Find a Specific Carbohydrate Diet Support Group Near You

Local support groups for the Specific Carbohydrate Diet (SCD) are popping  up. Check the following link to find one in your area, or start one in your area: https://www.scders.com/scd-support.html

The SCD has been helpful for many with Crohn's Disease, Ulcerative Colitis, Celiac Disease, autism, ADHD, autoimmune diseases.

Pecanbread...It's Not Just for Kids Anymore

Many of you know that Pecanbread is the SCD website for parents with children on the SCD. We started the SCD for my son in 2008, who has had GI issues since one week of age and regressive autism. Pecanbread has been a godsend for me, especially for kid friendly recipes and trouble shooting ideas. The website is designed for kid issues, however, there is so much valuable information that it is just as useful for grown ups too. If you are following the SCD and have never thought to poke around on it, you may be surprised. They also add new info from time to time. Here's a just a few of their interesting pages:

SCD and Detoxification
Stages (may be helpful for some)
Recipes in stages
Sample Menus
Food Preparation
Common Mistakes
Overcoming Difficulties
Improving Results
Yeast and SCD yeast protocol
Constipation
How to enhance the SCD (although I don't believe between GAPS and SCD one is better in general than the other, it all depends on the individual chemistry, for us starting SCD was the better option)
Probiotics

Dr. Ayers on Jimmy Moore's Low Carb Show

Jimmy Moore did an interview with one of my favorite non-foodie bloggers, Dr. Art Ayers' of Cooling Inflammation. His Anti-Inflammatory Diet recommendations are very similar to the SCD. When we first started the SCD diet I thought of it as temporary, until we were healed. After more research I now think it has it's advantages even in the absence of GI issues. Dr. Ayers blog has been full of information on the role of dietary inflammation on gut flora. In his interview with Jimmy Moore here, he discusses the role of starches and antibiotics on gut flora in allergies, autoimmunity, and constipation, and much more. The interview is 39 minutes into the podcast.

Gut Flora, Nutrition, and Immunity

He's a fascinating article on the importance of gut flora: Human nutrition, the gut microbiome and the immune system. I saw a link to this gem on Paul Whiteley's blog Feed Me Research. It's been said they you can't fully discuss nutrition without the role of the gut flora. This article discusses some of the nuts and bolts of this, and for the most part it is easy to follow for us laypersons. The article makes several points worth mentioning:

"During the past 30 or so years, the North American diet has also shifted in terms of the relative contributions of different foods to total energy intake. Since 1970, two dietary 'epochs' can be distinguished based on the contribution of grains to overall calories (the mean increase in daily carbohydrate intake for men and women during this period was 62.4 g and 67.7 g, respectively). The consumption of other food items has also changed: Spearman's rank correlations between food availability and time, followed by adjustments of P values to reflect false discovery rates, show that the representation of 177 out of 214 items tracked by the USDA has increased or decreased significantly in US diets since 1970. For example, Americans now eat less beef and more chicken, and corn-derived sweeteners have increased at the expense of cane and beet sugars. Furthermore, methods of food modification and preparation have changed."

I find this interesting because chronic autoimmune and digestive diseases are on the rise. As a SCD'er I can't help but wonder if the drastic uptake of grains and sugar are a factor. A fun look at this change can be seen by Tom Naughton here and here.

"The intestinal microbiota can synthesize several vitamins involved in myriad aspects of microbial and host metabolism, including cobalamin (vitamin B12), pyridoxal phosphate (the active form of vitamin B6), which is involved in several enzymatic interconversions in amino-acid metabolism, pantothenic acid (vitamin B5), niacin (vitamin B3), biotin, tetrahydrofolate and vitamin K. In addition to vitamin B12, gut microbes produce a range of related molecules (corrinoids) with altered 'lower ligands', including analogues such as methyladenine and p-cresol. More than 80% of non-absorbed dietary vitamin B12 is converted to these alternative corrinoids. There is preliminary evidence to suggest that syntrophic relationships among members of the human microbiota, and the fitness of some taxa, may be based on the ability to generate, use or further transform various corrinoids."

