Nature-cure, or the healing power of Nature, is the guiding principle behind naturopathic medicine. It is present in every living thing as the ability to restore health and balance: it keeps us alive. As inherent healing forces are not easy to measure using scientific instruments, this idea tends to be dismissed by science as a vitalistic concept, and as a result many of us have become distanced from the natural world.

For the innate therapeutic force to succeed, Nature should be free to work unhindered by the numerous barriers constructed by the human race. Depending on the vitality of the individual, Nature’s healing forces will be promoted by simple things that everyone should be able to take for granted: fresh air, pure water, sunlight, adequate exercise, rest and relaxation, correct thinking and a diet appropriate to the specific, environmental cultural and genetic needs of the individual.

These concepts sound simple enough at first, but to achieve them practically in today’s society may be virtually impossible: we breathe an atmosphere tainted by heavy metals and toxic chemicals; our water is polluted with dangerous contaminants either added by the water companies, by industrial processing or by consumers of cleaning materials, and then compressed in pipes until its vitality is destroyed; sunlight is dangerously high in radiation thanks to the destruction of the Earth’s protective ozone layer; exercise is a luxury when you have to subscribe to a gym or risk the polluted outdoor air and traffic in cities; most people’s idea of rest and relaxation is to slouch in front of a television or hunch by a computer games console. Even if our brains are not hampered by any of this, it is unusual to be able to think clearly in a materialistic Western society incessantly bombarded by media images of ‘normal’ and ‘desirable’ without being swallowed up by the tempo of the psyche of our times.

Nature has a lot to contend with these days: even from before birth, a deficiency in the diet of our grandmother during pregnancy may have influenced our nutritional makeup; the mercury in our mother’s teeth, along with the pesticides and PCBs accumulated in her body all become a part of us before we enter the world, and are accepted as normal; we may be bottle-fed from birth with pasteurised, denatured dried milk originally intended to supply the mucous production needed by calves; the multiple assaults on our immature immune systems by vaccination with toxic substances cultured on animal organs; the destruction of our sense of taste with sweet or salty foods and drinks in a culture of junk food; fruits and vegetables denatured by a forced growing environment; reliance on stimulant and relaxing drugs; the reductionistic overmedication of the population to suppress any symptoms that irritate or annoy us. There are numerous other travesties of humankind that deserve a mention here. Is it anything but a miracle that we are still alive in this jungle of modern society? I have often wondered how people maintain health in this environment without making it a full-time occupation.

If you have read this far without being distracted, disgusted or depressed, you are probably looking for the happy ending. Ultimately it is down to each individual to create his or her own future. Practitioners of natural medicine can help put people on the right path, but don’t expect a magic wand to be waved and suddenly everything will be all right. It is a full-time job keeping mind and body together in the face of all the barriers that humans encounter in daily life, and sometimes staying on the right track is not easy. Are you ready to share that journey?

Normally donors and recipients of blood transfusions need to be carefully matched to avoid a transfusion reaction - an immediate antibody-antigen reaction that can result in fever, low blood pressure, low back pain, a crushing sensation in the chest, nausea, vomiting and death. There are many different blood groups, but a transfusion reaction will only occur if an individual has acquired antibodies to a different blood group through exposure to the antigen that they don't have, and are then given blood with that antigen.

The best known blood group antigens are A, B and H (the O antigen). Exposure to these antigens occur through eating food that contains antigenic components identical to the blood group that the individual does not have. Antibodies to ABO blood groups are IgM, causing destruction of transfused red blood cells, which can then block the kidneys and cause acute tubular necrosis. In unsensitised individuals the reaction may develop over days or weeks as antibodies are produced, resulting in anaemia and jaundice. Reactions to white blood cells and platelets can occur, although the consequences are less serious.

Sensitisation to the Rhesus blood group, which includes the antigens C, c, D, d, E and e, can happen before or during birth, especially with Rhesus D, if the mother is Rhesus negative and her baby is Rhesus positive.

Individuals with blood group O Rhesus negative are considered universal donors, as their red cells do not carry antigens to A, B or D. Consequently O negative blood can generally be transfused to individuals of any blood group.

It is also possible to acquire antibodies to non-self blood groups following exposure to those antigens on some non-self tissue such as a graft or incompatible blood transfusion. Examples of other blood groups involved in transfusion reactions are Kell (K, k), Duffy (Fya, Fyb, Fy) and MN (M, N). Antibodies to Rhesus and other blood groups are IgG.

Scientists at the Albert Einstein College of Medicine, New York have now found a way to 'hide' the ABO and Rhesus antigens on the donor's red blood cells before transfusion to make their blood suitable for any recipient. Using polyethylene glycol (PEG), a polymer of the hydrocarbon ethylene oxide, stuck together with thiols to stick the PEG to the amino acid lysine on the surface of the red cell. The blood from individuals of any blood group will behave as if it is from a donor of blood group O negative. PEGylation has been used in other areas of medicine, such as PEGylated interferon, which remains in the body longer, prolonging its effectiveness. PEG has been found to be immunogenic and can induce antibodies that shorten survival of transfused PEG-RBCs in rabbits, so PEGylation may not be the best way to transfuse blood.

This is not the only way to alter red blood cells to create universal donor blood. Studies have been carried out on group B blood to remove the sugar galactose on the end of the B antigen with the enzyme galactosidase. The red blood cells from group B donors were found to be comparable to group O blood for safety and efficacy. This does not overcome the problem of Rhesus incompatibility, and also the researchers are still looking for a way to convert group A blood to group O.

The laboratory-manufactured universally compatible blood is still some way off. For now, it looks like it is best to get the closest match possible, and the best way to do that is to receive a transfusion of your own blood that you have stored prior to a scheduled operation.

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References:

Nacharaju P, Boctor FN, Manjula BN, and Acharya SA.

Surface decoration of red blood cells with maleimidophenyl-polyethylene glycol facilitated by thiolation with iminothiolane: an approach to mask A, B, and D antigens to generate universal red blood cells.

Transfusion, March 1, 2005; 45(3): 374-83.

PMID:

Garratty G.

Progress in modulating the RBC membrane to produce transfusable universal/stealth donor RBCs.

Transfus Med Rev. 2004 Oct;18(4):245-56.

PMID:

Garratty G, Telen MJ, Petz LD.

Red cell antigens as functional molecules and obstacles to transfusion.

Hematology (Am Soc Hematol Educ Program). 2002;:445-62. Review.

PMID:

Kruskall MS, AuBuchon JP, Anthony KY, Herschel L, Pickard C, Biehl R, Horowitz M, Brambilla DJ, Popovsky MA.

Transfusion to blood group A and O patients of group B RBCs that have been enzymatically converted to group O.

Transfusion. 2000 Nov;40(11):1290-8.

PMID:

Milk is a bovine secretion that is intended to allow rapid growth to calves following immediate consumption from their mother. It is widely consumed by humans, generally after pasteurisation and chilled storage, but may also be sterilised or further processed by heat treatment.

Research shows that one of the growth-promoting actions of this substance may be caused by the action of leptin in the body.

Leptin is a hormone secreted by body fat cells that adjusts food intake relative to energy expenditure. Leptin also plays a general role in regulating many of the physiological responses that are observed with changes in nutritional state.

Discovered by Jeffrey Friedman in 1994, Leptin has been shown to travel to the brain and other body tissues, causing fat loss and decreased appetite. In the brain, leptin affects food intake by acting on distinct classes of neurons in the hypothalamus that express the leptin receptor.

Leptin decreases both the desire to eat, and the deposit of fat in the body by acting on two classes of neurons. Leptin suppresses the activity of neuropeptide Y (NPY) neurons and it enhances the activity of proopiomelanocortin (POMC) neurons. Conversely, the absence of leptin increases both the desire to eat and the deposit of fat by exciting NPY neurons and suppressing the activity of POMC neurons.

In humans, leptin concentration in the blood correlates with body fat content and is usually higher in obese subjects, suggesting that human obesity is generally associated with insensitivity to leptin. However, 5–10 percent of obese individuals have relatively low levels of leptin, indicating a reduced rate of leptin production. The fact that some obese individuals have low leptin levels suggests that decreased production can also lead to obesity. This suggests that in most cases the cause of leptin resistance and obesity is equivalent to insulin resistance in type II diabetes.

Diet-induced weight loss in humans results in a decrease in leptin concentration. This may explain the high failure rate of dieting, as low levels of leptin appears to be a strong stimulus to weight gain.

When fasting on water only, appetite is generally suppressed after the first one to two days, when liver stores of glucose are used up and the body moves into ketosis (fat-burning). After a prolonged fast when all body fat stores are used up, starvation occurs. Starvation is the breakdown of essential body organs.

Research in the journal Diabetes shows that fat-containing milk, and of which fats are 98% triglycerides, immediately inhibits leptin transport across the blood-brain barrier. Fat-free milk does not have this effect. In this study both starvation and diet-induced obesity elevated triglycerides in the blood and decreased the transport of leptin across the BBB, whereas short-term fasting decreased triglycerides and increased leptin transport.

Triglyceride-mediated leptin resistance may have evolved as a mechanism to restore this fasting loss of appetite at the onset of starvation. Decreasing triglycerides may potentiate the effect of leptin to reduce appetite by enhancing leptin transport across the blood-brain barrier (BB.

The Complete Blood Type Encyclopedia outlines natural approaches to reducing triglycerides. ------------ References:

W.A. Banks et al., “Triglycerides induce leptin resistance at the blood–brain barrier,” Diabetes, 53:1253-1260, 2004.

A.J. Kastin, V. Akerstrom, “Fasting, but not adrenalectomy, reduces transport of leptin into the brain,” Peptides, 21:679–682, May 2000.

A paper published in the Journal 'Blood' entitled "HIV-1 incorporates ABO histo-blood group antigens that sensitise virions to complement-mediated inactivation" [1] 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 [2] 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 [3] 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 [4].



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.



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References:



1. Neil SJ, McKnight A , Gustafsson K, Weiss RA

HIV-1 incorporates ABO histo-blood group antigens that sensitise virions to complement-mediated inactivation.

Blood Online



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.

PMID 7851010



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.

PMID 8674246



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).



References:



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.

PMID 15609335



2. Pathbase