---
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title: "The Epigenetics Revolution: How Modern Biology is Rewriting Our Understanding of Genetics, Disease and Inheritance"
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# Data-driven gene expression analysis Comprehensive, authoritative biology text Cutting-edge epigenetics insights The Epigenetics Revolution: How Modern Biology is Rewriting Our Understanding of Genetics, Disease and Inheritance

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## Summary

> 🧠 Decode life’s hidden script with The Epigenetics Revolution!

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- **What is this?** The Epigenetics Revolution: How Modern Biology is Rewriting Our Understanding of Genetics, Disease and Inheritance
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## Key Features

- • **Bridge Science and Society:** Gain insights into mental health, evolution, and disease from a fresh perspective.
- • **Unlock the Future of Genetics:** Explore how epigenetics rewrites DNA's role beyond the blueprint.
- • **Master Complex Biological Codes:** Dive into DNA methylation and histone modifications with vivid illustrations.
- • **Understand Transgenerational Impact:** Discover how environment shapes gene expression across generations.
- • **Join the 21st Century Biology Revolution:** Stay ahead with the latest paradigm shift in genetics and inheritance.

## Overview

The Epigenetics Revolution offers a masterful, vividly illustrated exploration of how gene expression is regulated beyond DNA sequences. It reveals the profound impact of epigenetic mechanisms like DNA methylation and histone modifications on inheritance, disease, and evolution, making it essential reading for anyone eager to understand the cutting-edge science reshaping biology in the 21st century.

## Description

At the beginning of this century enormous progress had been made in genetics. The Human Genome Project finished sequencing human DNA. It seemed it was only a matter of time until we had all the answers to the secrets of life on this planet.