I found this one interesting because those of us with gi issues also tend to be lacking in these vitamins. Vitamin B6 has also been found to help in autism, again pointing to a possible gut issue. As well as anemia in both populations:

"Likewise, iron is an essential micronutrient for bacteria. Given the low solubility of Fe3+, microbes have evolved the capacity to produce several high-affinity iron-binding siderophores. Microbes take up soluble Fe3+–siderophore complexes by several active transporters. Early studies in gnotobiotic animals showed a link between the gut microbiota and the development of iron deficiency. Germ-free but not conventionally raised rats become anaemic when fed a low-iron diet. The germ-free rats also show increased loss of iron in their faeces compared with their conventionally raised counterparts54. The iron balance that exists between host and microbiota is disturbed in a mouse model of Crohn's disease in which tumour-necrosis factor-α (TNF-α) expression is dysregulated: oral (but not parenteral) iron supplementation in these animals causes a shift in the gut microbial community composition, as defined by 16S ribosomal-RNA-based surveys, and exacerbates their ileitis."

This article also discusses the role of gut flora in obesity and diabetes. I was curious about which type of fat they used in this study reference: "Mice fed a high-fat diet have increased serum levels of lipopolysaccharide".
It turns out the researchers used corn and lard for the 72 percent fat diet for the mice. (I suspect a lot of corn and corn oil in the modern diet may not be a good thing).

Study for Those With Crohn's Disease, Ulcerative Colitis, and IBD

This is a super easy study to participate in. Rush University is seeking volunteers for a study on IBD. They currently need controls, which in this case are folks with IBD who are NOT following a special diet. Here is the official release:

Do you have Crohn’s disease, ulcerative colitis or indeterminate
colitis? Would you like to have a free stool analysis to see what
bacteria, yeast and other microbes are in your gastrointestinal tract?

Rush University Medical Center’s Department of Gastroenterology is
conducting a study to determine if the Specific Carbohydrate Diet
changes the population of microbes in the gastrointestinal tract.
This is a popular dietary program amongst patients, but there are no
published studies on how the diet works. Your participation in this
study will contribute to scientific knowledge regarding how diet can
be used to manage the symptoms of inflammatory bowel disease.
Participation will entail completing a series of surveys and mailing
two stool samples and a urine sample. This study can be done
completely from home through the mail and does not require presence at
Rush University Medical Center.

We are currently looking for volunteers 8 years of age or older with a formal
diagnosis of Crohn’s disease, ulcerative colitis or indeterminate
colitis who are NOT on the Specific Carbohydrate Diet or a similar
diet. Subjects must be located in the United States. Volunteers who
qualify for the study will receive a DNA analysis of their stool.

The principal investigator for this study is
Ece Mutlu, MD
Rush University Medical Center Department of Gastroenterology
1725 W. Harrison St., Ste. 207
Chicago, IL 60612
If you are interested in participating or have questions, please contact
(312) 942-3466.
clinical_trials@rush.edu

Wheat Lectins, Soybean Lectins, and the GI Tract

Here is an interesting piece of research highlighted by David of Healthy Diets and Science. (David's site is fun to browse around in). The study is titled "Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity". In this study the researchers find the plant lectins wheat germ agglutinin (WGA) and soybean agglutinin (SGA) can not only inhibit repair of gi cells when damaged, they also can block mucus production that the body uses to lubricate damaged areas. Some interesting highlights:

"Areas of epithelial cell necrosis and even zones of complete epithelial cell denudation are seen in biopsies of the stomach and intestine of mammals and insects fed plant lectins. Indeed, the plant lectin may function as a natural insecticide. Epithelial cell microvilli particularly are affected by lectin exposure..."

"Epithelial cells lining the GI tract in vivo, unlike cells in vitro, are constantly exposed to mechanical stress and, consequently, frequently suffer plasma membrane disruptions. However, cell death is not the only outcome of this type of injury: cells are capable of rapidly repairing and thereby surviving plasma membrane disruptions. One key step of the repair mechanism, reviewed in, is exocytotic. For large disruptions, this exocytotic reaction functions by adding a ‘patch’ of intracellular membrane to plasma membrane surrounding the disruption site."

"Exocytosis, which is required for membrane repair, is likely targeted by this class of toxin: previous studies showed that lectins can inhibit exocytosis, and we show here that, in particular, mucin exocytosis, which is coupled to repair in the cells we have studied, is potently inhibited by lectins. Moreover, we have found (data not shown) that inhibition of repair is rapid in onset (<1 min after addition to cell medium) and rapidly reversed by lectin washoff ."

"Because lectins, based on the damage they do to the lining of the GI tract, and their hypertrophic effect, have been implicated in, respectively, celiac disease and cancer, knowledge of this mechanism may have implications beyond a better understanding of food poisoning."

