Category: Blood Type Diet
No single diet theory can address all aspects of our individuality, and only a fool would claim that soy, red meat, grains, coconut oil or anything else is universally good or universally bad for everyone.
For example, people who are blood type O appear to derive significant benefit from a diet including hormone and antibiotic free meats and poultry. There is a very basic physiologic reason for this: those with type O blood have almost three times the levels of an enzyme in their intestines called ‘intestinal alkaline phosphatase’ (IAP) . This enzyme performs two very important functions in the body. First, IAP splits dietary cholesterol into smaller fragments, allowing for their proper breakdown. Second, IAP enhances the absorption of calcium from the diet. Now you'd think this was cutting-edge, late-breaking news since it is obviously of tremendous interest in these nutrigenomic times. However, the first observations were made over four decades ago.
In addition to these two critical functions IAP is an important influence on the ability of the digestive tract to heal. Thus in most of our type O patients (44% of the population) we see a marked improvement in their IBS, colitis and Crohn’s disease when they increase their protein and cut back on their carbohydrates. 
Blood type B makes considerable amounts of IAP as well, but type A’s make very little. This probably explains why most studies that have looked at heart disease and blood type show a significantly higher rate of problems with blood type A individuals. These folks really should follow a Mediterranean-type diet.
Later studies showed that type A not only secreted almost no alkaline phosphatase in their intestines, but whatever little they did secrete was in and of itself inactivated by the presence of their own A antigen. 
Thus, we have here one of the strongest indications for the long term benefit of a low-fat diet in type A, both with regard to the susceptibility to cardiovascular disease, and (although not mentioned here) their additional susceptibility to cancer. Following the type A eating plan, with its emphasis on a healthy fats, low animal protein and the avoidance of foods high in phenylalanine, is the best method to maximize digestive efficiency in type As, lower their level of intestinal dysfunction, and to influence their susceptibility to cardiovascular disease.
I am aware that you may not answer this question, but I will attempt because I am very confused. I understand the concept of eating for your blood type. But, as a cancer survivor and a Type A - I'm having trouble connecting the soy issue. I read an answer you wrote on your web site, but it was so medically scientific I couldn't understand.
Do you believe that soy is linked to cancer? If so, do you believe it is linked to Type A's? How do you justify putting someone on a high soy diet and not be concerned about cancer?
Thank you for your time.
Soy is not linked to cancer. Some cancers are estrogen sensitive and the theory is that since soy contains a form of plant estrogen, these plant estrogens might work to stimulate cancer, just as the biological forms of estrogen do.
However, soy estrogens are very weak estrogens (tamoxifen, by the way, is also a weak estrogen) so in most situations they block the estrogen receptor, more than stimulate it. Soy also has two other functions which make it desirable in cancer patients, particularly those who are type A. It contains a protein, soy bean agglutinin, which can target cancer cells directly and help to kill them.
The flavones in soy, in particular genistein help keep genes methylated, which tends to suppress any cancer tendencies. Finally soy is rich in saponin molecules which has independent ant-cancer mechanisms of their own. A 2008 Japanese study was published on soy consumption and rates of breast cancer. This study looked at 24,226 Japanese women aged 40 to 69. Women who had the most consistently high levels of genistein had the lowest rates of breast cancer.Historically, breast cancer rates in the United States have been 4-7 times those in Asia, whereas isoflavone intake in the United States is less than 1% that in Asian populations.
You will hear and read a lot of garbage about soy on the internet. If you were to take the advice of some of these sites and authorities, you might as well give up most nuts, fruits and vegetables since they contribute more phytoestrogens into the average American diet than do soy products. Yet Americans have higher breast cancer rates than cultures where soy is a bigger part of the diet. Finally, many of the anti-soy crusaders point to a potential for soy to block mineral absorption, as it contains chemicals phytates. This might be true if soy were consumed in astronomical doses, but better evidence suggests that phytate containing foods also appear to block the development of colon cancer as well.
Bear in mind it is not a perfect food in everyone. However if you look at the dynamics of the type A immune system, it would appear to be a very useful food in these people.
