Category Archives: Epigenetics

New York City, NY: October 3, 2019 Published via (Wired Release) Global Epigenetics Market Research Report is an in-depth and professional document 2019:

A newly published market study by MarketResearch.biz, titled Global Epigenetics Market, is built up with a step by step analysis from expert research. The report provides accurate estimation, improvement criterias, action plans, and root ways. It has covered emerging market trends, key challenges, restraints, opportunities, future growth potentials, competitive outlook, and regional outlook, and value chain analysis. The top players/vendors of the global market are further covered in the report. The report presents a pin-point breakdown of Epigenetics on the basis of type, applications, and research regions. The latest data has been presented on the revenue numbers, product details, and sale of key companies.

For Better Understanding Go With this Free Sample Report Enabled with Respective Tables and Figureshttps://marketresearch.biz/report/epigenetics-market/request-sample

It aims to help customers in the decision making process. The manufacturers data is covered that includes shipment, price, revenue, gross profit, and business distribution. With this report, all the manufacturers and the vendors will be in aware of the threats, shortcomings that the market will offer in the next few years. The current and prospective growth of the market for 2019-2028 is also captured. Graphical data is integrated in the form of charts, diagrams and tables making the report well organized and understandable for the professionals.

We Have includedVital insights into Epigenetics Market Competition and StrategiesofCompetitors :

Bio-Rad Laboratories Inc, Thermo Fisher Scientific Inc, Diagenode, QIAGEN, Abcam Plc., New England Biolabs, Agilent Technologies, Zymo Research, PerkinElmer Inc, Active Motif

Outlook ofEpigenetics Market Segmentation:

Global epigenetics market segmentation, by product:ReagentsKitsInstrumentsEnzymes

Global epigenetics market segmentation, by technology:DNA MethylationHistone ModificationsRNA-Associated Silencing

Global epigenetics market segmentation, by application:OncologySolid TumorsLiquid TumorsNon OncologyCardiovascular diseasesInfectious diseasesInflammatory diseaseMetabolic diseases

Global epigenetics market segmentation, by end user:Academic and Research InstitutesPharmaceutical and Biotechnology CompaniesContract Research Organizations

Regional Coverage:

All the regions and countries of the world are covered that also shows a regional development status, Epigeneticsmarket size, volume, and value, as well as price data. The global demand for the Epigenetics market has been fragmented across several regions such as

Americas (United States, Canada, Brazil, and Mexico)

Middle East and Africa (Egypt, South Africa, Israel, Turkey, GCC Countries)

Europe (Germany, France, UK, Italy, Russia Spain)

APAC (China, Japan, Korea, Southeast Asia, India, Australia)

South America (Brazil, Colombia, Argentina, etc.)

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Main Features of The GlobalEpigeneticsMarket Research Report:

The report provides market values and anticipated growth rate of the global Epigenetics market for all years till 2028.

The report highlights the actual drivers of the market by considering risks and identifying and testing new tactics, manufacturing cost, raw material cost, downstream buyers, labor cost, and market channels.

The report assessed the market segments and provides the relative contribution to the development of the global Epigenetics market.

The report offers coverage of the competitive nature of the market and discusses various marketing strategies to stay ahead in the competition.

Its an essential tool to check the feasibility of a new project and geographical expansion of the company.

Browse Full Summary Research Report ofEpigeneticsMarket:https://marketresearch.biz/report/epigenetics-market/request-sample

There are 9 Chapters to deeply display the global Epigenetics market

Chapter One: Global Epigenetics Market Overview

1.1 Epigenetics Preface

Chapter Two: Global Epigenetics Market Analysis

2.1 Epigenetics Report Description

2.1.1 Epigenetics Market Definition and Scope

2.2 Epigenetics Executive Summary

2.2.1 Epigenetics Market Snapshot, [Segment 1]

2.2.2 Epigenetics Market Snapshot, [Segment 2]

2.2.3 Epigenetics Market Snapshot, [Segment 3]

2.2.4 Epigenetics Market Snapshot, [Region Segment]

2.3 Epigenetics Market Opportunity Analysis

Chapter Three: Global Epigenetics Market Dynamics

3.1 Drivers

3.2 Restraints

3.3 Opportunities

3.4 Trends

Chapter Four: Global Epigenetics Market Segment Analysis, by [Segment 1]

4.1 Epigenetics Overview

4.2 Epigenetics Segment Trends

4.3 Epigenetics Market Share and Forecast, and Y-o-Y Growth

Chapter Five: Global Epigenetics Market Segment Analysis, by [Segment 2]

