Nov 09 2011

When you point one finger, four usually point back at you.

There have been no shortage of supercilious, poorly researched articles about the blood type diets in the major media. They are usually provoked by a statement of support by some celebrity or media icon who has experienced success with the plan. Typically within a week my phone rings off the hook with one major media outlet or another needing ‘to talk with me as soon as possible because we are doing a story on your diet and are on deadline.’

This rushed approach characterizes almost every encounter I’ve had with major media. They gobble up whatever simple facts there are so as to explain the gist of the story, then go looking for an opposing viewpoint so they can get off being held responsible for any direct conclusions. This is called ‘balanced journalism.’

The article usually begins with a roll call of all the famous people who are following or have been on the diet. I usually have never heard of any of these folks, but my daughters often serve to tell me a bit about who they are. Then the diets are described, but never fully. Some reporters concentrate on the lectin-blood group specificity, others the anthropology, some the digestive differences in physiology. However, I’ve never seen a single article explain all aspects to some degree, which is of course the strongest argument for the theory: That it can be verified in multiple dimensions of analysis.

On the positive side, many articles feature a personal story about an average-type person who has had success with the diet. Usually the focus is weight loss, for obvious reasons. Very few of these articles profile people who have been cured of any physical diseases by adopting this way of eating. Again, this is due to legal issues. However, trying to heal or control a physical illness is the most common reason why people try the blood type diets.

Hard Facts from the Fiction Department

Finally, and this is almost always rolled out at the end, the article presents one or two nutrition experts to pass judgement on the merit, risk and need to follow a diet for your blood type. Unless the expert has had some exposure to the deeper, scientific basis for the theory (never) their comments are almost universally negative.

These comments usually fall into common categories:

  • The diets are dangerous. This statement is usually proffered by experts concerned that, by restricting certain foods by blood type, people will develop nutrient deficiencies. However, each diet variant (A, O, B and AB) is a carefully engineered balance of foods that ensures full nutritional value. This criticism has a long and hallowed record of institutional whoring for agribusiness: ‘whole grains are fine, except if you are gluten sensitive’, ‘high fructose corn syrup can be part of a balanced healthy diet’, etc. Curiously, this concern is often matched with the next:
  • Of course people get better, the diets are all healthy: If you tell someone to get off of diet soda, they will feel better. I actually have no problem owning this criticism. We do include a lot of good naturopathic food wisdom with the blood type recommendations. I fail to see the problem with that. Paradoxically, if one were to go back and read my earliest popular book, Eat Right For Your Type they would find perhaps some of the earliest references to the value of using grass-fed beef, spelt and sprouted breads, quinoa and amaranth grains and a host of other weird foods. Now these are all part of the popular culture, but back then nobody recommended these things. I’ve always thought that the basic benefit of using blood type as a guide to proper eating was its ability to let people know exactly which, of all the supposedly healthy diets, would be best for them.
  • There is no scientific validation. This criticism is particularly nefarious, since it says one thing but means another. To say that the blood type diet theory has not been tested in large numbers, via a double-blind study, at some neutral university, is in fact true. There are reasons why this has not occurred. One is the sheer size and cost of a study of this sort. Food and diet studies are notoriously difficult to control, require constant supervision, often must be pursed for years, and are enormously expensive. Now, on top of all that, multiply the work and expense by four. But let’s talk about what this criticism actually means. Most of the time what the critic is really implying is that the theory has no scientific basis, which is a form of intellectual dishonesty, since not one of theses critics has ever taken the time to read through the extensive collation of existing research, much of it freely available online, that supports the conclusions drawn to form the basis of the blood type diet. I don’t spend a lot of time writing critiques of other diet theories, but if I was planning to do so, I’d probably pick up the phone, call the other guy, explain my concerns and see if I’d gotten my facts straight. Yet in the last fifteen years I’ve never received any such phone call.
  • This is pseudoscience. This pejorative term is often used in conventional science to tar and feather ideas and practices that have no basis in accepted science, such as a theory that flouts the basic laws of physics. Of course, one man’s pseudoscience is another man’s frontier science, but that is the continual rub of forward progress and most honest scientists agree that it is part of the game. However, usage of the term has increasing become a favorite tactic of scoundrels to manufacture disinformation and stop interest and inquiry into a topic they might detest for any number of non-scientific reasons. By the way, there is nothing in the theory behind eating for your blood type that flouts the laws of physics, chemistry, immunology or physiology. On the contrary, that’s the problem: To talk intelligently about it requires that you know more than a little about these disciplines.

