Source:, Pierce the Disease Epigenetics Process Header

Learn How Diet Pierces the Disease Epigenetics Process!

SUMMARY:  This post explains the disease epigenetics process because most think your genes are your destiny.  That is actually not true. You are more than the genes you inherit from your parents!  Genes predispose you to the disease (~66% of “you” is determined by your genetics), but the remaining 33% is influenced by epigenetic changes to the genes, and that is one mechanism through which disease is triggered[Mellor, 2015 University of Oxford Podcasts]. That is why they study DNA identical twins having discordance for the same disease — they find epigenetic differences [Insights from Identical Twins]  [NovaScienceNow, Epigenetics]   While  it is often unknown if epigenetic differences are a cause or a consequence of disease, many  studies are providing evidence suggesting a potential role for epigenetic alterations in the pathophysiology (e.g. Type 2 Diabetes, asthma, brain disorders and neurodegeneration,  Alzheimer’s, autismLupusChronic Fatigue Syndrome colon and other cancersParkinson’sALS…).  The bottom line:  Even though you might be “predisposed” to disease (e.g. you have a genetic pre-disposition tendency to Alzheimer’s, anxiety, arthritis, autoimmune disorders, cardiovascular disease, depression, diabetes, hypertension, metabolic syndrome, obesity, and cancer — any disease with epigenetic involvement which seems to be all of them) you can STOP and REVERSE the epigenetic changes that trigger disease by modifying factors that affect epigenetics such as nutrition, stress, toxicity, exercise and drugs. [Mellor, 2015 University of Oxford Podcasts[NIH, NICHD[Moosav et al 2016]  [Szarc vel Szic et al 2015]  [Wopereis et al 2014]  [Hartzell et al 2012]  [University of Utah, Nutrition & EpigeneticsOne whopping impact of these factors is to pierce the disease epigenetic process by altering the microbiome. The microbiome is what makes identical twins, not identical! And it’s the microbiome consequent metabolites (which is where over 70% of our immunity resides) that can change epigenetic mechanisms (like methylation and histone modification — NOTE:  I won’t be “teaching” these mechanisms, I will however explain enough that you can EASILY understand the concept) which have onward effects including triggering or reversing disease in those predisposed What this means is that you actually have a say in if you turn on or off genes with consequent trigger (or reversal) of disease. The recognition that environment, not genetics, is the primary driver of health and disease carries a strong message of personal empowerment and responsibility. Thus, included is a special section — EPIGENETIC EXPERT SUGGESTIONS FOR EATING FOR YOUR EPIGENOME!  BAM — they sound a lot like those therapeutic diets I teach and blog about!  Don’t be duped.  A lot of disease is preventable — [WHO] says over 80% of all heart disease, stroke and type 2 diabetes AND over 40% of cancer!  From the grim stats below, if you don’t already have disease you likely will and sooner than you expect! A balanced lifestyle that includes a healthy diet, exercise, & avoiding exposure to contaminants, may in the long run create a healthy epigenome. [TedED, What is Epgenetics? -Carlos Guerrero Bosagna.] Time to empower yourself to use epigenetics modifications to keep or move yourself off diseasespan!

“Epigenetic modification of disease-related genes can contribute to diagnosis (biomarker) as well as disease prevention or progression.”   

[Szarc vel Szic et al 2015].

The Grim Disease Incidence Stats:  If you don’t have chronic disease now, you likely will, & sooner than you may expect.
  • More than half the population has one chronic disease (it is autoimmune for 20% of those, mostly women) AND almost a third of the population has multiple chronic diseases.
  • 67% of the working age 18 to 64 years have multiple chronic disease — 18% if aged 18 to 44 years, 49% if aged 45 to 64 years!
  • Even the young are not spared. 27% of 0 to 17 yr olds have one or more chronic disease!
  • The last slide shows what those diseases are by age!


WHO says, “The major causes of chronic diseases are known, and if these [known] risk factors were eliminated, at least 80% of all heart disease, stroke and type 2 diabetes AND over 40% of cancer would be prevented.  

