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Evolution leads to phenotypic changes through changes in DNA such as mutations. Mutations are transmitted to offspring. Cumulative mutational changes across many generations may cause evolution and speciation.
As far as I know, epigenetic changes causes an individual to change in how it appears (phenotypic changes). In turn, epigenetic changes may be transmitted to offspring, just as DNA mutations can be.
Is epigenetics a factor in evolution?
To start I will repost some of an answer I have previously posted, which will explain what evolution is:
Evolution is simply a process of change. It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection.
"Evolution means change, change in the form and behaviour of organisms between generations… When members of a population breed and produce the next generation we can imagine a lineage of populations, made up of a series of populations through time. Each population is ancestral to the descendant population in the next generation: a lineage is an ancestor-descendent series of populations. Evolution is then change between generations within a population lineage." - Ridley, Evolution
Evolution depends on the inheritance of information from the ancestral population to the descendant population. Much of the time we talk about information in the form of genetic variation, the information contained within the DNA. However, more and more we are realising that other forms of information transmission can occur, including epigenetic effects, and that these can contribute to evolution.
"Epigenetic modifications are a bit like ornaments on a Christmas tree; the tree (the DNA sequence) is still the same, but the decorations (epigenetic modifications) change how it's perceived."…
"Over the past few years, several studies have compared the epigenetic modifications of our genome with that of other great apes, leading to an emerging picture of the importance of epigenetics in our recent evolutionary history."…
"The role of epigenetics in evolution (particularly primate evolution) is an active and exciting area of research… " - Nature Scitable
The edited question is also broad in scope, but one can narrow it down by talking about specific conditions. For example, the role of epigenetics markers helping in survival under stress conditions, especially in A. thaliana, has begun to be much appreciated.
Epigenetics could also potentially be an important mechanism facilitating developmental plasticity-formation of two or more phenotypes from the same genotype, a process which helps organisms to adapt to changing environments (Developmental Plasticity and Evolution-Mary Jane West Eberhard, Oxford Univ. Press 2003).
Under both scenarios described above, epigenetic changes could favour a differential success in survival (e.g. under stress) and/or reproduction (e.g. flowering) of individuals in a population as compared to animals without these markers, thus leading to evolution in the next generation.
The prevailing view in science is that genetic mutations cause cancer. These changes to a gene’s sequence (which can be caused by bad luck, inheritance, or exposure to a carcinogen, such as cigarettes) can alter a gene’s function and behavior leading a cell to become cancerous. However, epigenetic changes to genes can alter behavior too. A story on Futurism discusses how — in patients with a rare brain tumor called ependymomas — alterations to histones may be driving the disease. The knowledge could lead to new treatments.
Schizophrenia has a 50 percent concordance rate of illness in monozygotic (identical) twins, which means the disease has a strong genetic component. But it also suggests that genes don’t tell the whole story. Augusta University psychiatrist Brian Miller has an excellent discussion in the Psychiatric Times of the potential epigenetic causes of schizophrenia. One piece of evidence Miller points to is a large genome-wide DNA methylation study which found that in people with the disease there are significant abnormal methylation levels on several genes thought to be involved with the onset of the disease.
In November, the Royal Society hosted a meeting entitled “New Trends in Evolutionary Biology.” The purpose was to discuss changes to the theory of evolution. Before creationists get too excited, it should be noted that the intent was not to throw out Darwin’s seminal theory of evolution by natural selection — but to consider updating it with new insights, data and technologies. It’s not the first time scientists have done this. In the mid-1900s scientists met to add new understandings from the (at the time) emerging field of genetics. They left with what is called the Modern Synthesis.
Denis Noble now sees a need for an Extended Evolutionary Synthesis.Credit: Tom Parker for Quanta Magazine
Kevin Laland, who co-hosted the Royal Society meeting, and his colleagues believe Modern Synthesis needs to be expanded to included transgenerational epigenetic inheritance. They call their new theory of evolution the Extended Evolutionary Synthesis. Carl Zimmer covered the meeting for Quanta, and described some of the evidence presented:
The evidence for this effect is strongest in plants. In one study, researchers were able to trace down altered methylation patterns for 31 generations in a plant called Arabidopsis. And this sort of inheritance can make a meaningful difference in how an organism works. In another study, researchers found that inherited methylation patterns could change the flowering time of Arabidopsis, as well as the size of its roots. The variation that these patterns created was even bigger than what ordinary mutations caused.