Case History

My office was recently contacted by Alexia Elejalde-Ruiz, a young reporter for the Chicago Tribune and told that they were doing an article on the blood type diet. Having given literally hundreds, if not thousands, of interviews at this point, my PR person usually begins the process with a few questions, such as what prompted the interest. In this case the interest appeared to stem from the health editor, who is apparently a type O vegan and somewhat distraught by the conclusions drawn from my theories. However the reporter was respectful and several emails went back and forth with the aim of addressing concerns from some of the nutrition experts. Since some were quite technical we directed the reporter to various links that discussed those point in detail. However, none of our corrections were turned into teaching points (for example, ‘a lot of people often think this about the diet, but in fact..’). Instead it seemed that they just went down their list to the next concern.

My Spidey senses were tingling, and I suspected that the article already had a preconceived agenda. Not surprisingly, when released the article pretty much went out of its way to diss the entire concept. Because of an association with Gannett Publishing, this article has appeared in other publications as well.

Famously, one of the experts firing the dreaded Parthian Shot, a Michael Greger, MD, who is touted as the head of something called, was quoted as the following:

Dr. Michael Greger, founder of, said the premise of the blood-type diet is wrong: The blood-type system, which predates humans, is far more complicated than just ABO, he said. “People crave individualized, personalized science, but this is pseudoscience,” said Greger, a general practitioner specializing in clinical nutrition.

I will not dwell on the stupendously ignorant basis of Dr. Greger’s criticism, since it betrays a complete lack of understanding about how blood types function in the body. You can read my answer to a similarly uninformed vegan doc here. What is interesting is the use of the pseudoscience label. Not simply because it is being applied by a person ignorant in the basic science, but rather because a quick look at Dr. Greger’s website ( and his ostensibly important job as head of the rather questionable show instead a vegan-biased, rather jaundiced army of one, and certainly not the vaunted expert the Tribune article purports him to be. Although I certainly acknowledge the value of vegan diets for some people (but certainly not everyone) others argue that the vegan diet theory itself is a pseudoscience, hence the title of this blog.

Conclusions, if any.

Media profilers of science and health need to start vetting their so-called experts. Here’s a news flash: Many critics of diet books have their own diet books and dietary agendas to protect. You’d think as professional news media this would cross their minds, but apparently it doesn’t. Balanced journalism should not mean that you just go out and find someone to disagree with the premise of your coverage.

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Nov 02 2011


Published by under Disease Links | Foods

Amaranth is a broad-leafed plant which produces multi-headed flowerets containing grain-like seed of extremely high nutritional value. The tiny seeds are a creamy tan in color and are about 1/32″ in diameter. Each plant produces 40,000-60,000 seeds. The amaranth seeds are used in their whole grain form, milled into flour or puffed into miniature kernels.

For centuries, the Aztecs and American Indians have known the benefits and diverse uses for amaranth.

Amaranthus, collectively known as amaranth, is a cosmopolitan genus of herbs. Approximately 60 species are recognized.

Not only is amaranth higher in protein than most commonly used grains, that protein, containing high levels of lysine and methionine, is better balanced and more complete. Amaranth, with 13-19% protein, scores closer to a perfect 100 on a theoretical protein score chart than do other grains. For example, amaranth’s 75 is significantly higher than wheat at 56.9, corn at 44, soybeans at 68 or even cow’s milk at 72.5.

Amaranth possesses a potent lectin that has been shown to identify colon cancer cells which are in the early stages of mutation.(1) As such a diet high in amaranth may well be protective against this common cancer, which is known to have a significantly higher incidence in blood group A.

Here are the Typebase values for amaranth.

Here’s a great recipe that uses amaranth flour to make a grain free bread:

Grain-Free Boston Brown Bread

Yield: 1 loaf

1 cup plus 2 tablespoons amaranth flour 1/4 cup arrowroot 1 teaspoon baking soda 1/2 teaspoon powdered ginger 1/2 cup currants 1/2 cup walnuts 3/4 cup boiling unsweetened fruit juice or water 1/4 cup honey or molasses 1 tablespoon lemon juice.

Generously oil a 1-quart mold or 1 pound coffee can. Fill a Dutch oven or stockpot with about 5 inches of water. Bring the water to a boil while you prepare the batter.

In a large bowl, combine the flour, arrowroot, baking soda and ginger. Stir in the currants.

In a blender, grind the walnuts to a fine powder. Add the juice or water, and blend 20 seconds. If the ingredients in the blender don’t reach the 1 -cup mark, add a little more liquid. With the blender running on low, add the honey or molasses and lemon juice.

Pour the liquid mixture into the flour bowl. Stir quickly to blend; do not overmix. Transfer to the prepared mold orcan. Cover with a square of foil or wax paper; tie the wax paper securely with a piece of string.

Place the mold in the boiling water. (It should come halfway up the sides.) Cover the pot tightly, and steam for 2 hours over medium-low heat. Do not remove the cover during that time.

Remove the mold from the pot. Cool the bread in the mold for 15 minutes, then turn out onto a wire rack to cool completely. For the best results, cut with a serated knife with a gentle sawing motion.

