Archives for: March 2004
I would like to know what you think of macrobiotic diet for Type A.I am Type A. I understand what ER4YT is about. Is it true that Type A should be on macrobiotic diet? I hope you explain me more about it.
Macroibiotics can work for type A, though you will have to double check for Type A avoids which may be avocated by macrobiotic philosophy. Lima beans, for example.
QUESTION: Why is peanut a poison for Type A, while peanuts and peanut butter are highly beneficial?
ANSWER: Blood group A in general has higher levels of cholesterol and significantly higher rates of heart disease. Peanut oil, while relatively unsaturated, is surprisingly atherogenic (causes atery plaque formation). This latter effect is not related to the level (6%) of long-chain saturated fatty acids (arachidic, behenic, lignoceric) present in peanut oil, but rather to its triglyceride structure.
Japanese white rabbits fed a restricted amount (100 g/head/day) of an atherogenic diet (AD) containing 6% peanut oil showed mild and persistent hypercholesterolemia (338 +/- 79 mg/dl). They developed atherosclerotic lesions at the 4th week of feeding.
Peanut oil apparently increases the amount of collagen and other proteins in atheroschlerotic lesions as well. Rates of arterial collagen and noncollagen protein synthesis were exaimined in rabbits maintained for 4 months on a control diet or the same diet supplemented with 2% peanut oil. Thoracic aortas from animals fed the atherogenic diet exhibited raised lesions covering 75% to 100% of the surface.
Cordain L. Atherogenic potential of peanut oil-based monounsaturated fatty acids diets. Lipids. 1998 Feb;33(2):229-30.
Kritchevsky D. Dietary fat and experimental atherosclerosis.Int J Tissue React 1991;13(2):59-65
Saso Y, Kitamura K, Yasoshima A, Iwasaki HO, Takashima K, Doi K, Morita T. Rapid induction of atherosclerosis in rabbits. Histol Histopathol 1992 Jul;7(3):315-20
Opsahl WP, DeLuca DJ, Ehrhart LA. Accelerated rates of collagen synthesis in atherosclerotic arteries quantified in vivo.Arteriosclerosis 1987 Sep-Oct;7(5):470-6
I'm concerned the higher level of beef suggested for O's maybe loading my system with gout triggering purines. As a gout prone O any thing to look out for in the O ER4YT plan?
Although red meat is high in purines (which can trigger gout), and purine are linked to uric acid metabolism, studies have repeatedly shown that the joints of gout sufferers have no higher levels of uric acid in them than non-gout patients, so the issue is far from clear-cut. In general, meats do acidify the system (but any perusal of the acid-alkaline charts will disclose that whole wheat is a close second)
Avoiding wheat and dairy should compensate for the addition of the purine rich red meats in a type O, especialy if the diet is high in other "alkaline" food such as black cherry juice, vegetables and other fruits.
As an additional insurance, 800mcg of folic acid can be added to the program.
Remember also, that gout crystals precipitate in the joints because they have reached their 'iso-electric point,' a point of saturation where the material begins to come out of solution. Anyone who has ever made rock candy as a kid would know what I was talking about! Anyway, the quickest and best way to lower one's isoelectric point is to drink plenty of water!
Your book stated, regarding the Indican Test, that "all commerical laboratories can do it. My doctor, even after looking at his Harvard Reference on Standard Lab Tests, could not find it. The Lab that did my blood test knew how to do it but the results were "L" (low?) without a number. Are more labs becoming familiar with this test after your book mentioned it? And should they report the results in numbers?
Indican can be a useful tool for monitoring degeneration or improvement in digestive efficiency of your system in dealing with protein.
Indican is formed by an abnormal metabolism of tryptophan. Indican is a by-product of putrefaction (protein degradation), usually in the intestine, but possibly in other locations as well. Putrefaction is the anaerobic bacterial decomposition of proteins - not ideally the healthy way for your body to deal with proteins.
When the product of this putrefaction (called indole) is absorbed into the blood stream, an increase in urinary indican is seen. This increase can also be seen if bacterial decomposition of body tissues or fluids occurs, as in gangrene, abscesses, etc.
Among the pathologic conditions in which urinary indican is likely to be elevated are hypochlorhydria (low stomach acid production), inhibited peristaltic movement (the involuntary muscular "waves" that move food through your bowel), and poor production of digestive bile secretions from the gall bladder and liver.
Elevated indican is rather rare in simple constipation, but often high with diarrhea. It is generally a good indicator for the poor breakdown of proteins accompanied by gastrointestinal permeability (the "leaky gut". A high lectin diet typically increase indican levels.
A few individuals can have high indican without symptoms, and some can have low indican with many symptoms. It is useful to use other complementary methods of testing bowel health simultaneously with indican to get a clear picture of your function.
Indican has been used for some time as a simple test for protein maldigestion. In the past, it has been measured with a color comparison chart which is graded 1-4. This has obvious drawbacks for accurate monitoring, so most labs will just report it as 'High' or 'Low."
STUDY: ABH and Lewis histo-blood group antigens in cancer.