Don’t be duped!  Albeit there likely are other mechanisms (viral and fungal links, the growing emphasis on mitochondrial issues, and even the role for those trillions of beasties [beyond those described in this post]) [Szarc vel Szic et al 2015],  getting epigenetics on track to result in best gene expression, using diet and lifestyle, RESOLVES MOST of the diseases I see and is spot on with what other experts and the evidence says. [Dr. Mark Hyman, Director Cleveland Clinic Center for Functional Medicine]  [Dr. David Katz, founder True Health Initiative and Director, Yale University Prevention Research Center; Griffin Hospital].  EVEN CONDITIONS where DRUGS FAIL are seeing vast improvement with DIETARY CHANGE (Autism  [Whiteley 2017 gluten and casein free, ketogenic] and Alzheimer’s: [Bredesen’s Approach reversing early onset AD [MIND Diet and Cognition Prevention, 2017, 3 year trial]   [Multicultural Healthy Diet 2017, 27 month trial]).  Even our response to CANCER treatment is changed by the composition of the microbiome. [Ledford 2017] Gut microbes can shape responses to cancer immunotherapy.

Learn the Disease Epigenetics Process the EASY way: Entertaining videos!

First, the difference between a genetic vs an epigenetic change is that the epigenetic change does NOT actually change the sequence:

Epigenetics and its Implications for Public Health, Genetic vs Epigenetic Change,
Epigenetics and its
Implications for Public Health, Genetic vs Epigenetic Change,

Now watch this video. I especially ♥ it because it shows what is actually changing epigenetically, What is Epigenetics?  An entertaining and educational primer”, GreenmedTV, April 2013,  or see its YouTube here.  As of today it has 1,591,038 views!  Add yours!       



  • Note ⇒  Don’t get hung up on understanding the specific methylation mechanism.  Key scientist concerns are that there not be too much focus on specific epigenetic mechanisms since epigenetics is cutting edge science (finding we do have more control over our genes then previously thought), there is a lot unknown, and the mechanisms now known may become outdated as the science progresses [Marriott Portland State University, Powerpoint].  
  • Pearl:  Just learn the concept — That environmental factors influence  epigenetics with consequent gene expression that makes the gene readable, or not.  I ♥ this video from the University of Utah Genetic Science Learning Center, “The Epigenome at a Glance” videoIt is interactive and allows you to wind and unwind genes as their histones and chemical tags  epigenetically react to environmental signals from diet, toxins (air, water, food, topicals), stress, sleep, etc! The process whereby environmental factors influence gene expression is called “epigenetics.”
Source:, Epigenetics
Source:, Epigenetics


  • If you sequence the genomes of a pair of identical twins every decade for fifty years, you get the same sequence over and over. But if you sequence the epigenomes of a pair of twins you find substantial differences: the pattern of epigenetic marks on the genomes of their various cells, virtually identical at the start of the experiment, diverges over time… It is a testament to the unsettling beauty of the genome that it can make the real world stick… Chance events—injuries, infections…, impinge on one twin and not on the other. Genes are turned on and off in response to these events, as epigenetic marks are gradually layered above genes, etching the genome with its own scars. [Mukherjee, 2016 New Yorker Magazine] 
  • One of the main processes switching genes on and off is an epigenetic process known as DNA methylation. By controlling which genes are on or off in any given cell, we are able to grow kidneys, heart, skin, etc. and control how these cells behave and what they look like. How Does Genetics Explain Non-identical identical twins?
  • “Methylation is [one] common and widely used mechanism for  epigenetic modifications in cells.  In methylation, methyl groups (CH3) stick to DNA and usually suppress gene expression.  Histones are the proteins DNA is wrapped tightly around. Histone modifications [are another mechanism that] usually involve attachment of an acetyl group (CH3CO.) Acetylation helps tightly coiled DNA unwind a bit, making genes easier to get to and turn on.”  [Moosav et al 2016]
  • Environmental exposures alter the expression of genes by tightly wrapping them making them unreadable (aka the gene is turned OFF), or relaxing genes so that the gene is easily accessible for attachment to chemical tags on the histone (aka gene is turned ON), thereby altering the mRNA and protein production.  Proteins perform important functions for the cells.  To function correctly, each cell depends on thousands of proteins to do their jobs in the right places at the right times.  Epigenetics does not change the DNA, it reads the DNA differently and alters protein production which alters cell behavior and function[Wopereis et al 2014] 
  • I ♥ this analogy:  The methyl groups hang off the DNA string like Christmas ornaments, and specific proteins add and remove the ornaments, in effect “decorating” the genome. The most heavily methylated parts of the genome tend to be dampened in their activity.  [Mukherjee, 2016 New Yorker Magazine] 
  • The cell epigenome is dynamic and can be affected by genetic and environmental factors. Furthermore, epigenetic modifications can be REVERSIBLE, which makes the genome flexible to respond to environment changes such as nutrition, stress, toxicity, exercise, and drugs [].   [Moosav et al 2016]
  • Epigenetic changes can be transmitted to your children It is our past, present, and future on disease risk — aka ‘developmental origin of health and disease’ (DOHaD) Individuals with metabolic syndrome, obesity, type 2 diabetes, and cardiovascular disease may show a LIFETIME imbalance between energy intake and expenditure due to incorrect epigenetic programming during their EARLY development as a result of placental insufficiency, inadequate maternal nutrition, metabolic disturbances, or neonatal medication.  [Szarc vel Szic et al 2015
  • Epigenetic changes during pregnancy can affect the health of future generations (epigenetic transgenerational inheritance).   An example for asthma transgenerational inheritance is:   Environmental Pollution Exposure during Pregnancy Increases Asthma Risk for Three Generations, American Physiological Society, 2017 and High-Fat Diet during Pregnancy Compromises Offspring’s Lung Health [increasing asthma and allergies], American Physiological Society, 2017.
  • Here is a great epigenetics 5 minute recap:  TedED, What is Epgenetics? -Carlos Guerrero Bosagna. 

