A great article about odds and illness

I just read this wonderful essay in the NYT by a regular guy - a guy who is at the same time a husband and a doctor - watching his wife having a chemo infusion for the first time. The article centers on the risks involved in chemo infusions of Taxol, a drug used to treat breast cancer, and the rare but potentially fatal allergic reactions to the drug.

I liked this article for two reasons. First, I think it addresses the fear that any of us who take Remicade, or any other strong and dangerous drug, experience. Infusion reactions are lurking possibilities that could occur at any time. The reaction to Taxol can be far more serious than those for Remicade, but the fear he and his wife experience echo my own.

Second, the addresses something that all of us with unusual illnesses struggle with. Odds.

The author, Dr. Peter Bach, writes about the risks and odds he has encountered with his wife during her fight with cancer:

Each time we heard “that rarely happens,” we knew that whatever it was – fevers requiring hospital admission, mouth ulcers that would stop you from eating, overpowering fatigue, hair coming back a different color – it could actually happen. Each time the odds were in our favor, but the odds on the other side were not zero.

Our disease, Psoriatic Arthritis, is not common - roughly only one in 200 Americans have it. Put one way, you could say we beat the odds when we got our diagnoses. But instead of making us feel lucky, I suspect beating the odds makes most of us feel more vulnerable. As someone with multiple diagnoses, I take each new ache or odd sensation a little more seriously - because I never know when I'll beat the odds yet again.

Dr. Bach puts it nicely.

The odds that Ruth would get breast cancer before she reached age 43 were about 100 to 1. Odds seem a lot different once you’ve come up on the short end.

Chances are I couldn't say it better - so I won't even try.

I'm going on a diet, and here's why...

An article in the New York Times caught my eye today. It inspired me to get out of my back to school and so much to catch up on so why the heck did I get that puppy when the cat died funk, and start writing again.

(yes, we got a puppy. By the way: puppy + psoriatic arthritis = really achy joints, a few second thoughts and lots of laughing. Back to the science - more on puppy later.)

The NYT's front page story was on autophagy, which was described as:

Our cells ... perpetually devouring themselves, shredding their own complex molecules to pieces and recycling them for new parts.

Apparently, we all have proteasomes and lysosomes, two types of small structures inside of cells that are recycling machines. They work day and night eating cells and spitting out the remains, which are used to build new cells. One scientist was quoted saying that we get an entirely new heart every 3 days due to the continual cell destruction and re-creation. WOW.

Scientists are now starting to believe that autophagy (or the lessening of autophagy as we get older) has a lot to do with the development of Alzheimer's and cancer. While autophagy doesn't necessarily cease as we age, it slows down, causing more and more cells to live longer and therefore mutate, leading to illness. The current thinking is that if we can control autophagy, we may live longer.

OK, fellow autoimmune specialists... doesn't "autophagy" remind you of another cellular process we're all really familiar with? Isn't autoimmune disease caused when our immune system (different cells, I know, but...) destroys our own cells mistakenly? Couldn't autoimmune disease be related to autophagy? And, could this slew of new research also support research in autoimmune disease?

It turns out that scientists are starting to connect the dots between autophagy and autoimmunity. While the NYT article doesn't mention autoimmune disease, there is some great work out along these lines:

The connection between autophagy and immunity should be emphasized in that autophagy contributes to the defense against microbial agents [5, 12], promotes antigen presentation through MHC class II [13, 14], is induced by cytokines [5, 15, 16], may regulate T lymphocyte survival and function [17], and may be stimulated by serum autoantibodies [18].

This is from an article by a ton of docs (Ana Lleo, MD, Pietro Invernizzi, MD PhD, Carlo Selmi, MD PhD, Ross L. Coppel, MD, Gianfranco Alpini, PhD, Mauro Podda, MD, Ian R. Mackay, MD, and M. Eric Gershwin, MD) linking autoimmunity and autophagy in the Journal of Autoimmunity (2007). The article is long and complex, so I'll cut to the chase. They conclude:

In the context of immunity, there is clear evidence for participation of autophagy in intracellular defense against infectious agents and also perhaps, in disposal of unwanted e.g. misfolded self proteins, although there is no evidence yet for an ensuing inflammatory response to such disposal.

As always, lots to learn on this topic, but there are some smart people out there trying to put all these pieces together. I'll keep watching, and will write more when I learn more.

OK, so I can hear you asking: "why the diet?".

Here's why. Autophagy kicks in when our bodies have fewer new proteins coming in... you've all heard of the process where our body starts "eating" itself when it has less food. And it is well documented that people on permanently lower calorie diet are healthier... turns out semi-starvation is kinda good for you. Scientists think that inducing this "cannibalism" increases the destruction of older, dysfunctional cells - those that cause Alzheimer's and cancer. So I wonder if the same is true of autoimmunity. In short:

Would a lower calorie diet induce autophagy, and help our bodies destroy those cells that are mis-firing and causing our immune systems to act up?

BTW, because of the dog, I've lost 3 pounds, just from walking. I look fabulous. And if I just stop eating, I'll apparently be able to walk the dog 'til I'm 150.

Where's the leash?

Getting up to speed on health care reform...

