Archives for: June 2004
QUESTION: Do you have any evidence that eating the incorrect diet can cause Peyronie's Disease? If so can the problem be reversed by correct eating for my blood type?
ANSWER: Peyronie's disease, a condition of uncertain cause, is characterized by a plaque, or hard lump, that forms on the penis. The plaque develops on the upper or lower side of the penis in layers containing erectile tissue. It begins as a localized inflammation and can develop into a hardened scar.
Peyronie's disease often occurs in a mild form that heals without treatment in 6 to 15 months. But in severe cases, the hardened plaque reduces flexibility, causing pain and forcing the penis to bend or arc during erection.
Because the plaque of Peyronie's disease often shrinks or disappears without treatment, medical experts suggest waiting 1 to 2 years or longer before attempting to correct it surgically. During that wait, patients often are willing to undergo treatments that have unproven effectiveness.
Some researchers have given men with Peyronie's disease vitamin E orally in small-scale studies and have reported improvements. Similar success has been attributed to oral application of para-aminobenzoate (PABA), a substance belonging to the family of B-complex molecules.
An analysis of the world literature shows surprisingly a 75% improvement by vitamin E therapy and almost a 60% amelioration by p-aminobenzoic acid. (1)
I've also told patients to take the pineapple enzyme bromelain, which helps digest scar tissue, 250mg away from meals twice daily. This has also helped about 60% of the patients.
A search of MEDLINE disclosed no ABO blood group distinctions.
1. Wagenknecht LV, Meyer WH, Wiskemann A. [Value of various therapeutic procedures in penile induration]. Urol Int. 1982;37(5):335-48.
QUESTION: I live in Germany and was diagnosed with Lyme decease beginning of June. I am A negative. The lyme disease was treated with 5 weeks of oral penicillin. Apart from general fatigue and malaise initially I had early knee joint involvement. I am now just on a protocol of vitamin supplements and I get acupuncture, which has helped my immune system as well as the joint problems. I would like to know what vitamin/mineral/herbal supplements you would specifically recommend for lyme and blood group A.
ANSWER: Lyme Disease is a systemic, tick-borne illness caused by the spirochete (a helical-shaped bacteria) Borrelia burgdorferi. It can affect almost any organ or system in the body. Lyme Disease is not new, and there are varying schools of thought in the treatment of Lyme Disease.
I have used an extract of the herb Sarsparilla (Smilax spp.) to help many of my patients with Lymes. The herb contain waxy-like substance called saponins which have in prior studies been shown to inhibit other types of similiar bacteria, called Spirochetes.(1) I use the solid extract of Sarsparilla.
In addition I've used larch arabinogalactan (ARA6) as a general immune tonic.
Other doctors of natural medicine has advocated using colloidal silver preparations for Lyme disease, but I have not seen any benefit from their use. In addition, there are potential toxicity problems from accumulation of silver in the tissues of the body.
1. Bernardo RR, Pinto AV, Parente JP. Steroidal saponins from Smilax officinalis. Phytochemistry. 1996 Sep;43(2):465-9.
QUESTION: I have a question about (fill in the blank: so-and-so's criticism; a discrepancy between 'Book A' and 'Book B', etc. etc.) How come you have never answered my question?
ANSWER: Probably because it was already answered. Before you ask a question, check the previously answered questions.
QUESTION: I was about to buy zinc on my lunch break today, on account of my enlarged heart, and Steve Shapiro's Food Lists say that zinc is an Avoid. A gentleman responded to my post a while ago, and said he met The Good Doctor at a book signing and said Dr. D suggested he take zinc supplements for his cardiomyopathy. I don't understand. What supplements should I take now, if zinc is no good for O's with this condition?
ANSWER: You should use zinc. Your clinical situation supplants the long- range recommendations for your blood type, which is to avoid long-term zinc administration as its cummulative effects are suppressive on the immune system rather than augmentative. Your condition creates a long-term drain on your zinc resources so the 'epidemiologic' effects are moot.
By the way, cardiomyopathy (an inflammation of the heart tissue) is also benefited by proper doses of the amino acid l-taurine, which is the one amino acid found to be consistently low in the diets of vegans, but quite abundant in the type O diet. Taurine is the amino acid found in highest concentration in the "free amino acid pool' in heart tissue; apparently it is used extensively in rebuilding heart muscle. You may even want to supplement with 500mg additional to the diet.
