Category: Personalized Medicine
I write a weekly email to the ND students on my shift at the University of Bridgeport Health Science Center. If in the course of working with a patient a concept arises that appears to require more in-depth knowledge I often specify certain research articles for the students to read in preparation for the next shift. This is not typical of clinic shifts and my shift is thought to be among the more demanding. Despite (or perhaps because of) this, a place on the shift rotation is always in high demand.
Recently the discussion came round to two concepts related to both cancer and inflammation: endoplasmic reticulum stress (ER stress), which results in poorly manufactured proteins; and the subsequent unfolded protein response (UFR), which occurs as a result of the dangerous aspects these improperly folded proteins pose to the cell.
After providing the students with 6-7 key studies, I began to suspect that they might need some cheering-up. So I appended this little ditty to the email:
A polymath is someone who is interested in everything, and nothing else.'
A polymath (Greek πολυμαθής, polymathēs, "having learned much") is a person whose expertise spans a significant number of different subject areas. In less formal terms, a polymath (or polymathic person) may simply be someone who is very knowledgeable. Most ancient scientists were polymaths by today's standards.
How do YOU propose to become a polymath? What might you need or observe?
Firstly, and this might be obvious, there must occur a huge leap in self-confidence. If you are easily intimidated by learning new things, or think you are somehow less smart than others, becoming polymathic will not be easy.
The learning-intimidated state is overcome by taking the first few baby steps in developing a new appreciation of just what you are capable of being aware of. This might be as simple as arriving at the conclusion that, since you are (at the very least) in control of your own life, who else is better capable?
I once had to do an interview with
Well of course I got all bent out of shape. The guy is like one of the smartest people on the planet. etc. etc. etc. string theory, etc. etc. etc. skeptic, etc.etc. etc.
As I got more twisted and twisted, I went to dinner at an old friend's house. These people were once our next door neighbors and we've kept in touch over the years, despite (or perhaps because) we don't have very much in common. On hearing my lament, the husband listened and simplified the whole thing for me by identifying the one basic truism:
'He may be smart, but he don't know what you know.'
Anyway, we couldn't get a time that worked for both of us and the interview never took place, but I did learn something about myself.
2. Rush/ Don't rush.
How often do we use time to avoid something? To just get 'it' over? However, far from telling you to slow down, I'm suggesting that you rush with a purpose. Not just to 'get it over with ', but rather to 'just to get to the end of it.' Then, instead of just moving on, going back and revisit that notion that caught your eye. Getting to the end of something lets the brain 'pin the four corners' of the concept and set aside space for conceptualization and context.
This observation has an important metaphor about disease and health buried within it.
Health is often like a car speeding down the highway: scenery flying by, but just barely noticed. Windows up. AC on. Favorite tunes playing. The conversation centering on some arcane subject. However, the timing belt breaks. So now we are going zero miles per hour, perched aside a forlorn stretch of highway. Initially we can only think about getting out of here ASAP. But soon other senses intervene and we begin to mesh with this new reality. Perhaps a tall copse of Shepherd's Purse. The sound of a small stream heard but not seen. The alluring shade of a nearby tree.
Disease as metaphor, disease as teacher.
3. Quantity has a quality all of its own.
Think of it like this: if you were pouring a concrete floor, it would be rather silly to start in one corner, pour a one-foot-square area, wait for it to cure and dry, and then move on to the next square. Not only would it be inefficient, but the floor itself would have very little structural integrity.
What should we do instead?
We'd pour 'skim coats' over the entire area, perhaps in several layers, trying to cover as much of the entire area as possible. Now, if I were insecure about my 'footing', and had to make the choice between standing on a one by one-foot-square of concrete or the first layer of a thin skim coat covering the entire area I might opt for the apparent security of the fully-completed one-foot square (and indeed, most testing is done on a person's ability to make the 'most perfect' one-foot square). Trouble is, I'm on a square of concrete that doesn't allow me to move anywhere else.
That's the problem with developing polymathic knowledge: there is an initial 'awkward stage' that many people find troubling, especially if they are insecure, or have been led to believe that all things taught to them must have immediate 'meaning'. However, there is a fix for this and a few of you have already figured it out:
Wonder is often compared to the emotion of awe but unlike awe wonder inspires joy rather than fear or respect.
