A paper published in the Journal 'Blood' entitled "HIV-1 incorporates ABO histo-blood group antigens that sensitise virions to complement-mediated inactivation"  suggests that transmission of HIV-1 is modified by both ABO blood group and the immune system enzyme complement. The premise is based on research showing how the ABO antigen (blood group marker) of the infected person is incorporated into the HIV virus that is replicated in their cells. Because the virus is coated in the person's blood group antigen, it then acts in the same way a red blood cell would when someone with an incompatible blood group becomes exposed to it, and the part of the immune system that would normally cause an incompatible blood transfusion reaction is activated against the virus, helping to protect the recipient against infection. This would mean that it would be harder for an individual of blood group O (the 'universal donor') to contract HIV infection from people of any other blood group apart from blood group O, as the recipient will have both anti-A and anti-B antigens in their blood. Conversely those with blood group AB (the 'universal recipient') who have no opposing blood group antibodies would contract HIV infection more easily from people of any blood group.
This paper follows previous research  on how complement is activated by anti-B IgM (the immune complex involved in incompatible transfusion reactions where the donor is blood group B or AB and the recipient is blood group A or O) and other factors, in blood from HIV-negative donors. In the research by Saarloos et. al. complement was however more easily activated against HIV by antibodies to HIV itself as a result of HIV infection than by IgM.
Later research  suggests that the immune system of some people with AIDS (PWA) who are blood group A or AB may form anti-A IgA, IgG and IgM (antibodies against their own blood group).
The HIV virus made in cells of an HIV-infected person will show their blood group antigen only when the originating cell expresses ABO antigens or is a lymphocyte (white blood cell). As ABH non-secretors have fewer cells expressing their blood group, it follows that they may produce more HIV viruses without blood group antigens than would ABH secretors. This could mean that it is as easy to become infected with HIV-1 from non-secretors of any blood group as it is from secretors of transfusion-compatible blood groups.
ABH non-secretors would be at some disadvantage in protection against HIV infection transmitted via mucous membranes, as they secrete lower levels of immune-protective substances .
HIV positive individuals and PWA should always take steps to avoid transmission of the HIV virus, whatever their blood group or secretor status. Neil and colleagues have however demonstrated a key concept in the relationship between blood groups and immunity, which is mirrored in numerous other blood group-disease connections. It also gives new meaning to the idea of universality in terms of blood group transfusion with relation to infection susceptibility.
1. Neil SJ, McKnight A , Gustafsson K, Weiss RA
HIV-1 incorporates ABO histo-blood group antigens that sensitise virions to complement-mediated inactivation.
2. Saarloos MN, Lint TF, Spear GT
Efficacy of HIV-specific and 'antibody-independent' mechanisms for complement activation by HIV-infected cells.
Clin Exp Immunol. 1995 Feb;99(2):189-95.
3. Friedli F, Rieben R, Wegmuller E et. al.
Normal levels of allo- but increased levels of potentially autoreactive antibodies against ABO histo-blood group antigens in AIDS patients.
Clin Immunol Immunopathol. 1996 Jul;80(1):96-100.
4. D'Adamo PJ.
Eat Right 4 Your Type Complete Blood Type Encyclopedia. p.320.
Pub. Penguin, 2002.
Research at the University of Wisconsin (1) has found an antioxidant present in green tea to be useful against malignant melanoma, the type of skin cancer with the highest mortality rate. Epigallocatechin-3-gallate (EGCG), the a polyphenolic antioxidant present in green tea decreased growth and proliferation of melanoma cells in vitro. The authors conclude that "EGCG, alone or in conjunction with current therapies, could be useful for the management of melanoma".
Melanoma accounts for only about 4% of all skin cancer cases, but most of skin cancer-related deaths. Although most types of cancer are more common in individuals of blood group A and AB, those of blood group O tend to have a lower survival rate from melanoma (2).
1. Nihal M, Ahmad N, Mukhtar H, Wood GS.
Anti-proliferative and proapoptotic effects of (-)-epigallocatechin-3-gallate on human melanoma: Possible implications for the chemoprevention of melanoma.
Int J Cancer. 2005 Apr 20;114(4):513-21.