QUESTION: I'm looking for a pracitioner who is supportive of your theories. I live in London, England. Any recommendations?
ANSWER: You can check the Practitioner Register. There are several practitioner listings for the UK (in addition to several other countries) and virtually every US state.
QUESTION: Please name a clinic or Naturopath in the Northwest (Seattle?) or Southwest (Yuma AZ?)where I can receive treatment for D'Adamo blood typing, diet, etc. I am a snowbird and live in the southwest and northwest.
ANSWER: Fortunately, both Arizona and Washington state have quite a few practitioners who use the system in their practices. In Arizona, you can contact the South West College of Naturopathic Medicine, who can supply you with the contact details for several local doctors. In Washington state, a good reference is: Healing Garden Clinic Ken Carlin, ND 10532 12th Ave NE Seattle, WA 98125-7557 (206) 505-9596
QUESTION: Rooibos tea is a herbal tea well known in South Africa. Can it be used by type O blood?
ANSWER: Yes, I though so highly of its health properties for type O that I included it in the 'Sip Right 4 Your Type' tea formulas for type O that we developed with The Republic of Tea. In particular I find Rooibos effective in 'tempering' the slightly over-enthusiastic type O immune system, leading to diminished allergies and autoiimmune problems.
Rooibos has significant anti-HIV activity (1) and appears to be somewhat protective against UV damage,(2) probably because of its anti-oxidant activity. The anti-oxidant activity in the plant also seems to suppress the age-related accumulation of lipid peroxides in th brain, at least in test animals. (3)
Rooibos has no caffiene, so it appears to be a good substitute in situations where the caffiene contain in green tea may prohibit its use. Like green tea, rooibos inhbits polyamine formation by blocking the enzyme ornithine decarboxlase. (4)
1. Nakano M, Itoh Y, Mizuno T, Nakashima H.Polysaccharide from Aspalathus linearis with strong anti-HIV activity. Biosci Biotechnol Biochem. 1997 Feb;61(2):267-71.
2. Shimoi K, Masuda S, Shen B, Furugori M, Kinae N. Radioprotective effects of antioxidative plant flavonoids in mice. Mutat Res. 1996 Feb 19;350(1):153-61.
3.Inanami O, Asanuma T, Inukai N, Jin T, Shimokawa S, Kasai N, Nakano M, Sato F, Kuwabara M. The suppression of age-related accumulation of lipid peroxides in rat brain by administration of Rooibos tea (Aspalathus linearis).
4. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol 1997 Jan;116(1):39-45 Effect of Rooibos tea (Aspalathus linearis) on chick skeletal muscle cell growth in culture. Lamosova D, Jurani M, Greksak M, Nakano M, Vanekova M
QUESTION: Is there a relationship between secretor status and aphthous stomatitis?
ANSWER: In general, non-secretors predominate over secretors with regard to oral problems, this is probably the result of:
1. Not having any free blood type antigen in their saliva. Free blood type antigen blocks bacterial attachment to the tooth and gum surfaces.
2. Non-secretors have lower levels of secretory IgA an antibody which tends to protect the mucous membranes.
Although known from the 1960's this association has again been shown in a recent journal article:
J Oral Rehabil 1999 Feb;26(2):177-82
Examining the secretor status in the saliva of patients with oral pre-cancerous lesions.
Vidas I, Delajlija M, Temmer-Vuksan B, Stipetic-Mravak M, Cindric N, Maricic D.
Department of Stomatology, Faculty of Medicine, University of Rijeka, Croatia.
