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IT’S A FACT: RLS occurs most often in the third trimester of pregnancy. Inflammation occurs most often in the third trimester of pregnancy.

Etymology: L, trimestris, three months
One of the three periods of approximately 3 months into which pregnancy is divided. The first trimester includes the time from the first day of the last menstrual period to the end of 12 weeks. The second trimester, closer to 4 months in length than 3, extends from the twelfth to the twenty-eighth week of gestation. The third trimester begins at the twenty-eighth week and extends to the time of delivery.
(from the Free Online Medical Dictionary)

Below are 3 studies confirming that RLS occurs most often in the third trimester of pregnancy.restless-legs-syndrome-pregnant

“Restless legs syndrome (RLS) is common in the third trimester of pregnancy. In this case-control study, 22.5% of 211 women had RLS. The RLS cases had a history of growing pains (GP) more frequently than controls (P = 0.042). A family history of GP (P = 0.025) and RLS (P = 0.018) was more frequent among cases than controls. RLS in pregnancy is predicted by family history of RLS and GP, and by childhood history of GP.”

“A common sleep disorder in pregnancy: Restless legs syndrome and its predictors.” Balendran J, Champion D, Jaaniste T, Welsh A. Aust N Z J Obstet Gynaecol. 2011 Jun;51(3):262-4. doi: 10.1111/j.1479-828X.2011.01294.x. Epub 2011 Mar 16.

“1,022 pregnant women living in a French town were included in our study. 24% of women were affected by RLS during their pregnancy. The disease was strongly related to the third trimester of pregnancy and had a significant impact on sleep leading to severe nocturnal and diurnal consequences with a high consumption of sleep medication.”

“Restless legs syndrome and pregnancy: a questionnaire study in the Poitiers District, France.” Neau JP, Porcheron A, Mathis S, Julian A, Meurice JC, Paquereau J, Godeneche G, Ciron J, Bouche G. Eur Neurol. 2010;64(5):268-74. Epub 2010 Oct 27.

“RLS prevalence increased from 0 during preconception to 23% (n = 7) during the third trimester of pregnancy.”

“Restless legs syndrome and sleep disturbance during pregnancy: the role of folate and iron.” Lee KA, Zaffke ME, Baratte-Beebe K. J Womens Health Gend Based Med. 2001 May;10(4):335-41.

100480667Below are 3 studies confirming that inflammation occurs most often in the third trimester of pregnancy.

“A significant increase of proinflammatory cytokines (IL-6 and IL-8) is produced in the third trimester. These cytokines act as chemoattractants of polymorphonuclear leukocytes stimulating the expression of prostaglandins in response to delivery preparation.”

“Vaginal cytokines in normal pregnancy.” G. Gilbert, G. Donders, A. Vereecken, E. Bosmans, and B. Spitz, American Journal of Obstetrics and Gynecology, vol. 189, no. 5, pp. 1433–1438, 2003.

“Pregnancy is a complex process which leads to a number of systemic changes. During normal pregnancy all these changes are very well regulated. Preeclampsia is a very common disorder of pregnancy and is characterized by hypertension and proteinuria that begins at more than 20 weeks of gestation. Poor placentation with inadequate cytotrophoblast invasion results in widespread maternal endothelial dysfunction. There is increasing evidence that preeclampsia is accompanied by exaggerated maternal systemic inflammatory response to this poor placentation.”

“C Reactive Protein levels are elevated in the Third Trimester in Preeclamptic pregnant Women.” Zaima Ali, Saima Zak, Ambreen Tauseef, Ayesha Akmal. Dept. of Physiology, Lahore Medical and Dental College, Department of Obstetrics and Gynecology, Jinnah Hospital, Lahore.

“Prokineticin-1 (PK1) is a recently described protein with a wide range of functions, including tissue-specific angiogenesis, modulation of inflammatory responses, and regulation of hemopoiesis. The aim of this study was to investigate the localization and expression of PK1 and PK receptor-1 (PKR1), their signaling pathways, and the effect of PK1 on expression of the inflammatory mediators cyclooxygenase (COX)-2 and IL-8 in third-trimester placenta.

Our study demonstrates that PK1 and PKR1 are highly expressed in third-trimester placenta with PK1 up-regulating expression of IL-8 and COX-2 potentially via activation of PKR1 and cross-talk with EGFR. The latter finding is supported by double-immunofluorescent immunohistochemistry studies that show that PKR1 colocalizes with IL-8 and COX-2 in placenta. Together, these data suggest that PK1 may be a novel paracrine mediator of the inflammatory response in third-trimester placenta.”

“Prokineticin-1: A Novel Mediator of the Inflammatory Response in Third-Trimester Human Placenta. Fiona C. Denison, Sharon Battersby, Anne E. King, Michael Szuber, and Henry N. Jabbour. Endocrinology. 2008 July; 149(7): 3470–3477. doi:  10.1210/en.2007-1695

to-summarizeIT’S A FACT!

RLS occurs most often in the third trimester of pregnancy. Inflammation occurs most often in the third trimester of pregnancy.

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RLS is NOT Hereditary: Welcome to the AMAZING World of Epigenetics! (PART ONE: Introduction)

ImageSeveral years ago someone in my book club suggested that we read “The Biology of Belief” by Bruce Lipton.

It turned out to be a life-changing event. The book had such an huge impact on me that I excitedly wrote a letter to Mr. Lipton congratulating him on his discoveries and his courage to bring his ideas forth to the scientific community – a community that doesn’t accept change lightly. I’ve never done that for any other author.

He had introduced me to a new field of science called “Epigenetics,” a deeper level of science that blew the lid off all that we had previously learned about genetics, including our firm beliefs of how our genes control our behaviour and traits.

When I first read the book, epigenetics seemed like an off-Broadway type of science that had a few enthusiastic followers, but probably wasn’t going to go anywhere. These radical views were far too outrageous for mainstream science to ever embrace.

BUt, here we are, many years later, and Epigenetics IS the new science. Its popularity is SOARING around the globe! The new possibilities that it offers to fight diseases, including Restless Legs Syndrome, are unlimited.

As you can see from the above graphics, epigenetics is front page news for dozens of magazines and journals. There are also a growing number of books on epigenetics being published.

To hold on to the old ideas about genetics is like holding on to the idea that the earth is flat. The old genetics we held so tightly to is officially dead. It’s time to move on.

ImageEpigenetics is to genetics … as a jet aircraft is to a rowboat.

“Our health is not controlled by genetics. Conventional medicine is operating from an archaic view that we’re controlled by genes. This misunderstands the nature of how biology works.

Medicine does miracles, but it’s limited to trauma. The AMA protocol is to regard our physical body like a machine, in the same way that an auto mechanic regards a car. When the parts break, you replace them—a transplant, synthetic joints, and so on—and those are medical miracles.

ImageThe problem is that while they have an understanding that the mechanism isn’t working, they’re blaming the vehicle for what went wrong. They believe that the vehicle, in this case our bodies, is controlled by genes.

But guess what? They don’t take into consideration that there’s actually a driver in that car. The new science, epigenetics, reveals that the vehicles—or the genes—aren’t responsible for the breakdown. It’s the driver.

Dr. Dean Ornish, physician and Clinical Professor of Medicine at the University of California, San Francisco. has taken conventional cardiovascular patients, provided them with important lifestyle insights (better diet, stress-reduction techniques, and so on), and without drugs, the cardiovascular disease was resolved. Ornish relayed that if he’d gotten the same results with a drug, every doctor would be prescribing it.” Bruce Lipton, PhD


There is a common prognosis that medical professionals tend to use. It’s a SINGLE WORD that brings in countless BILLIONS of dollars to pharmaceutical companies each year.

That word is “HEREDITARY.”

Loosely translated it means “There’s nothing that can be done about your condition. This is the hand you were dealt. You’ll need to take medication for the rest of your life in order to deal with the symptoms.”