Review: Epigenetics: phenomenology and molecular underpinning - The book is masterly in its treatment of this young, exciting, and profoundly significant field of biological research. The author's writing is clear, substantive, vivid, acutely insightful in matters relating to evolution, witty while her frequent use of analogy exemplary. In the course of the book, the author revisits topics in varying contexts but far from this being repetitious on the contrary it refreshes and embeds concepts in the mind of the reader and enhances its interconnection. Another positive element in the book is that on several instances there is a pictorial illustration of the issue raised by the author so that the reader has the benefit to visually follow the sequence of events on the issue raised. I have, however, to warn the prospective reader that the preceding notwithstanding the book is intrinsically not an easy read due to its conceptual richness, the multiplicity, subtlety, intricate sequence of interactions and the complexity of the epigenetic code - especially as related to histone modifications as opposed to DNA methylation - much of it presently understood only in broad outline. Until the turn of the century DNA was viewed as a blueprint or a template but since then there was a paradigm shift and we now correctly view it as a script and as such identical starting points may lead to different outcomes. It is possible without change in DNA (mutation) for life histories to be changed irrevocably in response to the environment through epigenetic changes in our genome. We infer that a phenomenon is likely to be influenced by epigenetic alterations in DNA and its accompanying proteins if one or both of the following are met: two things are genetically identical, but phenotypically variable; an organism continues to be influenced by an event long after the initiating event has occurred. Since all phenotypic variation has a physical basis, we can define epigenetics at the molecular level as the set of modifications to our genetic material that change the ways of gene expression - switch on, switch off, or some intermediate stage - but which does not alter our genome which we can transmit in all its purity to our descendants. The above also solved the mystery that only 2 per cent of our genome codes for proteins while 98 per cent does not code for proteins but as we now realize codes for something else which is connected with regulating gene expression through epigenetic mechanisms. We have similarly come to the realization that the complexity of living organisms scales much better with the percentage that does not code for proteins than it does with the number of base pairs coding for proteins. Further it has been argued that the difference between humans and our chimpanzee relatives may well be due to a special class of ncRNA (non coding RNA) which has an immense capacity of editing itself. Evolution seems to have solved the problem of creating more complex and sophisticated organisms by altering the regulation of the organisms than altering the proteins themselves. And this is exactly what has been achieved by using complicated networks of ncRNAs molecules to influence how, when and to what degree specific proteins are expressed. I shall now reconnect to an earlier part of the review to present epigenetics in action both when two individuals are genetically identical but phenotypically different and when individuals continue to be influenced by an event long after the initiating event has occurred. The scientific term for identical twins is monozygotic (MZ)twins. They were both derived from the same single-cell zygote formed from the fusion of one egg and one sperm. (MZ) twins allow us to explore mathematically the link between the sequences of our genes (genotype) and what we are like (phenotype). In genetically identical monozygotic twins, the concordance for schizophrenia does not reach 100 per cent but is only 50 per cent. The Dutch Hunger Winter lasted from the start of November 1944 to the late spring of 1945. The effects of the famine on the birth weights of children who had been in the womb during that terrible period were: if a mother was well-fed around the time of conception and malnourished only for the last few months few months of the pregnancy, her baby was likely to be small. If, on the other hand, the mother suffered malnutrition for the first three moths of the pregnancy, but then was well fed, she was likely to have a baby with a normal body weight. But then came the really surprising:babies who were born small tended to stay small all their lives - even though they were properly nourished - with lower obesity rates than the general population. Even more unexpectedly, the children whose mothers had been malnourished only early in pregnancy, had higher obesity rates than normal. And the truly stunning, some of these effects seem to be present in the children of this group, that is the grandchildren of women who were malnourished during the first three months of their pregnancy. Something suggesting Lamarckian inheritance and this is indeed what happened and has a name 'transgenerational inheritance'. But I want to reassure the reader because in the overwhelming number of cases, Darwinian evolution prevails. A child, less than three years old, is abused and neglected by his parents but subsequently is treated normally. Often such children who suffered from abuse or neglect in their early years have substantially higher risk as adults of mental health problems than the general population. All too often the child grows up into an adult at high risk of depression, self harm, alcohol and drug abuse, and suicide. We shall now turn our attention to the epigenetic modifications at the molecular level which influence gene and protein expression. The epigenetic regulation of gene expression occurs through different cells having the same DNA blueprint but carrying molecular modifications which can be transmitted from mother cell to daughter cell during somatic cell division. We shall examine in some detail DNA methylation and histone modifications. DNA methylation: Cytosine is the only one of the four DNA bases that gets methylated, to form 5-methylcytosine through one of three enzymes called DNA methyltransferases. The DNMTs are examples of epigenetic 'writers' - enzymes that create the epigenetic code. Most of the time these enzymes will only add a methyl group to a C (Cytosine) that is followed by G (Guanine). C followed by G is known as CpG. The chemical group is 'stuck onto' DNA but does not alter the underlying genetic sequence. DNA methylation has profound effects on how genes are expressed and ultimately on cellular, tissue and whole-body functions. CpG pairs are concentrated in the promoter region. Promoters are the stretches of the genome where transcription complexes bind and start copying DNA to form RNA. Regions where there is a high concentration of CpG motifs are called CpG islands. When genes are active, the levels of methylation in the CpG islands is low. The CpG islands tend to be highly methylated only when the genes are switched off. DNA methylation is clearly really important. Defects in reading DNA methylation can lead to a complex and devastating neurological disorder that leaves children with Rett syndrome severely disabled throughout their lives. DNA methylation is also important for maintaining the correct patterns of gene expression in different cell types, either for several decades in the case of our long-lived neurons or in all daughters of a stem cell in a tissue that is constantly replaced such as skin. Histone modifications: More than fifty different epigenetic histone modifications have been identified. These modifications all alter gene expression but not always in the same way. Some histone modifications push gene expression up, others drive it down. The pattern of modifications is referred to as a histone code and is extraordinarily difficult to read. This complexity contrasts with the fairly all-or-nothing effect of DNA methylation. As to why organisms evoved such complex patterns of histone modifications to regulate gene expression, the author offers an elegant explanation. She argues that complexity likely allows sophisticated fine-tuning of gene expression. Because of this, cells and organisms can adapt their gene expression appropriately in response to changes in their environment. I find it fitting to conclude the review with an apt comment of the author: In biology Darwin and Mendel came to define the 19th century as the era of evolution and genetics; Watson and Crick defined the 20th century as the era of DNA, and the functional understanding of how genetics and evolution interact. But in the 21st century it is the new scientific discipline of epigenetics that is unraveling so much of what we took as dogma and rebuilding it in an infinitely more varied, more complex and even more beautiful fashion.
Review: Fantastic book - A good book and really well written. It's a great way for anyone with a basic interest in genetics to start to understand that genetics is so much more than just the basic code of DNA. Fascinating in parts, but I wanted more depth to it and a bit more high level knowledge. But it's aimed at the casual science reader and for that I love it! Brilliant book and should be read by anyone with even a vague interest in genetics.

