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?

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.

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.

Humor me, but don't kiss me

My dog-eared copy of The Autoimmune Epidemic has me in its clutches again today. I'm bursting with hypotheses, but I'm realizing that my lack of a PhD in biochemistry or genomics or super-brainiac-science-chickness is getting in my way. Nevertheless, I will persevere in my attempt to be the psoriatic Sherlock Holmes.

In "The Autoimmune Epidemic" (starting on page 127) Jackson Nakazawa introduces the work of Drs. John Harley and Judi James. These two maverick researchers discovered a strong link between Epstein-Barr Virus (EBV) (which causes mononucleosis - the kissing disease) and the onset of lupus, which is another autoimmune disease. Jackson Nakazawa discusses how Harley and James were able to:

...travel back in time and show that the autoimmune reaction in lupus patients was a slow-brew reaction to an Epstein-Barr exposure that had occurred months, years or even decades before. (page 134)

Why did this tickle my brain, you may ask?

As I mentioned in an earlier post, my husband and I both suffered from a strange bout of sickness about 4 years ago. Our doctors at first thought it was lymphoma, but then settled on Epstein-Barr/mono (our test results were equivocal).

About 2 years after my husband had mono, he had his first Crohn's disease flare (Crohn's is an autoimmune illness). Also, about 2 years after I had mono, my knees, hands, and wrists flared with psoriatic arthritis.

I haven't had time yet to do a thorough scan of the the research journals, but at first glance there is not a lot out there about PsA and EBV. However, I did find this recent article about the possible link between EBV and our sister disease, Rheumatoid Arthritis. There's something to this, I think.

BTW, 95% of people will have EBV by the time they are 35-40. But most people get EBV, and mono, in their teens (I guess neither of us got enough action in high school). Did our late exposure to EBV trigger our bad genetics, and cause an autoimmune reaction?

More to come. But 'til then... be careful who you kiss, Watson.

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.

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.

A rose by any other name... would be something else?

The New York Times had a fascinating article in their magazine this weekend about the Undiagnosed Diseases Program sponsored by the N.I.H. The article focused on a 31 year old woman named Summer Stiers in declining health, who has spent the last 20 being undiagnosed or misdiagnosed by well-intentioned physicians. She was frequently misdiagnosed with autoimmune conditions, because her symptoms just scream "autoimmune".

The article followed her disease progression, and her experiences in Bethesda, MD being examined by a constellation of specialists from the N.I.H.

There were countless fascinating aspects of this article - I recommend you take the time to read through it. However, what stood out most to me was the difficulty physicians have in making accurate diagnoses, even now, with all of our tools and experience. The article highlights how the N.I.H. is trying to advance knowledge about both specific illnesses and the diagnostic process through the Undiagnosed Diseases Program, and it brings home how complicated the jobs of physicians AND patients are when addressed a complicated array of symptoms.

A few weeks ago I wrote about how fractured and fragmented our current of system of diagnostics are, and the article on Summer Stiers included a great discussion of this problem. Forgive the long quote - this is from page 5 - but I found this so interesting, esp in light of diagnostics in the field of autoimmunology (italics mine):

The balkanization of medicine accounts for an increasingly constrained approach to diagnosis — an approach that... is defined by a specialist’s focused knowledge rather than by some broader understanding of the patient. “This is partly because of how medicine is taught — how it has to be taught,” said Kathryn Montgomery, professor of medical humanities and bioethics and of medicine at the Northwestern University medical school in Chicago, when we spoke by telephone. “Doctors get educated to solve problems in their own terms. They’ve got only a certain set of information and experience at their disposal.”

Few physicians are trained to look at the patient as a whole, Montgomery says, with the exception of generalists like internists and pediatricians. ...

But the problem is not just overspecialization, Montgomery says; it’s the complex nature of diagnosis itself, and the difficulty of trying to teach the process in medical school. Because diagnosis involves so many intersecting and often incompatible parts, medical students have traditionally been taught to do opposite things at once when they meet a new patient: suspend judgment, but form an initial impression; look for a single diagnosis to explain all symptoms, but watch for co-morbidities; avoid the anecdotal, but pay attention to stories; expect the diagnosis to be a common disease, but don’t forget the rare ones. This dissonant approach was recently modified in some medical schools, according to Montgomery, with students now taught to begin with a “working diagnosis” that they refine as they accumulate data that either confirm or refute their first guess. But while the working-diagnosis method might clarify some things, Montgomery worries about what might be lost: a sense, as she wrote in her 2006 book, “How Doctors Think: Clinical Judgment and the Practice of Medicine,” of an alternative pathway. Because of the inherent contradictions traditionally taught in medical school, she wrote, new doctors have been able to achieve “a certain balance, a consciousness that, no matter which way they may work through a diagnosis, there is another way.”