I've been out of the loop for a couple of months - being home with the kids has taken more out of me, mentally and physically, than I expected. School started yesterday and my days are empty again - how can it be that I already I miss the noise, the fighting and the noontime cuddles?

But I've also missed a lot of the health care debate - and it's important for me to get up to speed. Psoriatic Arthritis is a chronic condition... and many of us with PsA are looking at huge medical and drug expenses for the rest of our lives. The decisions being made right now in Washington could deeply influence my health (and many of yours) for the long term.

So, yesterday, at my favorite gluten free cafe, I turned to the conservative writers that every liberal loves to love (Andrew Sullivan and David Brooks). And they both spoke very highly of Atlantic Monthly's cover article, called "How American Healthcare Killed My Father", written by David Goldhill... they both suggested that Obama should read it as he moves forward with health care reform.

So I read it too... and I hope the president reads it. It's long. It's heartbreaking. It's complicated. And it is really good. Goldhill pushes past the current focus on financing health insurance, and digs deep into what is really faulty at many levels with America's health care system, including:

A wasteful insurance system; distorted incentives; a bias toward treatment; moral hazard; hidden costs and a lack of transparency; curbed competition; service to the wrong customer. These are the problems at the foundation of our health-care system, resulting in a slow rot and requiring more and more money just to keep the system from collapsing.

And his solution goes much farther than the solution Obama presented last night - he would like to see more consumer-centered health care system which would:

not rely on a single form of financing for health-care purchases; it would make use of different sorts of financing for different elements of care—with routine care funded largely out of our incomes; major, predictable expenses (including much end-of-life care) funded by savings and credit; and massive, unpredictable expenses funded by insurance.

If you skip to page 6 of this article, you'll find thorough description of his plan for a more consumer driven health care system. It isn't a perfect plan (which he admits) but it is a compelling one. As someone who has huge monthly medical bills, I was first terrified by his plan - what? I'd pay for my Remicade out of my savings? But the more I read, and the more I thought about my year and a half trying tackling treatment for Psoriatic Arthritis, the more his plan made sense. Goldhill calculates that if we took all the money we spend in our lifetimes to pay for health insurance and sock it away, we would have over 1.7 million dollars each, to spend on our own health care. And if we have control over where we spend that money, hospitals and clinics would have to become more competitive (and transparent), raising quality.

Imagine, all of us with Psoriatic Arthritis, with 1.77 million each to spend on our health care. What changes could we make, in the quality of our clinics, our rheumatologists, the drugs we're offered, merely by having more choice? I'm getting all tingly just thinking about it.

Take a look at the article. It's a revolutionary idea, and educational. I liked it.

Is Psoriatic Arthritis underdiagnosed?

We all know the numbers - it is estimated that only 10-30% of people with Psoriasis will be diagnosed with Psoriatic Arthritis. But is the low rate of co-incidence because people with P(soriasis) don't usually develop Ps(oriatic) A(rthritis), or because many people with P don't realize they also have PsA? I tend to think the latter, and I think research is starting to back me up.

A recent Canadian research survey on people with Psoriasis (not Psoriatic Arthritis), called the SKIN study (cute) suggests that PsA could be widely underdiagnosed. The article I read about the study states:

The SKIN survey reveals that half of all respondents [with Psoriasis] reported that they had developed joint pain or stiffness, but only 18 per cent of these respondents had ever received a diagnosis of psoriatic arthritis.

and...

Respondents reporting no psoriatic arthritis diagnosis indicated that they experienced stiffness in the knees, shoulders and hips (48 per cent), followed by pain or stiffness in the finger joints (38 per cent) and toe joints (23 per cent).

Underdiagnosis concerns me for two reasons - firstly, of course, I don't want anyone else to experience the pain I experience. But secondly, fewer people diagnosed with PsA means the research community will be less likely to study PsA.

A while back I wrote about the lack of research and basic information about Psoriatic Arthritis, as compared to Rheumatoid Arthritis and Psoriasis. Here's the link.

Here's my point: fewer scholarly articles on PsA will lead doctors to make fewer diagnoses, AND, the lack of PsA diagnoses certainly has an effect on how much research is undertaken.

So if you're out there with P, and think you have PsA, please consider getting a definitive diagnosis.

You know what they say about the squeaky wheel, after all. I'm up for some grease (and I'm not talking another ointment).

Health Care in America, Part II

LILI SACKS, a primary care doctor in Seattle, says she began thinking differently about her work on the day she realized she was beginning each appointment with the words, “Sorry I’m late.”

The above is a quote from a recent article in the New York Times on health care... it is a perfect follow up to the New Yorker article I talked about a few weeks ago. Here's what follows that quote:

Scheduled to see as many as 25 patients a day at a large clinic, she lacked the time for thorough examinations and discussions. Because of this, she said, primary care doctors are often forced to order tests and send patients to specialists.

“Could I have helped some people without specialists and tests? Absolutely,” said Dr. Sacks. “Would it have saved the patient and the insurance company both money? Absolutely. Is the system set up for the best care and cost efficiency? Absolutely not.”

Dr. Sacks said she worried that seeing so many patients would lead to errors.

Much of this article talks about the "direct practice" model of medicine, which for many physicians translates to: each patient pays them a monthly fee, but then gets to see the doc for no cost, including many tests, pretty much as soon as and as often as needed. Dr. Sacks, in this article, switches her practice to a direct-practice model, and speaks very highly of it in the article.