So you might say that wonder is curiosity tinged with the prospect of potential joy.
Thus we have two choices with this week's assignments. We can moan about the amount of reading on what (after all) is just a clinic shift; start with the first article, tediously plow through it in workmanlike fashion, and then move onto the next, and the next.
This will take hours.
Or we can isolate the key concepts (in this instance I've supplied them: molecular chaperones and the process of n-glycation) gain a cursory understanding of these concepts and then skim through the articles, 'wondrously' luxuriating in areas that catch our attention and/or fit our model of the big picture. Each iteration (or skim coat) deepens knowledge and allows for the creation of more and more interconnectedness.
So, as you might gather, far from being onerous, polymathic behavior is a labor-saving device.
The British biologist Conrad Hal Waddington conceived of genotype (your genetic plan) passing through environment into phenotype (the physical you) as a walk through an 'Epigenetic Landscape'. He conceived a mode of visualizing this process, in which phenotype development is seen as marbles rolling downhill. In the beginning development is plastic, and a cell can become many fates. However, as development proceeds, certain decisions cannot be reversed. This Landscape has hills, valleys, and basins and marbles compete for the grooves on the slope, and eventually coming to rest at the lowest points, which represent the eventual types of tissues they become.
The Epigenetic Landscape. (After Waddington, C. H., 1956, Principles of Embryology)
Waddington was a big thinker. Not only did he visualize development as passing through the peaks, slopes and valleys of the Epigenetic Landscape, he considered this process one of increasing constraint, or as being "canalizedâ€? as he referred to it: That the early choices influence the later options. If we think of the canals of Venice, the analogy works even better; our little gondola floats from one canal into another and then another. Each choice leaves it fewer options than before, and since gondolas need water, so we can't just pick it up and put plunk it into another canal.
Now just for a moment visualize a newly fertilized egg. It already contains all the wisdom and information needed to eventually go on to produce a completely formed human being in its DNA, but over time it must develop various cell lines (called germ layers) that can then go off and further distinguish themselves as arteries, nerves and organs. Its unfolding is stochastic (a process that is non-deterministic in the sense that the current state state does not fully determine its next state.).
"Stochastic" is one of those great words that is more often misunderstood than understood. It is often quoted as being synonymous with random, but the actual Greek seems to imply something closer to "unknowable." It's often used in the arts (very often in music composition.)
In short: We know it's going to happen; we just don't know what is going to happen.
Your journey from genetic imprinting (the genes that were determined at conception) to full phenotype (the physical you) is to a great degree a stochastic process. which is why Waddington's metaphor is so great. Any architect will tell you that a house almost never winds up like that original plans. Environmental variables (cost of materials, availability) alter reality as the construction project moves from one stage to the other. We cannot always predict the eventual outcome, but we can describe and learn about the landscape in which it takes place and that, to a degree allows us to understand things.
Hindsight is always 20/20, because the outcome almost always describes the process.
That journey started long before your conception, since epigenetic gene control is hereditable.
You are in essence, not what you eat, but rather what your parents, grand parents and even great grandparents ate. Unlike defective genes, which are damaged for life, epigenetically controlled genes can be repaired. And, activation and silencing tags that are knocked off can be regained via nutrients, drugs, and enriching experiences. (1)
Conceivably the cancer you may get today may have been caused by your grandmother's exposure to an industrial poison 50 years ago, even though your grandmother's genes were not changed by the exposureâ€¦ or the mercury you're eating today in fish may not harm you directly, but may harm your grandchildren (2)
These inherited traits can continue to influence the onset of diseases like diabetes, obesity, mental illness and heart disease, from generation to generation.
All in all, the next few years should prove most interesting...
The post-genomic era, which is fueled by automation and other technologies, provokes a change in our grossly naive view of genetic determinism (that single genes govern complex traits) to the obvious reality that most human diseases are complex entities. Gene(s), although necessary, contribute only partially to disease, while environmental factors, lifestyles, epigenetics and epistasis significantly influence pathophysiology and, eventually, the expression of transient biomarkers that can be utilized for diagnosis and prognosis. Human osteoarthritis and rheumatoid arthritis are multifactorial, complex diseases. The genetic inheritance of these diseases remains elusive, although they tend to run in families wherein some siblings have a two- to tenfold increased risk of developing the diseases.