JOURNAL: APMIS 2001 Jan;109(1):9-31
AUTHORS: Le Pendu J, Marionneau S, Cailleau-Thomas A, Rocher J, Le Moullac-Vaidye B, Clement M.
ABSTRACT: Antigens of the ABH and Lewis histo-blood group family can be found on many normal cells, mainly of epithelial type. In carcinomas, altered expression of the various carbohydrate epitopes of this family occur, and are often strongly associated with either a good or bad prognosis. A review of the available data on these tumor-associated markers, their biosynthesis and their prognostic value is proposed here. For a long time it has been unclear whether their presence could affect the behavior of carcinoma cells. Recent data, however, indicate that they play biological roles in the course of tumor progression. The presence of sialyl-Le(a) or sialyl-Le(x), which are ligands for selectins, promotes the metastatic process by facilitating interaction with the endothelium of distant organs. The loss of A and B antigens increases cellular motility, while the presence of H epitopes increases resistance to apoptosis by mechanisms that remain to be defined. The Le(y) antigen has procoagulant and angiogenic activities. All these observations are used to present a model that may account for the described associations between the presence or loss of these markers and the outcome of disease.
COMMENTARY: We know that the presence of blood group antigens in our earliest hours of embryonic existence serve to channel the growth of the rapidly dividing cells into a cohesive living organism. Thus it is not unreasonable to assume that the lost of these same antigens later on in life could wreak havoc by giving rogue cancer cells the ability to spread (metastasize). Clearly studies aimed at reinstalling lost ABH antigens could represent a potentially useful therapy for cancer.
QUESTION: Can I use DEFLECT for arthritis? I do not have any weight to lose, thanks to the type A diet (33 kilos!) Many thanks and God Bless!
ANSWER: Perspectives on some nutritional supplements for arthritis through a blood type looking glass.
In the past few years, the use of supplements such as glucosamine sulfate, N-acetylglucosamine, chondroitin sulfate, and gelatin have gained increasing notoriety for their ability to improve some of the symptoms of arthritis (inflammation or degeneration of joints). While all of these products can work quite well for some people, unfortunately many individuals experience only modest to no improvements in their joint symptoms. An intersting observation of several practitioners I have spoken with is that chondroitin sulfate seems to work well in some people when glucosamine sulfate did not work (and vise-versa). While this seems to be a fairly common observation, I don't recall ever receiving an adequate explanation of why this might be the case.
In the past two years, combinations of these different compounds mixed together have begun to reach the shelves in ever increasing quantities in many retail stores. The questions that still need to be answered include; do these combinations work better than the single ingredients? Who do they work best for? Who does best on chondroitin sulfate? Who does better on glucosamine? or N-acetylglucosamine? Should certain individuals avoid any of these products? I believe the blood type paradigm just might provide some insights into these questions.
In order to understand the rationale behind the application of these nutritional supplements, let's take a quick tour of the biochemistry of joint health.
Joint cartilage consists of cells embedded in a collagen matrix within a concentrated water-proteoglycan gel. Proteoglycans are in a very general sense long branching chains made from a combination of chains of simple sugars and protein sugars. Chondroitin sulfate is an example of one of these long chains of protein sugars. Glucosamine or N-acetylglucosamine, on the other hand, are among the several most simplified segments or building blocks of these chains of protein sugars. Gelatin is basically this entire collagen and proteoglycan matrix.
In order for a joint to function properly, this matrix must be intact which means your joints must have adequate nutrition to build this joint matrix. Picture for a moment a bowl of jello. If you bump the jello or shake the bowl, the jello will move or wiggle in a characteristically jello-like manner. Healthy joints should also be able to withstand the impact of walking, or running by absorbing shock because of the jello-like activity of the collagen-proteoglycan substance.
Based on the biochemical knowledge of healthy joints, it has been reasoned that providing the builing blocks of the joint matrix as nutritional supplements should result in better joint health. In many respects this reasoning appears to hold true, since studies do show benefits from the oral use of these supplements. In fact a high percentage of glucosamine is absorbed and seems to boost the synthesis of joint building blocks. N-acetylglucosamine also appears to be absorbed intact. Chondroitin sulfate is largely broken down into its repeating components, N-acetylgalactosamine and glucuronic acid. Evidence indicates little to none of the entire chondroitin sulfate makes it to the blood or joint, however, it appears that some of the N-acetylgalactosamine or glucuronic acid must stimulate synthesis of joint proteoglycans.
Several researchers who studied the oral supplementation of chondroitin sulfate concluded that benefits "...after ingestion of chondroitin sulfate should be sought at the level of the gastrointestinal rather than the plasmatic or the articular cartilage level." (1)
Looking at these substances as potentially having an impact on arthritis or joint health not by what they do in the blood or at the joint, but rather by what they do in the stomach and intestines is indeed an interesting thought. As a matter of fact, Naturopathic physicians have long observed that arthritis often improves with diet and with a concurrent improvement of digestive function. This is where the blood type looking glass arrives.
As some of you readers might know, an interesting thing about the ABO blood types is that they are not just blood types, in fact they are also tissue types. This means if you are a blood type A for example, the antigen that makes your blood type A also lines your digestive system. As you no doubt also remember, the terminal component of the A antigen is n-acetylgalactosamine; the same protein sugar that is a building block of chondroitin sulfate. Glucosamine on the other hand can be readily converted into galactosamine, the terminal residue of the B antigen.
