Report of the UK and Eire IfHI Members Symposium, 7th April 2006

Part I

The first meeting of UK and Eire IfHI members was hosted by Stuart and Elspeth Semple, who offered attendees a warm welcome at their practice in Inveresk, Edinburgh. Most of the attendees were IfHI fellows or masters, and many reunited for the first time since the IfHI conferences in Phoenix.

Nick bowler, FIfHI, former biochemist and CEO of NAP Europe, lead the discussion for the morning, with a presentation based on his research over the last two years. Entitled “Surfing the genome with a blood type microscope,” and giving attendees a taste of what may be to come in future developments, he described the functional genomics of critical illness and injury in relation to blood group. The basis behind many of the studies that have found such a link is the haplotype, a set of single nucleotide polymorphisms (SNPs) found to be statistically associated as a group on a single chromatid (half of a chromosome). In terms of blood group, a haplotype in someone who is blood group O would be OO, the same as their genotype, one O gene inherited from each parent. The haplotype for someone who is AB could be AB or BA, depending on which gene was expressed more strongly. The haplotype for someone who is blood group A would be AA if they are homozygous, but a heterozygous individual with blood group A could have a haplotype of AO or OA. The strength of expression of certain genes may depend on environmental conditions.

This view of genetic expression is now challenging the existing dominant/recessive theory of blood groups (A and B being co-dominant and O being recessive), which was based on agglutination for transfusion purposes: if you have a gene for blood group A, you can’t receive blood from someone with the B antigen as you will certainly have strong IgM antibodies to B (from eating foods containing GalNAc (the A antigen) as a baby, which your immune system does not recognise as ‘self’). Whether you are Ao, AA or A1A2 does not matter in transfusion terms, you can still safely receive blood from a donor with any of those versions of blood group A1. This led to the concept of ‘dominance’ of blood groups A or B over O. Now functional gene expression is considered more important than the dominant and recessive theories, which means having Ao blood may give an individual different characteristics to AA blood. Even those with Ao blood could be different to each other depending on whether they express the A or O gene more strongly, effectively being ‘Ao’ or ‘Oa’, and the characteristics that go with each of those genes that we all relate to individuals with either blood groups O or A.

Nick Bowler then drew a link with Ayurvedic system of dosha categories being a possible ancient haplotyping system, with the 6 different ABO genotypes and the 9 possible haplotypes corresponding with the doshas vata, pitta and kapha, including possible combinations such as vata-pitta and pitta-vata as well as pure vata, for example. He pointed out that there are 82 verified genes at the 9q34 locus, the home of ABO blood group, controlling many characteristics that could give significant differences between individuals depending on blood group expression.

If ABO is interesting in genetic terms, ABH secretor status is even more so. Secretion of ABH antigens is under control of two linked genes on gene locus 19q13, another haplotype: a mutation (SNP variant) in one always goes with a mutation in the other. Presence of the secretor gene adds the H antigen (fucose) to red blood cells and body secretions. If this genetic code for secreting H is absent in the genetic material inherited from both parents, the individual will not secrete their red blood cell antigens into their body tissues, which is what we know as an ABH non-secretor. If they inherit the secretor gene from one parent only, they may still have some of the characteristics of a non-secretor: even though they secrete their ABH antigens, it was postulated that they may have some of the metabolic disease associations connected with being a non-secretor (but not necessarily the cell surface antigen-related ones). 19q13 has 288 verified genes related to this locus, even more than the ABO locus. Chromosome 19 has the highest gene density of all human chromosomes, and many of these relate to how the immune system works, which explains the difference between immune response of secretors and non-secretors: the humoral vs. the cellular response (TH1 and TH2). Other potentially genes on this chromosome relate to insulin-dependent diabetes, familial hypercholesterolaemia, and repair of other genes relating to repairing DNA damage from exposure to radiation and to other environmental pollutants.

