A study by Karlic et. al. [1] found that a vegetarian diet has a significant impact on a gene regulating carnitine metabolism. Carnitine is an amino acid (protein constituent) and a conditionally essential nutrient that plays a vital role in energy production and fatty acid metabolism. A “conditionally essential” nutrient is one that can be manufactured in the body, but the requirements of individuals might exceed dietary intake during specific disease states. Carnitine not obtained from food is synthesized in the body from two essential amino acids, lysine and methionine. Carnitine is found in higher levels in meat products as it is present in high levels in muscle tissue.

Vegetarian diets therefore contain less carnitine, and also often contain more carbodydrate than omnivorous diets as sources of concentrated vegetable proteins are not so readily available as animal proteins.

The study found increased expression of a gene [2] called Organic Cation Transporter 2 (OCTN2) in vegetarians which caused elevated levels of OCTN2 in cell membranes, compensating for lower carnitine levels obtained from the diet. Thus a vegetarian lifestyle has an impact on fat metabolism causing a remarkable stimulation of carnitine uptake.

The bioavailability of L-carnitine varies due to dietary composition. Bioavailability of L-carnitine in vegetarians who are adapted to low-carnitine diets is higher (66% to 86% of available carnitine) than regular red-meat eaters adapted to high-carnitine diets (54% to 72% of available carnitine). Carnitine influences carbohydrate metabolism. Abnormal carnitine regulation is implicated in complications of diabetes mellitus, cardiomyopathy, obesity, endocrine imbalances and other disorders. [3]

According to The Blood Type Diet and The GenoType Diet, individuals with a particular genetic characteristic and the associated metabolic consequences may be recommended to reduce the amount of red meat in their diets. This may be due to specific disease susceptibility and/or reduced ability to digest and metabolise red meats. Some of the consequences of increased carbohydrate intake in these individuals may be compensated for by the natural epigenetic effect of lowered carnitine intake on the gene that enhances the concentration of this nutrient and resultant increased bioavailability.

References:
1. Karlic H, Schuster D, Varga F, Klindert G, Lapin A, Haslberger A, Handschur M: "Vegetarian Diet Affects Genes of Oxidative Metabolism and Collagen Synthesis." Ann Nutr Metab 2008;53:29-32. Pubmed 18772587

2. OMIM OCTN2

3. Flanagan JL, Simmons PA, Vehige J, Willcox MDP, Garrett Q: "Role of carnitine in disease." Nutrition & Metabolism 2010, 7:30 doi:10.1186/1743-7075-7-30

Dear Dr. Greenfield,

I have decided to try the blood type diet (A). I am aware that Dr. D'Adamo suggests avoiding smoked meat and seafood. I am assuming this is due to the nitrate/nitrite added to the food. However, I shop at Whole Foods Market and they smoke their seafood in house, naturally, without any preservatives. Would this be okay to eat on the blood type diet?

Thank you,

Jennifer

Smoking is a way of preserving foods using smoke typically from hardwood burnt at low temperatures: Certain compounds given off by burning wood have a preservative or antimicrobial effect on the food, and add flavour. Other compounds, such as polycyclic aromatic hydrocarbons (PAHs) may have a detrimental effect on human health at levels found in cooked foods, they are certainly a risk for workers occupationally exposed to PAHs, and also for cigarette smokers. Certain PAHs may become more toxic when metabolised, and metabolism can be dependent on individual polymorphisms. For example, cytochrome P450 1A1 (CYP1A1) is the primary cytochrome P-450 isoenzyme that biologically activates benzopyrene, a tetracyclic hydrocarbon present in smoked food, and the main carcinogen in cigarette smoke. Charbroiled and smoked meats and fish contain more PAHs than uncooked products, with up to 2.0 µg/kg of benzopyrene detected in smoked fish.[1]

Some people may be more at risk from eating smoked foods or other exposure to PAHs: Genetic polymorphisms in CYP1A1 inducibility has been implicated as a factor for susceptibility to lung and laryngeal cancer. CYP1A1 may be induced by other substances. The mechanism by which PAH causes cancer is thought to be via the binding of metabolites to DNA. Infants may be at risk for exposure to PAHs: Animal studies have shown that PAHs and metabolites cross the placenta; Because PAHs are excreted in breast milk, nursing infants of exposed mothers can be exposed through breastfeeding. Polymorphisms causing glutathione transferase deficiencies (GSTM1) may result in elevated breast cancer risk from PAHs.[2] Other risk factors may include blood group, with type A individuals having a greater risk of certain types of cancer, although this can be masked by other genetic factors overriding the blood group phenotype.[3]

Sodium nitrite (E250) is a preservative added to meats, which can form carcinogenic nitrosamines when exposed to high temperatures. Nitrosamine formation can be inhibited by the addition of vitamin C.[4]

The Blood Type Diet™ is based on naturopathic principles, and as such advocates avoiding or minimising consumption of foods that may enhance disease risk either for the individual or for the population in general.