Last year, she moved to a clinic that focuses on longer patient appointments, 30 to 60 minutes. This translates to 10 to 12 patients a day. Patients also communicate directly with her by phone or e-mail.

During those longer appointments, Dr. Sacks can perform basic lab tests and simple procedures, so patients see fewer specialists.

I've been skeptical of this kind of service - worried about an even further separation between the wealthy and the poor in the type of health care they receive. But here's an argument from this article that I think makes a great deal of sense (italics mine):

Dr. Sacks said the financial mechanics of the direct-practice model match her medical goals. When she was compensated based on insurance, she was paid every time she saw a patient. Now, if she can use education and prevention to reduce office visits, she and her patients benefit, she said.

One thing (among many) required to make this model work would be a welcoming atmosphere... a "we want to see you" kind of attitude... at the doctor's office. Preventative care requires a doctor be able to see patients before diseases strike or progress too far. However, I can imagine if I was paying $100 a month for health care out of pocket, on top of insurance, I'd want to feel free to walk into my doc's office anytime I darn well felt like it.

Is anyone using this model? Do you like it?

I'm all about reducing the cost of health care. Imagine if it came with better care too!

Universities, beef, and some education on the side...

In the last few days two articles have come out in the New York Times that I think are relevant to this blog, despite the fact that neither of them is about psoriatic arthritis or psoriasis. Humor me... I do have a point...

The first is an opinion piece called End the University as We Know It, by Mark C. Taylor. It calls for a systemic reorganization of the university system, most specifically in graduate education, because:

Most graduate programs in American universities produce a product for which there is no market (candidates for teaching positions that do not exist) and develop skills for which there is diminishing demand (research in subfields within subfields and publication in journals read by no one other than a few like-minded colleagues), all at a rapidly rising cost (sometimes well over $100,000 in student loans).

Why is this relevant to PsA, you might ask? It was these paragraphs that hit me:

Responsible teaching and scholarship must become cross-disciplinary and cross-cultural.

Just a few weeks ago, I attended a meeting of political scientists who had gathered to discuss why international relations theory had never considered the role of religion in society. Given the state of the world today, this is a significant oversight. There can be no adequate understanding of the most important issues we face when disciplines are cloistered from one another and operate on their own premises.

It would be far more effective to bring together people working on questions of religion, politics, history, economics, anthropology, sociology, literature, art, religion and philosophy to engage in comparative analysis of common problems. As the curriculum is restructured, fields of inquiry and methods of investigation will be transformed.

Ok, so sub out the words "religion, politics, history, economics, anthropology, sociology" etc. etc. and put in "rheumatology, dermatology, immunology, gastroenterology" etc. etc. The more I learn about how deeply connected autoimmune diseases are, the more I wish that these, and other, fields of medicine were working more closely together.

Now I know I have it really good - my rheumatologist consults with my dermatologist on almost everything she does, and visa versa. But I'm assuming that that is not true for many of you, and certainly neither of them has talked to my gastroenterologist. I do like the idea of a new area of clinical (meaning, not in a lab- they see patients) specialization - autoimmunology - but boy folks in that field had better have great communication skills.

Anyway, go read the article. It really makes you think.

That second article? Here - Paying a Price for Loving Red Meat, written by Jane E. Brody. Apparently, a new study demonstrates that the more red meat consumed, the more likely you are to die early.

This article struck me because of the increased risk for heart disease that psoriasis patients (and, in theory, psoriatic arthritis patients) have. Here's my thinking - I'm already at increased risk for heart disease... and red meat consumption increases that risk further! I want to protect my body, and I want all of my readers to, too. So I thought I'd share this data...

For lunch today, I'll be eating lentils while reading the paper. What about you?

The business behind the disease

Was I the only one who was surprised, when starting Humira, that you could get a payment plan to reduce the cost of co-pays to pretty much nothing for the first 6 months on the drug? It came in the form of a card, given to my rheumatologist to give to me, which I could then use with the pharmacy to get that co-pay covered by Abbott, who makes Humira. Was Abbott encouraging me through that plan to use their drug?

In the words of my favorite Alaskan Governor - "You betcha".

The business behind big-pharma and biotech is fascinating. As I noted in a recent post, we've come a long way in our genomic research, (which leads to the development of effective biologic drugs) but we still have a long way to go. It's easy to think about a set of good-willed researchers in their white coats worrying about our joints and striving for the good of science to cure us. I know many of these researchers (I'm married to someone who used to be one). I'm grateful to them.

It's also easy to forget that good science is also about good business.