“This strategy is to produce rapid evolutionary genome change in response to the unfavorable environment,” Oxford researcher Dennis Noble explained to the audience. “It’s a self-maintaining system that enables a particular characteristic to occur independent of the DNA.”
However, not everyone was convinced. David Shuker of the University of St. Andrews stood up and challenged Noble to explain a biological mechanism. It was something, Zimmer said, Noble struggled to do.
Douglas Futuyma of Stony Brook University in New York presented the opposing view, which he joked was “the Jurassic view of evolution.” Futuyma argued that the core principals of Modern Synthesis are strong. He left the door open for dialogue, but made a strong call for data over rhetoric, saying: “I think what we find emotionally or aesthetically more appealing is not the basis for science…There have been enough essays and position papers.”
Laland agrees, “It’s doing the research, which is what our critics are telling us to do. Go find the evidence.”
Epigenetic control mechanisms have been grouped into three broad classes, such as posttranslational histone modifications and chromatin remodeling, DNA methylation, and ncRNA interactions. The interplay of these mechanisms in intra- and internucleosomal interactions over short and long distances generate a variety of chromatin states. The sum of these mechanisms is fundamental to the regulation of diverse cellular processes through differential transcriptional readout of the same genetic material. The importance of epigenetics is underscored by many diseases that can develop due to mutations in epigenetic regulatory proteins, misregulation of the epigenetic machinery, and aberrant placement or removal of epigenetic marks. The reversible nature of epigenetic alterations is an attractive target for therapeutics that can help reset the epigenome to the normal state. The fact that some of these epigenetic drugs have been efficacious in the treatment of cancers, such as hematological malignancies reinforces the importance of epigenetics. The recent developments in high throughput sequencing techniques have enabled epigenome profiling of various cell types in their normal or pathological states. These epigenome signatures can be valuable for disease diagnosis, prognosis, and treatment opportunities. Ongoing and future research in the field hopes to shed light on epigenetic changes from a host of inputs, such as aging, metabolic, nutritional, physiological states, environmental conditions, early and late life exposures, chemical, and immunological challenges.
Epigenetics: a new discipline
A new discipline was born, the study of epigenetics (over, or above genetics). One of those doing research on this intriguing mechanism, Dr Bas Heijmans, says, &ldquoEpigenetics could be a mechanism which allows an individual to adapt rapidly to changed circumstances &hellip It could be that the metabolism of children of the Hunger Winter has been set at a more economical level, driven by epigenetic changes.&rdquo 4 Tel Aviv University neurobiologist Oded Rechavi stated that &ldquothe children of Dutch famine victims showed various effects of their heredity that appeared to be a kind of compensation for their parents&rsquo starvation.&rdquo 5
Research pointing to changes in the access to genetic information in the DNA (genotype) driven by outside or environmental stimuli, and resulting in a change in the organism (phenotype), is proliferating. Experiments have been done on worms: &ldquoPreviously, nobody had yet shown that it&rsquos enough to change the worms&rsquo environmental conditions to cause heredity that isn&rsquot dependent on DNA &hellip Because restricting calorie intake apparently extends life, the great-grandchildren of our famished worms lived 1.5 times longer than ordinary worms&mdashdespite the fact that they ate no less than any other worm.&rdquo 6
In another example, an RNA silencer, induced in worms as a response to an introduced virus, continued to express itself for more than 100 generations. 7
Studies on bison bones found in permafrost in a Canadian gold mine indicated that epigenetic changes in the bison population enabled them to adapt rapidly to changes in climate. These are changes far too rapid for traditional Darwinian models of natural selection to explain. &ldquoThe bones play a key role in a world-first study, led by University of Adelaide researchers, which analyses special genetic modifications that turn genes on and off, without altering the DNA sequence itself. These &lsquoepigenetic&rsquo changes can occur rapidly between generations&mdashwithout requiring the time for standard evolutionary processes.&rdquo 8
Scientists conducting experiments on agouti mice found that by manipulating nutrition they could switch off a certain gene. When the gene is active (&lsquoon&rsquo) the mice are normally obese and a yellowish colour by switching the gene off the mice are of a normal, slim appearance, and brown. By feeding a combination of nutrients including vitamin B12 to the mother before mating, the gene was able to be turned off in the babies. 9
Evolutionists holding to the paradigm of the Modern Synthesis (neo-Darwinism that mutations and natural selection explain the diversity of life on earth) have tended to resist strongly the conclusions coming from epigenetic research. In their view, evolution is a slow process of random mutations in the genome, resulting sometimes in a tiny advantage in the phenotype. This is favoured by natural selection, and passed on by Mendelian inheritance to future generations. The gene is seen as the master that controls the outward expression in the cell and the larger organism, an idea made popular in Dawkins&rsquo book, The Selfish Gene. The idea that the interaction of the outward form of an organism with the environment passes information back to the genome, or even just affects how the genome &lsquoacts&rsquo, is anathema to them.
