A database of blood group correlations to common diseases
Total number of records: 145 Matching records: 1
|Description:||There is a very distinct difference among the blood types with regard to their incidence of heart disease. Type O and Type B are less likely to generate heart disease as a result of high cholesterol. Their pathway is carbohydrate intolerance. Type A and Type AB follow a more conventional path, through high cholesterol. Each of these pathways lead to a very different lifestyle plan and diet in order to stay heart healthy. |
Type A and Type AB: The Blood Type-Cholesterol Factor
A number of studies show that Type As and Type ABs are more likely to be at risk of heart disease and death by virtue of elevated cholesterol:
The relationship between blood type and total serum cholesterol level was examined in a Japanese population to determine whether elevated cholesterol levels are associated with Type A, as has been demonstrated in many Western European populations. The results showed that cholesterol levels were very significantly elevated in the Type A group compared to other blood types.
A study examining a total of 380 marker/risk factor combinations found associations between Type A and both total serum cholesterol and LDL cholesterol, while a negative association was found between Type B and total serum cholesterol.
A Hungarian study measured the cholesterol of 653 patients who underwent coronary angiography between 1980 and 1985 at the Hungarian Institute of Cardiology. The results showed that Type A was more frequent and Type O was less frequent than normally seen in the Hungarian population, and that there were differences between the blood types as to the areas of the vessels where the narrowing of the coronary arteries had occurred.
Several forms of elevated lipoproteins are inherited. One of the more common forms of hyperlipoproteinemia is called Type IIB, and it is characterized by increased LDL and VLDL (really bad cholesterol). Type IIB hyperlipoproteinemia results in premature hardening of the arteries, obstruction of the carotid artery (the artery which supplies blood to the head and brain), peripheral artery disease, heart attack, and stroke. Since all of these disorders show higher rates of occurrence in Type As, it is not surprising that studies have found a significant connection between hyperlipoproteinaemia IIb and Type A in both newborns and in patients who have suffered heart attacks.
Type O and Type B: The Blood Type-Carbohydrate Intolerance Factor
For Type Os and Type Bs, the leading risk factor for heart disease is not so much the fat in the food as the fat on the person. In other words, the elevated risk factor is due to carbohydrate intolerance. When Type Os and Type Bs adopt low-fat diets rich in metabolically inactivating lectins, they gain weight. This particular kind of weight gain is a major risk factor for heart disease.
For many years, heart experts have been saying that high triglycerides are not an independent risk for heart diseaseűonly in combination with other factors. However, increasing evidence is pointing to elevated triglycerides as a risk factor on their own, and this partially explains the anomaly of the Type O and Type B pathway to heart disease. The link between obesity, triglycerides, and bad lipoproteins has been evidenced in Type Os. In a French study of blood donors, serum triglycerides and lipoproteins were shown to correlate with both obesity and Blood Type O in a study screening for cardio-or cerebro-vascular disease. There is also a connection between non-secretors and high triglyceride levels, as well as insulin resistance.
Nature has provided Type O and Type B with an additional secret weapon to allow them to benefit from those higher protein levels. That weapon is intestinal alkaline phosphatase, an enzyme manufactured in the small intestine, which has the primary function of splitting dietary cholesterol and fats. Numerous studies since the mid-1960s have shown that Type O and Type B have higher levels of this enzyme--especially Type O and Type B secretors. Conversely, Type A and Type AB have lower levels of this enzyme. Recent studies suggest that it is the inability to break down dietary fat which in part predisposed Type A and Type AB to higher cholesterol and more heart attacks; while the opposite is true for Type O and Type B, who are aided in the breakdown of dietary fat by high amounts of intestinal alkaline phosphatase.
