The Scientist

I am an enthusiastic embracer of the broad concept of evolution. The only unasailable definition it that I have been able to reconcile myself to is "change." Aside from that definition, the details in contest are controverted hotly, with each side claiming its unfalsifiable first premise to be self-evident. With all due respect for Sir Isaac, any holder of any scientific model that is unfalsifiable, and who gets emotional about it is dogmatic. Whenever I pose questions such as those I am about to pose, I seem to find myself being attacked by both philosophical-only polarities. I say, let evidence speak for itself, and let interpretations be free of unfalsifiable biases. That having been said, perhaps the following questions that agonize me be stood on their own feet. Okay? Thank you. Now here is something that digs and digs at my curiosity: Why do some writers (some claiming scientific expertize, and others claiming a duty and an obligation to write whatever will sell to the general public, and still "report" what is going on in science somewhat reliably) talk about "adaptation" as though members of a species, or a species as an aggregation of all its members, do something to adapt? In genetics, it seems empirically "established" that germ line cells, despite being influenced by some epigenetic factors, are unable to observe, measure, appraise, evaluate... or otherwise have any awareness of the particularities of environmental stresses on their hosts. Correct me if I'm wrong, but we do agree, do we not, that, insofar as "determining" what mutations will occur is concerned, germline cells are totally out of touch. If we agree on that, then let me go another step and ask this: Do we not also agree that the entire idea of fitness surrounds longterm, that is multi-generational reproductive success... or, make that success in proportion to "competing" species for any given niche, or spectrum of niches. Please bear with me, but this is all leading up to a question is IS PERTINENT TO THE SUBJECT ARTICLE. It just requires at least this much background to put it into perspective. Continue then to the issue that if mutations are random, then any species gets the luck of the draw. Most mutations are deleterious in one way or another. Some, are neither beneficial nor deleterious, but are just a little different phenotype. That kind of thing may, indeed, lead to a situation, over many, many such changes, wherein some birds of one color no longer get erotic over their cousins of another. That makes sense to me. But here is where I am unable to follow things said, or implied, by some writers (from inside and/or outside research)... Now, to further elucidate the complexity surrounding my bottom-line question, let me assert that it makes sense to me that, while the idea of random mutation is often credited with providing to a member of a species an advantage, it is not likely to be "preferentially conserved" unless it yields immediate advantage. Nothing original about that. Once the enormous odds against a random mutation not causing cancer, or providing some phenotype that doesn't make a darn one way or another, along comes one that yields a distinct immediate advantage. As each of these subsumptive "requirements" is added to the "adaptation" picture, the odds jump up, don't they? I'm not arguing that they do. I'm asking. So now comes my bottom-line question: Oh, wait, there is one more subsumptive that demands attention. Hopefully we agree that adaptation is not a straight-line process in which successive advantageous mutated phenotypes out-compete (sexual reproduction-wise)to the point of becoming the norm for the species, rather than the occasional anomaly, such that all species get more and more "fit." On the contrary, climate changes and competitive dynamics change over time and HENCE mutations that are conserved and proliferous are those that change their species in such a way as to CHASE the changes going on in the environment (or as a result of increasing so as to require new, and different territory, and thus to "radiate" into new conditions. Okay. Sorry it took so much background, but now I can ask the question that bugs me, and bugs me, and bugs me... It is this: ADDED TO ALL THE FOREGOING SUBSUMPTIVE REQUIREMENTS FOR SERENDIPITOUS RANDOM MUTATIONS TO COME ALONG AND SAVE THE DAY FOR A SPECIES, WHAT ABOUT THE ADDITIONAL ODDS-AGAINST FACTOR OF... are you with me here... ADAPTATION CHALLENGE-APPROPRIATE mutations. Picture a black polar bear species going through all sorts of mutations as what once was a warm north turning into "the frozen north." Members could get cancer. Members could grow a beak (and probably fail). Members could grow tusks. Members could grow longer