Food as Epigenetic Medicine:  The next challenge is to determine which adverse epigenomic disease marks are reversible by specific diets, lifestyle changes, or drugs.

But you don’t need to wait for the researchers.  What do you have to lose?  Just try the tenets of Therapeutic Diets because…

MANY diseases have altered epigenetic methylation including (not exhaustive listing):

  • Different cancers, autoimmune   disorders, neurological disorders including Fragile X syndrome, Huntington, Alzheimer, and Parkinson diseases and schizophrenia.  [Moosav et al 2016]
  • Type 2 Diabetes [Elliott et al 2017].
  • Asthma.  Over two dozen genes regulate the antibody IgE which provokes allergic reactions… the epigenetic mechanism of low methylation occurring at 36 places in 34 genes.  This mechanism, low methylation. meant the genes didn’t get turned off so there was overproduction of IgE antibodies that trigger asthma attacks.  [Liang et al 2015].
  • Brain Disorders and Neurodegeneration.  A high fiber diet in the gut can alter gene expression in the brain to prevent neurodegeneration and promote regeneration… This paper integrates evidence from the disparate fields of gastroenterology and neuroscience to hypothesize that gut bacteria ferment fiber to produce butyrate, a short-chain fatty acid (SCFA), that can alter gene expression in the brain to improve brain health.  See below, Fig. 2. The proposed mechanisms for the neuroprotective effects of butyrate and the diseases [Alzheimer’s, Parkinson’s, Huntington’s, Mitochondrial Encephalopathy, Adrenoleuko-dystrophy, metabolic disorders, insulin resistance in brain, stroke, autism, psychological disorders] which may benefit from butyrate treatment or a high fiber diet. We can no longer overlook the importance of the gut-brain axis and nutrition in disease pathogenesis and treatment.   [Bourass et al, 2016].


  • Alzheimer’s [Qazi TJ et al 2017}.
  • Autism [Hartzell et al 2012Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?
  • Lupus [Richardson] DNA methylation and autoimmune disease. 
  • Chronic Fatigue Syndrome1,192 CpG sites were identified as differentially methylated between CFS patients and healthy control subjects, corresponding to 826 genes. [Wilfred C. de Vega et al 2014].
  • Parkinson’s [Miranda-Morales et al 2017].
  • ALS.   This study found widespread changes in methylation patterns in ALS-affected co-twins, consistent with an epigenetic contribution to disease. [Young et al 2017].
  • Colon and other Cancers.  Butyrate can modify histones which in turn can regulate the expression of miRNAs in colon and other cancers.  [Bishop et al 2017].   As cells become malignant, or cancerous, epigenetic modifications can deactivate tumour
    suppressor genes, which prevent excessive cell proliferation [Esteller, 2007].