What does this mean in practical terms? Well, since most lectins that are specifically detrimental to blood type A are bound and inactivated by N-acetylglalactosamine, this means that chondroitin sulfate is an excellent strategy for an A or and AB. But since blood type O and B are not impacted negatively from blood type A specific lectins and because O and B make antibodies against things that look like blood type A, chondroitin sulfate might not work as well for these people.
Glucosamine since it can be made into a variety of protein sugars, should theoretically benefit a greater percentage of the population (note: this is what studies have consistently shown). One of the simplest biochemical reactions that occurs to glucosamine results in the formation of galactosamine, a substance that with tend to protect B or AB from lectins with blood type B specificity. Glucosamine can also be acetylated to form N-acetylglucosamine, the protein sugar specific for binding the very disruptive lectin found in wheat. Since wheat seems to be particularly difficult on blood type O, binding this lectin is a good strategy for O's with arthritis. Giving N-acetylglucosamine directly would probably be an even better strategy for O's.
You can read about DEFLECT lectin blocking products here.
<1> Baici A, Horler D, Moser B, et al. Analysis of glycosaminoglycans in human serum after oral administration of chondroitin sulfate. Rheumatol Int 1992;12:81-88.
QUESTION: I have followed the type O non-secretor diet faithfully for over a year and have recieved tremendous results. My problem, however, is that I have reaccuring cervical dysplasia. I wondered if there was any connection between non-secretors and cervical dyspasia? I have tried everything from antioxidants to large doses of folic acid. Is this a non-secretor problem and can anything be done. I dred going in for another colposcopy.
ANSWER: When abnormal cells are found on the cervix this condition is called dysplasia. Cervical dysplasia is considered to be a pre-cancerous condition. The exact cause of cervical dysplasia is not known, but a number of different factors have been identified. For example, the risk of developing cervical dysplasia appears to be slightly higher after exposure to those types of human papilloma virus (HPV) that cause genital warts. Other risk factors for the development of cervical dysplasia include unprotected sex at an early age, unprotected sex with many partners, and becoming pregnant before age 20. However, exactly how these risk factors are connected to cervical dysplasia is unknown. Smoking also increases the risk of developing cervical dysplasia.
There is evidence that ABO and secretor type have a profound effect on the secretory cells of the cervical glands. (1). In cervical neoplasia, the progressive descent of the squamous mucosa into a precancerous state is mirrored by loss of both Lewis a and Lewis b expression. (2) In oral dysplasia, one study found the occurrence of epithelial dysplasia was found exclusively in the non-secretor group.
Non-secretor status has been linked to a variety of microbial susceptibilities in the female vaginal tract, including the composition of vaginal fluid, a prime defense against many pathogens. Earlier studies done in the 1960's documented a link between non-secretor status and lower levels of mucous membrane protecting IgA antibodies. (3) Most experts feel that cervical dysplasia typically has an element of diminished resistance to either viruses, such as HPV or other microorganisms, such as Chlamydia.
A common treatment used in naturopathic medicine is the escharotic treatment, pioneered by my friend Tori Hudson. Antioxidants and high levels of folic acid and beta carotene work in some women, but not all. There is some evidence that the broader group of carotene (such as one encounters when consuming a carotenoid-rich diet) may be protective against cervical dysplasia. Isolates, such as beta carotene (often synthetic) were ineffectual. Homepaths typically might prescribe the remedies Thuja or Acidum Nitricum, though neither have been clinically documented.
1. Okamura Y. Heterogeneity of the blood group ABH antigens and variation in the expression of these antigens of secretory granules in human cervical glands. An electron microscopic observation using lectins and monoclonal antibodies. Histochemistry 1990;94(5):489-96
2. Sanders DS, Milne DM, Kerr MA. The expression of Lewis(a) and Lewis(b) antigens reflects changes in fucosylation between normal and neoplastic cervical squamous epithelium. J Pathol 1990 Sep;162(1):23-8
3. Grundbacher FJ. Immunoglobulins, secretor status, and the incidence of rheumatic fever and rheumatic heart disease. Hum Hered. 1972;22(4):399-404
I was diagnosed with Crohn's disease 7 years ago and had surgery 2 years ago that removed a foot of my small intestine (including the terminal ileum) and a 1/2 foot of the large. I am an O blood type (and currently do not eat red meat, but some fish and a little poultry) and am curious if following your recommendations would help to improve my day to day health. I do not eat dairy currently, but do not otherwise follow this diet now. My general health is ok but do feel sluggish overall and am very able to notice problems with digestion of much of the food I eat. Curious to know your feedback.
Typical O things: wheat, corn and dairy avoidance, the use of the amino sugar n-acetyl glucosamine (not glucosamine sulphate) and the product "Seacure" (a peptide made from whitefish) have been the most successful strategies I've used in my practice. Also, NAP's 'Deflect' products can be very helpful. All of these should be securable from a good pharmacy or health food store.