eyelashes, or different colored eyes, or, more veins in the pads of the feet. But what are the odds against the adaptation challenge-appropriate mutations that would provide camouflage on snow, or provide a heavy enough coat to survive (and therefore be able to reproduce competitively) in temperatures double digits below freezing. Do you see the arithmetic or statistical nature of this question? Now, bringing this around to the article? It is really exciting to me to see at least one small new idea to how "adaptation" might have something besides random mutation to sever in place of germ line cells being able to observe, measure, analyze, and STRATEGIZE... which, although we often see articles and research papers using the term "adapt" almost as if it were a PROACTIVE process. But, here again, what are the ODDS that the changes wrought by new exposure of an imported species to local micro-organisms would chance to find serendipitous, adaptation challenge-appropriate "opportunistic" symbioses?\nI'm not saying it cannot happen. Something happens. But elephants' germ line cells, and those of tigers, and a few other endangered species, seem not to have a clue. They don't seem to have assessed the situation of being crowded out being sufficiently "needed" in the context of human population's doublings and redoublings. Of course, that's not how it works. In fact, I'm not sure anybody knows any solution to the rapid disappearance of species these days. But it's sort of sad, isn't it. Here they've come up with random mutations, just in the nick of time, again and again and again, over centuries, millenia, millions of years... else, they wouldn't be here. But now they don't seem prone to come up with anything impacting their germ cells that is adaptation challenge-appropriate. Maybe some mutation-selection vector might be the missing factor. Whatever writers of research papers may think, or those who are said to so-often get it wrong as to how biologists have things like this so well understood, on basis of a model that has all the answers. Gee whiz. I don't know the answer. But that's just half of it. I don't think any of us do... at least... not yet.

The evolution of sex ratios in the Sternorrhyncha (scales and relatives) is quite diverse and fascinating. Here is an example of how a symbiont might drive all sorts of evolutionary developments in one species and you sort of wonder whether there are more such dynamics elsewhere that might have led to the sessile life-style of some.

Randomness paradoxically gives organisms the opportunity to adaptively mutate each other.

is MARTHA S Hunter, not Molly.\n\nLink to the paper is dead.

I agree with Lawton. After Lamarck,s theory on evolution, in The Origin of Species, Darwin wrote: ?Natural selection can act only by taking advantage of slight successive variations; it can never take a leap, but must advance by the shortest and slowest steps?. Julian Huxley, a British scientist, published his landmark Monograph; ?Evolution: The Modern Synthesis in 1942?. This monograph brought Darwin?s ideas into the 20th century and incorporated a knowledge of genes that was emerging in this century in the light of Gregor Mendel?s experiments on inheritance (Monograph: Experiments with Plant Hybrids) at Hynčice (Vra?né) in the now Czech Republic. In the mid-century, Barbara McClintock discovered transposable elements where parts of the genome can jump around and cause mutations or alter the gene expression, skewing Mendelian ratios and inheritance patterns. \n It is well known that genotype manifests due to interaction of environment on genes resulting into phenotypes. These authors have discussed, for the last two decades, those environmental factors in general and nutrition in particular, could be important in the pathobiology of genetic variations and epigenetic inheritance, leading to emergence of chronic diseases of affluence (1,2) (Figure 1). In the Origin of Species, Darwin did not mention the role of nutrition in the evolution (3). However, it is not yet clear if the increase in chronic diseases is due to epigenetic inheritance or development of a phenotypes such as proinflammatory cytokines and transcription factors, due to interaction of thrifty gene (developed during scarcity) with environmental factors; excess of fat, refined carbohydrates in the diet (4) (Figure 2). It is possible that alteration in the methylation of genes can influence epigenetic inheritance. It has been proposed that dramatic adaptations can also occur, for instance in the form of major morphological changes which appear to be the cause of changes in structure from apes to man and various human races. It is not clear whether such adaptations may be responsible for the development of diseases or health or for development of man to humans.