From: Future of genomics in diagnosis of human arthritis: the hype, hope and metamorphosis for tomorrow
Ashok R Amin?, Seth D Thompson? & Shailey A Amin
August 2007, Vol. 2, No. 4, Pages 385-389
Epigenetic alterations have been known to be of importance in cancer for ~2 decades. This has made it possible to decipher epigenetic codes and machinery and has led to the development of a new generation of drugs now in clinical trials. Although less conspicuous, epigenetic alterations have also been progressively shown to be relevant to common diseases such as atherosclerosis and type 2 diabetes. Imprinted genes, with their key roles in controlling feto-placental nutrient supply and demand and their epigenetic lability in response to nutrients, may play an important role in adaptation/evolution. The combination of these various lines of research on epigenetic programming processes has highlighted new possibilities for the prevention and treatment of metabolic syndrome.
From: Nutritional Epigenomics of Metabolic Syndrome
Catherine Gallou-Kabani, and Claudine Junien
Diabetes 54:1899-1906, 2005
1. Asim K. Duttaroy Evolution, Epigenetics, and Maternal Nutrition 2006 Darwin Day Celebration.
2. Montague T. A New Way to Inherit Environmental Harm. Synthesis/Regeneration 39 (Winter 2006)
This Transfusion: Sword swallowers and sore throats | ABO in Neanderthals| Blood groups and endometriosis | Nutrigenomics and personalized diets | This News This Week
Welcome to The Weekly Transfusion, 1.6 for the week of April 26, 2009.
Sore throats more common in sword swallowers
Sword swallowers run a higher risk of injury when they are distracted or adding embellishments to their performance, but injured performers have a better prognosis than patients who suffer iatrogenic perforation....Major gastrointestinal bleeding sometimes occurs, and occasional chest pains tend to be treated without medical advice. Sword swallowers without healthcare coverage expose themselves to financial as well as physical risk.
I guess it is just that old 'occupational hazard' story, sort of like the study that discovered that woodpeckers don't seem to get headaches.
Genetic characterization of the ABO blood group in Neanderthals
The high polymorphism rate in the human ABO blood group gene seems to be related to susceptibility to different pathogens. It has been estimated that all genetic variation underlying the human ABO alleles appeared along the human lineage, after the divergence from the chimpanzee lineage. A paleogenetic analysis of the ABO blood group gene in Neandertals allows us to directly test for the presence of the ABO alleles in these extinct humans. We have analysed two male Neandertals that were retrieved under controlled conditions at the El Sidron site in Asturias (Spain) and that appeared to be almost free of modern human DNA contamination. We find a human specific diagnostic deletion for blood group O (O01 haplotype) in both Neandertal individuals. These results suggest that the genetic change responsible for the O blood group in humans predates the human and Neandertal divergence. A potential selective event associated with the emergence of the O allele may have therefore occurred after humans separated from their common ancestor with chimpanzees and before the human-Neandertal population divergence.
Certainly one of the major evolutionary advantages of being blood type O was their double-barreled antibodies; this blood type being the only one that reacts to both “A things” and “B things” in the environment. This probably provided an extra layer of protection against any number of epidemic diseases (plague, smallpox) and many endemic ones (flukes and parasites) as well. If this immune “hyper-vigilance” would go on to increase the rates of inflammation and auto-immune disease in their modern descendants, it should also be remembered that these are often diseases of later life, typically past child bearing and rearing age. Thus if it were a late-model alteration, it certainly provided a significant survival advantage. The Founder Effect can be seen in the characteristics and distribution of the genes for Rhesus Negative and O blood type among the early Mesolithic Period during the so called- ‘Happy Paleo’ period, which also shows some correlation with the ancestral haplogroups R1b and I. On the other hand blood type A seems to have conveyed a better chance of surviving the ‘lean’ period of the early Neolithic; a slightly different, perhaps better way to starve. Type A’s more tolerant immune system may have given them the benefit when it came widening the diet and exploring new foods.
ABO and Rh blood groups distribution in patients with endometriosis.