It has been demonstrated in a number of earlier studies on the aetiology and pathogenesis of certain diseases that the patients' secretor status (ABO (H) blood group antigens) may possibly be a factor influencing the development of systemic oral diseases. This likelihood has prompted the present study, to examine the differences in the saliva secretor status by comparing patients with oral pre-cancerous lesions on the one hand, and the healthy population on the other; (i) in relation to the intensity of the clinical manifestation of diseases and (ii) in relation to the intensity of epithelial dysplasia of patients with oral pre-cancerous lesions. In total 122 subjects were examined, half of whom suffered from oral pre-cancerous lesions (excluding Candida albicans in oral smears), while the other half were the healthy control group. All were subjected to clinical oral examinations and standard evaluation tests in order to establish the secretor status of their saliva. In the group of patients with oral pre-cancerous lesions (experimental group), a pathohistological examination of the oral mucosa was performed. The results have demonstrated that the large majority of the people examined in both groups were secretors and no significant difference between secretors and non-secretors was found in the comparison between the experimental group and the healthy control group. However, (i) we found a higher intensity of oral disease in the non-secretor group, and (ii) the occurrence of epithelial dysplasia was found exclusively in the non-secretor group.
My sister is type A and is battling breast cancer. I am thinking of getting her some of the Helix product, but how do I explain to her why she should take it.
Defects in surface glycosylation (the elaboration of long sugar chains) which in normal cells are very tightly restricted, is a characteristic of cancer cells. This results in the elaboration of tremendous amounts of glycoproteins, many of which (CA-125, CA15-3, CA 19-9, Lex) have clinical and diagnostic relevance. As neoplastic breast cells become malignantly competent, their surface glycosylation products alter, resulting in elaboration of structures characterized by the presence of GalNAc. It is the presence of these glycosylation products that allow for metastatic spread and poor prognosis. This molecule, an obscure ligand-like complex
(LLC) , is apparently absent from normal and early (non-metastatic) breast cancer cells. LLC can be considered a sort of "internal passport" for the breast cancer cells; allowing them free transit through the body. This complex shares many structural similarities with both A and M blood groups and may explain their particular succeptibility to breast cancer.
The common snail "Large Burgundy" contains a unique lectin called Helix pomatia agglutinin (HPA) which is capable of recognizing a ligand-like complex (LLC) elaborated as a surface glycosylation product on some tumor cells. Thus the consumption of this species of snail may serve as a very potent protective agent, as both these blood group antigens are associated with a higher risk of many of these cancers.
In 1987 and 1991 Brooks and co-workers (1, 2) reported that it is possible to predict lymph node involvement in women with breast cancer by the detection of altered glycosylation. Their 1991 study was performed on paraffin-embedded sections of 373 primary breast cancers, in a 24 year retrospective study, which were stained for the binding of Helix pomatia lectin. This lectin is nominally specific for N-acetyl-galactosamine (GalNAc). Brooks reported a strong association between HPA binding and the presence of lymph node metastases and proposed that HPA recognizes a glycoprotein associated with metastasis to axillary nodes and subsequent poor prognosis.
Springer (3) had earlier suggested that it may be related to the Tn blood group precursor substance, which is generally absent from normal tissue, yet detectable in a high proportion of breast cancer tissue. LLC also appears to display antigenic similarities to blood group A (the terminal antigen of which is GalNAc) and blood group M.
It has been shown that breast tumor cells which do not produce LLC tend to stay localized. These cells would not per se be susceptible to HPA agglutination. Interestingly, it would appear that HPA becomes active in an inverse ratio to tumor staging, i.e. as the malignancy worsens and LLC is increasingly elaborated, the tumor cells become paradoxically more susceptible to agglutination by HPA.
It is available from the shopping mall on this website.
1. Brooks SA. Lancet May 9, 1987: 1054-56
2. Brooks SA and Leathem AJC. Lancet, 8759, 338 (1991): 71-74
3. Springer G. J. Nat. Cancer Inst. 54,2 (1975):335-39
4. Schumacher DU. et al. Eur. J. Surgical Oncology; 22(6) 1996:618-620
How do you know if you are a secretor or non-secretor?
There are two ways to determine your secretor status: one that looks for blood type antigens in saliva, and another which uses another blood group system as a 'proxy.'
North American Pharmacal is developing a simple saliva based secretor test in association with Great Smokies Laboratories. They hope to have this test available by early winter.
You can also determine secretor status by using blood. Secretor status (whether you are genetically programmed to secrete your blood type antigen in your body fluids) is determined by a gene (FUT2) on chromosome 19 versus ABO which is one chromosome 9. FUT2 controls an enzyme which also controls the conversion of the Lewis blood group A antigen (LewisA) into Lewis blood group B antigen (Lewis.