\n Phenotypic changes have been observed to occur rapidly in the last 100 years, among many species (1-6), although The Modern Synthesis emphasized that ? populations containing some level of genetic variations evolve via changes in gene frequency, induced mostly by natural selection. Evolutionary biology, biochemistry, genomics, developmental biology, systems biology and the impact of the environment on genes concerning mechanism of evolution have grown significantly. It is possible that some lineages have greater ?evolvability? than others, independent of how much baseline genetic variation is present. In this connection, heritable phenotype variations may depend on the biology and biochemistry of the genes as well as on their status of methylation and remethylation. Some populations have more genetic variations and greater susceptibility to environmental factors and enormous evolvability for adaptations than others. Therefore, they are expected to generate phenotypic variation more rapidly within a few generations. The influence of photosynthesis, flight and multicellularity can enhance the evolvability resulting into rapid inheritance. The ability to evolve at a different speed than other species needs some particular characteristics related to epigenetic inheritance.\n Epigenetic mechanisms, such as DNA methylation, can cause stable alterations in gene activity without changes in the underlying DNA sequence. DNA methylation is associated with silencing of transposons, imprinting and silencing of both transgenes and endogenous genes. DNA methylation can cause heritable phenotypic modifications in the absence of changes in DNA sequence. Environmental stresses can trigger methylation\nchanges and this may have evolutionary consequences, even in the absence of\nsequence variation. However, it remains largely unknown to what extent environmentally induced methylation changes are transmitted to offspring, and whether\nobserved methylation variation is truly independent. In mammals, resetting of DNA methylation takes place during early embryonic development. However in plants a considerable proportion of DNA methylation marks can be stably transmitted from parents to offspring for development of segregating phenotypes. In one experiment (5), genetically identical apomictic dandelion ( Taraxacum officinale ) plants were exposed to different ecological stresses, and apomictic offspring were raised in the common unstressed environment. Only methylation-sensitive amplified fragment length polymorphism markers were used to screen genome-wide methylation alterations\ntriggered by stress treatments to assess the heritability of induced changes. Various stresses, most notably chemical induction of herbivore and pathogen defenses, triggered considerable methylation variation throughout the genome and several modifications were faithfully transmitted to offspring. Stresses caused some epigenetic divergence between treatment and controls, but also increased epigenetic variation among plants within treatments. The findings indicated that stress-induced methylation changes are\ncommon and are mostly heritable and sequence-independent, and autonomous methylation variation may be readily produced. This highlights the potential of epigenetic inheritance to play an independent role in evolutionary processes, which superimposed on the system of genetic inheritance. \n A prion that results from the mis-folding of the Sup35 protein in the yeast; Saccharomyces cerevisiae, may serve as a conduit for evolution of novel traits and as molecular vehicle for evolvability. The functional domain of Sup35 is highly conserved in a variety of organismal groups which serves as a translation termination factor. It may also help ribosomes to recognize stop codons on mRNA and thus mediates the normal translation of proteins. The yeast cells, which have aggregates of prions, read through about 5 to 10 % of stop codons in a given cell, so the mis-folded prions are not able to function correctly. The mRNA may stick around longer in cells enabling the expression of more proteins, so the cells with prions can express normally silent sequences beyond the termini of genes or express different levels of normal proteins. These cells are capable of expressing a wide variety of phenotypes (6). This study (6) found that nearly half of the conditions having the prion (PSI) led to significant phenotypic effects in some of the strains, which uncovered previously-hidden phenotypic variation in the yeast cells. This variation was advantageous in some of the conditions to which yeast cells were subjected. It is possible that prion (PSI) may act as capacitor and potentiator