Intestinal alkaline phosphatase activity rises following the ingestion of a fat-containing meal, especially if the triglycerides in the meal are long-chain fatty acids. In a study of volunteers given different test meals, the after-meal rise in serum intestinal alkaline phosphatase activity was significantly greater following the long-chain fatty acid meal than following the medium-chain fatty acid meal, and significantly higher in Type O and Type B over Type A and Type AB. Paradoxically, it appears that intestinal alkaline phosphatase gives Type O and Type B metabolic advantages when they eat high protein meals. Studies show that the consumption of protein further increases the levels of alkaline phosphatase in the intestines of Type Os and Type Bs. Without protein in their diets, Type Os and Type Bs do not gain the benefits of the specialized fat busting enzymes in their intestines. This explains why these blood types can lower their cholesterol by adopting high protein diets.
Recently, an intriguing study helped to cast some light on why Type As and Type ABs have such low levels of alkaline phosphatase activity. In an article entitled 'Intestinal alkaline phosphatase and the ABO blood group system--a new aspect' researchers presented evidence that the Blood Type A antigen may itself inactivate alkaline phosphatase. It may be the case that the lower levels of this enzyme, and the subsequent inability to break down dietary fats, may not be genetically linked to blood type. Instead, this reaction is to the physical expression of the A antigen. The authors found that the red cells of Type A and Type AB bind almost all intestinal alkaline phosphatase, while the red cells of Type O and Type B did so to a much lesser degree.
|References:||1. Wong FL, Kodama K, Sasaki H, Yamada M, Hamilton HB. Longitudinal study of the association between ABO phenotype and total serum cholesterol level in a Japanese cohort. Genet Epidemiol 1992;9(6):405-418 2. George VT, Elston RC, Amos CI, Ward LJ, Berenson GS. Association between polymorphic blood markers and risk factors for cardiovascular disease in a large pedigree. Genet Epidemiol 1987;4(4):267-275 |
3. Tarjan Z, Tonelli M, Duba J, Zorandi A [Correlation between ABO and Rh blood groups, serum cholesterol and ischemic heart disease in patients undergoing coronarography]. Orv Hetil 1995 Apr 9;136(15):767-9
4.Kipschidse NN, Schawgulidse NA [Arteriosclerosis and blood lipids]. Z Gesamte Inn Med 1989 Mar 15;44(6):175-6
5.Contiero E, Chinello GE, Folin M. Serum lipids and lipoproteins associations with ABO blood groups. Anthropol Anz 1994 Sep;52(3):221-30
6.Borecki IB, Elston RC, Rosenbaum PA, Srinivasan SR, Berenson GS. ABO associations with blood pressure, serum lipids and lipoproteins, and anthropometric measures. Hum Hered 1985;35(3):161-70
7.Lewis GF, Steiner G Acute effects of insulin in the control of VLDL production in humans. Implications for the insulin-resistant state. Diabetes Care 1996 Apr;19(4):390-3
8.Arfors, K. E., Beckman, L., Lundin, L. G. Acta Genet. Statist. Med. 1963,13,89
9.Hodson, A. W., Larner, A. L., Raine, L. Clin. chim. Acta, 1962, 7,255.
10.Shreffler, D. C. Am. J. Hum. Genet. 1965, 17, 71.
11.Bamford, K. F., Harris, H., Luffman, J. E., Robson, E. B., Cleghorn, T. E. Lancet, 1965, i, 530.
12.Langman, M. J. S., Leuthold, E., Robson, E. B. Harris, J.. Luffman, J. E., Harris, H. Nature, Lond. 1966, 212, 4 1.
13.Keiding, N. R. Clin. Sci. 1964, 26, 29 1. 27. Blornstrand, R., Werner, W. Acta chir. Scand. 1965, 129.
14.Domar U, Hirano K, Stigbrand T. Serum levels of human alkaline phosphatase isozymes in relation to blood groups. Clin Chim Acta 1991 Dec 16;203(2-3):305-313
15.Nakata N, Tozawa T. [The ABO blood groups-dependent reference intervals for serum alkaline phosphatase isozymes and total activity in individuals 20-39 years of age]. Rinsho Byori 1995 May;43(5):508-512
16.Day AP, Feher MD, Chopra R, Mayne PD Triglyceride fatty acid chain length influences the post prandial rise in serum intestinal alkaline phosphatase activity. Ann Clin Biochem 1992 May;29 ( Pt 3):287-91
17.Stepan J, Graubaum HJ, Meurer W, Wagenknecht C [Isoenzymes of alkaline phosphatase - reference values in young people and effects of protein diet]. Experientia 1976;32(7):832-834
18.Bayer PM, Hotschek H, Knoth E. Intestinal alkaline phosphatase and the ABO blood group system--a new aspect. Clin Chim Acta 1980 Nov 20;108(1):81-87
19.Jick H, et al. Venous thromboembolic disease and ABO blood type. A cooperative study. Lancet. 1969 Mar 15;1(7594):539-42. No abstract available.