Even worse for evolutionists, epigenetics suggests that latent genetic information of sorts is sitting in the DNA waiting for a particular environment in order to be switched on or off. It is like information in a book with certain pages stapled together, only to be opened and the information acted upon in certain environmental circumstances. If evolution occurs by natural selection, via the environment culling or conserving the effect of random mutations, how can there possibly be a &lsquosuite&rsquo of genetic information just waiting there to be switched on by an environment to which the organism has yet to be exposed? It poses another &lsquochicken or egg&rsquo conundrum to the myriad that already challenge evolutionists.
The Role of Epigenetics in Evolution: The Extended Synthesis
In 1942, Julian Huxley wrote an influential book Evolution: The Modern Synthesis that influenced generations of geneticists to today. The basis of the “modern synthesis,” also called the “new synthesis,” is that it addresses the question of whether Mendelian genetics could be reconciled with gradual evolution by means of natural selection of existing genetic variation. The modern synthesis states that “genetic assimilation” of existing variation can explain adaptation to a stressful environment and the evolution of new species. We propose an “ultramodern synthesis” that incorporates a range of responses an organism makes to environmental change or uncertainty, the timescales of these processes, the potential for reversibility, and the interplay between individual and population processes. Epigenetics is not an alternative to genetically-based adaptation. Rather, it is a mechanism by which an individual adjusts his biology in response to some stimulus and potentially transmits that change across generations.
We invite authors to submit original research articles as well as review articles in the following topics for both human and model organism evolution. Potential topics include, but are not limited to:
- Transgeneration epigenetics
- How epigenetic effects contribute to phenotypic variation and ecological breadth in native and invasive plants
- Experimental evolution of epigenetic effects in Arabidopsis
- Phenotypic plasticity in natural and agricultural systems in changing environments
- Bioinformatics evidence for epigenetic changes leading to genetic changes
- Bioinformatics evidence that prions are involved in epigenetic inheritance
- Epigenetic contributions to repeat expansions and contractions in the genome
- Hsp90 as an epigenetic capacitor for morphological evolution
- Quantitative epigenetics and the epigenetic assimilation of metastable epialleles
- Hybrid incompatibilities, evolution, and epigenetics
- Heterochromatin evolution
- Neocentromere evolution
- The role of imprinting in evolution
- The role of X-chromosome inactivation in evolution
Articles published in this special issue will not be subject to the journal's Article Processing Charges.
Epigenetic mechanisms allow native Peruvians to thrive at high altitudes
Humans inhabit an incredible range of environments across the globe, from arid deserts to frozen tundra, tropical rainforests, and some of the highest peaks on Earth. Indigenous populations that have lived in these extreme environments for thousands of years have adapted to confront the unique challenges that they present. Approximately 2% of people worldwide live permanently at high altitudes of over 2,500 meters (1.5 miles), where oxygen is sparse, UV radiation is high, and temperatures are low. Native Andeans, Tibetans, Mongolians, and Ethiopians exhibit adaptations that improve their ability to survive such conditions. Andeans, for example, display increased chest circumference, elevated oxygen saturation, and a low hypoxic ventilatory response, enabling them to thrive at exceptionally high elevations. While it is clear that there is a genetic component to these adaptations, exposure to high altitudes during early development is also known to play a role, although the underlying mechanism for this remains poorly understood. In a new study in Genome Biology and Evolution titled "Genome-Wide Epigenetic Signatures of Adaptive Developmental Plasticity in the Andes", Ainash Childebayeva, a doctoral student at the University of Michigan at the time of the study, and her colleagues sought to answer this question by studying members of the Peruvian Quechua, who live at high altitudes in the Andes. Their work reveals that mechanisms like DNA methylation may be involved in adaptation to high altitudes, and their findings have potential implications for the long-term health of those living at such heights.
