Beating Crohn's

IBD Less Common in Sunny States

2012-01-17T00:34:00.003-05:00

I've blogged about this before, but there was a recent study that revealed that people who live in sunnier regions of the United States are less likely to develop IBD. It confirms previous research conducted in Europe that generated the similar results. The study followed over 200k participants that began the study without symptoms of IBD.

The basic explanation for this is Vitamin D. There's a strong role for Vitamin D in the immune response and IBD patients (including myself) often have low Vitamin D levels. So stop postponing that vacation to Hawaii already!

Here's an excerpt:

"A leading explanation for this north-south gradient in the risk of ulcerative colitis and Crohn's disease may be differences in exposure to sunlight, or UVB radiation, which is generally greater in southern latitudes," wrote Dr. Hamed Khalili, of Massachusetts General Hospital in Boston, and colleagues.
"UV radiation is the greatest environmental determinant of plasma vitamin D, and there is substantial experimental data supporting a role for vitamin D in the innate immunity and regulation of inflammatory response," they noted.

Could Sucralose (Splenda) Be A Contributor?

2011-11-13T14:07:00.004-05:00

Saw an interesting article that suggested that Splenda (sucralose) was potentially to blame for the rapid rise in IBD in Canada.

I've never historically eaten any foods with Splenda in them, but perhaps other artificial sweeteners have a similar effect on the gut.

An excerpt:

The theory that Splenda may be a culprit in the rise of inflammatory bowel disease (IBD) appears to be a reasonable one, echoing the results from a 2008 study published in the Journal of Toxicology and Environmental Health, which discovered that Splenda:
Increases the pH level in your intestines, and
Reduces the amount of good bacteria in your intestines by 50 percent!

Bilberries May Help Control IBD

2011-11-13T13:59:00.002-05:00

Bilberries (or huckleberries) may help control symptoms of inflammatory bowel disease. Researchers in Europe suggest positive results (see article) from a study of colitis in mice. Blueberries are a close relative to bilberries, so they might serve as a more accessible alternative.

Here's an excerpt:

Bilberries, which are a close relative to blueberries, contain anthocyanins, pigments that have antioxidant, anticancer, and anti-inflammatory properties. Previous studies show bilberries are effective in the management of diarrhea, which is one of the main characteristics of inflammatory bowel disease.

Crohn's Disease Genes Linked to Multiple Illnesses

2011-11-13T13:51:00.003-05:00

According to a study from the University of Edinburgh, apparently some of the genes linked to Crohn's Disease are also linked to breast and prostate cancer, Hodgkin's lymphoma, high cholesterol, and obesity. Obviously, if you're suffering from Crohn's, you're probably thinking ... "Oh man, what else is going to get thrown at me!". But it's important to know that your genes may cause other problems with your health and it lets you be on the lookout for them (along with taking preventative action).

Here's an excerpt from the article linked to above:

The study by the University of Edinburgh has found that genes responsible for Crohn’s disease are linked with other conditions including breast and prostate cancer, Hodgkin’s lymphoma, high cholesterol and obesity.
Knowing how diseases are genetically connected could aid efforts to develop medicines and potential side-effects could be predicted and avoided.

The Low FODMAP Diet

2011-11-08T23:50:00.004-05:00

IBD and IBS must be becoming more widespread (or at least there must be more awareness about them), because I read an article in the Wall Street Journal about a new diet meant to address IBS. It's called the Low FODMAP's diet.

Here's an excerpt from the article:

The theory is that many people with IBS have trouble absorbing certain carbohydrates in their small intestines. Large molecules of those foods travel to the colon, where they are attacked by bacteria and ferment, creating the telltale IBS symptoms of gas, bloating, constipation or diarrhea.
A long list of foods—including dairy products, some fruits and vegetables, wheat, rye, corn syrup and artificial sweeteners—can potentially create such problems in susceptible people. Collectively, they're known as Fodmaps, an acronym that for stands for Fermentable Oligosaccharides, Disaccharides, Monosaccharides and Polyols.

The general theories behind this aren't anything new. In fact, they are very similar to the Specific Carbohydrate Diet in some ways. But if you look at what's "legal" vs. "illegal", there are some serious contradictions between the diets. I suppose that's not necessarily surprising, though, as IBS and IBD are different. But just interesting that one diet doesn't address both. I wonder if that hints to the cause at all?

At any rate, here's the graphic from the WSJ article that covers some of the low and high FODMAP foods:

Crohn's Disease, the Rise of Agriculture, and Gene Expression

2011-08-16T02:02:00.004-04:00

Just read a really complicated article that went way over my head in Discover Magazine, but thought I'd share it as there are some interesting theories presented.

Here's an excerpt:

So what happened? The authors posit that the 503F allele was selectively favored at some point in the past, and flanking it were the Crohn’s disease risk elevating variants of IRF1 and IL5. All things equal it is best not to have a risk for this disease, but all things are not equal. If there was a strong enough selective pressure on the target, 503F, then the downsides of the fact that it came as a “total package” with some deleterious alleles would be irrelevant. Over a long enough evolutionary time the deleterious alleles would be purified through negative selection because recombination does break apart associations, but there’s a lot of reality which consists of being between beginnings and ends.

Basically, the idea is that agriculture put a selective pressure on the genome that brought along genes that increased risk of Crohn's disease. To put that in more plain words, the rapid change in environment caused by the rise of agriculture (e.g. living off of certain grains), put pressure on the natural selection of genes. Certain gene variants (mutations) were favored in the new environment and so flourished. Unfortunately, those positive gene variants (which helped humans deal with the benefits of agriculture) brought with them negative gene variants (which increased risk of disease).

Interesting theory. The writer that's critiquing the article doesn't completely agree with the conclusion, but definitely some interesting analysis.

Been a while since I posted ...

2011-08-16T01:11:00.003-04:00

It's been quite a while since I've posted anything up here. I moved, started a new job, wife had a baby, and just generally been swamped. I've been really behind on doing any research on IBD and Crohn's but I'll likely start picking it up again. Appreciate the questions that I've been getting on here over the past couple months. Sorry for not responding to them all.

In other news, I'm coming up on two years on the Specific Carbohydrate Diet. It's been working pretty well so far (but it's time consuming!).

Broccoli Fiber Combats Crohn's Disease

2010-11-10T15:58:00.003-05:00

Saw this article in Life Extension magazine about broccoli:

An article published online on August 25, 2010 in the journal Gut reveals that fibers found in broccoli and plantain block a stage in the development of the Crohn's disease, an inflammatory bowel disease. The stage involves a process known as translocation, which is the invasion of microfold cells (M-cells) lining the colon by bacteria, particularly E. Coli, which tend to adhere to one another.
Crohn’s disease is uncommon in countries whose citizens regularly consume fibrous fruits and vegetables, while the incidence of the disease has increased in Japan with the rise of Westernized dietary habits. Additionally, some enteral feeds have been shown to result in clinical remission. “It is therefore a plausible hypothesis that dietary factors may have either harmful or protective roles in Crohn’s pathogenesis as a consequence of their effects on the interaction between the host epithelia and intestinal microbiota,” the authors write.
Dr Barry J. Campbell of the University of Liverpool and his associates tested the effects of soluble fiber from leeks, apples, broccoli and plantain in cultured human M-cells. Concentrations of 5 and 50 milligrams per milliliter plantain fiber, and broccoli fiber concentration of greater than 0.5 milligrams per milliliter helped inhibit E. Coli translocation. While apple and leek failed to show an inhibitory effect, translocation of E. Coli was enhanced by the fat emulsifier polysorbate 80, which is included in some enteral feed solutions administered to Crohn’s disease patients and is a common dietary additive. The results were confirmed in epithelial tissue samples derived from humans who underwent surgery for colon cancer or colonoscopy.
“These studies show that different dietary components may have powerful and contrasting effects on bacterial translocation across intestinal M-cells,” the authors conclude. “These effects may be relevant to the role of environmental factors in the pathogenesis of Crohn’s disease and suggest possible novel therapeutic approaches.”

This is related to an earlier post I had about broccoli. Eat your broccoli!

Caltech Researchers Discover that Gut Bacteria Affect Multiple Sclerosis

2010-08-02T22:08:00.003-04:00

I've had a couple blog posts about multiple sclerosis (MS), including links to both viral and bacterial infections. I just came across another study, this one from Caltech, that found that gut bacteria can affect the onset of MS. The researchers found that gut bacteria could influence the creation of Th17 cells (certain kinds of immune helper cells).

The bacteria aren't necessarily the entire cause of the disease, but they may represent the "environmental" component that when combined with genetic susceptibility causes the disease to kick into gear. Here's an excerpt:

Mazmanian and his colleagues don't, however, suggest that gut bacteria are the direct cause of multiple sclerosis, which is known to be genetically linked. Rather, the bacteria may be helping to shape the immune system's inflammatory response, thus creating conditions that could allow the disease to develop. Indeed, multiple sclerosis also has a strong environmental component; identical twins, who possess the same genome and share all of their genes, only have a 25 percent chance of sharing the disease. "We would like to suggest that gut bacteria may be the missing environmental component," he says.

It's amazing that inflammation of something as sterile as the central nervous system and brain could be impacted by what's going on in your gut. But there does indeed seem to be a connection. Hopefully they can find the bacteria (or type of bacteria) that triggers Crohn's Disease as well.

Key proteins that cause Celiac disease discovered

2010-08-02T21:57:00.003-04:00

Saw a few articles (ABC News, Geek System) about a study in Melbourne that identified several proteins that cause Celiac Disease. There are apparently three or four different protein fragments that can trigger the disease. Celiac is caused due to an allergic reaction to these proteins. The researchers hope to create an immunotherapy treatment where patients can build up immunity to those proteins. Very interesting development and certainly gives hope for the more than 2 million people in the US that suffer from the disease.

Here's an excerpt about the potential immunotherapy treatment:

Professor Anderson says the findings are being used to develop a new class of drugs, called peptide-based immunotherapy.
This involves injecting patients with a small amount of the toxic peptides to "desensitise" their body to them.
The researchers say the first phase of trials of the therapy to assess safety and tolerability were completed in June, and final results are expected in coming months.

Definitely great news.

Controversial treatment for MS - and another angle for research of IBD

2010-07-13T22:26:00.006-04:00

I don't know much about multiple sclerosis, but I see articles about it all the time as I monitor news about autoimmune diseases. I came across an article about a controversial treatment for MS that a person in Britain couldn't get because it hasn't been officially sanctioned by the government yet via clinical trials. For a person with IBD, I found the treatment less interesting than what it suggests about the potential cause of the disease.

Here's a really short excerpt just to give you an idea:

In 2005, Zamboni’s wife Elena was diagnosed with MS and he embarked on a mission to find out everything about it, from poring over medical literature dating back 100 years or more, to using state-of-the-art body-imaging techniques.
His conclusion was that this wasn’t only an autoimmune disease, but also a vascular one, caused by restricted, blocked, malformed or twisted veins in the trunk and neck. A small study showed that 90 per cent of his patients had venous obstruction. He named the condition chronic cerebrospinal venous insufficiency (CCSVI) and went further, postulating that an excess of iron, which causes inflammation and cell death, was responsible for tipping the immune system out of balance, resulting in MS symptoms.

The treatment was to unblock these twisted or malformed veins (similar to an angioplasty). What I found interesting is that an autoimmune disease, in this case MS, might not just be caused by the environment or genetic susceptibility, it might also include a physical malformation in the body that can be reversed! Might there be something similar with IBD? They should add that to the list of things to research.

UPDATE (8/2/2010): Saw an article in the WSJ about a study that refutes the Zamboni theory regarding jugular vein blockage. Jury is still out I suppose.

Why some people with IBD may not respond to corticosteroids

2010-07-13T21:18:00.004-04:00

We all know that corticosteroids are one of the first drugs prescribed to deal with IBD. But it doesn't always work for everyone. Why?

I just came across a press release about new research that uncovered why many people with lupus (another autoimmune disease) do not respond to corticosteroids - or at least steroids in high doses. An excerpt that explains why this is the case:

Currently, those with lupus and other autoimmune diseases, commonly treat the condition with corticosteroids to suppress their overactive immune system and prevent it from attacking healthy tissues which can result in symptoms such as inflammation, pain and organ damage.
These steroid treatments work by killing certain immune system cells, including plasmacytoid dendritic cells (PDCs) that overproduce type 1 interferons, an immune system substance that contributes to lupus and other autoimmune diseases. However, unlike other conditions, steroid treatments are not as effective against these cells in those with lupus.
By largely studying children with systemic lupus erythematosus (SLE), BRI scientists in collaboration with scientists at Dynavax in Berkeley, CA, were able to solve the mystery behind the resistance. They determined that two immune system proteins known as toll-receptor 7 (TLR7) and toll-receptor 9 (TLR9), cause an activation of PDCs—the very cells steroids target—negating the effects of treatment. BRI scientists reported their findings in the June issue of the journal Nature.

A similar resistance mechanism might be at play with people with IBD (and other autoimmune diseases). It hasn't been proven yet obviously, but it's certainly something to consider when you're working with your doctor to deal with a serious flare-up. The traditional prednisone or budesonide (Entocort) may not work for you simply because your body works against the mechanism of the drugs.

Two new drugs that could be used for autoimmune and inflammatory diseases

2010-07-09T02:29:00.003-04:00

Saw two recent articles about new drugs that could be used to treat autoimmune and inflammatory diseases, including multiple sclerosis, inflammatory bowel disease, arthritis, and others.

The first article was about a cancer drug, bortezomib, that was used in an animal study to treat inflammatory disease. The cancer drug induced cell death in only the harmful (active and proliferating) T-cells.

The second article was about a new protein from Compugen called CGEN-15001 that was found to abolish recurring relapses of multiple sclerosis in an animal study. The protein also delayed the onset of the disease. The protein apparently has some effect on the regulatory pathways in the immune system.

Both seem pretty interesting.

Virus Plus Gene Mutation Spurs Crohn's Disease in Mice

2010-07-08T23:17:00.004-04:00

Saw an article about a new study that found a specific link between a gene mutation and virus that caused Crohn's Disease in mice. The study found that mice that had a gene variant linked to Crohn's Disease only developed Crohn's symptoms when they were infected by a specific, common norovirus called MNV.

Here's an excerpt:

Two years ago, the researchers at Washington University School of Medicine in St. Louis and others discovered that mice with an ATG16L1 gene variant associated with Crohn's disease in humans develop similar abnormalities in gut immune cells called Paneth cells. But the mutation alone wasn't enough to trigger Crohn's disease.
In a routine screening, the team later found that mice with the gene variant developed Crohn's disease symptoms within seven days after exposure to the MNV norovirus.
The study appears in the June 25 issue of the journal Cell.
It's been suspected that autoimmune and other diseases might be influenced by viral infections, but "this is the first really clear indication of a disease caused by a susceptibility gene and a specific virus," study co-leader Thaddeus Stappenback said in a journal news release.

That last statement is important. They found a specific viral infection that can trigger the disease for a specific genetic predisposition. Given there are many genetic markers for CD, there may be many possible viral infections (or bacterial infections) that can trigger the disease. So there is lots of research still to be done. But this is an important finding. As an aside, I had another recent post about a bacteria triggering arthritis in mice, so there are many angles on this research.

Nice overview of IBD, CD, and UC from Duke Research

2010-07-08T22:44:00.006-04:00

Came across this nice 50 min overview video from Duke (my alma mater) covering different types of manifestations and management recommendations for inflammatory bowel disease, including both Crohn's Disease and Ulcerative Colitis. Highlights of note:

minute 36:00 - The speaker comments on clinical protocol for inducing remission right around minute 36. Gives you an idea of what your doctor is basing their recommendations on.
minute 39:30 - Non-Anti-TNF agents that are under clinical trial and study for treatment of IBD. Everything from helminthic therapy to stem cell treatment.

Broccoli extract effective against IBD and UC

2010-07-07T03:30:00.004-04:00

Saw an article about how a plant-derived compound called Phenethylisothiocyanate (PEITC) showed potential anti-inflammatory activity and reversed many symptoms of ulcerative colitis. The PEITC compound is found naturally in the Brassica genus of plants, which includes cabbage, cauliflower, watercress, and broccoli.

An excerpt:

"I tested this substance in a mouse model that is already established and widely used. What we found is that it not only alleviates several clinical signs of ulcerative colitis — for example, it attenuates the damage that occurs in the colon tissues and colon epithelium, as well as the clinical signs like diarrhea and blood in stool. The weight loss is a major sign in colitis and that was alleviated, too," Dey added.