Individuals who are non-secretors lack the enzyme needed to convert LewisA into LewisB. Thus you can use the Lewis blood group as a 'quick and dirty way' to determine ABH secretor status. Thus Lewis A-B+ individuals are ABH secretors, and Lewis A+B- individuals are non-secretors. A small percentage of individuals are Lewis A-B-, which makes it impossible to determine their secretor status. However, metabolically 'double negative Lewis' individals are perhaps even more metabolically 'non-secretors' than anyone else.
A recent study showed that Lewis A+ non-secretors snore more than secretors. Looking at men who had their own bedroom due to snoring (habitual snorers only) the factor most strongly separating those with their own bedroom due to snoring from those without were the Lewis blood group phenotype, Le(a+b-)p < 0.001. The results of this study indicate that snoring, to some extent, is hereditary.
Jennum P, Hein HO, Suadicani P, Sorensen H, Gyntelberg F. Snoring, family history, and genetic markers in men. The Copenhagen Male Study.Chest 1995 May;107(5):1289-93
QUESTION: In ER4YT you highly recommend hawthorn but give no guidelines as to dosage. Advice, please. P.S. This AB body has shown some remarkable changes. Thank you.
ANSWER: In general, hawthorn can be used in a variety of forms and doses. Perhaps the simplest is something like the tea, which can be found in a variety of stores. Other forms include standardized extracts (such as the NAP product) and solid extracts (which are extremely concentrated forms of the herb best used under physician supervision. It is probably best to avoid alcoholic tinctures, as many of the flavones in hawthorn, though responsible for much of its medical activity, are not soulable in alcohol.
STUDY: Vitamin D: a natural inhibitor of multiple sclerosis.
JOURNAL: Proc Nutr Soc 2000 Nov;59(4):531-5
AUTHORS: Hayes CE.
ABSTRACT: Inheriting genetic risk factors for multiple sclerosis (MS) is not sufficient to cause this demyelinating disease of the central nervous system; exposure to environmental risk factors is also required. MS may be preventable if these unidentified environmental factors can be avoided. We have proposed that vitamin D may protect genetically-susceptible individuals from developing MS. Evidence consistent with this hypothesis comes not only from geographic studies, but also genetic and biological studies. Over-representation of the vitamin D receptor gene b allele was found in Japanese MS patients, suggesting it may confer MS susceptibility. However, the clearest evidence that vitamin D may be a natural inhibitor of MS comes from experiments with experimental autoimmune encephalomyelitis (EAE), a model of MS. Treatment of mice with 1,25-(OH)2D3 completely inhibited EAE induction and progression. The hormone stimulated the synthesis of two anti-encephalitogenic cytokines, interleukin 4 and transforming growth factor beta-1, and influenced inflammatory cell trafficking or apoptosis. If vitamin D is a natural inhibitor of MS, providing supplemental vitamin D to individuals who are at risk for MS would be advisable.
COMMENTARY: Although commonly called a 'vitamin' because it must be supplied from the diet, vitamin D (1, 25-dihydroxycholecalciferol) is acutally a hormone, and the author of this article makes a strong case (both biochemically and demographically) that physicians should be thinking about vitamin D therapy for their MS patients. Fish oil is an excellent vitamin D source, and diets rich in fish may lower MS prevalence or severity.
Vitamin D deficiency afflicts most MS patients, as demonstrated by their low bone mass and high fracture rates. MS prevalence increases with decreasing sunlight (i.e the rates of MS are higher in northern Europe versus southern Europe) suggesting that sunlight may be protective in MS.
QUESTION: Could you help? My husband has had muscle spasms, continuously, for several months now. They don't allow him to led even a partially normal life. He can't sit for more than 45 minutes before his back swells up and he is in continuous pain. We've been following your advice for about two weeks and no change. Thank you.
ANSWER: Although you did not leave your husband's blood type, two recommendations can be given that are reasonably effective, rational and safe:
1. Magnesium. 500mg of supplemental magnesium taken every 3-4 hours can help, (1) especially if your husband is one of the many individuals with back spasm who tend towards magnesium deficiency.