Adaptations are typically thought of as genetic changes leading to the manifestation of a certain physiological trait, or phenotype. In a phenomenon known as developmental adaptation or adaptive plasticity, however, a certain genetic background merely serves as the prerequisite, and exposure to a certain environmental stimulus--generally during early development--is further required for the trait to be expressed. According to Childebayeva and co-authors, "There are several examples of Andean high-altitude adaptive phenotypes where developmental adaptation plays a key role in the manifestation of the adult phenotype." For example, Andeans who are lifelong residents of high altitude display greater lung volumes than those of Andean ancestry who were born and raised at sea level.
To reveal the biological mechanisms enabling this interplay between environment, development, and genetics, Childebayeva and her collaborators focused on epigenetics, the study of modifications that alter the DNA molecule without changing the order of nucleotides. Methylation is one type of epigenetic mark in which a methyl group is added to the cytosine nucleotides contained in DNA. Methylation suppresses the transcription of associated genes, thereby influencing an organism's biology by regulating protein expression. Importantly, DNA methylation patterns are established prenatally and in the early postnatal period, after which they remain relatively stable, providing an early developmental window during which environmental exposures may help shape an individual's phenotype.
The Quechua, an indigenous group native to Peru, have lived on the Andean Altiplano at an average elevation of 12,000 feet (over 3,600 m) for 11,000 years. In order to investigate the potential role of epigenetics in developmental adaptation to high altitudes, the study's authors evaluated DNA methylation patterns across the genome in three groups of Peruvian Quechua with different altitude exposures: high-altitude Quechua, who had lifetime exposure to high altitude migrant Quechua, who were born at high altitude but subsequently moved to low altitudes and low-altitude Quechua, who were lifelong residents of low altitude, despite the fact that their parents and both sets of grandparents were of highland Quechua ancestry. By comparing which DNA positions were methylated in high-altitude and migrant Quechua, who shared early childhood exposure to high altitudes, with those methylated in low-altitude Quechua, who shared ancestry but were not exposed in childhood, the authors were able to untangle the effects of developmental exposure to altitude and genetics.
The study identified specific positions and regions of DNA in which methylation was associated with either lifelong or early altitude exposure. Some of these regions were associated with genes previously linked to high-altitude adaptation, such as those involved in red blood cell production, glucose metabolism, and skeletal muscle development. In particular, some of these genes have been previously implicated in scans of genetic adaptations in other high-altitude populations, such as Tibetans and Mongolians, indicating that both genetic and epigenetic mechanisms may be acting on similar pathways in multiple high-altitude groups. These findings support the idea that epigenetics are involved in developmental adaptation and that early developmental exposures can have persistent impacts on DNA methylation patterns.
The study's findings also have implications for the health of high-altitude populations. For example, two of the methylated regions associated with high altitude overlapped genes linked to idiopathic pulmonary fibrosis, a condition characterized by irreversible fibrosis of the lung that is known to be associated with hypoxia (lack of oxygen). This suggests that high-altitude populations may have different susceptibilities to this condition or distinct pathological features compared to low-altitude populations. Moreover, the authors estimated the "epigenetic age" of the three groups of Quechua, a phenomenon that reflects the state of the epigenetic maintenance system and can serve as a marker of premature biological aging. They found that those with lifelong exposure to high altitude showed accelerated epigenetic aging compared to those who were lifelong residents of low altitude, likely reflecting the strain that hypoxia places on the cellular machinery.
According to Childebayeva, the resources and collaborators at the Cerro de Pasco High-Altitude laboratory, associated with the Cayetano Heredia University in Lima, Peru, were key to the completion of this project. Researchers have been studying high-altitude adaptation in Cerro de Pasco for almost one hundred years, with one of the first studies taking place in 1921-1922. Now in the Department of Archaeogenetics at the Max Planck Institute for the Study of Human History, Childebayeva hopes to one day extend this work by studying developmental adaptation in the high-altitude populations of Central Asia, shedding further light on the epigenetic mechanisms that allow humans to push the upper limits of high-altitude habitation.