Q: I am A+ secretor and take warfarin due to incidents of spontaneous DVTs (I have the Factor V Leiden gene deficiency). As such, I've had to lay off my beloved green tea and generally be careful of other supplements. I would like to begin taking A-friendly supplements from NAP, but am wondering if there are things I should avoid or watch for? Thanks for your help, Elizabeth
Venous Thromboembolism (VTE) is when a blood clot has formed in a blood vessel and then dislodges from its site of origin, blocking a vein. Blood clot formation may result from injury, or be associated with infections. In the US the incidence of VTE is more than 1 in 1000. Of these, 30% die within 30 days; one-fifth suffer sudden death due to pulmonary embolism. Independent risk factors for VTE in the US include increasing age, male gender, surgery, trauma, hospital or nursing home confinement, malignancy, neurological disease with arm or leg paralysis, prior superficial vein thrombosis and varicose veins; among women, risk factors include pregnancy, oral contraceptives and hormone replacement therapy. About 30% of surviving cases develop recurrent VTE within ten years. Independent predictors for recurrence include increasing age, obesity, malignant neoplasm, and arm or leg paralysis (1).
Deep Vein Thrombosis (DVT), a type of VTE usually in the deep veins of the legs or pelvis, may occur in people recovering from childbirth, surgery, or other conditions requiring prolonged bedrest, or after long haul flights; the clotting mechanism is thought to be impaired when the legs are immobilised. A danger is that a clot originating in the leg vein may dislodge and travel to the lung (pulmonary embolism). Redness, warmth, pain, swelling or tenderness of the leg can all be signs of DVT, but may not all be present. Doppler ultrasound may confirm the presence of a DVT.
Factor V is a clotting factor protein, whose normal role is to help blood to clot when an appropriate trigger is present. Like all steps in the clotting cascade however, Factor V is subject to regulation to keep it under control, preventing clots from forming too easily or too quickly. Factor V Leiden (FVL) is a genetic variant form of the Factor V clotting protein, where the inactivating protein APC cannot work to prevent excessive clotting by Factor V.
FVL is the most common hereditary blood coagulation disorder, affecting 5% of Caucasians in the US, and about 2 to 4% of the Dutch population, 7% of the Swedish population and 8% of the German population. FVL increases the risk of VTE 3-8 times for heterozygous (FVL gene inherited from one parent), and substantially more, 30-140 times, for homozygous (FVL gene inherited from both parents) individuals within the population as a whole (2).
Other genetic polymorphisms can affect blood clotting, the most common being an individual's sex and ABO and Lewis blood group (secretor status) (3,4).
Being blood group A or AB (and to a lesser extent , puts that person at greater risk of blood clotting due to an increase in plasma concentration of the clotting factors von Willebrand factor antigen (vWf) and Factor VIII. An estimated 30% of the genetically determined variance in plasma concentration of vWf is directly related to ABO blood group. Also ABH non-secretors, and in particular Lewis negative individuals have a higher tendency to blood clotting. These genetic factors can multiply together, increasing risk of VTE:
"ABH non-secretors are reported to have shorter bleeding times and a tendency toward higher factor VIII and vWf. This relationship appears to be another example of blood type synergy between ABO and Secretor/Non-secretor phenotypes. In fact, secretor genetics appear to interact with ABO genetics to influence as much as 60 percent of the variance of the plasma concentration of vWf, with secretors (Le(a-b+)) having the lowest vWf concentrations" (4).
As it is expression of the H antigen that mediates the ABO effect on plasma vWF concentration, it will make a difference as to whether an individual’s blood group A phenotype consists of a genotype of A1A1, which has higher levels than in A1O genotype, which has higher levels than in A2O genotype (3). Knowing your parents’ blood groups and getting a test for the A1/A2 subgroup may give further clarification of genotype and related risk factor.
Age-related difference in ABO-relative risk of VTE decreases with advancing age (6). It has also been suggested that high plasma homocysteine (Hcy) levels may also be a significant risk factor for VTE, particularly with those under 60 (7), as Hcy tends to increase with age. For individuals high Hcy levels, a supplement such as NAP Methyl B12 Plus may help to reduce Hcy.
Hormone replacement therapy and the contraceptive pill both increase the risk of VTEs, but women heterozygous for FVL on either type of hormonal intervention the risk is increased between two and six times, and monozygotes for FVL between fifteen and thirty times (8,9).
Statin drugs, and therefore natural statin mimetic substances such as red rice yeast may also decrease the risk of VTE, but aspirin therapy alone does not significantly reduce the risk (10).
Blood groups A and AB appear to be associated with increased risk estimates for both DVT and pulmonary embolism compared with blood group O during and after pregnancy (11).