of ?evolvability?, because switching into the PSI state sensitizes the yeast more efficiently to produce phenotypic diversity, with change in nutrition and other environmental conditions (6). \n The low ω-6/ω-3 fatty acid ratio, aminoacids and coenzyme Q10 present in the cell membrane to which species adapted during evolution, may have beneficial effects on DNA methylation and therefore on this phenotypic diversity. The prion (PSI) can pass from mother to daughter yeast cells when they divide either mitotically or meiotically despite lineage where they revert back to non-prion state selection, resulting into beneficial adaptations (6). Depending on the strain, this occurs naturally at every 100,000-1000, 000 cell divisions or so depending on the strain. There are more extreme phenotypes, if the cell is stressed-out of an organism, compared to a benign environment which may possibly be independent of natural selection but this is not yet established. It is also possible that ?natural selection? may not actually be ?natural? but it is our ignorance about the environmental factors that are causing phenotypic variations. This may be clearer from the evidence on the facilitation of genetic variation in a perspective of health and development of phenotypes related to diseases.\n\nENVIRONMENTAL FACTORS AND GENETIC VARIATION.\n\n About 15 million years ago our ancestor apes were eating mostly fruits, vegetables and seeds without any significant fat in the diet. Therefore, they adapted by evolving mutation for conversion of fructose from the fruit based diet to fat for metabolic functions, which allowed the apes to survive seasonal periods of famine, when the fruit and vegetable plants went bare. This epigenetic enheritance has become an adverse genetic variation for the modern man, although it was protective for the survival of apes. High fructose corn syrups and sugar, refined starches are rapidly converted to fat in the modern man because of this mutation, resulting into obese phenotype causing obesity, insulin resistance, type 2 diabetes and cardiovascular disease (CVD). Similar epigenetic enheritance has been observed among populations when they migrate from rural areas to urban environment and from developing countries of South Asia to developed countries, wherever South Asians have settled. The South Asians are known to be highly susceptible for central obesity, type 2 diabetes, insulin resistance and CVDs.\n A complex set of physical and chemical factors, coming into play during development, which can influence structures and functions that are beyond simple genome to phenotype translation (6-10). Several mechanisms have been proposed to explain facilitated variations including those related to oscillations of certain regulatory elements affecting segmentation in embryo and chemicals acting during development which can cause patterns of stripes or spots in the organism. In this connection, the role of nutrients causing birth defects and other biochemical phenotypes appear to be important. It seems that nutritional status of mothers and the psychological and physical environment during the perinatal period could be important influencers in the facilitated variations. These variations may spark faster evolutionary alterations compared to random mutations, because developmental changes can create additional phenotypes upon which selection can act. However, many of these random mutations may be due to less known environmental factors and astrochronobiological factors like solar activity, geomagnetic forces and nutrients excess or deficiency, developing according to time structures (1-4,11). These environmental factors may be important in the pathogenesis epigenetic enheritance. The basal metabolic rate, heart rate, blood pressures, platelet aggregation are greater in the morning in association with increased sympathetic activity whereas in the night, there is a reduction in these manifestations with increase in melatonin and parasympathetic activity (11). These circadian rhythms were evolved during evolution to adapt and to coordinate physiological needs during early period of development.