely heavily on doctors’ recommendations, which sadly were pretty gloomy and a bit much for a teenager to handle.

Fast forward to today. When I have a question, I connect with my local chapter of the Scleroderma Foundation, either by e-mailing a board member or by attending a support group meeting. I also go online to the Raynauds Association, Scleroderma Foundation and Pulmonary Hypertension Association. Above all it’s important to find a rheumatologist who is not only knowledgeable about scleroderma, but has a good grasp of its complexities and is willing to help you get the results you need. Trust me – they are out there!

Back in 2004, I decided it was time to get a new rheumatologist. I asked around for recommendations from my personal network and a friend with rheumatoid arthritis suggested I see her physician. Before meeting the doctor, I looked at his online reviews from other patients and his curriculum vitae to get a sense of his academic and professional experience and achievements. When meeting with a new physician, it’s important to ask if she/he has treated other scleroderma patients, gauge their knowledge of clinical trials, find out if they are up to date on the medications being used to treat the different facets of the disease, and make sure they understand the importance of certain annual tests.

When I switched rheumatologists, I had a particular problem I needed to solve. For the most part my illness had become stable, but I had one pesky ulcer that was truly relentless! I tried various calcium channel blockers, ACE Inhibitors, and Vasodilators, and nothing worked. The infections were getting out of control, even though I did my best to stay on top of it. My frustration reached a point where I asked my doctor to “please, remove the first flange of my index finger.” Thankfully he refused and said, “No, we’re not going to give up.”

Continue Reading »

Autoimmune Disease, Chronic Disease, Patient Care, Pediatrics

A wake-up call from a young e-patient: “I need to be heard”

We’ve partnered with Inspire, a company that builds and manages online support communities for patients and caregivers, to launch a patient-focused series here on Scope. Once a month, patients affected by serious and often chronic diseases share their unique stories. Our latest comes from 15-year-old Morgan Gleason, who lives with the autoimmune disease juvenile dermatomyositis. 

Before June 18, 2010, the day I was diagnosed, I knew the medical system the way that most kids do. I went to the doctor for immunizations, physicals, sore throats and bones that might be broken. Then, I developed a rash on my joints. I started sleeping more than normal, was very weak in my muscles, and experienced frequent stomachaches and headaches.

At the age of 11, after a year of these symptoms, I was diagnosed with a rare autoimmune disease called juvenile dermatomyositis. I suddenly was in a whole new medical system. I had to learn to swallow pills, wait for hours in doctors offices, spend nights in the hospital, worry about what was happening, deal with some not-so-nice doctors and nurses, and endure a lot of pain. I also watched my parents get frustrated with figuring out medical bills and trying to understand all of the claim statements and appeal denials.

Now I take 21 pills a day, get two infusions a month by an IV, and give myself an injection once a week. I have more specialists than my grandparents, and I spend a lot of time as a patient.

This January, I was hospitalized for the second time in four months for meningitis due to a reaction from a treatment I received. After four days of little sleep and an excruciating headache, I made a video about my hospital experience and posted it online. To my surprise, the video got a lot of attention. Forbes, Time, the Huffington Post and other outlets wrote about it. I believe that the video was popular because my experience was a common one and struck a nerve with others.

I am appreciative of the care I have been given. I love the hospital where I get my treatment, and I think it’s a great hospital. The medical students, residents, attending physicians, and specialists are great doctors. The nurses are also really great. This is not an issue with the individual people or hospitals. The issue is much bigger, and it’s the way the system as a whole is designed.

My video had a few main points. I was frustrated that I couldn’t get any rest in the hospital. The system is designed around the schedules of the doctors and the desire to discharge patients by noon instead of around the circumstances and needs of the patient. Second, the doctors come in individually instead of coming together and addressing all the concerns at one time. Third, when patients are awoken from deep sleep, they’re not going to be as engaged as they would be when they are alert and comfortable. Finally, patients, and even children and teenagers, appreciate having the doctor talk with them instead of having the doctors talk over them or away from them in the hallway.