As patients, we see similar contradictions in our roles of finding the right doctors. Do I find an older doctor... someone with lots of clinical experience? Or should I turn to someone who is fairly new out of school, who has fresh knowledge on the most modern techniques and research? Do I find a generalist or a specialist? Do I look to someone who is alternative in their approach, or have two separate doctors, one representing the "western" approach and one representing an alternative approach? When meeting a doctor for the first time, do I tell them my whole complicated history, or just focus on the day's issues?

This makes me more and more convinced that I am my own boss re: my health (see "I'm canceling everybody"). Doctors, by the very fact that they are human with limited brain-space, are fallible. We have to be our own agents, and rely on our doctors as we would rely on consultants. We have to be our own Chief Information Officers.

Sadly, the plot thickens

I'm back to reading The Autoimmune Epidemic religiously. In a previous post I discuss this book's main theme - that we are seeing an increase in autoimmune disease in our country in part because of an increase in exposure to toxic elements in our environment... from pesticides, chemicals, etc. The author provides compelling evidence that autoimmune diseases cluster in environments with more toxic waste.

I'm focused on this book because in the last few days I found out my beloved old cat, George, is pretty sick. Its his liver, his kidney, his heart, he's lost 4 pounds in 6 months... systemic yucky. Well, all the tests so far point to an autoimmune disease. No sign of cancer, no sign of thyroid problems, no heart disease.

I'm trying desperately hard not to be hysteric about this. I choose to rely on data and science, when I can. And, I'm a firm believer in "Med Student's Disease": when you read about a disease, you pretty much tend to think you have it. I'm anti-hypochondriasis...

But the coincidences demand a second glance.

• My cat probably has an autoimmune disease.
• My husband got diagnosed with Crohn's Disease (an autoimmune disease) 3 years ago.
• I was diagnosed with Psoriatic Arthritis (an autoimmune disease) in the last year.
• I had weird autoimmune like symptoms over the last few years: mono like symptoms one year, and then the next year crazy leg and foot swelling and horrible pain, and low grade fever and fatigue. The docs never quite figured out what it was - but my husband had a version of it too...

Now, I'm not a hysteric. I'm a scientist. But I'm not going to let this one go... not yet. Let's see how George's tests come out tomorrow.

Salmonella and arthritis

Ok, ok, so I wasn't going to write on the weekends. But I want to make sure to write this one down before I forget it in the haze of my day.

I'm reading the Sunday Paper, and just came across an article on the national salmonella outbreak. Apparently, some victims have now developed arthritis from the salmonella. To quote:

Dr. W. Hayes Wilson, chief of rheumatology and Piedmont Hospital in Atlanta, said some people born with the HLA-B27 antigen on their cells are predisposed to developing reactive arthritis after suffering from bacterial infections, including salmonellosis.

"Genetics are the loaded gun. Salmonella pulls the trigger" Wilson said.

I'm not quite sure what to make of this yet, but it seems like a relevant piece of the puzzle. I can only assume that either the salmonella continues to live in the body, causing the arthritis, OR more likely - the antigen triggers the autoimmune process.

Autoimmune emergency

I'm now simultaneously reading three books - the two mentioned in my post on Tuesday, and a new one - the Autoimmune Epidemic by Donna Jackson Nakazawa. In the introduction, Douglas Kerr, MD, PhD (he's the director of the John's Hopkins Transverse Myelitis Center) compares this book to Al Gore's Inconvenient Truth. He claims that Autoimmune Disease is becoming an epidemic in this country. One in 12 Americans, (and one in 9 women) will be diagnosed with an autoimmune disease. Those numbers are higher than our country's cancer rates and rates of heart disease. Even more shocking, in the last 30 years, the occurrence of these diseases has more than doubled, and may continue to increase if we don't put a stop to what may be causing this epidemic - environmental toxins.

Ms. Nazakawa, who has autoimmune disease herself, has written an incredible book. She cites both the most current research, and some of the best and brightest scientists in this field, to conclusively demonstrate that toxins in our everyday environment are causing an increase in autoimmune disease. Toxins like... pesticides on our food, plastics, chemicals in hair dye and in the foam mattresses we sleep on, exhaust from cars. And she's got the data to go along with it.