The probability of having a particular combination of two specific alleles at a given locus can be calculated using a mathematical formula, which suggests that 2/3 of the general population will be heterozygous for secretor status (i.e. having both secretor and non-secretor genes), which may have a significance in itself when compared with homozygote secretors and non-secretors.

Lewis blood group status becomes significant in terms of the less common Lewis negative individuals (5-15%), those who express neither Lewis a nor Lewis b antigens. This is a separate system from ABH expression, but when combined with ABH haplotype and secretor haplotype, there are 20 possible combinations, including variations of the rare Bombay blood group (those who do not express the H antigen on their red blood cells). Using the probability formula described, nearly half the population having a Lewis positive expression (Lewis a+ b- non-secretors, and Lewis a- b+ secretors) will be heterozygous for the Lewis negative allele. The evolution of the blood group genes was discussed, with the linkages of each gene to the survival needs of different groups of people.

The final part of Nick Bowler’s talk related to cancer, with a review of the unitarian or trophoblastic theory that suggests cancerous cells are similar to trophoblasts, a type of embryonic stem cell that attaches the fertilised ovum to the wall of the uterus. Cancerous cells develop in anaerobic conditions as a result of continuous inflammation and not all tumour cells have the capability of inducing new cancers, only the ones which are similar to embryonic stem cells. The most primitive cells are A-like in structure. Loss of cell surface antigens in cancer leads to exposure of the Thompson Friedenreich (T) antigen, the body’s auto antigen against itself. The connection with the T antigen and blood groups A and M appears to relate to a failure of the immune system in individuals with these blood groups to identify the cancer cells, perhaps due to the similarity between primitive embryonic cells and the A and M antigens. There was a lot more information on this topic, which may be detailed in a later entry.

With the morning presentation completed, the assembled company then proceeded to attend to the most important event of the symposium, the lunch provided by Elspeth Semple. A tasty quinoa and vegetable soup, 100% Demeter rye bread/rice cakes/oatcakes, chicken, a selection of goats’ cheeses and other delicacies catered amply for the individuals of various blood groups and secretor status in attendance.

Part II later...

Question from Dr. Peter J Williams DC

Dr. Greenfield: I attended April, 2005, IFHI Conference and rec'd certification. Have been reading and practicing the BTD for years... recently retired from active chiropractic practice to teach and administer this work on a permanent basis. I visited an M.D. earlier this week and although he is at this point very curious he keeps asking questions and the latest one is: "...are there any morbidity or mortality rates in the general populace [as it concerns] the btd"? Do you have a good answer for this doctor? I told him to visit the dadamo web site and just start to read the seven research modules as well as Database 1. I further told him that such a question w/o attaching the application of the diet to any diseased state in a clinically controlled research environment, wherein the morbidity factors could be analyzed along with the outcomes, i.e. mortality rates, would be quite difficult, if not impossible. Can you add any insights to this as I keep the communication going with this curious M.D.? Thank you.

It is correct that a clinical trial of this nature would be very difficult to set up properly: to answer the question about morbidity and mortality in connection with the BTD requires some joined up thinking. The Blood Type Diet has not been around for that long in comparitive terms, and it takes many years to do mortality studies of adequate size relating to a specific subject. For a realistic representation of the situation any comprehensive clinical trial specific to the BTD would have to look at diet start date, compliance level (how do you accurately measure that over a period of years?), pre-existing illness and family history, blood group, secretor status and other minor blood groups, as well as other polymorphic data such as dermatoglyphic information etc. Then you would have to wait for people to die of natural or disease causes (i.e. not accidental death, unless you want to prove that one blood group is more accident-prone than another). Morbidity would be similar, but you just wait for those people to get sick, they don't have to die. Another issue that would be difficult to factor into such a trial is this: many people following a particular dietary régime may already have health problems, or concerns due to family history. Actively caring for oneself on a daily basis through selective food choice while rejecting societal pressures to conform to a stereotypical dietary 'norm' is a form of self-empowerment. How do you have a control group that takes account of this influence?