This Transfusion: Sword swallowers and sore throats | ABO in Neanderthals| Blood groups and endometriosis | Nutrigenomics and personalized diets | This News This Week
Welcome to The Weekly Transfusion, 1.6 for the week of April 26, 2009.
Sore throats more common in sword swallowers
Sword swallowers run a higher risk of injury when they are distracted or adding embellishments to their performance, but injured performers have a better prognosis than patients who suffer iatrogenic perforation....Major gastrointestinal bleeding sometimes occurs, and occasional chest pains tend to be treated without medical advice. Sword swallowers without healthcare coverage expose themselves to financial as well as physical risk.
I guess it is just that old 'occupational hazard' story, sort of like the study that discovered that woodpeckers don't seem to get headaches.
Genetic characterization of the ABO blood group in Neanderthals
The high polymorphism rate in the human ABO blood group gene seems to be related to susceptibility to different pathogens. It has been estimated that all genetic variation underlying the human ABO alleles appeared along the human lineage, after the divergence from the chimpanzee lineage. A paleogenetic analysis of the ABO blood group gene in Neandertals allows us to directly test for the presence of the ABO alleles in these extinct humans. We have analysed two male Neandertals that were retrieved under controlled conditions at the El Sidron site in Asturias (Spain) and that appeared to be almost free of modern human DNA contamination. We find a human specific diagnostic deletion for blood group O (O01 haplotype) in both Neandertal individuals. These results suggest that the genetic change responsible for the O blood group in humans predates the human and Neandertal divergence. A potential selective event associated with the emergence of the O allele may have therefore occurred after humans separated from their common ancestor with chimpanzees and before the human-Neandertal population divergence.
Certainly one of the major evolutionary advantages of being blood type O was their double-barreled antibodies; this blood type being the only one that reacts to both “A things” and “B things” in the environment. This probably provided an extra layer of protection against any number of epidemic diseases (plague, smallpox) and many endemic ones (flukes and parasites) as well. If this immune “hyper-vigilance” would go on to increase the rates of inflammation and auto-immune disease in their modern descendants, it should also be remembered that these are often diseases of later life, typically past child bearing and rearing age. Thus if it were a late-model alteration, it certainly provided a significant survival advantage. The Founder Effect can be seen in the characteristics and distribution of the genes for Rhesus Negative and O blood type among the early Mesolithic Period during the so called- ‘Happy Paleo’ period, which also shows some correlation with the ancestral haplogroups R1b and I. On the other hand blood type A seems to have conveyed a better chance of surviving the ‘lean’ period of the early Neolithic; a slightly different, perhaps better way to starve. Type A’s more tolerant immune system may have given them the benefit when it came widening the diet and exploring new foods.
ABO and Rh blood groups distribution in patients with endometriosis.
The blood group A was more predominant in women with endometriosis, while blood group O was less predominant. The overall risk of women with endometriosis and A blood group was 2.89 (95%CI, 1.85-4.52). No significant difference was detected in ABO and Rh blood groups in women with endometriosis according to the severity of disease. CONCLUSION: Women with endometriosis have a 2.9-fold increased risk in the A blood group distribution. The role of blood groups in the development of endometriosis remains to be determined.
I verified the observation back in 1988, when we were observing whether increases in opposing blood group antibodies were associated with any reproductive illnesses. We observed that in our small endometriosis group, all women were type A, and all virtually had elevated antibodies to foreign blood types (in their case, blood type B ). It did seem at he time to be an area ripe for future research, but I never got back to it. It is nice to see that others have observed the same tendencies.
The antibodies in the ABO system (isoagglutinins) called anti-A and anti-B are not normally present at birth. The antibodies develop between 3-6 months of age due to the stimulation of the newborn’s immune system by microbes and foods that possess antigens of an opposing blood type. In, for example, type O children, they will begin forming to type A and B red cell antigens as soon as the child starts eating food, because the A and B antigens are actually found in quite a number of plants. So, as soon as the child starts eating plant food, she'll be exposed to those antigens and start making antibodies against them.