Warfarin is a standard treatment for thinning the blood to break up clots and prevent new clots from forming. Generally accepted side effects of warfarin include haemorrhage, hypersensitivity, rash, alopecia, diarrhoea, unexplained drop in haematocrit, ‘purple toes', skin necrosis, jaundice, hepatic dysfunction; also rarely reported are nausea, vomiting, and pancreatitis. Some other reported side effects include: hair thinning, hair loss, fatigue, taking longer to recover from cuts or bruises, sunburn or sensitivity to light, depression.
There are alternatives to Warfarin such as fish oils, gingko biloba and garlic tablets, but as with Warfarin, supplement intake and blood clotting time must be monitored regularly and supervised by a physician, preferably a naturopath.
Other factors that prevent DVT include the following:
Keep moving your legs, don't take sleeping pills (these cause immobility), wear loose-fitting clothing, keep the legs uncrossed, keep hydrated by drinking normally, avoid alcohol to prevent dehydration, wear graduated compression stockings.
Excess caffeine may cause dehydration, but green tea, which is traditionally brewed for less than a minute, contains relatively low levels of caffeine, and should not cause dehydration if drunk in moderation as well as water.
(1) Heit JA, Silverstein MD, Mohr DN, et. al. The epidemiology of venous thromboembolism in the community. Thromb Haemost. 2001 Jul;86(1):452-63. PMID: 11487036
(2) Folsom AR, Cushman M, Tsai MY, et. al. A prospective study of venous thromboembolism in relation to factor V Leiden and related factors. Blood. 2002 Apr 15;99(8):2720-5. PMID: 1192975
(3) Robinson WM, Roisenberg I. Venous thromboembolism and ABO blood groups in a Brazilian population. Hum Genet. 1980;55(1):129-31. PMID: 7450749
(4) D’Adamo PJ, Kelly GS. Metabolic and Immunologic Consequences of ABH Secretor and Lewis Subtype Status Altern Med Rev 2001;6(4):390-405 PMID: 11578255
(5) O’Donnell J, Boulton FE, Manning RA, Laffan MA Amount of H Antigen Expressed on Circulating von Willebrand Factor Is Modified by ABO Blood Group Genotype and Is a Major Determinant of Plasma von Willebrand Factor Antigen Levels Atherosclerosis. 1976 Jan-Feb;23(1):141-2. PMID: 11834538
(6) Allan TM. ABO blood groups and age groups in surgical venous thromboembolism. Atherosclerosis. 1976 Jan-Feb;23(1):141-2 PMID: 1078393
(7) Ray JG. Meta-analysis of hyperhomocysteinemia as a risk factor for venous thromboembolic disease. Arch Intern Med. 1998 Oct 26;158(19):2101-6. PMID: 9801176
(8) Herrington DM, Vittinghoff E, Howard TD, et. al. Factor V Leiden, hormone replacement therapy, and risk of venous thromboembolic events in women with coronary disease. Arterioscler Thromb Vasc Biol. 2002 Jun 1;22(6):1012-7 PMID: 12067913
(9) Spannagl M, Heinemann LA, Schramm W. Are factor V Leiden carriers who use oral contraceptives at extreme risk for venous thromboembolism? Eur J Contracept Reprod Health Care. 2000 Jun;5(2):105-12. PMID: 10943572
(10) Lacut K, Oger E, Le Gal G, et. al. Statins but not fibrates are associated with a reduced risk of venous thromboembolism: a hospital-based case-control study. Fundam Clin Pharmacol. 2004 Aug;18(4):477-82. PMID: 15312155
(11) Larsen TB, Johnsen SP, Gislum M, et. al. ABO blood groups and risk of venous thromboembolism during pregnancy and the puerperium. A population-based, nested case-control study. J Thromb Haemost. 2005 Feb;3(2):300-4. PMID: 15670036
(12) Ursavas A, Ozyardimci N. Travel and pulmonary thromboembolism Tuberk Toraks. 2004;52(1):98-102. PMID: 1514338
The consequences of severe human zinc deficiency have been known since the 1960s, but only more recently have the effects of milder degrees of zinc deficiency, which are highly prevalent, been recognized. Trials have shown that zinc supplementation results in improved growth in children, lower rates of diarrhoea, malaria, and pneumonia, and reduced child mortality. In total about 800 000 child deaths per year are attributable to zinc deficiency (1).
It has been shown that in people with zinc deficiency, activity of serum thymulin (a thymus specific hormone involved in T cell function) is decreased, an imbalance between T helper cell (Th1) and Th2 function develops, and lytic activity of natural killer cells (destructive action on enemy cells) is decreased (2).