Good evidence to suggest that you should eat your greens! If you hate broccoli, you'll just have to get over it cause it's good for you.

Alopecia Areata and Narcolepsy both confirmed as autoimmune diseases

2010-07-07T02:52:00.005-04:00

The list of health issues that are being categorized as autoimmune diseases are just stacking up! Saw an article a couple weeks ago that alopecia areata, a disease that causes hair loss and baldness, was caused by an autoimmune response. And a more recent article confirmed that narcolepsy is also autoimmune.

In alopecia areata, they found that some genes which attract killer immune cells are overexpressed in hair follicles. The immune cells attack the follicles and lead to rapid hair loss. In narcolepsy, the body's immune system attacks cells responsible for creating a certain hormone (hypocretin) in people's brains that's responsible for keeping people awake. The lack of hypocretin causes people to randomly and unexpectedly fall asleep.

It's amazing how many health problems are falling under the autoimmune category.

Chinese Fungus a Potential Immunosuppressant to Treat MS

2010-06-23T23:24:00.002-04:00

Saw an interesting article in the Wall Street Journal about a new drug being introduced by Novartis called fingolimod. The drug is used to suppress the immune system, treating some of the symptoms of multiple sclerosis. I'm generally not a big fan of immunosuppressants, but the article does suggest why many alternative therapies work.

The drug is based on a fungus known as "winter-insect-summer-plants". An excerpt describing the fungus:

Dr. Fujita says he reasoned that an even more powerful immunosuppressant chemical ought to be present in a group of Asian fungi known in Chinese and Japanese as "winter-insect-summer-plants." These fungi attack insects in the winter with their chemical arsenal. By summertime, the insect is dead and its corpse has been transformed into a vessel for the blooming fungus. Ironically, the same properties that make the chemical deadly in the insect world may also have a helpful side for people suffering from certain autoimmune diseases, in which an overactive immune-system response causes the body to attack its own cells.

There are many natural remedies used in Chinese and Japanese medicine, including herbs and fungus. Perhaps many of these work because they are immunosuppressive.

When Good Germs Go Bad - Friendly Bacteria Triggers Arthritis in Mice

2010-06-23T22:52:00.003-04:00

Saw a really interesting article in Scientific American about a study regarding a link between a specific strain of bacteria and rheumatoid arthritis (RA) in mice. The study found that the introduction of a single type of bacteria could increase the amount of IL-17 (interleukin 17), a protein that signals the immune system to cause inflammation, in the mouse. The "friendly" bacteria that causes this accelerated the onset of arthritis in the mice. The mice were selected to already be genetically predisposed to having arthritis, so all mice in the study developed arthritis. But the mice that were given the bacteria developed RA much more quickly.

Why is this important? This could mean that exposure to even a single bacteria or virus could trigger an autoimmune reaction in genetically susceptible individuals. Here's an excerpt:

Mathis emphasized that one should not take away from these mouse studies "that mice or humans can 'catch' an autoimmune disease or arthritis," she says. She added that the better way to think about it is that individuals have varying degrees of genetic susceptibility, and when exposed to certain environmental factors may then go on to develop disease. "It's really an interaction between genetics and environment," Mathis says.

Crohn's Disease or Inflammatory Bowel Disease (IBD) may have a similar pattern to RA. It could also mean that there is a single bacteria or virus responsible for the disease. Or ... it could also mean that there are any number of bacteria or viruses that trigger the disease. Either way, it's a very study and reinforces previous theories and studies I've seen.

Prostaglandin D2 a potential treatment for Ulcerative Colitis

2010-06-21T21:59:00.003-04:00

A recent study may suggest a new treatment for ulcerative colitis. The study, to be published in the journal Proceedings of the National Academy of Sciences, found that people with ulcerative colitis that have been in remission for a long time-period have higher levels of Prostaglandin D2 than those that don't. It's unclear whether the higher levels of the chemical are a result of being in remission or the cause of the remission, but the study is interesting nonetheless as it suggests follow-on research.

FDA requires cancer warning on TNF blockers (old news)

2010-06-21T21:38:00.004-04:00

I've thought for a while that TNF blockers and other immunosuppressive drugs may actually be counterproductive in the long-run in treating Crohn's Disease and IBD. The point of TNF-alpha in the immune system is to promote the fight against tumors (TNF = tumor necrosis factor). What happens if you suppress that immune response? Your body may be missing tumors that it should be fighting. A recent article prompted me to take a look at the FDA warnings for TNF-alpha blockers. Apparently, the FDA started requiring cancer warnings on TNF blockers back in August of 2009 -- here's the FDA press release. I think dozens of cancer cases in children taking TNF-blockers prompted the FDA to add the box warning.

I definitely see the value of these drugs in the short-term to help get the inflammation under control, but long-term use doesn't seem like a solution. (Hence why I'm avoiding them!)

Why Pregnancy Pushes Autoimmune Diseases into Remission

2010-06-17T21:44:00.006-04:00

A friend of a friend of mine has had Crohn's for many years. But when talking to her, she mentioned that during her pregnancy all her Crohn's symptoms completely subsided and she was in "remission". Why? This apparently is a common phenomenon for pregnant women with autoimmune diseases -- during pregnancy their diseases go into remission.

A new study from the University of Michigan may explain why. Apparently the expression of an enzyme called pyruvate kinase is reduced in immune cells in pregnant women. The reduction in this enzyme "dials-down" the immune system supporting the acceptance of the fetus.

An excerpt from the article:

In his search to explain the phenomenon, Dr. Petty knew to look for a metabolic pathway ormechanism with two characteristics. It had to "dial down" the intensity of the normal immune response, an action needed so that a pregnant woman does not reject the fetus, which has proteins from the father that are "foreign" to the mother. At the same time, such a mechanism must support cell growth needed by the developing fetus.

The activity of the enzyme pyruvate kinase–and its product, pyruvate–fills both roles: promoting cell growth while modifying the immune response. Because pyruvate kinase activity is depressed duringpregnancy, cell metabolism supports an increased production of lipids, carbohydrates, amino acids, and other substances that support cell growth.

This suggests an interesting alternative therapy or treatment option for the future (and I'm not suggesting that you just go get pregnant!). There may be a way to use this immune pathway in a drug therapy. It doesn't necessarily identify or address the root cause of IBD, but it could lead to another alternative therapy.

Gene Mutations Offer Clues to Autoimmune Disease

2010-06-17T20:52:00.003-04:00

Saw a couple articles (BusinessWeek, Wired.com, ScienceNews) commenting on a story in Nature about a study that found that variations in a single gene could result in different types of autoimmune diseases, including Crohn's Disease and diabetes.

An excerpt:

The gene in question encodes an enzyme called sialic acid acetylesterase or SIAE, which regulates the activity of the immune system’s antibody-producing B cells. About 2 percent to 3 percent of people with autoimmune disorders have defects in the enzyme that allow B cells to run amok and make antibodies that attack the body, a team led by Shiv Pillai of Massachusetts General Hospital in Charlestown and Harvard Medical School reports online June 16 inNature.
“It’s a seminal paper because it is so applicable to a wide variety of autoimmune diseases, says Judy Cho, a Yale geneticist not associated with the study. The finding suggests that enhancing the enzyme’s activity could help treat disease in people with autoimmune disorders.

Definitely an interesting finding!

Resveratrol Improves Inflammatory Bowel Disease Symptoms

2010-06-17T20:37:00.003-04:00

Saw an article about a new study that found that resveratrol, an antioxidant found in grapes, improved symptoms of inflammatory bowel disease (IBD).

Here's an excerpt from the article:

Resveratrol is a phytonutrient (phyto means “plant”) that is the subject of considerable research because of its anti-inflammatory, antioxidant, anti-tumor, and immune system boosting properties. Previous studies have suggested that resveratrol enhances brain function and builds resistance to stroke, helps withweight loss, inhibits prostate cancer cell growth, and protects against diabetes.
Resveratrol’s anti-inflammatory abilities are of special interest for possible treatment and prevention of inflammatory bowel disease, of which ulcerative colitis and Crohn’s disease are the two most common types. In the current study, which appears in theEuropean Journal of Pharmacology, researchers conducted a placebo-controlled study in which one group of mice were given 20 mg of resveratrol per kilogram of food and the other group received placebo. The study period lasted 30 days.

Grape juice is my primary dietary source of carbohydrates (because it is SCD compliant), so this is encouraging news. It also reinforces why the SCD diet may work.

Virus infection may trigger unusual immune cells to attack the brain and spinal cord in multiple sclerosis

2010-06-16T00:10:00.003-04:00

I came across a really interesting article regarding a possible causative mechanism for multiple sclerosis (MS). As you most likely know, MS is an autoimmune disease (similar to IBD and Crohn's) where immune cells misguidedly attack the body's own cells. In the case of MS, the body is attacking the protective sheath around major nerves. In the case of IBD, the body is attacking your intestinal tissue.

The above mentioned article found that a viral infection could incite certain rare immune cells to be released in the body that attack both the virus and (in the case of MS) nerve cells. The rare immune cells do this because they have receptors for both the virus' proteins and proteins present in nerve tissue (myelin). I found this research interesting given the recent talk from Amy Proal that I blogged about regarding the viral and bacterial metagenome and the recent study (similar to the MS one) that found a possible link between errant T-cells and diabetes.

The study about MS suggests that there's not necessarily a single virus that causes the disease, but instead a combination of factors that generate the errant T-cells:

The authors explained that it's possible that multiple viruses could influence susceptibility to multiple sclerosis. The ability of any particular virus to contribute to the disease could depend on an individual's own repertoire of other predisposing genes, exposure to other predisposing environmental factors, and the random chance that T cells had been generated that recognize a myelin protein and a pathogen.

Receptors on T cells are randomly generated during their development. This observation helps explain why multiple sclerosis is partly a matter of chance. Some people with a genetic predisposition and environmental exposure develop the disease, while others with similar genetic predisposition and environmental exposure do not.

This suggests some really interesting (and challenging) directions for future research. Many current studies are focusing on finding a single bacteria or virus (e.g. MAP) that someone is infected with or a single genetic mutation (e.g. NOD2) that cause IBD. This is a potentially flawed approach, though. This study suggests that even after the infection is cleared, the errant T-cells that cause the autoimmune reaction may persist (i.e. there's no smoking gun). It certainly makes finding the root-cause difficult! But it suggests a different direction to take research.

Teaching Kids to Cope with IBD

2010-06-15T23:48:00.003-04:00

Saw this article about a study conducted at the University of Georgia with teenage girls suffering from IBD. They found that teaching the young girls "coping" and "community" skills had a positive impact on their physical symptoms. They also found that mental distress decreased -- as they called it "catastrophic thoughts" (pretty scary sounding if you ask me).

Here's an excerpt:

"We saw significant improvements in these adolescents' physical symptoms and coping strategies following treatment," said Ronald Blount, professor of clinical psychology at UGA and an author of the study. "Parents, who were also involved in the study, reported reductions in catastrophic thoughts related to their daughters' pain and improved behavioral reactions related to their daughters' physical symptoms. We aimed to teach parents to become coaches for their daughters to help them better manage their symptoms."

Inflammatory bowel disease is a pretty life changing illness, though, and one quite difficult to talk about with others (particularly if you're a teenager), so I can certainly appreciate how important it is to teach young people these coping strategies. Stress certainly may play a contributing role in the disease, so stress reduction strategies may be helpful. The next step for the researchers is to expand the study to a larger population.

Meat Proteins Linked to Bowel Disease in Women

2010-06-07T13:15:00.007-04:00

A new study from France revealed that eating lots of animal protein appears to increase the risk of inflammatory bowel disease (IBD) in women. The study was conducted on 67,000 women in France over a long time period to find risk factors for different diseases, including cancer and other common illnesses. There are no conclusions that are being drawn from the study, but it does suggest that diet does potentially play a role in the disease.

An excerpt:

Women who consumed the most protein were at more than triple the risk of being diagnosed with IBD, the researchers found; animal protein accounted for most of the risk. Risk was specifically associated with high intake of meat and fish, but not with dairy products or eggs.
While experts have long suspected that diet might play a role in inflammatory bowel disease, Carbonnel and his colleagues note, the only links identified previously were with eating a lot of fats and certain kinds of sugars. Those studies were more prone to error than forward-looking or prospective studies like the current investigation. There have also been several studies linking vitamin D deficiency to IBD.

Another excerpt regarding the potential link to IBD:

Meat could contribute to inflammatory bowel disease risk because digestion of animal protein produces many potentially toxic "end products," such as hydrogen sulfide and ammonia, the researchers note. Also, Carbonnel pointed out, a high-protein diet could alter the mix of bacteria that live in the colon.

The article doesn't comment on it, but I would argue that there is potentially another possible causation here. The reasons suggested are that the high intake of proteins is either generating toxic end-products or causing dysbiosis of the bacterial mix. If that were the case, though, this type of correlation would be present with other types of animal protein sources, including dairy and eggs. But there was not. (As an aside, I would also expect that other food types - e.g. starches, sugars, etc. - also produce these types of toxic end-products as well). I think another alternative cause could be the bacteria present in meat and fish stocks. Contamination from these food sources (e.g. MAP), could also be an explanation. Hopefully that's a third alternative they'll do additional research on. Either way, interesting study.

Probiotic in breastmilk reduces painful cramps

2010-06-03T14:01:00.003-04:00

Thought this one was interesting. Apparently the bacteria Lactobacillus reuteri found in breastmilk decreases the force of muscle contractions associated with inflammatory bowel disease (IBD). It is passed on from mother to baby in breastfeeding. Interesting, but might be a tough one to add to your supplement list.

Here's an excerpt:

"It might not be possible for most of us to get breast milk from the tap," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "but we can still benefit from some of the life-supporting substances it carries. This research shows that the relationship between humans and microbes can be beneficial for both. The Lactobacillus finds a new home, and we're no longer up tight."

Amy Proal on Viral and Bacterial Metagenome

2010-06-02T12:09:00.004-04:00

Just watched a really interesting talk by Amy Proal about how the interaction and symbiosis (i.e. reinforcing relationship) between bacteria and viruses could lead to autoimmune disorders by interfering with Vitamin-D receptors (VDR's). I've embedded the video below, but here's a link to the post. It looks like she's working on some really interesting research.

The idea is that autoimmune disorders are caused by multiple bacteria and viruses working together to suppress the immune response. This causes a vicious cycle as it supports additional bacterial and viral infection. She suggests that traditional therapies like immunosuppression (which I have mentioned repeatedly seems counterintuitive) may actually prolong and worsen diseases in the long run. They have been working on alternative therapies that are meant to boost the innate immune response. Her blog seems pretty interesting as well, so worth a look as well: http://bacteriality.com/.

Crohn's Disease on the Rise in Scotland

2010-05-18T12:18:00.004-04:00

Saw an article in BBC News about how the incidence of inflammatory bowel disease has doubled in Scotland since 1980. It's unclear why there has been such an increase in that particular region relative to other European countries. But at this point, Scots are apparently the most likely Europeans to develop Crohn's Disease.

Antibiotics in Infancy Potentially Linked to IBD Risk

2010-05-10T19:35:00.003-04:00

A small study showed that there might be an increased risk of IBD for infants that are given antibiotics in their 1st year of life. The study compared 36 children with IBD with 360 children that did not have IBD. 60% of the group with IBD had been given antibiotics compared to only 40% for the non-IBD group. The difference was even more pronounced for boys than girls. The study suggests a possible root cause or causative agent in the development of the disease. But again, this was a very small study, so this just suggests areas for additional research.

Anti-TNF Decreases Presence of MAP

2010-05-06T16:40:00.003-04:00

I only saw the abstract of this one. There was a study that found that taking anti-TNF drugs, in this case infliximab (i.e. Remicade), reduced the occurrence of mycobacterium avium paratuberculosis (MAP) bacteria in people suffering from Crohn's. Specifically, they just measured the change in MAP antibodies in the blood, but it would suggest that Remicade supported the body's fight against any MAP infection. I've had a couple posts on MAP, so I like to monitor research in this area. Interesting finding that supports the efficacy of these drugs (although admittedly I don't take them).