Variations: Replace the honey or molasses with 1/3 cup maple syrup. Instead of the currants, use dried unsweetened pineapple, apples, prunes or ther dried fruit; use the corresponding juice as the liquid.

(1)Boland CR, Chen YF, Rinderle SJ, Resau JH, Luk GD, Lynch HT. Use of the lectin from Amaranthus caudatus as a histochemical probe of proliferating colonic epithelial cells. Cancer Res. 1991 Jan 15;51(2):657-65.

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Feb 23 2011

On Blood Groups and Heart Disease

A recent Lancet article has resuscitated some interest about the influence of ABO blood groups and one’s chances of developing coronary atherosclerosis. Like a lot of earlier studies that documented the influence of blood group phenotypic influences on disease incidence, the researchers a.) went in looking for one correlation and wound up finding another; and b.) possibly produced an oversimplification in the rationale of the results.

Historical Aspects

There is a clear-cut association with having A and AB phenotype and an increased risk for heart disease. This has been reported continuously in the scientific literature over the last 50 years. Individuals who are blood group A have higher rates of heart attack across all age groups, both the genders, and all ethnic and national groups.

In 1962, the Framingham Heart Study blood grouped the surviving 4125 members of the original study group of 5209 people first examined in 1948-51. The most striking observance was the lower rates of non-fatal heart disease in men ages 39-72 that were blood group O versus blood group A. (1) A 1994 Polish study on by-pass surgery patients with highly advanced arteriosclerosis of the coronary arteries found a significantly higher number of cases with group AB and a deficiency in group O. (2) A 1981 German study of 13,175 patients showed a prevalence of A blood group in all types of heart disease examined. (3)

In a study of 191 coronary artery bypass candidates, investigators paradoxically found an excess of type O over type A. When they examined the data more closely, they concluded that that the tendency of type A to develop blood clots more readily (“thrombotic proneness”) caused a poorer prognosis. In essence, the blood group A subjects were missing from the study because they had already died in greater numbers, leaving a disproportionate excess of type O among the long-term survivors. (4) In a study of male survivors of heart disease, researchers found that there were fewer type A patients before age 55 than otherwise would have been expected. (5)

An Italian study in 1975 of 746 patients with high blood pressure, 3258 with congenital heart disease, 4503 with a history of heart attack, found a significant lack of patients with type O blood, and a significant excess of blood group A in patients with myocardial infarction. The study also showed an excess of blood group A patients with high blood pressure, and a lack of patients who were blood group B. (6)

A study of 255 women published in the Journal of the American Medical Association originally to study the effects of smoking on the rates of heart attack in women also found several other factors significantly associated with heart attacks in this group, including hypertension, angina pectoris, family history, diabetes mellitus and blood group A. (7)

A 1985 study looked at blood group and heart attacks in two different age groups. The patients were divided into two groups: those who were 65 years old or older and younger patients. The predominance of blood group A in patients with cardiac infarction was “highly significant” in both age groups (P less than 0.005). This study was unique in that other risk factors, such as smoking, high blood pressure, diabetes, and high cholesterol levels, were excluded from the study. When the researchers looked specifically at the more elderly population, the predominance of blood group A in the older patients with cardiac infarction was even higher (P less than 0.001). The researchers concluded, “Our investigation strongly suggests the existence of a genetic factor associated with blood group A and independent of the other risk factors, which is also responsible for a greater incidence of cardiac infarction.” (8)

An eight-year study of 7662 men published in the British Medical Journal found blood group A is linked to the incidence of ischemic heart disease, as well as having higher total serum cholesterol concentrations. (9)

Intestinal alkaline phosphatase

Gene products, which may be expressed under plastic conditions, can contribute to further downstream gene expression by ecological elements. Beginning around 1965 researchers began to notice that people had different levels of an enzyme in their intestinal tract called intestinal alkaline phosphatase (IAP) and that the levels of this enzyme varied according to ABO blood group and secretor status. (10) Type A non-secretors have the lowest levels, and type O secretors the highest, with type B’s somewhere in the middle. The activity of intestinal alkaline phosphatase and serum alkaline phosphatase is strongly correlated with ABH secretor phenotypes. Independent of ABO blood group, ABH non-secretors have lower alkaline phosphatase activity than ABH secretors. It has been estimated that the serum alkaline phosphatase activity of non-secretors is only about 20% of the activity in the secretor groups. It appears likely that the ABO and secretor genes influence the rate at which the intestinal phosphatase enters the blood, or its catabolism, rather than its synthesis in the intestine. (11,12)

IAP has several important functions. During fetal development, IAP is the enzyme with the highest blood concentration during the critical period when the gut lining is developing. IAP also helps to split cholesterol and long chain fatty acids from food into smaller fatty acids. Finally, it also enhances the absorption of calcium from food. The concentration of the intestinal phosphatase is lowest in the serum during fasting and rises after ingestion of fat, reaching a peak at about seven to eight hours. The concentration of intestinal alkaline phosphatase in human thoracic-duct lymph rises after a fatty meal; and presumably, most of the intestinal phosphatase enters the blood by way of the lymphatic system.