This post is linked to Grain-Free Tuesdays and Fight Back Fridays.

Bakers Yeast Allergy (ASCA): Lesser Known but Just as Nasty

It's Curious Role In Crohn's, Behcet's, Celiacs and Autoimmunity

As with all of my posts, if you want to get right to the research and skip my babble, just scroll down. I am not a doctor, I draw stuff for a living. This blog is my interpretation of the research. Please research these things on behalf of your health that of your loved ones, and discuss them with your doctor or nutritionist.


It seems as though Gluten and Casein are getting alot of attention these days. This is great news. Many folks have been suffering months, years, decades with mysterious afflictions only to find out it was something they ate. There are many reports that children with Autism and ADHD seem to have trouble with at least one of these. Both of these have also been known to be genetic in some families, but not always.

For years the traditional medical community has strictly considered "allergies" to consist of hives, redness, swelling of the face or throat, and involve something called IgE antibodies produced by the immune system. Allergists would usually use skin prick tests to find these allergens. Researchers, however, would sometimes wind up scratching their heads (no pun intended). Some foods, or other items, where clearly causing a negative reaction in some people, but they were not able to get a response to a skin scratch test. They knew something else was going on. We now know that IgG antibodies were probably involved. They are an immune response with a different type of antibody, and tend to can cause more internal grief that can sometimes take a few days to develop, making them difficult to track down, or even suspect. IgG responses can cause a runny nose, chronic inflammation, migraine headaches, reflux, joint and muscular pain, digestive problems, canker sores, behavior problems, and the list goes on.... and you can develop IgG allergens to almost anything. They cannot be detected on a typical skin scratch test, but IgG's to food can be detected with a very simple blood test called an ELISA IgG Food Panel. One vial of blood can be run against 80 to 120 foods, depending on which labratory is used.

In 2007 Austrian researchers studying metastic renal cell carcinoma, a.k.a.kidney cancer, wanted to see if any cereal grains may be causing problems for these patients. They did an ELISA IgG Food panel for 113 foods and found one ingredient that stood out from the rest, and it wasn't a grain at all. Those with anti-Saccharomyces cerevisiae mannan antibodies (ASCA), a.k.a. bakers yeast allergy, had their median survival rate cut in more than half. The study concluded that ASCA alone was a source of "immune deviation and impaired immunosurveillance in predisposed RCC patients".

Although it does not have the notoriety of casein and gluten, bakers yeast allergy, known as anti-Saccharomyces cerevisiae mannan antibodies (ASCA), justly deserves a spotlight all it's own. In 1999 the commercial test for IgG ASCA became available. Since then researchers have been finding it in lots of places, especially in autoimmunity, and it's not always an innocent bystander. ASCA can be especially destructive in the GI tract. Just as a banana allergy can cross react and cause an allergy to latex, ASCA can cross react and make an individual allergic to yeast found in their own intestinal flora. ASCA appears to be one of the markers for Crohn's disease, an inflammatory bowel disease. While not all Crohn's patients have ASCA, studies have found up to 65 to 80 percent of them do. What's more, numerous studies have found that early age of onset plus having ASCA makes a patient at high risk for a severe course of the disease and a high chance of surgery. A 2003 study from John Hopkins School of Medicine, found that "ASCA titer was significantly associated with stricturing and penetrating CD".

ASCA has also been showing up in other bowel disorders as well, including Ulcerative Colitis and Celiac's Disease. Many researchers have come to the conclusion that anytime blood work reveals ASCA,and the patient has any gi tract issues, further testing for Inflammatory Bowel Disease, needs to be done.

Behcet's disease, an autoimmune disorder with chronic canker sores, vasculitis, and sometimes gi tract involvement, also tends to have ASCA. Another condition also plagued by canker sores is called Reccurent Aphthous Stomatis (RAS). Unlike Behcet's and Crohn's patients, RAS folks typically have canker sores and usually no gi involvement. Researchers, looking for a way to distinguish between Behcet's and RAS looked into ASCA, but found it in both. What's interesting is that Crohn's and Celiac's patients can be prone to canker sores and throat ulcers as well. Anyone plagued by frequent canker sores may want to consider the possibility of a bakers yeast allergy (or just get an ELISA IgG Food Panel to find any other food culprits).