5.1 Epigenetics Overview

5.2 Epigenetics Segment Trends

5.3 Epigenetics Market Share and Forecast, and Y-o-Y Growth

Chapter Six: Global Epigenetics Market Segment Analysis, by [Segment 3]

6.1 Epigenetics Overview

6.2 Epigenetics Segment Trends

6.3 Epigenetics Market Share and Forecast, and Y-o-Y Growth

Chapter Seven: Global Epigenetics Market Segment Analysis, by [Region Segment]

7.1 Epigenetics Overview

7.2 Epigenetics Regional Trends

7.3 Epigenetics Market Share and Forecast, and Y-o-Y Growth

Chapter Eight: Global Epigenetics Market Company Profiles

8.1 Companies

8.1.1 Company Overview

8.1.2 Product Portfolio

8.1.3 Financial Overview

8.1.4 Key Developments

8.1.5 SWOT Analysis

Chapter Nine: Global Epigenetics Market

9.1 Research Methodology

9.2 About Us

It further demonstrates a comprehensive view of the marketplace with subsequent information. The latest mechanical enhancements and new releases delivered in the report will help customers settle on taught business decisions and complete their requisite executions in the future. In the conclusion part of this report, you will find research findings, market size, worldwide market share, consumer needs along with customer preference change, and data source.

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In light of the rapid increases in opioid overdose deaths, there is an urgent need to develop better treatment options for pain and addiction, according to a summary of key messages and discussion from a 2-day event titled The Opioid Crisis and the Future of Addiction and Pain Therapeutics: Opportunities, Tools, and Technologies Symposium, held at the National Institutes of Health in Gaithersburg, Maryland, which was published in the Journal of Pharmacology and Experimental Therapeutics.

In order to develop new pain treatments, it is imperative to have a better understanding of the circuits, pathways, genetics, transcriptional and epigenetic mechanisms, and targets involved in both pain and opioid addiction.

Opioid misuse and addiction now represent a public health crisis with a debilitating social and economic impact on individuals, and associated mortality. The symposium aimed to address concerns regarding pain and addiction and was unique in that it brought together experts from 2 research disciplines: addiction and pain.

Attempts to identify novel targets that could lead to effective pain treatments without involvement of the -opioid receptor were unsuccessful and only a limited number of targets exist for pain management, most which have been known for decades. It is important to recognize the complexity and diversity of pain and the pain experience, involving distinct mechanisms that require different therapeutic interventions.

Although drugs that have the potential for misuse initially act at the synapses, addiction requires repeated drug exposure and can therefore be considered drug-induced neural plasticity that involves changes in gene expression. Approximately half of the risk for addiction is thought to be due to genetic factors, with hundreds of genes each contributing a small fraction, and half due to environmental factors.

Negative emotional states cause physical and emotional pain that may act as a driving force in addiction. There is significant overlap in the neural pathways that mediate negative emotional states (eg, hyperkatifeia) and pain.

Natural products, including capsaicin, menthol, isothiocyanates, and thiosulfinates, elicit irritation or pain by activating nociceptors. Studies examining the mechanisms of action of these compounds led to the identification of transient receptor potential (TRP) ion channels that represent promising targets for novel analgesics. Current work aims at identifying antagonist molecules to TRP channels that may represent alternatives to opioid analgesics.

Research into venomous toxins, including Hm1a/b spider toxins, has revealed a role for the Nav1.1 voltage-gated channel in pain. Cannabinoids and the opioid receptor agonist mitragynine (derived from kratom) are also gaining attention as potential targets for pain.

Efforts to identify inhibitors selective for the Nav1.7 channel have proved challenging due to factors that include the IC50 value of the receptor being inferior to concentrations required to block action potentials in nociceptors.

-opioid receptor antagonists may represent an effective therapeutic strategy to alleviate the affective dimension of chronic pain, as these can restore dopamine release.

Digital therapeutic options also lead to effective chronic pain therapy. With the use of data derived from smartphones, connected sensors, wearables, and voice input, there is the potential to better assess and understand a patients health and to identify biomarkers. Finally, behavioral epigenetics can be used to understand the interplay between life experience and brain function.

Given the rapidly growing occurrence of opioid use disorder and associated overdose deaths, as well as the lengthy time required for new targets to reach patients in need, there is a renewed urgency to develop better treatments for pain and addiction, concluded the authors.