Today, I found a European news article online that links to a report called: The Autoimmune Market Outlook to 2013: Competitive landscape, pipeline analysis and growth opportunities. I couldn't get access to the whole report, because it looks to cost a bundle. But here are some excerpts on the page describing the report:

-The global autoimmune market generated sales of $31.9bn in 2007, an increase of 14.4% over 2006 sales. The market is forecast to grow at a CAGR of 8.1% to reach a total value of $51.0bn in 2013.
-Immunosuppressant drugs dominate the automimnune [sic] market, with four products from this class accounting for 40.3% of total market sales. The highest selling immunosuppressant drug was J&J/Schering-Plough's Remicade, with 42.1% of total sales in this class.

and:

Use this report to:

- Assess patient potential, treatment trends and sales patterns of major autoimmune indications over the period 2009-13, with this report's coverage of osteoarthritis, rheumatoid arthritis, crohn's disease, systemic lupus erythematosus, ulcerative colitis and multiple sclerosis markets across Japan, France, Germany, Italy, Spain, the UK and the US.
- Discover the market dynamics of the autoimmune area and understand the impact of recent events by assessing key market trends, growth drivers and the latest issues affecting product development.

I'm glad there are market analyses being done regarding both autoimmune diseases and the drugs that treat them. And, of course, I worry whenever big money is involved, esp given our economic climate. Mostly, though, it is important for those of us who are health consumers to understand the multiple motivations behind good science. Money talks.

Make 'em laugh, doc!

We all know psoriatic arthritis is no laughing matter, but it appears that if we can find the funny side of our disease, we'll do better.

The Bio-Medicine website has a great article today about a research study showing that laughter can affect your disease course. Researchers took a group of diabetics, put them all on the same medication, but made only half of the diabetics watch a humorous video (of their choice) for a half an hour each day. The other half were not prescribed humor.

The folks who watched the funny videos:

had lower epinephrine and norepinephrine levels by the second month, suggesting lower stress levels. They had increased HDL (good) cholesterol. The laughter group also had lower levels of TNF-α, IFN-γ, IL-6 and hs-CRP levels, indicating lower levels of inflammation.

Crazy cool - laughter may reduce inflammation. Now I have to figure out what TV show makes me laugh for 30 minutes straight... finding one may be harder than giving myself that methotrexate shot!

Genomic research update - we've got a ways to go.

The New England Journal of Medicine published several articles this week about the current state of research on the human genome. The articles were especially focused on whether greater understanding of the genome will lead to greater understanding of how humans develop certain diseases.

(If you, like me, need to run to the dictionary every time you hear the word "genome" to find out why it is different from "gene" or "chromosome" - here's a good link. In short - the genome is the complete set of genes in a particular organism).

Kraft and Hunter, in an article they title "Genetic Risk Prediction: Are we there yet?", state pessimistically:

We are still too early in the cycle of discovery for most tests that are based on newly discovered associations to provide stable estimates of genetic risk for many diseases. Although the major findings are highly unlikely to be false positives, the identified variants do not contribute more than a small fraction of the inherited predisposition. ...Estimates are poor predictors of risk, both in absolute terms and in relation to risk estimators that will be available when more of the remaining locus associations are discovered.

In other words, to answer their title question - no, we're not there yet. The New York Times has a great review today about the NEJM series of articles that explains this far better than I can. But, basically - researchers and drug companies thought that if we could examine the genomes of people with illnesses and compare them with genomes of people who are well, one or two genes in the genome would essentially "light up" as the key genes causing these diseases. Drugs could then be made that would alter these genetic sequences, thus curing those diseases.

Turns out we're more complicated than that - much more complicated. When one or a few genes are implicated in a disease, usually these genes can only predict the disease some of the time, for some people. There seems to be a lot more going on in our bodies besides genes in the development of a disease. AND, often, there are hundreds, instead of tens, of genes involved in a disease, which makes the development of a targeted drug really difficult.

It's very smart for these scientists to be taking a step back to think about whether or not the genomic research they are doing is going to pay off in the short run (or long run). If you look at the NEJM articles, you can see some differing of opinions - some folks sound more optimistic than others... some are wisely watching their wallets, and some are ambitiously still looking into the future.

I fear we have a long way to go.

Celiac Disease and Psoriatic Arthritis

I was trolling around PubMed today and came across this topic... frankly, I'm surprised at myself for not looking at it before, considering my history.

A study was published in the Journal Rheumatology in 2002 linking psoriatic arthritis to celiac disease. The researchers found that there was a higher rate of celiac disease in their PsA patients. They state:

An increased prevalence of coeliac disease in patients with PsoA has not been reported previously. Among our patients, 4.4% had coeliac disease (ascertained by the presence of villous atrophy) compared with 0.4% in a large Swedish adult population of blood donors.

also:

Patients with PsoA have an increased prevalence of raised serum IgA AGA and of coeliac disease. Patients with raised IgA AGA seem to have more pronounced inflammation than those with a low IgA AGA concentration.

Celiac Disease (or coeliac disease, if you live in Europe), is an autoimmune disease in which the body confuses gluten (a protein found in wheat, barley and rye, as well as some other grains) with toxins. If a "celiac" ingests gluten, the body produces antibodies to break down the intestinal wall, destroying the villi which are used to digest food, in a flawed effort to save itself from toxins. When you lose those villi, you get super sick - anemic, weak, skinny. The only known treatment is complete adherence to a gluten free diet.

What this study is saying is that people with psoriatic arthritis are more likely to have celiac disease, and that patients with more acute inflammation in their psoriatic arthritis could possible also have worse celiac disease.