But that’s yesterday’s news.

Image“Roll over, Mendel. Watson and Crick. They are so your old man’s version of DNA. And that big multibillion-dollar hullabaloo called the Human Genome Project? To some scientists, it’s beginning to look like an expensive genetic floor pad for a much more intricate – and dynamic – tapestry of life that lies on top of it.” Newsweek Magazine, June 2009

People with chronic ailments can no longer use genetics as an excuse to NOT take action to lessen their condition. The old belief that an “inherited condition” is unchangeable is no longer supported by science.

This certainly applies to those with Restless Legs Syndrome. The excuse to not take action because it’s your mother or father’s fault that you have the “RLS gene” – and there’s nothing you can do about it, is not an option anymore.

In fact, researchers in the field of epigenetics insist that you DO take action. That’s how the switches on your genes are changed for the better.

Image“The picture ingrained in the public mind is that genes determine everything from our physical characteristics to our behavior. Even many scientists still speak from the assumption that our genes form an immutable blueprint that our cells must forever follow. However, the new science of epigenetics tells us that “genes are merely blueprints, and it is the environment that determines genetic expression.”Bruce Lipton & Dawson Church

Epigenetics has blown the roof off the limitations of the human genome and through it shines a brilliant light of hope that THOUSANDS of scientists are recognizing and acting on.

Researchers around the world are scrambling with a childlike enthusiasm in order to tap into the giant universe of possibilities that epigenetics has brought forth.

ImageAs a Restless Legs sufferer, the information you’ll read in these posts about epigenetics should help lessen the hopelessness of your condition.

1. You will no longer be chained to the belief that RLS is genetic and that you’re STUCK with it.

2. You may realize that RLS is NOT incurable when you learn how a simple diet can be used to switch helpful genes “ON” and harmful genes “OFF”.

For definitions of some of the terms used in the upcoming posts, please visit

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RLS is NOT Hereditary: Welcome to the AMAZING World of Epigenetics! (PART TWO: What is Epigenetics?)

Image“The exploding science of epigenetics will transform our understanding of health and disease.” – Peter A. Jones, PhD, DSc. Professor of Urology and Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California

As you will read below, the science of epigenetics IS exploding onto the scene.  
And with that explosion comes a powerful new awareness that is freeing our minds and spirits as it continues to debunk the old myth that we are “stuck” with the genes that were passed on to us, including the genes that cause RLS.

And we’re only at the beginning. Hope has arrived!

from Randy Jirtle, Geneticist, Dept. of Radiation Oncology at Duke University

“Think of the genome as being like the hardware of a computer. The epigenome would be like the software that tells the computer when to work, how to work, and how much.”

from The Week “Epigenetics: How our experiences affect our offspring.” January 20, 2013    

“New research suggests that people’s experiences, not just their genes, can affect the biological legacy of their offspring

Isn’t our genetic legacy hardwired?

From Mendel and Darwin in the 19th century to Watson and Crick in the 20th, scientists have shown that chromosomes passed from parent to child form a genetic blueprint for development. But in a quiet scientific revolution, researchers have in recent years come to realize that genes aren’t a fixed, predetermined program simply passed from one generation to the next. Instead, genes can be turned on and off by experiences and environment. What we eat, how much stress we undergo, and what toxins we’re exposed to can all alter the genetic legacy we pass on to our children and even grandchildren. In this new science of “epigenetics,” researchers are exploring how nature and nurture combine to cause behavior, traits, and illnesses that genes alone can’t explain, ranging from sexual orientation to autism to cancer. “We were all brought up to think the genome was it,” said Rockefeller University molecular biologist C. David Allis. “It’s really been a watershed in understanding that there is something beyond the genome.”

What is epigenetics?

The word literally means “on top of genetics,” and it’s the study of how individual genes can be activated or deactivated by life experiences. Each one of our cells, from skin cells to neurons, contains an identical DNA blueprint, yet they perform vastly different functions. That’s because epigenetic “tags” block developing fetal cells from following any genetic instructions that don’t pertain to their intended roles. That biochemical process, scientists have discovered, occurs not just during gestation and early development but throughout adulthood, switching genes on or off and altering our mental and physical health.

How does that affect who we are?

We’re only beginning to find out. A woman’s diet during pregnancy seems to have a major impact on her baby’s epigenetic tags. Prenatal diets that are low in folic acid, vitamin B-12, and other nutrients containing “methyl groups” — a set of molecules that can tag genes and cause epigenetic changes — have been linked to an increased risk of asthma and brain and spinal cord defects in children. Stress, too, can alter fetal epigenetic tags. Pregnant women who were traumatized at the World Trade Center on 9/11 were far more likely than other women to give birth to infants who reacted with unusual levels of fear and stress when faced with loud noises, unfamiliar people, or new foods.

Are these insights yielding medical therapies?

Over the past five years, evidence that epigenetics plays a major role in cancer has become “absolutely rock solid,” says Robert A. Weinberg, a biologist at the Whitehead Institute in Cambridge, Mass. Andrew Feinberg, director of Johns Hopkins University’s Epigenetics Center, thinks it’s a factor in autism and diabetes as well. Drugs are in the works aimed at undoing cancerous epigenetic changes. Even eating foods rich in gene-altering methyl groups — such as soybeans, red grapes, and green tea — might protect against disease by silencing detrimental genes. In one famous experiment, researchers fed a methyl-rich diet to pregnant female mice that carried a gene that made them fat, yellow, and prone to cancer and diabetes. Though their offspring carried the same gene, they were born slim, brown, and disease-free. But researchers are still trying to work out how to use this powerful tool to address specific health problems. “Did this change in diet increase cancer risk?” asks McGill University pharmacologist Moshe Szyf. “Did it increase depression? Did it increase dementia or Alzheimer’s? We don’t know yet, and it will take some time to sort it out.”

Imagefrom Newsweek Magazine “Beyond the Book of Life.” Jun 26, 2009

“There’s a revolution sweeping biology today — begrudged by a few, but accepted by more and more biologists — that is changing scientific thinking about the way genes work, the way diseases arise and the way some of the most dreadful among them, including cancer, might be diagnosed and treated. This revolution is called epigenetics, and it is not only beginning to explain some of the biological mysteries that deepened with the Human Genome Project. Because of a series of accidental events, it is already prolonging the lives of human patients with deadly diseases.

Over the past several years, and largely without much public notice, physicians have reported success using epigenetic therapies against cancers of the blood and have even made progress against intractable solid-tumor malignancies like lung cancer. The story is still preliminary and unfolding (dozens of clinical trials using epigenetic drugs are currently underway), but Dr. Margaret Foti, chief executive officer of the American Association for Cancer Research, recently noted that epigenetics is already resulting in “significant improvements” in cancer diagnosis and therapy. “It’s really coming into its own now,” she said. Leaping on the bandwagon, the National Institutes of Health made epigenetics the focus of one of its cutting-edge “Roadmap” initiatives announced last fall.

“I think we were all brought up to think the genome was it,” says C. David Allis, a scientist at Rockefeller University whose research in the 1990s helped catalyze the current interest in epigenetics. “But even when the genome was a done deal, some people thought, ‘Is that the whole story?’ It’s really been a watershed in understanding that there is something beyond the genome.”

The emergence of epigenetics represents a fundamental rethinking of how molecular biology works. Scientists have learned that while DNA remains the basic text of life, the script is often controlled by stage directions embedded in a layer of biochemicals that, roughly speaking, sit on top of the DNA. These modifications, called epimutations, can turn genes on and off, often at inappropriate times. In other words, epigenetics has introduced the startling idea that it’s not just the book of life (in the form of DNA) that’s important, but how the book is packaged.“

from “Epigenetics, Methylation, and Gene Expression.” by Kevin Cann, April 10th, 2013

“Many of us think that we are doomed to a life of obesity or disease because of our genes. The truth is, we may be more genetically predisposed to certain metabolic conditions or disease states, but that does not mean there are not things we can do to alter this gene expression.  The idea that our genes react to environmental and internal stimuli is referred to as epigenetics. Our genetic code is wrapped up into our DNA and paired into 23 sets of chromosomes.