STUDY: A new function of green tea: prevention of lifestyle-related diseases.
JOURNAL: Ann N Y Acad Sci 2001 Apr;928:274-80
AUTHORS: Sueoka N, Suganuma M, Sueoka E, Okabe S, Matsuyama S, Imai K, Nakachi K, Fujiki H.
ABSTRACT: In the normal human life span, there occur lifestyle-related diseases that may be preventable with nontoxic agents. This paper deals with the preventive activity of green tea in some lifestyle-related diseases. Green tea is one of the most practical cancer preventives, as we have shown in various in vitro and in vivo experiments, along with epidemiological studies. Among various biological effects of green tea, we have focused on its inhibitory effect on TNF-alpha gene expression. Based on our recent results with TNF-alpha-deficient mice, TNF-alpha is an endogenous tumor promoter. TNF-alpha is also known to be a central mediator in chronic inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. We therefore hypothesized that green tea might be a preventive agent for chronic inflammatory diseases. To test this hypothesis, TNF-alpha transgenic mice, which overexpress TNF-alpha only in the lungs, were examined. The TNF-alpha transgenic mouse is an animal model of human idiopathic pulmonary fibrosis which also frequently develops lung cancer. Expressions of TNF-alpha and IL-6 were inhibited in the lungs of these mice after treatment with green tea in drinking water for 4 months. In addition, judging from the results of a prospective cohort study in Saitama Prefecture, Japan, green tea helps to prevent cardiovascular disease. In this study, a decreased relative risk of death from cardiovascular disease was found for people consuming over 10 cups of green tea a day, and green tea also had life-prolonging effects on cumulative survival. These data suggest that green tea has preventive effects on both chronic inflammatory diseases and lifestyle-related diseases (including cardiovascular disease and cancer), resulting in prolongation of life span.
COMMENTARY: Green tea continues to show great promise as a simple way to enhance your resistance to several common cancers. Further evidence now accumualting points to a key role for the frequent use of green tea as a preventive for cardiovascular disease, and possibly also multiple sclerosis and rheumatoid arthritis as well.
Green tea is actually the same plant as its more well-known cousin black tea; however, special processing retains a far greater antioxidant profile in green tea leaves, resulting in a far and away superior beverage for supporting health. Numerous scientific studies now document the tremendous benefits of drinking green tea.
QUESTION: Have a question about the nutrient content of a certain food?
ANSWER: Why not look it up on the new Nutrient Database here on www.dadamo.com. In a handy outline report, foods can be searched to reveal their water, protein, mineral, fiber, vitamin, cholesterol and fatty acid compositions. You can then cross reference the food with its ABO/secretor value by using the Food Value database.
QUESTION: On Page 98 of ER4YBT you state that "Wheat is a mixed factor in the Type A diet." My question is...what about "wheatgrass? May Type A's consume this and if so how much a day i.e., 1-3 teaspoons in concentrated form dissolved in water or juice. Thank you for taking the time to help us all!!!
ANSWER: The sprouting of wheat into wheat grass destroys the lectin that is problematic in wheat. Sprouting also beneficially changes the nutrient profile of this grain, resulting in a nutrient-dense, enzyme-rich superfood. Because of these factors, I consider wheat grass to be an excellent addition to the diet for all blood types. As far as an amount, use your own judgement. Because of the concentrated nature of this food, a little goes a long way, so if you have not enjoyed wheat grass juice before, start with a smaller amount.
QUESTION: I've begun to incorporate many of your recommendations and have begun to see marked differences in my health. Thank you. My question is, if types A's are supposed to eat peanuts, where does this put the issue of aflatoxin?
ANSWER: Recently, a well-known figure in alternative medicine, Dr. Andrew Weil, made several statements which cast doubt upon the safety of commercially available peanuts. As an answer to the question "Does peanut butter cause cancer?" the authority answered that 'it's relatively common for aflatoxin to cause a type of poisoning called aflatoxicosis."
This assertion is questionable at best. There are no reported incidences of aflatoxicosis in the United States contained in MEDLINE, the medical database, and only a few isolated instances in Third World countries (Uganda 1971, India 1975 and Malaysia 1991) where methods of storage and identification are suspect. Indeed, in even these reported 'outbreaks' none were associated with peanut consumption! In Uganda and India the cause was contaminated corn, and in Malaysia a type of noodle.
This does not sound 'relatively common' to me, nor does it directly implicate peanuts as a dangerous source of aflatoxin any more than corn or walnuts.
In the United States, the FDA regulates aflatoxin, and it because it can be avoided or minimized with proper agricultural and manufacturing practices. Aflatoxins are highly controlled in food products for consumption and the concern for safety has been reduced drastically. FDA's efforts to ensure the safety and quality of foods and feeds are complemented by control programs carried out by USDA, state departments of agriculture, and various industrial trade associations.
STUDY: Cadherins and tissue formation: integrating adhesion and signaling.
JOURNAL: Bioessays 1999 Mar;21(3):211-20
AUTHORS: Vleminckx K, Kemler R.