\n There are complex gene interactions and sudden morphological reorganizations occur during development, and in experiments and natural setups, there is discordance between genotype and phenotype. In one study, house finches which were natives to deserts began spreading throughout the United States in the 1940s through the pet trade (7). The birds were tracked for 19 generations over a span of 15 years at a study site in Montana which showed that the population of birds was developing unique beak morphologies as adaptations to the new environment related to availability of foods, at a surprisingly rapid rate (7). The evolvability of the flinch to adapt rapidly to survive is clear from this evidence, which is a useful adaptation against the environmental factors related to housing, and the food available in the new habitats. The interacting embryonic processes resulted in an initial level of phenotypic variation greater than that predicted from underlying genotypic variation (7). The selection was essentially blind, during development of the egg, to the creation of the initial pool of phenotypic variation because it occurred only later when young birds began feeding on the foods available in their new habitat. The selection was able to determine which beaks were more or less suited to the environment which was related to the availability of foods, without looking into developmental process, by which this beak was produced, due to opportunity for diversification. There is a need to study the the quality of the food or method of eating or nutrient content responsible for this inheritance. \n\nEPIGENETIC INHERITANCE, A NEW PRESPECTIVE. \n\n Passing of phenotypic change to subsequent generations in ways that are outside the genetic code of DNA are described as multilevel inheritance. It is known that chromatin structure, remodeled histone proteins or methylated DNA, often mediated by environmental factors, can pass from parent to offspring without changing the actual sequence of the inherited genome. If epigenetic inheritance plays any role in evolutionary change, it should be possible to demonstrate that the changes last and are stable and cause heritable effects through several generations (8). In a experiment, two groups of genetically identical Arabodopsis plants (Brassicaceae) were exposed to either hot or cold conditions for two; P and F1 generations (9). The next generation; F2 from both groups was grown at normal temperatures, but the offspring (F3) from both groups were grown in either hot or cold conditions. The F3 plants grown in hot conditions and descended from P and F1 plants also grown in hot conditions produced five-fold more seeds compared to F3 plants grown in hot conditions but descended from cold treated ancestors ((9). These mutations may have occurred, due to epigenetic factors affecting flower productions and early stage seed survival, due to molecular adaptations, in these plants.\n\nNUTRITION AND INHERITANCE. \n\n In mammals, the example for epigenetic inheritance is the yellow agouti mouse, an epigenetic biosensor for nutritional and environmental changes. These fat and yellow mice owe their appearance to epigenetic modification that removes methyl groups from the normally methylated agouti gene (10). In a developing mouse fetus, if the above modification occurs shortly after fertilization, the baby mouse may exhibit the yellow fur and obese phenotype with greater risk of developing cancer and diabetes (10). However, the genetic code remains unchanged from normal mice. In this study, Waterland and Jirtle (10) altered the nutrient intake to serve as methyl group donors in mouse mothers, to cause methylation or demethylation of the agouti gene. Increased supplementation of choline, betaine, folic acid and vitamin B12 in the diet of pregnant yellow agouti mice was able to decrease the incidence of deleterious phenotypes in offspring, by donating methyl group and allowing for the remethylation of the agouti gene. If these mice be born with the agouti phenotype, they can pass that deleterious epigenetic trait in their offspring, regardless of their diet during pregnancy. This landmark study indicates that nutrients can cause phenotypic changes which can pass on through cell division and mating to the offspring due to their possible influence on (natural) selection (10). It is possible therefore to say; that we are what we eat and what our parents ate, and potentially what our grand parents ate which would be modification of the old Sanskrit saying ?Aham Annam? from the ancient Vedas (5000BCE). It may be also important to emphasize advances in Astrochronobiology particularly; time of eating, accordingly, therefore we are not only ?what we eat? but also ?we are when we eat? and when our father and grand father were eating (11). There is a need to study the effects of low ω-6/ω-3 ratio diet, arginine, taurine, cysteine, coenzyme Q10 on the remethylation of the agouti gene and their effects on phenotypic variations. However this mode of inheritance needs to penetrate more than a few generations before it earns a place in evolutionary concept. Epigenetic inheritance appears to be widespread but it does not mean that it lasts and causes ?evolutionarily? important effects. It is not clear until now, that if epigenetic changes are not stable for 20 to 30 generations, it would be relevant to evolution.