Discovery Prompts New Theory on Cause of Autoimmune Diseases

2010-05-06T16:26:00.005-04:00

Saw an article in ScienceDaily about a new theory on the cause of autoimmune diseases, including Crohn's Disease. Researchers discovered a protein (or peptide) fragment that's capable of causing diabetes in mice. The basic hypothesis is that the unusual introduction of these peptides allows errant T-cells to escape the thymus and make there way to other parts of the body where they initiate immune responses associated with autoimmune diseases. These errant T-cells that are autoreactive (or that react to your body's own cells) are normally deleted by the immune system. However, the introduction of these rare peptides causes the deletion procedure to not work properly.

Here's an excerpt:

In the April 23, 2010, issue ofImmunity, Drs. Brian Stadinski, John Kappler and George Eisenbarth propose that the unusual and rare presentation of protein fragments (peptides) to the immune system allows autoreactive T cells to escape the thymus and trigger autoimmune disease. The findings could lead to a new strategy for preventing type 1 diabetes.
"The immune system normally deletes dangerous, autoreactive T cells that recognize 'self' peptides, which are a normal part of the organism," said Dr. Kappler, Professor of Immunology at National Jewish Health. "We believe autoreactive T cells in diabetes and other autoimmune diseases escape destruction in the thymus because they never see these poorly presented peptides there. But the T cells do encounter those peptides elsewhere in the body and trigger an autoimmune attack."

Pretty fascinating if the theory is correct. It could also suggest very new areas of research for treatment options.

Olive Oil Good, Aspirin Bad

2010-05-04T13:27:00.003-04:00

Saw results of two different studies. One was about how Olive Oil (specifically oleic acid) helps to prevent inflammatory bowel disease. The second was about how aspirin increases the risk of Crohn's Disease by five times!

Recent Review of Diet's Role in Inflammatory Bowel Disease

2010-05-01T15:50:00.003-04:00

Came across this recent survey (PDF) of the different dietary causes and treatments of inflammatory bowel disease, including Crohn's Disease. Nice article that touches on several different dietary alternatives and their efficacy (when tested in controlled studies). Here's the abstract of the article (cut-and-pasted):

Many studies have looked at connections between diet, etiology, signs and symptoms associated with inflammatory bowel disease (IBD). Although these connections are apparent to clinicians, they are difficult to prove qualitatively or quantitatively. Enteral feeding and polymeric diets are equally effective at bringing about remission in Crohn’s disease (CD). Parenteral feeding is also effective, although none of these methods is as effective as corticosteroid therapy. However, enteral feeding is preferred in the pediatric population because linear growth is more adequately maintained via this route. Exclusion diets in patients brought into remission using an elemental diet have been shown to maintain remission for longer periods. Studies that aim to isolate culpable food groups have shown that individuals react differently on exposure to or exclusion of various foods. The commonly identified food sensitivities are cereals, milk, eggs, vegetables and citrus fruits. Studies that have looked at gut mucosal antigen behavior have shown higher rectal blood flow, in response to specific food antigens, in those with CD over healthy subjects. Exclusion of sugar shows little evidence of amelioration in CD. Omega 3 fatty acids show promise in the treatment of IBD but await larger randomized controlled trials. Patients frequently notice that specific foods cause aggravation of their symptoms. Whilst it has been difficult to pinpoint specific foods, with advances in the laboratory tests and food supplements available, the aim is to prolong remission in these patients using dietary measures, and reduce the need for pharmacotherapy and surgical intervention.

Of course the conclusion of the study basically just says "we need to do more research", but that's to be expected.

PPAR-gamma Protein Key to Inflammatory Bowel Disease

2010-05-01T15:27:00.004-04:00

Researchers have found a new potential treatment option for inflammatory bowel disease. The protein PPAR-gamma was found to help restore the body's natural defenses against gut infections from bacteria and could be used as a treatment for Crohn's Disease.

Here's an excerpt:

Samples taken from the colons of humans diagnosed with Crohn's disease also show reduced levels of the antimicrobial peptides, or defenses, regulated by the PPAR-gamma protein, they wrote.
Chamaillard said foods or diets containing conjugated linoleic acid (CLA) can also boost PPAR-gamma activity and have been shown to improve colitis and colitis-associated cancer.
CLA is primarily found in milk and meat products.
"In the short-term, managing the disease is what we are looking at, but it may also be that in the future we could develop a way of stopping it," Chamaillard said.
But he added that curing Crohn's disease would mean being able to identify those at highest risk before they contracted it and then being able to boost PPAR gamma-related defenses to ward it off -- both areas that would need more research.

So how could you add more CLA to your diet? I checked out the CLA Wikipedia page and found the following:

Of all foods, kangaroo meat may have the highest concentration of CLA.^[34] Food products (e.g. mutton and beef) from grass-fed ruminants are good sources of CLA, and contain much more of it than those from grain-fed animals.^[35] In fact, meat and dairy products from grass-fed animals can produce 300-500% more CLA than those of cattle fed the usual diet of 50% hay and silage, and 50% grain.^[36]
Eggs are also rich in CLA, and it has been shown that CLA in eggs survives the temperatures encountered during frying.^[37]
Some mushrooms like Agaricus bisporus and Agaricus blazei, are rare vegetable sources of CLA.^[38]^[39]

Very exciting to see research being done (and producing results) regarding natural methods of treating Crohn's. I'm looking forward to seeing how this research advances. In the meantime, stock up on the kangaroo burgers.

Pathobionts, Dysbiosis, and IBD

2010-04-25T18:27:00.004-04:00

Saw an article about some research at Caltech. Biologists have identified bacteria that lie between the traditional categories of "symbionts" and "pathogens". An example is the Helicobacter hepaticus bacterium. An excerpt:

"The bacteria appear to have struck a deal with their host," Mazmanian says. They keep their own numbers low so they don't overwhelm the immune system, and in return, the immune system leaves them alone. "The bacteria need the secretion system to put the host in 'don't attack' mode." In return, the presence of the bacteria does not induce inflammation, as would be the case with a pathogen that has not evolved a similar "agreement."
"There has to be communication. It could be peaceful—as is the case for symbionts—or it could be an argument—as is the case for pathogens. But when this molecular dialogue breaks down, it's probably harmful to both microbe and man," Mazmanian says.
Disrupt that communication, and the balance gets thrown out of whack. "Inflammation leads to cancer, and this bacterium has been associated with inflammation and colon cancer in animals," he says. Understanding if dysbiosis causes disease in humans could lead to therapies based on restoring the healthy microbial balance in the gut.

Stress Aggravates IBD

2010-04-18T10:55:00.004-04:00

Saw this article commenting on an upcoming study that will be published in the American Journal of Gasteroenterology. The study found that stress was linked to a more than twofold increase in the risk of symptom flare ups in IBD sufferers. Here's an excerpt:

Stress had long been among the main environmental factors linked to the flare-up of symptoms in some individuals. This theory, however, had never been clinically proven.

According to the study published in the American Journal of Gastroenterology, stress is associated with a more than twofold increase in the risk of symptom flare ups in sufferers.

Such a link was not seen in other factors suspected of triggering IBD symptoms such as the use of antibiotics or non-steroidal anti-inflammatory painkillers, and infections including colds, pneumonia and urinary tract infections.

"This is among the first evidence to show that the perception of stress had a direct association with disease course," said lead researcher Charles N. Bernstein, stressing that learning better stress management methods could help treat the condition more effectively.

Here's an excerpt from another article on the same topic suggesting a possible reason for the connection:

There are biological reasons to believe that a person's response to stress would trigger or worsen IBD symptoms, Bernstein and his colleagues note.

The sympathetic nervous system, which jumps into action during times of stress, acts on the lining of the colon, and might exacerbate existing inflammation. There is also evidence that stress hormones may help harmful bacteria take up residence in the intestines, which might, in turn, affect symptoms.

Combination Drug Therapy for Crohn's

2010-04-15T20:46:00.002-04:00

Read a few articles (USNews, WebMD) about a new study that showed that a combination of azathioprine and biologics are more effective in treating Crohn's Disease than taking each individually in succession. Normally doctors treat Crohn's by prescribing steroids. If steroids don't work, doctors will move on to azathioprines and then finally biologics if the other two don't work.

Here's an excerpt:

Doctors now start treatment of Crohn's disease with steroids, Sandborn said. If the steroids do not provide relief from the abdominal pain, nausea, fever, weight loss, diarrhea and othersymptoms of the condition, the next step is to use azathioprine, which reduces immune system activity broadly. Only if that fails will they try biologics, newer treatments that include monoclonal antibodies such as infliximab (Remicade). These drugs target a specific part of the immune system.
The trial showed that the azathioprine-alone step should be skipped. "This study suggests that the therapy that follows steroids should include a biologic," Sandborn added.
Therapy with both azathioprine and infliximab appears to be the treatment of choice if steroids are not effective, Sandborn said.
"What this trial shows is that the most effective strategy is combination therapy," he said.

Definitely an interesting finding and good that doctors are finding a more optimal way to treat with traditional medicine.

Genetic Variation Not the Only Cause of Crohn's Disease

2010-04-07T13:32:00.003-04:00

Saw an article that commented on a recent study of Danish people and thought it was interesting. The basic conclusion was that the NOD2/CARD15 gene variations previously considered a marker for Crohn's Disease actually do not have a statistically significant association with the disease ... at least for the Danish population. This certainly runs counter to previous studies.

Here's an excerpt:

The study, was conducted to estimate the likelihood that three particular genetic variants in the NOD2/CARD15 gene are related to the risk Crohn disease in the general population.
The population-based study genotyped 43 596 Danish people followed between January 1976 and July 2007. Using a logistic regression model (used to predict the probability of an occurrence) physicians estimated the risk of Crohn disease in the general population.
"Surprisingly, we found no statistically significant association between NOD2/CARD15 genetic variants and Crohn disease in either of the two general population studies that we analyzed, which suggests a low penetrance of the genetic variants in the European general population," write Dr. Børge G. Nordestgaard, Herlev Hospital, University of Copenhagen, Denmark and coauthors. (Penetrance is the degree to which the gene causes the disease.)
The authors conclude that the penetrance of NO2D/CARD15 genetic variants in relation to risk of Crohn for the Danish population was lower than might have been expected from previous European case-control studies. This should be considered when advising healthy individuals in whom these genetic variants are discovered.

What might this mean? Does this mean that genetic variations do not play a role in Crohn's Disease. Not necessarily. More likely it means that there are many contributing factors and many possible causes - not just one genetic variation. Another excerpt from the note:

In a related commentary http://www.cmaj.ca/embargo/cmaj100300.pdf, Dr. Katherine A. Siminovitch and coauthors write that these research findings reinforce the fact that common diseases have many causes and that in these diseases, the effect of any single gene variant on risk is usually small. This underscores the current challenge in realizing the potential of personalized medicine (use of an individual's specific information to select or optimize preventive care and therapy).

It'll be interesting to see how the research community comments on this in relation to previous studies.

Nlrp3 protein and Crohn's disease

2010-03-20T14:12:00.002-04:00

Saw an article about the Nlrp3 protein and it's relationship to Crohn's and Colitis. Here's the full press release. Here's an excerpt:

Researchers demonstrated that in a mouse model of colitis, Nlrp3 plays a pivotal role in keeping the intestinal tract intact, thus preventing further damage that occurs if intestinal bacteria leak into the body.

Nlrp3 works by anchoring a large, multi-protein complex known as the Nlrp3 inflammasome where the messenger protein interleukin 18 (IL-18) is made.

IL-18 belongs to a family of molecules known as cytokines, which shape the body's immune response. In this study, researchers showed IL-18 produced by the Nlrp3 inflammasome helped mice maintain healthy colon by triggering production of more epithelial cells to compensate for those damaged or destroyed by colitis.

"This paper provides the basis for more effective, potentially disease-modifying approaches to treatment," Kanneganti said.

Helminthic Therapy Spot on CBS 5 News

2010-03-07T16:39:00.003-05:00

This is a pretty old spot from CBS 5 in San Francisco, but thought it was interesting. For more info on this topic, see my old post - "I'll Take a Parasite Please: Helminthic Therapy and the Hygiene Hypothesis".

Gene Sequencing Yields Picture of Human Gut

2010-03-06T00:49:00.002-05:00

Read this article in Business Week about how researchers have identified 160 different species of bacteria in the gut. One interesting finding - people with inflammatory bowel disease (IBD) have 25% fewer bacterial genes than healthy people, indicating that those with IBD have less diversity in their gut.

An excerpt:

"This is so rich. It could help in so many different ways. It could help us understand diseases like inflammatory bowel disease [IBD], Crohn's and ulcerative colitis. It could help us with problems like malnutrition and obesity. It could help us understand many different metabolic problems from liver disease to kidney to heart disease," said Dr. Martin Blaser, chairman of the department of medicine at New York University Langone Medical Center and a professor of microbiology at New York University School of Medicine in New York City. "This is really a landmark study."

Italian researchers discover a possible onset mechanism for Multiple Sclerosis

2010-02-27T11:54:00.003-05:00

I just read an interesting article on how bacterium might be a trigger for the onset of Multiple Sclerosis. One theory regarding the cause of MS is that it is an autoimmune triggered. A recent study in mice found that a harmless bacterium made to look like a nerve cell allows T-cells to modify to the point where they can repeatedly break into the central nervous system. Normally, T-cells can not do this. However, in mice where this modified bacterium has been introduced, the T-cells modify in the inflammatory response. These modified T-cells persist well after the bacterium has been killed and continue to cause inflammation in the central nervous system.

I think it's interesting to see how other immune disorders operate as there may be analogs in Crohn's.

Here's an excerpt:

This is the hypothesis that the researchers coming from the Institutes of General Pathology, Microbiology and Anatomy of the Catholic University of Rome have been testing with their two-year long work. To demonstrate the viability of this idea, scientists have fooled the mouse immune system, modifying subtly a bacterium of the common family of mycobacteria (the same family to which also the bacterium causing tuberculosis belongs) to make it look like to myelin, the protein coating nerve cells. This modified mycobacterium is completely innocuous. As all external agents, though, it is capable to trigger the reaction of the T-cells of the immune systems. They intervene to destroy it. Since they are innocuous bacteria, although very common in the environment, and since they induce an immune reaction, they are the ideal bacteria scientists can use to study the environmental factor contributing, together with the genetic factor, to cause multiple sclerosis.

"Normally, T-cells cannot penetrate into the Central Nervous System", adds Rea, "because the hematoencephalic barrier prevents them from doing so. But the bacterium modifies the characteristics of the T-cells and allows them to overcome the barrier. In 15 days the bacterium disappears completely from the body".

Yet these T-cells can now enter into the brain. This way, they begin to attack the myelin of the nerve cells, and here is how the immune disease breaks out.

"We basically demonstrate – explains Rea – that in an animal model it is possible to be infected with something not carrying any disease, and later on develop a purely autoimmune disease".

Pretty interesting.

Alberta a 'hot spot' for Crohn's

2010-02-25T17:02:00.002-05:00

Saw this article about the high prevalence of Crohn's and Colitis in Alberta and thought it was interesting. They are planning to undertake a large research study there to look for common reasons that could be contributing factors. Looking forward to seeing the results.

TRPV2 Protein Trips Up Germs

2010-02-20T12:39:00.002-05:00

Another article on proteins related to the immune response. TRPV2 allows macrophages to get a better grip on bacteria, allowing the immune response to be more effective. There's no direct relationship found at this point with autoimmune diseases like Crohn's, but you never know. So thought I'd post it.

Here's an excerpt:

Citing the fact that TRPV2 is important not only in helping macrophages to bind to germs, but also in clearing bacterial infection, Caterina noted its potential as a useful drug target. And in cases of autoimmune diseases -- arthritis, lupus and asthma, for example -- it's possible that the inhibition of TRPV2 might help pull back an overactive immune system.
"We think there are going to be a lot of implications beyond just prevention of infectious diseases where this research about TRPV2's function in macrophages might be relevant," Link adds. "Macrophages consume cholesterol and contribute to hardening of the arteries. They also clear out debris when nerves are injured so that new nerves can grow through that area."

GM-CSF Protein Appears Key to Intestinal Balance

2010-02-20T12:21:00.003-05:00

Saw this article and thought it was interesting. It's about a protein called granulocyte-macrophage colony-stimulating factor (GM-CSF) that helps regulate gut inflammation.