ABSTRACT: Cadherins and other cell-substrate and cell-cell adhesion molecules play an essential role during development. Through their cytoplasmic interaction with the cytoskeleton, cell adhesion molecules physically link cells with the extracellular matrix and/or with each other. These interactions create architectural and structural entities that enable the tissues in the embryo to restrain the physical forces encountered during development. Regulated cell adhesion is also often the driving force of morphogenetic movements. This review goes beyond the adhesive aspect of cadherins, focusing on their roles as signaling molecules in development. We discuss how cadherins, through their effects on cell proliferation, cell death, cell polarization, and differentiation, play a role in the formation of tissues and organs in the developing embryo.
COMMENTARY: Cadherins are a class of adhesion molecules, typically part of the 'tight junction' that hold cells together. These tight junctions also tend to keep cells from misbehaving, due to the phenomena of 'contact inhibition.' Thus it is logical for defects in cancer cells, such as the ability to metastasize, to be linked with defects in cadherin synthesis. One cadherin in particular, E-cadherin, is associated with the development of metastasis in sevral common cancers, including prostate (1), breast(2) and stomach(3). Since it has been speculated that metastasis of cancer cells through the blood stream is inherrently hostile, and that fewer than 10,000 cancer cells may be involved in the initial metastatic event, development of strategies to re-establish cadherin integrity are on the forefront of medical research.
1.Arenas MI, Romo E, Royuela M, Fraile B, Paniagua R. E-, N- and P-cadherin, and alpha-, beta- and gamma-catenin protein expression in normal, hyperplastic and carcinomatous human prostate. Histochem J. 2000 Nov;32(11):659-67.
2.Madhavan M, Srinivas P, Abraham E, Ahmed I, Mathew A, Vijayalekshmi NR, Balaram P. Cadherins as predictive markers of nodal metastasis in breast cancer. Mod Pathol. 2001 May;14(5):423-7
3.Chan AO, Lam SK, Chu KM, Lam CM, Kwok E, Leung SY, Yuen ST, Law SY, Hui WM, Lai KC, Wong CY, Hu HC, Lai CL, Wong J. Soluble E-cadherin is a valid prognostic marker in gastric carcinoma. Gut. 2001 Jun;48(6):808-11.
I would also like to ask...if it is OK to take COQ10, as every person in my tribe has died of heart disease, my father at 48, or will I not need to do that later? I will understand if this note cannot be answered, but I just wanted to thank you.
Type O's can certainly take CoQ10. The typical dose is 30-90mg daily. You might also want to consider taking a bit of zinc, as it tends to amplify the effects. Co Q10 also absorbs better when taken with a meal containing some fat.
QUESTION: What helps with non-diseased receding gums? (I'm an O- with primary biliary cirrhosis and just found ER4YT three weeks ago. I feel better already just eliminating wheat & dairy and eating more meat-Thanks!)
ANSWER: Gum repair is one of the most energy-intensive functions performed by the body, and gum (or gingival) tissue is one of the most sensitive to the efects of free-radical damage. Since your gum loss id 'non-diseased' you may want to examine the problem from a whole body perspective.
I would recommend that you get your antioxidant levels checked. A simple, inexpensive way to do that is the use the Oxystress Test from NAP. If you level of oxidative stress is high (and I suspect it is becasue of the history of biliary cirrhosis) you can try a few of the suggestions below:
1. Crit Rev Oral Biol Med 1999;10(4):458-76 Oxidative injury and inflammatory periodontal diseases: the challenge of anti-oxidants to free radicals and reactive oxygen species. Battino M, Bullon P, Wilson M, Newman H
2. Pathol Biol (Paris) 1998 Sep;46(7):571-6 Morphometric analysis of human gingival elastic fibres degradation by human leukocyte elastase protective effect of avocado and soybean unsaponifiables (ASU).
3. J Clin Periodontol 1994 Jan;21(1):45-7 Reduction of collagen degradation in experimental granulation tissue by vitamin E and selenium. Asman B, Wijkander P, Hjerpe A
4. J Clin Periodontol 1984 Oct;11(9):619-28 Folate mouthwash: effects on established gingivitis in periodontal patients. Pack AR
A relative's friend is a 26 year oldType B female with Rheumatoid Arthritis diagnosed 5 years now and already having moderate deformity in hands (swan neck deformity?). She's Japanese, living there, so my information is limited.
Get your friend to follow the B diet, with perhaps more emphasis on wheat avoidance. Let her experiment with the "Membrane Fluidizer" cocktail in the AM.
QUESTION: I'm holding thumbs that you will have time to answer. My deadline for a Masters paper for the year 30.11.00. Question: Could I maintain that my blood, my very own blood not my TYPE blood, ran through Cro-magnon's veins? I'm busy with attacking relativism, and propounding universalism and individualism.
ANSWER: I don't think that the cellular elements carry over, since blood cycles from fully mature cellular elements to embryonic elements and back again. However the genetic studies make it almost certain that your gene base is greatly similiar to Cro-Magnon.
On a slightly different note:
Q: Do you know what the odds are that your next breath will contain at least one molecule of Julius Caesar's dying gasp?
A: 100% certainty.
QUESTION: Why does smoking or curing foods produce nitrates or nitrites?