\n Several experiments related to epigenetics are underway to establish the role of environmental factors in inheritance. Observing inheritance in 3 to 4 or more generations among patients of obesity, type 2 diabetes, hypertension and coronary artery disease appears to be important which would be clear from following cases.\n\nCASE 1. In 1975, we (RBS) examined a patient of obesity ( body mass index 27Kg/M2) and type 2 diabetes mellitus presented to us whose father also had a history of diabetes mellitus and died a sudden death. This 48 years old patient was, while under treatment (RBS) developed tightness in the chest and his electrocardiogram showed changes indicating myocardial ischaemia. He was treated and recovered but after a few months died a sudden cardiac death in 1977. His son who was about 40 years and obese presented with type 2 diabetes mellitus, while under treatment, also died a sudden cardiac death next year. Diet and lifestyle history showed that they have /had a wholesale business of selling clarified butter (anhydrous milk fat) during the time of the 1st generation, clarified butter and hydrogenated fat, during the 2nd generation which continued during the 3rd generation. Thus, albeit a single family, all the three generations were sedentary and were consuming more than 40% of calories from clarified butter which may have caused inheritance of deleterious phenotypes in the offspring, resulting in to type 2 diabetes and sudden death. The adverse effects of trans fat (unsaturated fats with trans-isomer fatty acids). and oxidized cholesterol present in the clarified butter consumed by the last three generations, on proinflammatory cytokines are well known and inflammation has been demonstrated to cause genetic damage. Sedentary behavior also enhances inflammation by its adverse effects on adiponectin, leptin and brain derived neurotrophic factor which are anti-inflammatory. Inflammation could be important in the pathobiology of epigenetic inheritance. Now RBS is tracking the son (4th generation) who is about 30 years, to look for type 2 diabetes mellitus and coronary artery disease who may be a future candidate for sudden cardiac death in the 4th degeneration because he and his baby are consuming clarified butter and high ω-6/ω-3 ratio diet by using sun flower oil and they continue to be sedentary. \n\nCASE 2. A 45 year old obese man presented in 1975 with hypertension (>150/95 mmHg) and albumineria and family history of hypertension and stroke causing death of his father. He had a heart attack in 1985 and died a sudden cardiac death after few months. His son presented with obesity and hypertension at the age of 29 years in 1995.\nWe need to study genetic markers in the 3rd and 4th generation to support this view. However, we need many more such observations and research because sufficient examples of transgenerational epigenetics are lacking. Most of the time, epigenetic characters are not inherited past one or two generations.\n\nTHE EVOLUTIONARY DIET, ENVIRONMENT AND DISEASES:\n\n During human development from apes to man, a fundamental view of evolution has been that the genetic makeup of contemporary humans shows only minor difference from that of the modern human, who appeared in Africa between 100,000 and 50,000 years ago (12, 13,16). However, during the past 50,000 years, the human evolution has been comparatively rapid as revealed by the molecular geneticists . There have been marked changes in the food supply with the development of agriculture about 10,000 years ago from now. However, only non-significant change in our genes occurred, during the past 10 centuries, due to presence of ω-3 fatty acids, amino acids, vitamins and minerals in the diet and non-significant changes in the environment (12-15). There have been some structural modifications in individual DNA sequences, and altered gene regulation has been the dominant mechanism involved. Increased evolutionary rapidity in humans compared with rates for other primates, has resulted from unprecedented demographic expansion, which has provided a far larger pool of mutations, upon which natural selection can operate. The human Diaspora which has exposed humans to environmental changes appears to be quite different from those of their ancestral land in Africa and this rapid change may predispose deleterious epigenetic inheritance (13-17). \n The spontaneous mutation rate for nuclear DNA is estimated at 0.5% per million years. Hence, over the past 10,000 years there has been time for very little change in our genes, possibly 0.005%. Our genes appear to be similar to the genes of our ancestors during the Paleolithic period 40,000 years ago, the time when our