Archives for: January 2008
A possible reason why the long headed GT5 Warriors are often taller than GT3 Teachers and GT4 Explorers:
In the article the development of skull measurements and head measurements (length and breadth) and of the cephalic index, calculated from these measurements, since the Neolithic period are presented. The results obtained from the historical material are compared with those of living persons. The measurements as well of the skull as of the head show secular changes. The following general trend was found: an increase of body height is connected with a debrachycephalisation* and a decrease of body height is connected with a brachycephalisation. It can be emphasized that brachycephalisation/debrachycephalisation are part of the secular trend. Therefore environmental factors are responsible for the described changes of measurements of the skull and the head in a broadest sense.
* Debrachycephalisation: the tendency for head shapes to become less 'square-like' and more elongated over succeeding generations. Brachycephalisation is the opposite.
Is head size modified by environmental factors? Z Morphol Anthropol. 1998;82(1):59-66.
A hypothesis is framed about which any influences of the nutrition may cause variations of the cranium, but concerning physiological data, kinds of nutrition and special victuals' ingredients cannot still be mentioned. If such connexions are proved, at last the well known brachycephalization among European populations since the Middle Ages and the beginning debrachycephalization in the present time could partially be interpreted.
The brachycephalisation problem, a nutrition constitutional problem? Gegenbaurs Morphol Jahrb. 1989;135(5):689-96.
Probably why GT4 Explorers usually are thicker boned than GT1 Hunters:
A growing body of archeological evidence suggests that the dramatic climatic events of the Last Glacial Maximum in Europe triggered important changes in foraging behavior, involving a significant decrease in mobility. In general, changes in mobility alter patterns of bending of the midshaft femur and tibia, resulting in changes in diaphyseal robusticity and shape. This relationship between levels of mobility and lower limb diaphyseal structure was used to test the hypothesized decrease in mobility. Cross-sectional geometric data were obtained for 81 Upper Paleolithic and Mesolithic European femora and tibiae. The sample was divided into three time periods: Early Upper Paleolithic (EUP), Late Upper Paleolithic (LUP), and Mesolithic (Meso). In addition, because decreased mobility often results in changes in sex roles, males and females were analyzed separately. All indicators of bending strength decrease steadily through time, although few of the changes reach statistical significance. There is, however, a highly significant change in midshaft femur shape, with LUP and Meso groups more circular in cross-section than the EUP sample, supporting archeologically based predictions of decreased mobility. Sexual dimorphism levels in diaphyseal strength remain low throughout the three time periods, suggesting a departure in Upper Paleolithic and Mesolithic foragers away from the pattern of division of labor by sex observed in modern hunter-gatherers. Results confirm that the onset of the Last Glacial Maximum represents a crucial stage in Late Pleistocene human evolution, and signals the appearance of some of the behavioral adaptations that are usually associated with the Neolithic, such as sedentism.
Mobility in Upper Paleolithic and Mesolithic Europe: evidence from the lower limb. Am J Phys Anthropol. 2003 Nov;122(3):200-15.
However marauding GT1 Hunters are on average, taller than glacial refugee GT4 Explorers:
Long bone lengths of all available European Upper Paleolithic (41 males, 25 females) and Mesolithic (171 males, 118 females) remains have been transformed into stature estimates by means of new regression equations derived from Early Holocene skeletal samples using "Fully's anatomical stature" and the major axis regression technique (Formicola & Franceschi, 1996). Statistical analysis of the data, with reference both to time and space parameters, indicates that: (1) Early Upper Paleolithic samples (pre-Glacial Maximum) are very tall; (2) Late Upper Paleolithic groups (post-Glacial Maximum) from Western Europe, compared to their ancestors, show a marked decrease in height; (3) a further, although not significant, reduction of stature affects Western Mesolithics. Evaluation of possible causes for the great stature of the Early Upper Paleolithic samples points to high nutritional standards as the most important factor. Results obtained on later groups clearly indicate that the Last Glacial Maximum, rather than the Mesolithic transition, is the critical phase in the negative trend affecting Western European populations. While changes in the quality of the diet, and in particular decreased protein intake, provide a likely explanation for that trend, variations in levels of gene flow probably also played a role. Reasons for the West-East Mesolithic dichotomy remain unclear and lack of information for the Late Upper Paleolithic of Eastern Europe prevents insight into the remote origins of this phenomenon. Analysis of regional differentiation of stature, particularly well supported by data from Mesolithic sites, points to the absence of today's latitudinal gradients and suggests a relative homogeneity in dietary, cultural and biodemographic patterns for the last hunter-gatherer populations of Western Europe.
Evolutionary trends of stature in upper Paleolithic and Mesolithic Europe. J Hum Evol. 1999 Mar;36(3):319-33.
Not because of shorter upper legs, but rather shorter lower ones..
Among recent humans brachial and crural indices* are positively correlated with mean annual temperature, such that high indices are found in tropical groups. However, despite inhabiting glacial Europe, the Upper Paleolithic Europeans possessed high indices, prompting Trinkaus (1981) to argue for gene flow from warmer regions associated with modern human emergence in Europe. In contrast, Frayer et al. (1993) point out that Late Upper Paleolithic and Mesolithic Europeans should not exhibit tropically-adapted limb proportions, since, even assuming replacement, their ancestors had experienced cold stress in glacial Europe for at least 12 millennia. This study investigates three questions tied to the brachial and crural indices among Late Pleistocene and recent humans. First, which limb segments (either proximal or distal) are primarily responsible for variation in brachial and crural indices? Second, are these indices reflective of overall limb elongation? And finally, do the Late Upper Paleolithic and Mesolithic Europeans retain relatively and/or absolutely long limbs? Results indicate that in the lower limb, the distal limb segment contributes most of the variability to intralimb proportions, while in the upper limb the proximal and distal limb segments appear to be equally variable. Additionally, brachial and crural indices do not appear to be a good measure of overall limb length, and thus, while the Late Upper Paleolithic and Mesolithic humans have significantly higher (i.e., tropically-adapted) brachial and crural indices than do recent Europeans, they also have shorter (i.e., cold-adapted) limbs. The somewhat paradoxical retention of "tropical" indices in the context of more "cold-adapted" limb length is best explained as evidence for Replacement in the European Late Pleistocene, followed by gradual cold adaptation in glacial Europe.
* Crural index is the result of multiplying the length of the lower leg (tibia) by 100 and dividing it by the length of the upper leg (femur).
Brachial and crural indices of European late Upper Paleolithic and Mesolithic humans. J Hum Evol. 1999 May;36(5):549-66.
Here 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):
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.
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.
Even 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.
Twelve 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 â€˜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. 1466â€“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 exposureâ€¦ 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.