I googled 'a diet rich in methyl groups' as mentioned in the Nova episode study on mice.

Summary of mice study:

Quote

Both mice and people have a gene called agouti. When a mouse's agouti gene is completely unmethylated it has a yellow coat color, is obese and prone to diabetes and cancer. When the agouti gene is methylated (as it is in normal mice) the coat color is brown and the mouse has a low disease risk. Fat yellow mice and skinny brown are genetically identical. You can think of the fat yellow mice as looking different because they have an epigenetic "mutation."

Results:
http://learn.genetic...tics/nutrition/

It's mostly your sulfur containing amino acids such as methionine and cysteine and other sulfur compounds like the sulfurophane in the veggies we are always telling you to eat. But other nutrients are also required/beneficial as methyl donors and to aid in histone acetylation (which I haven't googled yet, but apparently it's a less understood factor):

Quote

Methionine

Sesame seeds, brazil nuts, fish, peppers, spinach

SAM synthesis

Folic Acid

Leafy vegetables, sunflower seeds, baker's yeast, liver

Methionine synthesis

Vitamin B12

Meat, liver, shellfish, milk

Methionine synthesis

Vitamin B6

Meats, whole grain products, vegetables, nuts

Methionine synthesis

SAM-e (SAM)

Popular dietary supplement pill; unstable in food

Enzymes transfer methyl groups from SAM directly to the DNA

Choline

Egg yolks, liver, soy, cooked beef, chicken, veal and turkey

Methyl donor to SAM

Betaine

Wheat, spinach, shellfish, and sugar beets

Break down the toxic byproducts of SAM synthesis

Resveratrol

Red wine

Removes acetyl groups from histones, improving health (shown in lab mice)

Genistein

Soy, soy products

Increased methylation, cancer prevention, unknown mechanism

Sulforaphane

Broccoli (and all the other members of the brassica family and more)

Increased histone acetylation turning on anti-cancer genes

Butyrate

A compound produced in the intestine when dietary fiber is fermented

Increased histone acetylation turning on 'protective' genes, increased lifespan (shown in the lab in flies)

Diallyl sulphide (DADS)

Garlic, (and everything else in the onion family)

Increased histone acetylation turning on anti-cancer genes

And not listed on that site:

epigallocatechin-3-gallate (EGCG), the major polyphenol from green tea, can prevent deleterious methylation dimmer switches from landing on (and shutting down) certain genes.

Also, more on the badness of plastics - how BPA screws with your genes:

Quote

Of Toxins and Supplements

Chemicals and additives that enter our bodies can also affect the epigenome. Bisphenol A (BPA) is a compound used to make polycarbonate plastic. It is in many consumer products including water bottles and tin cans. ...

When pregnant yellow agouti mothers were fed BPA, more yellow, unhealthy babies were born than normal. Exposure to BPA during early development had caused decreased methylation of the agouti gene. However, when BPA-exposed, pregnant yellow mice were fed methyl-rich foods, the offspring were predominantly brown. The maternal nutrient supplementation had counteracted the negative effects of exposure.

Of course, those mice studies are about what your mother ate does to you. We need more on what we can do.

Homecysteine is something that can be tested to measure if you don't have enough methylation going on.

Quote

when your body uses the amino acid, methionine to join with your body's proteins and DNA, it produces a bi-product called homocysteine which needs to be methylated, or joined with methyl-related nutrients in order to convert it back to methionine. If methylation does not occur, homocysteine's presence increases your risk of heart disease, high cholesterol, Alzheimers, liver disease and depression. Methylation processes are happening throughout your body to keep your systems running well.

Read more: http://www.livestron.../#ixzz1qLo5iON3

Another summary of nutrients:

Quote

Methyl-related nutrients are found in three groups of compounds: B Vitamins, Betaine and SAMe, S-Adenosyl-Methionine. In food sources, methyl-related nutrients can be found in foods rich in natural folate, or Vitamin B9, including strawberries, citrus fruits and leafy green vegetables. Good sources of Vitamin B12 are fish, meat, milk, and eggs. Choline oxidizes to form a source of methyl called Betaine, which is found in its highest concentration in beef liver. Toasted wheat germ and eggs are also excellent sources of choline, with cod, beef, brussel sprouts, broccoli, shrimp and salmon being good sources as well. Two large eggs contain 252 mg choline, nearly half of the recommended 550 mg per day for men.

Read more: http://www.livestron.../#ixzz1qLo5iON3

And a fairly neat explanation of the whole thing:

Quote

Human Genome

The human genome describes the unique nucleotide sequence that makes up your DNA. In the nucleus of every cell, the approximately 3 billion nucleotides that make up your DNA are arranged in units called genes. Genes contain all the information to produce the proteins necessary to create your cells and tissues and to sustain life.

[Link Removed] Weight Watchers

Gene Expression

The process of creating a new protein in your cells is referred to as gene expression. Gene expression is highly regulated by your body to ensure the correct protein is produced in the correct amount, and at the appropriate time. Mistakes in gene expression have the potential to lead to illnesses such as cancer. There are many levels of control of gene expression. According to an article published in the February 2010 issue of "Nutrition Reviews," one type of regulation is linked to the epigenetic structure of the genome.
Epigenetics

Epigenetic modifications are changes made to the genome without changing the nucleotide sequence. A common type of epigenetic modification is the addition of methyl groups to DNA. A methyl group is simply a carbon with three hydrogens attached to it. The epigenetic addition or removal of methyl groups to DNA physically alters the structure of the DNA. According to the article in "Nutrition Reviews," this can have effects on gene expression. Environmental interactions with your genome, including dietary components, can alter the methylation pattern of your DNA.
Diet and Epigenetics

The effects of diet on epigenetic changes are currently being researched. As reported by an article published in the Novemeber 2010 issue of "Advances in Nutrition," several dietary components such as resveratrol from red wine, genistein from soy and the vitamins folate and B12 have all been shown to have an effect on DNA methylation and other epigenetic modifications. Experts in nutrition believe these epigenetic changes can affect the expression of certain genes. This could have implications for fetal development, cancer, aging and other biological processes. The research in this field is in the early stages and much is still unknown about this area of nutrition. However as researchers learn more, they will have a better understanding of the best dietary recommendations to reduce the risk of disease and improve health.

Read more: http://www.livestron.../#ixzz1qLp3okWL

And another from this discovery mag article [Link Removed]

Quote

genes themselves need instructions for what to do, and where and when to do it. A human liver cell contains the same DNA as a brain cell, yet somehow it knows to code only those proteins needed for the functioning of the liver. Those instructions are found not in the letters of the DNA itself but on it, in an array of chemical markers and switches, known collectively as the epigenome, that lie along the length of the double helix. These epigenetic switches and markers in turn help switch on or off the expression of particular genes. Think of the epigenome as a complex software code, capable of inducing the DNA hardware to manufacture an impressive variety of proteins, cell types, and individuals. ....

More and more, researchers are finding that an extra bit of a vitamin, a brief exposure to a toxin, even an added dose of mothering can tweak the epigenomeand thereby alter the software of our genesin ways that affect an individual's body and brain for life.

The even greater surprise is the recent discovery that epigenetic signals from the environment can be passed on from one generation to the next, sometimes for several generations, without changing a single gene sequence....

One form of epigenetic change physically blocks access to the genes by altering what is called the histone code. The DNA in every cell is tightly wound around proteins known as histones and must be unwound to be transcribed. Alterations to this packaging cause certain genes to be more or less available to the cell's chemical machinery and so determine whether those genes are expressed or silenced. A second, well-understood form of epigenetic signaling, called DNA methylation, involves the addition of a methyl groupa carbon atom plus three hydrogen atomsto particular bases in the DNA sequence. This interferes with the chemical signals that would put the gene into action and thus effectively silences the gene.

Until recently, the pattern of an individual's epigenome was thought to be firmly established during early fetal development. Although that is still seen as a critical period, scientists have lately discovered that the epigenome can change in response to the environment throughout an individual's lifetime.

...

a gene with a defective methylation pattern might very well be encouraged to reestablish a healthy pattern and continue to function. Already one epigenetic drug, 5-azacytidine, has been approved by the Food and Drug Administration for use against myelodysplastic syndrome, also known as preleukemia or smoldering leukemia. At least eight other epigenetic drugs are currently in different stages of development or human trials....

Others have published data on animal subjects suggesting an epigenetic component to inflammatory diseases like rheumatoid arthritis, neurodegenerative diseases, and diabetes.

* ^ Ah ha - now they are getting close to something that might be of interest to us. But the article doesn't say any more on that subject.*

The article then goes on to discuss research into methylation diets, bringing up research into green tea which wasn't mentioned in the other sites. And then about how epigenetic changes can be passed on to the next generation. And a new take on the old nature (genes) vs nurture debate. It's not either/or because diet and environmental factors change the epigenome.

But nurturing definitely has an affect on the epigenome too. One example: Mother mice licking their offspring 'causes them to release serotonin in the pup's brain, which activates serotonin receptors in the hippocampus. These receptors send proteins called transcription factors to turn on the gene that inhibits stress responses.' Also, 'adults who reported in a questionnaire that they had a poor relationship with their mother were found to have hippocampi that were significantly smaller than average. Those adults who reported having had a close relationship with their mother, however, showed perfectly normal size hippocampi. '

And then some about the impact on society, especially on those affected by things like poverty or war.

Quote

'

early child-parent bonding is made more difficult by the effects of poverty, dislocation, and social strife. Those factors can certainly affect the cognitive development of the children directly involved. Might they also affect the development of future generations through epigenetic signaling?'

...

Lawrence Harper [Link Removed],a psychologist at the University of California at Davis, suggests that a wide array of personality traits, including temperament and intelligence, may be affected by epigenetic inheritance. "If you have a generation of poor people who suffer from bad nutrition, it may take two or three generations for that population to recover from that hardship and reach its full potential," Harper says. "Because of epigenetic inheritance, it may take several generations to turn around the impact of poverty or war or dislocation on a population."

Here's a brief explanation on histone modification of the epigenome

Quote

The nucleosome
There are four core histone proteins that form the nucleosome, a structure which is used to package the DNA in the nucleus. Histone proteins can be modified at a number of different sites by adding or taking away either small chemical groups, termed acetyl-, methyl-, and phosphate-, or larger protein attachments, termed ubiquityl-. The effect of these modifications is to change the nature of the nucleosome in a manner that affects amongst other things how open or closed the chromatinis. There is evidence suggesting that specific combinations of histone modification can be read like a code, determining for example whether the associated gene should be on or off. This is thought to involve a set of factors that recognise and bind to a given modification present at a specific position on a specific histone. In addition to histone modifications there are a number of variant histones, related to one of the four core histones but with specific properties, for example helping to make a nucleosome more open or closed. Finally there is the linker histone, termed H1, that has an important role in regulating how tightly nucleosomes are packaged. Histone modifications and histone variants are central players in epigenetic processes in all organisms.

DNA methylation
DNA is made up of four different bases that represent the four letters of the genetic code, adenine, cytosine, guanine, and thymine. Sometimes the small chemical group termed methyl- is added to a base, conferring an extra level of information. In higher organisms (i.e not bacteria) methylation is largely confined to the base cytosine. Methylated cytosine is associated with formation of closed chromatin and therefore with switching genes off. This is thought to involve a set of factors that recognise and bind to the modified base. Cytosine methylation is thought to have first arisen as a defence against invading DNA elements, termed transposons. It has since been co-opted as a mechanism for epigenetic gene regulation. An important feature of DNA methylation is that it can be faithfully copied during the process of DNA replication, i.e. when cells double their chromosomes in readiness for cell division. This provides a nice example of how epigenetic information is transmitted from one cell generation to the next. DNA methylation occurs in many, but not all, higher organisms.

So at the bottom of the Discover mag article it says something about the guy/organization that's doing the research on the agouti mice is also investigating the gene that codes for stupidity. I wish them luck.

http://circleof13.blogspot.com/2009/05/epigenetics-most-surprising-thing-about.html

 

Anyone who studied a little genetics in high school has heard of adenine, thymine, guanine and cytosine the A,T,G and C that make up the DNA code. But those are not the whole story.

The rise of epigenetics in the past decade has drawn attention to a fifth nucleotide, 5-methylcytosine (5-mC), that sometimes replaces cytosine in the famous DNA double helix to regulate which genes are expressed. And now there's a sixth. In experiments to be published online Thursday by Science, researchers reveal an additional character in the mammalian DNA code, opening an entirely new front in epigenetic research....

Social Stress Changes Immune System Gene Expression in Primates

ScienceDaily (Apr. 9, 2012) The ranking of a monkey within her social environment and the stress accompanying that status dramatically alters the expression of nearly 1,000 genes, a new scientific study reports. The research is the first to demonstrate a link between social status and genetic regulation in primates on a genome-wide scale, revealing a strong, plastic link between social environment and biology.

http://www.sciencedaily.com/releases/2012/04/120409164513.htm

Oh, the things that I've researched, posted about , and then completely forgotten. It looks like I was starting to get some kind of handle on methylation, which apparently is what causes epigenetic changes. But, it's all gone from my head now.

also, I was recently posting something in some other thread wondering if accutane causes epigenetic changes in some people, and I've posted info on that here in the past.

anyway, bumping because it's interesting.

Today's Mercola Newsletter has this article about Epigenetics and how your diet and habits are more important than your genes and how you change your gene expression every day with what you do to yourself. It's about methylation, that thing I haven't managed to grasp yet. And somewhere on this board there is an article about how some people might be under or over-methylators and perhaps that is a reason why some people take longer to get results from their diet and lifestyle changes.

http://articles.mercola.com/sites/articles/archive/2010/07/08/your-diet-could-be-more-important-than-your-genes.aspx

Great News: Your Genes Can Be Influenced!

 

 

 

Epigenetic "malleability" helps to explain why identical twins become distinct as they age, health-wise, and it explains how you can actually tweak your genes for better or worse, too.

 

In fact,

you ARE changing your genetics daily

and perhaps even hourly from

the foods you eat

, the air you breathe, and even by the thoughts you think.

 

You are the "caretaker" of your genetic roadmap.

 

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.

 

The secret is in the methyl groups that overlie the DNA molecule, which is the realm of the epigenome.

 

When a gene is turned off epigenetically, the DNA has usually been "methylated." When methyl groups adhere to a segment of DNA, they inhibit the gene from being expressed.

 

For the most part you do not manifest disease merely by a defective gene, but by the regulation or expression of your gene by epigenetic influences.

 

This is good news as scientists have discovered it is easier to make epigenetic changes than to fix damaged genes. Your epigenome becomes dysfunctional easier -- but its also easier to fix.

 

Thats good news -- it means you arent doomed by bad genes!

 

 

Study on twins that suggested that sebum output was genetic but acne lesion formation was controlled by environmental factors. There's only an extremely brief abstract at this link. http://www.ncbi.nlm.nih.gov/pubmed/2965597

And, I must point out that many of us, myself included, have found that their sebum output is affected by diet and activities. Which also affect sebum composition.

This is such an important thread. I was reading somewhere that this is the first generation of kids that are worse off than the previous generation. And this would explain why, as our diets have become so toxic/genetically modified.

This is such an important thread. I was reading somewhere that this is the first generation of kids that are worse off than the previous generation. And this would explain why, as our diets have become so toxic/genetically modified.

And you are being born to parents that were already pretty far down that path. My parents were older. Sure there was Cambpells soup and sliced mushy white bread and coca cola. But they mostly ate real food and Coke was something you only occasionally. And my mother started out on a farm on home grown food.

And yeah, I need to reread this all the time. For example, the methylation stuff is yet one more reason why greens are so beneficial and people get good results from green smoothies. I never remember that. I usually just remember how they are food for liver health and just plain good sources of nutrients.

Wow, this is really interesting. I actually just started learning about epigenetics in my college Genetics class.

 

I actually read a study that looked at women who were pregnant in NYC during 9/11. Both the women and their children showed signs of post traumatic stress disorder. I've also heard that there are similar symptoms for descendants of Holocaust survivors.

 

People keep mentioning methylation, and I don't know if it's already been defined in this topic, but from my understanding it's the addition of methyl groups (CH3) to DNA causing it to pack tightly together. This in turn prevents the DNA from being transcribed and translated into proteins. Essentially the methylated gene is silenced.

 

Similar epigenetic regulation comes from the way the DNA is packed to either increase or decrease it's expression.

So methylation is what turns a gene on or off.

So at the bottom of the Discover mag article it says something about the guy/organization that's doing the research on the agouti mice is also investigating the gene that codes for stupidity. I wish them luck.

Bumping, by quoting one of my favorite posts I've ever made.

You can't blame your genes.

After the mapping was done, it turns out we have far fewer genes than previously thought. Not nearly enough to account for all the activity going on in your body.

Following the completion of the Human Genome Project (HGP) in 2003 it is no longer accurate to say that our genes "cause" disease, any more than it is accurate to say that DNA is sufficient to account for all the proteins in our body. Despite initial expectations, the HGP revealed that there are only 20,000-25,000 genes in human DNA (genome), rather than the 100,000 + believed necessary to encode the 100,000 + proteins found in the human body (proteome).

Did you follow that? There are not even enough genes in the human body to account for the existence of the basic protein building blocks that make it possible, much less explain the behavior of these proteins in health and disease states!

The "blueprint" model of genetics: one gene -> one protein -> one cellular behavior, which was once the holy grail of biology, has now been supplanted by a model of the cell where epigenetic factors (literally: "beyond the control of the gene") are primary in determining how DNA will be interpreted, translated and expressed. A single gene can be used by the cell to express a multitude of proteins and it is not the DNA itself that determines how or what genes will be expressed.

Rather, we must look to the epigenetic factors to understand what makes a liver cell different from a skin cell or brain cell. All of these cells share the exact same 3 billion base pairs that make up our genetic code, but it is the epigenetic factors, e.g. regulatory proteins and post-translational modifications, that make the determination as to which genes to turn on and which to silence, resulting in each cell's unique phenotype.

Moreover, epigenetic factors are directly and indirectly influenced by the presence or absence of key nutrients in the diet, as well as exposures to chemicals, pathogens and other environmental influences. Thoughts and emotions also play a role in how these epigenetic factors are articulated, indicating that the flow of genetic information, once thought to be strictly vertical (passage of genetic information from one cell or individual organism to its progeny by conventional heredity mechanisms), also flows horizontally and bi-directionally, opening the door back up for the human soul to return to biological science, having been reduced to a mere "ghost in the machine," since Rene Descartes (1596-1650), the French philosopher and mathematician, split body and soul asunder, almost five centuries ago.

*In a nutshell, what we eat and what we are exposed to in our environment directly affects our DNA and its expression.**

Within the scope of this new perspective even classical monogenic diseases like Cystic Fibrosis (CF) can be viewed in a new, more promising light. In CF many of the adverse changes that result from the defective expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene may be preventable or reversible, owing to the fact that the misfolding of the CFTR gene product has been shown to undergo partial or full correction (in the rodent model) when exposed to phytochemicals found in turmeric, cayenne, and soybean.

Moreover, nutritional deficiencies of seleniun, zinc, riboflavin, vitamin e, etc. in the womb or early in life, may "trigger" the faulty expression or folding patterns of the CFTR gene in Cystic Fibrosis which might otherwise have avoided epigenetic activation. This would explain why it is possible to live into one's late seventies with this condition, as was the case for Katherine Shores (1925-2004).

The implications of these findings are rather extraordinary: epigenetic and not genetic factors are primary in determining disease outcome. Even if we exclude the possibility of reversing certain monogenic diseases, the basic lesson from the post-Genomic era is that we can't blame our DNA for causing disease. Rather, it may have more to do with what we choose to expose our DNA to, and even more surprisingly: how we choose to think and feel about our embodiment.

http://www.greenmedinfo.com/blog/defective-genes-cause-less-1-all-disease

I wish there was a 'love' feature. Cause i'd love this last post. Thanks for sharing this alternativista

http://greenmedinfo.us1.list-manage1.com/track/click?u=7f494613c5ad4db1b93e647ad&id=11d8cf3f9d&e=bb6c9e5ae0

This article about 5 cancer and disease fighting foods or spices makes this statement about turmeric:

Turmeric has been scientifically documented to have over 500 applications in disease prevention and treatment. It also has been shown to modulate over 150 distinct biological and genetic/epigenetic pathways of value in health, demonstrating a complexity as well as gentleness that no drug on the planet has ever been shown to possess.

They don't site any studies in the article, but mention they have over 1500 studies on turmeric on their site. Something to look into. I have 20 other things open right now though...

Interesting article about Angeline Jolie's reaction to having a mutated gene:

http://www.greenmedinfo.com/blog/did-angelina-jolie-make-mistake-acting-breast-cancer-gene-theory?utm_source=GreenMedInfo+Weekly&utm_campaign=669eea2cde-Greenmedinfo&utm_medium=email&utm_term=0_62bb7ef31e-669eea2cde-86852581

The gist of which is that doctors of all sorts are still operating on faulty pre-genomic mapping beliefs. (kind of like how your derm is operating on what was in their non-updated textbooks they used back in med school when telling you diet has nothing to do with acne, despite all the proof otherwise. some of which goes back many decades.)

Excerpts: The first bit is what I've already posted here. It turns out our bodies do not have nearly enough genes to account for all the things happening to us.

Despite the commonplace refusal of so-called 'evidence-based medicine' to acknowledge the actual evidence of genetics, we moved into a Post-Genomic era over a decade ago following the completion of first draft of the entire human genome in 2000. At that moment, the central dogma of molecular biology that our DNA controls protein expression, and therefore disease risk was disproved. Our genome was found to contain roughly 20,000 genetic instructions not even enough to account for the 100,000 proteins in the human body!

As a result, we must now accept that factors beyond the control of the gene, known as epigenetic factors, and largely determined by a combination of nutrition, psychospiritual states that feed back into our physiology, lifestyle factors, and environmental exposures, constitute as high as 95% of what determines any disease risk. In fact, even the psychological trauma associated with being diagnosed with cancer can drive malignancy via adrenaline-mediated multi-drug resistance, and according to a recent NEJM study, lead up to a 26-fold increased risk of heart-related deaths in the seven days following diagnosis.[ii]

Given this fact, Jolie's decision to have a bilateral mastectomy in order to excise from her body the breast tissue that contains BRCA1/BRCA2 genes which are known to interfere with the repair of radiation-induced DNA damage, rather than focusing on reducing or eliminating all future radiation exposure from her breasts, or incorporating hundreds of nutritional components experimentally confirmed to protect against radiation and associated genotoxic insults to the breast, reflects a iron clad faith in the inevitability of gene-driven cancer vis-a-vis a fundamentally powerless subject, versus trust in the body's ability to prevent and heal all disease, assuming it has the right conditions.

and

Another common misconception is that you either have, or don't have the "BRACA genes," as if they were monolithic entities, ascertained with the black and white certainty of a pregnancy test. It is a little known fact that thousands of "mutations" in the BRCA1 and BRCA2 genes have already been identified and ..

These mutations are technically known as gene polymorphisms which are naturally occurring variations of a gene present in more than 1% of the populations. It will come to many as a surprise to learn that some of these so-called "mutations" actually REDUCE the risk of breast cancer.

And then it goes on to talk about the common overdiagnosis and overtreatment of breast cancer.

On the other hand, in a woman's health magazine online article I found a statement that said in the case of a BCRA gene, there was a portion missing and nothing to turn on or off and that it was an exception to how your lifestyle/environment can change gene expression and reduce your likelihood of developing the cancer you are genetically predisposed to. But they provided no support for that claim or any other.

http://articles.mercola.com/sites/articles/archive/2013/03/18/fat-soluble-vitamins.aspx?e_cid=20130318_DNL_art_2&utm_source=dnl&utm_medium=email&utm_content=art2&utm_campaign=20130318

Magnesium contributes to more than three hundred specific chemical reactions that occur within our bodies, including every reaction that depends on ATP, the universal energy currency of our cells.¹³Magnesium also activates the enzyme that makes copies of DNA, as well as the enzyme that makes RNA, which is responsible for translating the codes contained within our genes into the production of every protein within our body. This process of translating the DNA code in order to produce proteins is called gene expression.

Vitamins A and D carry out most of their functions by regulating gene expression, which means they rely directly on magnesium to carry out these functions. They also rely indirectly on magnesium because our cells can only produce their receptors and all the proteins with which they interact with the assistance of this critical mineral.

Zinc is an essential structural component of many vitamin A-related proteins, including the primary protein that transports vitamin A through the blood, the enzyme that carries out the first step in the activation of vitamin A to retinoic acid, and the nuclear receptor that binds to retinoic acid and allows it to regulate gene expression.

Although less well studied, zinc also interacts with vitamin D. Vitamin D and zinc most likely promote each others intestinal absorption.¹⁸ In rats, dietary zinc supports the production of the vitamin D receptor.¹⁹ Once the receptor is formed, zinc provides it with essential structural support. Although in the absence of this structural support the receptor still binds to vitamin D, the structural support is needed to allow this vitamin-receptor complex to bind to DNA.²⁰ Studies with isolated cells illustrate the importance of this interaction: adding zinc to these cells increases the rate at which vitamin D activates the expression of genes.²¹

Altogether, these results suggest that vitamins A and D can only fulfill their functions in the presence of adequate zinc.

Exercise can bring about epigenetic changes

http://www.sciencedaily.com/releases/2012/03/120306131254.htm

The underlying genetic code in human muscle isn't changed with exercise, but the DNA molecules within those muscles are chemically and structurally altered in very important ways. Those modifications to the DNA at precise locations appear to be early events in the genetic reprogramming of muscle for strength and, ultimately, in the structural and metabolic benefits of exercise.
The DNA changes in question are known as epigenetic modifications and involve the gain or loss of chemical marks on DNA over and above the familiar sequence of As, Gs, Ts, and Cs.

Citing study

Romain Barres, Jie Yan, Brendan Egan, Jonas Thue Treebak, Morten Rasmussen, Tomas Fritz, Kenneth Caidahl, Anna Krook, Donal J. O'Gorman, Juleen R. Zierath. Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle. Cell Metabolism, 2012; 15 (3): 405 DOI: 10.1016/j.cmet.2012.01.001

articles on research on the effects of inflammation on epigenetic changes

Quote

Epigenetics is the study of heritable changes in gene expression that do not involve changes in the DNA sequence. Epigenetic mechanisms play important roles in development from a fertilized egg into a complex human being, as well as in aging and in various diseases (including cancer). Study topics such as DNA methylation, histone modification, RNAi, cancer epigenetics, stem cells and the environment (for example, nutrition and stress) as potential modifiers of the human epigenome.

Quote

http://www.news-medical.net/news/20130328/Inflammation-and-epigenetics-an-interview-with-Dr-Belkina-and-Dr-Denis-Boston-University-School-of-Medicine.aspx Please can you give a brief introduction to epigenetics?

Epigenetics refers to processes of inheritance that are not directly dependent on DNA sequences and mutations, such as the mechanisms that cause children born to metabolically stressed mothers to develop metabolic disease when the children reach adulthood.

Epigenetics can also refer to the interactions of proteins with chromatin, the packaging material of DNA; these interactions also do not depend directly on the DNA sequences, but on the nature of the packaging material itself. DNA sequencing and human genomic information can tell us almost nothing about an epigenetic process.

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[Link removed] 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. .... info in study on mice that indicate its chronic inflammation not obesity that lead to diabetes.......then...

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.

http://www.news-medical.net/news/20130328/Inflammation-and-epigenetics-an-interview-with-Dr-Belkina-and-Dr-Denis-Boston-University-School-of-Medicine.aspx

Maximizing Methylation: The Key to Healthy Aging

http://drhyman.com/blog/2011/02/08/maximizing-methylation-the-key-to-healthy-aging-2/#close

Dr. Hyman is one of the rare doctors that recognize the connection between diet and acne and wrote one of the best articles I've seen for the masses in the Huffington Post.

I notice he doesn't mention methionine, a sulfur containing amino acid that's abundant in the greens he recommends. I'm confused about the methionine because i expected abundant methionine to be desirable, but here's a study on low methionine diets increasing longevity http://www.ncbi.nlm.nih.gov/pubmed/18789600

Quote

1. Eat more dark, leafy greens You want to eat l cup a day of vegetables like bok choy, escarole, Swiss chard, kale, watercress, spinach, or dandelion, mustard, collard, or beet greens. These are among the most abundant sources of the nutrients needed for optimal methylation
2. Get more Bs in your diet Good food sources include sunflower seeds and wheat germ (vitamin B6); fish and eggs (vitamin B6 and B12); cheese (B12); beans and walnuts (vitamin B6 and folate); leafy dark green vegetables; asparagus, almonds, and whole grains (folate); and liver (all three)
3. Minimize animal protein, sugar, and saturated fat Animal protein directly increases homocysteine. Sugar and saturated fat deplete your bodys vitamin stores
4. Avoid processed foods and canned foods These are depleted in vitamins
5. Avoid caffeine Excess amounts can deplete your B vitamin levels
6. Limit alcohol to 3 drinks a week More than this can deplete your B vitamin levels
7. Dont smoke As noted above, smoking inactivates vitamin B6
8. Avoid medications that interfere with methylation See notes on this above
9. Keep the bacteria in your gut healthy Take probiotic supplements and use other measures to make sure the bacteria in your gut are healthy so you can properly absorb the vitamins you do get
10. Improve stomach acid Use herbal digestives (bitters) or taking supplemental HCl
11. Take supplements that prevent damage from homocysteine Antioxidants protect you from homocysteine damage. Also make sure you support methylation with supplements like magnesium and zinc
12. Supplement to help support proper homocysteine metabolism Talk to your doctor to determine the best doses and forms for you. Here are a few suggestions:
    Folate (folic acid): Amounts can vary based on individual needs from 200 mcg to 1 mg. Some people may also need to take preformed folate (folinic acid or 5 formylTHF) to bypass some of the steps in activating folic acid
    Vitamin B6: Take 2 to 5 mg a day. Some people may need up to 250 mg or even special active B6 (pyridoxyl-5-phosphate) to achieve the greatest effect. Doses higher than 500 mg may cause nerve injury
    Vitamin B12: Doses of 500 mcg may be needed to protect against heart disease. Oral vitamin B12 isnt well absorbed; you may need up to 1 or 2 mg daily. Ask your doctor about B12 shots
    Betaine: This amino acid derivative is needed in doses from 500 to 3,000 mg a day, depending on the person

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Measuring Your Own Methylation Process

To find out if your methylation process is optimal, ask your doctor for the following tests:

• Complete blood count Like our friend Mr. Roberts, large red blood cells or anemia can be a sign of poor methylation. Red blood cells with a mean corpuscular volume (MCV) greater than 95 can signal a methylation problem
• Homocysteine This is one of the most important tests you can ask for. The normal level is less than 13, but the ideal level is likely between 6 and 8
• Serum or urinary methylmalonic acid This is a more specific test for vitamin B12 insufficiency. Your levels may be elevated even if you have a normal serum vitamin B12 or homocysteine level
• Specific urinary amino acids These can be used to look for unusual metabolism disorders involving vitamins B6 or B12 or folate, which may not show up just by checking methylmalonic acid or homocysteine

This guy wrote some interesting articles on this suite101 site, but i don't know who he is or about the validity.

Eating to Enhance One's Epigenome (DNA Methylation)
[Link removed]

In case anyone wanted to know about the gene expression that affects your fasting blood glucose and thus your ability to survive famine/tendency to develop type II diabetes.

Your genetic makeup may also affect your response to intermittent fasting. Many people of Asian and European ancestry (myself included) have a mutation in the SNP rs2291725 that is associated with higher fasting blood glucose. This mutation probably became widespread in some populations thousands of years ago as a response to the inevitable lean times that came with a switch to agricultural food production. Women with this mutation were more likely to maintain their pregnancies during times of food scarcity. These days, the same mutation is associated with a higher risk of developing Type 2 diabetes and/or gestational diabetes. I wonder if having this mutation also makes intermittent fasting more comfortable (due to higher fasting blood glucose levels)?

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alternativista, I appreciate this post thanks again for all the info. I'm curious, there's a lot of talk about magnesium, zinc and vitamin D. If one has acne due to something they have 'done' in their life that has 'activated' the gene (rather than it being an allergy etc), is it being suggested that taking these three supplements may just help 'deactivate' the acne gene in that particular person?

I'm curious on your thoughts as I think I have something interesting to add..

Note how studies these days always explore gene expression. Not genes. Gene expression. Because that's what matters when it comes to health conditions and gene expression is affected by the things you do to yourself.

alternativista, I appreciate this post thanks again for all the info. I'm curious, there's a lot of talk about magnesium, zinc and vitamin D. If one has acne due to something they have 'done' in their life that has 'activated' the gene (rather than it being an allergy etc), is it being suggested that taking these three supplements may just help 'deactivate' the acne gene in that particular person?

I'm curious on your thoughts as I think I have something interesting to add..

Well, epigenetics is about changes in expression that your parents may have passed on to you or that you may pass on to your children. And that's what most of the info I've posted here is about. I'm not sure how much evidence has been found of anyone switching anything on and off. I think some of those studies on the yellow obese agouti mice might have included changes that occured within the mouse's lifetime. And I know there are books and posted some titles that certainly make claims that you can activate or deactivate a gene. Who knows, maybe whenever someone reverses insulin resistance they've flipped a switch.

Maybe I'll see if any of those books are in the library.

alternativista, I appreciate this post thanks again for all the info. I'm curious, there's a lot of talk about magnesium, zinc and vitamin D. If one has acne due to something they have 'done' in their life that has 'activated' the gene (rather than it being an allergy etc), is it being suggested that taking these three supplements may just help 'deactivate' the acne gene in that particular person?

I'm curious on your thoughts as I think I have something interesting to add..

I don't know about those supplements, other than of course they play major roles in cell proliferation and hormone regulation and more. And well, zinc and mag at least have much to do with methylation which means they have much to do with gene expression.

But this paper says that avoiding habits that elevate growth factors (or growing out of puberty) changes expression of genes involved in acne.

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J Dtsch Dermatol Ges. 2010 Feb;8(2):105-14. doi: 10.1111/j.1610-0387.2010.07344.x.

FoxO1 - the key for the pathogenesis and therapy of acne?

[Article in English, German]

Melnik BC.

Source

Department of Dermatology, Enviromental Medicine and Health Theory, University of Osnabruck, Germany. [email protected]

Abstract

Five main factors play a pivotal role in the pathogenesis of acne: androgen dependence, follicular retention hyperkeratosis, increased sebaceous lipogenesis, increased colonization with P. acnes, and inflammatory events. This paper offers a solution for the pathogenesis of acne and explains all major pathogenic factors at the genomic level by a relative deficiency of the nuclear transcription factor FoxO1. Nuclear FoxO1 suppresses androgen receptor, other important nuclear receptors and key genes of cell proliferation, lipid biosynthesis and inflammatory cytokines. Elevated growth factors during puberty and persistent growth factor signals due to Western life style stimulate the export of FoxO1 out of the nucleus into the cytoplasm via activation of the phos-phoinositide-3-kinase (PI3K)/Akt pathway. By this mechanism, genes and nuclear receptors involved in acne are derepressed leading to increased androgen receptor-mediated signal transduction, increased cell proliferation of androgen-dependent cells, induction of sebaceous lipogenesis and upregulation of Toll-like-receptor-2-dependent inflammatory cytokines. All known acne-inducing factors exert their action by reduction of nuclear FoxO1 levels. In contrast, retinoids, antibiotics and dietary intervention will increase the nuclear content of FoxO1, thereby normalizing increased transcription of genes involved in acne. Various receptor-mediated growth factor signals are integrated at the level of PI3K/Akt activation which finally results in nuclear FoxO1 deficiency.

So, they name 5 major factors in the pathogenesis of acne:

androgen dependence, follicular retention hyperkeratosis, increased sebaceous lipogenesis, increased colonization with P. acnes, and inflammatory events.