The blood group A was more predominant in women with endometriosis, while blood group O was less predominant. The overall risk of women with endometriosis and A blood group was 2.89 (95%CI, 1.85-4.52). No significant difference was detected in ABO and Rh blood groups in women with endometriosis according to the severity of disease. CONCLUSION: Women with endometriosis have a 2.9-fold increased risk in the A blood group distribution. The role of blood groups in the development of endometriosis remains to be determined.
I verified the observation back in 1988, when we were observing whether increases in opposing blood group antibodies were associated with any reproductive illnesses. We observed that in our small endometriosis group, all women were type A, and all virtually had elevated antibodies to foreign blood types (in their case, blood type B ). It did seem at he time to be an area ripe for future research, but I never got back to it. It is nice to see that others have observed the same tendencies.
The antibodies in the ABO system (isoagglutinins) called anti-A and anti-B are not normally present at birth. The antibodies develop between 3-6 months of age due to the stimulation of the newborn’s immune system by microbes and foods that possess antigens of an opposing blood type. In, for example, type O children, they will begin forming to type A and B red cell antigens as soon as the child starts eating food, because the A and B antigens are actually found in quite a number of plants. So, as soon as the child starts eating plant food, she'll be exposed to those antigens and start making antibodies against them.
Nutrigenomics and Personalized Diet: From Molecule to Intervention and Nutri-ethics
The relationships between food, nutrition science, and health outcomes have been intensively analyzed over the past century. Genomic variation among individuals and populations is a new factor that enriches and challenges our understanding of these complex relationships. Hence, the rapidly emerging intersection of nutritional science and genomics - nutrigenomics - was the focus of a special issue of OMICS: A Journal of Integrative Biology in December 2008 (Part 1). The OMICS Nutrigenomics Special Issue (Part 2) February 2009 is The relationships between food, nutrition science, and health outcomes have been intensively analyzed over the past century. Genomic variation among individuals and populations is a new factor that enriches and challenges our understanding of these complex relationships. Hence, the rapidly emerging intersection of nutritional science and genomics - nutrigenomics - was the focus of a special issue of OMICS: A Journal of Integrative Biology in December 2008 (Part 1). The OMICS Nutrigenomics Special Issue (Part 2) February 2009 is now available free online
Two entire issues on personalized nutrition with virtually no mention of any of the bio-markers that really determine individualized dietary functionality: ABO blood groups and secretor status. Maybe these bio-markers are just too low-tech for the average scientist. More likely, the nay-sayers behind the smear campaign I've had to endure over the last ten years have had their desired effects.
No matter, if you read enough history you soon realize that Billy Shakespeare had it right: 'Truth will out.'
News of the Week
- April 28 2009: Dr. Peter D'Adamo - Lecture at Backus Hospitalthe basics of 'Eating Right For Your Type.' Open to the general public. More information
- June 5-7 2009: Personalized Medicine in Form and Function. A weekend intensive seminar with naturopathic physician, scientist and author, Dr. Peter J. D'Adamo in Norwalk, CT. This seminar provides training in personalized nutrition determination using blood grouping, secretor status, epigenetic indicators, dermatoglyphics and biometrics. Extensive overview of the latest clinical and laboratory techniques, information systems and pharmacology. Certification will also be offered. Presented by the Institute for Human Individuality. CME's may be available. More information. SEATING IS EXTREMELY LIMITED. RESERVE YOUR SEATS NOW!
Until next time.
This Transfusion: Parachutes and death from gravitational challenge | Hawthorn and heart disease | Blood group A and ovarian hyperstimulation syndrome | Rh blood group and hearing loss | Epigenetics, diet and super oxide dismutase (SOD)
Welcome to The Weekly Transfusion, 1.5 for the week of April 13, 2009.
Insufficient evidence for parachute use to prevent death and major trauma related to gravitational challenge
As with many interventions intended to prevent ill health, the effectiveness of parachutes has not been subjected to rigorous evaluation by using randomised controlled trials. Advocates of evidence based medicine have criticised the adoption of interventions evaluated by using only observational data. We think that everyone might benefit if the most radical protagonists of evidence based medicine organised and participated in a double blind, randomised, placebo controlled, crossover trial of the parachute.
Evidence based medicine is the buzz-phrase of the moment, the idea being that you scour the medical literature on a particular association,for example using the herb Hawthorn to treat chronic heart failure. You set the selection criteria, such as the type of study (placebo controlled, etc.) and the amalgamate the data. Evidence Basis has some very important advantages, namely that it gives the most accurate current assessment of a treatment or strategy since you are pooling all the available data.
