Tags: genotype diet
Here it is.. another Monday and another research grab-bag.
Five daily portions of fruits and vegetables raise serum antioxidants in three months
To explore the effects of increasing fruit and vegetable intake and the resulting effects on levels of circulating micronutrients in a community-dwelling population with an already high consumption of fruits and vegetables, 112 volunteers (86% women) underwent targeted dietary counseling for three months. At the beginning of the study and after 4, 8 and 12 weeks a food frequency questionnaire was filled in, and plasma levels of dietary antioxidants as well as biomarkers of oxidative lipid and protein damage were determined. Compared to baseline, especially the intake of fruits was significantly improved after 3 months of intervention, and mean plasma levels of lutein, zeaxanthin, β-cryptoxanthin, lycopene, α- and β-carotene, retinol, α-tocopherol, vitamin C and vitamin B6 were increased. Biomarkers of oxidative stress remained unchanged. Thus, a nutritional counseling program is capable of improving plasma levels of antioxidants even in a health-conscious population.
What is especially interesting about this study was that they used individuals who were already eating a pretty healthy diet, which just goes to show that even if you follow the BTD or GTD in terms of food choices, something as basic as making sure that you get the required amounts of recommended fruits and vegetables can make a big difference.
Schizophrenia, gluten, and low-carbohydrate, ketogenic diets
We report the unexpected resolution of longstanding schizophrenic symptoms after starting a low-carbohydrate, ketogenic diet. After a review of the literature, possible reasons for this include the metabolic consequences from the elimination of gluten from the diet, and the modulation of the disease of schizophrenia at the cellular level.
Previously, Dohan (Acta Psych Scand 1966, 42(2):125-152) observed a decrease in hospital admissions for schizophrenia in countries that had limited bread consumption during World War II, which suggested a possible relationship between bread and schizophrenia. Early work with lectins clearly showed that the brains of schizophrenics bind lectins differently than the brain tissue of non-schizoprhenics, which appears to make sense in that the carbohydrate content of schizophrenic brain tissue (in addition to dementia and a few other illnesses) revealed the existence of spherical deposits in the inner and middle molecular layers of the dentate gyrus in the hippocampal formation which contained fucose, galactose, N-acetyl galactosamine, N-acetyl glucosamine, sialic acid, mannose and chondroitin sulfate; many of these blood group active carbohydrates with known lectin binding affinities (link).
Over the years some of the most stirring letters I've received from book readers have centered around improvements in family members with schizophrenia. Almost all of these letters have been from or about blood type O schizophrenics, which may mean that the nutritional approach to schizophrenia might necessarily differ by foods and blood type. We are now only beginning to understand the effects of tissue glycosylation on the development and maintenance of brain neural networks (in particular those utilizing the blood group O specific antigen fucose).
Lectin-epithelial interactions in the human colon.
Similar changes in glycosylation occur in the colonic epithelium in inflammatory conditions such as ulcerative colitis and Crohn's disease and also in colon cancer and precancerous adenomatous polyps...Tools are now available to allow fast and accurate elucidation of glycosylation changes in epithelial disease, characterization of their potential lectin ligands, whether dietary, microbial or human, and determination of the functional significance of their interactions. This should prove a very fruitful area for future research with relevance to infectious, inflammatory and cancerous diseases of the epithelia.
In years past I've written about the effects of some dietary lectins on the cells of the colon, in particular the lectins found in mushrooms, fava beans and jackfruit. Most of the plant lectins are specific for the Thomsen-Friedenreich Antigen (T antigen) a pseudo blood group antigen which is often expressed in pre-malignant cells of the colon.
Here is a quote from a study examining fava (broad) bean lectin:
VFA stimulated an undifferentiated colon cancer cell line to differentiate into gland like structures. The adhesion molecule epCAM is involved in this. Dietary or therapeutic VFA may slow progression of colon cancer.
Here is a quote from a study examining standard commercial supermarket mushroom lectin:
Agaricus bisporus agglutinin (ABA) isolated from edible mushroom has a potent anti-proliferative effect on malignant colon cells with considerable therapeutic potential as an anti-neoplastic agent.
Here is a quote from a study examining jackfruit lectin:
(Jacalin) Lectin binding to human colonocytes can predict the presence of malignant and premalignant lesions of the colon, and has potential as a noninvasive screening tool for colorectal neoplasms.
If you have a family history of colon cancer, or have been diagnosed with colon abnormalities (such as polyps) you may want to investigate adding more of these foods to you diet (using the BTD as a guide to which would be best for you)
Human pseudogenes of the ABO family show a complex evolutionary dynamics and loss of function.