I have had celiac disease and have been on a gluten-free diet for 16 years. I continually struggle with the autoimmune diet (no dairy, alcohol, sugar, etc - boring!) but the gluten-free part of the autoimmune diet has been easy. Gluten makes me very, very ill, and I'm never tempted to cheat. Its not worth it. When we're better friends I'll describe what happens to my gut when I eat wheat. But not yet. I don't know you well enough.

The researchers state, at the end of their article:

Studies of the gastrointestinal mucosa in PsoA patients are therefore needed. Controlled studies of the effects of a gluten-free diet on the severity of PsoA are also required.

In short, more psoriatic arthritics should go on gluten-free diets to see if they get better. In a research setting, with control subjects eating gluten, etc. etc.

Of course, the plot thickens. Here in the U.S.A, another study was conducted which looked at the prevalence of IgA antibodies to gliadin (in other words, celiac disease) in folks with psoriasis and psoriatic arthritis. Their results found no increase in these antibodies in psoriasis and psoriatic arthritis patients. They state:

We found no support for the results of prior studies showing that elevated AGAs occur with increased frequency in patients with psoriasis.

I'm not convinced. Look at this abstract if you want to have your mind blown. It lists many, many skin manifestations in auto-immune diseases - from Grave's to Crohn's to celiac disease. It is apparent our skin, as one of the organs of our bodies, is greatly affected by our immune system, especially when it is in havoc. I'm continually astounded by the links between all of these autoimmune diseases, and by how so much of this science is still in its infancy. And it appears that our skin disease, and our joint disease, may be related to a gut disease.

Hm. I meant for this to be a short blog post. But isn't this stuff fascinating? And here's another piece in my puzzle:

I have no idea if a gluten-free diet would work on my PsA, because guess what... the year I developed celiac disease was the year my knees first showed signs of arthritis. Autoimmune diseases can be triggered by something in the environment, and in 2003 I had just come back from Tonga with a bad case of giardia, a parasite. We think it triggered the celiac disease, and I know now what I didn't realize then - I was developing two diseases back in 2003 instead of one. At the time I had some physical therapy, but ended up ignoring my knees in order to focus on my gut. After a while, the knee pain was pretty manageable.

So here's my question: Did the giardia trigger two diseases, and did the new gluten free diet slow the disease process in my knees?

A final note: I've not had a single bout of ... um... unmentionable gastrointestinal troubles ... since I went on Humira for my arthritis. Go figure.

Chicken or the egg?

Those of you who get Google alerts for the word psoriasis will have noticed this headline popping up all over this morning - "Psoriasis may reflect systemic inflammation, heart disease".

The article this headline links to is on the American Medical News website, and refers to a key theme from the American Academy of Dermatology meeting in San Francisco in March. At this annual meeting, several forums focused on whether psoriasis should be considered a systemic disease (a disease which affects multiple parts of the body, instead of just the skin), and especially considered cardiac risks in people with psoriasis. The article states:

This meeting is the latest to highlight a burgeoning body of scientific literature, data and expert opinion that psoriasis is related to more than a lower quality of life. Like other inflammatory conditions, it is linked to a shorter lifespan and a range of significant health problems. The theory is that inflammation on the skin may be a reflection or cause of additional inflammation throughout the body.

Look at that last sentence of the paragraph I quote above, and note the words "reflection or cause". Those are the key words, right there, and suggest some important questions: Does the skin inflammation cause other portions of the body (like the heart) to experience inflammation? Or is it the reverse - is skin psoriasis the result of other inflammation (like in the heart)? Or, is there a third factor at play that causes both skin and heart inflammation?

This article also did a great job explaining the complexities of of studying psoriasis in humans, especially when you're trying to include how psychology affects these studies. Sometimes we smoke, sometimes we get overweight, sometimes we're non-compliant. Do we act this way because of our disease, or do these behaviors cause the disease?

Watch out, though... here comes my soapbox again. I found NO mention of the ugly stepsister in this article - not one reference to psoriatic arthritis was included. Time for my megaphone: Hello!!! What about the inflammatory disease closely related to psoriasis? We have quality of life issues. We experience depression and obesity due to pain and immobility. Don't forget us!

You know they talked about psoriatic arthritis at the March meeting. But the press didn't pick it up. I find that a bit frustrating.

Ok, soap box is going back in the closet. Check out the article, though. I liked it anyway.

Are autoimmune diseases connected? I think yes!

A fellow Psoriatic Arthritis patient asked me to explain whether (and why) if someone has one autoimmune disease, they are more likely to get a second one. For example, in my case, is there some reason other than chance that I have both Psoriatic Arthritis and Celiac Disease?

To tell the truth... if I could answer that question I could win the Nobel prize and run a whole lot of people out of work. The immune system is incredibly complex, and a layperson like me can only skim the surface of understanding it.

Here's what I do know, however, after doing some sleuthing.

Yes, autoimmune diseases come in multi-packs, like underwear from Target. If you have one, you're likely to get two or three. This is called co-morbidity, btw. Just last month, an article in the American Journal of Epidemiology discussed some researchers' attempts to demonstrate autoimmune co-morbidity. The authors used public records to see how often rheumatoid arthritis, multiple sclerosis, autoimmune thyroiditis and insulin-dependent diabetes mellitus were present in the same individual. And they found that there was a high co-occurrence between rheumatoid arthritis, insulin-dependent diabetes mellitus and autoimmune thyroiditis. BUT... they found that there was an inverse relationship between RA and MS - which means that if you had one, you were LESS likely to have the other! Go figure. This reverse relationship does speak to a relationship... but what kind of relationship?