Follow @ClinicalPainAdv

Reference

Coussens NP, Sittampalam GS, Jonson SG, et al. The opioid crisis and the future of addiction and pain therapeutics [Published online September 3, 2019]. J Pharmacol Exp Ther. doi: 10.1124/jpet.119.259408

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Challenges in Developing Therapeutics for Addiction and Pain - Clinical Pain Advisor

Hollywood is really, really good at killing the bad guys. And even though they haven't quite gotten to ISIS just yet, there is a trail of bloody, dismembered evil in the wake of action stars like Jason Statham, Sylvester Stallone, and everyone else who may have been considered for a part in The Expendables.

Despite Hot Shots! Part Deux and Charlie Sheen's claim to the contrary, there is an undisputed number one deadliest action star in the annals of Hollywood military history. That title goes to the Terminator: Arnold Schwarzenegger.

Who was also in the Expendables. Three times.

(Lionsgate)

Big Data is back to settle the debates about everything we love. Just like the time a statistical analysis settled who was the best general in history, another data enthusiast set out to determine who was the deadliest onscreen action star in cinema history.

Granted, this is before the Expendables 3 and the newest Rambo movie, but unless Rambo kills an entire Colombian drug cartel (which I admit, he might), the winner should still be pretty clear.

Randal Olson, a data scientist at Life Epigenetics, merges cutting edge epigenetics research with advanced machine learning methods to improve life expectancy predictions. He put data collected from MovieBodyCounts.com to put together data visualizations for the deadliest action heroes. At the top, was the star of Predator, Total Recall, and my personal favorite, True Lies.

Thank you, sir.

As of Olson's 2013 writing, Arnold was at the top of the list with 369 kills. His highest single movie record came in Commando where in the final island scene alone, he managed to off 74 guys, mostly using firearms but featuring the best use of a toolshed. Hey, Alyssa Milano ain't gonna rescue herself.

Of the 200 actors listed in the data, the top ten include Chow Yun-Fat in second, Sylvester Stallone in third, and then Dolph Lundgren (thanks, Punisher!), Clint Eastwood, Nic Cage, Jet Li, Clive Owen, and Wesley Snipes. In fourth place comes Tomisaburo Wakayama, who got 150 of his 266 onscreen kills in a single movie, 1974's Lone Wolf and Cub: White Heaven in Hell.

The top 25 deadliest actors, visualized.

(Randal Olson)

Olson notes that the deadliest woman onscreen is Uma Thurman, who has 77 kills because remember: the Crazy 88s only had 40 members.

From Your Site Articles

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This is Hollywood's deadliest action star - We Are The Mighty

Hypersexual disorder, sometimes referred to as sex addiction, affects around 3 to 6 percent of the global population.

The World Health Organization lists hypersexual disorder as an impulse disorder characterized by obsessive thoughts revolving around sex, feeling out of control, and engaging in risky sexual behavior disregarding personal health and safety.

There is some controversy as to whether hypersexual disorder can be classified as such, or if its simply an extension or manifestation of another mental health issue. Without a clear understanding of hypersexual disorder, it can result in stigma, misleading information, and prevent people from seeking treatment or help.

Very little research has been done on the neurobiology behind hypersexual disorder.

Researchers from Uppsala University and Karolinska Institutet in Sweden may have identified biological mechanisms that drive hypersexual disorder.

The researchers focused on epigenetic or heritable changes that influence gene expression without altering DNA sequences.

We set out to investigate the epigenetic regulatory mechanisms behind hypersexual disorder so we could determine whether it has any hallmarks that make it distinct from other health issues, said Adrian Bostrm, the lead author of the study.

The researchers analyzed blood samples from 60 patients with hypersexual disorder and 30 patients who werent diagnosed with the disorder.

In the blood samples, the researchers measured DNA methylation patterns or modifications that affect gene expression.

Two regions of DNA were altered in the blood of the patients with hypersexual disorder, and the changes may result in unregulated and elevated production of oxytocin (the love hormone), but the researchers say that more work is needed to confirm this connection.

Further research will be needed to investigate the role of microRNA-4456 and oxytocin in hypersexual disorder, but our results suggest it could be worthwhile to examine the benefits of drug and psychotherapy to reduce the activity of oxytocin, said Professor Jussi Jokinen, an author of the study.

The researchers published their findings in the journal Epigenetics.

By Kay Vandette, Earth.com Staff Writer

Image Credit: Shutterstock/Vasilyev Alexandr

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Is sex addiction rooted in the unregulated production of oxytocin? - Earth.com

Introduction

For decades, scientists have known the basic structure of our DNA, the building blocks that make up our genes. Although nearly every cell in the human body has the same set of genes, why is it that different types of cells, such as those from brain or skin, look and behave so differently?