The DNA then wraps itself around alkaline proteins called histones. These histones then give the DNA structure. These newly formed structures are referred to as nucleosomes. On the outside of these histones are chemical messengers that listen for cues from the environment and from our internal systems. This whole structure is known as the epigenome. When the chemical messengers receive a stimuli, they will react by tightening themselves around certain genes to make them inactive so that they cannot be read by other cells. On the other hand they will relax themselves around other genes so that they are easily accessible. Our DNA we are stuck with, but our gene expression can be altered.

Our bodies turn off genes through a process called methylation. To keep it simple this is adding a methyl group to the DNA. As of late researchers have been looking at methylation as a primary role player in the onset of certain diseases. It is believed that methylation plays an important role in the stability of trinucleotides. In a trinucleotide repeat disorder such as Huntington’s Disease, this is important to understand. There are germinal and somatic cells within our system, and methylation is in charge of maintaining their stability.”
from The University of Utah Genetic Science Learning Center “What is Epigenetics”

“The development and maintenance of an organism is orchestrated by a set of chemical reactions that switch parts of the genome off and on at strategic times and locations. Epigenetics is the study of these reactions and the factors that influence them.”
Imagefrom Science Watch “Epigenetics: 20 Years and Rising.” by Jeremy Cherfas   

“Over a 20-year period, there has been an eight-fold increase of papers on epigenetics from just over 1,000 papers in 1992 to more than 8,500 in 2011.
Following on this steady rise, epigenetics as a research field will undoubtedly get a further boost from the 2012 Nobel Prize in Physiology or Medicine, awarded to John B. Gurdon and Shinya Yamanaka. Gurdon showed that an adult frog nucleus contains all the genetic information needed to develop into a mature frog. Yamanaka discovered that just four genes could reprogram an adult skin cell into a pluripotent stem cell, capable of differentiating into all the specialized cell lines of an adult mouse. Both were effectively reversing a lifetime of epigenetic modifications to the cell.”

from NOVA scienceNOW “Epigenetics.” July, 2007

“Once nurture seemed clearly distinct from nature. Now it appears that our diets and lifestyles can change the expression of our genes. How? By influencing a network of chemical switches within our cells collectively known as the epigenome. This new understanding may lead us to potent new medical therapies. Epigenetic cancer therapy, for one, already seems to be yielding promising results.

Our lifestyles might affect the health of our children and even grandchildren.”

from The New York Times “Why Fathers Really Matter.” by Judith Shulevitz, September 8, 2012

“Epigenetics means that our physical and mental tendencies were not set in stone during the Pleistocene age, as evolutionary psychology sometimes seems to claim. Rather, they’re shaped by the life we lead and the world we live in right now. Epigenetics proves that we are the products of history, public as well as private, in parts of us that are so intimately ours that few people ever imagined that history could reach them.”

from The University of Utah Genetic Science Learning Center “The Epigenome Learns from its Experiences.”

“Epigenetic tags act as a kind of cellular memory. A cell’s epigenetic profile — a collection of tags that tell genes whether to be on or off — is the sum of the signals it has received during its lifetime.

As a fertilized egg develops into a baby, dozens of signals received over days, weeks, and months cause incremental changes in gene expression patterns. Epigenetic tags record the cell’s experiences on the DNA, helping to stabilize gene expression. Each signal shuts down some genes and activates others as it nudges a cell toward its final fate. Different experiences cause the epigenetic profiles of each cell type to grow increasingly different over time. In the end, hundreds of cell types form, each with a distinct identity and a specialized function.“

Imagefrom The New York Times “Study Finds How Genes That Cause Illness Work.” by Gina Kolata, January 20, 2013

“In a pathbreaking paper, researchers at the Johns Hopkins University School of Medicine and the Karolinska Institute in Sweden report a way to evaluate one gene-regulation system: chemical tags that tell genes to be active or not. Their test case was of patients with rheumatoid arthritis, a crippling autoimmune disease that affects 1.5 million Americans.

Researchers know a gene will remain stable, but the chemical tags that turn the genes on and off are not so reliable. Their presence can be affected by the environment or medications or even the activity of other, distant genes. They can be a consequence of a disease or set off a disease.

The researchers reported measurement techniques that enabled them to sort things out. They found hundreds of chemical tags but only four that seemed truly related to the disease. Those four were in a cluster of genes that controls the immune response and that was known to affect the risk of rheumatoid arthritis, said Dr. Andrew Feinberg of Johns Hopkins, a lead author of the study. In particular, the tags were in a gene called C6orf10 whose function is unknown.

The chemical tags may help determine if a person with a gene that increases risk of developing a disease actually gets the disease. There were people in the control group who had gene variations associated with arthritis risk, but they did not have those four chemical tags and did not have the disease.”

from The Washington Post “Emerging science aims to manipulate human DNA.” by Rachel Saslow, December 15, 2009

“Two mice. One weighs 20 grams and has brown fur. The other is a hefty 60 grams with yellow fur and is prone to diabetes and cancer. They’re identical twins, with identical DNA.

So what accounts for the differences?

It turns out that their varying traits are controlled by a mediator between nature and nurture known as epigenetics. A group of molecules that sit atop our DNA, the epigenome tells genes when to turn on and off.

A growing body of research has some scientists rethinking humans’ genetic destinies. Is our hereditary fate — bipolar disorder or cancer at age 70, for example — sealed upon the formation of our double helices, or are there things we can do to change it? Are we recipients of our DNA, or caretakers of it?

Last year, the National Institutes of Health announced that it would invest $190 million to accelerate epigenetic research. The list of illnesses to be studied in the resulting grants reveals the scope of the emerging field: cancer, Alzheimer’s disease, autism, bipolar disorder, schizophrenia, asthma, kidney disease, glaucoma, muscular dystrophy and more.”

“Prostaglandin E2 promotes intestinal tumor growth via DNA methylation.” by Dianren Xia, Dingzhi Wang, Sun-Hee Kim, Hiroshi Katoh & Raymond N DuBois. Nature Medicine 18, 224–226 (2012). doi:10.1038/nm.2608

“The difference between genetics and epigenetics can be compared to the difference between writing and reading a book. Once a book is written the text (genes or DNA sequence) will be the same in all copies distributed to the audience. However, each individual reader of a book may interpret the story slightly differently, with varying emotions and projections.

In a similar manner, epigenetics would allow different interpretations of a fixed template and result in different read-outs dependent on the variable conditions under which the template is interrogated.”
from “Why Your DNA Isn’t Your Destiny.” January 23, 2010

“For decades, we have stumbled around massive Darwinian roadblocks. DNA, we thought, was an ironclad code that we and our children and their children had to live by. Now we can imagine a world in which we can tinker with DNA, bend it to our will.

It will take geneticists and ethicists many years to work out all the implications, but be assured: the age of epigenetics has arrived.

ImageYour Genetics Are Malleable — Like Clay

Epigenetic “malleability” helps to explain why identical twins become distinct as they age.

Why does one identical twin develop cancer and the other remain healthy when they have identical DNA? Why does one twin become obese and another remain lean?

As you age, your genome does not change but your epigenome changes dramatically, especially during critical periods of life, such as adolescence. It is influenced by physical and emotional stresses — how you respond to everything that happens in your environment, from climate change to childhood abuse.

You do not manifest disease merely by a defective gene, but by your epigenome. In other words, whether or not you develop disease is determined by how your genome is being directed to express itself. There are also “master genes” that can switch on and off clusters of other genes.

Scientists have discovered it is easier to make epigenetic changes than to fix damaged genes. Your epigenome is easier to mess up — but it’s also easier to fix.

That’s good news — you aren’t doomed by bad genes!

Epigenetic therapy, which is essentially the curing of disease by epigenetic manipulation, involves changing the instructions to your cells — reactivating desirable genes and deactivating undesirable ones. This emerging field, now in its infancy, may represent the future of medicine.”

from The New York Times “Genes as Mirrors of Life Experiences.” by Benedict Carey, November 8, 2010

“By studying genes at the “epi” level, scientists are hoping to discover patterns that have been elusive at the level of the genes — and ideally to find targets for calibrated treatments that would not simply shut off errant genes but would gradually turn their activity up or down, like adjusting the balance on a stereo.”

from LiveScience “Why Your DNA May Not Be Your Destiny.” by Denise Chow, June 04, 2013  

“Ten years ago, when researchers completed the first map of all the genes of human beings, the immense undertaking promised to revolutionize the field of molecular medicine. It did, but something was still missing.

“By sequencing the 3 billion chemical base pairs that make up human DNA, scientists were able to glean new information about genes and how they are expressed. Yet there were hints that something else might be controlling which genes are turned on and off” said Jean-Pierre Issa, director of the Fels Institute for Cancer Research and professor of molecular biology at Temple University in Philadelphia.

“When the human genome was sequenced, some scientists were saying, ‘That’s the end. We’re going to understand every disease. We’re going to understand every behavior.'” Issa said. “And it turns out, we didn’t, because the sequence of the DNA isn’t enough to explain behavior. It isn’t enough to explain diseases.”

In the 1950s, an English developmental biologist named Conrad Waddington suggested that something was working on top of the DNA sequence to modulate gene expression.

Scientists who advanced Waddington’s hypothesis began investigating whether experiences or a person’s environment could trigger genetic changes. This work came to be known as epigenetics, and it suggested that human development was not completely hardwired in DNA.

“When you think of nurture and nature, what epigenetics represents is the interface between those two influences,” said Frances Champagne, a behavioral scientist at Columbia University in New York.”
from The Scientist “Decoding DNA: New Twists and Turns.”

“From my perspective,” says Victoria Richon, Vice President, Discovery and Preclinical Research, Sanofi. “I think the reason why we’re really seeing the explosion of information about this field is that we now understand the enzymes and really the machinery that’s catalyzing the … different modifications, which previously we didn’t.”

Imagefrom Jean Pierre Issa M.D. Anderson Cancer Center  

“The idea of epigenetic therapy is to stay away from killing the cell. Rather, what we are trying to do is diplomacy, trying to change the instructions of the cells, reminding the cell, “Hey, you’re a human cell. You shouldn’t be behaving this way.” And we try to do that by reactivating genes.”

from “Phenocopies in families with essential tremor and restless legs syndrome challenge Mendelian laws. Epigenetics might provide answers.” by Zimprich A.  Parkinsonism Relat Disord. 2012 Jul;18(6):711-6. doi: 10.1016/j.parkreldis.2012.03.019.  

“Inheritance of epigenetic mutations along with paramutational events have the potential to explain the non-mendelian features in the genetics of restless legs syndrome.”

from Scientific American “How Acquired Diseases Become Hereditary Illnesses.” by JR Minkel, August 9, 2010

“One of the primary goals of genetics over the past decade has been to understand human health and disease in terms of differences in DNA from person to person. But even a relatively straightforward trait such as height has resisted attempts to reduce it to a particular combination of genes. In light of this shortcoming, some investigators see room for an increased focus on an alternative explanation for heritable traits: epigenetics, the molecular processes that control a gene’s potential to act. Evidence now suggests that epigenetics can lead to inherited forms of obesity and cancer.

The best-studied form of epigenetic regulation is methylation, the addition of clusters of atoms made of carbon and hydrogen (methyl groups) to DNA. Depending on where they are placed, methyl groups direct the cell to ignore any genes present in a stretch of DNA. During embryonic development, undifferentiated stem cells accumulate methyl groups and other epigenetic marks that funnel them into one of the three germ layers, each of which gives rise to a different set of adult tissues. In 2008 the National Institutes of Health launched the $190-million Roadmap Epigenomics Project with the goal of cataloguing the epigenetic marks in the major human cell types and tissues.”

from Potential Magazine “Research Frontiers: The Study of Epigenetics.” by Martie Callaghan, Spring 2009

Are your genes turned on?

“We know that epigenetic phenomena can be transmitted from generation to generation,” says Dr. Walter Kaufmann of the Kennedy Krieger Institute. “We must now identify specific diets or other lifestyle dynamics that can influence and potentially reverse these epigenetic labels that you inherited from your ancestors.”

The implications and applications of epigenetics reach even farther.

“We use a lot of medications in young children and many times there is no alternative but to do that,” Dr. Kaufmann says. “We may be able to think about interventions that are more environment based.”

Imagefrom The Sydney Morning Herald “You are what your mother ate.” by Sarah Berry, March 15, 2012

“Unlike genes, which can take hundreds of years to change, epigenetic changes can occur relatively quickly.”

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RLS is NOT Hereditary: Welcome to the AMAZING World of Epigenetics! (PART THREE: Inflammation and Epigenetics)

ImageAs a society we are faced with an epidemic of chronic inflammation.

Epigenetics’ role in lessening this condition is of the highest interest to restless legs sufferers.

Scientists have reached a level where the “cause” of diseases can actually be determined and altered.

Unfortunately, at this time, RLS is not a high priority for researchers when it comes to tapping into the vast healing powers of epigenetics.

Obviously, cancer is at the top of the list. It is followed by other heavy-hitters such as Alzeimer’s, depression, obesity etc.

But that’s still good news for you. Cancer and RLS have something in common – they are both deeply connected to inflammation.
Therefore, whatever switches are discovered that lessen the inflammation involved with cancer, could also be of help to RLS sufferers.

As you’ll read below in the interview with Doctors Belkina and Denis that “changes to one master regulator can affect many different, apparently unrelated, diseases.”

In other words, people with inflammatory diseases other than cancer, such as RLS, could still benefit from any major discoveries made in epigenetic cancer research.

Image“Inflammation and epigenetics: an interview with Dr Belkina and Dr Denis, Boston University School of Medicine.” Interview conducted by April Cashin-Garbutt, BA Hons (Cantab). Published on March 28, 2013.

“What diseases are associated with inflammation?

Inflammation can be thought of as taking two major forms: acute or chronic.

Acute inflammation, which can be painful, usually arises quickly and resolves quickly. It accompanies bacterial infections, traumatic injury and is useful to fight infections and promote healing. But unresolved, severe, acute inflammation can be fatal, such as acute respiratory distress syndrome or influenza, where the lungs develop edema; or sepsis, where ‘cytokine storms’ cause organ damage and shock.

Chronic inflammation is a low-grade form that fails to resolve and can persist over years. Cardiovascular disease, insulin resistance, Type 2 diabetes are good examples; this inflammation is often not acutely painful in a way that might warn the sufferer. Its subtle nature renders it dangerous, and associated with sudden death due to cardiac arrest or stroke. Chronic inflammation can be a serious problem in older, obese humans and has been linked to obesity-associated cancer.

What are macrophages and how do they cause inflammation?

Macrophages differentiate from blood monocytes, they are recruited to different organs in response to signals called chemokines; or they permanently reside in tissues, and so are called ‘resident macrophages’. These cells produce small proteins called cytokines that promote inflammation in the tissue or help with wound healing, tissue remodelling or other kinds of housekeeping.

In acute and chronic inflammatory diseases, the net output of inflammatory cytokines results in organ dysfunction, pain, deteriorating health and even cellular death.

How can genetically identical cells express their genes differently without DNA sequence changes?

The controlling regions of genes, called ‘promoters’ or ‘enhancers’ are packaged into chromatin, which can be permanently marked by epigenetic ‘writer’ enzymes, such as histone acetylases, and read in daughter cells by ‘reader’ proteins, such as bromodomain proteins. These marks can dramatically affect gene expression in otherwise genetically identical cells.

DNA itself can be marked by epigenetic writer enzymes, such as DNA methylases, and read by yet other proteins to change gene expression. Yet in none of these cases has the DNA been mutated or the genetic sequences altered; so that daughter cells can have very different gene expression, yet be genetically identical.

What epigenetic mechanisms did your research into inflammation identify?

We found that the BET family of double bromodomain-containing ‘reader’ proteins is essential for transcriptional regulation of a broad array of genes that produce inflammatory cytokines.

We found that one BET protein in particular, Brd2, is a ‘master regulator’ of many different inflammatory cytokine genes. Thus, if one inhibits this master regulator of inflammation, it’s like throwing a bucket of cold water on the inflammatory fire.

What epigenetic mechanisms did your research into inflammation identify?

We found that the BET family of double bromodomain-containing ‘reader’ proteins is essential for transcriptional regulation of a broad array of genes that produce inflammatory cytokines.

We found that one BET protein in particular, Brd2, is a ‘master regulator’ of many different inflammatory cytokine genes. Thus, if one inhibits this master regulator of inflammation, it’s like throwing a bucket of cold water on the inflammatory fire.

How did your research into the epigenetic mechanisms that connect diseases associated with inflammation originate?

We had been studying Brd2 for many years, and knew that high level expression of Brd2 and other BET family proteins causes cancer. We expected that when we deleted Brd2 in mice that they would not be viable, but got a huge shock when not only did they live, but they became obese.

We experienced an even bigger shock when we found that they did not develop glucose intolerance or insulin resistance, despite their incredible obesity, which was the human equivalent of 600 pounds.

We discovered that their reduced inflammatory profile, brought about by low Brd2 levels, rather than zero Brd2 levels, paradoxically kept them alive, made them fat, and protected their metabolism from inflammatory complications.

There are humans like this, e.g., ‘metabolically healthy obese’ patients who actually perplex their physicians because, although they may be severely obese, they actually preserve many metabolic features of lean and healthy people, including lower risks for cardiovascular disease and Type 2 diabetes, in part because they have a reduced inflammatory profile.

We felt we had no choice but to pursue this amazing, accidental discovery.

Does your research suggest that the different diseases associated with inflammation are linked?

The ‘master regulators’ form a very limited set of proteins that share control of many diverse genes. Thus, changes to one master regulator can affect many different, apparently unrelated, diseases.

By analogy, if you want to cut power quickly to numerous household appliances, you could just trip the master circuit breaker, rather than running around the house and turning off each appliance individually.

Do you think that the current division of medical specialities will need to change in the future to reflect this?

Yes. It will be necessary for cardiologists and endocrinologists to attend immunology meetings, for oncologists to attend endocrinology meetings, and for everyone to ‘think outside of the box’.

Our research shows that many diseases such as atherosclerosis, insulin-resistant obesity, obesity-associated cancer, Type 2 diabetes and other chronic inflammatory diseases are deeply related through common mechanisms of shared networks that control chromatin.

What impact do you think your research will have on controlling the inflammatory response associated with diseases such as type 2 diabetes, cancer and so forth?

New BET protein inhibitors are in the pipeline in a number of research groups and pharmaceutical companies. Some of these agents, if shown to be safe and on target, might become excellent new drugs to treat problems in insulin production, insulin resistance or chronic inflammation, which often accompany obesity and exacerbate risks for obesity-associated cancers.

However, these safety issues are complex and will not be straightforward to overcome.

How important do you think the study of epigenetics will be in the future of medicine?

Epigenetics is a critical new area of research. The Dutch ‘Hunger Winter’ of 1944 – 1945 taught us about the importance and long-lasting impact of maternal starvation, which apparently transmitted cardiometabolic risk epigenetically from the deprived, pregnant mothers to their unborn children.

New research with rodent models is showing us that inflammation in the uterine environment can epigenetically reprogram the young into unhealthy metabolic patterns after birth. Therefore, proper support for maternal health and metabolism will be shown to matter all the more, and we may be able to define specific steps to protect the fetus.

Best of all, we may be able to develop epigenetic drugs that will ultimately be useful to correct these epigenetically transmitted diseases. Until then, there is no cure for the adult children of the Dutch ‘Hunger Winter’ mothers, or patients like them.”

Imagefrom Nature “Unravelling the cancer code.” by Vicki Brower, March 2011  

“A prime candidate at the interface of environment and genetics is chronic inflammation, which is known to precede the development of numerous types of precancerous lesions — and indeed certain cancers themselves, including oesophageal, liver and colon cancers. Inflammation has been linked with increased DNA methylation in otherwise healthy looking tissue. Jean-Pierre Issa, an epigeneticist at the MD Anderson Cancer Center in Houston, and a researcher on the Cancer Genome Project calls chronic inflammation “a truly epigenetic phenomenon.”

“Induction of epigenetic alterations by chronic inflammation and its significance on carcinogenesis.” by Niwa T, Ushijima T. Carcinogenesis Division, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan. Adv Genet. 2010;71:41-56. doi: 10.1016/B978-0-12-380864-6.00002-X.

“Chronic inflammation is deeply involved in development of human cancers, such as gastric and liver cancers. Induction of cell proliferation, production of reactive oxygen species, and direct stimulation of epithelial cells by inflammation-inducing factors have been considered as mechanisms involved. Inflammation-related cancers are known for their multiple occurrences, and aberrant DNA methylation is known to be present even in noncancerous tissues. Importantly, for some cancers, the degree of accumulation has been demonstrated to be correlated with risk of developing cancers. This indicates that inflammation induces aberrant epigenetic alterations in a tissue early in the process of carcinogenesis, and accumulation of such alterations forms “an epigenetic field for cancerization.” This also suggests that inhibition of induction of epigenetic alterations and removal of the accumulated alterations are novel approaches to cancer prevention. Disturbances in cytokine and chemokine signals and induction of cell proliferations are important mechanisms of how inflammation induces aberrant DNA methylation.“

“Role of epigenetics in inflammation-associated diseases.” by Shanmugam MK, Sethi G. Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore. Subcell Biochem. 2012;61:627-57. doi: 10.1007/978-94-007-4525-4_27.

“There is considerable evidence suggesting that epigenetic mechanisms may mediate development of chronic inflammation by modulating the expression of pro-inflammatory cytokine TNF-α, interleukins, tumor suppressor genes, oncogenes and autocrine and paracrine activation of the transcription factor NF-κB. These molecules are constitutively produced by a variety of cells under chronic inflammatory conditions, which in turn leads to the development of major diseases such as autoimmune disorders, chronic obstructive pulmonary diseases, neurodegenerative diseases and cancer. Distinct or global changes in the epigenetic landscape are hallmarks of chronic inflammation driven diseases.“

Imagefrom “Inflammatory signalling as mediator of epigenetic modulation in tissue-specific chronic inflammation.” Liselotte Backdahl, Andrew Bushell & Stephan Beck. Medical Genomics Group. 09/2008; 41(1):176-84. DOI:10.1016/j.biocel.2008.08.023

“Recent successes of therapeutic intervention in chronic inflammatory diseases using epigenetic modifiers such as histone deacetylase inhibitors and inhibitors of DNA methylation suggest that epigenetic reprogramming plays a role in the aetiology of these diseases. The epigenetic signature of a given immune cell is reflected in the history of modifications from different signals the cell has been subjected to during differentiation. Like other cells, differentiating immune cells are dependent on a complex combination of inter- and intracell signalling as well as transcription machineries to modulate their epigenomes in order to mediate differentiation.”

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RLS is NOT Hereditary: Welcome to the AMAZING World of Epigenetics! (PART FOUR: Diet and Epigenetics)

ImageRecognizing the importance of diet is one of the incredible gifts that epigenetics has given us.

Incredible, because researchers have discovered, through pure science, that the best way to turn ON the “helpful” genes and turn OFF the “harmful” genes is through a proper diet.

There has never been an intersection point in modern history where scientists and nutritionists have met with such like minds.

Sure, most scientists are researching with the goal of developing a drug that will throw ON the good switches … but until those drugs are developed, the best methods they have discovered to turn on the good genes is a healthy and balanced diet, with the addition of some key supplements.

Many of their recommendations are listed in the excerpts below.

from The University of Utah Genetic Science Learning Center “Nutrition and the Epigenome.”

“Unlike behavior or stress, diet is one of the more easily studied, and therefore better understood, environmental factors in epigenetic change.

The nutrients we extract from food enter metabolic pathways where they are manipulated, modified and molded into molecules the body can use. One such pathway is responsible for making methyl groups – important epigenetic tags that silence genes.

Familiar nutrients like folic acid, B vitamins and SAM-e (S-Adenosyl methionine, a popular over-the-counter supplement) are key components of this methyl-making pathway. Diets high in these methyl-donating nutrients can rapidly alter gene expression, especially during early development when the epigenome is first being established.

ImageDiet During Early Development Can Cause Changes Lasting Into Adulthood

Your mother’s diet during pregnancy and what you’re fed as an infant can cause critical changes that stick with you into adulthood. Animal studies have shown that deficiency of methyl-donating folate or choline during late fetal or early postnatal development causes certain regions of the genome to be under-methylated for life.

For adults, a methyl deficient diet still leads to a decrease in DNA methylation, but the changes are reversible with resumption of a normal diet.

The Emerging Field of Nutrigenomics

As we better understand the connections between diet and the epigenome, the opportunity arises for clinical applications. Just as mapping our gene variations gives us a window into our personalized medical needs, so might a profile of one’s unique epigenome.

Formed through a lifetime of experiences beginning in the womb, our epigenome may provide a wealth of information about how to eat better. Enter the future field of nutrigenomics, where nutritionists take a look at your methylation pattern and design a personalized nutrition plan. While we’re not quite to that point yet, your doctor can already tell a lot about the your disease risk by looking at your family health history.”

from “Epigenetics, Methylation, and Gene Expression.” by Kevin Cann, April 10th, 2013

“The elasticity of our epigenome is critical for human survival.  It allows us to adapt and survive in changing environments. Diet and stress play an important role in gene expression. An interesting study just came out of UMASS Medical School and was published in the journal Cell regarding diet and gene expression.  The researchers concluded their study by saying even the smallest amount of food can alter gene expression.  The interesting piece is that the gene regulators that were affected by nutrition in the study also play a role in maintaining human circadian rhythm, and they react very quickly to food choices. This is important to the individuals that are genetically predisposed to obesity or disease and/or making lifestyle choices that are causing negative gene expression. Everything in moderation is not the key. This is also important for those that may have a genetic disorder.

Altered circadian rhythm and increased oxidative stress are largely responsible for the onset of symptoms seen in Huntington’s Disease. This concept becomes extremely important for those that tested positive for the abnormal gene.  Every wrong food choice, as well as a failure to deal with stress, can speed up the onset of symptoms.  This goes for the other direction too.  Every good food choice and the ability to manage stress can go a long way to prolonging positive gene expression. Maintaining an appropriate circadian rhythm is critical to overall health for the entire population. Disruption of circadian rhythm has been linked to heart disease, diabetes, obesity, thrombosis and inflammation.”  
from “Nature or nurture: Let food be your epigenetic medicine in chronic inflammatory disorders.” by Katarzyna Szarc vel Szica, Matladi N. Ndlovua, Guy Haegemana & Wim Vanden Berghea. Biochem Pharmacol. 2010 Dec 15;80(12):1816-32. doi: 10.1016/j.bcp.2010.07.029. Epub 2010   

“Numerous clinical, physiopathological and epidemiological studies have underlined the detrimental or beneficial role of nutritional factors in complex inflammation related disorders such as allergy, asthma, obesity, type 2 diabetes, cardiovascular disease, rheumatoid arthritis and cancer.

Today, nutritional research has shifted from alleviating nutrient deficiencies to chronic disease prevention. It is known that lifestyle, environmental conditions and nutritional compounds influence gene expression. Gene expression states are set by transcriptional activators and repressors and are often locked in by cell-heritable chromatin states. Only recently, it has been observed that the environmental conditions and daily diet can affect transgenerational gene expression via “reversible” heritable epigenetic mechanisms. Epigenetic changes in DNA methylation patterns at CpG sites (epimutations) or corrupt chromatin states of key inflammatory genes and noncoding RNAs, recently emerged as major governing factors in cancer, chronic inflammatory and metabolic disorders. Reciprocally, inflammation, metabolic stress and diet composition can also change activities of the epigenetic machinery and indirectly or directly change chromatin marks. This has recently launched re-exploration of anti-inflammatory bioactive food components for characterization of their effects on epigenome modifying enzymatic activities (acetylation, methylation, phosphorylation, ribosylation, oxidation, ubiquitination, sumoylation). This may allow to improve healthy aging by reversing disease prone epimutations involved in chronic inflammatory and metabolic disorders.”
Imagefrom The Toronto Globe and Mail “Eat your broccoli and ward off cancer.” by Leslie Beck, April 05, 2011

“Looks like Mom was right. Broccoli and cauliflower are good for you. According to a recent review, they’re key ingredients in an eating plan – called the epigenetics diet – designed to fend off cancer.

The epigenetics diet also includes soybeans, red grapes and green tea, foods with active ingredients that influence genes involved in the cancer process.

While genetics is the study of inherited genes, epigenetics looks at changes in the activity of genes. Epigenetics investigates how environmental agents – including the foods you eat – influence which genes are turned on or off.

The traditional view of cancer is that the disease is caused by damage to genes and DNA mutations.

But scientists are learning that other forces – diet, stresses, toxins – have the power to change gene activity in healthy, undamaged cells and ultimately alter cancer risk.

Turns out your diet has the potential to reverse negative changes to gene expression, changes that could, over time, lead to cancer as well as other diseases.

The review by scientists from the University of Alabama at Birmingham outlines how specific components in foods can activate genes that suppress tumour growth and silence genes that promote cancer development.

The epigenetics diet, a term coined after the report’s publication in March, is a daily diet that includes food components that turn on or off a gene’s natural defences against cancer. And it’s easy to adopt since the amounts of active ingredients in foods needed for cancer prevention are very achievable.”

“Diet and the epigenetic (re)programming of phenotypic differences in behavior.” by Patrick O. McGowana, Michael J. Meaneya & Moshe Szyf. Brain Research. Volume 1237, 27 October 2008, Pages 12–24. 

“Epidemiological data suggest that dietary changes in methyl contents could affect DNA methylation and gene expression programming. Nutritional restriction during gestation could affect epigenetic programming in the brain. These findings provide evidence for a stable yet dynamic epigenome capable of regulating phenotypic plasticity through epigenetic programming.”

from “Falling for This Myth Could Give You Cancer.” by Dr. Mercola, April 11, 2012

“How Nutrition Alters Genetic Expression

A study performed by the Linus Pauling Institute at Oregon State University was showcased at the annual Experimental Biology convention. The study demonstrated how “histone modifications” can impact the expression of many degenerative diseases, ranging from cancer and heart disease to biopolar disorder and even aging itself.

According to Rod Dashwood, a professor of environmental and molecular toxicology and head of LPI’s Cancer Chemoprotection Program “We believe that many diseases that have aberrant gene expression at their root can be linked to how DNA is packaged, and the actions of enzymes such as histone deacetylases, or HDACs. As recently as 10 years ago we knew almost nothing about HDAC dysregulation in cancer or other diseases, but it’s now one of the most promising areas of health-related research.”