2. GABA or gamma amino butyric acid, is an inhibitory neurotransmitter - a chemical involved in nerve regulation which serves to inhibit excessive bioelectrical activity. GABA is the prime inhibitory neurotransmitter in the brain. It is a derivative of the amino acid glutamic acid and is related to the sleep-enhancing biochemical Gamma Hydroxy Butyrate. The function of GABA is to decrease neuron activity and inhibit nerve cells from overfiring. Together with other chemicals, GABA prevents anxiety and stress-related messages from reaching the motor centers of the brain by occupying the receptor sites for these messages. (2) GABA brings to the source what nerves need to stay calm. The nutrient GABA can be taken to calm the body in much the same way as these pharmaceuticals but without the fear of addiction. Supplemental GABA can quiet anxiety and reduce muscle tensions. Typical doses are 250-750mg daily. Avoid higher doses.
1. Rossier P, van Erven S, Wade DT. CLINICAL CORRESPONDENCE: the effect of magnesium oral therapy on spasticity in a patient with multiple sclerosis. Eur J Neurol. 2000 Nov;7(6):741-4.
2. Waagepetersen HS, Sonnewald U, Schousboe A. The GABA paradox: multiple roles as metabolite, neurotransmitter, and neurodifferentiative agent. J Neurochem 1999;73:1335–42.
QUESTION: My conservative, normally omnivorous brother pointed to this website which jumps all over your program. Have you answered any of this guy's concerns? By the way, I find your program for Type A works great!
ANSWER: That is a very old and biased article that was cross-posted to several vegetarian websites. It was answered long ago.
Its major problem with my theory is that I allow some blood types to eat animal protein; thus the author's gripe is not just with me, but also with all the other 'high protein diets' out there as well. I suppose if I had just published the type A diet he would have not had much of a problem with my theory.
His points that attempt to refute the thousands of published studies linking blood type to many diseases and biological functions are simplistic and display no great appreciation or understanding of much of the material that he attempts to contradict.
Unfortunately it was not the science that resulted in his critique, but rather the conclusions.
Started Type A diet late March; lost 40 lbs. reached goal of 105 end of Sept. Last two months have been continually plagued with sugar cravings and binges, whether or not I stick strictly to the eating plan. Have always had a sugar habit; am concerned about diabetes. Have tried adding back more "good" fat; works for a day or so. Any advice appreciated. Recommended your book to many friends and coworkers. All except one who have tried their type diets have had great success! I am only one with sugar problem. Thanks so much from all of us!
Very often this type of sugar reaction complicates an otherwise nice result from the diet. Usually it just a that the liver is having some problems adjusting to the new way of eating, and needs some rehabilitation. Try taking the herb "Milk Thistle" for a while (commonly available at most health food stores) and having a cup of licorice root tea at about 10AM and 2PM. Usually a few weeks of this suffices to get things back on tract. Do not use licorice without physician supervision if you suffer from high blood pressure. "Celestial Seasoning" and "Stash Teas" are two good brands.
QUESTION: I ahev just been diganosed with open angle glaucoma. Is there any link to blood type? Thanks for a WONDERFUL website!
ANSWER: Glaucoma is a specific pattern of optic nerve damage and visual field loss caused by a number of different eye diseases which can affect the eye. Most, but not all of these diseases, are characterized by elevated intra-eye pressure, which is not the disease itself, but the most important risk factor for the development of glaucoma.
Primary Open-Angle Glaucoma (POAG). Approximately one percent of all Americans have this form of glaucoma, making it the most common form of glaucoma in our country. It occurs mainly in the over 50 age group. There are no symptoms associated with POAG. The pressure in the eye slowly rises and the cornea adapts without swelling. If the cornea were to swell, which is usually a signal that something is wrong, symptoms would be present. But as this is not the case, this disease often goes undetected. It is painless, and the patient often does not realize that he or she is slowly losing vision until the later stages of the disease. However, by the time the vision is impaired, the damage is irreversible.