The answer is epigenetics, a rapidly growing area of science that focuses on the processes that help direct when individual genes are turned on or off. While the cells DNA provides the instruction manual, genes also need specific instructions. In essence, epigenetic processes tell the cell to read specific pages of the instruction manual at distinct times.

Some epigenetic changes are stable and last a lifetime, and some may be passed on from one generation to the next, without changing the genes.

Several epigenetic processes involve chemical compounds that attach, or bind, to DNA or to proteins that package the DNA within cells called histones. When a chemical compound binds to DNA, certain genes switch on or off, selecting which proteins are made.

For example, the epigenetic process of DNA methylation involves the binding of a chemical compound called a methyl group to certain locations on the DNA. This binding changes the structure of DNA, making genes more or less active in their role of making proteins.

Another process called histone modification involves chemical compounds that bind to histone proteins. Ribonucleic acids, or RNAs, are also present in cells and can participate in epigenetic processes that regulate the activity of genes.

DNA methylation and histone modification are normal processes within cells and play a role in development, by instructing stem cells, or cells capable of turning into more specialized cells, like brain or skin cells.

Epigenetic processes are particularly important in early life when cells are first receiving the instructions that will dictate their future development and specialization. These processes can also be initiated or disrupted by environmental factors, such as diet, stress, aging, and pollutants.

In 2005, a team of Italian researchers provided the first concrete evidence for the role of environmental epigenetics in explaining why twins with the same genetic background can have vastly different disease susceptibilities.1 The researchers showed that, at birth, pairs of identical twins have similar epigenetic patterns, including DNA methylation and histone modifications.

However, over time, the epigenetic patterns of individuals become different, even in twins. Since identical twins are the same genetically, the differences are thought to result from a combination of different environmental influences that each individual experiences over a lifetime.

Investigating the effects of the environment on the epigenetic regulation of biological processes and disease susceptibility is a goal in the NIEHS 2012-2017 Strategic Plan.

NIEHS is currently supporting epigenetics research that is accelerating the understanding of human biology and the role of the environment in disease. These discoveries may lead to the development of new ways to prevent and treat diseases for which the environment is believed to be a factor.

In 2003, NIEHS-supported researchers made an important discovery that demonstrated the role of environmental epigenetics in development and disease.2 They used the agouti mouse in their study. The mouse has an altered version of the agouti gene, which causes them to be yellow, obese, and highly susceptible to developing diseases, such as cancer and diabetes.

The researchers fed the mice a diet rich in methyl groups. Through epigenetic processes, the methyl groups attached to the mothers DNA, and turned off the agouti gene. As a result, most of the offspring were born lean and brown, and no longer prone to disease.

This study was the first to demonstrate that it is not just our genes that determine our health, but also our environment and what we eat.

While researchers have known, for quite some time, the sequence of DNA that make up all human genes, collectively known as the genome, the same could not be said for the human epigenome, until recently. The epigenome refers to all of the chemical compounds added to the genetic material of an organism that regulate its function.

NIEHS and the National Institute on Drug Abuse (NIDA) co-led a national effort, through the NIH Roadmap Epigenomics Program, to create a series of epigenomic maps representing locations on the DNA where chemical compounds attached in more than 100 different tissue and cell types, including blood, lung, heart, gastrointestinal tract, brain, and stem cells. The groundbreaking work was featured in a 2015 article in the journal Nature.3

By comparing the epigenomic map of a healthy cell or tissue, with the map of the same cell or tissue after an environmental exposure or in relation to a specific disease, NIEHS scientists can better understand how the environment affects genes through epigenetic processes. The epigenomic maps are available to the entire scientific community through the Washington University Epigenome Browser.

NIEHS-supported researchers at Harvard T.H. Chan School of Public Health have shown that human exposure to environmental air pollutants and toxic metals, such as arsenic, can cause damage to cells that may lead to cardiovascular disease. The research team has been tracking abnormalities in blood, as well as epigenetic changes, which may serve as indicators, or markers, of exposure to air pollution and toxic metals at levels that can increase the risk of cardiovascular disease, particularly in elderly men. These markers may help in the early detection and prevention of cardiovascular and other diseases.4,5

Grantees at Beth Israel Deaconess Medical Center used epigenetics to define the link between environmental exposure to smoke, mercury, and lead, and reproductive outcomes, such as preterm birth.6,7 Their results are important, since more than one in 10 infants worldwide is born prematurely, increasing their chances of having health problems later in life.8 The study also found that epigenetic changes may serve as markers for maternal chemical exposure during pregnancy.