Dr. Noel Rose wrote an essay called The Common Thread discussing the etiology (the cause) of autoimmune diseases and the need for more research on the links between them. You can find the paper on the American Autoimmune Related Diseases Association website. Dr. Rose states:

Autoimmunity is an etiology: it is a cause of disease. Anatomically, autoimmune disease is very diverse; and that's why we see specialists in so many areas of medicine studying autoimmunity. They may be rheumatologists who are interested in joints; they may be dermatologists who are interested in skin; they may be cardiologists who are interested in the heart; they may be gastroenterologists who are interested in the gastrointestinal tract. But the common etiology for all of these disease--for Crohn's disease of the gut; for lupus of the skin; for rheumatoid arthritis of the joint--the common etiology that brings together all of these diseases is autoimmunity.

Dr. Rose doesn't necessarily say that one disease can cause another, but that's not what we're talking about. We're talking about whether they occur at the same time, and whether autoimmune diseases are all just one disorder with multiple symptoms. It does make sense that if you are having a problem with your immune system in general, that the problem won't always limit itself to one organ or region, but can be systemic. But how do we prove that all of these autoimmune diseases are related, or perhaps one underlying disease?

Here's one data point that suggests a connection: many different autoimmune diseases can be treated by the same medication - and I'm not just talking about diseases that look similar, like psoriatic arthritis and rheumatoid arthritis. For example, my husband and I could get Abbott labs to give us a bulk discount - Humira treats PsA and Crohn's Disease. Humira is a TNF-alpha blocker - and both of our diseases can be linked to an excess of TNF-alpha. On the other hand, so far, Humira doesn't seem to treat every auto-immune disease.

In their book "The Autoimmune Connection" Rita Baron-Faust, Jill P. Buyon, M.D. hypothesize about some of the reasons autoimmune diseases may co-occur, or may perhaps be one disease with multiple symptoms. They say:

While autoimmune diseases may target different areas of the body, the genes that affect immune responses may be the same. For example, genes that govern cytokines may have a mutation that causes too many inflammatory molecules to be released. Defective genes common to autoimmune diseases may also affect the way T-cells are programmed to recognize antigens, the number of receptors they carry, the number of T-cells with a faulty memory, or how many defective T-cells are eliminated.

Researchers are now trying to demonstrate, on a genetic level, that many autoimmune diseases are related. A group of researchers looked across 42 separate studies of 11 autoimmune diseases to see if they could find underlying genetic links. They found that several diseases shared some common genetic fingerprints (the HLA region of chromosome 6 lit up for many autoimmune diseases, as did many parts of chromosome 16). On the other hand, there were several genes that seemed to be involved with only one disease. This is from the Feb 2009 issue of the European Journal of Human Genetics - you can read the abstract here.

So, ok, what do we know about autoimmune co-morbidity? What do we think? Here's what I've learned:

• Many autoimmune diseases are likely to co-occur in the same person, but some aren't.
• Many researchers think that separate autoimmune diseases have a shared etiology, or cause, and may possibly be one disease. Some evidence supports this, but some doesn't.
  
• Many autoimmune diseases share similar genetic links, but not in all cases.

What does this mean? Folks, it means that we need more research. And of course, this means we need more funding for research. If you haven't yet, find some way to support research on your disease(s), or autoimmune disease in general. Go to the NPF website, or the AARDA website. Do something, and keep talking.

It also speaks to something I've discussed before in my blog - the fact that humans' compulsions to put things in boxes - to categorize - may limit how we understand disease. Maybe autoimmune diseases are all just one disease... maybe they aren't, but they just share a lot of qualities or root causes. Do the diagnostics get in the way of knowledge? I think yes, sometimes. Perhaps a more holistic approach to research, diagnosis, and treatment would help use understand these symptoms (not diseases) better.

It also means I have a lot more to learn before I ever attempt to write a logical post about this topic again. This is complicated stuff.

What's your buzz cut?

Today's New York Times has a beautiful article about self-image and illness, written by Dana Jennings, a blogger/writer who has prostate cancer and has gotten a buzz cut to help get through. He says:

In a time of utter vulnerability — having already weathered three months of post-diagnosis ups-and-downs — I needed the primal ferocity that a buzz cut proclaims. I needed to look like a soccer thug or an extra from “Prison Break” to help get me through surgery, the physical indignities of post-op life, and my subsequent radiation and hormone therapy. I still do. My prostate cancer and its treatment have transformed me — in body and spirit — and the buzz cut has helped me cope with those changes.

For many people, including myself, chronic illness profoundly changes who you think you are. Jennings quotes Dr. Robert Klitzman, an associate professor of clinical psychiatry at Columbia University Medical Center, who aptly says:

“The challenge with cancer is to find a new sense of self... because the narrative of yourself has been disrupted".

I think this is true of chronic illness as well. I know I have struggled immensely with my personal narrative since October, when I found out I have three inflammatory and chronic diseases (celiac disease, psoriatic arthritis, lymphocytic colitis). My childlike belief in my own invulnerability has been exchanged for a terrifying sense of my own mortality. While externally I'm talking and writing and "being" my disease, internally I cringe when I think of myself as someone who ONLY is sick. The other identities - aspiring writer, competent mom, non-profit professional, loving wife, all seem to hide behind the title "sick person".