One problem with evidence based medicine is the simple reality that evidence and benefit are not always the same thing. As shown by this slightly tongue in cheek study, there is still an insufficient evidence basis to conclude that parachutes are effective in preventing major trauma related to gravitational challenge. The researchers failed to find suitable studies showing the effects of using a parachute during free fall, despite setting logical criteria (death or major trauma, defined as an injury severity score > 15) and scouring he available literature.
Setting artificial standards can also impeded the workings of common sense: Edward Murphy put it best in his classic The Logic of Medicine: 'Only a fool would require a double-blind study to see if it was raining outside.'
Lack of evidence is not evidence of lack.
Evidence based medicine has potential to revolutionize day to day health care. However I think an even bigger revolution lurks under the surface: The reinterpretation and reorganization of medical facts derived under the older 'disease-care paradigm' by evolving paradigms that better fit new real-world circumstances.
A common argument against the need for heterodoxy in medicine is that 'when facts are proven, they stop being alternative.' This may well be true, but it neglects that facts themselves are forever open to reevaluation, deconstruction and recycling. Much of my work with the ABO polymorphisms was the simple reappraisal and restructuring of the conventional biomedical literature on the subject --but done with an eye to its ulterior benefits in naturopathic circumstances. Had they not been subjected to the 'naturopathic lens' these facts may well still be floating in their own splendid isolation.
Hawthorn extract for treating chronic heart failure
For the physiologic outcome of maximal workload, treatment with hawthorn extract was more beneficial than placebo... Exercise tolerance were significantly increased by hawthorn extract... The pressure-heart rate product, an index of cardiac oxygen consumption, also showed a beneficial decrease with hawthorn treatment... Symptoms such as shortness of breath and fatigue improved significantly with hawthorn treatment as compared with placebo...These results suggest that there is a significant benefit in symptom control and physiologic outcomes from hawthorn extract as an adjunctive treatment for chronic heart failure.
I first wrote about Hawthorn (Crataegus spp.) in my book Eat Right For Your Type over thirteen years ago, making specific reference to its benefit for blood group A individuals with cardiovascular problems. In general the plant has a good track record, especially, if used in quite low doses for extended periods of time. The herb seems to allow cardiac patients to derive extra benefit from exercise (link), has some very nice effects on the artery lining (link) and has been shown to lower blood pressure in patients taking diabetic medication. (link)
Hawthorn was shown to be well tolerated and safe. However, it should not be used as a substitute medication in circumstances of active heart disease or concurrently with other cardiac medicines unless under the supervision of a physician trained in its use. In one study, it actually seemed that the hawthorn group had a worse outcome than the placebo group. (link) Hawthorn also does produce occasional side-effects, though they appear uncommon and rather mild.(link) Perhaps this is the darker side of the biochemical individuality revolution; it's no longer acceptable to claim that all natural products are safe in every person. Anything that can add to the personalization of herbal recommendations can only help to increase their safety profile.
Blood type A women get more complications from fertility treatment
Ovarian hyperstimulation syndrome is a potentially life-threatening complication during controlled ovarian stimulation for fertility treatment. Since no association of this condition with ABO blood groups was known, we compared ABO antigens with severity and onset of symptoms in a case-control study...The odds ratio for patients undergoing controlled ovarian stimulation with blood group A versus O to develop the early-onset form of this condition was 2.171 (p-value 0.002). Blood group A may be associated with early-onset ovarian hyper-stimulation syndrome in Caucasians...This possible association may be considered for an individualized hormone dosing in controlled ovarian stimulation.
Ovarian hyperstimulation syndrome (OHSS) is a complication from some forms of fertility medication. Most cases are mild, but a small proportion is severe. Symptoms can range from a more mild form that includes abdominal bloating and feeling of fullness, nausea, diarrhea, and slight weight gain to a more severe form that includes and fullness/bloating above the waist, shortness of breath, urination significantly darker or cessation of urination altogether, calf and chest pains, marked abdominal bloating or distention, and lower abdominal pains. This study looked at 127 Caucasian patients hospitalized because of ovarian hyperstimulation syndrome after receiving in vitro fertilization, in the period from January 2000 to February 2007 and found that blood group A was markedly more frequent and blood group O less frequent in patients with ovarian hyperstimulation syndrome.