genetic profile was established. Man appears to live in a nutritional environment which completely differs from that for which our genetic constitution was selected. However, it was only during the last 100-160 years that dietary intakes and environment have changed significantly, causing increased intake of saturated fatty acids (SFA), trans fat and linoleic acid, and decrease in ω-3 fatty acids, from grain fed cattle, tamed at farmhouses, rather than meat from running animals. The food and nutrient intake among hunter-gatherers and during the Paleolithic period showed no remarkable differences. However, during the last 160 years, there is marked reduction in consumption of ω-3 fatty acids, vitamins and antioxidants and proteins and significant increase in the intakes of carbohydrates, (mainly refined,), fat ( saturated, trans fat, linoleic acid) and salt compared to Paleolithic period (1-4,12-19). There are also marked changes in the environmental factors and quality of food and nutrients which may also have deleterious effects on epigenetic inheritance (16-19).\n Humans evolved on a diet that was low in saturated fat and the amount of ω-3 and ω-6 fatty acids was quite equal.(14) Nature recommends to ingest fatty acids in a balanced ratio (polyunsaturated:saturated: ω-6:ω-3=1:1) as part of dietary lipid pattern in which monounsaturated fatty acids is the major fat(P:M:S=1:6:1).These ratios represent the overall distribution of fats in a natural untamed environment. (www.columbus-concept.com). Circulating plasma fatty acids, such as ω-6/ω-3 fatty acid ratio, gives an indication of proinflammatory status of blood vessels. Of major importance appear to be the essential dietary nutrients (essential amino acids, fatty acids, antioxidant vitamins and minerals) and the functional component of the regimen(diet, sport, spiritualism, etc) because these factors may be important in the epigenetic inheritance. An example is given of an essential dietary nutrient and of a functional component of man?s regimen that affect health in a predictive way derived from the 3D representation of blood cholesterol. Caption The Columbus Concept and its 3D representation of blood lipoprotein behaviours. "Bad" LDL-C, "good" HDLC, and "healthy" LDL-CC:HDL-CC ratios. CC= Columbus Concept. The Tsim Tsoum Concept is an extension of the Columbus concept. The word Tsim Tsoum is derived from Hebrew and it is similar to ?ying yang? in Chinese. (http://www.tsimtsoum.net/ editorials/tsimtsoum_editorial_2009-Kosice-14th-WCCN-and-5th-ICCD.pdf). It includes the simultaneous approach of controlling of Mind-brain- body connection and interactions of leptin, cholecystokinin, polyunsaturated fatty acid CoA, incretins, brain derived neurotrophic factor and neuropeptide Y secreted in the hypothalamus (16-19). The Tsim Tsoum Concept also presumes that if, and only if, diet and environmental factors are designed holistically, for individuals and populations or for any species, for several generations, they may be responsible for the alteration in biological functions causing epigenetic inheritance, resulting in the development of man to human and thence to superhuman. \n Recent studies indicate that food and nutrient intake, energy expenditure and body adiposity are homeostatically regulated (18,19). Central and peripheral Various signals from central and peripheral areas communicate information about the current state of energy balance to key brain regions, including the hypothalamus and brainstem (19). Hunger and satiety represent coordinated responses to these signals, which include neural and hormonal messages from the gut. Our understanding of how neural and hormonal brain?gut signalling regulates energy homeostasis has advanced considerably and it is possible that gut-brain- body connection may be regulated by genes. Gut hormones have various physiological functions that include specifically targeting the brain to regulate appetite. New research suggests that gut hormones can be used to specifically regulate energy homeostasis in humans, and offer a target for genetic modulation.\n In brief, it is possible that diet, mental strain, tobacco, alcoholism, radiation, pollutants, geomagnetic activity can induce adverse biological functions including genetic variations. If these environmental changes are subjected to species for several generations, they might predispose epigenetic inheritance of diseases. However, supplementation of w-6:w-3 fatty acids to achieve a ratio of 1:1 in the tissues with adequet choline, betaine, folic acid, and vitamin B12 as well as other essential amino acids, antioxidants and vitamins can modulate methylation of DNA resulting in to reduction in phenotypes for type 2 diabetes, obesity and CVD by epigenetic inheritance. More evidence is necessary to demonstrate the role of environment in the epigenetic inheritance for the development of obesity, insulin resistance, type 2 diabetes and CVD in this new perspective for health and diseases.