I despaired in October, as you can tell if you read the first few posts on this blog. I wallowed. I grieved deeply for the me that I felt (and still feel) was lost.

This blog may be my buzz cut. I can't be silent. I'm writing in order to create the new me - a me who is sick, but is also many other things: a researcher, an advocate, a writer. Dana Jennings says about his true self:

I am basically a cream puff. But I like the contradiction, the tension, that the buzz cut seems to represent between my inner and outer lives.

The buzz cut is a kind of veil or, perhaps, a mask hiding my secret identities: one of which is being a cancer patient.

But to be honest, I don’t think I’m hiding anyone. We are, all of us, a bundle of apparent contradictions. Even though I’m a dreamy pragmatist, I need the guy with the glare, the shaved skull and the brutishly broad forehead to help me through the day.

I need to write to get through my day. What's your contradiction? What's your buzz cut?

Burn, baby, burn

Just a quick note... I'm going to be starting laser treatment for my psoriasis soon, if my insurance allows. Here's an article on it from the WSJ. This is extremely exciting new technology. My dermatologist said during each of the 10 treatments, they will only use the laser 'til my skin turns red. They have to be careful that my skin doesn't blister (although she also said that blistering works faster... eeeewwww).

I can't imagine not feeling embarrassed about my elbows this summer.

Our little club is getting bigger

After writing so much about the increased incidence of autoimmune diseases, and also about potential triggers for Psoriatic Arthritis, I wanted to make sure I wasn't barking up a non-existent tree. Are Psoriatic Arthritis incidence rates really on the rise?

The answer is... most probably yes.

In this opinion article from the Feb 2009 issue of the Journal of Rheumatology, Dr. Vinod Chandran from Toronto Western Hospital discusses a current study (in the same issue) that demonstrates that PsA rates are in the rise. He also devotes a bunch of page space to the diagnostic challenges of PsA, which profoundly affect how well we can measure incidence rates.

Here's a summary quote from the article, but I recommend going in and reading the whole piece:

...the prevalence of both psoriasis and PsA is increasing, and environmental rather than genetic factors are probably responsible.

So, why do I state above that the rates are "probably" rising? Because of the nature of research and available data. The quoted study was done only on people in one smallish area in Minnesota - so while we can assume this increase is true across the country, we can't be sure. Maybe there is something in Minnesota that is causing an increase - something not present elsewhere. The author also refers to our inability to truly understand why these rates are rising:

Genetic or ethnicity related factors are unlikely to be responsible for the observed change since there has not been any significant immigration or emigration from this “captive” population. It would be interesting to study how environmental factors have changed over the years to give us an explanation. However, such studies are best done prospectively.

(prospectively meaning: not after-the-fact)

I admire Dr. Chandran's analysis of the frustrations preventing true understanding of the prevalence rates of PsA. He cites weaknesses in diagnostics or "classification criteria", which is a reflection of how recently scientists have begun studying Psoriatic Arthritis. Until doctors and scientists nationwide agree on what PsA signs and symptoms really are, it is hard to compare epidemiological studies from different regions. And, of course, it's financially challenging to develop a nation-wide study.

Once again, I'm struck with how much PsA remains the "ugly stepsister" to Psoriasis and Rheumatoid Arthritis. I wish the science behind this disease wasn't still so hit-and-miss. I admire, and appreciate, those scientists and doctors dedicated to this disease, but I wish there were more of them. It may take more and more of us being diagnosed to generate more PsA researchers.

And unfortunately or fortunately, my wishes may be coming true.

Morbidity and comorbidity

The National Psoriasis Foundation recently headlined a news article about the long term risks of psoriasis because of its highly inflammatory nature. At the recent Annual Meeting of the American Academy of Dermatology, Dr. Joel M. Gelfand (a dermatologist) explained:

that for the last two decades, research has shown that excessive inflammation is a critical feature of psoriasis... Excess inflammation also is present in other common conditions, such as hardening of the arteries, heart attacks, stroke, obesity and diabetes - which may explain why some psoriasis patients may be at an increased risk for developing these other serious conditions.

He goes on to say that people with severe psoriasis are likely to die 5-7 years earlier than those without.

Upon reading this, I went racing off to PubMed to try to locate some of this comorbidity research that Gelfand is talking about (especially the stuff that says I'm gonna croak soon), and ran across this 2008 article. Here are some highlights from the abstract (italics mine):

The risk factors of cardiovascular disease and other disease comorbidities appear to be more common in patients with psoriasis compared with the general population. To support this concept, the association between psoriasis and cardiovascular disease and other comorbidities was analyzed... from 1127 patients with psoriasis and a matched cohort of nonpsoriasis patients. Psoriasis patients were significantly more likely to have cardiovascular comorbidities... compared with nonpsoriasis patients. Other comorbidities significantly associated with psoriasis were arthritis, depression, sleep disorder/insomnia, chronic obstructive pulmonary disease, and gastroesophageal reflux disease. Responses to this large survey confirm that patients with psoriasis have a higher rate of cardiovascular risk factors and other comorbidities compared with patients without psoriasis.