## Features

- ICON BOOKS

## Technical Specifications

| Specification | Value |
|---------------|-------|
| Best Sellers Rank | 28,064 in Books ( See Top 100 in Books ) 15 in Genetics in Popular Science 166 in Biology (Books) |
| Customer Reviews | 4.5 out of 5 stars 1,736 Reviews |

## Images

![The Epigenetics Revolution: How Modern Biology is Rewriting Our Understanding of Genetics, Disease and Inheritance - Image 1](https://m.media-amazon.com/images/I/71jeBfjA1AL.jpg)

## Customer Reviews

### ⭐⭐⭐⭐⭐ Epigenetics: phenomenology and molecular underpinning
*by S***T on 8 November 2013*

The book is masterly in its treatment of this young, exciting, and profoundly significant field of biological research. The author's writing is clear, substantive, vivid, acutely insightful in matters relating to evolution, witty while her frequent use of analogy exemplary. In the course of the book, the author revisits topics in varying contexts but far from this being repetitious on the contrary it refreshes and embeds concepts in the mind of the reader and enhances its interconnection. Another positive element in the book is that on several instances there is a pictorial illustration of the issue raised by the author so that the reader has the benefit to visually follow the sequence of events on the issue raised. I have, however, to warn the prospective reader that the preceding notwithstanding the book is intrinsically not an easy read due to its conceptual richness, the multiplicity, subtlety, intricate sequence of interactions and the complexity of the epigenetic code - especially as related to histone modifications as opposed to DNA methylation - much of it presently understood only in broad outline. Until the turn of the century DNA was viewed as a blueprint or a template but since then there was a paradigm shift and we now correctly view it as a script and as such identical starting points may lead to different outcomes. It is possible without change in DNA (mutation) for life histories to be changed irrevocably in response to the environment through epigenetic changes in our genome. We infer that a phenomenon is likely to be influenced by epigenetic alterations in DNA and its accompanying proteins if one or both of the following are met: two things are genetically identical, but phenotypically variable; an organism continues to be influenced by an event long after the initiating event has occurred. Since all phenotypic variation has a physical basis, we can define epigenetics at the molecular level as the set of modifications to our genetic material that change the ways of gene expression - switch on, switch off, or some intermediate stage - but which does not alter our genome which we can transmit in all its purity to our descendants. The above also solved the mystery that only 2 per cent of our genome codes for proteins while 98 per cent does not code for proteins but as we now realize codes for something else which is connected with regulating gene expression through epigenetic mechanisms. We have similarly come to the realization that the complexity of living organisms scales much better with the percentage that does not code for proteins than it does with the number of base pairs coding for proteins. Further it has been argued that the difference between humans and our chimpanzee relatives may well be due to a special class of ncRNA (non coding RNA) which has an immense capacity of editing itself. Evolution seems to have solved the problem of creating more complex and sophisticated organisms by altering the regulation of the organisms than altering the proteins themselves. And this is exactly what has been achieved by using complicated networks of ncRNAs molecules to influence how, when and to what degree specific proteins are expressed. I shall now reconnect to an earlier part of the review to present epigenetics in action both when two individuals are genetically identical but phenotypically different and when individuals continue to be influenced by an event long after the initiating event has occurred. The scientific term for identical twins is monozygotic (MZ)twins. They were both derived from the same single-cell zygote formed from the fusion of one egg and one sperm. (MZ) twins allow us to explore mathematically the link between the sequences of our genes (genotype) and what we are like (phenotype). In genetically identical monozygotic twins, the concordance for schizophrenia does not reach 100 per cent but is only 50 per cent. The Dutch Hunger Winter lasted from the start of November 1944 to the late spring of 1945. The effects of the famine on the birth weights of children who had been in the womb during that terrible period were: if a mother was well-fed around the time of conception and malnourished only for the last few months few months of the pregnancy, her baby was likely to be small. If, on the other hand, the mother suffered malnutrition for the first three moths of the pregnancy, but then was well