ASCA is also showing up in other areas, although it's role may not be as clear: cystic fibrosis, acute myocardial infarction, autoimmune hepatitis, primary biliary cirrhosis, ankylosing spondylitis, infertility. It can also show up temporarily during a bacterial or viral infection in healthy individuals.

There are different ways folks can acquire a bakers yeast allergy. In Celiacs disease it seems to go hand in hand with the amount of intestinal damage one has acquired, and it seems to lessen on a gluten-free diet. A Finnish study noted "that serum levels of ASCA correlated with the grade of mucosal morphology, as the ASCA serum levels declined in accordance with mucosal healing". Researchers have also found that infections from another strain of yeast, Candida albincans, can also cause ASCA, perhaps due to cross reaction. Candida is normally present in a healthy gi tract in small amounts, but can become pathogenic when given the opportunity. Modern day diet and medications have contributed to thriving Candida. The healthy bacteria in our intestines keep the Candida in check, but when antibiotics kill off these bacteria, there is nothing to stand in the way. Combine that with the modern high sugar and processed diet (a buffet for yeasts) and liken it to feeding stray cats...they multiply and poop all over your flower beds.

ASCA can also be inherited, much like a gluten allergy is inherited in Celiacs. There appears to be a genetic predispostion in Crohn's and Behcet's disease. There have been several studies finding ASCA in healthy relatives of these patients. What's more, the genetic mechanism that may be responsible is something called Mannan Binding Lectin (MBL) deficiency. Mannan Binding Lectins are a part of the Innate Immune System. They look similar to bouquets of tulips. The tulip portion is designed to latch on to the carbohydrate surface of yeasts and certain bacteria. Once latched on they can sweep the particle away or call out to other components of the immune sytem to help with disposal. Roughly 55 percent, or so, of the population has adequate MBL, about 40 percent of so are lower on MBL and roughly 5-10 percent are deficient. When an individual is low, another part of the immune system steps in to take up the slack, and it's usually antibodies that do this. And if I understand correctly (again, I just draw stuff for a living) this may also put one at a higher risk for autoimmunity. MBL sweeps the particles away, where as an antibody may just charge on the spot, also attacking the tissue (again, I might not be getting the correct jist, just my interpretation). MBL deficiency is found in Crohn'patients and their healthy relatives. Swiss researchers concluded "enhanced mannan exposure stimulates specific immune responses in a subgroup of CD patients with genetically determined low MBL concentrations. This enhanced exposure contributes to the generation of ASCA."
Low MBL is also found in Lupus, otitis media, and a slew of other health issues. (I will devote a future post to MBL's).

Research points to avoidance of Bakers Yeast as a good thing to do for those with ASCA's. But as with most food allergies, you may have to read between the lines to find out where it's hidden. First of all it's in most yeast breads. Sourdough breads, however, can have different strains of yeast, which some folks with ACSA can tolerate and some cannot. Bakers yeast also tends to show up in crackers and many other "flat" baked goods ( I found this list). Many broths, gravy and sauce mixes, marinades, frozen dinners, etc will also have yeast extract as an ingredient, this has been shown to cross react with ASCA's. There is also another source of bakers yeast that, surprisingly enough, even some doctors are not aware of: the hepatitis B vaccine given to newborns, and at six weeks of age and again at six months. The two brands of hep B vaccines used are Merck "RECOMBIVAX HB"! and the GlaxoSmithKline "ENGERIX-B" While it is not my intent to discuss vaccines, from a food allergy stand point it does raise some cause for concern, as ASCA seems to play a curious role in autoimmunity. There has also been some interesting research on untreated Celiacs and a non-response to this vaccine. Here's an interesting article link atCeliac.com I have a few links at the end pertaining to the Heb B virus.

Sometimes just avoiding Bakers Yeast is not enough and one can have problems with many yeasts. Avoiding sugars that feed intestinal yeasts and avoiding fermented foods that harbor other strains of yeast might be required. This is often known as a Yeast-Free diet. The Specific Carbohydrate Diet is highly recommended for rebalance of intestinal flora.

Research:

Serum antibodies against Saccharomyces cerevisiae : a new prognostic indicator in metastatic renal-cell carcinoma

Antibodies to Saccharomyces cerevisiae in Crohn's disease: Higher titers are associated with a greater frequency of mutant NOD2/CARD15 alleles and with a higher probability of complicated disease

IBD serological panels: Facts and perspectives


Anti-Saccharomyces cerevisiae antibodies in patients with Crohn's disease

Anti-Saccharomyces cerevisiae antibody (ASCA) positivity is associated with increased risk for early surgery in Crohn's disease.