References:
1. Grimmer G. 1968. "Carcinogenic hydrocarbons in the human environment". Dtsch Apoth Ztg 108:529.
2. van der Hel OL, Peeters PH, Hein DW, Doll MA, Grobbee DE, et al. "NAT2 slow acetylation and GSTM1 null genotypes may increase postmenopausal breast cancer risk in long-term smoking women." Pharmacogenetics. 2003 Jul;13(7):399-407. Pubmed.
3. Anderson DE, Haas C. "Blood type A and familial breast cancer." Cancer. 1984 Nov 1;54(9):1845-9. PubMed.
4. Mackerness CW, Leach SA, Thompson MH, Hill MJ. "The inhibition of bacterially mediated N-nitrosation by vitamin C: relevance to the inhibition of endogenous N-nitrosation in the achlorhydric stomach." Carcinogenesis 1989; 10(2) 397-399. PubMed.

Dear Dr. Greenfield,

I am a 42 year old woman with RLS. I have it since I was 20, with alternating good and bad periods.

It affects me especially in my sleep. I am a 0+, Gatherer.

Are there any natural supplements I can take which could make a difference?

Thanks and kind regards,

Petra

Restless legs syndrome (RLS) and periodic limb movement disorder are characterized during waking by an irresistible urge to move the legs while awake, and involuntary leg movements while asleep.

For people with a family history of RLS, it is worth considering whether there is a genetic influence on the condition: researchers have found several genetic loci associated with RLS in an autosomal dominant inheritance pattern [1].

One of the genetic influences may involve an increased need for folate [2]. Individuals with polymorphisms for folate metabolism often do better taking an active form of folic acid such as folinate, rather than the commonly available folic acid supplements. Although folic acid improves methylation in all GenoTypes, GT4 Explorers are more prone to folic acid deficiency anaemia; GT1 Hunters and GT6 Nomads may also need folate to slow down their rapidly aging genes [3].

Researchers have also found that iron supplementation may improve the symptoms of RLS [2], reducing fluctuations in dopamine levels in the brain at night. Patients with RLS have lower levels of dopamine and respond to iron administration [4]. Caffeine, nicotine, alcohol and medication that affects dopamine levels may induce RLS as a side effect. It is recommended to check ferritin (iron storage) levels before supplementing with iron, as ferritin levels are often lower than average in RLS sufferers. There are strong indications that a gene regulating dopamine beta hydroxylase activity is linked to the ABO blood group locus [5], and altered dopamine levels may be associated with blood type.

Finally, osteopathic manipulative therapy has been found to decrease spinal facilitation in a small pilot study, relieving symptoms in many patients with RLS [6].

References:
1. Dhawan V, Ali M, Chaudhuri KR. "Genetic aspects of restless legs syndrome." Postgrad Med J. 2006 Oct;82(972):626-9. PubMed
2. Lee KA, Zaffke ME, Baratte-Beebe K.J. "Restless legs syndrome and sleep disturbance during pregnancy: the role of folate and iron." Womens Health Gend Based Med. 2001 May;10(4):335-41. PubMed
3. Dadamp, P. The GenoType Diet. Broadway Books, 2007, ISBN 978-0-7679-2524-2
4. Patrick LR. "Restless legs syndrome: pathophysiology and the role of iron and folate." Altern Med Rev. 2007 Jun;12(2):101-12. PubMed
5. Wilson AF, Elston RC, Siervogel RM, Tran LD. "Linkage of a gene regulating dopamine-beta-hydroxylase activity and the ABO blood group locus". Am J Hum Genet 1988;42:160-166. PubMed
6. Peters T W, "Restless Legs", Osteopathy Today, October 2001. P12-13.

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

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

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