fed, she was likely to have a baby with a normal body weight. But then came the really surprising:babies who were born small tended to stay small all their lives - even though they were properly nourished - with lower obesity rates than the general population. Even more unexpectedly, the children whose mothers had been malnourished only early in pregnancy, had higher obesity rates than normal. And the truly stunning, some of these effects seem to be present in the children of this group, that is the grandchildren of women who were malnourished during the first three months of their pregnancy. Something suggesting Lamarckian inheritance and this is indeed what happened and has a name 'transgenerational inheritance'. But I want to reassure the reader because in the overwhelming number of cases, Darwinian evolution prevails. A child, less than three years old, is abused and neglected by his parents but subsequently is treated normally. Often such children who suffered from abuse or neglect in their early years have substantially higher risk as adults of mental health problems than the general population. All too often the child grows up into an adult at high risk of depression, self harm, alcohol and drug abuse, and suicide. We shall now turn our attention to the epigenetic modifications at the molecular level which influence gene and protein expression. The epigenetic regulation of gene expression occurs through different cells having the same DNA blueprint but carrying molecular modifications which can be transmitted from mother cell to daughter cell during somatic cell division. We shall examine in some detail DNA methylation and histone modifications. DNA methylation: Cytosine is the only one of the four DNA bases that gets methylated, to form 5-methylcytosine through one of three enzymes called DNA methyltransferases. The DNMTs are examples of epigenetic 'writers' - enzymes that create the epigenetic code. Most of the time these enzymes will only add a methyl group to a C (Cytosine) that is followed by G (Guanine). C followed by G is known as CpG. The chemical group is 'stuck onto' DNA but does not alter the underlying genetic sequence. DNA methylation has profound effects on how genes are expressed and ultimately on cellular, tissue and whole-body functions. CpG pairs are concentrated in the promoter region. Promoters are the stretches of the genome where transcription complexes bind and start copying DNA to form RNA. Regions where there is a high concentration of CpG motifs are called CpG islands. When genes are active, the levels of methylation in the CpG islands is low. The CpG islands tend to be highly methylated only when the genes are switched off. DNA methylation is clearly really important. Defects in reading DNA methylation can lead to a complex and devastating neurological disorder that leaves children with Rett syndrome severely disabled throughout their lives. DNA methylation is also important for maintaining the correct patterns of gene expression in different cell types, either for several decades in the case of our long-lived neurons or in all daughters of a stem cell in a tissue that is constantly replaced such as skin. Histone modifications: More than fifty different epigenetic histone modifications have been identified. These modifications all alter gene expression but not always in the same way. Some histone modifications push gene expression up, others drive it down. The pattern of modifications is referred to as a histone code and is extraordinarily difficult to read. This complexity contrasts with the fairly all-or-nothing effect of DNA methylation. As to why organisms evoved such complex patterns of histone modifications to regulate gene expression, the author offers an elegant explanation. She argues that complexity likely allows sophisticated fine-tuning of gene expression. Because of this, cells and organisms can adapt their gene expression appropriately in response to changes in their environment. I find it fitting to conclude the review with an apt comment of the author: In biology Darwin and Mendel came to define the 19th century as the era of evolution and genetics; Watson and Crick defined the 20th century as the era of DNA, and the functional understanding of how genetics and evolution interact. But in the 21st century it is the new scientific discipline of epigenetics that is unraveling so much of what we took as dogma and rebuilding it in an infinitely more varied, more complex and even more beautiful fashion.

### ⭐⭐⭐⭐ Fantastic book
*by A***. on 24 February 2026*

A good book and really well written. It's a great way for anyone with a basic interest in genetics to start to understand that genetics is so much more than just the basic code of DNA. Fascinating in parts, but I wanted more depth to it and a bit more high level knowledge. But it's aimed at the casual science reader and for that I love it! Brilliant book and should be read by anyone with even a vague interest in genetics.