ANSWER: Nitrate (NO3) is a naturally occurring form of nitrogen found in soil. Nitrogen is essential to all life, and most crop plants require large quantities to sustain high yields. The formation of nitrates is an integral part of the nitrogen cycle in our environment. In moderate amounts, nitrate is a harmless constituent of food and water. Normally, nitrates are converted to nitrites by bacteria in the saliva and the back of the tongue.
Nitrites are though to be problematic becasue they can be converted into nitrosamines compounds with known carcinogenicity. This reaction definitely occurs in the test tube: Whether it occurs in the human digestive tract is not yet clear. Research has demonstrated that vitamin C (ascorbic acid) can inhibit the reaction of nitrites with amines or amides. It competes with the amine for the nitrite, which inhibits carcinogenic compound formation. However, I would recommend the use of food-derived vitamin C (acerola or rose hips) over synthetic.
Nitrates and nitrites are compounds typically found in smoked or cured meats, though they can be found in many vegetables as well. The main significance of nitrites and nitrates is that they my be linked to cancer of the stomach. However, there may be evidence that this link is oversimplified. New research indicates that moderate amounts of nitrates are not only safe, but may protect humans and animals against potentially fatal infections from microbes such as salmonella, shigella and E. coli.
Cancer of the stomach, or gastric cancer, is a disease in which stomach cells become malignant (cancerous) and grow out of control, forming a tumor. Almost all (95%) of stomach cancers start in the glandular tissue that lines the stomach. The tumor may spread along the stomach wall or may grow directly through the wall and shed cells into the bloodstream or lymphatic system. Once beyond the stomach, cancer can spread to other organs.
The link between nitrates and stomach cancer is probably strongest for blood group A individuals, since that groups has been known since the 1950's to have higher levels of stomach cancer than the others. (1) Type A's with stomach cancer have the most uniform supression of anti-Tn antibodies. Anti-Tn antibodies usually serve to protect against the earliest changes in the mutational process.
It has been hypothesized that the mechanisms behind the association between blood group A and gastric carcinoma is that the carcinoma cells produce an antigen immunologically related to blood group A, which particularly in O-individuals may have a protective effect by preventing the growth and spread of the tumor.
If you are group O, the relationship with nitrosamines can be just as lethal, since H. pylori infection is associated with an increased risk of stomach cancer as well, and evidence suggests that group O individuals have a greater inflammatory response against H. pylori than the other blood groups.
Hoskins LC, Loux HA, Britten A, Zamcheck N. Distribution of ABO blood groups in patients with pernicious anemia, gastric carcinoma and gastric carcinoma associated with pernicious anemia.N Engl J Med. 1965 Sep 16;273(12):633-7.
I am 55 yr old woman with O+ and long history of recurrent major depression. Your suggestion to excercise vigorously, rather than just walking has improved my sense of well being. However, your site only speaks against St John's Wort. Am wondering whether you suggest any natural herbs for depression in Type O's? Thanks for all of your research and availability here. Do see that my body prefers type O foods for the most part. Craving sweets remains a problem though. Thanks again.
Type O's have lower levels of the enzyme MAO, and St. Johns Wort is an MAO inhibitor. This perhaps explains why many type Os on St Johns Wort say they feel "weird" or have disturbing dreams. I have however been finding that type O's with mild to moderate depression do benefit from the amino acid tyrosine (which can boost dopamine levels), and arginine (which is used to recycle nitrous oxide in the nervous system). Also, the gene for the enzyme dopamine beta hydroxylase sits right on top of the ABO gene and there are indications that this may cause psychiatric syndromes to be somewhat related to ABO blood group. Maybe those Japanese personality observations were not so off-the-wall after all? It is interesting that dopamine, a chemical which is closely linked with sense of well-being, when defficient also produces hypoglycemia, which you allude to at the end of your question. Perhaps even more interesting is that the chemical structure of dopamine resembles the ABO antigens.
What does blood type have to do with neurotransmitters and the neuro-hormonal response to stress? While the use of blood type as a determinant of personality traits has been prevalent in Japan, a lack of tangible scientific facts had relegated these cultural beliefs to the realm of fantasy. However, an increasing amount of evidence indicates that individuals of differing blood groups have extremely different responses to the same stressor. Equally surprising, the genetics of blood group also appear to alter your susceptibility to developing certain neuro-psychiatric disorders. Even the response to inhaled nitric oxide seems to be modulated along the lines of blood type.
Stress, brain chemicals, nitric oxide; the common ground these disparate observations share is that all are dependent on neuro-hormonal signals to moderate an appropriate response to environmental factors. This is where science meets magic, because these neuro-hormonal signals are all mediated by the availability of certain nutritional building blocks and the activity of specific enzymes to catalyze the transformation of neurotransmitters and stress hormones.
Supplement-wise, I've found that type O's with mild to moderate depression can do very well with additional levels of the amino acid L-TYROSINE (1) and the B vitamins FOLIC ACID (2) and METHYLCOBALAMIN, or "Active B12". (3)
Through the miracle of the human genome project, it has become possible to explore the very fabric of human genetics. Evidence indicates the gene that controls blood type expression is probably also linked to and controls inheritence of the genes that code for the activity of dopamine-beta hydroxylase, catechol-O-methyl transferase, and arginosuccinate synthetase. Coincidentally, these are all enzymes that influence our neuro-hormonal response to environmental factors.