Here's an excerpt:

Reduced levels of the protein — granulocyte-macrophage colony-stimulating factor (GM-CSF) — could be an underlying factor in severe illness caused by pathogens such as E. coli and intestinal inflammation in inflammatory bowel diseases such asCrohn’s disease, the researchers said.
“The gut normally is in a chronic state of low-grade inflammation that is beneficial,” study author Dr. Martin Kagnoff, professor emeritus of medicine and pediatrics at the University of California, San Diego, School of Medicine, said in a university news release.
“This study shows that GM-CSF has a profound influence in the regulation of cells that determine whether the gut lives in peace with this inflammation or becomes severely inflamed during infection,” he said. “Any time that delicate balance is disrupted, all heck can break loose.”
Kagnoff said the findings might help explain why some people with Crohn’s disease benefit from receiving GM-CSF. A greater understanding of the role of GM-CSF in the gut could lead to new treatments based on the protein, he added.

Link Between Inflammatory Disease and Premature Aging

2010-02-06T14:19:00.002-05:00

Some research from University of Arizona suggests that inflammatory diseases, including inflammatory bowel diseases like Crohn's Disease, could lead to a premature aging process. The researchers found that the Klotho gene, a gene which plays a vital role in aging, was down-regulated. This could speed the onset of age-related diseases like osteoporosis.

Here's one excerpt:

"We have made a novel discovery," said Dr. Fayez K. Ghishan, professor and director of the Steele Center. "Based on our research, it appears that chronic inflammation of the gut causes Klotho to down-regulate – or ‘turn off' – contributing to premature-aging diseases such as osteopenia, osteoporosis and atherosclerosis, to name a few."

And another excerpt:

"We can now theorize that if you have an inflammatory process going on, like IBD or rheumatoid arthritis, for example, you are likely to develop symptoms of premature aging," Kiela said. "Our findings lay the foundation for future work related to the contribution of Klotho to chronic inflammatory diseases in human patients – and how to better treat these diseases."

Distinct demographic profiles between Crohn's disease and ulcerative colitis

2010-02-06T14:14:00.002-05:00

Just read a short article on the demographic differences between UC and CD sufferers in the UK. Additional support for environmental differences being a contributing factor. Interesting that CD was more common among "deprived social groups". Perhaps a different diet in that group? Here's an excerpt:

They found that hospitalization for severe CD was more common among women than men and it peaked among younger people aged 16󈞉 years. UC was similar among men and women and was more common among older people. There was no link between social deprivation and UC, but CD was more common among more deprived social groups.
The differing demographic profiles between CD and UC, suggest that environmental factors play a more significant role in the etiology of CD. The findings of this large population-based study on the prevalence and mortality of IBD are also important for service planning and provision.

Vitamin D may help fight Crohn's Disease

2010-01-28T14:40:00.003-05:00

More evidence regarding the benefits of Vitamin D for Crohn's in this recent article. See my post from Sept 2009 for additional evidence - "Vitamin D and Why Immunosuppressants May Be Counterproductive".

Excerpt from the recent article:

“Our data suggests, for the first time, that Vitamin D deficiency can contribute to Crohn’s disease,” says Dr. White, a professor in McGill’s Department of Physiology, noting that people from northern countries, which receive less sunlight that is necessary for the fabrication of Vitamin D by the human body, are particularly vulnerable to Crohn’s disease.

Perhaps an argument to finally take that vacation to Hawaii.

Faecalibacterium prausnitzii and other butyric acid producing bacteria may be a treatment for IBD

2010-01-20T11:27:00.006-05:00

Saw this article ("Gut bug may hold key to inflammatory bowel disease treatment") today about trials in mice of F. prausnitzii that produced promising results in the treatment of inflammatory bowel disease (IBD). See my blog post from August 2009 on the initial findings related to F. prausnitzii - Lack of Faecalibacterium prausnitzii Bacteria May Contribute to Crohn's.

Here's an excerpt from the more recent article about the trials:

While the exact causes are unclear, IBD is known to be the result of an overactive immune response that is linked to an imbalance of the normal types of bacteria found in the gut.
Several recent studies have identified butyric acid as a potential therapeutic agent for IBD. Some gut bacteria produce butyric acid naturally in the intestines, but in IBD patients some of these strains are heavily depleted.
Trials in mice have shown that injecting one such strain Faecalibacterium prausnitzii into the digestive tract is effective at restoring normal levels of gut bacteria and treating the symptoms of IBD.
In addition, novel identified butyrate-producing strains, such as Butyricicoccus pullicaecorum, have been shown to exert similar effects.
Butyric acid has well-known anti-inflammatory effects and is able to strengthen intestinal wall cells - making it an ideal therapeutic agent against IBD.
In addition to butyric acid, it is hypothesized that strains such as F. prausnitzii and B.pullicaecorum secrete other anti-inflammatory compounds that may enhance the therapeutic effect.
Prof. Filip Van Immerseel, a medical microbiologist from Ghent University in Belgium said that a new treatment for IBD would be welcomed.
“Conventional drug therapy has limited effectiveness and considerable side effects. Probiotics are live bacterial supplements or food ingredients, which when taken in sufficient numbers confer health benefits to the host,” he said.

There are likely more strains of gut bacteria that produce butyric acid, so I wouldn't be surprised to see a probiotic treatment in the coming months or years.

The Hunt for an Autism Drug

2010-01-16T14:26:00.003-05:00

Just read an interesting article in Business Week ("The Hunt for an Autism Drug") about how many companies are seeking drugs to treat autism. Apparently, 1 in 110 8-year old children in the US falls someone on the autism scale. That's a pretty staggering statistic when you think about it. Obviously autism is a very different disease from Crohn's, so why am I mentioning this? When I was reading the book Breaking the Vicious Cycle, they mentioned how the Specific Carbohydrate Diet showed improvement in children with autism. One start-up drug maker is looking at this link:

One of the most promising treatments in this category is a drug called CM-AT made by a startup called Curemark. Dr. Joan Fallon, the company's founder and CEO, observed that many autistics show a strong preference for foods high in carbohydrates and low in protein. A diagnostic test revealed that some autistic children lack enzymes that digest protein. As a result, these children produce fewer of the essential amino acids that are the building blocks for brain development and neuroreception. Fallon believes this deficiency is linked to the most severe symptoms of autism, and she says an early observational study of CM-AT, an orally ingested powder that delivers protein-digesting protease, showed "significant improvements." Curemark is enrolling patients in phase III clinical trials at 10 to 12 sites—the largest autism trial to date.

Seemed related and interesting so thought I would mention it.

The other thing I found interesting was the mention of epigenetics, which I think I'm going to do some further research on. The basic premise is that the environment can influence gene expression. So many diseases may be a combination of both genetics and environmental influences (pollution, viruses, diet, etc.). Perhaps that's why it is so hard to pin down a single cause for Crohn's, autism, and many other diseases.

Good Bacteria - Lactobacillus Plantarum

2010-01-01T16:19:00.003-05:00

Read an article about a particular probiotic called Lactobacillus Plantarum. Here's an excerpt:

Lactobacillus plantarum is a resilient and highly adaptive bacterium that can survive at vast temperature ranges (1-60 degrees Celsius) and a wide scale of atmospheric pressures. The name "plantarum" indicates that this bacterium is a "species of the plants." According to several specialists, including Dr. Bengmark, the adhesive properties of L plantarum make it a powerful tool to fight off pathogenic bacteria such as E Coli, while repairing the intestinal lining.

Mannose-specific adhesions are common among gram negative strains, but not gram positive (lactobacillus). Interestingly, according to Dr. Bengmark's research, L-plantarum uses mannose-specific adhesions, which makes it possible that L plantarum can compete with both gram- positive and gram-negative pathogenic strains for receptor sites and valuable nutrients in the mucosal membrane. It also secretes anti-microbial substances that help to inhibit the formation of pathogenic gram-positive & negative colonies.

These characteristics make L plantarum a potent aide for irritable bowel syndrome, Crohn's disease, and Colitis. In fact, several studies have shown that L plantarum is able to survive through harsh environments including rounds of antibiotics. This is especially important for emergency situations when someone may have to take an antibiotic. According to Donna Gates, Body Ecology Diet, the L. plantarum in your intestines will survive the antibiotic onslaught, maintaining long-term health by ensuring that a yeast overgrowth will not occur.

Apparently only 25% of the Western population has this strain in their guts. So how do you get it? Another excerpt:

L. Plantarum is found in abundance in many fresh vegetables and fermented foods such as sauerkraut, kimchi, pickles, and brined olives. However, be careful of store-bought processed alternatives which use cheap vinegars to pickle vegetables. The real cultural dishes use natural fermentation or salted foods and/or put them in a brine solution, all methods which allow Lactobacillus plantarum to survive and thereby be ingested. Many of these dishes can easily be made at home on a continual basis.

Maybe time to add some kimchi.

MAP and its Relationship to Crohn's Disease

2009-12-31T17:49:00.004-05:00

I just read a really great paper ("Mycobacterium avium subspecies paratuberculosis and its relationship with Crohn’s disease") that summarized recent literature on the role of Mycobacterium avium paratuberculosis (MAP) in Crohn's Disease. I've had several previous posts regarding MAP's potential role in Crohn's and IBD, but this paper was much more comprehensive and cited studies I had not heard of.

It's really worth reading the whole thing if you're looking for background on this topic. Here were the topics covered:

Introduction
MAP - description and background on the MAP bacterium
Detection of Map in Crohn's Disease - intro of detection techniques
MAP Culture - different methods of culturing MAP and results of studies related to Crohn's
Detection of Insertion Sequence IS900 - methods of detecting the IS900 gene sequence (which is unique to MAP)
Serologic Studies of MAP - looking for antibodies in the blood of Crohn's patients
MAP and Genetic Susceptibility to Crohn's Disease - interaction between genetic susceptibility (via the NOD2/CARD15 Crohn's gene mutations) and MAP (e.g. overgrowth, etc.)
Anti-Mycobacterial Antibiotics for Crohn's Disease - review of studies that tried (unsuccessfully) to cause long-term remission of Crohn's through use of antibiotics. MAP is very resilient and the interaction between antibiotics and immunosuppressive agents (which may also impact MAP function) leave room for doubt in the studies.
Epidemiologic Evidence for MAP as a Cause of CD - lots of epidemiologic evidence for why MAP is likely not the cause of Crohn's, but some support of it being a cause.
Conclusion (full excerpt below)

For reference, I'm including an excerpt of the conclusion of the paper:

MAP is the causative agent of Johne’s disease. It seems likely that chronic infection with MAP does occasionally occur in humans. MAP is widely present in our food chain and the DNA of this organism can be recovered from the intestine of CD patients. Studies have shown that a high percentage of subjects with CD are infected with MAP, though whether the association of this bacterium and CD is causal or coincidental is not known. Epidemiologists have gathered enough information to indicate an association between MAP and CD. Nonetheless, the role of MAP in CD etiology is not known, and may be determined from consistent results of studies using improved methods of isolation and detection of MAP bacilli and/or MAP-elicited immune responses in the host.

Bacteroides ovatus (B. ovatus) May Help IBD Suffers

2009-12-31T16:58:00.004-05:00

Saw an article about some recent work regarding a bacteria called Bacteroides ovatus (B. ovatus) that helps repair the intestinal lining. Here's the excerpt:

The group focused on the bacterium Bacteroides ovatus (B. ovatus), which is one of an assortment of intestinal microflora in humans. B. ovatus thrives in the oxygen-free environment of the large intestine, where it breaks down xylan—a fiber found in plants—and other sugars for energy and growth.
The team created a strain of B. ovatus that used xylan to induce secretion of human keratinocyte growth factor, a protein that helps repair and restore the intestine’s delicate lining. This increased the ability of the intestine to repair IBD-inflicted damage.
The researchers found that IBD-affected mice treated with oral doses of xylan and the engineered strain of B. ovatus had intestinal tissues that healed more rapidly. This group of mice also lost less weight and had lower levels of rectal bleeding. In addition, dosing mice with B. ovatus provided protection from induced IBD and limited the development of subsequent intestinal inflammation.

Maybe this will end up as another probiotic supplement at some point in the future.

Probiotics May Help Prevent Crohn's Disease

2009-12-30T14:54:00.003-05:00

Saw an interesting mention of a research report in a Wall Street Journal article. Here's the excerpt:

Crohn's Disease: Probiotics—live microorganisms that appear to improve gastrointestinal health—may prevent the onset of Crohn's disease, according to a study in the Proceedings of the National Academy of Sciences. The researchers fed young mice, who had been bred to develop a Crohn's-like inflammatory bowel disease, diets that included a high dose of eight probiotic bacteria strains. The disease, ileitis, was entirely prevented in five of those 11 mice, and markedly less severe in five of the remaining six. A lower dose of the bacteria, given to another set of mice, provided little beneficial effect. The researchers suggested, based on necropsies of the mice, that the probiotics guarded against ileitis by stimulating the immune system of the gut lining.
Caveat: It's not known whether probiotics would prevent actual Crohn's disease in humans, or what dose would be required. (Read the Report)

This kind of raises an interesting question around the Specific Carbohyrdrate Diet (which I'm using). How do you train or sensitize your immune system to handle different types of gut bacteria if you're on a diet that is targeted at eliminating many strains of bacteria in the gut? Perhaps you slowly introduce new bacteria (or foods that allow those other bacteria to develop). That way your body can slowly develop (or re-develop) it's sensitivity to these.

A Potential Stem Cell Treatment for IBD from Pfizer

2009-12-25T01:15:00.010-05:00

Pfizer announced some news this week that could result in a stem cell treatment for inflammatory bowel disease (IBD), including Crohn's. On Monday, Pfizer struck a development and commercialization agreement with Athersys, Inc., a Cleveland biotech company. Pfizer plans to develop a therapy for IBD based on MultiStem, the Athersys adult stem cell product line.

From reading through the MultiStem website, the product seems to have great potential as a therapy. The really dumbed-down version of the therapy (I'm a dummy, so correct me if I'm wrong) would be to inject these cells into a sufferer of IBD and then the cells, based on the

local environment and specific type of inflammatory response, would produce molecules to help properly regulate the immune system. The stem cells would not be a permanent solution. Similar to other biologics (e.g. Cimzia), they would have a temporary impact on how the immune system functions and to continue to see benefits you would need to continue to take the drug. Here's an excerpt:

MultiStem consists of a special class of human stem cells that have the ability to express a range of therapeutically relevant proteins and other factors, as well as form multiple cell types. Factors expressed by MultiStem have the potential to deliver a therapeutic benefit in several ways, such as the reduction of inflammation, protection of damaged or injured tissue, and the formation of new blood vessels in regions of ischemic injury. These cells exhibit a drug-like profile in that they act primarily through the production of factors that regulate the immune system, protect damaged or injured cells, promote tissue repair and healing and most or all of the cells are cleared from the body over time.

The real unique thing about MultiStem versus other biologics is that it could actually have multiple methods of working (the beauty of stem cells). Here's an excerpt:

Though the cells have the potential to differentiate into a variety of cell types, in certain indications the primary mechanism of MultiStem appears to be the production of a physiologically relevant and complex set of therapeutic molecules in response to the local environment. In the initial indications Athersys is pursuing, the cells appear to minimize the inflammatory reaction that occurs in response to ischemic events (such as myocardial infarction or stroke) or the anti-host immune reaction seen in graft vs. host disease (GvHD), and promote healing and recovery. Unlike traditional pharmaceuticals, MultiStem cells are dynamically regulated, and have the potential to respond to signals of inflammation or tissue damage in multiple ways. Potential mechanisms of benefit include protection of damaged or injured cells, reduction of inflammation, stimulation of new blood vessels, and the recruitment of other cell types to promote tissue repair and healing.

Athersys claims that one of the benefits of the drug is that it can be scaled to be produced efficiently on a large scale. That could mean the drug could be made available to people on the same scale that traditional pharmaceuticals are. (Although I wouldn't expect the scale economies to translate into affordable prices).

Great news and looking forward to see what Pfizer brings to market. And in terms of bringing the product to market, here's a good excerpt from The Motley Fool ("Pfizer Swings for the Fences"):

MultiStem is being tested in several conditions, but Pfizer's license is specifically for the treatment of inflammatory bowel disease (IBD), a group of conditions that includes ulcerative colitis and Crohn's disease. The license is only costing Pfizer $6 million up front because the technology is still relatively unproven, having not entered clinical trials for IBD yet. Athersys can get milestones of up to $105 million and royalties as the drug passes through clinical trials and is commercialized.
Pfizer will pay for the phase 1 and 2 trials. Then, if it gets that far, Athersys will have the option of co-developing the drug -- sharing profits and losses -- or letting Pfizer proceed on its own and take the milestones and royalty payments.
Unlike traditional stem cell companies like Geron (Nasdaq: GERN) that are developing stem cells to regenerate tissue, MultiStem uses donated bone marrow cells to produce a product that promotes healing of the tissue through cell signaling. Essentially it has a more drug-like profile as the stem cells are cleared from the body.