The GT6 glycosyltransferases gene family, that includes the AB0 blood group, shows a complex evolution pattern, with multiple events of gain and loss in different mammal species.These results suggest that some of these GT6 human pseudogenes may still be functional and retain some valuable unknown function in humans, in some case even at the protein level. The evolutionary analysis of all members of the GT6 family in humans allows an insight in their functional history, a process likely due to the interaction of the host glycans that they synthesize with pathogens; the past process that can be unravelled through the footprints left by natural selection in the extant genome variation.
Pseudogenes have been defined as nonfunctional sequences of genomic DNA originally derived from functional genes and are sometimes referred to as 'Junk DNA.' However new finding are suggestive that these areas of non-coding DNA and RNA may be involved in developmental changes which differentiate the functions linked to the blood type genes that occur between the various species.
Another nail in the coffin for the 'animals have blood types and don't eat right for their type' criticism of the Blood Type Diet by the nincompoop Andrew Weil.
The Effect of ABO Blood Types on Periodontal Status.
A relatively higher percentage of A group patients was found in gingivitis group and relatively higher percentage of O group patients was found in periodontitis group. A significant relationship was also determined between Rh factor and gingivitis. ABO blood subgroups and Rh factor may constitute a risk factor on the development of periodontal disease. However, long-term studies are needed to make a more comprehensive assessment of the effects of ABO group on periodontal diseases.
I'm sure that secretor status had something to do with these results, since it has an effect on pellicle formation (link) I do however, agree with the results. In my own patients I have seen periodontal disease resolve easily in many type A's by simply getting their gingivitis under control. Type O's on the other hand have a harder time of things, especially if their protein intake is not adequate.
That's about it for this week.
A bit of news: I would be willing to entertain questions about topics that might be of interest to this community. Just drop a comment (link is below). I will not however, respond to questions of a personal medical nature, nor give medical advice. Thanks for respecting this caveat.
From Percept Mot Skills. 2008 Dec;107(3):737-46.
Twin and family study findings indicate a substantial heritability of digit ratio (2D:4D), a putative marker for the masculinizing effects of prenatal androgen exposure. Functional polymorphisms of the X-linked androgen receptor gene, i.e., androgen sensitivity, contribute somewhat to the expression of 2D:4D in men, but otherwise the genetics of 2D:4D is unknown. This study investigated differences in 2D:4D by self-reported ABO blood type and Rhesus factor, two easily collectible genetic traits, in two samples (combined N=1273). Effects of blood groups on 2D:4D were small and not significant in all tests in both samples; however, two consistent patterns emerged across samples. Of the ABO types, AB had the lowest right-hand 2D:4D, the highest left-hand 2D:4D, and the lowest right-minus-left difference in 2D:4D, and Rhesus factor Rh- had higher left-hand 2D:4D and lower right-minus-left difference in 2D:4D than Rh+. If replicable, this may suggest genes contributing to the expression of 2D:4D reside in the vicinity of the gene loci (chromosomal locations: 9q34.2 and 1p36.11) of these blood groups or pleiotropic effects of the blood-group genes.
The New York Times had an extensive discussion of epigenetics in their February 24 issue:
The ideal of regenerative medicine is to convert a patient’s normal body cells first back into the embryonic state, and then into the specific cells lost to disease. But to prepare such cells safely and effectively, researchers will probably need to learn how to control and manipulate the chromatin of the epigenome as well as the transcription factors that shape cell identity.
New research shows that sugar deposits may be the major cause of skin aging.
Skin science appears to have caught up with the humble sugar molecule. Wrinkles, sagging skin, and pigment deposits may stem less from the sun and more from one-way sugar molecules that we make as part of the aging process but cannot remove. With no small amount of serendipity, scientists call these wrong-way sugars ‘AGE molecules’ (the AGE stands for 'Advanced Glycation End-products').
AGE molecules are all around us, and often taste pretty good: Any time we brown an onion or caramelize sugar we are making AGE molecules. However, when you make these molecules under your skin, you’ll probably find much less to like about them.
Unlike most other complex sugars, AGE molecules are not easily removed from the body (Just think back to a time you tried to clean burnt sugar off of a piece of crockery!) And because they stay in place for years, the immune system can react to tissues they deposit in, causing inflammation, damage, and aging.
AGE molecules: Good on marshmallows, bad on people.
NAP recently released the next three D’Adamo Genoma Skin products, which now expands the line to four products:
The Day Light Face Crème is the original formula. We’ve has virtually 100% customer satisfaction with the product, including unsolicited comments from three users that it was the only product that worked on their facial rosacea.
To this base formula, I’ve added an AGE (Glycation inhibiting) toner, a rich night crème and a tissue cleanser that uses a few very interesting botanicals.
