Category Archives: Epigenetics

When I meditate, I literally can feel the neuropathways in my mind opening up. ~ Katy Perry, Elle.

One sees that science also rests on a faith. ~ Nietzsche

That whereof we cannot speak, thereof we must remain silent. ~ Wittgenstein

Over the past 30 years of seeking, I have heard meditation teachers, yoga teachers, self-help gurus and life coaches utter factoids in their classes such as

If your meditation teacher starts prattling on about his corpus callosum, prefrontal cortex, epigenetics, and/or neuroplasticity, you should run out of the room screaming. This person is either a liar, a charlatan, or a fucking idiot. Anyone who has not spent 1020 years in a laboratory analyzing human brains and conducting scientific research should not casually pepper lectures with factoids gleaned from the Internet or the copy of Psychology Today magazine sitting in his or her therapists waiting room.

In the summer of 1994 Peter Guber invited Deepak Chopra to speak at Sony Pictures and I was in the audience. If I remember correctly, Doctor Deep said something such as, Human beings have 50,00070,000 thoughts every day and most of them are redundant and negative. In case you dont already know, Deepak Chopra is a medical doctor who taught at Tufts and Boston University School of Medicine and was Chief of Staff at the New England Memorial Hospital in Stoneham, Massachusetts. For many years, when I was teaching at Esalen or Kripalu I would quote Doctor Deep to impress my students with this supposedly scientific ditty.

That is, until late 2016 when I sent the final draft of How To Survive Your Childhood Now That Youre An Adult to my editor at New World Library. She kindly asked me to send her the scientific studies demonstrating that human beings have 50,00070,000 thoughts every day and that most of them are redundant and negative.

Please take 30 seconds now to Google number of thoughts per day scientific study.

What did you find?

Ill tell you what you found. You found unscientific (unreplicable), tautological, self-serving psychobabble. Thats what you found. Nonetheless, I have been a student in over one hundred classes where teachers nonchalantly claim that every human being has 50,00070,000 thoughts every day and most of those thoughts are redundant and negative.

Just think about it: how would a neurologist even measure one thought? How could a scientist even define what constitutes a thought? And how would a scientist be able to discern if that thought was positive or negative? What were the criteria? Would A bear is chasing you. Run! be considered a positive or negative thought? Is The sky is blue a positive or negative thought? What if you are a farmer whose crops need rain or they will not grow and you will lose your farm? Is sky is blue universally positive?

OK, so if your meditation or yoga teacher mentions numbers of thoughts per day please ask him or her to cite the research studies I couldnt find any.

Because its a complete fiction, an urban legend.

Similarly, in my book I write, Human beings do not have direct introspection into brain states. At no time in your lifetime will you hear someone say, Synapses 85,932 and 700,774 just fired. I need to take an aspirin. So when Katy Perry states, When I meditate, I literally can feel the neuropathways in my mind opening up she is obviously delusional. Literally delusional (although I am uncertain to what literature she is referring). 1. There are no neural pathways in her mind for her to feel (the mind is non-local), and 2. not even His Holiness the Dalai Lama can feel inside his own brain not even with the perfect dose of LSD or ayahuasca.

To be clear, fMRI machines measure magnetic waves in the brain; EEG machines measure electricity. Then expert physicians and neurologists can witness patterns and discern abnormalities. But does a neuron firing an electrical stimulus correlate with a thought? Does a wave correspond with a thought?

Nobody knows. Not yet, at least.

So why is it that armchair neurologists (who have never seen a human brain except in a horror film) write or say things such as

Studies show that gratitude ACTIVATES the hypothalamus

The hypothalamus regulates all bodily mechanisms, one of which is sleep

Thus, gratitude improves sleep quality

What???

This is what I call a false syllogism. A plus B does not equal C. Can you discern the missing, direct causal link here? A scientific study would have to establish direct CAUSALITY between people expressing gratitude and the quality (quality? REM cycles how is sleep quality determined? Duration? Subjective retrospective recounting?) while eliminating or holding constant all other variables that could influence quality of sleep such as food, exercise, light, caffeine, relationships, alcohol, nicotine, previous amounts and types of sleep, levels of anxiety, brain chemistry, medications, talking, meditating etc.

I find it fascinating that so many hucksters can blatantly and egregiously misinterpret the pittance that neurologists know about the brain namely, studies show that gratitude activates the hypothalamus to arrive at grandiose conclusions such as, Gratitude improves sleep quality!

Speaking of which, this is another way to discern if your teacher is fucking idiot or not: neurologists say and write things such as, Studies SUGGEST SUGGEST SUGGEST while meditation teachers, yoga teachers, self-help gurus, and life coaches often say things such as, Studies PROVE Research DEMONSTRATES Studies SHOW or They have proven with this They being some mysterious yet authoritative, omniscient and definitive cabal of fellow human beings in lab coats with dubious facial hair arrangements hovering over Petri dishes in a windowless basement in Cambridge, Massachusetts.