Although several studies on highly select populations have yielded conflicting results (13,14), the consensus is that blood group A has a significantly higher basal cholesterol level than the other blood groups. The relationship between ABO blood phenotype and total serum cholesterol level was examined in a Japanese population to determine whether elevated cholesterol levels are associated with blood group A. Their results showed that cholesterol levels were very significantly elevated in the blood group A group compared to non-A group (P < 0.00001). (15) In a nationwide sample of more than 6000 black and white adolescents aged 12 to 17 years, ABO blood group and coronary risk factor levels were measured. Blood group A1 was associated with significantly higher serum total cholesterol levels in white females independent of all other risk factors, in white males independent of age and weight, and in southern black females independent of age and weight. (16) A separate study (the Bogalusa Heart Study) looked at 656 white and 371 black adolescents and found the same results with regard to cholesterol (A higher than others) and also showed higher levels of LDL lipoproteins in type A adolescents over the other blood groups. (17) Whether the association between group A and elevated cholesterol levels is through linkage or environmental factors, such as diet, remains to be determined. The aforementioned ABO variations in intestinal alkaline phosphatase levels have been posited as a potential causative factor.

Viscosity and rheological differences

Elevated Factor VIII (FVIII) levels contribute to venous thrombotic risk. FVIII levels are determined largely by levels of von Willebrand factor (VWF), its carrier protein that protects FVIII against proteolysis. (18) ABO polymorphism is one of the best-characterized genetic modifiers of plasma FVIII; it accounts for approximately 30% of the total genetic effect. (19) Subjects with blood group non-O have higher VWF and FVIII levels than do individuals with blood group O. (20)

Rheology is the science of deformation and flow. One common factor between solids, liquids, and all materials whose behavior is intermediate between solids and liquid is that if we apply a stress or load on any of them they will deform or strain. For our purposes, we will use the term to describe the dynamics between blood clotting (moving towards a solid state) and blood thinning (moving towards a liquid state). It might be tempting to substitute the word “viscosity” for rheology when talking about blood groups and clotting; but it does not cover the “dynamics” of how, when, and why blood can change texture; it only distinguishes one texture state form another.

There is evidence that the rheology of blood may play a role in a variety of chronic anxiety states. When compared to normal subjects, chronic depressive and schizoid patients had very significant differences in their blood rheology and in the ability of their red blood cells to aggregate. When patients having schizoid anxiety were compared to those having depressive anxiety, their ratio of albumin to globulin was increased. When patients were divided according to their ABO blood groups, significant differences were found in their albumin to fibrinogen ratio and their blood viscosity. This was particularly true for women who were type A and who suffered from depressive anxiety: their blood tended to be substantially “thicker” and have higher amounts of serum proteins in it than women with similar depression who were blood group O. (21)

Associations between the ABO phenotype and variations in blood rheology have been also reported in high blood pressure, (22) stress, (23) diabetes, (24) heart attack, cancer and thyroid disease, (25) renal failure (26) and malignant melanoma. (26-27)

Soluble adhesion factor E-selectin

Endothelial (E)-selectin (CD62E), formerly known as ELAM-1, is synthesized de novo by endothelial cells in response to IL-1, lipopolysaccharide, TNF-alpha, or G-CSF and is, therefore, detectable either after or concurrently with P-selectin to augment leukocyte recruitment. In humans, E-selectin is encoded by the SELE gene. E-selectin recognizes and binds to sialylated carbohydrates present on the surface proteins of certain leukocytes. These carbohydrates include members of the Lewis X and Lewis A families found on monocytes, granulocytes, and T-lymphocytes.

E-selectin is a heavily glycosylated transmembrane protein. E-selectin, recognizes several diverse and structurally distinct glycoconjugates on various hematopoietic and carcinomatous cells in affinity or binding assays. These ligands may include cutaneous lymphocyte-associated antigen (CLA) a distinct glycoform of P-selectin glycoprotein ligand-1 (PSGL-1), L-selectin, E-selectin ligand-1, CD43, hematopoietic cell E- and L-selectin ligand (a specialized glycoform of CD44), betaa-2 integrins, and glycolipids. (28) Recently, death receptor-3 (DR3) expressed on colon carcinoma cells has been identified as a new E-selectin ligand. (29)

During inflammation, E-selectin plays an important part in recruiting leukocytes to the site of injury. The local release of cytokines IL-1 and TNF by damaged cells induce the over-expression of E-selectin on endothelial cells of nearby blood vessels. Leukocytes in the blood, expressing the correct ligand, will bind with low affinity to E-selectin, causing the leukocytes to “roll” along the internal surface of the blood vessel as temporary interactions are made and broken. As the inflammatory response progresses, chemokines released by injured tissue enter the blood vessels and activate the rolling leukocytes, which are now able to tightly bind to the endothelial surface and begin making their way into the tissue. E-selectin binds sialyl Lewis X (SLeX).

