A recent study published in Complementary and Alternative Medicine (1) looked into the effect of fasting and diet on patients with rheumatoid arthritis (RA) and fibromyalgia (FM), and produced some interesting results. The investigation was carried out at an integrative medicine hospital in Germany, comparing the effects of a mostly vegetarian modified whole grain Mediterranean diet with a supervised modified fast of eight days on a small patient group. The researchers aimed to evaluate whether the Mediterranean diet or the 8-day fasting period were associated with changes in faecal flora, and whether changes in faecal flora might be associated with clinical improvements in the two diseases.
Although fasting is normally considered to be a period of consuming only water, the patients on the 8-day "modified fast" received free amounts of tea, 200 cl of fruit juice and small standardised quantities of light vegetable soup with a total maximum energy intake of 1255 kj (300 kcal)/day. Stool samples were sent for analysis of pH, mycology, bacteria and secretory IgA (sIgA) levels on admission to hospital, on the last day in hospital and at follow up after 3 months. There were no significant differences between the two groups, and "the results of this study do not suggest any relationship between diet, faecal culture analysis, sIgA and disease activity in patients with RA and FM" [The reason given was suggested to be due to the method of analysis used (quantitative stool culture), rather than gas-liquid chromatography, which had shown differences between omnivorous and vegan diets in a previous study(2)].
The results do however suggest that "the efficacy of fasting in the treatment of FM should be addressed in randomised trials, given that the clinical course in both, patients with FM and RA, appeared to be beneficially affected by fasting". The benefit was more apparent in the patients with RA (a result consistent with previous randomised trials). The authors point to specific effects of fasting on neuroendocrine regulation, central serotonin availability and quality of sleep from previous studies, but do not mention an obvious connection with fasting: it dramatically reduces the patient's lectin intake, when compared with a high lectin (Mediterranean = whole grain) diet. Additionally the study did not mention the blood group or secretor status of the patients, which can significantly alter levels of bacterial flora and sIgA.
For further information, see the book Arthritis - Fight it with the Blood Type Diet, by Dr. Peter D'Adamo
I would like to know an estimated time for the creation of antibodies against offending foods. I am getting ready to have a food allergy test done from Great Smokies Lab, and have been on a food rotation diet for a week. I want to give my body time to create these antibodies. Your input would be greatly appreciated.
Ailments resulting from ingestion of food and drink have been around for a long time: The first record of food sensitivity was by Hippocrates, who observed that milk could cause gastric upset and urticaria. In 200 A.D. Galen described a case of allergy to goat's milk, and in 1679 Willis observed that the ingestion of wine could bring on asthma. In the early 1900s, Shloss described several cases that established a strong correlation between food allergy and the development of atopic dermatitis. Duke was one of the first to make extensive observations of foods causing allergic responses. He linked food ingestion to bladder pain, Meniere's syndrome, colitis, gastrointestinal upset, and diarrhoea. Walzer then described experiments showing how ingested food antigens penetrate the intestinal lining and are transported through the bloodstream to mast cells in the skin. In the 1930s Rinkel first described food sensitivities that differed from the classic immediate anaphylactic reactions. The symptoms he described occurred hours or days after ingestion and could be masked or unmasked by the offending food. Rinkel's discovery has been confirmed by recent research demonstrating that delayed-type food allergies play a primary role in the immune system's response to ingestants. Brenman admits: "Involvement of the entire immune system is evident if the more prevalent delayed-type food allergy is to be explained"(1).
Rotation diets are one method used by individuals with reactions to foods for the prevention of new allergies from developing and to give their immune system a rest and the intestines a chance to heal. This type of diet may also significantly improve gastrointestinal symptoms in patients with concomitant environmental illness(2).
The basic concept of the diversified rotation diet is to achieve the following:
• Eliminate all major allergenic substances.
• Eat the remaining foods once every 4 days.
• Allow 2 to 4 days between food families.
A Rotation diet consists of eating tolerated foods at regularly spaced intervals of 4 to 7 days. This approach is based on the principle that infrequent consumption of tolerated foods is not likely to induce new sensitivities or increase any mild sensitivities, even in highly sensitized and immune-compromised individuals. As tolerance for eliminated foods returns, they may be added back into the rotation schedule without reactivation of the symptoms. Because individuals commonly experience difficulties in adhering to the diet, advice from a naturopath should be sought by anyone attempting to follow a rotation diet to assist with what may be a confusing process, as well to ensure proper nutritional intake.
Another, simpler way of dealing with food-related allergic symptoms is to follow a diet according to your blood group and secretor status, which can often be a good starting point for getting the immune system on track. For more information refer to 'Allergies - Fight them with the Blood Type Diet' By Dr. Peter D'Adamo, ISBN 0-399-15252-0.