Other studies have found a slightly greater incidence of ovarian cancer in women who are blood group A (link) and blood group antigens (as mucins or 'blood group substances') are known to be richly deposited on ovarian tissue. (link) Hopefully fertility specialists will consider individualizing hormonal treatment by blood group when working with fertility patients.
Four patients developed thrombosis (clots) in the jugular or subclavian vein, none of whom had blood group O; this correlates with earlier studies linking blood groups other that type O with an increased risk of thrombosis (link) at some of this clotting may in fact be due to enhanced sensitivity to estrogen, at least in women who are not blood group O.(link)
What was that? Being Rh positive may increase your risk of hearing loss
Noise-induced hearing loss (NIHL) is one of the most common occupational problems and is one of the main causes of deafness. Many factors cause NIHL. Individual susceptibility is one of them. Rhesus (Rh) antigens and ABO blood groups can be factors in determining individual susceptibility. In conclusion, we suggest that the people with Rh-positive blood group are more prone to develop NIHL.
The researchers looked at factory workers who had been exposed to a noise level more than 85 dB for 8 hours a day for a period of over 15 years. Two hundred and nineteen (55.4%) of Rh-positive workers and seventeen (39.5%) of Rh-negative workers have noise-induced hearing loss, and the difference between the two groups was statistically significant (P < 0.05). There was no link between hearing loss and ABO blood type.
If you are a rabid reader of this blog, you'd immediately notice that these results are just ever-so-slightly statistically significant (and not be much of a discovery) since given enough noise, virtually anyone will develop hearing loss. However we could speculate that something in being Rh positive influences the structure of the ear anatomy to make these people more likely to get hearing damage. Or on the other hand, what is it about being Rh negative that makes these people less likely to get hearing loss?
An earlier study with infants and adults also showed a higher incidence of hearing loss in Rh positive people, with a slightly better level of significance (0.01) if the mother was Rh negative blood type (which might support the idea that the problem would then be seen in the incompatible Rh-positive children). Another maternal influence via blood group!
Diet influences epigenetic regulation of super oxide dismutase (SOD) gene
The impact of nutrition on the epigenetic machinery has increasingly attracted interest. The aim of the present study was to demonstrate the effects of various diets on methylation and gene expression. The antioxidative enzyme mitochondrial superoxide dismutase (MnSOD) was chosen as the model system because epigenetic regulation has been previously shown in cell lines for this gene. A 3-fold increase in the expression of the MnSOD gene was associated with decreased CpG methylation of the analyzed promoter region in the vegetarian group compared with the age-matched omnivores group. These results indicate that diet affects the epigenetic regulation of human MnSOD.
The super oxide dismutases are a class of enzymes that catalyze the conversion of free radical superoxide molecules into oxygen and hydrogen peroxide. They are an important antioxidant defense in nearly all cells exposed to oxygen. SODs 'outcompete' healthy tissue for the damaging free radical molecules. They protect the cell in a way reminiscent of a common scene in the the old Laurel and Hardy movies where two soldiers in a trench hoist a helmet on a stick above their heads and then retrieve it having been shot full of bullet holes. Although SOD supplements are a common item on health food store shelves, oral SOD products are completely destroyed in the gut, so methods to increase the native (endogenous) production in our own cells would be optimal.
Epigenetics is best explained as the 'non-genomic' or 'post-genomic' control of gene expression, mechanisms such as DNA methylation, or histone acetylation, which act a 'volume controls' on the ability of the cell to read the section of DNA that contains that gene. In the case of this study, the vegetarian group has less methylation on the CpG section of promoter region of the SOD gene.
In English, what they are saying is that diet removed some of the restrictions (methyl groups) on the part of the gene that activates it (the promoter region). Removing methyl groups usually takes the brakes off a gene, especially when they are in the gene's cystine-rich 'front.'
Exciting stuff. Now we'll need to see exactly which specific foods have the maximum epigenetic effects on SOD.
Until next week.
Note to readers: By mistake I had uploaded an earlier, non-spell-checked version of this entry on Monday. I beg your indulgence on this matter. Although I am a reasonably good speller, if truth be told I am a terrible typist.
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.