For example, I have heard non-neurologists say, Epigenetics proves that thoughts change genes! which is patently false. Epigenetics studies the changes of gene expression the genes do not change, only their expressions change. Do you understand the difference and thus the myriad false claims (lies) hawkers make through ever-so slighltly altering their diction from suggest to show, prove or demonstrate?

Similarly, in scientific research journals, neurologists employ conditional terms such as may as in may or may not. For example, Practicing yoga MAY MAY MAY make people happier. But by the time this information reaches our ears while we hold Warrior II pose until our arms and legs go numb, our local yoga teacher is shouting, They proved it! Yoga makes people happy!

Really?

After class, you can ask who they are and what causality they unequivocally established between yoga and happiness. Thats not to say that I havent practiced yoga for 26 years and I wouldnt swear that it makes me happier within one or two standard deviations, notwithstanding the extremely limited statistical population and random variables such as what I ate for breakfast that morning. Trying to prove scientifically that yoga causes everyone to be happier would be analogous to trying to measure milk with a ruler.

It is obvious that many self-help gurus, meditation teachers, and life coaches consistently mistake research for conclusions, c.f. Amy Cuddy. What type of malarkey must one peddle to the masses to be asked to leave a tenure-track position at Harvard? Ask former Professor Cuddy.

So unless you have the spent the past 10-20 years like Jill Bolte Taylor in a laboratory with human brains sloshing around your gloved hands and the occupation box on the first page of your tax return reads Scientist, Neurologist, or Neuro-biologist, you may just want to take Ludwig Wittgensteins prescient advice to heart and shut the fuck up about neuroplasticity, epigenetics, your corpus callosum, or rewiring your mind.

For thereof non-neurologists must remain silent.

Namaste!

Oh yeah this quote by Michel Foucault may or may not pertain to the above: Ive met a lot of people who talk about the intellectual. And listening to them, Ive got some idea of what such an animal could be. Its not difficult hes quite personified. Hes guilty of pretty well everything: of speaking out and of keeping silent, of doing nothing and of getting involved in everything In short, the intellectual is raw material for a verdict, a sentence, a condemnation, an exclusion

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Why Neurologists and Research Psychologists Think that Meditation Teachers, Yoga Teachers, Self-Help Gurus, and Life Coaches Are Liars, Frauds, and...

In the past 25 years, the agricultural landscape has seen several significant changes, from the advent of herbicide-tolerant crops to precision agriculture systems and soil supplements. Many were dubbed game changers when they were introduced, and were glad to have them all, but they also met with unexpected issues like weed resistance, or they didnt evolve as fast as expected for other reasons.

The science of genetic alterations RNAi silencing or CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) technology has also come with great potential for improving plant breeding and enhanced traits. But it too has its challenges, including regulatory agencies in Canada.

The field of genomics is still in a state of growth as it searches for the best ways to enhance plant performance and productivity. At the same time, regulatory agencies are still haggling over definitions and applications. When is a genetic manipulation a plant novel trait (PNT)? When is the precautionary principle impairing scientific discovery to its detriment?

Epigenetics has been around for decades but its only been recently that researchers have started to manipulate it for field crop advantages, including the development of plants capable of withstanding stress such as drought, heat or cold.

Although there are questions surrounding the reaction of Health Canada or the Canadian Food Inspection Agency (CFIA), one U.S. researcher has uncovered a world of potential for this form of genetic manipulation.

Epigenetics is defined as the study of heritable changes in gene expression that do not involve changes to the underlying DNA sequence. In effect, it changes gene expression without altering the genetic makeup of the plant. These changes occur naturally and often in an organism. In humans, as we know, genes can be silent during childhood, then be activated as a person ages, and vice versa.

Another example is that some genes are active in an eye cell, for example, yet are completely silent in a kidney cell. Epigenetics is the vehicle for different tissues taking on specialized functions.

In plants, epigenetics can oversee alterations that shift reactions from normal growing conditions to ones that adapt to more stressful conditions, such as drought or cold tolerance. A control point for influencing these epigenetic traits was recently discovered in the plant gene MSH1, a discovery made by Dr. Sally Mackenzie and her colleagues in 2012. Mackenzie had been studying the role of the mitochondria that are responsible for respiration and energy generation in plant cells, trying to understand their influence on plant fertility and their ability to disrupt pollen development.

It was only later that we found out that MSH1 operates not just in mitochondria but in a different compartment: the chloroplasts, says Mackenzie, a professor of biology and plant science at Penn State University. That compartment has an ability to trigger epigenetic changes, and it was purely serendipitous that we discovered this, and we were off and running in a totally different direction.

Dr. Sally Mackenzie (right) with PhD candidate Hardik Kundariya (centre) and Dr. Xiaodong Yang (left) at work in the laboratory.photo: Courtesy Dr. Sally Mackenzie, Penn State University

In effect, her method silences the MSH1 gene in plants growing under normal conditions. Because of this, the plant behaves as though its growing under stressful conditions and it activates compensatory mechanisms that allow it to cope with temperature, drought and pathogen stress.

Manipulating these reprogrammed plants through crossing or grafting results in higher yields and greater resilience.