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
Epigenetics of Autism Spectrum Disorder
Autism spectrum disorder (ASD), one of the most common childhood neurodevelopmental disorders (NDDs), is diagnosed in 1 of every 68 children. ASD is incredibly heterogeneous both clinically and aetiologically. The etiopathogenesis of ASD is known to be complex, including genetic, environmental and epigenetic factors. Normal epigenetic marks modifiable by both genetics and environmental exposures can result in epigenetic alterations that disrupt the regulation of gene expression, negatively impacting biological pathways important for brain development. In this chapter we aim to summarize some of the important literature that supports a role for epigenetics in the underlying molecular mechanism of ASD. We provide evidence from work in genetics, from environmental exposures and finally from more recent studies aimed at directly determining ASD-specific epigenetic patterns, focusing mainly on DNA methylation (DNAm). Finally, we briefly discuss some of the implications of current research on potential epigenetic targets for therapeutics and novel avenues for future work.
Keywords: Aetiology Autism spectrum disorder DNAmethylation Epigenetics Genetics Heterogeneity Molecular mechanisms.
ASJC Scopus subject areas
Research output : Contribution to journal › Article › peer-review
T1 - Evolution of ontogeny
T2 - Linking epigenetic remodeling and genetic adaptation in skeletal structures
N1 - Funding Information: The authors are grateful to H. Heatwole and three anonymous reviewers for extensive comments on previous versions of this article and constructive suggestions. The authors also thank D. Acevedo Seaman, R. Duckworth, E. Landeen, K. Oh, J. Rutkowska, and E. Snell-Rood for discussions, and S. E. Vincent, S. P. Lailvaux, A. Herrel, and E. Taylor for the invitation to contribute to this symposium. This study was funded in part by the National Science Foundation grant (DEB-0608356) to R.L.Y. and by the David and Lucille Packard Fellowship to A.V.B.
N2 - Evolutionary diversifications are commonly attributed to the continued modifications of a conserved genetic toolkit of developmental pathways, such that complexity and convergence in organismal forms are assumed to be due to similarity in genetic mechanisms or environmental conditions. This approach, however, confounds the causes of organismal development with the causes of organismal differences and, as such, has only limited utility for addressing the cause of evolutionary change. Molecular mechanisms that are closely involved in both developmental response to environmental signals and major evolutionary innovations and diversifications are uniquely suited to bridge this gap by connecting explicitly the causes of within-generation variation with the causes of divergence of taxa. Developmental pathways of bone formation and a common role for bone morphogenetic proteins (BMPs) in both epigenetic bone remodeling and the evolution of major adaptive diversifications provide such opportunity. We show that variation in timing of ossification can result in similar phenotypic patterns through epigenetically induced changes in gene expression and propose that both genetic accommodation of environmentally induced developmental pathways and flexibility in development across environments evolve through heterochronic shifts in bone maturation relative to exposure to unpredictable environments. We suggest that such heterochronic shifts in ossification can not only buffer development under fluctuating environments while maintaining epigenetic sensitivity critical for normal skeletal formation, but also enable epigenetically induced gene expression to generate specialized morphological adaptations. We review studies of environmental sensitivity of BMP pathways and their regulation of formation, remodeling, and repair of cartilage and bone to examine the hypothesis that BMP-mediated skeletal adaptations are facilitated by evolved reactivity of BMPs to external signals. Surprisingly, no empirical study to date has identified the molecular mechanism behind developmental plasticity in skeletal traits. We outline a conceptual framework for future studies that focus on mediation of phenotypic plasticity in skeletal development by the patterns of BMP expression.
