The big finger
January 30th, 2008 , by adminHere are a few more scientific studies which could pass for the more outlandish claims of The GenoType Diet. Finger digit ratios (the comparison of the lengths of the ring and index fingers) correlate with other facial structures used in The GenoType Diet, such as jaw angle and other asymmetries. Put it all together and you get (drum roll, please):
A GenoType!
The second-to-fourth-digit ratio (2D:4D) may be related to prenatal testosterone and estrogen levels and pubertal face growth. Several studies have recently provided evidence that 2D:4D is associated with other-rated facial masculinity and dominance, but not with facialmetric measures of masculinity. We found that localized face shape differences, shown here to be sexually dimorphic* and related to ratings of dominance, were associated with direct and indirect measurements of 2D:4D. In this study we examined various localized features of the face, showing nose width, jaw angle, and lip height to be sexually dimorphic. We then had faces rated for dominance and saw that the most dimorphic characteristics were those most associated with rated dominance, with typically masculine characteristics tending to be associated with high ratings of dominance. Finally, 2D:4D measurements were made using three different techniques. High (feminine) values of 2D:4D were associated with feminine facial characteristics in women, but not in men. It was concluded that certain aspects of facial development are governed by factors that are established prenatally. These aspects may be associated with perceptions of the self by others that are important in the social environment, particularly in terms of intra-sexual competition and mate acquisition.
* Dimorphism is the systematic difference in form between individuals of different sex in the same species.
2D:4D and sexually dimorphic facial characteristics. Arch Sex Behav. 2007 Jun;36(3):377-84.
The average human male face differs from the average female face in size and shape of the jaws, cheek-bones, lips, eyes and nose. It is possible that this dimorphism is determined by sex steroids such as testosterone (T) and oestrogen (E), and several studies on the perception of such characteristics have been based on this assumption, but those studies focussed mainly on the relationship of male faces with circulating hormone levels; the corresponding biology of the female face remains mainly speculative. This paper is concerned with the relative importance of prenatal T and E levels (assessed via the 2D : 4D finger length ratio, a proxy for the ratio of T/E) and sex in the determination of facial form as characterized by 64 landmark points on facial photographs of 106 Austrians of college age. We found that (i) prenatal sex steroid ratios (in terms of 2D : 4D) and actual chromosomal sex dimorphism operate differently on faces, (ii) 2D : 4D affects male and female face shape by similar patterns, but (iii) is three times more intense in men than in women. There was no evidence that these effects were confounded by allometry or facial asymmetry. Our results suggest that studies on the perception of facial characteristics need to consider differential effects of prenatal hormone exposure and actual chromosomal gender in order to understand how characteristics have come to be rated 'masculine' or 'feminine' and the consequences of these perceptions in terms of mate preferences.
Second to fourth digit ratio and face shape. Proc Biol Sci. 2005 Oct 7;272(1576):1995-2001.
Sex steroids are supposed to moderate the differences between male and female facial characteristics. Studies on women's preferences for male faces reported increased preferences for facial architecture developed under the influence of testosterone as this may indicate masculinity, dominance and social status. Recent research demonstrates that facial sexual dimorphism does not only develop at puberty but may be organized much earlier in ontogeny. However, the actual cause and timing of variation in facial shape due to sex-steroids remains speculative. This study uses data from Neave and colleagues who measured digit ratio (2D:4D) as a proxy to prenatal testosterone and also salivary testosterone samples in order to study differential effects of androgens on perceived male facial shape. Male facial shape was regressed upon 2D:4D ratio and circulating levels of testosterone by means of geometric morphometric methods. We found some evidence for opposite effects of early androgen action (via 2D:4D ratio) on the upper and the lower face respectively (i.e. low 2D:4D ratio results in a relatively robust and prominent lower face), whereas circulating testosterone seems to cause a rather uniform elongation of the face. Local deformations primarily show pronounced and medially tailed eyebrows for the shapes associated with increasing salivary testosterone. These preliminary results suggest that prenatal and pubertal testosterone have differential effects on male facial shape that should be considered in future studies on women's preferences towards male facial appearance.
Visualizing facial shape regression upon 2nd to 4th digit ratio and testosterone. Coll Antropol. 2005 Dec;29(2):415-9.