In a one-year trial with an elite tomato variety, Mackenzie saw a 29 per cent yield boost under ideal conditions. Researchers have also seen striking gains in tomato plant resilience under heat stress conditions in the field.

Mackenzie believes that genetic enhancements under less-than-ideal conditions will result not only in better yield stability, but also enhanced resilience in the plant.

Although the MSH1 gene was originally cloned in 2003 for mitochondrial research, it wasnt until 2011 that Mackenzie and her lab colleagues made the discovery about its influence on chloroplasts. Since then, shes successfully applied the MSH1 method to sorghum, tomato and soybeans for enhanced field performance, and has begun greenhouse work in canola and strawberries. Shed also like to test alfalfa for increasing above-ground biomass, as well as grapes, various tree crops, cotton and potatoes, although for that she requires more funding.

Theres an urgency to Mackenzies work, as she believes agriculture isnt adjusting rapidly enough to really address climate change.

In the next 30 years, its clear that crop production strategies will have to adapt, but there isnt a lot invested in what that process should look like, Mackenzie says. Im hoping that people will reflect on the idea that epigenetics is one tool that we havent had in our toolbox that might offer, not a full solution, but at least one potential remedy. I worry that were going to keep our strategies the same and were going to get caught with larger losses each year when that flood or that drought comes, and we havent come up with crops that have a level of resilience to tolerate those changes.

The method by which these genetic manipulations can occur allows for two different breeding approaches. The first and the fastest is to graft an MSH1-modified line as rootstock to an unmodified line and harvest the seed from that combination. The modification has been introduced already, so imparting a genetic enhancement occurs by the next generation. The second approach is through conventional crossbreeding.

In crops that can be grafted, which would apply to soybeans, tomatoes and any dicot species as well as grapes and tree crops, it works wonderfully, and thats the most rapid way to introduce the method, says Mackenzie. There are lots of crops that offer something valuable to our studies as we find out how much impact this system can have on any individual crop that has the cultivation properties. Potatoes would be great because theyre vegetatively propagated, so once you carry out the manipulation and find the perfect crop features, you can propagate that in perpetuity because they never go through seed.

If breeders dont get serious about climate change, the losses in crops like soybeans may be catastrophic, Mackenzie says.photo: Supplied

Although shed like to work with wheat and corn, the two crops present different challenges, over and above sufficient funding. The wheat genome is a polyploidy, so it is unclear how effectively the current gene silencing method would work. On the corn side, she concedes theres reluctance within the sectors research and breeding efforts to focus on much aside from yield and the current F1 hybrid model. She notes that recent yield improvements in corn have been largely due to increased plant densities.

To me, that is not a long-term strategy, but as long as the industry is fixated on that, I dont see them looking for innovations in other areas, says Mackenzie. And because theyre so recalcitrant to change, weve been slower to move into corn.

The one constraint to introducing methods designed to stabilize yield in the face of climate instability (instead of just increasing yield) is that the industry is not yet open to novel, out-of-the-ordinary breeding strategies for stability. Newer methods, like MSH1, must conform to the standard breeding protocols within each crop. If the tomato sector uses a hybrid, then the method has to be hybrid-ready; if its a plant that breeders dont want to graft, then Mackenzie has to shift to crossing.

Often, they will only consider a method that gives them a predetermined yield gain, which doesnt consider yield stability as equally valuable, she says. While this is certainly the decision of an industry partner, it does imply that there is not yet a true sense of urgency regarding climate change.

The good news on epigenetic discovery is in its acceptance from a regulatory standpoint. According to Mackenzie, the standard practice when dealing with an agency such as the Animal and Plant Health Inspection Service (USDA-APHIS) is to fill out a submission form, send it in and await a decision. With her epigenetics method, APHIS representatives asked her to address their officers in person.

The technology we were using was so distinctly different from anything theyd ever evaluated that they needed to make sure they understood what we were doing, explains Mackenzie. I was in front of that panel for more than two hours, with question after question.

The ultimate question was, What exactly would we regulate? Mackenzies response was, Precisely.

Epigenetic changes in plants are constant. The only difference is the way Mackenzie induces it. The modified plant would be indistinguishable from a plant thats under extreme stress.

This isnt something you could regulate even if you wanted to, insofar as there isnt a genetic change that occurs, and although gene expression is altered, many of the alterations naturally occur in a plant thats under stress, Mackenzie says. How do you say that a plant undergoing these gene expression changes under stress is compositionally different from a plant where were creating that stress using this manipulation?

Its why the panel concluded there wasnt anything to regulate, since there hasnt been a tangible change in the crop to follow. Mackenzie reasons that if that same conversation played itself out in Canada, regulators might come to the same conclusion.

But it will take leadership, says Mackenzie. Part of the regulatory terrain has been complicated by the fact that various aspects of CRISPR and other cisgenic technologies are just now coming out, and until the dust settles on all of that, were kind of in limbo also.