DIET can Modulate Epigenetics by changing the Microbiome to Increase Production of Butyrate:

It is estimated that 90% of the cells in the human body are of microbial origin, and the vast majority of these microbiota are comprised of 15,000–36,000 species of commensal and symbiotic bacteria that reside within the lumen of the gut. [Frank et all 2007 [Stillling et al 2014].

The microbiota produce metabolites which include short-chain fatty acids (the most common are propionate, acetate and butyrate — butyrate is an important source of energy for colonic epithelial cells, may enhance epithelial barrier integrity, modulate the GI immune response, produce neurotransmitters (serotonin, dopamine, and GABA), alter epigenetic markers, and produce bioactive food components and energy metabolites.  Some microbe-derived metabolites enter the circulation and can cross the blood-brain barrier.  Butyrate biological functions include its ability to serve as a histone deacetylase (HDAC) inhibitor [epigenetic mechanism], an energy metabolite to produce ATP and a G protein-coupled receptor (GPCR) activator.  [Frank et all 2007]

♥ Certain Microbiota can produce butyrate:  2 major groups of butyrate-producing bacteria are Faecalibacterium prausnitzii  and Eubacterium rectale/Roseburia spp. [Bishop et al 2017]

♥ In addition to microbiota production of butyrate, diet can influence the production of butyrate (see pic below for relative proportions of SCFAs for various carbs).

“Much attention is currently focused on the modulation of hyper/hypomethylation of key inflammatory genes by dietary factors as an effective approach to chronic inflammatory disease management and general health benefits. In this respect, ‘Let food be your epigenetic medicine’ could represent a novel interpretation of what Hippocrates said twenty-five centuries ago.”  [Szarc vel Szic et al 2015]

  • Fiber having low ferment ability [are not fuel for the microbiota] include cellulose, lignin, and some insoluble fiber. [Bishop et al 2017]
  • Non-fiber foods naturally containing butyrate that can increase butyrate production in the colon include oligosaccharides acarbose and tributyrin, fatty acid oxidation and glucose metabolism, plant oils, and animal fats (ruminant animal milk products like butter).  Butter is the richest source of dietary butyrate containing 3-4% butyric acid in form of tributyrin. 1g/kg of tributyrin elevated rat portal vein concentrations of butyrate to 2.4 mM after 1 hour [18]. [Bishop et al 2017]
  • High fiber foods, summarized in Table 1 [below], enable butyrate producing bacteria such as Clostridium,  Eubacterium, and Butyrivibrio to thrive and includes resistant starches (e.g., whole grain and legumes) and fructo-oligosaccharides (FOS) (e.g., bananas, onions, and asparagus). In fact, within two weeks of a high FOS diet, rats showed increase butyrate in the large intestine without changing the total number of anaerobic bacteria. [Blay et al 1999 ].  Butyrate bloom was shown in rat studies for FOS & resistant starches. [Perrin et al 2001]

FOOD as Epigenetic Medicine Epigenetic Expert Suggestions for Eating for Your Epigenome

[University of Utah, Nutrition & Epigenetics] explains:  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 & SAM-e (S-Adenosyl methionine, popular OTC supplement) are key components of this methyl-making pathway. [♥ Their food list shown on the slide below:  sesame seeds, nuts — brazil nuts and others, garlic, fish, sunflower seeds, baker’s yeast, meats including liver, beef, chicken, veal, turkey, shellfish, milk [can be made less inflammatory by using A2 casein pasture sourced milk along with a long enough fermentation that it is lactose-free yogurt or cheese],   whole grain products including wheat [I’d add if properly prepared, if tolerated, and free of gut harming additives like emulsifiers and disease associated fats], vegs (specifically highlighted are broccoli, peppers, leafy vegs, spinach, sugar beets), eggs, soy [caution, recent studies find soybean oil inflammatory], and red wine [one glass, more decreases microbiome diversity].  [See the snippets below for epigenetic effects of nutrition. [Sang-Woon Choi et al 2010] [Szarc vel Szic et al 2015]. Diets high in these methyl-donating nutrients can rapidly alter gene expression, especially during early development when the epigenome is first being established [And,] a methyl-deficient diet leads to a decrease in DNA methylation, but the changes are REVERSIBLE when methyl is added back to diet. See this autism paper [Hartzell et al 2012] as an example! See the snippets below for the NUTRIENTS in epigenetic foods [Sang-Woon Choi et al 2010]   [Szarc vel Szic et al 2015]Methyl donors: Vitamin B12, folate, choline, betaine, methionine, serine, glycine. Phytochemicals:  Genistein, soy isoflavones, curcumin, reveratrol, sulphorophane, polyphenols. Fatty acids:  Butyrate, arachidonic acid, docosahexaenoic acid, eiconsapentaenoic acid. Vitaminsretinol, tocopherols, vitamin C. 