Nutrigenomics and Personalized Diet: From Molecule to Intervention and Nutri-ethics
The relationships between food, nutrition science, and health outcomes have been intensively analyzed over the past century. Genomic variation among individuals and populations is a new factor that enriches and challenges our understanding of these complex relationships. Hence, the rapidly emerging intersection of nutritional science and genomics - nutrigenomics - was the focus of a special issue of OMICS: A Journal of Integrative Biology in December 2008 (Part 1). The OMICS Nutrigenomics Special Issue (Part 2) February 2009 is The relationships between food, nutrition science, and health outcomes have been intensively analyzed over the past century. Genomic variation among individuals and populations is a new factor that enriches and challenges our understanding of these complex relationships. Hence, the rapidly emerging intersection of nutritional science and genomics - nutrigenomics - was the focus of a special issue of OMICS: A Journal of Integrative Biology in December 2008 (Part 1). The OMICS Nutrigenomics Special Issue (Part 2) February 2009 is now available free online
Two entire issues on personalized nutrition with virtually no mention of any of the bio-markers that really determine individualized dietary functionality: ABO blood groups and secretor status. Maybe these bio-markers are just too low-tech for the average scientist. More likely, the nay-sayers behind the smear campaign I've had to endure over the last ten years have had their desired effects.
No matter, if you read enough history you soon realize that Billy Shakespeare had it right: 'Truth will out.'
News of the Week
- April 28 2009: Dr. Peter D'Adamo - Lecture at Backus Hospitalthe basics of 'Eating Right For Your Type.' Open to the general public. More information
- June 5-7 2009: Personalized Medicine in Form and Function. A weekend intensive seminar with naturopathic physician, scientist and author, Dr. Peter J. D'Adamo in Norwalk, CT. This seminar provides training in personalized nutrition determination using blood grouping, secretor status, epigenetic indicators, dermatoglyphics and biometrics. Extensive overview of the latest clinical and laboratory techniques, information systems and pharmacology. Certification will also be offered. Presented by the Institute for Human Individuality. CME's may be available. More information. SEATING IS EXTREMELY LIMITED. RESERVE YOUR SEATS NOW!
Until next time.
Here it is.. another Monday and another research grab-bag.
Five daily portions of fruits and vegetables raise serum antioxidants in three months
To explore the effects of increasing fruit and vegetable intake and the resulting effects on levels of circulating micronutrients in a community-dwelling population with an already high consumption of fruits and vegetables, 112 volunteers (86% women) underwent targeted dietary counseling for three months. At the beginning of the study and after 4, 8 and 12 weeks a food frequency questionnaire was filled in, and plasma levels of dietary antioxidants as well as biomarkers of oxidative lipid and protein damage were determined. Compared to baseline, especially the intake of fruits was significantly improved after 3 months of intervention, and mean plasma levels of lutein, zeaxanthin, β-cryptoxanthin, lycopene, α- and β-carotene, retinol, α-tocopherol, vitamin C and vitamin B6 were increased. Biomarkers of oxidative stress remained unchanged. Thus, a nutritional counseling program is capable of improving plasma levels of antioxidants even in a health-conscious population.
What is especially interesting about this study was that they used individuals who were already eating a pretty healthy diet, which just goes to show that even if you follow the BTD or GTD in terms of food choices, something as basic as making sure that you get the required amounts of recommended fruits and vegetables can make a big difference.
Schizophrenia, gluten, and low-carbohydrate, ketogenic diets
We report the unexpected resolution of longstanding schizophrenic symptoms after starting a low-carbohydrate, ketogenic diet. After a review of the literature, possible reasons for this include the metabolic consequences from the elimination of gluten from the diet, and the modulation of the disease of schizophrenia at the cellular level.
Previously, Dohan (Acta Psych Scand 1966, 42(2):125-152) observed a decrease in hospital admissions for schizophrenia in countries that had limited bread consumption during World War II, which suggested a possible relationship between bread and schizophrenia. Early work with lectins clearly showed that the brains of schizophrenics bind lectins differently than the brain tissue of non-schizoprhenics, which appears to make sense in that the carbohydrate content of schizophrenic brain tissue (in addition to dementia and a few other illnesses) revealed the existence of spherical deposits in the inner and middle molecular layers of the dentate gyrus in the hippocampal formation which contained fucose, galactose, N-acetyl galactosamine, N-acetyl glucosamine, sialic acid, mannose and chondroitin sulfate; many of these blood group active carbohydrates with known lectin binding affinities (link).