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Is this what farmers have been waiting for? - Country Guide

A small Canadian biotechnology company has convinced the FDA to reward its sole experimental drug breakthrough therapy status as a preventative therapy for major adverse cardiac events, despite a failed late-stage study.

Last September, Calgary, Alberta-based Resverlogix Corp said its investigational apabetalone did not meet the main pivotal study goal of reducing major adverse cardiovascular events (MACE) defined as cardiovascular death, non-fatal myocardial infarction, and stroke when added to standard care in patients with type II diabetes, recent acute coronary syndrome, and low HDL cholesterol.

Apabetalone is a selective inhibitor of the BET family of proteins that play a role in the regulation of cell growth, differentiation, and inflammation. BET inhibition is an epigenetic mechanism and the drug is designed to restore biological functions, altered by serious illnesses, back to a healthy state.

If DNA is the hardware, epigenetics is the software. DNA contains the code that dictates what cells do while epigenetic changes modulate the effect of those messages, like a dimmer switch telling cells which proteins to make more of and where to limit protein production.

Detailed data from the 2,425-patient, placebo-controlled Phase III trial dubbed BETonMACE were disclosed in November. The results showed the MACE findings on the apabetalone arm were 10.3%, while the placebo patients chalked up 12.4% (p = 0.11). All other secondary goals, apart from stroke, favored the drug but did not induce a statistically significant effect.

Kausik Ray, the BETonMACE study chair and professor of public health and consultant cardiologist at Imperial College London, suggested that while apabetalone was not found superior to placebo the drug only just missed statistical significance and it appeared that the trial was a bit underpowered to show a benefit due to lower than expected event rates.

Given the promising signswe think this (drug) holds considerable promise, and perhaps a slightly larger study with a few more events would allow us to assess more robustly whether this drug will provide a 20% treatment effect in this patient population, he said in an interview with the American Heart Association.

As for Resverlogix, it is convinced the experimental therapy works. On its website the company says:

From data collected in our clinical trials, we now know that apabetalone through its effects on epigenetics benefits multiple processes which contribute to the onset and worsening of disease. This is consistent with observed reductions in major adverse cardiac events (MACE) in study participants. Patients who take apabetalone have fewer heart attacks, strokes, and cardiac-related deaths.

On Monday, the FDA granted the drug breakthrough status in combination with standard care for the secondary prevention of major adverse cardiac events in patients with type II diabetes mellitus and recent acute coronary syndrome.

Heart disease the leading killer in developed nations (although cancer is catching up) is a lucrative battleground for drugmakers big and small, although the field is littered with failure.

Resverlogix is also testing apabetalone in patients with Fabry disease.

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Failed pivotal study? You can still have breakthrough therapy status FDA signals to Resverlogix - Endpoints News

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There is so much we can do beyond medicine for our health and well-being. Let medicines do their work but, there are plenty of other tools that can improve our quality of life. One such tool is prayer, provided it is done the right way. Neither do you have to be a religious person nor do you need to visit a religious place to do a prayer. This is about honest spirituality and true prayer is free from all of this.

How do prayers work: Everything is energy. The food you eat, the water you drink, the air you breathe. We ourselves are a bundle of energy. We can create bad or good energy. Prayer done with a clean heart and intentions helps generate good energy or change the bad energy into good energy. So, imagine the amount of good energy you can create by praying and how that can be channelised for healing.

Prayers can affect us at a genetic level: They have the ability to awaken certain emotions in our system that has the ability to turn on and turn off certain genes. Our lifestyles have a huge role to play here. While clean lifestyle habits can turn on genes that have the ability to repair and heal you, unhealthy lifestyle habits can turn on genes that can bring about sickness and diseases. This is called epigenetics, where epi stands for the environment and how it can control the functionality of a certain gene. For example: watching a clip of a funny video, movie or a good laugh with friends can turn on over 700 genes that are related to our immune system. But a drag, anxious and angry lifestyle can also turn off those same 700 genes thereby dampening your immunity. Prayers work in a similar way, by evoking positive emotions in us that has the capacity to activate the good genes.

Why do most patients who have gone through their journey of cancer turn to spirituality? There are some who never ever prayed in their life but have now come down to praying heavily. What changes? Well, as the mysteries of life unfold and the journey gets challenging, most individuals tend to go through intense emotions of love, lost love, relationship issues, unforgiveness, anger and shifting their focus towards spirituality and prayer asking for safety and recovery. And it doesnt take a disease to lead to this. As kids and teens, visiting holy places disinterest us, then as we grow older, we gradually move to read holy books and spend time chanting. Some people experience this transition early in life and some later.

We go wrong when spirituality is practiced as a fad and we add more complexity to it. Prayers are not any other to-do list activity in your day. If you pray, let those prayers and their teachings slip into your daily life. The three most essentials when it comes to prayers is Faith, Belief, and Surrendering. So many of us pray fervently almost daily, visit different religious places, but are still anxious and worried about the very problems they prayed for. Instead, pray with utmost faith and belief and just surrender the outcome. Above all, keep practicing your prayers till you build so much faith that there is no room for fear.