“Food can be thy medicine,” or put more accurately, “food is Epigenetic Medicine” providing information to our cells. It is how we are designed. Eat right, and we can fix ourself!

Foods that Shape You:  How Diet can Change your Epigenome recommends:

Broccoli and other cruciferous vegetables contain isothiocyanates, which are able to increase histone acetylation. Soya, on the other hand, is a source of the isoflavone genistein, which is thought to decrease DNA methylation in certain genes. Found in green tea, the polyphenol compound epigallocatechin-3-gallate has many biological activities, including the inhibition of DNA methylation. Curcumin, a compound found in turmeric (Curcuma longa), can have multiple effects on gene activation, because it inhibits DNA methylation but also modulates histone acetylation. Figure 4 (below) shows further examples of epigenetically active molecules.

Eating for Your Epigenome recommends:

  • So if you’re keen to look after your epigenome, then you could try munching on foods that provide 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 [I’d add if properly prepared, if tolerated, and free of gut harming additives like emulsifiers and disease associated fats]. Choline comes from eggs, lettuce, peanuts & liver.
  • 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. Alternatively, try cheese, milk, meat, or… liver.
  • Finally, if you’re looking for something to wash down your meal, red wine seems like a good choice, given that its resveratrol might help to prevent cancer and ageing.
  • Until we understand more about the links between diet and epigenetics, the best advice seems to be to get lots of green veg, limit your alcohol intake, and eat liver!

The foods these experts list sound a lot like the Therapeutic Diets in clinical trials I lecture and blog about including MIND Diet and Dementia Prevention, SCD for IBD (and many other off–the–label conditions including autism), Wahl’s for MS, DASH for hypertension, Mediterranean…!  Also important, they eliminate processed foods.

Conclusion and PEARL of this post:  Your genes are not your destiny.  

Even though one might be “predisposed” to disease, we can STOP and REVERSE the epigenetic changes that trigger disease by IMPLEMENTING diet and lifestyle changes.

Diet alters the microbiome community ⇒  this targets the trillions of beasties in the gut microbiome (which is where over 70 percent of our immunity resides) and changes their metabolites (aka by-products). That alters epigenetics (including methylation and histone modification) with consequent change in gene expression.  This can change disease status.  

Implementing healing Therapeutic Diet tenets really means “food can be thy medicine,” or put more accurately, “food is Epigenetic Medicine.”

Bottom line:  Eat to support your cells AND THEIR epigenome.

Watch this Drew Berry video for a great visual of all our cells do, billions of time, right now, just to regenerate and split“Animations of Unseeable Biology,”  showing our incredible biology.


For further related reading, see below my signature:

  • Links to all 55 references, in order of appearance, used in this post
  • Pearls from NIH to better understand Genetic Predisposition.
  • The Top Five Reasons for Teaching  Epigenetics  [Marriott et al 2016].
  • Nestlé meeting of esteemed experts in human and animal health discussing the future of nutrition science with focus on epigenetics of nutrition.