20.Neumann JK, Chi DS, Arbogast BW, Kostrzewa RM, Harvill LM. Relationship between blood groups and behavior patterns in men who have had myocardial infarction. South Med J 1991 Feb;84(2):214-8
21.Miller AL. Botanical influences on cardiovascular disease. Altern Med Rev. 1998 Dec;3(6):422-31. Review.
22.Langsjoen PH, et al. Overview of the use of CoQ10 in cardiovascular disease.Biofactors. 1999;9(2-4):273-84. Review.
23.Maxwell SR. Can anti-oxidants prevent ischaemic heart disease? J Clin Pharm Ther. 1993 Apr;18(2):85-95.
24.Bertolini S, Donati C, Elicio N, et al. Lipoprotein changes induced by pantethine in hyperlipoproteinemic patients: adults and children. Int J Clin Pharmacol Ther Toxicol 1986;24:630-637
25.Zak A, et al [Effect of fish oils on plasma lipid risk factors and esterified fatty acids in primary hyperlipoproteinemia]. Sb Lek. 1997;98(3):213-24.
26.Shahar E, Folsom AR, Wu KK, Dennis BH, Shimakawa T, Conlan MG, Davis CE, Williams OD. Associations of fish intake and dietary n-3 polyunsaturated fatty acids with a hypocoagulable profile. The Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb 1993 Aug;13(8):1205-12
27. Olszewski AJ, McCully KS. Fish oil decreases serum homocysteine in hyperlipemic men. Coron Artery Dis 1993 Jan;4(1):53-60
28.Rustan AC, Nenseter MS, Drevon CA. Omega-3 and omega-6 fatty acids in the insulin resistance syndrome. Lipid and lipoprotein metabolism and atherosclerosis. Ann N Y Acad Sci 1997 Sep 20;827:310-26
29.McFadzean J, et al Nitric oxide ABO blood group difference in children. Lancet. 1999 Apr 24;353(9162):1414-5.
30.Weimann J, et al ABO blood group and inhaled nitric oxide in acute respiratory distress syndrome. Lancet. 1998 Jun 13;351(9118):1786-7
31.. Streeper RS, et al Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol. 1997 Jul;273(1 Pt 1)
32.Dhuley JN. Effect of ashwagandha on lipid peroxidation in stress-induced animals. J Ethnopharmacol. 1998 Mar;60(2):173-8.
33.Panda S, et al. Changes in thyroid hormone concentrations after administration of ashwagandha root extract to adult male mice. J Pharm Pharmacol. 1998 Sep;50(9):1065-8
34.Bhandari U, Sharma JN, Zafar R. The protective action of ethanolic ginger (Zingiber officinale) extract in cholesterol fed rabbits. J Ethnopharmacol 1998 Jun;61(2):167-71
35.Sharma RD, et al. Effect of fenugreek seeds on blood glucose and serum lipids in type I diabetes. Eur J Clin Nutr. 1990 Apr;44(4):301-6.
36.Tjokroprawiro A, Pikir BS, Budhiarta AA, Pranawa, Soewondo H, Donosepoetro M, Budhianto FX, Wibowo JA, Tanuwidjaja SJ, Pangemanan M, et al. Metabolic effects of onion and green beans on diabetic patients. Tohoku J Exp Med 1983 Dec;141 Suppl:671-6
37.Nityanand S, et al. Clinical trials with gugulipid. A new hypolipidaemic agent. J Assoc Physicians India. 1989 May;37(5):323-8.
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PathType is a searchable database of blood group and disease associations, clinical correlates and citations.
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