The simplest prayer: The simplest one could be to offer gratitude and count your blessings. It doesnt have to be a prayer for God. Prayer in any form, if done with faith and belief, counts. For example: Thank you for blessing the air that we breathe, the food that we eat and the water that we drink. Just because the results of prayers arent immediate doesnt mean its not powerful. The power of this simple act is immense, free and we mustnt take for granted what is free. Sometimes when life hits us through any challenge, financial, emotional, physicalall we need to do is step back, pray and ask for help. Teach this to your kids too.

The author is a Mumbai-based holistic lifestyle coach

Luke Coutinho

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The power of prayers - The New Indian Express

In an effort to identify genetic variants responsible for asthma, thousands of genetic studies have been performed. Of the potential answers to this dilemma, epigenetics represents a solution, according to a review published in Tuberculosis and Respiratory Diseases.

Familial clustering of asthmatics is indicative of a genetic component of asthma, a condition with up to 60% heritability. Over the last 3 decades, more than 100 loci have been identified as being linked with asthma, and recent genome-wide single nucleotide polymorphism (SNP) association studies have confirmed that SNPs on genes associated with antigen presentation, inflammation, and Th1/Th2 processes are strongly associated with asthma and its subphenotypes.

Worldwide asthma prevalence has increased over the past 30 years, but investigators note that changes in genetic variants of the disease have rarely occurred. They posit that exposure to changing exposomes large sets of environmental exposures including diet, toxins, and hormones have introduced several different phenotypes of asthma.

In 2007, epigenetics was defined via the following criteria: a change in the activity of a gene that does not involve a mutation; initiated by environment signals; and mitotically or meiotically inherited in the absence of the change in nucleotide sequence of genomic DNA. Epigenetic mechanisms include DNA CpG methylation, histone deformation, and non-coding RNA.

DNA methylation takes place in CpG occupying 1% of DNA bases in human somatic cells, resulting in a total number of CpG sites of approximately 28 million; 70% to 80% of the human DNA CpG bases are methylated. Considerable research has identified specific time periods during which individuals are more susceptible to the effects of environmental exposures and other asthma triggers, including during prenatal development, early childhood, and adolescence. Epigenetic modifications are more likely to develop during these times.

Both human skin and lungs have large surface areas exposed to external environments; surface area estimates depend on height, weight, and other factors. Both indoor and outdoor stimuli affect airway epithelium, with 2 methods that have been used to study DNA CpG methylation: candidate gene approaches and epigenome-wide association studies. One candidate CpG methylation approach utilized buccal mucosa of children with asthma on 1505 CpG loci across 807 genes, identifying a small number of DNA methylation signatures. Recent epigenome-wide association studies have been launched with the intention of searching for changes in global CpG methylations.

Many CpG methylation studies have relied on the use of DNA isolated from unfractionated peripheral blood leukocytes because they are widely available and easily accessed. New methods have been recently developed to infer the proportion of immune cell populations in these leukocytes using DNA methylation data. The major immunologic components of asthma pathogenesis and their epigenetic mechanisms specifically affect the expression of the transcription factors involved in the development of Th1, Th2, Th17, and regulatory T cells. Therefore, these DNA methylation profiles have been very useful in identifying the epigenetic change of immune status.

In terms of atmospheric environmental factors, smoking is the most important asthma risk factor. Through DNA damage and other mechanisms, cigarette smoke modulates gene expression; several epigenome-wide association studies have demonstrated that cigarette smoke results in global hypomethylation. In one study, smoke exposure was associated with a 2% increase in mean CpG methylation in the FERM domain containing 4A gene compared with no smoke exposure. Despite the potential for clinical relevance, the authors noted that the current interpretation of cross-sectional epigenetic studies is problematic because it is impossible to determine whether methylation alteration is a cause or consequence.

Because DNA CpG methylation changes are more reversible than DNA mutations, many treatment strategies are currently under investigation, the authors wrote, including dietary manipulation, which has demonstrated that methyl-rich diets have been associated with epigenome hypermethylation. These findings have generated interest, but clinical efficacy is still unclear.

Epigenetic influences and mechanisms have been clarified in allergic diseases and asthma, but there are still many questions to be solved yet, the researchers posit. The most complex situation is when both the gene and the environment are unknown. Additional information on exposomes, they added, is necessary, and data should be analyzed via multi-Omnic approaches.

The researchers concluded that If accurate influence and mechanisms of epigenetics are revealed, prevention and control strategies for asthma and its subtypes will be developed.

Reference

Bae D-J, Jun AE, Chang HS, Park JS, Park C-S. Epigenetic changes in asthma: role of DNA CpG methylation.Tuberc Respir Dis. 2020;83(1):1-13.

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Epigenetic Influences and Mechanisms in Asthma - Pulmonology Advisor

With the NFL Championship game this Sunday, all eyes turn to Whitehouse native and Kansas City Chiefs quarterback Patrick Mahomes.

Over the course of the last couple weeks, CBS19 has spoken to everyone from Mahomes father, Pat Mahomes Senior, his trainer at APEC, Bobby Stroupe, and fans across the region. Mahomes environment clearly helped forge him into a future NFL MVP.