Types of testing
As mentioned above, there are various different types of food allergy test available, and the most clinically relevant type of test can depend on the symptoms. The two most commonly used tests are for levels of immunoglobulins IgE (immediate hypersensitivity) and IgG (delayed hypersensitivity, or intolerance). Levels of IgG immunoglobulins may change with time and food intake, but there are a large number of variables that can influence this, see below. As a consequence, an allergy test might not always be the best way to approach food-related symptoms:
Intestinal permeability may be a related factor, as with increased gut permeability, greater quantities of antigens are allowed to penetrate the gut wall, resulting in an overly sensitised, reactive immune system in some individuals. Increased permeability has been implicated in various types of allergies(3). The converse may also be true, however, as in experimental models, IgG antibodies have been shown to increase intestinal permeability(4);
Blood group and secretor status can be an important factor when looking at allergies or intolerances, as certain foods containing lectins may have different effects on the individual according to their blood group, and autoimmune disease can be an issue as Lectins stimulate class II HLA antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells(5). Non-secretor status is associated with higher levels of IgE, intestinal permeability and insulin resistance, and lower Secretory IgA levels. These can all have implications for the effects of food ingestion;
Secretory IgA (sIgA) is the predominant immunoglobulin in intestinal secretions, the first-line defence against gastrointestinal pathogens including bacteria, parasites, fungi, toxins, and viruses. Normally abundant in saliva and other mucosal fluids, sIgA works by forming immune complexes with pathogenic microorganisms, allergenic food proteins, and carcinogens, preventing them from binding to the surface of absorptive cells. If sIgA response is impaired, mucosal tissue repair may be compromised, leading to reduced mucosal integrity, decreased tolerance mechanisms to foods, and reduced immunity against foreign invaders. Low sIgA levels can signal the presence of a previously unsuspected allergy or other autoimmune disorder. SIgA levels can be tested in the saliva or stool.
Appropriate bacterial colonisation is fundamental for adequate function of the intestine. The health-inducing bacteria are especially important because they suppress the growth of toxic bacteria. Reseeding the intestines is done through the use of probiotics and prebiotics, and the most appropriate varieties differ according to blood group. Probiotics are the normal bacteria found in the healthy intestines. Prebiotics are indigestible substances that help the healthy bacteria grow, such as larch arabinogalactan. Both prebiotics and probiotics also help by increasing the production of secretory IgA in the intestines, which also helps protect against bacteria and food allergens. Probiotic therapy has been shown to mitigate allergic inflammation, as demonstrated by the control of clinical symptoms and the reduction of local and systemic inflammatory markers. As such, probiotics can be used as tools to alleviate intestinal inflammation, normalize gut mucosal dysfunction, and downregulate hypersensitivity reactions, probably by increasing intestinal permeability and by improvement of the immunological barrier of the intestine(6). Intestinal bacterial colonisation can be assessed with a stool test.
The fingerprint test is a quick and easy way to check for intestinal integrity: if your fingerprint has white lines, it could be a sign of altered gut integrity. Butyrate as a supplement, or as butter ghee, may help to resolve this problem, as could taking anti-lectin supplements according to blood group(7).
Other nutrients may help decrease a local inflammatory reaction. Quercetin is a natural bioflavonoid that inhibits the release of inflammatory chemicals from sensitized mast cells, an especially useful effect for a sensitised gut. Quercetin and other bioflavonoids have been shown to decrease the release of intestinal prostaglandins and nitric oxide(8), inhibit the release of inflammatory chemicals from mast cells, scavenge free radicals, and inhibit irritability of the muscles of the intestines. It has also been shown to reduce the intestinal damage in animals caused by ingestion of food allergens(9).
Histamine levels may be important, as histamine is a prime mediator of allergy and asthma. It is generated in the central nervous system when the body is dehydrated. It is also released by mast cells located on the mucous membranes of the respiratory and gastrointestinal systems. Histamine works with the immune system, facilitating the movement of white blood cells to sites of microbe invasion. Anecdotal evidence confirms the efficacy of pure water as a therapeutic agent in this situation. Pure water should be a key component of regimens for states of hypersensitivity such as asthma and allergy.
[For references see link below]
A recent Japanese study (1) reasserts the correlation between ABO blood group and secretor status and intestinal alkaline phosphatase (IAP), an enzyme that aids digestion of fat in the diet. The study also concludes that evaluation of metabolic syndrome would be better if ABO blood group and secretor status are taken into account.
The abstact of the study, to be published in the journal Biochemical and Biophysical Research Communications, starts:
"Serum levels of intestinal alkaline phosphatase (IAP), a protein implicated in transcellular transport of chylomicrons, vary among ABO blood groups."