So certainly a ways out.

Frankincense a Treatment for Crohn's?

2009-12-25T00:48:00.003-05:00

Thought this article ("Frankincense and Myrrh: The Wise Men brought...healthcare?") was timely given it's the holiday season. Apparently frankincense has been studied as an anti-inflammatory and treatment for Crohn's disease. Here's an excerpt:

But frankincense (Boswellia serrata) is less commonly known as a traditional remedy. What does frankincense treat? It's been a remedy for children, and studied as an anti-tumor agent against bladder cancer. In terms of rigorous assessments, a British Medical Journal review of the data looked at all research results and found particularly notable "trials related to asthma, rheumatoid arthritis, Crohn's disease, osteoarthritis, and collagenous colitis. Results of all trials indicated that B. serrata extracts were clinically effective. Three studies were of good methodological quality. No serious safety issues were noted."

Maybe Santa will leave some in your stocking.

Autoimmune Disease Clusters and Crohn's

2009-12-25T00:31:00.003-05:00

Happy Holidays! Saw this article (GWAS Meta-Analysis Supports Existence of Autoimmune Disease Clusters) today about a study conducted by Stanford University researchers. They were trying to see if there were any connections between different auto-immune diseases. Specifically, they looked at six autoimmune diseases - type 1 diabetes, rheumatoid arthritis, Crohn's disease, multiple sclerosis, autoimmune thyroid disease, and ankylosing spondylitis - and five non-autoimmune diseases to see if genetic factors related these diseases with each other.

The researchers did find that diseases go together. However, Crohn's is not related to any of these other diseases. Here's the excerpt:

Based on their analyses, the researchers suggest autoimmune diseases fall into at least two different groups: one containing rheumatoid arthritis and ankylosing spondylitis and another containing multiple sclerosis and autoimmune thyroid disease.
Meanwhile, they reported, type 1 diabetes resembled both of the groups to a certain extent, sharing characteristics with autoimmune thyroid disease but not multiple sclerosis. Crohn's disease, on the other hand, did not cluster with either group.

I suppose we're just in a category of our own =)

Crohn's blamed on lazy immune cells

2009-11-21T18:30:00.002-05:00

Saw this article. Not necessarily anything new here.

It still wasn't clear, however, what caused the weakened immunity in the first place. So Segal's team focused on cells called macrophages, the immune system's whistle-blowers. In people with Crohn's disease, they found that macrophages secrete lower levels of cytokines, the chemicals that rally other immune cells to infection sites (Journal of Experimental Medicine, DOI: 10.1084/jem.20091683).
The team concluded that ineffectual rallying of immune cells in people with defective macrophages is what allows intestinal bacteria to run amok in the early stages of an infection, setting in motion the series of events that leads to Crohn's disease.

Johne's Disease (and MAP) in as Many as 70% of U.S. Herds

2009-10-31T23:41:00.002-04:00

I saw an article today that shared some startling news about the spread of Johne's Disease. In the last 15 years (from 1996 to 2009), the prevalence of Johne's has increased from only 22% to as much as 70% of U.S. dairy herds. Johne's Disease is caused by the MAP bacteria (see previous blog posts), which many people have found links with to Crohn's Disease.

Here's an excerpt:

"Studies showed that in 1996, Johne's disease was in about 22 percent of the U.S. herds, but because of rapid expansion of herds across the country, producers unknowingly purchased young heifers and older cows which were infected with the disease and thus has raised the prevalence of Johne's to be present in nearly 70 percent of the herds," she said.

Could the recent rise in Crohn's Disease be linked to this rise in the spread of MAP?

Anti-TNF Drugs Don't Seem to Increase Cancer Risk

2009-10-29T11:02:00.003-04:00

Good news for those that use TNF-blockers to manage their Crohn's disease. Long-term use of the drugs (at least for 6 years or less) does not appear to increase your risk of cancer. That's certainly a concern as TNF is part of the body's immune response in dealing with "tumor"-like cells. The study looked at both short and medium term use of these drugs for rheumatoid arthritis and didn't find any elevated risk of cancer.

UPDATE: (6/21/2010) - The FDA released a cancer warning for TNF-blockers back in August 2009. See this related post. Thanks to the anonymous person that commented!

Scientists Link Diet and Immune System

2009-10-29T10:54:00.002-04:00

Saw this article about Australian scientists that found a "direct link" between diet and how the immune system functions. The scientists found that a specific short-chain fatty acid (created when bacteria breaks down dietary fiber) binds with an immune cell receptor to influence immune response. The article didn't provide many details on the exact findings, but they were hopeful that it could help explain how dietary changes could be a contributing factor in the rise of autoimmune disorders.

Here's an excerpt:

"When (immune cells) go bad they cause inflammatory diseases, so asthma, rheumatoid arthritis, inflammatory bowel disease ..." Prof Mackay said.
"We think one of the mechanisms for their normal control is short chain fatty acids binding to this receptor.
"And if we were to speculate on the real significance of this, we believe firmly that the best explanation for the increase in inflammatory diseases in western countries ... is our changes in diet."
A lack of dietary fibre could also be behind the rise in type 1 diabetes, Prof Mackay said.
The research suggests that having a healthy diet rich in fruits, vegetables, grains, nuts and seeds would reduce a person's risk of autoimmune disease.

Gut Bacteria Linked to Immune Response

2009-10-21T17:57:00.002-04:00

Just read this article about a new finding of a bacteria linked to a specific immune response in mice. The bacteria induced higher Th17 response. The finding suggests additional bacteria to look at in the formation of autoimmune disease. Here's an excerpt:

If the effect is present in humans, it suggests a clinical use for the findings, Littman said. "So you can immediately see some practical application of this, if one can mimic the presence of these commensal bacteria to strengthen resistance to pathogenic microbes," he said.
On the other hand, the level of the microbes could also play a role in the development of autoimmune disease, he said. "You have to have the right balance," Littman said.

With hundreds of strains of bacteria, the "right balance" seems very difficult to find.

I'll Take a Parasite Please: Helminthic Therapy and the Hygiene Hypothesis

2009-10-08T13:53:00.000-04:00

I've been wanting to post on this topic for a while, but never got around to it. I just saw this article in ABCNews titled "Allergy Desperation: I'll Take a Parasite, Please" (linked to from this blog post). It includes a story of a guy named Jasper Lawrence who in desperation from long-term allergy problems decided to infect himself with hookworms. The result was that his symptoms were dramatically diminished (if not cured). Why?

Here's a good excerpt from the article that sums it up:

The hypothesis goes that until recently, humans were fighting off some sort of parasite or another for millions of years, ever since humans evolved into humans. That co-existence eventually led humans to evolving an immune system that worked with parasites.

"When you're born you have an immune system, but your immune system is a blank slate," said Weinstock.

Weinstock explained that just as humans create a functioning digestive system by populating their digestive system with bacteria, humans historically developed an immune designed to account for parasites in the body.

But in the last 150 years, the industrialized world's clean food supply and plumbing suddenly removed parasites from people's bodies. In response, researchers now widely think that people's immune systems stopped developing properly.

Weinstock said most people still have a powerful "attack" function of their immune system, but that many believe the immune system does not develop to regulate properly in the absence of helminthes (parasitic worms).

"People who are not exposed to helminthes have sloppy regulation," said Weinstock. As a result some people's immune systems go off kilter and misfire against their own bodies creating autoimmune disorders such as allergies, asthma, or inflammatory bowel disease.

There has been a lot of research into this area and the general "hypothesis" mentioned has been around since the 1980's. The theory is called the hygiene hypothesis. Basically, our overly hygienic lifestyles in developed nations (particularly in the northeast) means that our immune systems have not been properly balanced and exposed to regulating agents. The lack of this exposure causes all sorts of downstream effects when your body encounters mostly innocuous allergens -- basically it over-reacts. The type of therapy described in the article, helminthic therapy, is meant to correct this problem (albeit later in life than probably should have been the case).

In helminthic therapy, you purposely expose the body to parasites such as hookworms. This exposure forces the immune system to develop the proper regulation systems and as a result it no longer over-reacts.

Sounds great! Pass the bowl of hookworms over so I can load up. Perhaps not so fast. Immune development is really complex and many of these parasites can have serious side effects (... they are parasites after all ...), so it's likely wise to wait for many of the clinical trials underway to be completed. You never know, within a few years you may find hookworms in the same category as probiotics!

Wildlife May Cause Livestock Infections of MAP

2009-10-08T13:38:00.001-04:00

A study by Scottish researchers found a possible source of Mycobacterium avium paratuberculosis (MAP) infections in livestock -- wild animals. The transmission of infection may be from wild animals to livestock to humans.

DNA Test Results May Not Be As Reliable As They Appear

2009-10-08T13:30:00.000-04:00

Just saw an article in the LA Times about how much you can trust new consumer DNA tests. The article highlights a recent experiment that compared the results of two of the leading vendors in this space, Navigenics and 23andMe. The experiment found that in some cases the two vendors conclusions about disease susceptibility was in agreement, but in others it was wildly different. The reason: each company uses different research studies to draw their conclusions. So, one might say that you have a 25% chance of developing Crohn's while the other says something higher. So although both companies do a great job of reading your DNA correctly, the determination of disease susceptibility is simply not a perfect science. In many cases, particularly those where definitive cause is unclear (like Crohn's), it's far from perfect and can generate very different results.

CD39 and Gene Variant Linked to Crohn's

2009-09-29T19:57:00.000-04:00

Saw an article posted yesterday via WebMD about another potential genetic link found to Crohn's Disease. The gene variant, common in white people and those with European descent, causes a lower amount of the enzyme CD39 to be created in the gut. The enzyme dampens inflammation. Here's an excerpt:

All humans have a CD39 gene. But some have a version of the gene linked to lower CD39 levels. Friedman and colleagues identified a genetic marker for low CD39 production. They then looked for this marker in 1,748 patients with Crohn's disease and in 2,936 people without IBD.
They found that the genetic marker was significantly more common in people with Crohn's disease. Moreover, people without IBD were more likely to carry two copies of the high-CD39 gene, while those with Crohn's disease were more likely to carry two copies of the low-CD39 gene.
Genetics are not destiny. Not everyone with the low-CD39 gene has or will have IBD. Even having two copies of the gene only increases a person's risk of Crohn's disease by 27%.
But since about 40% of whites of European ancestry carry at least one copy of the gene, its effects across the entire population should be quite large.

It seems there may be many contributing factors to Crohn's. Perhaps that means it's an umbrella disorder with many possible causes (rather than one single cause).

Just Say No To Antibacterial Burgers

2009-09-28T22:32:00.000-04:00

Read a good Washington Post article about the extreme use of antibiotics in our livestock and food supply. An astonishing 70% of antibiotics used in the US are used for the raising of livestock (primarily in disease prevention rather than treatment). That means were are steadily getting small doses of antibiotics through our food supply our entire lives. But those antibiotics lets us keep our food cheap and accessible for the masses, right? How could we eliminate it? I thought this excerpt was good:

There's also the argument that the pennies we're saving on each burger are being spent in our hospitals. A 2005 study out of Tufts University estimated that antibiotic-resistant infections add $50 billion to the annual cost of American health care. On the other side of the coin, a National Academy of Sciences study found that eliminating non-therapeutic antibiotics from animals would cost only about $5 to $10 per person per year. I'd pay that for a lower risk of super-staphylococcus.

That's very reasonable.

50% of Type 1 Diabetics Show Adverse Immune Response to Wheat

2009-09-28T22:00:00.001-04:00

Saw this post on Celiac.com about a recent study in Ottawa that found that nearly half of people with Type 1 Diabetes showed an abnormal response to wheat proteins. Here's an excerpt:

Dr. Scott’s results offer the first suggestions that T cells

Small lymph cells created in the thymus which orchestrate the immune system\'s response to infected or malignant cells. Also known as T lymphocytes. T cells in the immune systems of type 1 diabetics are also more likely to have adverse immune reactions to wheat. His results also suggest that such over-reaction is tied to genes associated with type 1 diabetes.

According to Dr. Scott, the research suggests that "people with certain genes may be more likely to develop an over-reaction to wheat and possibly other foods in the gut and this may tip the balance with the immune system and make the body more likely to develop other immune problems, such as type 1 diabetes.”

Dr. Scott adds that the immune system has to find "the perfect balance to defend the body against foreign invaders without hurting itself or over-reacting to the environment and this can be particularly challenging in the gut, where there is an abundance of food and bacteria.”

In side comments that accompany the paper, diabetes expert Dr. Mikael Knip of Finland suggest that the team's results "add to the accumulating concept that the gut is an active player in the diabetes disease process.”

Nothing ultra-new here relative to previous studies that led to the SCD diet, but interesting to see this applied to Type 1 Diabetes.

Contamination of food products with Mycobacterium avium paratuberculosis: a systematic review

2009-09-28T21:45:00.000-04:00

A study published back in March 2009 conducted a systematic review of previous studies of the potential threats to exposure to the MAP bacteria. Here's the abstract from the research:

Although a causal link between Mycobacterium avium subspecies paratuberculosis (MAP) and Crohn's disease has not been proved, previous studies suggest that the potential routes of human exposure to MAP should be investigated. We conducted a systematic review of literature concerning the likelihood of contamination of food products with MAP and the likely changes in the quantity of MAP in dairy and meat products along their respective production chains. Relevant data were extracted from 65 research papers and synthesized qualitatively. Although estimates of the prevalence of Johne's disease are scarce, particularly for non-dairy herds, the available data suggest that the likelihood of contamination of raw milk with MAP in most studied regions is substantial. The presence of MAP in raw and pasteurized milk has been the subject of several studies which show that pasteurized milk is not always MAP-free and that the effectiveness of pasteurization in inactivating MAP depends on the initial concentration of the agent in raw milk. The most recent studies indicated that beef can be contaminated with MAP via dissemination of the pathogen in the tissues of infected animals. Currently available data suggests that the likelihood of dairy and meat products being contaminated with MAP on retail sale should not be ignored.

One of the tables that summarizes the rates of infection of MAP in livestock was pretty telling. In the US, rates of infection in herds ranged from 2% to 74%. Main take-away is that there is substantial risk to exposure to MAP in the US (and in most other countries - regardless of how developed they are).

Faces of Low Dose Naltrexone: New Book Explores Cutting-Edge Autoimmune Disease Treatment

2009-09-23T12:57:00.000-04:00

I saw this blog post on About.com regarding an e-book that someone published summarizing many of the findings related to low-dose naltrexone (LDN). I haven't read through it yet, but just bookmarking it to review later.

This slide caught my eye while I was skimming through the document. It's a summary of the mechanism of how LDN works:

Urban Cluster of Crohn's Potentially Explained by MAP

2009-09-23T12:36:00.000-04:00

I just came across a new research report published Sept 23, 2009 (Possible Transmission of Mycobacterium avium subspecies paratuberculosis through Potable Water: Lessons from an Urban Cluster of Crohn's Disease) that found a geographical cluster of people that developed Crohn's Disease.

Here's an excerpt that describes the clustering they found (only three people, but still warrants further research):

Despite the documented presence of MAP in tap water and its probable growth on tap water pipes, clusters of Crohn's disease have not previously been described in relationship to tap water pipes supplying patients' homes. This report describes three unrelated individuals who lived on the same block along a street in a midwestern American city and developed Crohn's disease within four years of each other in the 1960's. A common tap water pipe supplied their homes. This is the first reported cluster of Crohn's disease possibly linked to fully treated drinking water, and is consistent with previously reported clusters of Crohn's disease linked to an infectious microorganism in water.

The full article can be found here.