Continue Reading »

Ask Stanford Med, Autoimmune Disease, Chronic Disease

Join Ask Stanford Med for a live discussion about scleroderma on Wednesday

Join Ask Stanford Med for a live discussion about scleroderma on Wednesday

hands_laptop_033114Although scleroderma is derived from the Greek words meaning “hardness” and “skin,” its symptoms affect far more than patients’ epidermis. The complex, rare disease can cause damage to the vascular system, lungs, kidneys and gastrointestinal tract with potentially life-threatening consequences.

On Wednesday at 4:30 PM Pacific time, we’ll be hosting an Ask Stanford Med Google+ Hangout about scleroderma research and progress being made to enhance patients’ quality of life. The live video discussion was organized in partnership with the Scleroderma Foundation and Inspire, a company that builds and manages online support communities for patients and caregivers.

Our panel of special guests includes Lorinda Chung, MD, director of the Scleroderma Center and co-director of the Multidisciplinary Rheumatologic Dermatology Clinic at Stanford; Karen Gottesman, patient services director for the Scleroderma Foundation of Southern California; and Melissa Warde, who was diagnosed with scleroderma at age 15 and has lived with the disease for more than two decades.

Panelist will address a range of topics, including:

  • Recent modifications to the disease criteria used in diagnosing scleroderma
  • The importance of patients being screened for pulmonary hypertension
  • The use of rating skin-thickness progression to help determine prognosis
  • A patient’s perspective on participating in a clinical trial
  • Efforts to develop online tools that enhance quality of life
  • Tips on how patients can live life to the fullest despite this debilitating disease

To participate in the discussion, watch the broadcast on the Stanford Medicine YouTube channel. A link to the hangout will also be tweeted on the @SUMedicine feed and posted on the School of Medicine’s Facebook page once the broadcast begins. Only panelists will be featured on screen, so audience members don’t need to be camera ready to join the conversation.

The public is welcome to submit questions for panelists in advance of the discussion by posting them in the comments section below before 3 PM Pacific time tomorrow (Tuesday). Questions can also be submitted during the live video discussion via Twitter using the hashtag #AskSUMed.

Previously: Save the date: Ask Stanford Med Google+ Hangout on Scleroderma April 2Another piece of the pulmonary-hypertension puzzle gets plugged into place, Patients with rare diseases share their extraordinary stories and Restoring hand function with surgery 
Photo by Judit Klein

Ask Stanford Med, Autoimmune Disease, Chronic Disease

Save the date: Ask Stanford Med Google+ Hangout on Scleroderma April 2

Save the date: Ask Stanford Med Google+ Hangout on Scleroderma April 2

Updated 03-25-14: Readers are welcome to submit questions for our panelists in the comments section below. We’ll collect questions until 3 PM Pacific time on April 2. A selection of the questions will be answered during the live video conversation, which will be broadcast on the Stanford Medicine YouTube channel starting at 4:30 PM Pacific time. A future blog entry will provide details on how to watch the Google+ Hangout.

***

3-17-14: An estimated 300,000 Americans are living with scleroderma, a chronic connective tissue disease that is generally classified as one of the autoimmune rheumatic diseases. While hardening of the skin is the most visible manifestation of scleroderma, symptoms of the disease vary greatly among patients and the effects range from mild to life-threatening. Researchers are still working to determine the cause of scleroderma, and currently there is no cure for the disorder.