This begs the question "Does blood group in itself influence overall lifespan?" The results are conflicting. A study of Italian physicians showed a higher percentage of those over the age of 75 were blood group O (1), while two other studies showed that type B was associated with a longer lifespan (2), (3). It could be that group B individuals are healthier than their counterparts due to the typical modern diet being reasonably close to the ideal diet for those expressing the B antigen. Alternatively with regard to disease susceptibilities, as they tend to fall between groups A and O in this respect, this could be expected to translate into a higher percentage of group B individuals attaining a more advanced age. Either way, blood groups A and AB don't come off well in the longevity stakes.

Incidentally, the NN subtype of the MNSs blood grouping system may be associated with a slight increase in longevity (especially in women) (4). This could relate to the fact that the presence of the M antigen (absent in NN blood group) increases the incidence and mortality rates of many types of cancer due to a biochemical similarity to the A and TN antigens.

The question itself shows typical reductionist medical thinking: to put it another way, "Does following a specific diet according to one's blood group reduce illness and increase lifespan?" The fact is that the diet forms part of an entire programme that takes a person's individuality into account. It may be part of a comprehensive lifestyle strategy for natural preventive medicine in association with an ND. Patients are treated as individuals, not as a disease classification who should be a suitable candidate for some symptom-suppressive medication with side effects, or just to say: "Follow this diet as it is proven statistically that you will live longer and be healthier".

To see the bigger picture one needs to be able to connect two separate facts: firstly the hundreds of orthodox medical research papers showing physiological and psychological differences between individuals of varying blood groups, the connection between lectins and cell surface carbohydrates, the genetic linkage between ABO and other seemingly unrelated genes; secondly the millions of people who are following the BTD system worldwide because they have their own evidence of improvement in wellbeing. As in all holistic systems, the whole is more than the sum of the parts. It takes a little more than: "in the absence of any controlled clinical study to prove the existence of this concept it cannot exist in the real world."

Relevant studies are already being carried out on a small scale: The Southwest College of Naturopathic Medicine reported studies on diet and blood group at IfHI 2005, specifically the effect of ABO blood groups and soluble endothelial adhesion factors as a possible cause of atherogenesis. The Institute for Human Individuality is developing further study protocols.

Until the BTD has been around long enough and there are enough people following it to attract research money to design clinical trials that will satisfy the reductionist attitude, those seeking confirmation that the system works will have to use the outcome results of the hundreds of people who claim to have become healthier following this approach. Finally, whether or not a person lives longer or healthier, surely it is the quality of life that is more important?

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The British Medical Journal has published a study1 on how stress at work increases the risk of metabolic syndrome (or Syndrome X), a cluster of risk factors that increases the risk of heart disease and type 2 diabetes. Characteristics of the metabolic syndrome are abdominal obesity, signs that increase the likelihood of fatty deposits in the arteries (raised triglycerides, small LDL cholesterol particles, and low concentrations of HDL cholesterol), high blood pressure, insulin resistance (with or without glucose intolerance), and prothrombotic and proinflammatory states (three of these risk factors need to be present).

The results showed:

A dose-response relation was found between exposure to work stressors over 14 years and risk of the metabolic syndrome, independent of other relevant risk factors. Employees with chronic work stress (three or more exposures) were more than twice as likely to have the syndrome than those without work stress.

The authors conclude that the study provides evidence for the biological plausibility of the link between psychosocial stressors from everyday life and heart disease.

The connection between stress and disease was famously documented by Hans Selye2, and later by Dr. D'Adamo3.

Non-secretors of ABO blood group are statistically more at risk of metabolic syndrome and all its individual components, and also tend to respond differently to stress when compared with secretors of blood groups A and B. Non-secretors tend to have trouble clearing the catecholamines adrenaline and noradrenaline. Appropriate exercise, stress-reduction techniques and eating correctly according to secretor status as well as ABO blood group may help prevent the effects of work stress on heart disease risk factors.

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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

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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.

Valerie

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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]

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