Background: the body produces proteins which bind with lipids (fats) and are transported around the bloodstream together as lipoproteins, where the fats are needed or stored. One way of measuring the amount of lipids transported in the blood is by measuring the proteins associated with lipid transport. An apolipoprotein is the protein component that combines with a lipid to form a lipoprotein. Chylomicrons are lipoprotein particles that are created by cells in the small intestine. Chylomicrons transport lipids to adipose tissue.
Variation in IAP according to blood group has been known for decades from previous studies, and is one of the reasons why individuals of different blood groups vary in their tolerance and metabolism of dietary fats.
To determine whether IAP is associated with chylomicron secretion in humans as well as rats, the researchers used the following method:
"Serum samples from 40 healthy subjects were obtained after overnight fast and 3h after a high-fat meal, and assayed for IAP and apolipoprotein B-48 (apoB-48), both proteins exclusive to intestine, although only apoB-48 is found in chylomicrons.
"The two proteins were greater in subjects without blood antigen A (B and O) than in those with this antigen (A and A; 2.4- and 4.7-fold for IAP and 1.5- and 2.0-fold for apoB-48 before and after the meal, respectively."
This is a significant difference between IAP and apoB-48 levels even when fasting.
The study concludes:
"Moreover, IAP and apoB-48 levels were strongly correlated in the subjects with the secretor phenotype (r>0.81). These results indicate that IAP is strongly involved in chylomicron formation and fatty acid metabolism might change among ABO blood type."
"In addition, ABO blood type classification in apoB-48 measurement would improve the diagnostic value in the evaluation of metabolic syndrome."
In other words, this is a mechanism by which non-secretors are more likely to get syndrome X than are secretors, and can be monitored with blood tests for IAP and apoB-48.
Involvement of intestinal alkaline phosphatase in serum apolipoprotein B-48 level and its association with ABO and secretor blood group types.
Nakano T, Shimanuki T, Matsushita M, et. al.
Biochem Biophys Res Commun, January 5, 2006.
Pubmed [16412386 ]
Are there diet options that will assist in quit smoking? Most difficult hurdle to quit. Am 53 years of age and have smoked since 9 years of age. Tried every marketed product. What's the crazy 'noose' that holds this habit inside my life so strongly? Better, what is the solution to ridding of this nasty and lethal habit? Thanks for your advice.
The World Health Organization estimates that tobacco kills around 4.9 million people a year, and that this will rise to 10 million by 2030 (1).
Smoking predisposes and contributes to cell-damaging changes throughout the body. Smokers have a greater incidence of coronary heart disease, myocardial infarction, peripheral vascular disease and reduced healing rates. People with diabetes and women who use oral contraceptives are at higher risk of circulatory problems, and respiratory disease is higher among smokers. Smoking increases the risk and severity of oral cancer, periodontal disease, and premalignancy in the oral cavity (see previous article on smoking).
A study on how dentists can play a part in helping their patients to give up smoking using a point of care test for measuring salivary nicotine metabolites (2) improved smoking quit rates by 17% at eight weeks.
A saliva test carried out during the visit to the dentist gave patients a visual scale of the level of toxic substances in the blood. Patients were given verbal counselling on smoking cessation, information about the effects of smoking on oral health (including photographs of smoking related disease), and literature packs. They were then asked to attend the dental clinic eight weeks later, with the objective of smoking cessation as measured by self report and confirmed by a salivary nicotine metabolite value of zero.
At eight weeks the saliva test showed that quit rates had improved significantly, with 23% of cases quitting compared with 6% of controls (based on the number of patients who attended the follow-up).
The authors recommend: "The identification, documentation, screening, and treatment of every tobacco user should become standard practice in all healthcare environments."
It appears that personalised feedback on exposure to tobacco derived toxins can improve motivation to quit smoking. Immediate and personalised biofeedback from the test reinforced counselling and placed potential quitters in a more supportive environment.
You may wish to consult your dentist on stopping smoking, however your naturopath may be able to offer further assistance:
In natural medicine the herb Lobelia inflata has been used to help people stop smoking. An active ingredient in the lobelia plant, lobeline, is similar to nicotine in its effect on the body. Like nicotine, it stimulates nerves in the central nervous system. In fact, lobeline has been used as a nicotine substitute in many anti-smoking products and preparations designed to break the smoking habit. In 1993, however, the U.S. Food and Drug Administration (FDA) prohibited the sale of lobeline-containing smoking products because, according to the FDA report, they lacked effectiveness in helping people quit or reduce smoking.