To foster conversation about this complex, rare disease, we’re partnering with the Scleroderma Foundation and Inspire, a company that builds and manages online support communities for patients and caregivers, for a Google+ Hangout about scleroderma research and progress being made to enhance patients’ quality of life. Among the panel of special guests are:

  • Lorinda Chung, MD, director of the Scleroderma Center and co-director of the Multidisciplinary Rheumatologic Dermatology Clinic at Stanford. Chung is actively involved in clinical, translational, and epidemiologic research on systemic sclerosis and related connective tissue disease, and she’s the principal investigator on a number of clinical trials of new potential therapies for scleroderma patients.
  • Karen Gottesman, patient services director for the Scleroderma Foundation of Southern California. Both a patient and a long-standing patient advocate, she is author of The First Year – Scleroderma, An Essential Guide for the Newly Diagnosed. Gottesman is also a member of the Scleroderma Patient-centred Intervention Network (SPIN), an international consortium of scientific researchers and clinicians organized to develop, test and disseminate psychosocial interventions to improve the quality of life for scleroderma patients worldwide.

Audience members are welcome to submit questions during the live video discussion via Twitter using the hashtag #AskSUMed. Please save the date and join us on April 2 at 4:30 PM Pacific Time.

Previously: Another piece of the pulmonary-hypertension puzzle gets plugged into place, Rules for living with a chronic illness, Patients with rare diseases share their extraordinary stories and Restoring hand function with surgery

Ask Stanford Med, Autoimmune Disease

A closer look at the autoimmune disease vasculitis

When various forms of news media last week reported the cause of death of Harold Ramis, the writer/director/actor, as complications from the “rare autoimmune disorder vasculitis,” I can promise you there were many people who read that and said, “Huh?” for very personal reasons. These are people who, like me, knew that these reports weren’t quite right. Vasculitis is actually a family of at least 15 forms of this disease group and one not so rare when all those who have some form (perhaps as many as 3 million) are added together.

Research and clinical trials on vasculitis have been carried on in a handful of centers around the world. One long-time investigator in this area, also a teacher and clinician, is here at Stanford: Cornelia Weyand, MD, PhD, division chief of immunology and rheumatology. Wayand’s e-mail box was flooded last week, so we asked her to answer some basic questions here about the vasculitis family.

I understand the vasculitides are a family of diseases. Is there something all forms have in common?

A diagnosis of vasculitis means that there is inflammatory disease in the blood vessels.

All organ systems in the body have blood vessels. Therefore, all organ systems can be affected by vasculitis. Blood vessels provide oxygen and nutrients to the tissues. Inflamed blood vessels have a tendency to become blocked. In that case, the tissues do not get blood supply anymore, causing serious complications. In some cases, the inflamed blood vessel bursts, causing life-threatening bleeding. This complication is particularly serious if the body’s largest blood vessel, the aorta, is affected. A leak in the aorta is incompatible with life.

What insights into vasculitis have we gotten from research?

My research team has been involved in vasculitis research for the last decade. We have been trying to find answers to the questions most patients ask at one point in the course of their disease:

A. Why did I get this disease?

Vasculitis results from a faulty immune response. Cells of the immune system attack the blood vessel and cause tissue injury. The blood vessel responds to the attack by either closing up or by rupturing. We have been able to identify the immune cells that initiate and sustain vasculitis. Remarkably, cells that induce disease are identical to cells that protect the body. We have also learned that blood vessels have specialized sensor cells in them that keep a dialogue with the immune system and start the inflammation.

B. How can my disease be treated or prevented?

We cannot prevent vasculitis, but since the disease takes a course of flares and remission, we may be able to prevent the next disease flare.

Vasculitis is treated by suppressing the immune system. One of the most effective drugs is cortisone. Some patients need it in large doses and we are very cognizant of side effects.

We have devoted our research effort to develop new means of therapy. To accomplish that goal, we have developed a system in which we can induce vasculitis and then test new therapies. This system involves the transplantation of human blood vessels into mice. If such mice are supplied with immune cells from our patients, vasculitis develops in the engrafted blood vessel. We can treat that inflammation in the mice and can easily take a biopsy from the blood vessel to check what we have achieved and how therapy actually works.

C. How do you know whether my disease is active or not?

This is one of our greatest challenges as we take care of our patients. We cannot just go and take a tissue biopsy of our patients every time they come and see us. We have a research project in place which is aimed at developing biomarkers of vasculitis in a blood sample. We isolate out the immune cells of the patient and, by applying cutting edge technology, we assess these immune cells to get information how likely or unlikely these cells would cause inflammation.