Deviations of physical characteristics from bilateral symmetry, in otherwise symmetric individuals, are supposed to result from environmental perturbations during development. One cause of such perturbations may be sex steroids such as testosterone and estrogen. AIM: The study examined the relationship between second to fourth digit ratio (2D:4D), a putative negative correlate with prenatal testosterone and a positive correlate with prenatal estrogen, and asymmetry. METHODS: Eleven traits (including the second and fourth finger lengths) were measured in a sample of 680 English children aged 2-18 years, and second to fifth finger lengths in samples of 120 Austrian and English undergraduate students aged from 17 to 30 years and 213 Polish adults aged from 26 to 90 years. RESULTS: Significant U-shaped curvilinear associations between 2D:4D and all 11 traits were found in English children with the strongest associations between 2D:4D and composite asymmetry of second plus fourth digit, and second to fifth digits. Further investigation of the relation between 2D:4D and digit asymmetries in the sample of Austrian and English undergraduates and the Polish adults confirmed significant U-shaped relationships between 2D:4D and finger asymmetries. CONCLUSION: Our data show that both low 2D:4D (a marker of high prenatal testosterone) and high 2D:4D (a marker of high prenatal estrogen) are associated with elevated levels of asymmetry and this relationship applies particularly to finger asymmetry.
The second to fourth digit ratio and asymmetry. Ann Hum Biol. 2006 Jul-Aug;33(4):480-92.
Which diet system is best for you?
January 25th, 2008 , by admin
Perhaps you are a long time Blood Type Dieter and you're thinking of moving onto The GenoType Diet. Perhaps you've just heard about The GenoType Diet, but did not know about my New York Times bestseller, Eat Right For Your Type, the book about eating according to your blood type.
So.. which one is right for you?
Although they have very great similarities, the Blood Type Diet series of books and the new GenoType Diet book are actually two distinct dietary systems, which complement each other but work through different mechanisms.
Well, I've made it easy! Just complete the little quiz below and press the 'Find Out' Button. I'll tell you which book I think will be best suited for your needs.
Sound bites
January 24th, 2008 , by adminEven USA Today is getting into the finger measuring business, though their recommended technique is not very accurate. And some of the more recent articles on epigenetics appearing in Medline are reading like sound bites for The GenoType Diet:
Medical practice patterns which are designed to provide quick and effective amelioration of signs and symptoms are frequently not an enduring solution to many health afflictions and chronic disease states. Recent scientific discovery has rendered the drug-oriented algorithmic paradigm commonly found in contemporary evidence-based medicine to be a reductionist approach to clinical practice. Unfolding evidence appears to support a genetic predisposition model of health and illness rather than a fatalistic predestination construct - modifiable epigenetic and environmental factors have enormous potential to influence clinical outcomes. By understanding and applying fundamental clinical principles relating to the emerging fields of molecular medicine, nutrigenomics and human exposure assessment, doctors will be empowered to address causality of affliction when possible and achieve sustained reprieve for many suffering patients.
-'Our genes are not our destiny: incorporating molecular medicine into clinical practice.' J Eval Clin Pract. 2008 Feb;14(1):94-102.
A wealth of evidence points to the diet as one of the most important modifiable determinants of the risk of developing cancer, but a greater understanding of the interaction between diet and genes may help distinguish who will and will not respond to dietary interventions. The term nutrigenomics or nutritional genomics refers to the bidirectional interactions between genes and diet. Nutritional genomics encompasses an understanding about how the response to bioactive food components depends on an individual's genetic background (nutrigenetics), nutrient induced changes in DNA methylation, histone posttranslational modifications, and other chromatin alterations (nutritional epigenetics), and nutrient induced changes in gene expression (nutritional transcriptomics). These approaches to the study of nutrition will assist in understanding how genetic variation, epigenetic events, and regulation of gene expression alter requirements for, and responses to, nutrients. Recognition of the interplay between genes and diet could ultimately help identify modifiable molecular targets for preventing, delaying, or reducing the symptoms of cancer and other chronic diseases.
'Nutritional genomic approaches to cancer prevention research.' Exp Oncol. 2007 Dec;29(4):250-6
Obesity and type 2 diabetes arise from a set of complex gene-environment interactions. Explanations for the heritability of these syndromes and the environmental contribution to disease susceptibility are addressed by the "thrifty genotype" and the "thrifty phenotype" hypotheses. Here, the merits of both models are discussed and elements of them are used to synthesize a "thrifty epigenotype" hypothesis. I propose that: (1) metabolic thrift, the capacity for efficient acquisition, storage and use of energy, is an ancient, complex trait, (2) the environmentally responsive gene network encoding this trait is subject to genetic canalization and thereby has become robust against mutational perturbations, (3) DNA sequence polymorphisms play a minor role in the aetiology of obesity and type 2 diabetes-instead, disease susceptibility is predominantly determined by epigenetic variations, (4) corresponding epigenotypes have the potential to be inherited across generations, and (5) Leptin is a candidate gene for the acquisition of a thrifty epigenotype.