In a nutshell, we all have tumor suppressor genes, and these genes are capable of stopping cancer cells in their tracks. These genes are present in every cell in your body, but so are proteins called “histones.” As Dr. Jean-Pierre Issa at the M.D. Anderson Cancer Center explainsv , histones can “hug” DNA so tightly that it becomes “hidden from view for the cell.” If a tumor suppressor gene is hidden, it cannot be utilized, and in this way too much histone will “turn off” these cancer suppressors, and allow cancer cells to proliferate.

Now here’s where epigenetics comes in … certain foods, such as broccoli and other cruciferous vegetables, garlic, and onions contain substances that act as histone inhibitors, which essentially block the histone, allowing your tumor suppressor genes to activate and fight cancer. By regularly consuming these foods, you are naturally supporting your body’s ability to fight tumors.

Certain alternative oncologists also tap directly into the epigenetic mechanism, such as Dr. Nicholas Gonzalez, who uses a three-pronged approach to cancer based primarily on nutrition and detoxification, and Dr. Stanislaw Burzynski, who treats cancer with a gene-targeted approach. His treatment uses non-toxic peptides and amino acids, known as antineoplastons, which act as genetic switches that turn your tumor suppressor genes “on.”

ImageA Healthy Lifestyle Supports Healthy Genetic Expression

So the good news is that you are in control of your genes … You can alter them on a regular basis, depending on the foods you eat, the air you breathe, and the thoughts you think. It’s your environment and lifestyle that dictates your tendency to express disease, and this new realization is set to make major waves in the future of disease prevention — including one day educating people on how to fight disease at the epigenetic level. When a disease occurs, the solution, according to epigenetic therapy, is simply to “remind” your affected cells (change its environmental instructions) of its healthy function, so they can go back to being normal cells instead of  diseased cells.

You can begin to do this on your own, long before you manifest a disease. By leading a healthy lifestyle, with high quality nutrition, exercise, limited exposure to toxins, and a positive mental attitude, you encourage your genes to express positive, disease-fighting behaviors.

This is what preventive medicine is all about. It’s not about taking any one particular nutrient as a supplement to fix one specific “part” of your biological machinery… The more people become willing to embrace this simple truth, the healthier everyone will get.”

from Science Daily “Epigenetic Biomarkers May Predict If a Specific Diet and Exercise Regimen Will Work.” May 30, 2013

“Would you be more likely to try a diet and exercise regimen if you knew in advance if it would actually help you lose weight? Thanks to a report published in the June 2013 issue of The FASEB Journal, this could become a reality. In the report, scientists identify five epigenetic biomarkers in adolescents that were associated with a better weight loss at the beginning of a weight loss program. Not only could this could ultimately help predict an individual’s response to weight loss intervention, but it may offer therapeutic targets for enhancing a weight loss program’s effects.
“Successful obesity treatment during adolescence could reduce morbidity at later stages of life and lead to a better quality of life,” said Amelia Marti, Ph.D., Pharm. D., co-author of this study from the Department of Nutrition, Food Science, Physiology and Toxicology at the University of Navarra in Pamplona, Spain. “It is crucial to find new markers for obesity treatment.”  

“If you’ve ever wondered why some people seem to do so well on a diet and exercise plan and other fail so miserably, then now we know that the way that genes express themselves (via epigenetics) plays an important role,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “This report moves us a step closer when we will be able to prescribe a weight loss program tailored to more than just the lifestyle and conditioning level of the patient, but also to his or her particular genetic and epigenetic profile.”

from Charles A. Moss M.D.

“Epigenetics is possibly the most important and powerful new information on how to lose weight and prevent chronic illness that I have seen in my 35 year medical career.”

from The National Institute on Alcohol Abuse and Alcoholism (NIAAA) “Alcohol Metabolism and Epigenetic Changes.” by Samir Zakhari, Ph.D.

“Alcohol can influence gene expression, and specifically epigenetic regulatory processes that modify the activity of genes, through a variety of mechanisms. Some of these are related to the metabolism of alcohol in the cells. In general, several metabolites, such as nicotinamide-adenine dinucleotide (NAD) in its oxidized and reduced forms, acetyl-coenzyme A (acetyl-CoA), and S-adenosylmethionine (SAM) serve as cofactors for numerous reactions in the cell, including reactions related to epigenetic DNA and histone modifications. Changes in metabolite levels may impact epigenetic processes such as DNA methylation and histone acetylation.”

Imagefrom “Research shows junk-food diet is passed on to children in genes.” by Grant McArthur, January 15, 2009

“OVERWEIGHT parents are condemning their children to obesity and disease by damaging their genes with their own poor diets, scientists have found.

World-first research by the Australian team has revealed that obese sweet-tooths are reprogramming the controls over their DNA, passing on fatness and associated disease to generations of the future.

Scientists from the Baker IDI Heart and Diabetes Institute in Melbourne have proved that damage from unhealthy eating is “remembered” in people’s genetic controls, called epigenetics, turning off good genes needed to prevent diabetes, heart disease and other dangerous complications.

Lead researcher Assam El-Osta said the discovery meant eating a chocolate will not only go straight to your hips, but will also sit on your DNA.

“It is this idea that you are what you eat. Perhaps it’s a reflection of what your parents ate, and perhaps what your grandparents ate,” he said.

The scientists proved that a single sugar hit, such as eating a chocolate bar, damaged the controls regulating the body’s genes for two weeks.

But Professor El-Osta warned that regular poor eating meant the damage would last for months or years, and the real problems caused by an unhealthy diet were deferred until later life.

After having proved the impact of high-sugar foods, the Baker IDI team is now focusing efforts to determine if high fat foods, smoking and other lifestyle-related factors also cause long-term damage to genetic controls, which could then be passed along family bloodlines.

“If you had a Big Mac every day or a very poor diet for a month the consequences would be that you immediately put on weight, but long-term complications are that very serious changes would be remembered for many months or even years,” Professor El-Osta said.

The discovery could explain why some people put on weight or become sick after eating junk food more than others.

“This is not all doom and gloom, because we think there is good epigenetic memory as well for individuals who have a good diet, not only for themselves but potentially for future generations,” Professor El-Osta said.”

from “Epigenetics: A New Bridge between Nutrition and Health.” by Sang-Woon Choi and Simonetta Friso. doi: 10.3945/​an.110.1004. Adv Nutr vol. 1: 8-16, 2010.

“Nutrients can reverse or change epigenetic phenomena such as DNA methylation and histone modifications, thereby modifying the expression of critical genes associated with physiologic and pathologic processes, including embryonic development, aging, and carcinogenesis. It appears that nutrients and bioactive food components can influence epigenetic phenomena either by directly inhibiting enzymes that catalyze DNA methylation or histone modifications, or by altering the availability of substrates necessary for those enzymatic reactions. In this regard, nutritional epigenetics has been viewed as an attractive tool to prevent pediatric developmental diseases and cancer as well as to delay aging-associated processes. In recent years, epigenetics has become an emerging issue in a broad range of diseases such as type 2 diabetes mellitus, obesity, inflammation, and neurocognitive disorders.”

from Understanding Nutrition “A Primer on Epigenetics and Diet.”

“In the last decade, epigenetics has become one of the hottest topics in science.

The environment largely determines the epigenetic marks present on the DNA. The epigenetic marks improve the body’s ability to adapt to an environment

For example, the body has a set of machinery for processing carbohydrates and different a set of machinery for processing fat. If a person eats mostly carbohydrates, the carbohydrate-processing machinery will be up-regulated and the fat-processing machinery will be down-regulated. If the person switched to a high fat, low carbohydrate diet, they would likely feel sluggish for a few days. They might feel sugar cravings because their body is not yet adapted for using fat as the main fuel source. After a few days, their body would up-regulate the fat-processing machinery and down-regulate the carbohydrate-processing machinery. At that point, they would have adapted to new diet and become efficient at processing fat for fuel.