1. Meyers S. Related Articles Use of neurotransmitter precursors for treatment of depression. Altern Med Rev. 2000 Feb;5(1):64-71. Review.
2. Lee S, Wing YK, Fong S. A controlled study of folate levels in Chinese inpatients with major depression in Hong Kong. J Affect Disord. 1998 Apr;49(1):73-7.
3. Kelly GS. Folates: supplemental forms and therapeutic applications. Altern Med Rev. 1998 Jun;3(3):208-20. Review.
QUESTION: I've just read that soy can increase the rate of breast cancer. Your A diet recommends quite a bit of soy. How do you reconcile your theories with these new studies?
ANSWER: This was from a BB post I left a few weeks ago:
Man bites dog? I know Stephen has posted till he was blue in the face on the subject, but two additional thoughts on why if soy causes cancer, it certainly doesn't do it in type A's:
1. The relatively low methionine levels in some phytochemicals such as soy, limit the synthesis of polyamines necessary for tumor growth(1). Methionine is problematic for type A's in other areas as well: it is linked to elevated levels of homocysteine, a significant risk factor for artery disease.
2. Genistein and daidzein, the major phytoestrogens in soy are themselves 'aromatase inhibitors.'(2) This is true of many isoflavones. Aromatase is an enzyme which converts androgens to estrogens by altering the ring structure of the steroid. Aromatase is located in estrogen-producing cells including ovaries, placenta, testicular Sertoli and Leydig cells, adipose, and brain tissues. Aromatase inhibitors are increasingly the drug of choice for managing metastatic breast cancers which have retained estrogen sensitivity.
This may explain why certain plant estrogen rich foods (such as alfalfa) have always been viewed by naturopaths as 'estrogen modulating' rather than 'estrogen elevating'; the phytoestrogens simultaneously act both as estrogens and aromatase inhibitors. The particular effect may be variable in the individual, and because aromatase is part of the liver's cytochrome p-450 system, it is intimately linked up with many detoxification functions.
This is important anti-cancer stuff for type A's.
1. AU Cline J M, Hughes C L Jr IN Bowman Gray School of Medicine, Department of Comparative Medicine, Comprehensive Cancer Center of Wake Forest University, Winston-Salem, NC 27157, USA TI Phytochemicals for the prevention of breast and endometrial cancer SO Cancer-Treat-Res 1998, VOL: 94, P: 107-34
2. J Steroid Biochem Mol Biol 1993 Sep;46(3):381-8 Flavonoid inhibition of aromatase enzyme activity in human preadipocytes. Campbell DR, Kurzer MS
QUESTION: As a chemist and immunologist familiar with lectins, I immediately saw the potential relevance of your blood type diet. I started the type B diet a couple weeks ago. It has occured to me that some beneficial bacteria may be more beneficial than others for type B. Have you been able to sort this out? Which species should I favor? Thanks for your work!
ANSWER: ABO blood type antigens are quite prominent in the digestive tract. Also, in about 80% of individuals (secretors) they are distributed in the mucus that lines your digestive tract. Because of this, many of the bacteria in the digestive tract actually use ABO blood type antigens as a preferred food supply.
In fact, blood group specificity is common among intestinal bacteria with almost 1/2 of strains tested showing some blood type A, B, or O specificity. To give you an idea of the magnitude of the blood type influence on intestinal microflora, it has been estimated that someone with blood type B will have up to 50,000 times more of some strains of friendly bacteria than either blood type A or O individuals.
Some strains of unbeneficial bacteria actually can have lectin-like hemagglutinin activity directed against your blood type. There is good evidence that our intestinal flora can have very positive effects on the immune capabilities of bone marrow.
With this information, it is possible to design probiotic formulas that utilize blood type friendly prebiotics (substances needed to encourage the growth of helathy bacterial flora). These considerations are behind the design of the NAP Polyflora compounds.
QUESTION: The other day your 'next" question was to be about 'O' type and low platelets. This never appeared. Can we ever look to the day it will be one of the questions answered. I would really like to express my appreciation for you and this web site but I just can't find the words. So I'll just say a simple 'THANK YOU'. However, keep up this good work you are doing I really appreciate what you are doing and I believe you are BLESSED.
ANSWER: I apologize. The question did appear for a few hours and was then gobbled up by a bug in the program.
Immune Thrombocytopenic Purpura (ITP) is a disorder of the blood. The main symptom is bleeding, which can include bruising ("ecchymosis") and tiny red dots on the skin or mucous membranes ("petechiae"). In some instances bleeding from the nose, gums, digestive or urinary tracts may also occur.
Immune refers to the immune system's involvement in this disorder. Antibodies, part of the body's immunologic defense against infection, attach to blood platelet, cells that help stop bleeding, and cause their destruction. Thrombocytopenia refers to decrease in blood platelet. Purpura refers to the purplish- looking areas of the skin and mucous membranes (such as the lining of the mouth) where bleeding has occurred as a result of decreased platelet.