Best in health through increased awareness,Signature2

References, in order of appearance.
  1.  [Mellor, 2015 University of Oxford Podcasts] Epigenetics: What Makes You “You”?
  2. [Insights from Identical TwinsUniversity of Utah Genetic Science Learning Center.
  3. [NovaScienceNow, Epigenetics]  
  4. [Elliott et al 2017] Role of DNA Methylation in Type 2 Diabetes Etiology: Using Genotype as a Causal Anchor.
  5. [Liang et al 2015] An epigenome-wide association study of total serum immunoglobulin E concentration. Epigenetics and asthma.
  6. [Bourass et al, 2016] Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?   Brain Disorders and Neurodegeneration.
  7. [Qazi TJ et al 2017}  Epigenetics in Alzheimer’s Disease: Perspective of DNA Methylation.,
  8. [Hartzell et al 2012Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?
  9. [Richardson] DNA methylation and autoimmune disease with focus on Lupus.
  10.  [Wilfred C. de Vega et al 2014]  DNA Methylation Modifications Associated with Chronic Fatigue Syndrome.
  11. [Bishop et al 2017Epigenetic Regulation of Gene Expression Induced by Butyrate in Colorectal Cancer: Involvement of MicroRNA. Colon Cancer and other Cancers.
  12. [Miranda-Morales et al 2017Implications of DNA Methylation in Parkinson’s Disease.
  13.  [Young et al 2017, ALS epigenetic differences] Epigenetic differences between monozygotic twins discordant for amyotrophic lateral sclerosis (ALS) provide clues to disease pathogenesis.  ALS twin registry studies show the disease is discordant in over 90% of monozygotic twins which implies that susceptibility to the disease has a major epigenetic or environmental component.
  14. [NIH, NICHD Eunice Kennedy Shriver National Institute of Child Health and Human Development, What role do epigenetics & developmental epigenetics play in health & disease? Environmental factors affecting epigenetic change in gene expression (turns genes on or off with consequent trigger of disease) include diet and lifestyle. 
  15. [Moosav et al 2016Role of Epigenetics in Biology and Human Diseases.  
  16. [Szarc vel Szic et al 2015] From Inflammaging to healthy aging by dietary lifestyle choices: is epigenetics the key to personalized nutrition?
  17. [Wopereis et al 2014]   “The first thousand days – intestinal microbiology of early life: establishing a symbiosis.” 
  18.  [University of Utah, Nutrition & Epigenetics]
  19. [Vighi et al 2008] Allergy and the gastrointestinal system. Over 70% of our immune system resides.
  20. WHO, Overview – Preventing chronic diseases: a vital investment, Misunderstanding #4.
  21.  TedED, What is Epgenetics? -Carlos Guerrero Bosagna. 
  22. Other experts say [Dr. Mark Hyman, Cleveland Clinic Center for Functional Medicine]. Is Predispositon Our Destiny?
  23. [Dr. David Katz, founder True Health Initiative and Director, Yale University Prevention Research Center; Griffin Hospital]   Preventitive Medicine:  Why We Stay Fat and Can we Say What Diet is Best for Health?
  24. [Whiteley 2017] Gluten & Casein Free Diet vx Ketogenic Diet for Autism: Fight!
  25. Alzheimer’s [Bredesen’s Approach reversing early onset AD]. 
  26. Alzheimer’s [MIND Diet and Cognition Prevention, 2017 3yr trial]
  27. Alzheimer’s [Multicultural Healthy Diet 2017, 27month trial] NIH funds research to fight Alzheimer’s disease with anti-inflammatory diet
  28. [Ledford 2017] Gut microbes can shape responses to cancer immunotherapy.
  29. What is Epigenetics?  An entertaining and educational primer”, GreenmedTV, April 2013,  or the YouTube here.  
  30. [Marriott Portland State University, PowerpointEpigenetics and its Implications for Public Health.
  31. University of Utah Genetic Science Learning Center, “The Epigenome at a Glance” video.
  32. [Mukherjee, 2016 New Yorker Magazine] Same but Different, Breakthroughs in Epigenetics.
  33. How Does Genetics Explain Non-identical identical twins?
  34. Environmental Pollution Exposure during Pregnancy Increases Asthma Risk for Three Generations, American Physiological Society, 2017. 
  35.  High-Fat Diet during Pregnancy Compromises Offspring’s Lung Health [increasing asthma and allergies], American Physiological Society, 2017. 
  36. [Esteller, 2007 Epigenetic gene silencing in cancer: the DNA hypermethylome.
  37. [Frank et all 2007Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. 
  38. [Stillling et al 2014Microbial genes, brain & behaviour − epigenetic regulation of the gut-brain axis.
  39. [Blay et al 1999Prolonged intake of fructo-oligosaccharides induces a short-term elevation of lactic acid-producing bacteria and a persistent increase in cecal butyrate in rats.
  40. [Perrin et al 2001Only fibres promoting a stable butyrate producing colonic ecosystem decrease the rate of aberrant crypt foci in rats Butyrate bloom was shown in rat studies for FOS and resistant starches.
  41. CLA Grassfed SCD Yogurt Benefits, Cytokine Studies, Erivan & Whole Foods 365.
  42. Get SCD Cheese Right. It is Loaded with Nutrients & Bacteria!
  43.  Emulsifiers, Microbiome, Emulsifiers, IBD & Metabolic Syndrome.
  44. Disease associated fats,  Soybean oil, Corn Oil, Diabetes, Metabolic Syndrome, & P-450.
  45. Optimal Microbiome Diet from American Gut Data.
  46. [Sang-Woon Choi et al 2010] Epigenetics: A New Bridge between Nutrition and Health.
  47. Foods that shape you How Diet can change your epigenome.
  48. Eating for your epigenome. 
  49. MIND Diet and Dementia Prevention, CME Microbiome Questions & Answers.
  50. SCD for IBD, Concise Summary of SCD Studies.
  51.  “Animations of Unseeable Biology”
  52. NIH excerpts from “Genetics Home Reference, Your Guide to Understanding Genetic Conditions.”
  53.  “Microbiome Rules, What Is Microbiome?”
  54. [Marriott et al 2016] Epigenetics: A new science for middle school – and why you should teach it. Science Scope.
  55. Nestle meeting, How Diet Can Change Your DNA, Recent studies suggest that the food you eat could modify your genes and potentially your children’s.