Dr. Ushimbra Buford, a psychiatrist at UT Health Science Center at Tyler says there are crucial mental aspects of becoming an elite athlete.

Buford says the phrase nature vs nurture which references conflicting theories on whether the natural instincts with which people are born or the environment in which they are brought up has more of an impact on their development, is now somewhat outdated.

When I first started in medicine, we used to say things like nature and nurture and saw them as two different things. In the past several years with the advent and understanding of epigenetics, we understand now that the nurture aspect influences the nature, the environment influences your genetics, Buford said.

Buford says a persons development in all aspects, including athleticism, is heavily influenced by their environment, down to changes their body makes at a biological level.

From a genetic standpoint, that person may have a certain kind of capacity for the muscle fibers that they will produce that they were born with. But then they get into an environment where the expectation and the understanding and like the daily living is different from what their body is genetically set. Over time, their composition would change to reflect the activities they were involved in, and the potential reality exists that over time their genetics would change to reflect the new physical reality, Buford said.

This means growing up in an environment, such as in Mahomes case, where his father is a professional baseball player and he was immediately around athletics, can be incredibly beneficial. However, Buford says in athletics and in life, it always comes down to a choice to strive for greatness.

Every quarterback is saying we're going to the Super Bowl this year, but how many of them believe that?" Buford said. "How many of them really, truly feel that this is my going to be my reality? You almost have to be delusional like that to achieve greatness in a sense. You have to see and believe something before other people can or will."

This mentality is something everyone can implement in their daily lives. Buford says the sky is the limit when a persons head is in the right place.

We all have the ability to be incredible," Buford said. "You know, we really limit ourselves and I don't know if this is a societal thing, or it's just not receiving the right messages early enough in life. But don't ever think for a minute that anyone cannot become what they want to be. Only person stopping you is you.

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The Mental Game: Inside the mind of an elite athlete - CBS19.tv KYTX

6.8.1 DNA Hypermethylation in Cancer

CpG hypermethylation in gene promoters is the best characterized epigenetic abnormality in human malignancies. A common paradigm in cancer epigenetics is hypermethylation of the CpG-rich promoter regions of tumor-suppressor genes, resulting in epigenetic silencing of these genes (14). Indeed, for some of the most important tumor suppressorssuch as the CDKN2A gene encoding the p16 cell cycle inhibitorpromoter hypermethylation can be the most common mechanism underlying their functional loss during tumor formation, with the corresponding genetic pathways for loss of function (deletion/mutation) being utilized less commonly (230). Hypermethylated promoter DNA is associated with virtually every type of human tumor, with each type of tumor having its own signature of methylated genes, such as the methylation of GSTP1 in prostate cancer, the von HippelLandau syndrome gene VHL in renal cancer, the mismatch repair gene MLH1 in colon and endometrial cancers, and sometimes BRCA1 in breast cancer (231236). In some of these examples, the same tumor-suppressor gene is mutated or methylated as alternative pathways in the same tumor type: loss-of-function mutations in MLH1 and VHL are found in the germlines of patients with hereditary colon and renal cancer, respectively, and these same genes are hypermethylated and silenced in sporadic tumors of the same histologic type (231,237).

While gain of DNA methylation is often discussed as a late event in tumor progression, CpG hypermethylation in specific sequences often occurs early in cancer formation, sometimes preceding tumorigenesis. Examples of early epigenetic aberrations can also be cited in other adult malignancies: in cigarette smokers, CDKN2A promoter methylation occurs in dysplastic bronchial epithelial cells prior to the formation of overt lung cancers (238), promoter hypermethylation of tumor suppressor genes is already detectable in the pre-malignant lesion Barrett esophagus (239,240). One of the best substantiated examples of a very early epigenetic lesion predisposing to subsequent tumor formation is the gain of methylation of the H19 DMR on the maternal allele, which leads to the loss of imprinting of IGF2 expression and can often be detected in non-neoplastic kidney cells both in BWS-associated and sporadic cases of the pediatric kidney cancer Wilms tumor (227).

DNA hypermethylation has attracted much attention as a biomarker for cancer detection and classification. To be clinically applicable, an ideal tumor biomarker must be specific for cancer, and readily detectable in clinical specimens obtained through minimally invasive procedures. DNA hypermethylation seems to fulfill these requirements and has been considered to be a promising biomarker. Examining the methylation of a subset of genes (GSTP1, APC, RASSF1, and MDR1) distinguished primary prostate cancer from benign prostate tissues with sensitivities and specificities of greater than 90% (241,242). DNA methylation alterations can be detected and used as biomarkers in feces for colorectal cancer, urine for bladder cancer screening, and sputum to predict the occurrence of lung cancer (243245). However, for reasons that are complex but partly financial, these types of tests largely remain at the research stage and have not yet been widely adopted in clinical practice.