Normal Tension Glaucoma. Normal-tension glaucoma, also known as low-tension glaucoma, is characterized by progressive optic nerve damage and visual field loss with a statistically normal intraocular pressure. This form of glaucoma, which is being increasingly recognized, may account for as many as one-third of the cases of open-angle glaucoma in the United States. Normal-tension glaucoma is thought to be related, at least in part, to poor blood flow to the optic nerve, which leads to death of the cells which carry impulses from the retina to the brain. In addition, these eyes appear to be susceptible to pressure-related damage even in the high normal range, and therefore a pressure lower than normal is often necessary to prevent further visual loss.
Angle-Closure Glaucoma. Angle-closure glaucoma affects nearly half a million people in the United States. There is a tendency for this disease to be inherited, and often several members of a family will be afflicted. It is most common in people of Asian descent and people who are far-sighted. In people with a tendency to angle-closure glaucoma, the anterior chamber is smaller than average.
Exfoliation Syndrome. This common cause of glaucoma is found everywhere in the world, but is most common among people of European descent. In about 10% of the population over age 50, a whitish material, which looks on slit-lamp examination somewhat like tiny flakes of dandruff, builds up on the lens of the eye. This exfoliation material is rubbed off the lens by movement of the iris and at the same time, pigment is rubbed off the iris. Both pigment and exfoliation material clog the trabecular meshwork, leading to IOP elevation, sometimes to very high levels. Exfoliation syndrome can lead to both open-angle glaucoma and angle-closure glaucoma, often producing both kinds of glaucoma in the same individual.
There are some blood type associations with glaucoma. A series of 474 mixed cases of glaucoma was assessed to determine whether there were any genetic differences between different types of glaucoma. A careful distinction was made between chronic open angle glaucoma (COAG), acute and chronic angle closure glaucoma, ocular hypertension, low tension glaucoma, patients with large cup disc ratios, and various types of secondary glaucoma including pseudoexfoliation of the lens capsule, uveitic and traumatic glaucoma. Using ABO blood groups, Rhesus groups and ABH secretion or non-secretion the researchers identified certain differences.
The differences were significant decrease in Rh-negative patients in chronic closed angle glaucoma. Secretors had lower rates of in ocular hypertension and fewer HB secretors in patients with chronic open angle glaucoma. There was a significant lack of type A secretors and increase type B secretors in both pseudoexfoliation with raised intraocular pressure compared with chronic closed angle glaucoma.
I've found that medication is the only reliable way to control glaucoma. Although following the ER4YT principles and using prudent amounts of vitamin C and the herb Coleus forskolii have allowed many patients to keep their glaucoma under good control for many years.
Brooks AM, Gillies WE. Blood groups as genetic markers in glaucoma. Br J Ophthalmol 1988 Apr;72(4):270-3
QUESTION: My husband is A- and has phlebitis in his left ankle. We have been slowly incorporating the blood type principles into our lifestyle (I am A+). What else can be done to eliminate or lessen the phlebitis?
ANSWER: Phlebitis any condition where there is inflammation of a vein. It can refer to superficial veins in the legs or deep veins in the muscles of the leg or pelvis.
Phlebitis may be characterized by any of the following symptoms:
1. a hard, red vein visible in your leg; it may be warm and tender.
2. fever is possible and sleepless nights as the pain worsens.
3. a throbbing or burning sensation beneath the skin's surface.
4. pain deep inside the leg and swelling in the ankle
Often this condition is followed by thrombosis (clotting of the blood). Therefore phlebitis followed by thrombosis is called thrombophlebitis. These painful clots may partially or fully block blood flow in affected veins.
The superficial phlebitis is the most common form of phlebitis and occurs in veins near the skin's surface usually in the legs. This is usually harmless although painful and uncomfortable.
Deep phlebitis, on the other hand, is less common and more dangerous as it affects the internal veins of the legs. These clots tend to be larger and more able to loosen and travel to other areas. It is also possible for you not to realise you have this problem and it may go untreated.
Phebitis is typically treated by blood thinning agents, including low-dose aspririn therapy.
It has been found that having type O blood lessens the risk of phlebitis, especially in women and younger subjects. In one study 86 medical patients with a hospital discharge diagnosis of thrombophlebitis of the lower extremity, 70 (81%) were of blood type A,B, or AB (non-O).(1) There is typically an excess of blood group A in epidemiological studies of venous thrombosis.