ABO is a major locus for serum soluble E-selectin levels. E-selectin is higher in O/O than O/A heterozygotes, which likewise have higher levels than A/A genotypes. Analysis of subgroups of A alleles reveals heterogeneity in the association, and even after this was accounted for, an intron 1 SNP remained significantly associated. Additional findings indicate that the genetic variants at ABO locus affect plasma soluble E-selectin levels and diabetes risk. (30,31)


The Lancet researchers conclude that the propensity of ABO blood grousp to influence the course of heart disease “was attributable to the glycotransferase-deficient enzyme that encodes the ABO blood group O phenotype previously proposed to protect against myocardial infarction.”

This is indeed true. However there are a great many other factors related to ABO phenotype that interact together to produce clinical cardiovascular illness. Soluble adhesion factors like E-selectin best promote arterial inflammation when in the presence of clotting factors such as Factor VIII and even slightly elevated cholesterol.

Both of these factors are also known to be associated with the blood group A phenotype. Blood viscosity is known to alter most prominently in group A when under stress and a variety of health conditions often unrelated to heart disease.

The almost three-fold differences in intestinal alkaline phosphatase between group O and group A individuals and between ABH secretors and non-secretors points to the cardiovascular benefits of a lower protein diet in group A, especially group A individuals of the non-secretor phenotype; and suggests that secretor status should also be included in any analysis of blood group propensities towards cardiovascular disease.