For the rest of the month, at my request, NAP is offering the complete set of four products at a savings of 50%. I asked that they try to do this so that as many people as possible can try the line. If you are looking for a great skin care line at an unbelievable price, either as a holiday gift for someone or even yourself, you might want to look into these products.
However, do it before December 31, 2008.
This has been a busy time of things lecture-wise. Last month I lectured on 'Cancer Survivorship' at Backus Hospital in Norwich Connecticut, as part of their Fall Oncology Support Series. I really appreciate that Amy, the program coordinator (Center for Healthcare Integration) took the time to write a very nice thank you note:
Thank you so very much for the wonderful program you offered at Backus last week. Your use of metaphors to translate the scientific research is so effective and at the same time so much fun to listen to. I had many a-ha moments and between that lots of laughter. You are truly a gifted teacher.
It is a great support program from an imaginative hospital.
Immediately after this I lectured to a large group of doctors and nurses over at Soundview Medical Associates in Norwalk, Connecticut. This lecture was pretty much straight blood group science and physiology and despite some early technical glitches I was made most welcome, treated to an attentive and lively audience, and had a great time.
Early October featured a lecture at the Annual Conference of the New York Association of Naturopathic Physicians in Manhattan. This lecture was entitle 'Verisimilitude and Malignancy' and discussed how cancer systems often elude the immune system by posing as quasi blood type markers. Most naturopathic physicians were new to this type of information and as I looked out into the audience all I saw was a sea of heads pointed down as they furtively scribbled note after note.
At the conference I bumped into my old friend Dr. Russell Marz, one of the top naturopathic nutrition educators, whose 'Nutrition from Marz' is a standard nutrition text in the schools. Russell also write the nutrition reviews for NPLEX (the Naturopathic Licensing Exams). We're both expatriate New Yorkers and Russell always brings out the Brooklyn kid in me. Got a nice note afterward:
Good to see you and I just wanted to tell you how much I have appreciated your work. You really have created a whole new dimension in the field of nutrition and I believe especially in the area of cancer.
As I write this I'm preparing to leave for the airport and fly to Nashville, Tennessee for the first IFHI Micro Conference. I'll be lecturing for 3-4 hours throughout the day tomorrow. Hopefully the larynx holds up. Dr. Natalie Colicci is coming along to help with the certification, and tells me that she has already packed the lozenges.
After Tennessee things calm down a bit, which is great since I've discovered a few new veins of research that I want to pursue, and have just purchase a 1971 Volkswagon Bus that I am itching to restore.
Looming on the horizon is IFHI 2009, our biannual master conference. Unlike the prior 2005 and 2007 conferences I'll be doing most of the lecturing (something like nine hours total) by myself, with assistance from Drs. Tom Greenfield and Natalie Colicci. Again and again the feedback from prior conferences has been that, although the attendees have enjoyed the guest speakers, they would prefer that I spend more time on core curriculum and training. So here it is. I'm challenged by the idea of encapsulating an entire lifespan of work into such an information intensive format.
For the first time IFHI 2009 will be held on the east coast of the US (Norwalk Connecticut). It is close to our base of operations and affords a more easy access for the EU attendees, who comprise a rather large share of the audience. Proximity to NYC also allows folks to do some Manhattan site-seeing before or after the conference. Unlike prior conferences which held about 350 attendees, IFHI 2009 is limited to 125 on site and about 25 off site attendees. Also unlike the Buttes in Phoenix, the conference price is a 'soup to nuts package.'
I designed this little flyer for the conference. Almost prophetically it is the exact same model VW Bus that I'll be restoring. However my bus in in something over 1000 parts in over 50 crates.
I thought a recent abstract from one of the premiere nutrition journals did a pretty good job of catching up to, and explaining the theory behind The GenoType Diet:
Epigenetics encompasses changes to marks on the genome that are copied from one cell generation to the next, which may alter gene expression but which do not involve changes in the primary DNA sequence. These marks include DNA methylation and post-translational modifications (acetylation, methylation, phosphorylation and ubiquitination) of the histone tails protruding from nucleosome cores. The sum of genome-wide epigenetic patterns is known as the epigenome. It is hypothesised that altered epigenetic marking is a means through which evidence of environmental exposures (including nutritional status and dietary exposure) is received and recorded by the genome. At least some of these epigenetic marks are remembered through multiple cell generations and their effects may be revealed in altered gene expression and cell function. Altered epigenetic marking allows plasticity of phenotype in a fixed genotype. Despite their identical genotypes, monozygotic twins show increasing epigenetic diversity with age and with divergent lifestyles. Differences in epigenetic markings may explain some inter-individual variation in disease risk and in response to nutritional interventions.
Session 2: Personalised nutrition. Epigenomics: a basis for understanding individual differences? Mathers JC. Proc Nutr Soc. 2008 Nov;67(4):390-4.