NIEHS scientists in the Epigenetics and Stem Cell Biology Laboratory are examining how epigenetic mechanisms influence normal cell development, and contribute to biological processes involved in breast cancer and immune function. To date, they have uncovered many details of how the protein complex Mi-2/NuRD controls genes involved in breast cancer. Mi-2/NuRD is found in the nucleus of cells and includes enzymes that affect histone modifications that regulate gene activity.

The research is helping to identify what genes are regulated by the complex and how the complex alters epigenetic processes that may contribute to disease. Understanding the underlying mechanisms of disease may lead to the development of new methods to diagnose, prevent, and treat diseases, such as breast cancer, in the future.

NIEHS-supported researchers have found that early-life exposure to nutritional and dietary factors, maternal stress, and environmental chemicals can increase the likelihood of developing disease and poor health outcomes later in life. In addition, some of the effects of these exposures can be passed down for multiple generations, even after the original exposure has been removed, through a process known as transgenerational inheritance.

Researchers in the NIEHS Transgenerational Inheritance in Mammals After Environmental Exposure (TIME) Program are using mice and rats to investigate how transgenerational inheritance occurs after exposure to environmental exposures, whether the process is different in males and females, and when in development these events are most likely to occur. Understanding how transgenerational inheritance of effects from exposures occur in animals may shed light on similar processes in humans.

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Epigenetics - National Institute of Environmental Health ...

New scientific research shows that environmental influences can actually affect whether and how genes are expressed. In fact, scientists have discovered that early experiences can determine how genes are turned on and off and even whether some are expressed at all. Thus, the old ideas that genes are set in stone or that they alone determine development have been disproven. Nature vs. Nurture is no longer a debateits nearly always both!

Deep Dive: Gene-Environment InteractionLearn more about the physical and chemical processes that take place as part of the creation of the epigenome.

Working Paper 10: Early Experiences Can Alter Gene Expression and Affect Long-Term DevelopmentThis in-depth working paper explains how genes and the environment interact, and gives recommendations for ways that caregivers and policymakers can effectively respond to the science.

During development, the DNA that makes up our genes accumulates chemical marks that determine how much or little of the genes is expressed. This collection of chemical marks is known as the epigenome. The different experiences children have rearrange those chemical marks. This explains why genetically identical twins can exhibit different behaviors, skills, health, and achievement.

Until recently, the influences of genes were thought to be set, and the effects of childrens experiences and environments on brain architecture and long-term physical and mental health outcomes remained a mystery. That lack of understanding led to several misleading conclusions about the degree to which negative and positive environmental factors and experiences can affect the developing fetus and young child. The following misconceptions are particularly important to set straight.

The epigenome can be affected by positive experiences, such as supportive relationships and opportunities for learning, or negative influences, such as environmental toxins or stressful life circumstances, which leave a unique epigenetic signature on the genes. These signatures can be temporary or permanent and both types affect how easily the genes are switched on or off. Recent research demonstrates that there may be ways to reverse certain negative changes and restore healthy functioning, but that takes a lot more effort, may not be successful at changing all aspects of the signatures, and is costly. Thus, the very best strategy is to support responsive relationships and reduce stress to build strong brains from the beginning, helping children grow up to be healthy, productive members of society.

For more information:Early Experiences Can Alter Gene Expression and Affect Long-Term Development: Working Paper No. 10.

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What is Epigenetics? The Answer to the Nature vs. Nurture ...

What if the decisions you make today affect not just your health, but the health of your family for several generations to come? It sounds a bit crazy sure, your mid-afternoon sugar habit could lead to you packing on a few pounds over the years, but how in the world would it affect offspring you dont even have yet?

Welcome to the wild world of epigenetics.

Epigenetics is an emerging field of science that, eventually, could have massive implications on how we address our health and that of future generations. The world literally means on top of the genes, and that sums up the epigenomes role in the body.

All of us have DNA which, unless you have an identical twin, is completely unique. Almost every cell in our body contains all of our DNA and all of the genes that make us who we are; this is known as the genome. But obviously we are not all made up of just one type of cell. Our brain cells do different things from those in our heart, for instance, who behave differently than our skin cells. If all of our cells have the same information, how is it that they do different things?