  1. Havlik RJ, et al. Blood groups and coronary heart disease. Lancet. 1969 Aug 2; 2(7614):269-70.
  2. Slipko Z, Latuchowska B, Wojtkowska E. Body structure and ABO and Rh blood groups in patients with advanced coronary heart disease after aortocoronary bypass surgery. Pol Arch Med Wewn. 1994 Jan; 91(1):55-60.
  3. Meshalkin EN, Okuneva GN, Vlasov IuA, Vel’tmander NN. ABO and Rh blood groups in cardiovascular pathology. Kardiologiia. 1981 Apr; 21(4):46-50.
  4. Erikssen J, Thaulow E, Stormorken H, Brendemoen O, Hellem A. ABO blood groups and coronary heart disease (CHD). A study in subjects with severe and latent CHD. Thromb Haemost 1980 Jun 18; 43(2):137-140.
  5. Allan TM. ABO blood groups, age, and work in ischemic heart disease. Atherosclerosis. 1975 May; 21(3):459-461.
  6. Galeazzi L, Gualandri V. ABO blood-group phenotypes and pathogenesis of cardiovascular diseases. Congenital, rheumatic, and coronaric heart disease and arterial hypertension. Ital Cardiol. 1975; 5(5):744-751.
  7. Rosenberg L, Miller DR, Kaufman DW, Helmrich SP, Van de Carr S, Stolley PD, Shapiro S. Myocardial infarction in women under 50 years of age. JAMA. 1983 Nov 25; 250(20):2801-2806.
  8. Platt D, Muhlberg W, Kiehl L, Schmitt-Ruth R. ABO blood group system, age, sex, risk factors and cardiac infarction. Arch Gerontol Geriatr. 1985 Oct; 4(3):241-249.
  9. Whincup PH, Cook DG, Phillips AN, Shaper AG. ABO blood group and ischemic heart disease in British men. BMJ. 1990 Jun 30; 300(6741):1679-1682.
  10. Blood groups and The Intestine. Editorial. Lancet. 1966 Dec 3; 2(7475):1232-3.
  11. Arfors KE, Beckman L, Lundin LG. Genetic Studies of Blood Group-Associated Variations in a Human Serum Alkaline Phosphatase. Acta Genet Statist Med. 1965; 13, 89.
  12. Mehta NJ, Rege DV, Kulkarni MB. Total serum alkaline phosphatase (SAP) and serum cholesterol in relation to secretor status and blood groups in myocardial infarction patients. Indian Heart J. 1989 Mar;41(2):82-85
  13. Martin NG, Rowell DM, Whitfield JB. MN and Jk systems influence environmental variability in serum lipid levels. Clin Genet. 1983 Jul; 24(1):1-14.
  14. Gleiberman L, Gershowitz H, Harburg E, Schork MA. Blood pressure and blood group markers. Association with the MN locus. J Hypertens. 1984 Aug; 2(4):337-41.
  15. Reid ME. MNS blood group system: a review. Immunohematology. 2009; 25(3):95-101.
  16. Sharon R, Weinberg H, Husseini N. An unusually high incidence of homozygous MM in ankylosing spondylitis. J Bone Joint Surg Br. 1985 Jan; 67(1):122-3.
  17. Howard DR. Expression of T-antigen on polyagglutinable erythrocytes and carcinoma cells: preparation of T-activated erythrocytes, anti-T lectin, anti-T absorbed human serum and purified anti-T antibody. Vox Sang. 1979; 37(2):107-10.
  18. Platt D, Muhlberg W, Kiehl L, Schmitt-Ruth R. ABO blood group system, age, sex, risk factors and cardiac infarction. Arch Gerontol Geriatr. 1985 Oct; 4(3):241-249.
  19. Whincup PH, Cook DG, Phillips AN, Shaper AG. ABO blood group and ischemic heart disease in British men. BMJ. 1990 Jun 30; 300(6741):1679-1682.
  20. Jorgensen G. ABO blood groups in physicians more than 75 years old. On the hypothesis concerning “little more fitness of blood group O” MMW Munch Med Wochenschr. 1974 Mar 29; 116(13):649-52.
  21. Dintenfass L, et al. Blood rheology in patients with depressive and schizoid anxiety. Biorheology. 1976 Feb; 13(1):33-6.
  22. Dintenfass L, et al. Dynamic blood coagulation and viscosity and degradation of artificial thrombi in patients with hypertension. Cardiovasc Res. 1970 Jan; 4(1):50-60.
  23. Dintenfass L, et al. Effect of stress and anxiety on thrombus formation and blood viscosity factors. Bibl Haematol. 1975; (41):133-9.
  24. Dintenfass L, et al. Genetic and ethnic influences on blood viscosity and capillaries in diabetes mellitus. Microvasc Res. 1977 Sep; 14(2):161-72.
  25. Dintenfass L, et al. Effect of fibrinogen on aggregation of red cells and on apparent viscosity of artificial thrombi in hemophilia, myocardial infarction, thyroid disease, cancer and control systems: effect of ABO blood groups. Microvasc Res. 1975 Jan; 9(1):107-18.
  26. Dintenfass L, et al. Formation, consistency and degradation of artificial thrombi in severe renal failure. Effect of ABO blood groups. Thromb Diath Haemorrh. 1968 Nov 15; 20(1):267-84.
  27. Dintenfass L. Some aspects of hemorrheology of metastasis in malignant melanoma. Haematologia (Budap). 1977; 11(3-4):301-7.
  28. Barthel SR, Gavino JD, Descheny L, Dimitroff CJ. Targeting selectins and selectin ligands in inflammation and cancer. Expert Opin Ther Targets. 2007 Nov; 11(11):1473-91.
  29. Gout S. et al. Death receptor-3, a new E-selectin counter-receptor that confers migration and survival advantages to colon carcinoma cells by triggering p38 and ERK MAPK activation. Cancer Res. 2006; 66(18):9117–9124.
  30. Paterson AD, Lopes-Virella MF, Waggott D, Boright AP, Hosseini SM, Carter RE, Shen E, Mirea L, Bharaj B, Sun L, Bull SB. Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Genome-wide association identifies the ABO blood group as a major locus associated with serum levels of soluble E-selectin. Arterioscler Thromb Vasc Biol. 2009 Nov; 29(11):1958-67.
  31. Qi L, Cornelis MC, Kraft P, Jensen M, van Dam RM, Sun Q, Girman CJ, Laurie CC, Mirel DB, Hunter DJ, Rimm E, Hu FB. Genetic variants in ABO blood group region, plasma soluble E-selectin levels and risk of type 2 diabetes. Hum Mol Genet. 2010 May 1; 19(9):1856-62.

One response so far

Jan 09 2011

Blood groups and the intestine

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 group 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 group O blood have almost three times the levels of an enzyme in their intestines called intestinal alkaline phosphatase (IAP) [LINK]. 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. ABH secretor status plays a role in determining alkaline phosphatase levels: for example, Group O secretors secrete more IAP than group O non-secretors. So a spectrum of IAP secretion would extends from a high in group O secretors to a low in group A non-secretors.

Alkaline Phosphatases are a group of enzymes found primarily the liver, bone and the intestines. There are also small amounts produced by the placenta, and the kidneys. The primary importance of measuring alkaline phosphatase is to check the possibility of bone disease or liver disease so the bone and liver fractions are the most common diagnostic fractions. [LINK] Rosacea is a common inflammatory condition of the facial skin of unknown etiology, which frequently occurs in combination with gastrointestinal disorders. Many dietary and hormonal factors are known to affect the severity of rosacea symptoms, several of which also modulate the activity of the enzyme intestinal alkaline phosphatase (IAP). The role of IAP in inhibiting an inflammatory response to intestinal bacteria suggests a mechanism by which intestinal pathologies may be linked to the skin inflammation characteristic of rosacea. [LINK]IAP is involved in the maintenance of normal gut microbial homeostasis and may have
therapeutic potential against dysbiosis and pathogenic infections. [LINK]

IAP is critical to the health of the intestinal microvilli, delicate fingers of tissue that incrase absorption.