Serologic testing with ANCA, ASCA, and anti-OmpC in children and young adults with Crohn's disease and ulcerative colitis: diagnostic value and correlation with disease phenotype.

Diagnostic role and clinical correlates of anti-Saccharomyces cerevisiae antibodies (ASCA) and anti-neutrophil cytoplasmic antibodies (p-ANCA) in Italian patients with inflammatory bowel diseases.

Antineutrophil cytoplasmic antibodies, anti-Saccharomyces cerevisiae antibodies, and specific IgE to food allergens in children with inflammatory bowel diseases.

Anti-Saccharomyces cerevisiae antibodies in inflammatory bowel disease: a family study.

Clinical significance of anti-Saccharomyces cerevisiae antibody (ASCA) in Korean patients with Crohn's disease and its relationship to the disease clinical course.

Anti-Saccharomyces cerevisiae antibodies status is associated with oral involvement and disease severity in Crohn disease.

Predictive value of serologic markers in a population-based Norwegian cohort with inflammatory bowel disease.

Familial expression of anti-Saccharomyces cerevisiae mannan antibodies in affected and unaffected relatives of patients with Crohn's disease.

Seroreactivity against Saccharomyces cerevisiae in patients with Crohn's disease and celiac disease

Diagnostic value of anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies for inflammatory bowel disease: high prevalence in patients with celiac disease.

Elevated serum anti-Saccharomyces cerevisiae, anti-I2 and anti-OmpW antibody levels in patients with suspicion of celiac disease.

Serological responses to microbial antigens in celiac disease patients during a gluten-free diet.

Anti-Saccharomyces cerevisiae antibodies in coeliac disease.

Anti-Saccharomyces cerevisiae antibodies in Behçet's disease--a familial study.

Comparison of Behcet's Disease and Recurrent Aphthous Ulcer According to Characteristics of Gastrointestinal Symptoms

Anti-Saccharomyces cerevisiae antibodies - A novel serologic
marker for Behçet’s disease

Frequency of ASCA seropositivity in children with cystic fibrosis.

Anti-Saccharomyces cerevisiae antibodies in acute myocardial infarction.

Anti-Saccharomyces cerevisiae IgA antibodies are raised in ankylosing spondylitis and undifferentiated spondyloarthropathy

Yeast Antibodies Predict More Severe AS

Anti-Saccharomyces cerevisiae as unusual antibodies in autoimmune hepatitis.

Anti-Saccharomyces cerevisiae antibodies in primary biliary cirrhosis.

Autoantibodies and prediction of reproductive failure.

Autoantibodies in nonautoimmune individuals during infections

ASCA: genetic marker, predictor of disease, or marker of a response to an environmental antigen?

Candida albicans is an immunogen for anti-Saccharomyces cerevisiae antibody markers of Crohn's disease.

Colonization of mice by Candida albicans is promoted by chemically induced colitis and augments inflammatory responses through galectin-3.

Candida albicans is an immunogen for anti-Saccharomyces cerevisiae antibody markers of Crohn's disease.

Microbial mannan inhibits bacterial killing by macrophages: a possible pathogenic mechanism for Crohn's disease.

Pathogenic agents in inflammatory bowel diseases.

The dyspeptic macrophage 30 years later: an update in the pathogenesis of Crohn's disease

Association of Deficiency for Mannan-binding Lectin with Antimannan
Antibodies in Crohn’s Disease: A Family Study

Food-induced immune responses as origin of bowel disease?

Serum mannose-binding lectin levels are decreased in behcet's disease and associated with disease severity.

Association of HYPA haplotype in the mannose-binding lectin gene-2 with Behçet's disease

Association of mannose-binding lectin gene variation with disease severity and infections in a population-based cohort of systemic lupus erythematosus patients.

Genetic variants of the mannan-binding lectin are associated with immune reactivity to mannans in Crohn's disease.

Mannose-binding lectin deficiency is associated with early onset of polyarticular juvenile rheumatoid arthritis: a cohort study

Concurrent HLA-related response factors mediate recombinant hepatitis B vaccine major adverse events.

The development of rheumatoid arthritis after recombinant hepatitis B vaccination.

Humoral response to recombinant hepatitis B virus vaccine at birth: role of HLA and beyond