We are beginning to understand that diet has a big impact on which genes are up – or down-regulated, and this, in turn, has a big impact on our health. A poor diet doesn’t make us unhealthy simply from the consequences of being malnourished or overweight, the diet actually affects the expression of our genes. Certain diets could up-regulate cancer-causing genes and other diets may up-regulate cancer-resistance genes.”  

from Epigenetics “Eating for your epigenome.” by Brona McVittie

“If you’re keen to look after your epigenome, then you could try munching on foods that provide the building blocks for methylation in the body. For example, leaf vegetables, peas and beans, sunflower seeds and liver are good sources of folic acid, as are fortified bread and breakfast cereals. Choline comes from eggs, lettuce, peanuts and liver (again! My mother was right after all).

To boost your intake of methionine try spinach, garlic, brazil nuts, kidney beans or tofu. And if you fancy something non-veggie, chicken, beef and fish are all good sources. For zinc, splash out on a plate of oysters. And while you’re on a seafood tip, get some vitamin B12 from fish.”  

Imagefrom the Biotechnology and Biological Sciences Research Council (BBSRC).”New evidence for epigenetic effects of diet on healthy ageing.” December 2012

“New research in human volunteers has shown that molecular changes to our genes, known as epigenetic marks, are driven mainly by ageing but are also affected by what we eat.

The study showed that whilst age had the biggest effects on these molecular changes, selenium and vitamin D status reduced the accumulation of epigenetic changes, and high blood folate and obesity increased them. These findings support the idea that healthy ageing is affected by what we eat.

Researchers from the Institute of Food Research led by Dr Nigel Belshaw, working with Prof John Mathers and colleagues from Newcastle University, examined the cells lining the gut wall from volunteers attending colonoscopy clinic.
The study volunteers were free from cancer or inflammatory bowel disease and consumed their usual diet without any supplements. The researchers looked for specific epigenetic modifications of the volunteers’ genes that have been associated with the earliest signs of the onset of bowel cancer – an age-related disease.

The investigators studied the relationship between the occurrence of these epigenetic marks at genes known to be affected in cancer, and factors including the volunteers’ age, sex, body size and the levels of some nutrients in the volunteers’ blood. The biggest influence on gene methylation was age. This fits with the fact that the biggest risk factor for bowel cancer is age, with risk increasing exponentially over 50 years old.

The findings, published in the journal Aging Cell, showed that men tended to have a higher frequency of these epigenetic changes than women, which is consistent with men being at a greater risk of bowel cancer. Volunteers with higher vitamin D status tended to show lower levels of methylation, and a similar effect was observed for selenium status. Again, this is consistent with the known links between higher vitamin D and selenium and reduced bowel cancer risk.

The B vitamin folate is essential for health, but in this study, high folate status was associated with increased levels of epigenetic changes linked with bowel cancer. These findings are consistent with some epidemiological studies suggesting that excessive folate intakes may increase risk in some people. The researchers intend to investigate the mechanism for the observed effect of folate on DNA methylation in a follow-up study.

Obesity is also a risk factor for bowel cancer. This study found relationships between body size (height, weight and waist circumference) and epigenetic changes. How excess body weight induces these epigenetic changes, and the consequences for gut health, are currently being investigated at IFR and in Newcastle University.

In summary, the results of this study support the hypothesis that ageing affects the epigenetic status of some genes and that these effects can be modulated by diet and body fatness.”

from Digital Journal “Vegetables in the diet have epigenetic effect to fight cancer.” by Kathleen Blanchard, Mar 8, 2011

Scientists say compounds in vegetables can prevent and even reverse cancer, in what they call an ‘epigenetics’ diet. The researchers say the diet is easily attainable and can prevent aging related diseases and lead to healthier “lives.

Investigators from the University of Alabama at Birmingham explain epigenetics is the study of how gene expression changes over time, leading to cancer and other diseases including Alzheimer’s.

In a study review, published in the journal Clinical Epigenetics, the scientists found compounds in vegetables have been identified from global studies, showing vegetable compounds can help prevent potentially debilitating diseases and boost protection from cancer.

Lead author Syed Meeran, Ph.D., a research assistant professor in Tollefsbol’s UAB Department of Biology laboratory says you don’t have to eat a lot of vegetables to achieve the desired effect. For instance, three cups of green tea might help prevent breast cancer, shown in mouse studies, and a daily cup of broccoli sprouts with the cancer-fighting compound sulforaphane could prevent a variety of cancer types.”

Tollefsbol says, “Our review article has drawn everything together from global studies, and the common theme is that compounds in the epigenetics diet foods can, at the very least, help us lead healthier lives and help our bodies prevent potentially debilitating diseases like breast cancer and Alzheimer’s.”

The notion that vegetables fight cancer and disease is not new. The current study shows why eating vegetables can help prevent cancer and other diseases because compounds in veggies prevent gene aberrations, or epigenetic changes that occur over time in the way genes are expressed.”

Imagefrom “Epigenetics Diet – broccoli, cabbage help prevent and treat cancer, Alzheimer’s.” by Amy Rabinovitz, March 12, 2011

“An Epigenetics Diet is a daily diet that includes foods that turn on or off a gene’s natural defenses to these cancers and age-related diseases.

Vegetables such as broccoli and cabbage are part of the Epigenetics Diet, as are soybeans, cauliflower, green tea, fava beans, kale, grapes and the spice turmeric.

Meeran says sipping tea compounds called polyphenols in daily amounts that are equivalent to approximately three cups of green tea has been shown to reverse breast cancer in laboratory mice by suppressing the gene that triggers the disease. Similarly, a daily cup of broccoli sprouts, which has sulforaphane as an active compound, has been shown to reduce the risk of developing many cancers.”

from Newsweek Magazine “Controlling Your Genes.” by Sharon Begley, Jan 13, 2010

“Scientists are now making specific, actionable discoveries in epigenetics. This week, for instance, researchers are reporting that eating leafy green vegetables, folate (found in these veggies as well as in some fruits and in dried beans and peas), and multivitamins can affect the epigenetics of genes involved in lung cancer in a way that could reduce the risk of getting the disease, especially from smoking.

As Steven Belinsky of the Lovelace Respiratory Research Institute in Albuquerque and his team describe in a new paper posted online in the journal Cancer Research, they found that eating a lot of leafy green vegetables, folate, and taking multivitamins containing vitamin C, carotenoids, lutein, folic acid, and vitamins A and K was strongly associated with lower methylation of these cancer-related genes.

“A mere 12 servings a month of leafy greens reduced DNA methylation in these genes about 20 percent; taking a multivitamin reduced it almost 50 percent” says Belinsky. “As a result of lower methylation, these beneficial genes—suppressing cancer and repairing DNA—remained on. So it seems that these foods and vitamins can counteract the effect of cigarettes on DNA: although the carcinogens in smoke turn off the beneficial genes, these foods keep them in the game.”

And it isn’t just cancer. A new study from scientists at Cambridge University found a connection between heart disease and DNA methylation. In a nutshell, they found that particular regions of the DNA in the diseased hearts contained DNA-silencing marks—methylation—while healthy hearts did not. “There is already good evidence that these [methylation] marks are strongly influenced by environment and diet,” said Cambridge’s Roger Foo. “We found that this process is different in diseased and normal hearts. Linking all these things together suggests this may be the ‘missing link’ between environmental factors and heart failure.”

Imagefrom The University of Leicester – Virtual Genetics Education Centre “Epigenetics, diet and pregnancy.”

“An unbalanced, high-fat, low-protein or energy-restricted diet can modify epigenetic marks, which are associated detrimental health effects in offspring in both animal and human models (Brait et al., 2009, van Straten et al., 2010, Widiker et al., 2010).”

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