Thrombocytopenic purpura is considered chronic when it has lasted more than 6 months. The onset of illness may be at any age. Adults more often have the chronic disorder and females are affected two to three times more than males. The onset of illness may be at any age.
The treatment of idiopathic thrombocytopenic purpura is determined by the severity of the symptoms. In some cases, no therapy is needed. In most cases, drugs that alter the immune system's attack on the platelet are prescribed. These include corticosteroids (i.e., prednisone) and/or intravenous infusions of immune globulin. Another treatment that usually results in an increased number of platelet is removal of the spleen, the organ that destroys antibody-coated platelet.
Another treatment involves the use of intravenous gamma globulin serum (IVIG) and in one study there were no significant differences in response rate or clinical outcome by ABO blood group or Rh type in children with ITP who received IVIG monotherapy as their initial treatment. (1)
Although you identify yourself as type O, one study showed an increased incidence of blood group A was found in ITP patients (64 vs. 37.98% in the control population), especially in those with acute ITP (84.7%), an association I've verified in my own clinic. (2)
As far as treatment is concerned, I've always seen rewarding results when the patients have stuck to the right diet for their blood type. I've also used the herb Berberis vulgaris (Barberry) as a front-line treatment.
In one study, the authors recommend berberine bisulfate (the active ingredient in Barberry) for use as a thrombocytopoiesis (platelet growth) stimulator in thrombocytopenias as they have found secondary therapeutic property of this drug--to increase platelet count in patients with primary and secondary thrombocytopenia. The drug was given as 3 times a day for 15 days in a dose 5 mg 20 min before meals. (3)
I've also found moderate doses of the anti-oxidant selenium (100-200mcg daily) to be effective as well (4)
(1) Sturgill MG, Nagabandi SR, Drachtman RA, Ettinger AG, Rubin J, Ettinger LJ . The effect of ABO and Rh blood type on the response to intravenous immune globulin (IVIG) in children with immune thrombocytopenic purpura (ITP). J Pediatr Hematol Oncol 1997 Nov-Dec;19(6):523-5
(2) el-Khateeb MS, Awidi AS, Tarawneh MS, Abu-Khalaf M. HLA antigens, blood groups and immunoglobulin levels in idiopathic thrombocytopenic purpura. Acta Haematol 1986;76(2-3):110-4
(3) Chekalina SI, Umurzakova RZ, Saliev KK, Abdurakhmanov TR. [Effect of berberine bisulfate on platelet hemostasis in thrombocytopenia patients]. Gematol Transfuziol. 1994 Sep-Oct;39(5):33-5. Russian.
(4) Hampel G, Schaller KH, Rosenmuller M, Oefele C. Selenium-deficiency as contributing factor to anemia and thrombocytopenia in dialysis patients. Life Support Syst. 1985;3 Suppl 1:36-40.
I am curious about the incidence of dental caries as it relates to the different blood types. Understanding the variety of organisms that can inhabit the mouth and proliferate causing oral disease,your comments about this as it relates to blood types and the incidence of caries would be appreciated. I am type A-, age 36, and tend to have "pits" in my molars which seem to last about 10+ years before a dentist decides to fill them as surface cavities. So far, I have only had 4 surface "cavities". Thank you!
There are a few studies on blood type and dental caries (cavities), and in general it appears that blood group A may have lower levels of cavities than the other blood groups, especially if the group A subjects(1) were SECRETORS.(2) It appears that the secretion of our ABO(h) antigens into saliva probably inhibits the ability of bacteria to attach to the tooth surface,(3) since many of these bacteria possess lectins on their surface which they use to attach to body surfaces, and many of these lectins are ABO(h) specific. Also, non-secretors tend to have lower levels of the IgA class antibodies in their saliva, which may compromise their ability to keep bacteria counts low.
It has been noted that many groups with high rates of caries have low rates of periodontal disease, and vice versa. This may be true of blood groups as well. Type O has been known to have lower frequencies of periodontal disease (4) perhaps because they carry both anti-A and anti-B antibodies, thus being protected again more strains of periodontitis-causing bacteria than A, B or AB.(5)
1. Arneberg P, Kornstad L, Nordbo H, Gjermo P. Less dental caries among secretors than among non-secretors of blood group substance. Scand J Dent Res. 1976 Nov;84(6):362-6.
2. Holbrook WP, Blackwell CC. Secretor status and dental caries in Iceland. FEMS Microbiol Immunol. 1989 Jun;1(6-7):397-9. PMID: 2631879; UI: 90212306
3. Haertig A, Krainic K, Vaillant JM, Derobert L. [Medicolegal identification : teeth and blood groups]. Rev Stomatol Chir Maxillofac. 1980;81(6):361-3. French.
4.Kaslick RS, West TL, Chasens AI. Association between ABO blood groups, HL-A antigens and periodontal diseases in young adults: a follow-up study.J Periodontol 1980 Jun;51(6):339-42
5. De Tomasi A. Related Articles[Agglutinogens and isoagglutinins in human saliva]. Rass Trimest Odontoiatr. 1970 Jul-Sep;51(3):137-46. Italian.