### ⭐⭐⭐⭐⭐ Fascinating, but she jumps to conclusions too readily
*by L***D on 9 February 2015*

This is a great book for anyone who like me, is trying to make sense of what is really going on in the genome, in that it brings together many facts from research papers. I've given it five stars for this reason, and despite my many criticisms below, because it tackles an incredibly complex subject in an understandable and fascinating way. The criticisms come from my intense prior involvement in the subject, and are challenges to some of the ideas which I hope might help other readers. The book fails to put over the central story regarding the big question, "what is going on in the genome and to what ends?" I say this because the reader is led to believe that epigenetics explains many things that could not be explained before, such as how cells acquire their individual identity and retain it over decades. Methylation, we are told here, has been said to be virtually irreversible, so it fits the bill, but as we are later told the effects of methylation can be undone by further addition. Notable for their absence are the terms 'transcription factor', and ''genetic cascade' (they are not even in the index), though they are the bedrock of genetic theory; complex books have been written explaining cell fate and development in these terms, and we have no reason to dump the existing theory. A gene can make a protein which is a transcription factor, which can turn off another gene, and there is no reason why that gene cannot go on doing that in a cell and it's copies, through various mechanisms, ad infinitum - no need for methylation to suppress the gene. We should really be asking what methylation adds to the existing processes. It may be 'belt and braces', or it may be, as I think, much more complex than that. Again, later in the book, it is suggested that the permanence of methylation makes it the ideal candidate as the cause of PTSD (post traumatic stress disorder). Only after this idea has been developed in detail is it stated that memory may also be epigenetically determined. Memory, of course, is a far bigger subject than PTSD, and a very complicated one in which the growth of both new connections and new synapses (and possibly glial cells) has long been recognised as a perfectly good explanation of how neurons build and strengthen association. These processes may indeed be under control of epigenetics, but epigenetics isn't necessary for an explanation - again transcription factor cascades, or just the fact that synapses remain once they have been induced to form by neural firing are sufficient. PTSD undoubtedly arises out of memory; and especially emotional memory which appears to get separated from other memories, but memory is a much more complex process than can just be put down to epigenetics. I'm not saying that epigenetics isn't important - I think it's hugely important; just that Carey tends to jump to conclusions in a less than thorough way. There is much mention of 'mental illness' in the book, again with methylation implicated especially in the 'diseases' of PTSD and 'depression'. While the author does a great, and much needed job of explaining how paradigm shifts can take a long time in science because of inertia in the system which resists the overthrow of established ideas, she is clearly unaware of the paradigm shift that has long been underway in the field of so called 'mental illness', especially in the UK, where DSM (the Diagnostic Statistical Manual) has long been viewed with disdain by many psychiatrists, clinical psychogist, and therapists. I suspect that the author's involvement in the pharmaceuticals field has blinded her to this. Many experts, such as Professor Richard Bental ('Doctoring the Minds' and 'Madness Explained') regard depression and even schizophrenia as understandable consequences of pressure from society and family (see also R D Laing's 'Politics of the Family' etc and Bateson's double bind hypothesis). Carey's search for a simple 'cause', though valid to some degree, is much too crude, and ignores so many complex factors. Her quoting of identical twin studies (too often glibly trotted out in general) needs to be questioned. Even twins who grow up together don't share the same experiences - one might have been traumatised, chastised, or otherwise changed in a fleeting moment while the other was absent - this is what creates differing personalities, and it does so through memory, the functioning of the mind, and even psychosomatic effects. All of these are down to neural networks, and we don't understand the functioning of neural networks yet, even at a quite basic level. It's jumping to conclusions to think that epigenetics is suddenly the key to 'mental illness'. An interesting fact about PTSD which caught my attention years ago, is that the commonly prescribed beta-blocker, propranolol, has been found to prevent PTSD if given to soldiers prior to battle. It is also said to 'kill conscience', and there is considerable evidence from research that emotional memories are erased and then put back when we remember events, and that re-living traumatic events while taking propranolol can block that 'putting back'. This poses serious questions for the role of methylation - how is the methylation in neurons involved in emotional memories undone every time we remember something; and if memories are constantly erased and put back, even those causing PTSD, doesn't that rather conflict with the argument that the permanence of methylation is the key? And does propranolol in fact affect methylation or some process around it (a topic for research)? As I said, I'm not the average reader, having been passionately involved in these subjects for thirty or more years, and I know just how mind-bogglingly complicated they are becoming. All the more credit to Nessa Carey for tackling them in a book now, because studying papers is exhausting and takes time, even when you have access to them, and we need books that try to summarise, and access to other's ideas, if what E O Wilson calls 'consilience' across science disciplines is to be achieved. A great book, and I look forward to reading the next one on 'Junk' DNA when it comes out.

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