Dr. Tom Greenfield

Blood Typers wanting to get a Blood Type certification in Europe will be able to take the IfHI test in Ireland on Independence day. A certification exam will be offered to those who have completed the two-day training with Dr. Prannie Rhatigan at the Nutri Centre in Dublin. A successful introductory day has already been held, another introductory day for those who missed the first one will be scheduled. Day two will be the Preparation for Level 1 (Fellow) certification and distribution of exam papers on Saturday 4th July 2009, Time 10am -4.30.

Guest lecturers scheduled to speak at Day Two are Nick Bowler, biochemist and head of NAP Europe, and Tom Greenfield ND, blood type practitioner from Canterbury, UK.

... more details to follow shortly.

The UK Food Standards Agency (FSA) has issued a press release advising pregnant mothers to limit their intake of coffee and caffeine-containing substances.[1] "Pregnant women are advised to limit their daily caffeine intake to 200mg a day – roughly two mugs of coffee a day" due to a potential link with Foetal Growth Retardation (FGR). This is a reduction from the previous advice of 300 mg per day, following an updated report from the FSA's independent Committee on Toxicity (COT).[2] According to the committee, if there is a causal link then there may be no lower 'safe' limit, but a caffeine intake of less than 200 mg per day during pregnancy may reduce the risk of FGR to less than 2%. FGR is defined as failure of the baby to attain its growth potential as determined by genetic and environmental factors.

The FSA funded research published by the British Medical Journal[3] which measured caffeine intake from all sources (coffee, tea, colas and medication) in pregnant women, and then measured their babies when they were born. The xenobiotic caffeine can be detoxified from the body in four main ways, 3-demethylation being quantitatively the most important: caffeine is converted to paraxanthine by the enzyme cytochrome P450 1A2 (CYP1A2). This is one of the enzymes which often has low activity in the GT4 Explorer GenoType, and is responsible for Explorers being up all night after drinking coffee. The researchers measured the CYP1A2 enzyme activity as the main form of caffeine clearance in the mothers taking part in the study. They found that the mothers with the highest CYP1A2 activity passed the most caffeine and caffeine metabolites to their foetus via the placenta. CYP1A2 activity is absent in the placenta and the fetus.[4] This means that like the GT4 Explorer, the unborn baby won't get much sleep after their mother has drunk coffee.

What is the problem with having smaller babies? It is a well known epigenetic risk factor, as the COT study says:

FGR is an important outcome because it is associated with an increased risk of perinatal mortality and morbidity, including perinatal asphyxia. Moreover, there is epidemiological evidence that FGR correlates with adverse effects in adult life. For example, affected individuals have an increased incidence of metabolic syndrome, manifesting as obesity, hypertension, hypercholesterolemia, cardiovascular disease, and type 2 diabetes.

Smoking and alcohol intake also have a significant effect on the risk of FGR.

References:

1. Food Standards Agency. "Food Standards Agency publishes new caffeine advice for pregnant women." Press release, Monday 3 November 2008.
2. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment. "Statement on the reproductive effects of caffeine". COT statement 2008/04
3. CARE Study Group. "Maternal caffeine intake during pregnancy and risk of fetal growth restriction: a large prospective observational study" BMJ 2008;337:a2332
4. Aldridge A, Aranda JV, Neims AH. "Caffeine metabolism in the newborn." Clin Pharmacol Ther. 1979 Apr;25(4):447-53. PMID: 428190

With great fanfare, the establishment medical journal The New England Journal of Medicine (NEJM) published a paper "Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein."[1] Rosuvastatin (Crestor) is a drug marketed by the pharmaceutical company AstraZeneca as a HMG-CoA reductase inhibitor (they called it a 'super-statin'). AstraZeneca funded this study, and the lead author is one of the patent holders for the high sensitivity C-Reactive Protein test (hs-CRP),[2] a sensitive blood marker of inflammation. Of course there are no real vested interests apart from the health of the nation, and as such, the American Heart Association meeting wondered whether it should be "put in the water".[3] This harks back to the PolyPill hypothesis,[4] where it was suggested everyone should take pharmaceutical medication before they inevitably get ill. Shares in AstraZeneca rose since the NEJM publication,[3] as it would cost $116 USD per month for an individual (over $1,300 USD per year) to take it daily, according to USA Today.[5] This means that each life saved would cost approximately $557,000 (if you believe the studies). AND that does not include the cost of the patented hs-CRP test (more expensive than a cholesterol test). And according to The Blog of Michael R Eades MD,[6] the drug might only give a little protection to a very few people:

If you believe the data from this study..., it indicates that men over 50 and women over 60 with normal LDL-cholesterol levels AND elevated C-reactive protein levels who took the very expensive ($3.50 per day) statin drug rosuvastatin (Crestor) minimally reduced their risk of developing heart disease or dying of any cause as compared to those who took placebo.

So what else should we put in the water - the toxic chemical fluoride? But that's another story ...

What is counted by medics as 'high' cholesterol has been gradually dropping over the years as drug companies push the 'benefits' of statins as a simple magic bullet to the ubiquitous deaths from heart disease. Yet simple epigenetic cardiovascular disease risks such as low birth weight in males who regain a normal or above average Body Mass Index in childhood,[7] or men with shorter legs[8] or shorter index fingers than ring fingers[9] (high 2D:4D ratio) are ignored until the individual becomes a patient with heart disease later in life.