Here's what I found fascinating...It wasn't until roughly 50 years ago that it was recognized that our bodies could turn on themselves, which is essentially what autoimmune disease is. Instead of fighting toxins, our T cells (and other parts of our complex immune system) turn on our own cells, mistaking them for enemies within. But once the autoimmune process was demonstrated in the lab, each medical specialty laid claim on the autoimmune diseases closest to their work: e.g. rheumatology took the arthritises, gastro took crohns and celiac, derma took psoriasis. Unfortunately, there weren't many people left looking at autoimmune disease in general, at how it works, and how can it be controlled and prevented. So we're a bit behind in understanding the autoimmune process, let alone the immune system in general. But meanwhile - in the last 50 years, we have increased our use of environmental chemicals exponentially.

Fortunately, there are a few fabulous scientists out there studying the autoimmune process in our bodies, and in the last 10 years there has been a huge increase in research, especially in immunotoxicology. Ms. Nakazawa describes in lay language many current findings - she does a great job making a complicated process understandable.

I really recommend this book. It will scare the pants off of you.

Mistakes were made

Like our fabulous new president, I'm not afraid to admit when I don't do my homework and make an assumptions about those close to me. Like Obama, I can admit a mistake. In Obama's case, it was Tom Daschle. In my case, it was Lymphocytic Colitis (LC - damn it's hard to type Lymphocytic Colitis).

In a previous post, I mentioned that I had several auto-immune disorders, including LC. However, according to the American Autoimmune Related Diseases Association (AARDA), LC is not an autoimmune disorder. Or at least it's not listed on their website as an autoimmune disease.

Not yet, anyway.

According to the Mayo Clinic, LC occurs frequently in folks who already have other autoimmune issues, including Rheumatoid Arthritis and Celiac Disease. LC is, for many people, a mild and treatable condition. But it also involves inflammation, which I'm learning is a hallmark of many autoimmune diseases. I suspect it will make the AARDA list soon.

BTW - I'm recently enamored of the AARDA.

Thanks Mom

My lovely husband sent me this article in the NYT yesterday (here) . I'll let you all read it for yourselves, but the gist of the article is:

Researchers have long wondered how pregnant women might shape their fetuses’ development — by protecting them against later disease, perhaps, or instilling an appreciation of Mozart.

Now a group in California has discovered a surprising new mechanism by which women train their fetuses’ budding immune systems: the mother’s cells slip across the placenta, enter the fetus’s body and teach it to treat these cells as its own.

A crucial task of the developing immune system is to learn to distinguish between foreign substances and the self. It is tricky: the system must respond to outside threats but not overreact to harmless stimuli or the body’s own tissues.

The new findings show “how Mom is helping to tune that whole system early on,” said William J. Burlingham, an immunologist at the University of Wisconsin, who is not connected with the research. “It’s a major advance, very new and very exciting.”

The work could have relevance to research on topics as diverse as organ transplantation, mother-to-child transmission of H.I.V. and autoimmune disorders like Type 1 diabetes.

Now, I haven't started talking about T cells here yet - I still don't get it all myself. I'm learning that the immune system is incredibly complicated, and every book I read describes it differently. I'll write more about it as I understand it more. BUT... the take away I got from this article was:

1) our first immune responses are learned from our mothers, when we are in utero. This research will greatly enhance our understanding about how these first lessons are taught, and maybe how the immune system learns in general.

This article also illustrates the reverse of what I was talking about in yesterday's post. Not only does the mother's immune system have to be tolerant of the child it is hosting, but the child's immune system has to learn to be tolerant of its mother.

Now if I could only get Zoe to tolerate me!

New Directions

Recently I've become convinced that I don't have Celiac Disease, AND Psoriatic Arthritis, AND Psoriasis, AND Lymphocytic Colitis, AND a tendency towards Lymphoedema, AND some female irregularities. I'm certain that these are merely symptoms, and I've got a bigger problem on my hands. It turns out all of my fun conditions are auto-immune related. As I mentioned in an earlier post, I feel like all of these diseases are a gang of thugs... and I want to find the leader of the pack, and give him or her a black eye.

So for the next few weeks I'm going to be doing a lot of reading and writing about Auto-Immune Diseases. I'm currently reading two books on Women and Autoimmune disease (here and here), and am amazed by what I'm finding out. Women suffer from autoimmune diseases far more often then men, and it is hypothesized (by the authors of these two books) that this is in part because of our ability to bear children. Just think - for 9 months our bodies house a child who is made up of 50% foreign substance - and our bodies have to recognize that and not destroy that foreigner. Therefore, our immune systems are much more complicated then men's. And, as Lahita and Yalof mention - a machine with lots of buttons is more likely to break than a machine with just a few. We girls are just more complicated.

Well, anyone could have told you that...