Now you’d think this was cutting-edge, late-breaking news since it is obviously of tremendous interest in these nutrigenomic heavy times. However, the first observations were made over four decades ago.[LINK] In almost thirty years of practice, I’ve never met a physician who was aware of this association until I had first told them.

In addition to these two critical functions IAP is an important influence on the ability of the digestive tract to heal. In fact during the fetal period levels of IAP rise so high that they are temporarily the most abundant enzyme in the body. Thus in most of our group 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. [LINK]

Blood group 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 group A individuals. These folks really should follow a Mediterranean-type diet.

Later studies showed that blood group 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. [LINK]

Thus, we have here one of the strongest indications for the long term benefit of a low-fat diet in blood group A, both with regard to the susceptibility to cardiovascular disease, and (although not mentioned here) their additional susceptibility to cancer. Following the group 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 group A, lower their level of intestinal dysfunction, and to influence their susceptibility to cardiovascular disease.

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Jan 08 2011

Get My Drift

Published by under Anthropology | Genetics

One of the great chin-scratchers of modern physical anthropology revolves around blood type, in particular why most indigenous populations of the New World have such incredibly high percentages of the gene for type O. Sometimes, especially as you move south of the modern US-Mexico border, the percentages almost reach 100%.

Since almost everyone agrees that human habitation of the New World began with migrations out of the Siberia, across the Bering Sea, and the population on the Russian Asiatic side shows no similar high percentage of type O; if anything the percentage frequency of the type O gene drops as we move further and further north and east. Several theories have been advanced to explain the apparent ‘Bering Sea Bottleneck’.

The most often suggested is the genetic drift theory. The basic idea behind genetic drift is easy enough to understand. If you flip a coin two hundred times, there is a very good chance that your results will be somewhere close to 100 times coming up heads, and another 100 times coming up tails. Indeed, the more you flip a coin, the more likely (given that you have an honest coin) the results will be 50% head and 50% tails.

However, suppose that you instead only flipped the coin seven times; would it not be feasible on any given Sunday to flip five heads and two tails? Sure it is. That is how Las Vegas stays in business. Genetic drift is like that: A small population may have an uncharacteristic gene distribution simply because the genetic coin did not flip enough to have things even out.

So the Genetic Drift Theory of the ‘Bering Bottleneck Type O Anomaly’ posits that a small band of folks swam, walked or boated over the Bering Strait, and because their numbers were so small, the genes for A and B did not come along with the coin flip. This small number of colonist determined the future gene pool for the continent due to their exerting a ‘founder effect‘.

It’s not a bad theory, except that in order to accomplish this, the numbers of Asian immigrants to the New World must be very small; along the order of a dozen or less, so that there is an even slight statistical chance that they could all be type O. However, even if the original colonizers of the New World numbered, say ten or eleven, the odds of those entire ten or eleven colonist being type O is about one in a thousand. Even if the number of colonists is dropped to five the odds only drop to one in thirty-two. (1) And that also assumes that there was one boatload or band of colonists, when common sense tells us that there must have been numerous attempts, though perhaps not all successful, to migrate to the New World.

The second theory is that of Natural Selection, which a lot of people equate with evolution, but it’s not. Natural selection posits that perhaps a mixture of all blood types were part of the original migration, but for some reason, probably infectious disease, the type A and type B colonists died out. Of the two, Natural Selection is perhaps the stronger theory since there a definite likes between ABO type and susceptibility to small pox, syphilis, E. coli and tuberculosis, all of which probably killed lots of people back then.

However, as any honest exterminator will tell you, it’s hard to kill them all.

A.E. Mourant addressed this issue in his book Blood Relations

“Like the absence of B in the Australian aborigines, the lack of B in the northern zone and of A and B in the southern zone raises a problem of world-wide importance. Was the B gene totally absent from the original populations from eastern Asia that ultimately reached Australia and America, or was the gene lost on the way? If so, was this due to genetic drift in relatively small isolated populations, or to natural selection? Early blood-group workers suggested that when man left Asia for Australia and America mutations for the A and B genes had not yet occurred. However, analogous if not identical genes occur in the higher apes at least, and so are several million years old. In the light of the discussion of O frequencies in Europe it is not difficult to see how, as a result of the elimination of A and B fetuses of O mothers, first the gene B (which is rarer than A) could have tended to disappear, and then A itself.”(2)

Now, it has been know for a while (3) that human and primate ABO genes are somewhat analogous, let’s just say that they are similar enough for our purposes, which is to say that the individual genes for A, B and (by default) O are ‘old’. However, does it automatically lead us to assume that just because genes share a long history, does that mean we can assume that they will always exist in the percentage numbers? Of course not, we just say that with Genetic Drift: percentages change.