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Epigenetics - an overview | ScienceDirect Topics

By Alma Laney and Alison Bernstein

This post is the first in a series about transgenerational inheritance, epigenetics, and glyphosate that address questions raised by the publication of the paper, Assessment of Glyphosate Induced Epigenetic Transgenerational Inheritance of Pathologies and Sperm Epimutations: Generational Toxicology.

Transgenerational inheritance is the concept that traits can be passed on from parent to great-grandchildren. In the context of toxicology, this hypothesis can be described as ancestral environmental exposures to non-mutagenic agents can exert effects in unexposed descendants. If you imagine a person being exposed to some substance, their reproductive cells are exposed so their children are also exposed (intergenerational inheritance). If that person is a pregnant female, the reproductive cells of their offspring are exposed so the grandchildren are also exposed (multigenerational inheritance). Thus, true transgenerational inheritance can only be observed in the great-grandchildrens generation (transgenerational inheritance).

Transgenerational inheritance can occur through epigenetic, ecological, or cultural mechanisms (See Figure 1 of the linked paper below).

The focus of the paper under discussion is the epigenetic mechanisms through the germline, or transgenerational epigenetic inheritance. In any experiment of transgenerational inheritance, it is critical to use a careful study design to separate the epigenetic piece from the other mechanisms.

Epigenetics can be defined as: the processes and marks on or around the DNA processes that control the activity of the genome and can be mitotically and/or meiotically inherited. It encompasses a set of mechanisms that regulate gene expression and that can be inherited from cell to cell within an organism. Sometimes, if they occur in germline cells, these mechanisms may also be inherited from parent to offspring. Epigenetic mechanisms can also be sensitive to environmental inputs. Because they can be modified by the environment and may be inherited from parent to offspring, epigenetic mechanisms are a prime candidate for the mediating transgenerational inheritance.

Epigenetics generally refers to four mechanisms.

These four mechanisms do not exist in isolation. They form a network of interacting mechanisms that all work together to affect gene expression. For an overview on these mechanisms of epigenetics, please visit the Intro to Epigenetics series at Mommy, PhD.

Transgenerational epigenetic inheritance is well documented in plants and the commonly used model organisms, such as C. elegans (roundworms) and D. melanogaster (fruit flies). However, whether transgenerational inheritance occurs in mammals is still unclear.

The existence of transgenerational epigenetic inheritance remains unclear in mammals. There are a few reasons why this is hard to answer.

First, humans are complicated. When we have evidence of transgenerational inheritance of a trait in people, it is nearly impossible to separate the cultural and ecological effects from the epigenetic effects to definitively say if that inheritance occurs partly or exclusively through a biological mechanism. In humans, exposures are rarely isolated to the original generation only, making it extremely difficult to separate out true transgenerational effections. In addition, even when exposures are isolated, those exposures often produce differences that have their own effects. In the example of the Holocaust, it is difficult to separate the effects of trauma from living through the Holocaust on offspring from the effect of having a parent who lived through the Holocaust on offspring.

In order to determine if transgenerational inheritance occurs, scientists must stop the exposure in the original generation to isolate the exposure. While this can be done in model organisms in the lab, exposures are rarely isolated to a single generation in humans. Even when they are, the genetic, ecological and cultural confounders are so complex that it is extraordinarily difficult to conclusively identify transgenerational epigenetic inheritance in humans.

Second, experimental design is extremely complicated. We can use model organisms (such as mice or rats) to control for some of these factors to determine if transgenerational epigenetic inheritance occurs in mammals. However, when properly designed, these experiments are extremely complicated, expensive, and time-consuming, as described in A guide to designing germline-dependent epigenetic inheritance experiments in mammals. These experiments can be done, but at this point in time, very few studies are properly designed to actually be able to answer this question. We will discuss this in more detail below when we get to the methods of the paper under discussion.

Third, germline reprogramming clears (erases) many epigenetic marks twice during mammalian development. First, DNA methylation marks are cleared during germ-cell development. There is a second wave of demethylation following fertilization; the timing of this demethylation and the reestablishment of methylation patterns is different for maternal and paternal chromosomes. A subset of genes (mostly imprinted genes) do not undergo this second wave of demethylation and are more sensitive to environmental regulation. Thus, only a subset of the genome could be undergoing translational epigenetic inheritance. While research in the area is still evolving, it is clear that more of the genome than previously thought is protected from this second wave of demethylation. But transgenerational epigenetic inheritance seems unlikely to be a genome-wide phenomenon.

This 2018 state of the science report on transgenerational inheritance from the National Toxicology Program cites 21 papers from the lab that published the current glyphosate study. It summarizes the weaknesses of the existing evidence and underscores the need for well-designed studies.

In conclusion, a broad range of exposures and outcomes have been reported to support transgenerational inheritance of health effects. Over 80 different agents have been tested in a transgenerational experimental design; and this state of the science review collected and categorized the literature into a systematic evidence map for transgenerational inheritance by broad health effect categories, exposures, and evidence streams. This scoping review and evidence map identifies serious limitations in the available bodies of evidence to support a systematic review for reaching hazard conclusions or even rating certainty in the bodies of evidence under evidence to decision frameworks such as the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach.