Continue Reading »

Autoimmune Disease, Chronic Disease, Dermatology

My two-decade battle with psoriasis

My two-decade battle with psoriasis

We’ve partnered with Inspire, a company that builds and manages online support communities for patients and caregivers, to launch a patient-focused series here on Scope. Once a month, patients affected by serious and often rare diseases share their unique stories; the latest comes from Alisha Bridges.

Psoriasis has affected every aspect and transition of life that I’ve encountered thus far. I’ve had the itchy, flaky, non-contagious autoimmune disease since I was 7 years old; I’m now 26. As I approach the 20-year anniversary of encountering the disease, I think of how my treatment has evolved, and as I reflect on the differences in treatment between then and now, it’s a Catch-22 in some ways.

It all started after a bad case of chicken pox. My scars weren’t healing correctly. They looked crusty and inflamed. After more than 90 percent of my body remained covered with this mysterious rash, my grandmother decided it was time for me to see the doctor, who diagnosed me with psoriasis. The positive side was that I had Medicaid as insurance, and it covered any and everything I needed. But unfortunately, due to my age, there weren’t many treatment options. From the age of seven to 19, I was prescribed an array of topical treatments and UVA light treatment, none of which were really effective in ridding me of psoriasis. The treatments just kept it at bay.

Once I went to college, treatment became more challenging. First, I went out of state for college, so the only time I could get treatment was when I came home for winter vacation. This particular treatment required me to stay in the hospital for three weeks, which was basically my entire winter break. Once I realized a treatment twice a year wasn’t going to be effective, my family attempted to find me a doctor near my school. The only caveat then was that Medicaid is state-to-state; therefore I was removed from hometown Michigan Medicaid and required to apply for Alabama Medicaid where I attended school. I wasn’t approved for Alabama Medicaid, though, which caused me to go essentially without insurance, aside from the simple coverage the school offered for emergencies.

After a few years of being in school without any insurance, I finally landed a job with coverage and started my routine doctor visits. This time I had more options. As a child I couldn’t consider biologic injections and oral medications, but as a working adult these options became available to me. The flip side was and remains that the medicine is harder to get because of high deductibles and regulations by insurance. I’ve also found that it’s harder to maintain insurance due to life situations such as layoffs or career changes.

There are vast differences between having this disease as a child through adulthood, yet there are a few similarities that I experienced in both phases of life. Doctors have fought to get me treatment no matter what age. As a teenager with severe psoriasis, doctors attempted to get me approved for Enbrel, which has only been authorized for adults over 18. I’ve even had doctors battle the insurance company to gain approval and decrease the cost of various medicines.

Though there have been many things that have changed there is one aspect of psoriasis that is too often neglected. From childhood until now there have been no coping strategies offered to me when dealing with this disease. Out of the approximately ten doctors I’ve seen in regards to my psoriasis, not one inquired on how the condition affected me psychologically. Although this disease appears to be a battle from the outside, the mental anguish faced as a psoriasis patient is life-altering and can even be virtually paralyzing. Patients need to know that there are other people in the world with this disease, and that there are resources outside of medicine to help them cope. Coping strategies are just as important as treatment. Although I have found organizations such as the National Psoriasis Foundation to help manage this disease, it wasn’t because of professional recommendation. I found them on my own at the age of 24.

I can only fathom how having support would have enhanced the overall quality of life for me if a doctor would have made me aware of these organizations at the age of seven. Although I have struggled to find a successful treatment, knowing that there’s support for the mental aspect of psoriasis will give me peace until a cure is found.

Now, psoriasis does not define me - I define it.

Alisha Bridges is the creator of Beingmeinmyownskin.com, where she blogs about life with psoriasis. She’s a community ambassador and volunteer for the National Psoriasis Foundation.

Stanford Medicine Resources: