An debate in the International Breastfeeding Journal  has revealed how a US government agency designed to safeguard the health of low-income women, infants and children could be putting the lives of over 700 babies per year at risk, exploits the government-funded distribution network as a promotional and brand loyalty tool, encourages inflated retail prices and may even contravene human rights.
The article focuses on the WIC program (The United States' Special Supplemental Nutrition Program for Women, Infants and Children), launched in 1974 and administered by the Food and Nutrition Service of the US Department of Agriculture. The WIC program “serves to safeguard the health of low-income women, infants, & children up to age 5 who are at nutritional risk by providing nutritious foods to supplement diets, information on healthy eating, and referrals to health care”.
The WIC provides free formula milk to the needy if: 1) they are individually determined by a competent professional to be in need of the special supplemental foods supplied by the program because of nutritional risk; and 2) meet an income standard, or receive or have certain family members that receive benefits under the Food Stamp, Medicaid or Temporary Assistance for Needy Families Program. The total cost of the WIC program in the 2004 financial year was US$4,890,200,000 for 7,904,000 participants.
The cost of the formula milk was rebated to the WIC at between 85 to 98 percent of the wholesale price in 2000 financial year, and for the US as a whole, net prices averaged 18 cents per can of milk-based liquid concentrate that year. The manufacturers of the formula are paying most of the cost of the actual product, the author suggests, for the following reasons: low product cost, inflated retail prices, brand loyalty, and expanded reach. This is corroborated by the following facts: during the 1970's, one company paid a million dollars to the City of New York for the privilege of donating free formula to all of the City hospitals; In 1989, Abbott Laboratories and Bristol Myers got into a bidding war in Canada over the exclusive right to supply free formula to Canada’s largest maternity hospital.
It is universally accepted that breastfeeding is preferable to formula feeding in most cases. The infant mortality associated with not breastfeeding is relatively small in richer countries, but it is not negligible. Recent studies indicate that formula feeding in the US causes substantial numbers of excess infant deaths. The risk of post-neonatal (29-365 days of age) mortality is about 27% higher among infants who are never breastfed compared to infants who are ever breastfed. On this basis, about 720 infant deaths in the US would be averted each year if all infants were breastfed. WIC has a vigorous and effective program for promoting breastfeeding, resulting in steadily increasing breastfeeding rates among clients. However, a USDA report acknowledges: Although breastfeeding rates are increasing among women participating in WIC—both while in the hospital immediately after giving birth, and 6 months after giving birth—the rates continue to be lower than those of non-WIC women. Although some have questioned whether WIC provides a disincentive to breastfeeding by supplying free infant formula, the women most likely to participate in WIC, including mothers who are poor and have low education levels, are less likely to breastfeed their children in general. WIC has a breastfeeding promotion program, but its positive impact is diluted by WIC’s infant formula program. It is difficult to see how offering free formula could fail to be an incentive to use formula. The inducement is not simply that something of value is being offered at no cost. Even if it is unspoken, there is the implicit message of endorsement: if a government agency is handing out this product, it must be good.
It is also suggested that the WIC program may contravene human rights law: The most directly applicable international human rights agreement is the Convention on the Rights of the Child, an international human rights agreement that came into force in 1990, which states, “States Parties recognize the right of the child to the highest attainable standard of health” and they shall take appropriate measures “to combat disease and
malnutrition . . . through the provision of adequate nutritious foods, clean drinking water, and health care.” It also says States Parties shall take appropriate measures “To ensure that all segments of society, in particular parents and children, are informed, have access to education and are supported in the use of basic knowledge of child health and nutrition [and] the advantages of breastfeeding . . .” and that States Parties shall "take appropriate measures to diminish infant and child mortality.”
The author concludes:
"If infant formula could be demonstrated to produce better infant health, there might be a reason to distribute it without cost to those who could not otherwise afford it. However, there is no evidence to support the generalization that the use of infant formula results in better infant health than breastfeeding. On the contrary, the evidence clearly and consistently shows that the use of infant formula increases the risks of morbidity and mortality throughout the life cycle. The use of infant formula has been shown to be harmful to the health of mothers as well. The inescapable conclusion is that the government should not be distributing free infant formula... WIC could reasonably provide infant formula, but only in exceptional cases, if that is recommended for a specific reason by a physician or a lactation counselor. An initial list of acceptable reasons could be drawn from the Lawrence study of contraindications to breastfeeding. The rebate program should be ended. The WIC program should stop providing free infant formula to the majority of its clients, and should be limited to providing infant formula to no more than a small percentage of its clients... Currently, WIC acts in a way that benefits commercial enterprises at the expense of infants. The government should not risk infants’ health in order to support commercial enterprises."
The book Eat Right 4 Your Baby  gives suggestions on how to encourage and promote a good flow of breast milk, and where necessary, the use of soya-based formula milk is gaining popularity due to colic and digestive problems from cows' milk. Predigested protein is also available. The best formula for your baby should be decided in conjunction with your paediatrician.
Report of the UK and Eire IfHI Members Symposium, 7th April 2006
After lunch I gave a presentation of lab testing facilities for blood type practitioners. This included a basic review of blood groups, UK distribution, disease and dietary significance of Rhesus, Lewis negative and minor blood groups A2 and A3, MN, and postal serology services offered by nature-cure lab services. Other useful laboratory tests were discussed: salivary secretor status test; the indican test; oxidative stress urine test; secretory IgA; anti-A and anti-B agglutinin titre; various stool markers; blood group specific markers in the standard biochemistry assay such as ALP (alkaline phosphatase) and BUN (blood urea nitrogen). There is a choice of labs for most of these tests for UK practitioners.
New information on subgroups of A was presented: As discussed in part I, many individuals of blood group A phenotype may have the genotype AO (it may be as high as 90%). Of these individuals, AO secretors are therefore capable of secreting the H antigen (of blood group O) into their stomach as well as the A antigen, allowing bacterial infestation, i.e. H. pylori (1). Low stomach acid, common in individuals with group A blood, additionally increases the potential for bacterial growth.
It has been known since the 1950’s (2) that individuals of blood group O are more prone to gastric ulcers, and it has been hypothesised that the connection relates to secretion of the H antigen and H. pylori cellular adhesion. Also those with blood group O tend to be hospitalised as a result of gastric ulceration more frequently than individuals with other blood groups due to the thinner O blood. Non-secretors of all types are also more prone to H. pylori, due to the similarity of Lewis a (Le a) to H antigen, although it has been found that some strains of H. pylori prefer Lewis b (Le b). A recent study (3) suggests that due to the diversity of H. pylori strains, their varying preferences for cell membrane antigens and the possibility of several mechanisms of attachment to the cell surface may make this type of study of H. pylori inappropriate for epidemiological research.
The question may arise “how do you know if you are AO or AA?” Mendelian genetics can be applied in certain cases to give an answer: if one parent is O the child typed blood group A1 must be A1O, (who may be more prone to bacterial overgrowth than AA). Similarly if two parents of blood group A have a child who is typed as blood group O, both parents must be AO.
If an individual is typed as A2, which can only be A2O or A2A2, they may have susceptibility to H. pylori beyond that of A1O: a recent study found that individuals with the A2 phenotype, as well as individuals of blood group O, are also more prone to gastric ulcers (4).
The A2 blood group may have some structural differences when compared with A1 – there are several similar A antigens on the surface of red blood cells of individuals with blood group A, individuals with the A2 phenotype express only one of these.
The afternoon coffee and green tea break also included a selection of NAP Unibars and Elspeth Semple’s amazingly tasty wheat-free fruit cake and chocolate cake, as well as fresh and dried fruit and nuts.
Then followed a presentation on herbs by Carole Symons MIfHI, medical herbalist. Carole listed selected herbs and their suitability for individuals of particular blood groups, including some used in NAP formulations. Where a particular herb might not be suitable for a specific patient, alternatives were given with similar actions. It was noted that Echinacea is not suitable for prevention of bird flu, as it is likely to overstimulate the cytokine burst. This was a topical subject, as the previous day a dead swan had been found to have the H5N1 strain of bird flu in Scotland. Elderberry products may be a better approach, than Echinacea, in combination with selenium, zinc and olive leaf. For someone with flu, the recommended dosage for an elderberry product such as Proberry liquid is 4 tablespoons (15 ml) 3 times per day.
Dr. Stuart Semple MBChB, FFHom, MIfHI presented a discourse on homoeopathy and the BTD. After 40 years of involvement in homoeopathy, he now uses blood grouping as a first line approach. He described how initially changing a client’s diet at the first appointment before deciding on a constitutional remedy at the second consultation tends to clarify the remedy picture in that individual and allows for more accurate prescribing. A former student of Marjorie Blackie, Dr. Semple explained that there are only 20 constitutional remedies, and that 60 % of the population have personalities that fit these remedy pictures. It would be an area ripe for research in the homoeopathic world to explore the correlation between the 8 basic blood groups and their subcategories, and these constitutional remedies, in the same way that the link was drawn earlier with the dosha/haplotype connection. This would also raise the question as to whether certain blood groups might react better or worse to a particular constitutional remedy.
Another area of interest to Dr. semple is lectinology, and the lectin-binding content of certain foods. He hypothesised the extent to which certain traditional food combinations or preparation methods coule neutralise, destroy or otherwise disable the lectins in foods, in what he called “therapeutic cooking”.
The discussion then opened out to the floor. Naturopath Ken Green noted how Hahnemann, the founder of homoeopathy, ate several kinds of animal protein at every meal. His test subjects, while proving a homoeopathic remedy, had to keep to a very limited diet to avoid confusing the effects of certain foods with that of the homoeopathic proving.
Dr Prannie Rhatigan MD, MIfHI mentioned a forthcoming course she is presenting in conjunction with naturopath Dr. Gaby Wieland: “Exploring the links between blood group and diet”, as part of a cooking weekend at the Organic Centre, 22-23 April 206. www.theorganiccentre.ie
That evening, the group met at one of the Howies restaurants in central Edinburgh, courtesy of NAP Europe. Dr. Semple had been ‘training’ the restaurant staff to provide suitable food for the party comprising individuals of 3 different blood types (the Semples’ usual restaurant had recently changed hands). Everyone was very well catered for, and it was a fitting close to an educational and informative day. The new information presented at this symposium will surely be enough food for thought until the next IfHI meeting, in May 2007, Phoenix, AZ.
Report of the UK and Eire IfHI Members Symposium, 7th April 2006
The first meeting of UK and Eire IfHI members was hosted by Stuart and Elspeth Semple, who offered attendees a warm welcome at their practice in Inveresk, Edinburgh. Most of the attendees were IfHI fellows or masters, and many reunited for the first time since the IfHI conferences in Phoenix.
Nick bowler, FIfHI, former biochemist and CEO of NAP Europe, lead the discussion for the morning, with a presentation based on his research over the last two years. Entitled “Surfing the genome with a blood type microscope,” and giving attendees a taste of what may be to come in future developments, he described the functional genomics of critical illness and injury in relation to blood group. The basis behind many of the studies that have found such a link is the haplotype, a set of single nucleotide polymorphisms (SNPs) found to be statistically associated as a group on a single chromatid (half of a chromosome). In terms of blood group, a haplotype in someone who is blood group O would be OO, the same as their genotype, one O gene inherited from each parent. The haplotype for someone who is AB could be AB or BA, depending on which gene was expressed more strongly. The haplotype for someone who is blood group A would be AA if they are homozygous, but a heterozygous individual with blood group A could have a haplotype of AO or OA. The strength of expression of certain genes may depend on environmental conditions.
This view of genetic expression is now challenging the existing dominant/recessive theory of blood groups (A and B being co-dominant and O being recessive), which was based on agglutination for transfusion purposes: if you have a gene for blood group A, you can’t receive blood from someone with the B antigen as you will certainly have strong IgM antibodies to B (from eating foods containing GalNAc (the A antigen) as a baby, which your immune system does not recognise as ‘self’). Whether you are Ao, AA or A1A2 does not matter in transfusion terms, you can still safely receive blood from a donor with any of those versions of blood group A1. This led to the concept of ‘dominance’ of blood groups A or B over O. Now functional gene expression is considered more important than the dominant and recessive theories, which means having Ao blood may give an individual different characteristics to AA blood. Even those with Ao blood could be different to each other depending on whether they express the A or O gene more strongly, effectively being ‘Ao’ or ‘Oa’, and the characteristics that go with each of those genes that we all relate to individuals with either blood groups O or A.
Nick Bowler then drew a link with Ayurvedic system of dosha categories being a possible ancient haplotyping system, with the 6 different ABO genotypes and the 9 possible haplotypes corresponding with the doshas vata, pitta and kapha, including possible combinations such as vata-pitta and pitta-vata as well as pure vata, for example. He pointed out that there are 82 verified genes at the 9q34 locus, the home of ABO blood group, controlling many characteristics that could give significant differences between individuals depending on blood group expression.
If ABO is interesting in genetic terms, ABH secretor status is even more so. Secretion of ABH antigens is under control of two linked genes on gene locus 19q13, another haplotype: a mutation (SNP variant) in one always goes with a mutation in the other. Presence of the secretor gene adds the H antigen (fucose) to red blood cells and body secretions. If this genetic code for secreting H is absent in the genetic material inherited from both parents, the individual will not secrete their red blood cell antigens into their body tissues, which is what we know as an ABH non-secretor. If they inherit the secretor gene from one parent only, they may still have some of the characteristics of a non-secretor: even though they secrete their ABH antigens, it was postulated that they may have some of the metabolic disease associations connected with being a non-secretor (but not necessarily the cell surface antigen-related ones). 19q13 has 288 verified genes related to this locus, even more than the ABO locus. Chromosome 19 has the highest gene density of all human chromosomes, and many of these relate to how the immune system works, which explains the difference between immune response of secretors and non-secretors: the humoral vs. the cellular response (TH1 and TH2). Other potentially genes on this chromosome relate to insulin-dependent diabetes, familial hypercholesterolaemia, and repair of other genes relating to repairing DNA damage from exposure to radiation and to other environmental pollutants.
The probability of having a particular combination of two specific alleles at a given locus can be calculated using a mathematical formula, which suggests that 2/3 of the general population will be heterozygous for secretor status (i.e. having both secretor and non-secretor genes), which may have a significance in itself when compared with homozygote secretors and non-secretors.
Lewis blood group status becomes significant in terms of the less common Lewis negative individuals (5-15%), those who express neither Lewis a nor Lewis b antigens. This is a separate system from ABH expression, but when combined with ABH haplotype and secretor haplotype, there are 20 possible combinations, including variations of the rare Bombay blood group (those who do not express the H antigen on their red blood cells). Using the probability formula described, nearly half the population having a Lewis positive expression (Lewis a+ b- non-secretors, and Lewis a- b+ secretors) will be heterozygous for the Lewis negative allele. The evolution of the blood group genes was discussed, with the linkages of each gene to the survival needs of different groups of people.
The final part of Nick Bowler’s talk related to cancer, with a review of the unitarian or trophoblastic theory that suggests cancerous cells are similar to trophoblasts, a type of embryonic stem cell that attaches the fertilised ovum to the wall of the uterus. Cancerous cells develop in anaerobic conditions as a result of continuous inflammation and not all tumour cells have the capability of inducing new cancers, only the ones which are similar to embryonic stem cells. The most primitive cells are A-like in structure. Loss of cell surface antigens in cancer leads to exposure of the Thompson Friedenreich (T) antigen, the body’s auto antigen against itself. The connection with the T antigen and blood groups A and M appears to relate to a failure of the immune system in individuals with these blood groups to identify the cancer cells, perhaps due to the similarity between primitive embryonic cells and the A and M antigens. There was a lot more information on this topic, which may be detailed in a later entry.
With the morning presentation completed, the assembled company then proceeded to attend to the most important event of the symposium, the lunch provided by Elspeth Semple. A tasty quinoa and vegetable soup, 100% Demeter rye bread/rice cakes/oatcakes, chicken, a selection of goats’ cheeses and other delicacies catered amply for the individuals of various blood groups and secretor status in attendance.
Part II later...
Question from Dr. Peter J Williams DC
Dr. Greenfield: I attended April, 2005, IFHI Conference and rec'd certification. Have been reading and practicing the BTD for years... recently retired from active chiropractic practice to teach and administer this work on a permanent basis. I visited an M.D. earlier this week and although he is at this point very curious he keeps asking questions and the latest one is: "...are there any morbidity or mortality rates in the general populace [as it concerns] the btd"? Do you have a good answer for this doctor? I told him to visit the dadamo web site and just start to read the seven research modules as well as Database 1. I further told him that such a question w/o attaching the application of the diet to any diseased state in a clinically controlled research environment, wherein the morbidity factors could be analyzed along with the outcomes, i.e. mortality rates, would be quite difficult, if not impossible. Can you add any insights to this as I keep the communication going with this curious M.D.? Thank you.
It is correct that a clinical trial of this nature would be very difficult to set up properly: to answer the question about morbidity and mortality in connection with the BTD requires some joined up thinking. The Blood Type Diet has not been around for that long in comparitive terms, and it takes many years to do mortality studies of adequate size relating to a specific subject. For a realistic representation of the situation any comprehensive clinical trial specific to the BTD would have to look at diet start date, compliance level (how do you accurately measure that over a period of years?), pre-existing illness and family history, blood group, secretor status and other minor blood groups, as well as other polymorphic data such as dermatoglyphic information etc. Then you would have to wait for people to die of natural or disease causes (i.e. not accidental death, unless you want to prove that one blood group is more accident-prone than another). Morbidity would be similar, but you just wait for those people to get sick, they don't have to die. Another issue that would be difficult to factor into such a trial is this: many people following a particular dietary régime may already have health problems, or concerns due to family history. Actively caring for oneself on a daily basis through selective food choice while rejecting societal pressures to conform to a stereotypical dietary 'norm' is a form of self-empowerment. How do you have a control group that takes account of this influence?
This begs the question "Does blood group in itself influence overall lifespan?" The results are conflicting. A study of Italian physicians showed a higher percentage of those over the age of 75 were blood group O (1), while two other studies showed that type B was associated with a longer lifespan (2), (3). It could be that group B individuals are healthier than their counterparts due to the typical modern diet being reasonably close to the ideal diet for those expressing the B antigen. Alternatively with regard to disease susceptibilities, as they tend to fall between groups A and O in this respect, this could be expected to translate into a higher percentage of group B individuals attaining a more advanced age. Either way, blood groups A and AB don't come off well in the longevity stakes.
Incidentally, the NN subtype of the MNSs blood grouping system may be associated with a slight increase in longevity (especially in women) (4). This could relate to the fact that the presence of the M antigen (absent in NN blood group) increases the incidence and mortality rates of many types of cancer due to a biochemical similarity to the A and TN antigens.
The question itself shows typical reductionist medical thinking: to put it another way, "Does following a specific diet according to one's blood group reduce illness and increase lifespan?" The fact is that the diet forms part of an entire programme that takes a person's individuality into account. It may be part of a comprehensive lifestyle strategy for natural preventive medicine in association with an ND. Patients are treated as individuals, not as a disease classification who should be a suitable candidate for some symptom-suppressive medication with side effects, or just to say: "Follow this diet as it is proven statistically that you will live longer and be healthier".
To see the bigger picture one needs to be able to connect two separate facts: firstly the hundreds of orthodox medical research papers showing physiological and psychological differences between individuals of varying blood groups, the connection between lectins and cell surface carbohydrates, the genetic linkage between ABO and other seemingly unrelated genes; secondly the millions of people who are following the BTD system worldwide because they have their own evidence of improvement in wellbeing. As in all holistic systems, the whole is more than the sum of the parts. It takes a little more than: "in the absence of any controlled clinical study to prove the existence of this concept it cannot exist in the real world."
Relevant studies are already being carried out on a small scale: The Southwest College of Naturopathic Medicine reported studies on diet and blood group at IfHI 2005, specifically the effect of ABO blood groups and soluble endothelial adhesion factors as a possible cause of atherogenesis. The Institute for Human Individuality is developing further study protocols.
Until the BTD has been around long enough and there are enough people following it to attract research money to design clinical trials that will satisfy the reductionist attitude, those seeking confirmation that the system works will have to use the outcome results of the hundreds of people who claim to have become healthier following this approach. Finally, whether or not a person lives longer or healthier, surely it is the quality of life that is more important?
The British Medical Journal has published a study1 on how stress at work increases the risk of metabolic syndrome (or Syndrome X), a cluster of risk factors that increases the risk of heart disease and type 2 diabetes. Characteristics of the metabolic syndrome are abdominal obesity, signs that increase the likelihood of fatty deposits in the arteries (raised triglycerides, small LDL cholesterol particles, and low concentrations of HDL cholesterol), high blood pressure, insulin resistance (with or without glucose intolerance), and prothrombotic and proinflammatory states (three of these risk factors need to be present).
The results showed:
A dose-response relation was found between exposure to work stressors over 14 years and risk of the metabolic syndrome, independent of other relevant risk factors. Employees with chronic work stress (three or more exposures) were more than twice as likely to have the syndrome than those without work stress.
The authors conclude that the study provides evidence for the biological plausibility of the link between psychosocial stressors from everyday life and heart disease.
The connection between stress and disease was famously documented by Hans Selye2, and later by Dr. D'Adamo3.
Non-secretors of ABO blood group are statistically more at risk of metabolic syndrome and all its individual components, and also tend to respond differently to stress when compared with secretors of blood groups A and B. Non-secretors tend to have trouble clearing the catecholamines adrenaline and noradrenaline. Appropriate exercise, stress-reduction techniques and eating correctly according to secretor status as well as ABO blood group may help prevent the effects of work stress on heart disease risk factors.