This is where epigenetics comes in. Its basically a layer of instruction on top of our DNA that tells it what to switch on, how to perform and so forth. You can think of it like an orchestra: our DNA is the music, and the epigenome is the conductor, telling the cells what to do and when. Everyones personal orchestra is a little bit different. So while the epigenome doesnt change our DNA, its responsible for deciding what genes will be expressed in your bodys cells.

Heres how it works: each cell with all of your DNA waits for outside instruction to give it instructions. This comes in the form of a methyl group, a compound made from carbon and hydrogen. These methyl groups bind to the genes, letting them know when to express themselves and when to stay dormant, and they bind differently depending on where in the body the DNA is. Smart, eh?

Histones also play a role in epigenetics and how genes express themselves. Histones are the protein molecules that DNA wind itself around. How tightly wound the DNA is around the histone plays a role in how strongly a gene expresses itself. So the methyl groups tell the cell what it is (youre a skin cell, and heres what you do), and histones decide how much the cell is going to crank up the volume, so to speak. Every cell in your body has this methyl and histone combination, instructing it what to do and how much to do. Without the epigenome giving instructions to your cells, the genome, our bodies wouldnt know what to do.

What makes this interesting is that while our genome is the same from the time we are born to when we die, our epigenome changes throughout our lifetime, deciding what genes need to be turned on or off (expressed or not expressed). Sometimes these changes happen during major physical changes to our body, like when we hit puberty or when women are pregnant. But, as science is beginning to discover, external factors to our environment can prompt epigenetic changes as well.

Things like how much physical activity we engage in, what and how much we eat, our stress levels, whether we smoke or drink heavily and more can all make changes to our epigenome by affecting how methyl groups attach to the cells. In turn, changing the way methyl bonds to the cells can cause mistakes, which can lead to disease and other disorders.

It seems like because the epigenome is constantly changing, that each new human would start with a clean, fresh epigenome slate that is, that parents wouldnt pass their epigenomes on to their offspring. And while thats what should happen, sometimes these epigenetic changes get stuck on the genes and are passed down to future generations.

One example of this is the Dutch Hunger Winter Syndrome. Babies who were exposed to famine prenatally during World War II in the Netherlands had an increased risk of metabolic disease later in life and had different DNA methylation of a particular gene when compared to their same-sex siblings who were not exposed to famine. These changes persisted six decades later. (1)

Another study found that while identical twins are largely epigenetically indistinguishable from each other when theyre first born, as they aged, there were vast differences in their methyl groups and histones, affecting how their genes express themselves, and accounting for differences in their health. (2)

Damaged or weakened DNA that is replicated can inevitably create alternative epigenetic expression states that can affect several generations. A 2017 study discovered impaired DNA replication in roundworms increased expression from a non-expressed transgene or natural genetic material that has the potential to change the physical characteristics of an organism. Additionally, impaired DNA replication during embryonic or prenatal development has epigenetic consequences for a genomeor the organisms complete set of DNA. (3)

So far, it sounds like epigenetics is just kind of scary the worst of our habits or life situations being passed down not only to our children, but perhaps even our grandchildren. While epigenetics is still very much in its infancy, there is a lot to be excited about.

1. It could change the way we treat disease. Because the epigenome controls how genes behave, an erroneous epigenome can behave like a genetic mutation. This can lead to an increased risk for diseases like cancer or autoimmune disorders, even if the genes below the epigenome are perfectly normal. As we learn more about what causes those epigenetic errors, scientists can develop drugs that would manipulate the methyl groups or histones that are causing the epigenomic errors, potentially finding a cure for the subset of diseases caused by epigenetics.

2. It could change the way we treat addiction. We already know that some people are more vulnerable to addiction than others. But there is no one addiction gene, as its a combination of inherited and environmental factors that lead to addiction. Researchers have now found that epigenetic mechanisms play a role in the brain when it comes to addiction, influencing how the genes express themselves to develop addiction and also how the predisposition to addiction is passed along to future generations. (4) (5)

A better understanding of how the epigenome affects addiction could mean changing the way addiction is treated in order to prevent a persons offspring from an increased risk of addiction.

3. It could change the way we address trauma. One of the earlier theories around epigenetics is how traumatic events like surviving the Holocaust might change a person epigenome, along with that of their offspring. One small study suggests that the children of Holocaust survivors inherited a specific response to stress. (6)

Another found that children of women pregnant during the September 11 attacks had lower levels of cortisol, which could leave them more vulnerable to post-traumatic stress disorder. (7) These were both small studies and have their detractors, but while these studies might not be conclusive, its not a stretch to think that major traumatic events could find a way of altering someones epigenome enough to pass down to offspring.