With apologies to Edward Tufte, let’s take a look at the snazzy graphic I just did:

What you are looking at is the northeast corner of Asia and the northwest corner of North America at the Bering Strait, across and under-which one day your kids may be able to drive their cars. Not surprisingly, the colors of the map mean things: For example, the darker green the land is colored, the higher the frequency of the gene for type O; the lighter the color, the lower the percentage (less type O genes)

Now, first of all, note that these are indigenous populations, so the modern-day Alaskans and Siberians don’t figure here that much here. What sticks out at you? Yup, there is lots of O gene the further east (the right side of ther map) you travel! But what else? Normally we might expect the trail of O genes to drift nicely along, but in our map the distribution is bi-modal: The incidence of O gene is higher at both ends of the map and lower in the middle. You can see that by looking at the bar graphs below, which not only looks at the relative ‘percentage if each percentage’ but also the percentage of land versus water: Each bar graph is actually a snapshot of one of the sixteen ‘slices’ of the map, the black lines.

So if anything, the more constricted that land mass became, the less you find the type O gene.

Interestingly, look at the red numbers on the map. They are the percentages of type B gene. Notice as well that the Asian side of the Strait has some of the highest percentage of Type B gene on the planet. What about on the American side?

Virtually no type B gene.

Now, to me this implies that there may well have been two waves, a ‘First Wave’ that contained very high percentages of type O gene and which had a relatively easy time getting across the Bering Strait (which may well have still been a land bridge) and who created the ‘Founder Effect’ in America, and a ‘Second Wave’ somewhat higher in Type A and much higher in Type B which followed but got stymied by the ecological changes and the closing of the land bridge.

So what I think is that both the Genetic Drift and the Natural Selection theories are correct, but I’m more inclined to move both of their occurrences with regard to blood type further back in time and much further west. In that case, rather than having crossed before the advent of the genes for A and B, our first American colonists would have walked across before the rest of Asia had a chance to recover from the results of its own initial ‘flip of the coin.’

By which time there was no more walking there.

  1. L. Luca Cavalli-Sforza. Genes People and Languages. University of California Press, 2000
  2. Mourant, AE. Blood Relations, Blood Groups and Anthropology. Oxford University Press, Oxford, UK 1983.
  3. Saitou N, Yamamoto F. Evolution of primate ABO blood group genes and their homologous genes. Mol Biol Evol. 1997 Apr;14(4):399-411
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Jan 06 2011

Blood group and complications from fertility treatment

Published by under Disease Links

Ovarian hyperstimulation syndrome is a potentially life-threatening complication during controlled ovarian stimulation for fertility treatment. Since no association of this condition with ABO blood groups was known, we compared ABO antigens with severity and onset of symptoms in a case-control study…The odds ratio for patients undergoing controlled ovarian stimulation with blood group A versus O to develop the early-onset form of this condition was 2.171 (p-value 0.002). Blood group A may be associated with early-onset ovarian hyper-stimulation syndrome in Caucasians…This possible association may be considered for an individualized hormone dosing in controlled ovarian stimulation.

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Ovarian hyperstimulation syndrome (OHSS) is a complication from some forms of fertility medication. Most cases are mild, but a small proportion is severe. Symptoms can range from a more mild form that includes abdominal bloating and feeling of fullness, nausea, diarrhea, and slight weight gain to a more severe form that includes and fullness/bloating above the waist, shortness of breath, urination significantly darker or cessation of urination altogether, calf and chest pains, marked abdominal bloating or distention, and lower abdominal pains. This study looked at 127 Caucasian patients hospitalized because of ovarian hyperstimulation syndrome after receiving in vitro fertilization, in the period from January 2000 to February 2007 and found that blood group A was markedly more frequent and blood group O less frequent in patients with ovarian hyperstimulation syndrome.

Other studies have found a slightly greater incidence of ovarian cancer in women who are blood group A (link) and blood group antigens (as mucins or ‘blood group substances’) are known to be richly deposited on ovarian tissue. (link) Hopefully fertility specialists will consider individualizing hormonal treatment by blood group when working with fertility patients.

Four patients developed thrombosis (clots) in the jugular or subclavian vein, none of whom had blood group O; this correlates with earlier studies linking blood groups other that type O with an increased risk of thrombosis (link) at some of this clotting may in fact be due to enhanced sensitivity to estrogen, at least in women who are not blood group O. (link)

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