Foods For Healthy Weight Gain

2009-09-13T01:34:00.001-04:00

Just read this post about how to gain weight when dealing with diseases like Crohn's. Obviously everything about eating pasta, rice, potatoes, and such won't quite work on the SCD diet. But I thought the calorie counts were very interesting. Here's the excerpt:

Plan to eat about 6 meals daily, and eat about 500 calories a day more than usual. Sugary products like milkshakes (which could be made with skim milk and low-fat ice cream), jellies, jams, cakes and cookies can accomplish that goal easily, short-term.
Eating a balanced diet and managing weight long-term should be done thoughtfully. You don’t want to only gain fat and no muscle. Any kind of SAFE dieting program suggests eating healthy foods while exercising, to keep the body at an ideal weight while building muscle.
Know your recommended weight for your height and body type. The average 165-pound man, between 19 to 24 years old, needs 3000 calories a day to maintain his weight. But, as we age, we need fewer calories, so that same man will only require 2700 calories daily from the age of 25 to 49. And even less beyond that.
An average woman, ages 19 to 24, will need 2100 calories daily to maintain a weight of 127 pounds. As she ages, up to 49, she will only need 1900 calories.

Good guidance. The article also mentions to work with a nutritionist along side your doctor. It's tough to get 3000 to 3500 calories a day on the SCD, but I suppose I'll have to find a way.

Is Soy Bad? Type 1 Diabetes and Leaky Gut

2009-09-12T00:07:00.000-04:00

I came across a blog post about Type 1 Diabetes (again thanks to Google Alerts) where the author talks about why Soy is bad and how it may have contributed to the recent (i.e. last 30 - 40 years) growth in Type 1 Diabetes or other autoimmune disorders. I thought it was pretty interesting. The idea (regarding Type 1 Diabetes) is that soy damanges the gut mucosa, causing a leaky gut, thereby allowing large proteins (e.g. gluten) directly into the bloodstream where they cause an immune response around the body.

Now, I don't have Type 1 Diabetes so that's only partially interesting for me. But the process described in the post raises some interesting questions. One of the things mentioned was that there are diabetes related genes that have been found (and that have been present for decades), but recent environmental (or in this case diet) changes are making those genes get expressed more than they previously were. Could something similar be happening in Crohn's? I need to research leaky gut syndrome some more and perhaps it makes sense to continue broadening my research beyond Crohn's to other auto-immune disorders.

Fecal Bacteriotherapy

2009-09-11T23:28:00.000-04:00

In reading through a recent report on the autoimmune disease treatment options (mostly from a market sizing perspective), I came across a therapy called fecal bacteriotherapy. The treatment is a last resort option for patients with pseudomembranous colitis or ulcerative colitis. The therapy is based on the premise that these diseases are caused by imbalances of bacteria in the colon or small intestine and so by transplanting fecal bacteria from a healthy individual (i.e. microflora from someone that doesn't have any GI issues) to an afflicted patient you restore the balance of bacteria in the gut. By introducing a "healthy" mix of bacteria, you can replace whatever pathogenic bacteria is there (e.g. Clostridium difficile in the case of pseudomembranous colitis) with healthy, probiotic bacteria. It's not unlike other probiotic therapies, but this one literally uses all the bacteria from a healthy person rather than just a subset.

I found this interesting for two reasons. One is that it's interesting to see a related disorder where they have pinpointed the bacterial agent that causes the disease. And second, it might be another last resort option for people for Crohn's or UC.

SCD Website - "No More Crohn's For Me"

2009-09-10T22:01:00.000-04:00

Came across this website sharing best practices (recipes, etc.) for he Specific Carbohydrate Diet.

Vitamin D and Why Immunosuppressants May Be Counterproductive

2009-09-09T15:01:00.000-04:00

I just saw a post from the Napa County Science News Examiner (thank Google Alerts for that) commenting on an upcoming research paper that will be published in the September issue of "Annals of the New York Academy of Sciences" regarding Vitamin D's role in auto-immune diseases. The post talks about a recent research paper that discusses why Vitamin D may be even more important for women than in men (and could also explain higher rates of auto-immune diseases in women). The paper found that women have a higher number of Vitamin D receptors in their body, in particular in the endometrial cells (lining of the uterus). When Vitamin D binds with these receptors, many genes are expressed that help kick-up the immune system.

Here's an excerpt:

The key to how vitamin D plays its part is to understand what the VDR does. When the correct form of vitamin D (a form known as 1,25-D or calcitriol) binds to VDR, VDR then directly causes the expression of over 900 genes to occur. Two of the genes that are turned on produce proteins that are directly responsible for kicking the immune response into active mode. The reason for VDR in the endometrium is that it provides protection against infection for the developing fetus.

Another key to the puzzle has been the growing evidence that bacteria may play a role in the development of autoimmune disease. If so, why wouldn’t women, who have more VDRs, be better off than men? The problem is that bacteria of various kinds can interfere with VDRs and prevent vitamin D from binding. If vitamin is unable to bind, then the immune response is disrupted. Not only is the immune system affected, but thyroid hormone problems can result too.

There are many clear links that have been established between Crohn's and bacteria. However, this finding could point to why immunosuppressants could be hurting rather than helping the problem. Here's another excerpt:

Although these results do not provide a clear path to treatment, “the potential role of persistent pathogens in autoimmune disease mandates reconsideration of the use of corticosteroids as a first-line treatment for many autoimmune diseases. Corticosteroids effectively reduce the ability of the immune system to respond to pathogens, including persistent microbiota, which is counterproductive to recovery.”

This would suggest that Vitamin D supplementation, particularly in women, is important in recovery. Plus, it really calls into question usage of corticosteroids as a treatment for Crohn's.

With all that said, though, you don't want too much Vitamin D apparently. Another study (from 2004) conducted at UCLA found that people with Crohn's had very high levels of Vitamin D in their blood. The high Vitamin D level (contrary to what you would think) actually causes loss of bone density, which could lead to osteoperosis. Here's the excerpt:

ISLAMABAD: Contrary to expectations, people with the inflammatory bowel condition Crohn’s disease are likely to have excessive levels of the active form of vitamin D in their blood, researchers have found. This is associated with low bone mineral density, they report.
Dr. Maria T. Abreu from the Inflammatory Bowel Disease Center at Cedars-Sinai Medical Center in Los Angeles led the study. She told Reuters Health, "Most doctors think that Crohn’s patients automatically have decreased vitamin D levels and encourage supplementation with vitamin D. We would like to urge doctors to check vitamin D levels before making that recommendation."
As Abreu’s team explains in the medical journal Gut, under certain circumstances too much active vitamin D can actually contribute to the breakdown of bone, leading to osteoporosis. The researchers found "inappropriately high" blood levels of the active form of vitamin D in 42 percent of the 138 people they studied with Crohn’s disease. This was true of only 7 percent of 29 patients with ulcerative colitis, another type of inflammatory bowel disease.
Also, the higher the blood levels of active vitamin D in Crohn’s patients, the lower was their bone density -- regardless of whether they were treated with steroids -- the investigators found. "We believe that high vitamin D levels are most likely a manifestation of the underlying gut inflammation," Abreu said. A high vitamin D level is "an additional risk factor predisposing to development of osteoporosis" for some Crohn’s disease patients, the team concludes. Treatment of the underlying inflammation, "may improve metabolic bone disease."

I suppose it's a mixed verdict then. But at the very least it's worth getting your Vitamin D level checked to see where you are and then only supplement if necessary.

Rifaximin (Xifaxan) Antibiotic Used to Treat Crohn's

2009-09-05T22:40:00.000-04:00

I came across a drug called Rifaximin (Xifaxan) via a post about IBD drugs in the pipeline in the About.com IBD blog.

The drug has been around and used for over 20 years to treat travelers' diarrhea. The drug is an antibiotic that works exclusively in the GI tract and does not enter the bloodstream. Here's the excerpt from the About.com blog that comments on its efficacy:

Rifaximin (Xifaxan) is currently being studied for use in treating severe Crohn’s disease. This drug, manufactured by Salix Pharmaceuticals, is an antibiotic currently approved for use in traveler’s diarrhea. Rifaximin is not absorbed into the bloodstream like other antibiotics, but instead affects the digestive tract directly. The theory is that intestinal bacteria may have a connection to the inflammation in Crohn’s disease, and an antibiotic may be effective if it kills these bacteria.
In a 16-week study of rifaximin, 78 percent of the patients with Crohn’s disease experienced an improvement in their disease, and 59 percent went into remission.
This drug is also being studied for use in treating pouchitis, a complication that can occur after j-pouch surgery. In one study, 11 patients for whom other therapies had failed received either 400 mg of rifaximin twice a day or 200 mg three times a day -- both groups showed improvement.

I investigated the efficacy of this drug a bit more in terms of its use for Crohn's. I came across a website where folks post their experiences with drugs. There were two pages that were relevant, one for primary treatment of Crohn's and the other (with more responses) regarding maintenance of Crohn's.

From reading through the reviews, it appears that the drug provides quick relief of symptoms, but that relief appears to be temporary if you stop taking the drug (and even if you continue taking it). One person, for instance, went on a regimen combining Xifaxan, probiotics, and Boswellia serrata. Here's an excerpt from that person's experience I thought was worth capturing:

Xifaxan for Crohn's I take this med for Crohn's disease, my doc is trying it although it isn't a "recognized" Crohn's drug yet. I take 2-200mg pills twice a day. It is very easy to take, coated tablets do not taste bad although they are on the larger side. I do not feel nauseous on them or anything, no side effects at all. Can be taken with or without food. After 24 hrs on this (two doses) I had my first solid "BM" in a very long time, it worked like a charm. It continued to work for 4-5 days when I started getting BMs more frequently and less solid. I realized that this is probably killing off the good bacteria so I started supplementing with a several-strain probiotic which has helped (I take the probiotics between the doses of Xifaxan, not at the same time which would be useless).

One huge drawback of this medicine is the cost. My insurance has told me they won't cover it, so I am in the process of appealing that and hopefully they will cover it because a one month's supply costs $1100.00. Nope I'm not kidding. There is no generic.

Overall I think it has done me some good and hopefully my results will continue to be positive. Looking forward to reading about other people's experiences with this drug.

**Update 6/26/05
I have continued taking this drug along with Boswellia serrata capsules, probiotics, and a multivitamin and as of 2 days ago I was officially in remission! I am very pleased with the results and would encourage others to try it. Please read my rating on boswellia too because I truly believe that boswellia had a big impact on my remission as well as this antibiotic. Also, my insurance did eventually cover the entire cost of this medicine but my dr had to send a letter before they would do it.

Another person combined use of the Xifaxan with the Specific Carbohydrate Diet and probiotics and seemed to have positive results as well:

I was diagnosed with Crohn's disease in 2002. Since then I have tried just about everything to cure myself of this disease. Through my journey I have discovered that the Specific Carb Diet combined with a course of Xifaxan and high quality six strain probiotics (powder form) from customprobiotics.com has put me very close to remission. The first few days in Xifaxan caused severe painful bloating (die off of the bad bacteria) and then I was ok. You must stay way from bad carbs (ie. sugar, bread, cereal) and dairy if you want to get well.

The drug, combined with other regimens, certainly appears to have promising results and hence warrants further investigation. However, the use of antibiotics long-term is rather disconcerting to me. My assumption is that you need more than just a few strains of probiotics in your intestines to be really healthy (e.g. creation of Vitamin K). Can you really live your entire life taking antibiotics?

A Link Between Food Poisoning and Crohn's

2009-09-05T22:31:00.000-04:00

Another one I saw off of the About.com IBD blog (post). A recent study conducted in Denmark found a connection between certain types of food poisoning and increased rates of IBD.

Here is the excerpt:

Increased Risk of Inflammatory Bowel Disease After Salmonella or Campylobacter Gastroenteritis: A Population-Based Study (Abstract #80)
Researchers in Denmark have discovered a link between inflammatory bowel disease (IBD) and an initial bacterial infection with either salmonella or campylobacter gastroenteritis, an important step in understanding the development of IBD that may help explain the increasing incidence of IBD over the past decade.
Denmark’s system of tracking its citizens with individual identification numbers allowed researchers to examine patient interaction with the health-care system over a 15 year period. Investigators examined how many patients in a control group would develop IBD and compared them with those who have been exposed to bacteria in the past. They found that over 15 years, three times as many patients who had been exposed to bacteria later developed IBD as those who had not been exposed.
“This is the first time we are able to make such a clear association with an initial exposure to bacteria and subsequent development of IBD in the long term,” said Nielsen Henrik, MD, professor of infectious diseases at Aalborg Hospital in Denmark. “Our research has important implications for food safety and disease prevention. If we can reduce and prevent the spread of food bacteria and infections, we may reduce or even largely eliminate IBD in the long term.”
Dr. Nielsen is hopeful that further research will go beyond the association between bacteria exposure and IBD established in his study and attempt to prove causality by studying in detail the biology of individual patients.

I find this very interesting as I was recently thinking about several severe bouts of food poisoning I had about 5 years before being diagnosed with Crohn's. Such episodes would no doubt have some impact on the microflora in your gut.

A possible link here could be that those severe bacterial infections caused dysbiosis or some other imbalance of bacteria in the gut - perhaps killing off some good bacteria that helped to regulate the immune response in the gut. Over time, the problem that was introduced at that point compounded (or at least makes you susceptible) to other bacteria or pathogens that cause of the problem.

Cases of Crohn's Rising in Scotland, Canada (Ontario), and Northern France

2009-09-05T22:11:00.001-04:00

I read three posts in the About.com IBD blog about recent epidemiology studies pointing to rising cases of Crohn's in Scotland and Ontario, Canada. Also came across a study that showed rising cases in youth (0 - 19 yrs) in Northern France.

Here's the post about Scotland:

Scotland Has High Incidence of Pediatric IBD
Monday July 13, 2009
Researchers in Scotland are puzzled by the dramatic increase of pediatric cases of inflammatory bowel disease (IBD) in recent years. IBD is increasing all over Europe, but the 4-fold increase in Crohn's disease in Scotland has been the most dramatic. Scottish researchers are currently recruiting for a new study to determine what may be causing the rise in IBD cases. The research will focus on the role bacteria may play in the onset of IBD. The BISCUIT (Bacteria in Inflammatory bowel disease in Scottish Children Undergoing Investigation before Treatment) Study is underway at the Royal Aberdeen Children's Hospital, with plans to expand to hospitals in Dundee, Edinburgh, and Glasgow.

And here's the post about Ontario:

Increased Rate of IBD in Ontario Children
Monday August 10, 2009
A new population-based study has shown that the rate of inflammatory bowel disease (IBD) in children in Ontario, Canada is increasing. The rate of IBD in children under the age of 18 increased from 42.1 per 100,000 in 1994 to 56.3 per 100,000 in 2005. The most striking increases occurred in preschool and school-aged children. The rates in pre-teens and teenagers showed no significant change. The authors stress that even at the increased rate, IBD is still considered rare in children.
It's already known that Canada has a very high rate of IBD, and especially pediatric IBD. The authors of this study indicate that the high immigration rates from south Asia to Ontario may be partly responsible. Research has shown that Asian immigrants to Ontario have a higher risk of developing IBD. The theory is that being exposed to the Western environment increases the likelihood of developing IBD.

And a much earlier post about Canada in general:

O Canada! Why So Much IBD?
Monday November 20, 2006
Inflammatory bowel disease (IBD) is known to be a “western” disease. In other words, it largely affects people who live in western societies. Canada appears to be a hotbed for IBD. Crohn’s disease appears to be particularly prevalent, with 13.4 per 100,000 people in Canada having the disease. In the United States, about 10 people per 100,000 have IBD. An estimated 0.5% of all Canadians have one of the two major forms of IBD. What can explain this?
The theory is that it’s the cold. The cold temperatures create a “sterile” environment which is inhospitable to bacteria. It is thought that when children are raised in an environment where they are exposed to too few bacteria, the risk of IBD is higher. Low exposure to bacteria can also occur in “too hygienic” conditions as well as cold climates.
The authors of the study published in American Journal of Gastroenterology that reported these findings indicate that hygiene and other factors may influence the development of IBD. They stress, however, that the exact cause(s) of IBD are not yet clear.

I thought the second (highlighted) paragraph in the last post was interesting. I have read elsewhere that rates of IBD are higher in northeastern areas. That's an interesting explanation for why it might be the case. Also, it could also be interesting to test dairy products in those regions to see if there is an increased presence of MAP.