'The thrifty epigenotype: An acquired and heritable predisposition for obesity and diabetes?' Bioessays. 2008 Feb;30(2):156-66.
Compared to other periods of life, infancy is a period of rapid growth, but the relative relationships among rates of linear growth, weight accretion and brain growth vary greatly during the first years of life. Additionally, while the energy requirements for body tissue deposition as a fraction of daily energy needs decrease dramatically during infancy, brain energy demands, measured as the cerebral rate of glucose utilization, increase markedly during the same period. There is now substantial evidence that postnatal growth in infancy is associated with various consequences detrimental to health in adult life, particularly hypertension, cardiovascular disease, obesity and type 2 diabetes, but the relationships vary depending on whether one takes growth to mean statural growth or ponderal growth, as well as on the specific period of infant growth. Recently, several mechanisms have surfaced that might account for the relationships observed. These include epigenetic effects on gene expression, alterations in neuronal signaling because of inappropriate dendritic pruning, and gut microbiota effects on fat storage.
'Growth in the first two years of life.' Nestle Nutr Workshop Ser Pediatr Program. 2008;61:135-44.
Reversible karma
January 18th, 2008 , by adminTwelve years ago when I was writing Eat Right For Your Type I used to Google (although there was no actual Google at the time; I used Excite) the phrases personalized medicine and personalized nutrition. At the time there were virtually no references. Now they number in the tens of thousands. However, Eat Right For Your Type was among the first books to ever use this concept.
With the The GenoType Diet, I've been instead googling the phrase Intergenerational Medicine and seeing about as much. Mark my words: in ten years you will see this phrase also appearing in the tens if not hundreds of thousands.
I often quote these citations when I lecture. Of course it would be most interesting to eventually learn what the author of the last abstract might consider an enriching experience.
Environmental influences can be inherited even without any mutations in the genes themselves. If genetic mutations are ‘typos' and relatively easy to test for, epigenetic changes are analogous to the formatting of the text (e.g. font, size, and color) and are much less well understood.
- Montague T. A New Way to Inherit Environmental Harm. Synthesis/Regeneration 39 (Winter 2006)
Mother rats exposed to hormone-mimicking chemicals during pregnancy gave birth to four successive generations of male offspring with significantly reduced fertility. Only the first generation of mothers was exposed to a toxin, yet four generations later the toxic effect could still be detected .
- M. Anway, A. Cupp, M. Uzumcu, and M. Skinner, Epigenetic Transgenerational Actions of Endocrine Disruptors and Male Fertility, Science Vol. 308, June 3, 2005, pp. 1466–1469.
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 exposure… or the mercury you're eating today in fish may not harm you directly, but may harm your grandchildren. These inherited traits can continue to influence the onset of diseases like diabetes, obesity, mental illness and heart disease, from generation to generation.
- Montague T. A New Way to Inherit Environmental Harm. Synthesis/Regeneration 39 (Winter 2006)
Global decrease in methylation levels is commonly observed in aging cells, as well as in neoplasia (early event.) The causes of this hypomethylation are not known. Contributes to chromosomal instability in cancer and to increased expression of selected affected genes. Unlike defective genes, which are damaged for life, methylated genes can be demethylated. And, methyl tags that are knocked off can be regained via nutrients, drugs, and enriching experiences.
- Asim K. Duttaroy Evolution, Epigenetics, and Maternal Nutrition 2006 Darwin Day Celebration.
Who heals is right!
January 17th, 2008 , by adminLast night I gave a second lecture at the Wilton Library. This was sponsored by the library and open to the general public, so I was surprised and pleased to see standing room only. Despite the fact that I wasn't exactly feeling all that terrific (exhaustion from doing 17 radio interviews the day before and perhaps a bit of food poisoning as well) I gave what I think was one of my best lectures ever. Funny how all the fatigue, aches and pains disappear in me when it's time to talk about this material. Expression really is the best medicine. Signed a lot of books, which were supplied by the local town book shoppe, who sold out their stock. This is a really good thing since Wilton is one of the few towns that still has a local bookseller, versus most towns with their B&Ns and Borders, who have taken over the industry.