Epigenetics is still extremely young, and many of the studies around the topic are quite small, so its hard to say anything is conclusive. Additionally, sometimes epigenetics seems like just one more thing that women who might potentially one become pregnant must worry about (though investigators believe that fathers could pass down epigenetic information at the time of conception, not enough research in humans has been done yet). This could get morally murky in terms of how we dictate what women can and cannot do because they might someday bear children.

No one is sure just how much what we do influences the epigenome, either. While doing all of the usual things like sticking to a healthy diet, exercising regularly, limiting alcohol will all positively affect your health, can they reverse previous damage to the epigenome? Its still unclear in humans. Most of the work done on epigenetics thus far has been on animals, and how much this translates to people remains to be seen.

There is one glimmer of hope in the animal world, though. A study done on rats found that the babies of mothers who were attentive were happier than those with inattentive mothers. There was a difference in the methylation levels between the happy and less happy baby rats, which affected how the gene that controlled their stress response was expressed. But when the less happy babies were adopted by the more attentive rat mothers, they actually grew up to be happier that is, the methyl differences werent permanent and were able to be changed. (8)

Read Next: Telomeres Can Unlock the Key to Longevity

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Epigenetics: Will It Change the Way We Treat Disease? - Dr. Axe

DNA modifications that do not change the DNA sequence can affect gene activity. Chemical compounds that are added to single genes can regulate their activity; these modifications are known as epigenetic changes. The epigenome comprises all of the chemical compounds that have been added to the entirety of ones DNA (genome) as a way to regulate the activity (expression) of all the genes within the genome. The chemical compounds of the epigenome are not part of the DNA sequence, but are on or attached to DNA (epi- means above in Greek). Epigenetic modifications remain as cells divide and in some cases can be inherited through the generations. Environmental influences, such as a persons diet and exposure to pollutants, can also impact the epigenome.

Epigenetic changes can help determine whether genes are turned on or off and can influence the production of proteins in certain cells, ensuring that only necessary proteins are produced. For example, proteins that promote bone growth are not produced in muscle cells. Patterns of epigenetic modification vary among individuals, different tissues within an individual, and even different cells.

A common type of epigenetic modification is called methylation. Methylation involves attaching small molecules called methyl groups, each consisting of one carbon atom and three hydrogen atoms, to segments of DNA. When methyl groups are added to a particular gene, that gene is turned off or silenced, and no protein is produced from that gene.

Because errors in the epigenetic process, such as modifying the wrong gene or failing to add a compound to a gene, can lead to abnormal gene activity or inactivity, they can cause genetic disorders. Conditions including cancers, metabolic disorders, and degenerative disorders have all been found to be related to epigenetic errors.

Scientists continue to explore the relationship between the genome and the chemical compounds that modify it. In particular, they are studying what effect the modifications have on gene function, protein production, and human health.

Read more here:
What is epigenetics? - Genetics Home Reference - NIH

Depiction of cytosines methylation and demethylation processes. The different modified forms of cytosine along with the corresponding enzymes responsible for each modification are shown.

DNA methylation is an epigenetic mechanism that occurs by the addition of a methyl (CH3) group to DNA, thereby oftenmodifying the function of the genes and affecting gene expression. The most widely characterized DNA methylation process is the covalent addition of the methyl groupat the 5-carbon of the cytosine ring resulting in 5-methylcytosine (5-mC), also informally known as the fifth base of DNA. These methyl groups project into the major groove of DNA and inhibit transcription.

In human DNA, 5-methylcytosine is found in approximately 1.5% of genomic DNA.In somatic cells, 5-mC occurs almost exclusively in the context of paired symmetrical methylation of a CpG site, in which a cytosine nucleotide is located next to a guanidine nucleotide. An exception to this is seen in embryonic stem (ES) cells, where a substantial amount of 5-mC is also observed in non-CpG contexts. In the bulk of genomic DNA, most CpG sites are heavily methylated while CpG islands (sites of CpG clusters) in germ-line tissues and located near promoters of normal somatic cells, remain unmethylated, thus allowing gene expression to occur. When a CpG island in the promoter region of a gene is methylated, expression of the gene is repressed (it is turned off).