Here's the text of the final study about children in Northern France:

The Changing Pattern of Crohn’s Disease Incidence According to Age in Northern France: A Constant Increase in the 0-19 Years Age Group (Abstract #114)
A population-based study of residents in northern France finds that the incidence of Crohn’s disease (CD) is on the rise, most dramatically among young people less than 19 years of age. The findings raise a number of questions about the likely causes of the increase, which the investigators say could be related to environmental factors.
Investigators from the EPIMAD registry in France tracked rates of CD among nearly six million patients in northern France between 1988 and 2005. They found that the incidence of CD among all patients increased 20.7 percent but that rates had stabilized 10 years into the study. Among young people less than 19 years of age however, the incidence of CD increased linearly by 48.5 percent.
The cause of the increased incidence of CD among young people is unknown, but investigators say aggravating factors like environmental pollution and changes in diet or smoking habits could be culprits.
“Since we now know that CD disproportionately affects young people, future studies to uncover its cause should focus on this age group,” said Guillaume Savoye, MD, EPIMAD registry and department of gastroenterology, University Hospital, Rouen, France.

All very interesting (and yet troubling) trends.

Additional Genes Linked to Crohn's - IL23R and 30 Others

2009-09-05T22:07:00.001-04:00

Saw two posts on an About.com IBD blog (post one, post two) about new studies that found several genes that could be linked to Crohn's Disease. The first study pointed to the IL23R gene. The second study pointed to over 30 possible genes. It's seems to be unclear at this point how these genes are expressed in the body to contribute to the disease, but I assume that's the next step.

Microbial Symbiosis (e.g. B. fragilis) May Prevent Intestinal Inflammatory Disease

2009-09-05T21:46:00.000-04:00

As discussed in previous posts (see Reduced Diversity of Faecal Microbiota in Crohn's Disease, Localized Dysbiosis of lactobacilli and the Clostridium leptum Subgroup May Be Related to UC, Lack of Faecalibacterium prausnitzii Bacteria May Contribute to Crohn's), imbalances or reduced numbers of certain types of bacteria in the gut have been linked to Crohn's disease.

A further example of this was demonstrated by researchers in regard to the Bacteroides fragilis bacteria. When the bacteria was not present in the gut and a pathogenic bacteria, in this case Helicobacter hepaticus, was introduced, intestinal inflammation was induced. The B. fragilis bacteria produces Polysaccharide A (PSA), which suppresses the inflammatory response of the immune system (by suppressing IL-17 production).

With hundreds of bacteria in the gut, it's unclear which ones are needed to have a "normal" balance. And it's also unclear what is "normal" based on genetic pre-disposition. Nonetheless, it does highlight the need for further investigation into how all of these bacteria interact and how exposure, diet, and other factors can influence the balance of those interactions.

Myoconda (Anti-Biotic) Kills MAP as a Treatment for Crohn's

2009-09-05T19:45:00.000-04:00

A follow-up to my last post about the body of evidence pointing towards MAP as a contributing cause to Crohn's, I came across a commercial anti-biotic being used in the treatment of the disease. The drug, Myoconda, is a combination of three already used and registered anti-biotics. More from the manufacturer's website (Giaconda Ltd):

Myoconda®, the Company’s therapy for the treatment of Crohn’s Disease is a combination of three registered antibiotics - rifabutin, clarithromycin and clofazimine. These three drugs are widely marketed world-wide for the treatment of mycobacterial and other infections. Myoconda® presents these three compounds in a specific patented combination.

Myoconda® is based on the proposition that Crohn’s Disease is caused by infection. Prof. Borody has long been at the forefront of this approach, which is gaining increasing acceptance among gastrointestinal specialists worldwide. Prof. Borody has published significant data demonstrating that patients treated with Myoconda®’s antibiotic combination experience long-term remission of clinical symptoms and inflammation, some for up to nine years.
The results of a Phase II clinical trial of Myoconda®, conducted at the Centre for Digestive Diseases (CDD), were published in 2002. This was followed up with a full retrospective analysis of all CDD Crohn’s patients treated for at least six months with anti-MAP therapy. This analysis of 52 patients demonstrated a remission rate of 65% with a clinical response of almost 95%. These results exceed those of any Crohn’s therapy on the market by major margins.

Myoconda's Investigational New Drug (IND) application was approved by the US FDA in April 2007, allowing it to proceed with Phase 2/3 trials of the drug. It doesn't quite seem to be the silver bullet yet, but certainly is a very promising start.

Link Between Mycobacterium avium paratuberculosis (MAP) Bacteria and Crohn's

2009-09-05T17:04:00.001-04:00

Someone on one of the HealingWell.com message boards was pretty passionate about a strong link between a bacteria called Mycobacterium avium paratuberculosis (MAP) and Crohn's Disease. The bacteria is found in milk and beef from cows and is known to cause a very similar disease (in terms of symptoms) in cows called Johne's Disease.

Here's an excerpt about Johne's Disease and how people may get exposed to MAP:

The microorganism, mycobacterium avium subspecies paratuberculosis, has been established in the veterinary literature to be the cause for Johne's disease, a disease causing colitis in cattle, sheep, and subhuman primate species. This disease resembles, clinically, Crohn’s disease in humans and acts very much the same. Studies in England and in Wales have shown the presence of mycobacterium paratuberculosis in milk and water supplies. It is known that infected cows secrete this bacteria in milk and hence, milk borne infection appears to be theoretically possible.

Here's an excerpt from a Science Daily article (Dec 2007):

It is thought that the Mycobacteria make their way into the body’s system via cows’ milk and other dairy products. In cattle it can cause an illness called Johne's disease - a wasting, diarrhoeal condition. Until now, however, it has been unclear how this bacterium could trigger intestinal inflammation in humans.
Professor Jon Rhodes, from the University’s School of Clinical Sciences, explains: “Mycobacterium paratuberculosis has been found within Crohn’s disease tissue but there has been much controversy concerning its role in the disease. We have now shown that these Mycobacteria release a complex molecule containing a sugar, called mannose. This molecule prevents a type of white blood cells, called macrophages, from killing internalised E.Coli.”
Scientists have previously shown that people with Crohn’s disease have increased numbers of a ‘sticky’ type of E.coli and weakened ability to fight off intestinal bacteria. The suppressive effect of the Mycobacterial molecule on this type of white blood cell suggests it is a likely mechanism for weakening the body’s defence against the bacteria.
Professor Rhodes added: "We also found that this bacterium is a likely trigger for a circulating antibody protein (ASCA) that is found in about two thirds of patients with Crohn's disease, suggesting that these people may have been infected by the Mycobacterium."

MAP could release mannose (a sugar that acts as an immune inhibitor), which could then allow other bacteria to get overgrown (e.g. E. Coli).

Given today's milk processing, you might think that the pasteurization process would kill all bacteria in retail sold milk, including MAP. So how could someone ever be exposed to this type of bacteria in the first place? You'd be wrong, though. An excerpt from a Canada.com article commenting on milk in the U.S. and the possible link between MAP and Crohn's mentions how 3% of US retail milk has live MAP bacteria:

As part of his research, Dr. Rioux is focusing on the MAP bacteria. He believes it's plausible the bacteria may be a trigger for Crohn's disease. A recent study showed it was present in the intestines of some Crohn's patients.

"It found there was a significant association, finding this mycobacterium in Crohn's patients versus those who do not have Crohn's disease...we can see the footprints of this organism associated with Crohn's disease, but we can't really prove it's at the scene of the crime so to speak," adds Dr. Rioux.

The Dairy Farmers of Canada says a Guelph, Ontario study in 2002 found the bacteria in Ontario milk, though it wasn't alive. Yet a 2005 study in the United States did find live bacteria in almost 3% of retail milk sampled.

"It can survive pasteurization in a limited number of samples, and only in low numbers, so that would not explain the high numbers of Crohn's disease patients we have in the developed world at all," says Barkema.

The Food Directorate of Health Canada calls MAP an "emerging organism of concern." At a recent meeting in Ottawa, it called for more research and testing of food products, to see just how often MAP is found in the products we consume.

Other theories about milk actually go even further, suggesting that any bacteria presence, dead or alive, can contribute to Crohn's disease. Even the bacteria that are killed during the pasteurization process still cause problems. Apparently, although the bacteria are dead, the cell walls and remnants of the bacteria are still present in the milk. These fragments would most certainly be present throughout your GI tract as well as around the body due to leakage through the intestinal wall and circulation around the body via the blood-stream. For example, the fragments could get lodged in your joints in your hands, leading to an immune response there, which would cause arthritis.

There do appear to be some trials being conducted to use antibiotic mixes to kill the MAP infection. Worth looking into more.

Reduced Diversity of Faecal Microbiota in Crohn's Disease

2009-08-31T00:28:00.000-04:00

Another research study (related to previous posts) found that:

... a reduced complexity of the bacterial phylum Firmicutes as a signature of the faecal microbiota in patients with CD. It also indicated the presence of new bacterial species.

The question is why is there less of that bacteria? Overgrowth from other bacteria? Lack of exposure to that bacteria? Hyper-immune response to that bacteria that result in immune imbalances due to the reduction in modulating or regulating effects of the bacteria?

Another interesting thing to follow-up on: small bowel bacterial overgrowth syndrome. Could there be a relationship with Crohns?

Localized Dysbiosis of lactobacilli and the Clostridium leptum Subgroup May Be Related to UC

2009-08-31T00:12:00.000-04:00

This study (related to my previous post) highlights how there is localized dysbiosis (i.e. bacterial imbalances) in ulcerative colitis patients. Specifically, the lactobacilli and Clostridium leptum subgroups are lower than expected.

Also, the concentration of these bacteria were actually different within the same patient from site to site within their colon.

Here's the excerpt:

The data revealed that lactobacilli and the Clostridium leptum subgroup were significantly different between the ulcerated and the nonulcerated regions. It also was noted that for lactobacilli, the composition varied significantly between biopsy sites irrespective of the location of UC in the gut but that the composition of the Clostridium leptum subgroup showed significant differences between paired samples from UC in the rectum and not in the left colon. Localized dysbiosis of the mucosa-associated intestinal microflora, especially for lactobacilli and the Clostridium leptum subgroup, may be closely related to UC.

Lack of Faecalibacterium prausnitzii Bacteria May Contribute to Crohn's

2009-08-30T23:26:00.000-04:00

Interesting research from last year.

Here's the text of the article:

Washington, Oct 21 (ANI): Lack of a specific bacterium in the gut may be a cause of Crohn’’s disease, an inflammatorygastrointestinal disorder, according to a team of French researchers.
Researchers from the Institut National de la Recherche Agronomique have highlighted the bug, Faecalibacterium prausnitzii, which they show secretes biochemicals that reduce inflammation.
The researchers have already shown that patients with Crohn’’s disease have a marked deficiency in bacteria from the Clostridium leptum group.
Now, their latest study shows that F. prausnitzii, a major component of this group, accounts for a large part of the deficit.
The researchers found that Crohn’’s patients who underwent bowel surgery were more likely to experience a recurrence of the condition if they had low levels of F. prausnitzii.
And in experiments on cultured cells, they showed that liquid in which F. prausnitzii had been grown provided an anti-inflammatory effect.
According to researchers, if the ongoing animal trials prove successful, human patients could benefit from a probiotic treatment with F. prausnitzii.
Dr Anton Emmanuel, medical director of the digestive disorders charity Core, agreed that the study raised the possibility of a therapeutic replacement therapy.
“It would be interesting to see how this finding relates to the emerging body of evidence looking at genetic changes in some patients with Crohn’’s disease, with the known abnormal gene being one that codes for the body’’s ability to recognise foreign bacteria,” BBC quoted Emmanuel, as saying.
The study appears in Proceedings of the National Academy of Sciences. (ANI)

Another quick article on the topic.

Some Interesting Blogs and Forums

2009-08-28T18:58:00.000-04:00

Upon doing a Google search for "gaining weight on the Specific Carbohydrate Diet", I came across several pretty interesting blogs and forums. Here they are (short list):

HealingWell.com Crohn's Disease Articles - array of articles on IBD and Crohn's
HealingWell.com Crohn's Disease Forum - seems to be quite a bit of activity on there, including folks that are very well read up on the latest IBD research studies. I was pretty impressed by people's knowledge.
Fanatical Adherence - blog from a young man on his attempt to have a "fanatical adherence" to the SCD diet. Interesting note, he regrets having taken himself off meds too soon as he developed a stricture in his colon as a result of excessive inflammation -- leading to a resection surgery. He continues his diet. He's 5'10" and at one point was as low as 115 lbs, but now a healthy 150 lbs. (Although, ominously, he hasn't posted anything in about a year).
Living With Crohn's Disease - collection of blog postings via WordPress that cover a wide range of topics from the basics of the disease, to treatment options, to drug side-effects, to dealing with your doctor, etc.

Dr. Hoffman on Crohn's Disease and Ulcerative Colitis

2009-08-26T18:55:00.001-04:00

I came across several great articles from Dr. Hoffman on the topic of IBD, specifically Crohn's and Ulcerative Colitis. Hoffman runs a center that combines both modern and natural medicines in treating illnesses. I'm still reading these articles, but they are so helpful I thought I would forward them on. I found the first article off of the scdiet.org website, which is also great. Not a coincidence that Hoffman wrote the foreword on the Breaking the Vicious Cycle book.

Here are links to a few articles:

Crohn's Disease and Ulcerative Colitis - great article from 1995 that highlights the Specific Carbohydrate Diet and even new therapies like low-dose naltrexone
Addressing inflammatory bowel disease - includes a very long list of treatment options with discussion of each
Candida - discussion of candida overgrowth / infections and its link to IBS. This is why I am currently drinking Chamamille tea (as it is an anti-fungal).
Inflammatory bowel disease update - similar to the first article listed above, but also includes a few success stories that are quite interesting (all involving IV treatment which I had not thought of)
How Does Dr. Hoffman Treat Crohn's and Ulcerative Colitis? - discussion of treatment approach that Dr. Homman might take (excerpt included below)

And here's a sample of a treatment program:

An example of our treatment program is described below.
TESTING:
IgG RAST food panel, Candida antibodies, anti-gliadin antibodies, Vitamin D, B12, folic acid, homocysteine, zinc, iron, ferritin, testosterone (healing in men), and DHEA (healing in both sexes)
DIET:
Specific Carbohydrate Diet (tailored to reflect results of IgG RAST)
SUPPLEMENTS:
SCD-Compliant Probiotics, Vitamin D, Enteric-coated Fish Oil, EGCG, Curcumin, Zinc, L-glutamine, Methylcobalamin, Methylfolate, DHEA
OTHER THERAPIES:
Low-dose Naltrexone, Chrohn's/Colitis intravenous "drips", antifungal medication (Nystatin, Diflucan, etc.), bio-identical testosterone

There was a very long list of potential therapies and supplements in the above articles that I will likely be investigating more and experimenting with myself. His services don't seem too expensive, but he doesn't accept any forms of insurance, so its all out of pocket. They appear to have offices in Manhattan (New York) only.

Dr. Whitaker on Crohn's Treatment Options

2009-08-20T00:33:00.000-04:00

I mentioned that Dr. Whitaker recently commented in his newsletter on the latest treatment options for Crohn's. I thought I would post that here:

A reader wrote in and asked:
Would you supply me with whatever information you have on dealing with Crohn's disease? I have had it for 36 years and they want to do surgery and remove my large bowel. I don't want to go that route. Any nutritional information you can give me would be helpful. --Pastor David, NE

Dr Whitaker wrote back:
The first thing I would recommend isn't a nutrient but a safe, effective drug that your doctor probably doesn't know about: LOW-DOSE NALTREXONE (LDN). In a recent pilot study, Jill Smith, MD, of the Pennsylvania State College of Medicine treated patients with Crohn's disease with 4.5 MG of LDN at bedtime for 12 weeks, and then followed them for an additonal month. Eighty-nine percent of the participants responded to LDN, and 67 percent went into remission. Dr Smith is now conducting a large phase II placebo-controlled trial of LDN involving children with Crohn's. To learn more vist lowdosenaltrexone.org

Diet modifications are also helpful. But now, you likely know what foods exacerbate your symptoms. If you aren't sure, try eliminating common problematic items such as milk, gluten, citrus, tomatoes, additives, preservatives, sugars, and starches.

Crohn's is associated with poor nutritional status, which means a good daily multivitamin is essential. Correcting vitamin D deficiencies alleviates symptoms in some patients, so make sure you get adequate sun exposure and talk to your doctor about testing your blood level of vitamin D (25(OH)D). If its below 50 ng/mL, take enough supplemental vitamin D to bring it into the optimal range.