Wait, wait... now I'm confused. Because I have psoriasis, I'm more likely to have arthritis? So...am I a patient with psoriasis, and the psoriasis is manifesting itself through the comorbidity of arthritis?

Or, am I a patient with psoriatic arthritis, which is an inflammatory condition similar to rheumatoid arthritis, but I also have some skin stuff going on too??

It's all just so blurry, and leads me back to questioning the diagnostic process again. I think I'm going to go back to reading those autoimmune books. While there's still time.

What am I hiding?

Even after 38 years with psoriasis and 15 years with swollen arthritic knees, if someone asked me if try to hide the physical traces of my disease, I would deny it outright. In my idealized view of the world we should be judged on who we are, not on how we look. For the sake of my daughter, I'd like to think that I live this ideal.

But truthfully, I do hide.

I didn't recognize how much until I read this article from WebMD on how to camouflage your psoriasis or psoriatic arthritis. I was truly surprised to realize that I do use many of the tricks recommended in this article. My wardrobe is the offspring of embarrassment and years of trial and error. I don't wear dark colors often. I won't wear shorts - haven't in years, because my knees are so huge. I wore long gloves at my wedding to cover my scabby elbows. As for cosmetics - well, that secret will stay with me.

I'll resist the urge to write a pedantic paragraph about women's obsessions with our body images, the powers of marketing, modern feminism, and "Our Bodies Ourselves". You have all heard it before, and I'm sure you'll just agree with me.

Instead, I'll just end with a question - why do we feel better physically when we look better?

More power to Tim Gunn.

Why am I so tired?

I'm REALLY tired today. I have the cold that won't quit, and the Humira has short-circuited my immune system so I'm not fighting the cold off as well as I could. Ironically, because I'm tired, I'm having a hard time getting the motivation together to write about an article on fatigue and inflammatory illnesses that I found last week. But this is really cool science... I've been excited to share it.

In short:

Although the brain is usually isolated from the immune system, the study suggests that certain behavioral changes suffered by those with chronic inflammatory diseases are caused by the infiltration of immune cells into the brain. The findings suggest possible new treatment avenues to improve patients' quality of life.

It was previously thought that immune cells couldn't make it to the brain... but this study shows that in folks with inflammatory illnesses, white blood cells called monocytes do get up into our noggins and make us feel sick. The researchers in this study were able to reduce "sickness behaviors"(fatigue, malaise, loss of social interest) in sick mice by blocking monocytes from the brain. And one way they were able to block these monocytes was by blocking TNF signals, which as we know is part of what Humira does.

I love the idea of these little mice suddenly exhibiting social interest. What, are they making martinis? Playing bridge? At least now I know that my Humira is making me sick and outgoing at the same time.

Generic biologics! Thanks, POTUS!

This just in from the WSJ - Obama's new budget includes increased funding to fast track the creation of generic biologic drugs. Here's the article.

Why is this exciting, you may ask? Biologics (like Humira, Embrel, and Remicade) are the newest form of treatment for many of us with autoimmune diseases, and they are also prohibitively expensive. I'm very lucky that our family's insurance covers my Humira shot twice a month. According to one website, the cost of Humira runs $1662 a month. That's almost as much as our mortgage. My co-pay for it is already $60 a shot.

This item in the budget is great news for those of use who lead more normal lives thanks to biologics.

However, note this line in the last paragraph of the WSJ article:

Makers of brand-name biotech drugs say the copies aren't identical to the originals and should undergo rigorous examinations to ensure safety.

If I understand it, the process for making biologics is very organic. These drugs are cooked up in big vats, all started from the same set of cells etc. And there's essentially just one vat for each unique drug. It reminds me a bit of Oompa-loompas, or yogurt starter - you gotta have a little bit of the magic goop to make that exact drug. And unless drug companies are willing to share their magic goop, the generic drugs won't be exactly the same as the originals. So I suspect these generics are long time coming... lots of research needs to go into each one to ensure that it is safe and that it works.

But still, thanks POTUS, for being forward thinking.

Take your medicine, folks!

A recent article in the Journal "Arthritis Research and Therapy" demonstrated, unsurprisingly, that folks with Rheumatoid Arthritis who were more consistent at taking their DMARDs (Disease Modifying Anti-Rheumatic Drugs) do have better prognoses - they feel better sooner, and have less structural damage. The subjects in this study had just been diagnosed, and were followed over two years.

The key point of this article was that younger patients were more likely to stay on their drugs than older patients.

My two cents - have any of you been on methotrexate? Many rheumatologists and patients love this drug, but it was my personal nightmare. I took it weekly for 6 weeks, and for three days each week I was nauseated, dizzy, exhausted, and had rampant diarrhea. I'm in my early 40s, and not frail by any means. I can imagine that for folks with compromised health already some of these drugs are worse than the disease. I think about my grandparents, who as they have gotten older are more forgetful and less tolerant of side effects. The article calls for more investigation into how to increase medication compliance - and this is especially true for older people.

So, if you can, don't give up on your meds too quickly. Build a support system to get yourself through the first few months, when both the pain and side effects are the worst. Many of these drugs do work. Just give them time...