AB - Evolutionary diversifications are commonly attributed to the continued modifications of a conserved genetic toolkit of developmental pathways, such that complexity and convergence in organismal forms are assumed to be due to similarity in genetic mechanisms or environmental conditions. This approach, however, confounds the causes of organismal development with the causes of organismal differences and, as such, has only limited utility for addressing the cause of evolutionary change. Molecular mechanisms that are closely involved in both developmental response to environmental signals and major evolutionary innovations and diversifications are uniquely suited to bridge this gap by connecting explicitly the causes of within-generation variation with the causes of divergence of taxa. Developmental pathways of bone formation and a common role for bone morphogenetic proteins (BMPs) in both epigenetic bone remodeling and the evolution of major adaptive diversifications provide such opportunity. We show that variation in timing of ossification can result in similar phenotypic patterns through epigenetically induced changes in gene expression and propose that both genetic accommodation of environmentally induced developmental pathways and flexibility in development across environments evolve through heterochronic shifts in bone maturation relative to exposure to unpredictable environments. We suggest that such heterochronic shifts in ossification can not only buffer development under fluctuating environments while maintaining epigenetic sensitivity critical for normal skeletal formation, but also enable epigenetically induced gene expression to generate specialized morphological adaptations. We review studies of environmental sensitivity of BMP pathways and their regulation of formation, remodeling, and repair of cartilage and bone to examine the hypothesis that BMP-mediated skeletal adaptations are facilitated by evolved reactivity of BMPs to external signals. Surprisingly, no empirical study to date has identified the molecular mechanism behind developmental plasticity in skeletal traits. We outline a conceptual framework for future studies that focus on mediation of phenotypic plasticity in skeletal development by the patterns of BMP expression.
End the Hype over Epigenetics & Lamarckian Evolution
You might recall from high school biology a scientist by the name of Jean-Baptiste Lamarck. He proposed a mechanism of evolution in which organisms pass on traits acquired during their lifetimes to their offspring. The textbook example is a proposed mechanism of giraffe evolution: If a giraffe stretches its neck to reach higher leaves on a tree, the giraffe would pass on a slightly longer neck to its offspring.
Lamarck's proposed mechanism of evolution was tested by August Weismann. He cut off the tails of mice and bred them. If Lamarck was correct, then the next generation of mice should be born without tails. Alas, the offspring had tails. Lamarck's theory therefore died and remained largely forgotten for over 100 years.
However, some scientists believe that new data may at least partially resurrect Lamarckian thinking. This recent resurgence is due to a new field called epigenetics. Unlike regular genetics, which studies changes in the sequence of the DNA letters (A, T, C, and G) that make up our genes, epigenetics examines small chemical tags placed on those letters. Environmental factors play an enormous role in determining where and when the tags are placed. This is a big deal because these chemical tags help determine whether or not a gene is turned "on" or "off." In other words, the environment can influence the presence of epigenetic tags, which in turn can influence gene expression.
That finding is certainly intriguing, but it isn't revolutionary. We've long known that the environment affects gene expression.
But, what is potentially revolutionary is the discovery that these epigenetic tags, in some organisms, can be passed on to the next generation. That means that environmental factors may not only affect gene expression in parents, but in their yet-to-be-born children (and possibly grandchildren), as well.
Yikes. Does that mean Lamarck was right? That question was addressed by Edith Heard and Robert Martienssen in a detailed review in the journal Cell.
Of particular concern is the idea that mammalian health can be affected by epigenetic tags received from parents or grandparents. For example, one group reported that pre-diabetic mice have different epigenetic tag patterns in their sperm and that their offspring have a higher chance of contracting diabetes. (Virginia Hughes has written an excellent article summarizing this and other related epigenetic studies.) A flurry of other biomedical and epidemiological research has strongly hinted that a susceptibility to obesity, diabetes, and heart disease can be passed on through epigenetic tags.
However, Heard & Martienssen are not convinced. In their Cell review, they admit that epigenetic inheritance has been demonstrated in plants and worms. But, mammals are completely different beasts, so to speak. Mammals go through two rounds of epigenetic "reprogramming" -- once after fertilization and again during the formation of gametes (sex cells) -- in which most of the chemical tags are wiped clean.
They insist that characteristics many researchers assume to be the result of epigenetic inheritance are actually caused by something else. The authors list four possibilities: Undetected mutations in the letters of the DNA sequence, behavioral changes (which themselves can trigger epigenetic tags), alterations in the microbiome, or transmission of metabolites from one generation to the next. The authors claim that most epigenetic research, particularly when it involves human health, fails to eliminate these possibilities.
It is true that environmental factors can influence epigenetic tags in children and developing fetuses in utero. What is far less clear, however, is whether or not these modifications truly are passed on to multiple generations. Even if we assume that epigenetic tags can be transmitted to children or even grandchildren, it is very unlikely that they are passed on to great-grandchildren and subsequent generations. The mammalian epigenetic "reprogramming" mechanisms are simply too robust.
Therefore, be very skeptical of studies which claim to have detected health effects due to epigenetic inheritance. The hype may soon fade, and the concept of Lamarckian evolution may once again return to the grave.