Over the years some of the most stirring letters I've received from book readers have centered around improvements in family members with schizophrenia. Almost all of these letters have been from or about blood type O schizophrenics, which may mean that the nutritional approach to schizophrenia might necessarily differ by foods and blood type. We are now only beginning to understand the effects of tissue glycosylation on the development and maintenance of brain neural networks (in particular those utilizing the blood group O specific antigen fucose).
Lectin-epithelial interactions in the human colon.
Similar changes in glycosylation occur in the colonic epithelium in inflammatory conditions such as ulcerative colitis and Crohn's disease and also in colon cancer and precancerous adenomatous polyps...Tools are now available to allow fast and accurate elucidation of glycosylation changes in epithelial disease, characterization of their potential lectin ligands, whether dietary, microbial or human, and determination of the functional significance of their interactions. This should prove a very fruitful area for future research with relevance to infectious, inflammatory and cancerous diseases of the epithelia.
In years past I've written about the effects of some dietary lectins on the cells of the colon, in particular the lectins found in mushrooms, fava beans and jackfruit. Most of the plant lectins are specific for the Thomsen-Friedenreich Antigen (T antigen) a pseudo blood group antigen which is often expressed in pre-malignant cells of the colon.
Here is a quote from a study examining fava (broad) bean lectin:
VFA stimulated an undifferentiated colon cancer cell line to differentiate into gland like structures. The adhesion molecule epCAM is involved in this. Dietary or therapeutic VFA may slow progression of colon cancer.
Here is a quote from a study examining standard commercial supermarket mushroom lectin:
Agaricus bisporus agglutinin (ABA) isolated from edible mushroom has a potent anti-proliferative effect on malignant colon cells with considerable therapeutic potential as an anti-neoplastic agent.
Here is a quote from a study examining jackfruit lectin:
(Jacalin) Lectin binding to human colonocytes can predict the presence of malignant and premalignant lesions of the colon, and has potential as a noninvasive screening tool for colorectal neoplasms.
If you have a family history of colon cancer, or have been diagnosed with colon abnormalities (such as polyps) you may want to investigate adding more of these foods to you diet (using the BTD as a guide to which would be best for you)
Human pseudogenes of the ABO family show a complex evolutionary dynamics and loss of function.
The GT6 glycosyltransferases gene family, that includes the AB0 blood group, shows a complex evolution pattern, with multiple events of gain and loss in different mammal species.These results suggest that some of these GT6 human pseudogenes may still be functional and retain some valuable unknown function in humans, in some case even at the protein level. The evolutionary analysis of all members of the GT6 family in humans allows an insight in their functional history, a process likely due to the interaction of the host glycans that they synthesize with pathogens; the past process that can be unravelled through the footprints left by natural selection in the extant genome variation.
Pseudogenes have been defined as nonfunctional sequences of genomic DNA originally derived from functional genes and are sometimes referred to as 'Junk DNA.' However new finding are suggestive that these areas of non-coding DNA and RNA may be involved in developmental changes which differentiate the functions linked to the blood type genes that occur between the various species.
Another nail in the coffin for the 'animals have blood types and don't eat right for their type' criticism of the Blood Type Diet by the nincompoop Andrew Weil.
The Effect of ABO Blood Types on Periodontal Status.
A relatively higher percentage of A group patients was found in gingivitis group and relatively higher percentage of O group patients was found in periodontitis group. A significant relationship was also determined between Rh factor and gingivitis. ABO blood subgroups and Rh factor may constitute a risk factor on the development of periodontal disease. However, long-term studies are needed to make a more comprehensive assessment of the effects of ABO group on periodontal diseases.
I'm sure that secretor status had something to do with these results, since it has an effect on pellicle formation (link) I do however, agree with the results. In my own patients I have seen periodontal disease resolve easily in many type A's by simply getting their gingivitis under control. Type O's on the other hand have a harder time of things, especially if their protein intake is not adequate.
That's about it for this week.
A bit of news: I would be willing to entertain questions about topics that might be of interest to this community. Just drop a comment (link is below). I will not however, respond to questions of a personal medical nature, nor give medical advice. Thanks for respecting this caveat.