\n\nAcknowledgements are due to Tsim Tsoum Institute, Krakow, Poland and International College of Nutrition for the support to produce this work.\n\nREFERENCES.\n\n1. Singh RB, Mori H. Risk factors for coronary heart disease: synthesis of a new hypothesis through adaptation. Med Hypoth 1992; 39:334-341.\n2. Mishra S, Singh RB, Dwivedi SP, De Meester F, Rybar R, Pella D, Fedacko J, Juneja LR. Effects of nutraceuticals on gene expression. The Open Nutra J 2009; 2:70-80.\n3. Singh RB. Darwin, evolution and origin of species. The Open Nutr J 2009;2: 86-87.\n4. Singh RB, Moshiri M, De Meester F, Juneja L, Muthusamy V, Manoharan S. The evolution of low w-6/w-3 ratio dietary pattern and risk of cardiovascular diseases and diabetes. JAMR 2011;3: ( In Press)\n5. Verhoeven KJF, Jansen JJ, van Dijk PJ, Biere A. Stress induced DNA methylation, changes and their heritability in asexual dendilions. New Phyto 2010;1108-1118. \n6. True HL, Lindquist SL. A yeast prion provides a mechanism for genetic variation and Phenotypic diversity. Nature 2000; 407: 477-483.\n7. Badyaey A. The beak of the other finch : Coevolution of genetic covariance structure and developmental modularity during adaptive evolution. Phil Trans Royal Soc 2010; 365: (in press)\n8. Jablonka F, Raz G. Transgenerational epigenetic inheritance: prevalence, mechanisms and implications for the study of heredity and evolution. Q Rev Biol 2009; 84:131-176.\n9. Whittle CA, Otto SP, Johnston MO, Krochko JE. Adaptive epigenetic memory of ancestral temperature regime in Arabidopsis thaliana. Botany 2009; 87: 650-657.\n10. Waterland RA, Jirtle RL. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol 2003; 23: 5293-300.\n11. .Halberg F , Cornélissen G, Otsuka K, Siegelova J, Fi?er B , Du?ek J, Homolka J, Salvador S, Peña DL, Singh RB and the BIOCOS project. Extended consensus on need and means to detect vascular variability disorders (vvds) and vascular variability syndromes (vvss). Intl. J. of GERONTO-GERIATRICS, 2008;11: 119-146. \n12. .Eaton B. Evolution and cholesterol. World Rev Nutr Diet 2009; 100: 46-54.\n13. De Meester F. Progress in lipid nutrition: the Columbus concept addressing chronic diseases. World Rev Nutr Diet 2009;100: 110-21. \n14. .Simopolous AP, Genetic variation and dietary response: nutrigenetics/ nutrigenomics. Asia Pac J Clin Nutr 2002,11:S117-S128.\n15. Eaton SB, Eaton SB III, Sinclair AJ, Cordain I, Mann NJ. Dietary intake of long chain polyunsaturated fatty acids during the Paleolithic period. In Simopoulos AP edition. The return of w-3 fatty acids in the food supply. Land based Animal Food Products and their Health Effects. World Rev Nutr Dietetics 1998; 83: 12-23.\n16. Simopoulos A. Evolutionary aspects of the dietary omega-6/omega-3 fatty acid ratio : medical implications. World Rev Nutr Diet 2009; 100:1-21.\n17. Kwiatek AW, Singh RB, De Meester F. Nutrition and behaviour: the role of w-3 fatty acids. The Open Nutra J 2010; 3:119-128.\n18. Thaler JP, Cummings DF. Metabolism: food alert. Nature 2008; 452: 941-942.\n19. Wang PY, Caspi L, Lam CK, Chari M, Li X, Light PE, Gutierrez-Juarez R, Ang M, Schwartz GJ, Lam TK. Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production. Nature 2008;452:1012-16.\n\n\n\n\n\n\n\n\n\n\n \n \n

I do not see how this article is demonstrating "instant evolution". \n\nThis isn't evolution as far as I can see, or at least the data presented here does not address whether this is evolution. This is selection, it seems, infected flies do better. Evolution is a process that results in a reproductively stable transmission of traits, and distinction of the organism from its ancestors (at least for now it would seem that the fundamental differences between species are genetically based, epi or otherwise). There is no evidence of that here. As far as I can see if you infect any white fly with this bacterium it would be beneficial. If so no evolution, this is the way these flies are now. If the current infected population responds differently to the bacteria than separated populations not infected/colonized (for example, if you were to infect these non-infected populations and they didn't benefit similarly), then we might be talking about an evolutionary event or stage.

Thank you for your comment. The senior author, listed on the paper as Martha S. Hunter, goes by the first name Molly, used here in the article and also in a press release from the University of Arizona.\n\nThe link to Science has also been fixed. \n\n-Megan Scudellari, author