All those factors are related to a relative deficiency of the nuclear transcription factor FoxO1.

Nuclear FoxO1 suppresses androgen receptors, genes involved in cell proliferation and lipid biosynthesis. and inflammatory cytokines.

Elevated growth factors due to puberty OR Western diet and lifestyle decrease Fox01

This leads to increased androgen receptor sensitivity, increased cell proliferation, and increase in inflammatory cytokines. I have to look into what 'induction of sebaceous lipogenesis' means, exactly.

Retinoids, antibiotics work by increasing FoxO1 and so will dietary interventions. I.e. avoiding high glycemic and insulinotropic diet habits.

'thereby normalizing increased transcription of genes involved in acne' - in other words, it changes genetic expression or 'flips some genetic switches'.

More Vocabulary:

The genotype of an organism is the inherited instructions it carries within its genetic code. Not all organisms with the same genotype look or act the same way because appearance and behavior are modified by environmental and developmental conditions.

A phenotype is the composite of an organism's observable characteristics. Phenotypes result from the expression of an organism's genes as well as the influence of environmental factors and the interactions between the two. This genotype-phenotype distinction was proposed by Wilhelm Johannsen in 1911 to make clear the difference between an organism's heredity and what that heredity produces.

genotype (G) + environment (E) + genotype & environment interactions (GE) phenotype (P)

environment means stuff you are exposed to which includes stuff you do to yourself.

Gene expression is the process by which information from a gene is used in the synthesis of a functional gene product. Gene regulation gives the cell control over structure and function, and is the basis for cellular differentiation, morphogenesis and the versatility and adaptability of any organism.

In genetics, gene expression is the most fundamental level at which the genotype gives rise to the phenotype. The genetic code stored in DNA is "interpreted" by gene expression, and the properties of the expression give rise to the organism's phenotype. Such phenotypes are often expressed by the synthesis of proteins that control the organism's shape, or that act as enzymes catalysing specific metabolic pathways characterising the organism.

Transcription is the first step of gene expression, in which a particular segment of DNA is copied into RNA by the enzyme, RNA polymerase. During transcription, a DNA sequence is read by an RNA polymerase, which produces a complementary, antiparallel RNA strand. As opposed to DNA replication, transcription results in an RNA complement that includes uracil (U) in all instances where thymine (T) would have occurred in a DNA complement. Also unlike DNA replication where DNA is synthesised, transcription does not involve an RNA primer to initiate RNA synthesis.

Transcription proceeds in 5 or 6 steps, each moving like a wave along the DNA.

Transcription factors are one of the groups of proteins that read and interpret the genetic "blueprint" in the DNA. They bind to the DNA and help initiate a program of increased or decreased gene transcription. Transcription factors bind to either enhancer or promoter regions of DNA adjacent to the genes that they regulate. Depending on the transcription factor, the transcription of the adjacent gene is either up- or down-regulated. The number of transcription factors found within an organism increases with genome size, and larger genomes tend to have more transcription factors per gene.^[9] There are approximately 2600 proteins in the human genome that contain DNA-binding domains, and most of these are presumed to function as transcription factors.,^[10]

DNA methylation is often utilized to silence and regulate genes without changing the original DNA sequence, an example of epigenetic modification. Methylation often occurs on nucleic bases in DNA or amino acids in protein structures. Methytransferases use a reactive methyl group bound to sulfur in S-adenosyl methionine (SAM) as the methyl donor.

Epigenetics Project Blog, subtitled 'Can our DNA be "Played" like a musical instrument?'

http://georgefebish.wordpress.com/2013/03/08/dairy-can-give-you-acne/ - post on dairy and acne. Not overly valuable post though.

They are selling a book 'Food For Thought - An Epigenetic Guide to Wellness [Link removed]

It looks like it has a pro-veganism slant so they probably only have research that support that idea.

On 7/2/2013 at 5:02 PM, alternativista said:

Epigenetics Project Blog, subtitled 'Can our DNA be "Played" like a musical instrument?'

http://georgefebish.wordpress.com/2013/03/08/dairy-can-give-you-acne/ - post on dairy and acne. Not overly valuable post though.

They are selling a book 'Food For Thought - An Epigenetic Guide to Wellness [Link removed]

It looks like it has a pro-veganism slant so they probably only have research that support that idea.

I love this topic - I think it's fascinating, and very important to acne healing.

I'm personally interested in the practical techniques that have been developed for making these Epigenetic changes happen, such as acupuncture, acupressure, EFT, TFT, and others.

I use EFT on a daily basis, and have cleared my acne entirely with with it. It's a very complex topic on the outside, but once you can break it down and understand what kind of daily practices you can do, it's incredible the kind of changes that can happen - that I've experienced, anyway.

Alternativista, have you heard of the book 'The Genie In Your Genes - Epigenetic Medicine and the New Biology of Intention' written by Dawson Church, Ph.D.?

It gives a very comprehensive look at this topic. At great introduction, and even includes some of the studies you've linked to here.

This is fascinating stuff, thanks for the reading recommendations. I only recently began practicing biofeedback exercises for stress, which is complementing acupuncture treatments nicely. I will need to look into other forms of epigenetics as well. I wonder if it is possible to permanently normalize acne genes, or if we are just suppressing those genes while following specific regimens long term.