Genetic Predisposition Pearls — NIH excerpts from “Genetics Home Reference, Your Guide to Understanding Genetic Conditions”

If you are not into technicalities, move on to the post “Microbiome Rules, What Is Microbiome?”

“A genetic predisposition (sometimes also called genetic susceptibility) is an increased likelihood of developing a particular disease based on a person’s genetic makeup. A genetic predisposition results from specific genetic variations that are often inherited from a parent. These genetic changes contribute to the development of a disease but do not directly cause it. Some people with a predisposing genetic variation will never get the disease while others will, even within the same family.

Current research is focused on identifying genetic changes that have a small effect on disease risk but are common in the general population. Although each of these variations only slightly increases a person’s risk, having changes in several different genes may combine to increase disease risk significantly. Changes in many genes, each with a small effect, may underlie susceptibility to many common diseases, including cancer, obesity, diabetes, heart disease, and mental illness.

In people with a genetic predisposition, the risk of disease can depend on multiple factors in addition to an identified genetic change. These include other genetic factors (sometimes called modifiers) as well as lifestyle and environmental factors. Diseases that are caused by a combination of factors are described as multifactorial. Although a person’s genetic makeup cannot be altered, some lifestyle and environmental modifications… may be able to reduce disease risk in people with a genetic predisposition.”

“To function correctly, each cell depends on thousands of proteins to do their jobs in the right places at the right times. Sometimes, gene mutations prevent one or more of these proteins from working properly. By changing a gene’s instructions for making a protein, a mutation can cause the protein to malfunction or to be missing entirely. When a mutation alters a protein that plays a critical role in the body, it can disrupt normal development or cause a medical condition.

“Only a small percentage of mutations cause genetic disorders—most have no impact on health or development. For example, some mutations alter a gene’s DNA sequence but do not change the function of the protein made by the gene.

Often, gene mutations that could cause a genetic disorder are repaired by certain enzymes before the gene is expressed and an altered protein is produced. Each cell has a number of pathways through which enzymes recognize and repair mistakes in DNA. Because DNA can be damaged or mutated in many ways, DNA repair is an important process by which the body protects itself from disease.

A very small percentage of all mutations actually have a positive effect. These mutations lead to new versions of proteins that help an individual better adapt to changes in his or her environment.”

“People have two copies of most genes, one copy inherited from each parent. In some cases, however, the number of copies varies—meaning that a person can be born with one, three, or more copies of particular genes. Less commonly, one or more genes may be entirely missing. This type of genetic difference is known as copy number variation (CNV).”