We know that ABO genetics has an influence on the production of Factor VIII and Von Willdebrand Factors, crucial blood clotting factors. Having group A blood and/or the Lewis a-b- phenotype increases the risk of coagulation difficulties dramatically. This may be the result of the action of the A blood group antigen directly on the platelets themselves.
Since anti-coagulation therapy is considered 'front-line' treatment for venous thrombosis, your husband may benefit from several natural alternatives. John Bastyr, the famous naturopathic icon, used to tell us students that the juice of several lemons had a demonstrable effect on inhibiting clot formation. The pineapple enzyme bromelain has proven anti-edematous, anti-inflammatory, anti-thrombotic and fibrinolytic (clot dissolving)activities.
Stress reduction may be more improtant for group A patients with phlebitis than commonly realized. Studies have shown a direct correlation between ABO blood group, blood viscosity (thickness) and a variety of conditions,including stress.(2,3) In all cases, group A had the highest blood viscosity.
1. Jick H, Porter J. Thrombophlebitis of the lower extremities and ABO blood type. Arch Intern Med. 1978 Oct;138(10):1566-7.
2. Dintenfass L. Blood rheology as diagnostic and predictive tool in cardiovascular diseases. Effect of ABO blood groups. Angiology. 1974 Jun;25(6):365-72
3. Dintenfass L. The role of ABO blood groups in dynamic coagulation and thrombus formation in vascular disease. An in vitro study. Haematologia (Budap). 1971;5(3):205-16.
I have two sons, a 3-month-old and a 3-year-old and I would like to get them started on the right track with their diet before they get used to eating foods that are wrong for their blood type. My question is, is your blood type testing kit appropriate for small children and how is it done? I'm not a nurse and the idea of testing their blood myself makes me nervous.
Lots of people have typed their families with the home test. It is very easy to do on a child. Unlike an adult you don't stick them on the finger, you stick them on the fat pad at the bottom of the heel of their foot. There are less nerve endings their so it doesn't hurt much, plus they can't see what you are doing if they're on their stomachs!
Have been on the diet for two months and my knee arthritis problems have improved immensely. I can jog again! As a type O woman, if thryoid function is sluggish ( enough to prevent me from losing any weight at all over my two months on the diet) does it show up on standard thyroid panels or is it like the cholesterol panels where they tested a large group of middle aged men and decided 220 was "normal" until they figured out they were dying of cardiac arrests.
The best measurement of thyroid function is the basal metabolic rate, which involves taking an axillary (armpit) reading every morning before rising from bed. Several days readings should be performed sequentially and averaged. A resting axillary temperature lower than 97.5 makes me start thinking about improper thyroid function.
QUESTION: My 21 month old grandson was born with a rare skin condition called Epidermolysis Bullosa or EB for short. The type is Dowling meara, simplex. It is a genetic disease and a cure has not been found as yet. I was wondering if you have any suggestions. The blisters are more prevalent on hands and feet and the baby has difficulty walking.
ANSWER: Epidermolysis Bullosa is a group of diseases characterized by blister formation after minor injury to the skin. This family of inherited disorders range in degree of severity from mild to very serious and disabling.
Daily skin care is a mainstay of treatment in EB, with avoidance of trauma a primary goal. Management of skin infections is an important part of EB patient care. Systemic antibiotics are frequently used for cutaneous infection and chronic wound colonization is managed best by regular cleansing and bathing in modified Dakin's solution and topical antibiotics as needed. Modified Dakin's solution is 2 teaspoons of Clorox per gallon of bath water.
In general, a good anti-oxidant based vitamin/mineral formula would be a very wise move, as many BE patients are nutrient-deficient (1), and the basis of the blistering reactions are related to excessive free radical activity. This is particularly true of vitamin E. (2,3)
1. Birge K. utrition management of patients with epidermolysis bullosa. J Am Diet Assoc. 1995 May;95(5):575-9.
2. Pehr K, Forsey RR. Why don't we use vitamin E in dermatology? CMAJ. 1993 Nov 1;149(9):1247-53.
3.Ayres S Jr. Epidermolysis bullosa controlled by vitamin E. Int J Dermatol. 1986 Dec;25(10):670-1.