It is important to note that lobelia is a potentially toxic herb. Lobelia can be safely used in very small doses (particularly homeopathic doses), but moderate to large doses can cause serious adverse effects ranging from dry mouth and nausea to convulsions and even coma. Under the guidance of a qualified healthcare practitioner, however, lobelia, in combination with other herbs that affect the respiratory system, is considered relatively safe.
In homoeopathy there are various other remedies that may be used to help individuals stop smoking, including Caladium Seguinum, Natrum Carbonicum and Sepia, depending on the clinical picture.
(1) World Health Organization. Annual report from WHO's tobacco free initiative. Geneva: WHO, 1999.
(2) Effect of incorporating a 10 minute point of care test for salivary nicotine metabolites into a general practice based smoking cessation programme: randomised controlled trial.
Barnfather KD, Cope GF, Chapple IL.
BMJ. 2005 Oct 29;331(7523):999.
Cœliac disease is believed to affect 0.3-1% of the population in almost all countries and ethnic groups where it has been investigated. Previously regarded largely as a childhood problem it is now recognised to affect mostly adults, with about 25% of diagnoses being made in people over 60 years of age. Typically the presenting features of malabsorption (diarrhoea and weight loss) are suggestive of cœliac disease, but case presentations in the BMJ indicate that often few or no gastrointestinal symptoms are present, and some people with the condition can even be obese. The condition may also present insidiously, for example, with iron deficiency anaemia, osteoporosis or neurological symptoms
Historically diagnosis is based on atrophy of the lining of the small intestine, which recovers on a gluten-free diet. An endoscopic examination is needed to see this. Since antibody testing has become available, anti-endomysial and anti-transglutaminase antibodies are often used as a preliminary and less invasive method of screening.
Where both intestinal atrophy and blood antibodies are found the diagnosis of cœliac disease is straightforward. Difficulties arise when one or other of these is not found, and the diagnosis is particularly difficult when both are negative. The objective of orthodox medical diagnosis of cœliac disease is to determine treatment, i.e. a gluten-free diet. Some individuals with cœliac disease have no symptoms and find a gluten-free diet very limiting. When the diagnosis is in doubt and individuals have few or no classical symptoms of cœliac disease, treatment approach is more problematic.
Intestinal biopsy needs expertise: the disease may be patchy, so biopsies from several sites in the upper intestine should be carried out, and although cœliac disease is regarded as an upper small intestinal disorder, it is possible for atrophy to be present at the far end of the small intestine. If endoscopy is carried out following a positive antibody test, the individual may have already started a gluten-free diet, and the results of endoscopy can then be negative.
The results of antibody testing in any area depend on the population used to standardise the test, the particular test used, and the laboratory expertise. A combination of anti-endomysial and anti-transglutaminase antibodies is often used, and can be highly predictive of the condition. Antibody negative cases of cœliac disease do occur, a possible reason for this is IgA deficiency. This is more common in cœliac disease and since anti-endomysial and anti-transglutaminase antibodies are normally measured as immunoglobulin A antibodies they will be absent in individuals with IgA deficiency. Therefore in patients with IgA deficiency, IgG anti-endomysial and anti-transglutaminase antibodies need to be checked.
There is a strong association between being an ABH non-secretor and having overt cœliac disease. Non secretors being about 200% more likely to be cœliacs than secretors. Non-secretors also have lower levels of IgA than secretors. One study reported that up to 48% of patients with cœliac disease were reported to be ABH non-secretors. This appears to be especially true for the Lewis negative (a-b-) phenotype. Evidence suggests an increased prevalence of complications and cœliac-associated abnormalities is also found in non-secreting and Lewis negative individuals with cœliac disease.
This may go some way to explaining the 'atypical' cases of cœliac disease reported in the BMJ. Gluten-free diets are usually heavily reliant on corn/maize-based substitutes. Using corn as a staple is likely to increase weight due to the inhibiting effect it has on insulin production, which may cause weight gain, particularly in non-secretors, who are more prone to syndrome X.
The possibility of cœliac disease should be borne in mind even with 'atypical' presentations and negative diagnostic results. It would appear that eating according to reccomendations of blood group and secretor status would still be of benefit when diagnosed as cœliac or not, although with a positive diagnosis of cœliac disease gluten should also be avoided.
Saunders DS, Hurlstone DP, McAlindon ME, Hadjivassiliou M, Cross SS, Wild G, et al.
Antibody negative coeliac disease presenting with coeliac crisis in the elderly people—an easily missed diagnosis.
BMJ 2005;330: 775-6.
Furse RM, Mee AS.
Atypical presentation of coeliac disease.
BMJ 2005;330: 773-4.
Pathbase 3.0 - Celiac disease