Zinc has been used effectively to treat Wilson's disease, hepatic encephalopathy, sickle cell disease, and the common cold. Zinc is an essential part of metalloproteins and transcription factors involved in gene expression of various proteins. Zinc activates nuclear factor-kappa B in T helper cells and in zinc deficiency binding of nuclear factor-kappa B to DNA is decreased, leading to decreased gene expression of interleukin 2 and its production (2).
Zinc deficiency commonly coexists with other micronutrient deficiencies including iron, making single supplements inappropriate. Authors of a paper in the British Medical Journal now suggest: "Until the results of trials of multiple micronutrient interventions are available, zinc supplements should be given to children with infections" (3).
As zinc is essential in the activation of the enzyme intestinal alkaline phosphatase (IAP) as demonstrated in the IAP of calves (4), it is particularly important for ABH salivary non-secretors to maintain adequate zinc levels due to their lower levels of IAP (5).
If taken in doses greater than 15 mg per day, zinc supplementation should be supervised by a physician.
1. BLACK, R.
Micronutrient deficiency: an underlying cause of morbidity and mortality.
Bull World Health Organ. [online]. 2003, vol.81, no.2, p.79-79.
Available from: . ISSN 0042-9686.
2. Prasad AS.
BMJ. 2003 Feb 22;326(7386):409-10.
3. Shrimpton R, Gross R, Darnton-Hill I, Young M
Zinc deficiency: what are the most appropriate interventions?
BMJ, Feb 2005; 330: 347 - 349.
4. Yan S, Liu Y, Tian X, Zhang Y, Zhou H.
Effect of extraneous zinc on calf intestinal alkaline phosphatase.
Protein Chem. 2003 May;22(4):371-5.
5. Matsushita M, Irino T, Stigbrand T, Nakajima T, Komoda T.
Changes in intestinal alkaline phosphatase isoforms in healthy subjects bearing the blood group secretor and non-secretor.
Clin Chim Acta. 1998 Sep 14;277(1):13-24.
Recent research (1) shows a significant difference in the prevalence of osteoporosis in postmenopausal women, suggesting that bone resorption is more active in women with non-O blood types during the post-menopausal period compared to women with blood type O. Further, osteoporosis was more frequently observed in blood type AB than in other blood types, particularly osteoporosis of the hip. The proximal femurs of AB women were 2.3 times more likely to have osteoporosis than that those belonging to women with O blood type. The findings are consistent with that of previous research (2), (3) cited in the Complete Blood Type Encyclopedia,which suggests that the reason blood types O and B are less susceptible to osteoporosis is due to a lower level of intestinal alkaline phosphatase.
For consistency, all the women were rhesus positive, and none were smokers or suffering from chronic obstructive pulmonary diseases and none were taking HRT (all of which factors can affect bone mineral density).
This study openly recognises the influence of ABO blood group and secretor status on disease incidence, and seeks to add to the wealth of information in this area. In this study the researchers admit that they could not measure objectively the behavioural habits, personality traits, or duration and intensity of physical exercise. This may be significant, as Physical activity, which is closely associated with personality and behavior patterns, is widely accepted as a favourable factor influencing bone mineral metabolism, and individuals with blood phenotype O show a significantly lower incidence of obsessional personality traits, compared to the blood types AB, A, and B. What the researchers failed to mention is the dietary habits of the South Korean women in the study, and whether their typical dietary intake may be more appropriate to the digestive capabilities of blood type O and less to those of blood type AB.
The researchers state that further research is needed to see if such findings are observed in elderly men or premenopausal women. Future studies might also find determination of secretor status, comparison of intestinal alkaline phosphatase levels and dietary intake useful markers in addition to ABO blood type, in determining the risk factors for osteoporosis, although at present it appears to be beyond the remit of scientists to think in these terms.
1. Choi JW, Pai SH. Associations between ABO blood groups and osteoporosis in postmenopausal women. Ann. Clin. Lab. Sci., March 1, 2004; 34(2): 150-3. PMID: 15228226
2. Kolodchenko VP. ABO, rhesus and MN system blood groups and spinal osteochondrosis. Tsitol Genet. 1979 Mar-Apr; 13(3):232-3.
3. Davidson BJ, MacMurray JP, Prakash V. ABO blood group differences in bone mineral density of recovering alcoholic males. Alcohol Clin Exp Res. 1990 Dec;14(6):906-8. PMID: 2088127