Other supplements with proven benefits for Crohn's disease include aloe vera (I've heard good things about AMP Floracel and Digestinol), the amino acid glutamine, fish oil, curcumin extract (10% of tumeric is curcumin and 90% something else), and probiotics. Look for these supplements in your health food store or call (800) 810-6655 to order.

To read more about Crohn's, visit the Subscriber Center at drwhitaker.com. I truly hope these suggestions will improve your condition. Give them a try and let me know how you're doing. -- JW

To list those out:

Low Dose Naltrexone
Diet modifications
Daily multivitamin
Vitamin D
Aloe vera
Glutamine
Fish oil
Curcumin extract
Probiotics

Low Dose Naltrexone (LDN) Could Help in Treating Crohn's

2009-08-19T23:49:00.000-04:00

In a recent Dr. Whitaker newsletter, Whitaker discussed some of the natural or alternative treatment options for Crohn's sufferers. The one that caught my eye was Low Dose Naltrexone (LDN). Naltrexone is an FDA approved drug from 1984 that has been used to help people overcome their addiction to herion and opium addictions. For that use, the drug is given in 50mg doses and helps to block the effects of the drugs. Researchers have been experimenting with lower dose uses (e.g. 3 - 5mg) of the drug to treat a variety of immune disorders from cancer to Crohn's with very promising results.

The drug works by boosting the immune system. Specifically, LDN increases the body's production of endorphins and enkephalin. These opiods apparently have some regulating effect on the immune system (although the exact effect appears to be unknown). From what I've gathered, there are other immune therapies, such as acupuncture, that may have a similar effect. Acupuncture, for instance, likely triggers the release of endorphins as well.

The recent study conducted at Pennsylvania State University to use LDN for Crohn's therapy used 4.5mg at night before bedtime and had great results. The positive results prompted additional NIH funding to proceed with clinical trials.

Another source of info (in addition to Wikipedia) is this website: http://lowdosenaltrexone.org/. It includes information on how and where to get low-dose naltrexone. Naltrexone is already widely available, but you need to get it altered to put it in low-dose form. There are a limited number of pharmacies that do this.

Another thought that this treatment prompts is that this treatment works in direct opposition to most traditional therapies. While most prescription drugs are meant to stop the immune system (i.e. immunosuppressants like Entocort or Prednisone), this treatment is meant to boost the immune system. Which way is right?

Low-carb, high protein diet

2009-08-02T04:56:00.000-04:00

I came across this via another web search. It's off of a ministry website. Perhaps the pastor is really into health? Here's the link to the diet. I only skimmed it, so will have to read it in more detail another time. There is a lot of content. Unclear how much of it is opinion vs. real research.

Glutamine helps heal stomach ulcers

2009-08-02T04:17:00.000-04:00

I came across a short article in Life Extension titled "Glutamine helps heal stomach ulcers" and thought it might be useful for dealing with Crohn's inflammation as well. Might be a stretch, but worth a try to add L-Glutamine (perhaps 500-mg per day) to see if there is any benefit.

Here is the text of the article:

In the May, 2009 of the Journal of Nutrition, researchers from Beth Israel Deaconess Medical Center and the Massachusetts Institute of Technology report that the amino acid glutamine could help heal the damage caused by H. pylori, the bacteria that causes stomach ulcers and many cases of stomach cancer.
In earlier research, Susan Hagen, PhD and her colleagues discovered that glutamine prevented the death of cultured stomach cells from H. pylori-produced ammonia. For the current experiment, they divided 105 mice to receive standard diets or diets in which L-glutamine replaced 5 percent of total calories. After two weeks, some of the mice in each group were infected with H. pylori. The animals were followed for 20 weeks, during which blood samples were analyzed for antibodies to immune cells that mediate the body’s response to H. Pylori. Additionally, tissue samples were obtained from the stomach and examined for damage, cancer progression and inflammation.
At the end of the 20 week period, infected animals that received L-glutamine had less inflammation than those that received the control diet. "Because many of the stomach pathologies during H. pylori infection are linked to high levels of inflammation, this result provides us with preliminary evidence that glutamine supplementation may be an alternative therapy for reducing the severity of infection," Dr Hagen explained.
"H. pylori bacteria infect more than half of the world's population and were recently identified as a Group 1 carcinogen by the World Health Organization," Dr Hagen added. "Approximately 5.5 percent of the entire global cancer burden is attributed to H. pylori infection and, worldwide, over 900,000 new cases of gastric cancer develop each year. The possibility that an inexpensive, easy-to-use treatment could be used to modify the damaging effects of H. pylori infection warrants further study in clinical trials."

NOD2 Gene Mutation and Crohn's

2009-07-26T03:02:00.000-04:00

There seems to be general consensus that Crohn's disease has some genetic component to it, so I figured it was worth learning more about it. As I discovered, studies have found that the NOD2 gene protein is somehow directly involved in a large percentage of Crohn's cases (25%). The NOD2 gene is expressed in the immune system leukocyte cells and plays a role in the body's immune response by recognizing some of the molecules (muramyl dipeptide - MDP) that are part of bacterial cell walls. In essence, they are a sensor for bacteria. And as we know, there are trillions of bacteria in the gut, so there are plenty of bacterial cell walls for them to respond to. The gene also has a connection with the NF-kB protein which regulates the immune system. Here is an excerpt from one of the articles I linked to:

Today, it is known that Nod2 expresses a protein that recognizesa building block of bacterial cell walls, called muramyl dipeptide(MDP), effectively making it a bacterial sensor. Nod2 is expressedprimarily by bone-marrow-derived macrophages. In addition, theprotein NOD2 appears to play a role in the activation of NF-B,a major regulator of the production of pro-inflammatory cytoinessuch as tumour necrosis factor- (TNF) and interleukin IL-1ß.The relation is relevant because patients with Crohn's diseaseoverproduce NF-B and cytokines, and anti-inflammatory drugsrepresent the mainstays of treatment. Nevertheless, how Nod2contributes to the pathology of Crohn's disease has been anopen question — one that the modelling of the diseasein mice is beginning to answer.

So if everyone has the NOD2 gene, why do only Crohn's patients have problems with it? The problem arises due to mutations in the gene. The premise is that normal responses to bacterial infection should not create an overabundance of pro-inflammatory cytokines and hence should not create the inflammation associated with Crohn's disease. The mutated NOD2 genes cause the problems. But keep in mind, those genes are just responding to the environment - they don't cause it. Having a mutation in the NOD2 gene, then, doesn't necessarily cause the disease but instead makes people susceptible to it. Here's an excerpt:

The results of these studies help to explain the associationbetween Nod2 mutations and Crohn's disease. In finding Nod2to be an important immune mediator in the intestine, the studiesalso fuel the notion that bacterial infection is an importantpathogenetic factor. Indeed, as Kobayashi and colleagues suggest,Nod2 mutations may not play a directly causative role but, rather,may create an environment in the gut that renders it susceptibleto Crohn's disease. Further research is required to confirmthis and to elucidate the link between Nod2 mutations and -defensin,one that has already been established in humans.⁶ It is hopedthat the results of this research will open future therapeuticavenues.

Obvious take-aways for future research (from the perspective of managing or preventing the disease) then are to look into how to undo or prevent mutations in the NOD2 gene. The stem cell treatment previously discussed is presumably (if I'm understanding it correctly) one way to undo these mutations (i.e. by creating all immune cells from scratch using stem cells). I'm curious to learn more about alternatives like nutrigenomics, though, for example that could help prevent mutations. But more on that in another post.

Entocort and Budesonide

2009-07-26T01:37:00.000-04:00

I came across a good video describing how EntocortEC works. Entocort is a corticosteroid formulated to localize its effect on the ileum and ascending colon through a delayed release mechanism. Most Crohn's disease patients have the majority of inflammation in that area, hence it is meant to be a targeted drug. Because of the targeted delivery mechanism, it is mostly metabolized before it has a chance to reach the rest of the body, limiting the side-effects that many other cortiosteroid drugs (like prednisone, etc.) can cause.

The specific drug used in Entocort is budesonide. I was quite surprised to find that it is also used to treat rhinitis (nasal inflammation).

Stem Cell Treatment for Crohn's

2009-07-26T01:07:00.000-04:00

In skimming through some of the forums on CCFA.org, I saw someone mention a treatment option involving stem cells. A quick Google search revealed this article. Researchers in Barcelona, Italy, and the US have treated a handful of patients with promising results - with 80% achieving remission after being followed for 6 years after their treatment. The basic idea is to "reset" your immune system by 1) destroying all of your leukocyte cells (i.e. immune-system cells) via chemotherapy so that you can then 2) replace them all via a stem cell transplant. The premise is that the leukocyte cells you currently have are not working properly - i.e. they are incorrectly attacking microflora in your gut causing inflammation - and hence you need to get rid of all of them and re-build all your immune cells from scratch.

From the article it sounds like they only try this on patients that don't respond to medication or surgery, so it's kind of a last resort. And from the sound of it, it really should be. Sounds extreme.

Dr. Whitaker on Natural Remedies

2009-07-20T21:29:00.000-04:00

Just read through Dr. Whitaker's website and his page on digestive health. He has a page on treating diarrhea using natural remedies. Here is the abbreviated list of what he recommends:

Drink plenty of water
Add soluble fiber (the kind in fruits and legumes)
Replenish the beneficial bactera (probiotics)
Take digestive enzymes
Eliminate foods you may have allergies to (perhaps via the Specific Carbohydrate Diet)
Take the herb Una de gato (cat's claw)

One of the products offered on his website is PearlBiotics. It is a specially formulated probiotic supplement (in tablet form) that has a special coating (made in Japan) that allows the bacteria to survive the stomach so that they make it alive to the intestines.

Probiotics

2009-07-19T18:41:00.001-04:00

I'm reading up on probiotics. Here are a collection of good articles on the topic with some interesting findings. There are numerous health benefits associated with probiotics (outlined in all of the articles below). But then again, the name itself means that the agent produces some benefit in the host, so by definition it must have health benefits.

Background and findings

Wikipedia article "Probiotic" - includes a history of how probiotics were discovered and research and a list of strains
NIH - "An Introduction to Probiotics" - covers much of the same stuff
Life Extension Magazine - "Optimizing Digestive Health" - this is a fantastic article and highlights the benefits of BACILLUS COAGULANS. Although many people take probiotics supplements, much of the effort can often be wasted because those probiotics are not able to survive and colonize in your gut. Part of the reason is that natural food sources with live cultures (e.g. yogurt) are often on the shelf too long. With supplements, many bacteria are not able to make it through the manufacturing process. Dead bacteria, no matter how many make it to the intestines, don't really help. The goal is to have colonization in the gut. Bacillus coagulans is a probiotic bacteria that is able to survive through the harsh conditions of the stomach to make it to your intenstines. It then quickly multiples via spores to colonize the intestines. An additional benefit of the bacteria is that it produces lactic acid which aids in digestion and helps to kill off other pathogens. For those three reasons, it is a superior probiotic to other alternatives.

Natural Food Sources:

eHow article - "Food Sources of Probiotics" -

From reading all this, it seems that the tablet form of Bacillus coagulans is worth a try, as is continued inclusion of natural forms of probiotics in the diet (yogurt, kimchi, etc.).

The Specific Carbohydrate Diet

2009-07-19T15:12:00.000-04:00

I read through the Specific Carbohydrate Diet website (Breaking the Vicious Cycle). The basic premise of the diet is that proper GI function is dependent on having an appropriate balance of bacteria and microflora. When that balance is damaged, a vicious cycle is started that leads to the failure of the GI tract, GI diseases, and other related diseases stemming from malnutrition and the increase in toxins.

The GI tract has over 400 different kinds of bacteria (5 to 7 lbs of it in fact). Much of that bacteria should be "good" bacteria - organisms that aid in the digestion of foods and creation of vitamins. There are also "bad" bacteria present. These bacteria compete for limited space in your digestive system. These bacteria come into play, in particular, when you eat food that your body can't digest on its own. Whatever bacteria is present will break down and digest the bacteria. Good bacteria does good things while digesting this material. Bad bacteria produce bad things - like gas, toxins, etc.

This is where the "vicious cycle" begins. The good bacteria are lost (likely due to a poor diet or antibiotic drugs that are taken for other illnesses). In the absence of good bacteria, the bad bacteria proliferate. These bad bacteria contribute to inflammation in the GI tract. That inflammation further decreases the digestive tracts ability to absorb nutrients into the body. The lack of nutrition weakens the immune system, decreasing the body's ability to deal with the bad bacteria. The inflammation and change in pH also contribute to the loss of good bacteria.

And then the result of all of this is disease first in the GI tract - Crohn's disease, IBD, collitis - and then disease throughout the body - arthritis, excema, psoriasis, etc. Here's an explanation from the website on the vicious cycle and how it works:

When the balance in the gut is disturbed, an overgrowth of intestinal flora can result. Microbes migrate to the small intestine and stomach, inhibiting digestion and competing for nutrients. The gut then becomes overloaded with the byproducts of their digestion. This bacterial overgrowth can be triggered by overuse of antacids, reduced stomach acidity due to aging, weakening of the immune system through malnutrition or poor diet, and alteration of the microbial environment through antibiotic therapy.

The components of our diet, particularly carbohydrates, play an enormous role in influencing the type and number of our intestinal flora. When carbohydrates are not fully digested and absorbed, they remain in our gut, and become nutrition for the microbes we host. The microbes themselves must digest these unused carbohydrates, and they do this through the process of fermentation. The waste products of fermentation are gases, such as methane, carbon dioxide & hydrogen, and both lactic & acetic acids, as well as toxins. All serve to irritate and damage the gut. There is evidence that increased acidity in the gut due to malabsorption and fermentation of carbohydrates, may lead common harmless intestinal bacteria to mutate into more harmful ones. Further, lactic acid produced during the fermentation process has been implicated in the abnormal brain function and behaviour sometimes associated with intestinal disorders. The overgrowth of bacteria into the small intestine triggers a worsening cycle of gas and acid production, which further inhibits absorption and leads to yet more harmful byproducts of fermentation. The enzymes on the surface of the small intestines are destroyed by the now present bacteria, and this further disrupts the digestion and absorption of carbohydrates, leading to further bacterial overgrowth. As both the microbial flora and their byproducts damage the mucosal layer of the small intestine, it is provoked to produce excessive protective mucus, which further inhibits digestion and absorption.

Damage to the mucosal layer involves injury to the microvilli of our absorptive cells. These microvilli act as the last barrier between the nutrition we take in and our bloodstream. As our absorption is inhibited, folic acid and vitamin B12 deficiency can lead to impaired development of microvilli, while an abnormally thick layer of mucus prevents contact between microvilli enzymes and the carbohydrates we ingest. The small intestine responds to this spiraling irritation by producing more goblet (mucus-making) cells, creating yet more mucus. Finally, as the goblet cells become exhausted, the intestinal surface is laid bare, and is further damaged, and possibly ulcerated. As more carbohydrates are left in the gut, they cause water and nutrients to be pulled from the body into the colon, resulting in chronic diarrhea. Absorption is further hindered as diarrhea increases the rate with which food travels through the gut.

The Specific Carbohydrate Diet is intended to restore the proper balance in your system by 1) starving the bad bacteria, 2) introducing good bacteria, and 3) feeding the good bacteria so that it proliferates.

Here's an excerpt from the website with an explanation from them:

The allowed carbohydrates are monosaccharides and have a single molecule structure that allow them to be easily absorbed by the intestine wall. Complex carbohydrates which are disaccharides (double molecules) and polysaccharides (chain molecules) are not allowed. Complex carbohydrates that are not easily digested feed harmful bacteria in our intestines causing them to overgrow producing by products and inflaming the intestine wall. The diet works by starving out these bacteria and restoring the balance of bacteria in our gut.

The Specific Carbohydrate Diet™ is biologically correct because it is species appropriate. The allowed foods are mainly those that early man ate before agriculture began. The diet we evolved to eat over millions of years was predominantly one of meat, fish, eggs, vegetables, nuts, low-sugar fruits. Our modern diet including starches, grains, pasta, legumes, and breads has only been consumed for a mere 10,000 years. In the last hundred years the increase in complex sugars and chemical additives in the diet has led to a huge increase in health problems ranging from severe bowel disorders to obesity and brain function disorders. We have not adapted to eat this modern diet as there has not been enough time for natural selection to operate. It therefore makes sense to eat the diet we evolved with.

It certainly seems to make sense.