Random House has made available a small number of signed first editions of The GenoType Diet. You can read more about it here. They cost a bit more than the jacket price of the book, but I will be donating any of my royalties to a wonderful charity in Africa that helps women develop entrepreneurial skills. Teach an person to fish.. and all that.
Yesterday featured an interesting day of sorts. The amazon.com 'Health Bestsellers' featured 5 books that I have written as part of their top 25 bestselling health books. Cool.
Got a very nice note from Professor Gerhard Uhlenbruck, who had received his copy of The GenoType Diet. The good professor (the only scientist I have meet who has read Emil Cioran) shared these thoughts:
When I worked in the earlier sixties at the Lister Institute of Preventive Medicine in London, my famous teacher, Prof. Dr. W.T.J. Morgan, who elucidated the biochemical structure of the ABH(O) and Lewis blood group antigens, used to say at various occasions: "Its all in the genes!". In fact, having experience in more than 50 years in clinical science and immunochemical research, I was so often confronted with this sentence, that it became a credo to me with the value of a proverb, which explained so many phenomena of patients and their very different reactivity to the susceptibility of illnesses, chronic diseases and early aging processes. When I first heard of Peter D'Adamo's blood group diet, of course I was very skeptical: Should we have missed in our book (Prokop/ Uhlenbruck: Human Blood and Serum Groups) such an important aspect? But years later, my interest switched to the nutritional field while working on the so-called Metabolic Syndrome, my interest increased in studying the role of genes in metabolic processes. I found out, that Peter D'Adamo's blood group orientated diet could probably be a first step in the right direction, however it could not be the whole story.
So I was not surprised at all, when now a book on The Genotype Diet by him was published as a next step in this new area. And I am sure it will not be the last one by him, as the role of genes and a subsequent personal, individual view of illness, diseases and health, including aging problems, has widened the approach of medical treatment, lifestyle change and a healthy nutrition.. We all live driven by our genes, sometimes feeling to suffer under their government,, and sometimes having the wish to change over our genetic outfit, to jump over the hurdle of genes or to influence their expression. Fat is not fate! I can confirm Peter D'Adamo in so far, as I have own experience in sport medicine, exercise immunology and in treating the Metabolic Syndrome.
According to the vision of D'Adamo, it seems also to me, that we can switch on the "good genes" and turn off the bad ones. In this context we must keep in mind that more than fifty percent of all illnesses are due to an inadequate nutrition. We know now much about anti-aging genes, which can be influenced by lifestyle (exercise) or by nutrition (as a curious example the action of red winew has been investigated). Looking on Peter D'Adamo's six Genotypes, being a medical doctor too, I must admit and I am a little bit amused, that one has so often met such types in the general medical practice. In any case, the book of D'Adamo is very stimulating, full of new ideas and creative concepts. Of course it will rise criticism and controversy, but at least I have observed, that people are very faithful to these diet suggestions, much more than to other diet programs: Who heals is right?
The sentence "Its all in the genes" has to be enlarged in that way that "its all in genes we ca influence". In this respect, Peter D'Adamo's approach is very optimistic, but this may be good in order to motivate people. To alter the genetic destiny is an old dream of mankind. What can be done in this direction, is limited but very understandably outlined in this book, written in a fascinating language and produced with many pictures and tables. It demonstrates also the profound knowledge of the author, its not a superficial "quicky", but with the aim not to become something like a dogmatic "bible", but a guidance book: Health as a creative process by activating personal thoughts and ideas about a longer healthy life, which is not permanent under the threat of disease. Life-style change means a revolution in the
personal life history.We generally have the freedom to decide on our health. This book is showing a way, walking this way we must do alone, personally, guided by the genes we activate or suppress. Let me put it together: A person can keep healthy, fit and wise, by doing his diet and daily exercise! What motivates him maybe modified individually and in future. So I can recommend this book of my colleague as a start for a personal, individual life-style change. And
for that it is never too late.
What I so like about this guy (and surprisingly for an academic) is that he understands that there is a bigger game to be played, a greater goal to be achieved, in writing books such as the GTD than just winning some sort of nebulous intellectual argument between scholars. That is important too, but more often than not it is also irrelevant.
Who heals is right. Gotta love that.