“Researchers were surprised to learn that copy number variation accounts for a significant amount of genetic difference between people. More than 10 percent of human DNA appears to contain these differences in gene copy number. While much of this variation does not affect health or development, some differences likely influence a person’s risk of disease and response to certain drugs. Future research will focus on the consequences of copy number variation in different parts of the genome and study the contribution of these variations to many types of disease.”                                                   Gene Mutations and Health

“Mitochondria (illustration) are structures within cells that convert the energy from food into a form that cells can use. Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA (known as mitochondrial DNA or mtDNA). In some cases, inherited changes in mitochondrial DNA can cause problems with growth, development, and function of the body’s systems. These mutations disrupt the mitochondria’s ability to generate energy efficiently for the cell.

Conditions caused by mutations in mitochondrial DNA often involve multiple organ systems. The effects of these conditions are most pronounced in organs and tissues that require a lot of energy (such as the heart, brain, and muscles). Although the health consequences of inherited mitochondrial DNA mutations vary widely, frequently observed features include muscle weakness and wasting, problems with movement, diabetes, kidney failure, heart disease, loss of intellectual functions (dementia), hearing loss, and abnormalities involving the eyes and vision.

Mitochondrial DNA is also prone to somatic mutations, which are not inherited. Somatic mutations occur in the DNA of certain cells during a person’s lifetime and typically are not passed to future generations. Because mitochondrial DNA has a limited ability to repair itself when it is damaged, these mutations tend to build up over time. A buildup of somatic mutations in mitochondrial DNA has been associated with some forms of cancer and an increased risk of certain age-related disorders such as heart disease, Alzheimer disease, and Parkinson disease. Additionally, research suggests that the progressive accumulation of these mutations over a person’s lifetime may play a role in the normal process of aging.”

The Top Five Reasons for Teaching  Epigenetics  [Marriott et al 2016]
  1. It’s the science of why a person’s choices matter.
  2. Science is constantly advancing. Don’t be naive enough to ever think you know it all just because you have the sheepskin on the wall.  This is the evolving “nature of science”.
  3. Epigenetics Impacts Generational Society and can be taught so that the concept is understood by all.  Epigenetic science finds that famine, wartime stress, and toxins can all affect generation DNA functions. Knowing this, we have a vast amount of information to frame the implications of world events. What obligations do we have to ourselves and others?
  4. It helps to think how to be critical consumers of information – False claims with new products? Overreaching interpretations?
  5. It is our past, present, and future on disease risk —  ‘developmental origin of health and disease’ (DOHaD). 

Nestlé meeting This winter Nestlé convened esteemed experts in human and animal health to talk about the future of nutrition science.  One theme to emerge was the epigenetic impact of diet and lifestyle on individual health. Epigenetics is the study of how different biological and environmental signals affect gene expression.  Rather than change DNA itself, epigenetic signals can, for example, prompt changes in the number of methyl chemical groups attached to a gene, turning it on or off. A person’s diet is an important source of epigenetic signals…   investigating how eating habits modify gene expression in adults and their offspring… could help researchers identify nutritional elements that might help prevent or treat diseases such as obesity, diabetes, coronary artery disease, cancer and Alzheimer’s.

  • Nestlé and EpiGen are not the only groups investigating the epigenetic impact of diet. In a study conducted at the German Research Center for Environmental Health and published in Nature Genetics in 2016, genetically identical mice that consumed a high-fat diet were more likely to produce obese offspring with impaired glucose tolerance, an early sign of type 2 diabetes.
  • Nor are epigenetic impacts limited to obesity and diabetes. A 2014 study in Science conducted by the University of Cambridge revealed that undernourished pregnant mice bore offspring with glucose intolerance and pancreatic issues. Moshe Szyf, a geneticist at McGill University Medical School in Montreal, is investigating the epigenetic basis of multiple diseases, including depression and Alzheimer’s. He recently contributed to a paper in Biological Psychiatry in February 2017 on the connection between maternal infection in pregnant mice and the risk of neurodevelopmental disorders in their offspring.
  • Read more here, How Diet Can Change Your DNA, Recent studies suggest that the food you eat could modify your genes and potentially your children’s.

Last updated: January 17, 2018 at 7:19 am editorial.

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