The addition of methyl groups is controlled at several different levels in cells and is carried out by a family of enzymes called DNA methyltransferases (DNMTs). Three DNMTs (DNMT1, DNMT3a and DNMT3b) are required for establishment and maintenance of DNA methylation patterns. Two additional enzymes (DNMT2 and DNMT3L) may also have more specialized but related functions. DNMT1 appears to be responsible for the maintenance of established patterns of DNA methylation, while DNMT3a and 3b seem to mediate establishment of new or de novo DNA methylation patterns. Diseased cells such as cancer cells may be different in that DNMT1 alone is not responsible for maintaining normal gene hypermethylation (an increase in global DNA methylation) and both DNMTs 1 and 3b may cooperate for this function.

DNA demethylation is the removal of a methyl group from DNA. This mechanism is equally as important and coupled with DNA methylation. The demethylation process is necessary for epigenetic reprogramming of genes and is also directly involved in many important disease mechanisms such as tumor progression. Demethylation of DNA can either be passive or active, or a combination of both. Passive DNA demethylation usually takes place on newly synthesized DNA strands via DNMT1 during replication rounds. Active DNA demethylation mainly occurs by the removal of 5-methylcytosine via the sequential modification of cytosine bases that have been converted by TET enzyme-mediated oxidation. The ten-eleven translocation (TET) family of 5-mC hydroxylases includes TET1, TET2 and TET3. These proteins may promote DNA demethylation by binding to CpG rich regions to prevent unwanted DNA methyltransferase activity, and by converting 5-mC to 5-hmC, 5-hmC to 5-fC (5-formylcytosine), and 5-fC to 5-caC (5-carboxylcytosine) through hydroxylase activity. The TET proteins have been shown to function in transcriptional activation and repression (TET1), tumor suppression (TET2), and DNA methylation reprogramming processes (TET3).

The biological importance of 5-mC as a major epigenetic modification in phenotype and gene expression has been widely recognized. For example DNA hypomethylation, the decrease in global DNA methylation, is likely caused by methyl-deficiency due to a variety of environmental influences and has been proposed as a molecular marker in multiple biological processes such as cancer. The quantification of 5-mC content or global methylation in diseased or environmentally impacted cells could provide useful information for detection and analysis of disease. Furthermore, the detection of the DNA demethylation intermediate 5-fC in various tissues and cells may also be used as a marker to indicate active DNA demethylation. 5-fC can also be directly excised by thymine DNA glycosylase (TDG) to allow subsequent base excision repair (BER) processing which converts modified cytosine back to its unmodified state.

Differentially methylated regions (DMRs) are areas of DNA that have significantly different methylation status between multiple samples. Researchers will often perform genome-wide methylation profiling to identify DMRs between treated or untreated samples, revealing functional regions that may be involved in gene transcriptional regulation. There can be DMRs specific to tissues, cells, individuals, and so on. Differentially methylated regions may also be used as biomarkers or potential targets of epigenetic therapy.

Continue to the next page to learn about DNA methylation tools of the trade.

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DNA Methylation | What is Epigenetics?

Epigenetic mechanisms act at the interface of genetic and environmental factors regulating brain development and determining autism risk. Analysis of postmortem brain tissue, for example, shows thatepigenetic markers varyin people with autismcompared with controls.

Epigenetic modifications, particularly DNA methylation, can be influenced by chemical exposures in the environment, hormones, thefiring patterns of neurons, and diet. Folate, a B vitamin that we absorb from food and is included in prenatal vitamins, is necessary for DNA synthesis and methylation. Preconception use of prenatal vitamins was found to be protective for autism, particularly in mothers with genetic susceptibility in methyl-group metabolism.

Pinpointing epigenetic differences between healthy and diseased cells at progressive stages of development could reveal the roots of neurodevelopmental dysfunction.

Epigenetic changes can occur in adult brain cells and can be activity-dependent that is, triggered by brain activity in response to experience. Such neural responses to changes in the environment are an essential component of adaptivebrainfunction. Therefore, dysregulation of this capacity could lead to maladaptive behavior.

Some studies suggest that when one identical twin has autism, the other will also have it about 40 to 90 percent of the time. A better understanding of how the prenatal environment influences epigenetics could help pinpoint earlyenvironmental risk factors for autism and help explain those cases in which only one twin has autism.

Mapping the epigenome in the brain throughout the lifespan is important for understanding epigenomic changes in autism. In 2013, scientists unveiled the first comprehensive maps of human and mouse DNA methylation patterns from fetal development through adulthood. Aten-year effort known as theInternational Human Epigenome Consortiumaims to catalog and examine epigenetic maps for all cell types throughout the course of development.

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Epigenetics | Spectrum | Autism Research News