Back to the paper, which was dubbed the JUPITER trial: "The primary objective of the Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) was to investigate whether treatment with rosuvastatin, 20 mg daily, as compared with placebo, would decrease the rate of first major cardiovascular events." Eades translates this as "by God we’re going to prove that statins prevent something. "[6]

And what it did prove is that more people taking Crestor got diabetes than the people not taking Crestor:

We did detect a small but significant increase in the rate of physician-reported diabetes with rosuvastatin, as well as a small, though significant, increase in the median value of glycated hemoglobin. Increases in glucose and glycated hemoglobin levels, the incidence of newly diagnosed diabetes, and worsening glycemic control have been reported in previous trials of pravastatin, simvastatin, and atorvastatin.

Even though physician-reported diabetes was been significantly increased in this and previous Crestor studies, and statins are given to people who have diabetes because they have diabetes, the authors say that "further study is needed before any causative effect can be established or refuted." Eades suggests that this is why the study was stopped when it was by outside observers. Ok, let's further poison our water supply with an expensive drug that gives people diabetes (not to mention muscle pain) all in the name of health.

References:

1. Ridker PM, Danielson E, Fonseca FA, et. al. Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein. N Engl J Med. 2008 Nov 9.

2. US Patent 6040147 - Systemic inflammatory markers as diagnostic tools in the prevention of atherosclerotic diseases and as tools to aid in the selection of agents to be used for the prevention and treatment of atherosclerotic disease. Paul M Ridker.

3. "Cholesterol Pills in the Water? Crestor Market Widens (Update3)". Bloomberg.com news, Nov 10 2008.

4. Wald NJ, Law MR. "A strategy to reduce cardiovascular disease by more than 80%". BMJ 2003;326:1419 (28 June), doi:10.1136/bmj.326.7404.1419

5. "Crestor would save lives at $500,000 each" Steve Sternberg, USA Today, Nov 10 2008.

6. Eades, M. Weblog: "Truth versus hype in the Jupiter study" 10. November 2008.

7. Eriksson JG, Forsén T, Tuomilehto J, Winter PD, Osmond C, Barker DJP "Catch­up growth in childhood and death from coronary heart disease: longitudinal study." BMJ 1999;318;427-431

8. Davey Smith G, Greenwood R, Gunnell D, Sweetnam P, Yarnell J, Elwood P. "Leg length, insulin resistance, and coronary heart disease risk: The Caerphilly Study." J. Epidemiol. Community Health 2001;55;867-872 doi:10.1136/jech.55.12.867

9. Manning JT, Bundred PE, Flanagan BF. "The ratio of 2nd to 4th digit length: a proxy for transactivation activity of the androgen receptor gene?" Med Hypotheses. 2002 Sep;59(3):334-6. Pubmed 12208164

Dear Dr. Greenfield,

I own the English original of "Eat right for your type". I recently bought a German translation for a friend. The lists of food stuff are not the same. E.g. in the type O beneficial fruit list it has cherries, blueberries and mangoes in addition to figs and plums. Did Dr. D'Adamo change the lists or were the German translators inventive?

Thanks in advance,

Best, Claudia

The German edition of Eat Right 4 Your Type, published as 4 Blutgruppen - Vier Strategien für ein gesundes Leben was published in hardback in 1998, and then in paperback in January 2001. The later German edition appears to have been updated with the new food lists that were available after new research for the American publication of Live Right 4 Your Type (and English The Eat Right Diet), the Complete Blood Type Encyclopedia, and online in Typebase 4. The American and English editions of Eat Right 4 Your Type have not been updated since they were published. Also read this clarification about differences between the books.

A new study to be published in Schizophrenia Research[1] has found that markings on the hand may be a sensitive marker for genetic and environmental factors in schizophrenia.

Anthropologists in Barcelona, Spain studied the hand patterns of patients with schizophrenia, their relatives and healthy 'control' subjects. They looked at A-B ridge count, which is the number of ridges between two points on the palm called A and B (defined by specific areas where patterns converge under the second and third digits). There was no overall difference in A-B ridge count, but A-B ridge count was lower (fewer ridges) in schizophrenic patients with a low birth weight, and also in patients who did not have a family history of schizophrenia.

According to the study, the frequency of ectodermic derivates abnormalities (that is, Ridge Dissociation [RD] and/or Abnormal Palmar Flexion Creases [APFC] - abnormalities originating from the embryonic ectodermal layer of tissue, including the epidermis) appeared to be higher in patients and relatives than in controls. Ridge dissociation refers to short broken segments of lines that cover the patterns of dermatoglyphic areas in a disorganized way. Examples of abnormal palmar flexion creases are the Simian line, the Sydney line, clear broken proximal and distal palmar creases, and very rudimentary creases. Associations of this kind studying RD and APFC have been found in previous studies, one of them[2] concluding that factors affecting early foetal development may increase the risk for psychotic disorder. In this new study males had more of these abnormalities than females, which also shows the potential influence of male hormones in response to stress. Males also had more fluctuating asymmetry of their A-B ridge count (difference between left and right hands).

Overall these studies show the importance of maintaining a peaceful and stress-free environment for the unborn child, as well as highlighting a potentially observable risk factor for schizophrenia.

References:
1: Fatjó-Vilas M, Gourion D, Campanera S, et. al.
"New evidences of gene and environment interactions affecting prenatal neurodevelopment in schizophrenia-spectrum disorders: A family dermatoglyphic study."
Schizophr Res. 2008 Jun 24.
PMID: 18583099

2: Rosa A, Fañanas L, Bracha HS, Torrey EF, van Os J.
Am J Psychiatry. 2000 Sep;157(9):1511-3.
Congenital dermatoglyphic malformations and psychosis: a twin study.
PMID: 10964873

Read more »