This report includes assessments of potential bias in the studies that do exist. The images below show a summary of their assessment of bias in animals studies (top) and specifically in animal studies of vinclozolin (bottom). The top panel shows that the probability of bias is probably high for many papers on many measures, with more than half of papers showing a definitely high risk of bias for confidence in the exposure characterization. The bottom panel shows the risk of bias from individual studies.

You can see from these images that much of the risk of bias seems to arise from the failure to report specific aspects of the methods and results. Nine of the fifteen papers listed in this panel are from the lab that performed the study in question. The areas identified as being of high risk for bias are also problematic in the current study as we will go through in detail below. This doesnt necessarily mean that the studies are flawed or the results are biased, but it does mean that the results cannot be accurately interpreted and it is not possible to determine if they are flawed or valid.

View the other parts of our series on transgenerational epigenetic inheritance:

Read this article:
Part 1: What is Transgenerational Epigenetic Inheritance? - Biofortified Blog

By Alison Bernstein and Alma Laney

The paper Assessment of Glyphosate Induced Epigenetic Transgenerational Inheritance of Pathologies and Sperm Epimutations: Generational Toxicology reported transgenerational epigenetic inheritance and increased disease rates after glyphosate exposure. Not surprisingly, the paper generated a lot of attention and discussion. Due to the focus on glyphosate by activist groups and recent lawsuits, weve taken an in-depth look at the state of the science on transgenerational epigenetic inheritance, the data in this paper, and the larger body of work from this lab.

Whether glyphosate exposure causes health problems through transgenerational epigenetic inheritance is an important research question. The original EPA reference dose is based on a transgenerational phenotype, even though this result has been determined to be spurious and unrelated to treatment since more extensive evaluations in subsequent reproduction studies conducted at much higher doses did not replicate the offspring effects (as explained in the draft human health assessment for glyphosate).

In this series, we address questions about transgenerational inheritance and epigenetics in general, and this glyphosate study in particular.

See original here:
Transgenerational Epigenetic Inheritance and Glyphosate - Biofortified Blog

Sameer Joshi Call: +912067274191Email: [emailprotected]Pune, January 9,2020

Premium Market Insights has announced the addition of the Epigenetics Market . The report focuses on global major leading industry players with information such as company profiles, product picture and specification.

The Epigenetics market is driven by the driving factor such as declining prices of sequencing, and is likely to drive the market in the coming years. The declining costs associated with different strategies and methods for sequencing supports to influence the scale and scope of almost all genomic research projects. In 2000, cost for sequencing was US$ 3.7 billion, which dropped down to US$ 10 million in 2006 and declined to US$ 5,000 in 2012. Owing to factors such as advances in the field of genomics, development in different methods and strategies for sequencing, there is a notable decline in the cost of sequencing, that upsurge the growth of the market.The market is likely to restrain its growth due to the factors such as high cost of advanced technologies. Companies such as Illumina and PacBio offer instruments with high cost. For instance, Illumina MiSeq cost for US$ 128,000 and PacBio RS cost for US$ 695,000. Thus, the high cost of next generation sequencers is hindering the growth of the market for in the future. Whereas the use of the neuroepigenetics to diagnose the neurodevelopmental disorders is likely to contribute a potential market growth in the forecast period.

The Epigenetics market as per the product the segment is segmented as reagents, kits, enzymes, instruments and consumables and bioinformatics tools. The market of kits has the highest market share in 2017, contributing a market share of 29.8% and is expected to retain its dominance during the forecast period from 2018 to 2025. The epigenetic kits allows researchers to perform experiments, researchers to analyze epigenetic modifications efficiently and reliably by using antibodies directed against epitope tags or RNA-binding proteins. Thus holding the major market share. Likewise the reagents contributed 26.2% of the market share in the year 2017 and is expected to be the fastest growing market in the coming near future.

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The Technology segment of the epigenetics market includes histone modification, DNA methylation and other technologies. The DNA methylation segment for the epigenetics market was valued at US$ 506.29 Mn in 2017 and is estimated to grow at a CAGR of 13.9% during the forecast period from 2017 to 2025, to reach US$ 1,361.67.0 Mn by 2025. The DNA methylation segments is likely to dominate the market in the coming future as it supports the development of therapies for diseases including cancer, lupus, muscular dystrophy and various congenital defects. Thus the DNA methylation segment is expected to hold major share and is also the fastest growing segment during the forecast period.

Some of the major primary and secondary sources included in the report epigenetics market are National Institute of Environmental Health Sciences (NIEHS), Epidemiology and Genomics Research Program (EGRP), Canadian Institutes of Health Research (CIHR), Synthetic Biology Leadership Council, Chinese Academy of Sciences, World Health Organization, European Union, Food and Drug Administration and more.

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Contact Info:Name: Sameer JoshiEmail:[emailprotected]Organization: Premium Market InsightsPhone: +1-646-491-9876

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Epigenetics Market Expected to Reach US$ 2,611.57 Mn By 2025 - Merck, Thermo Fisher, Abcam, Agilent, Active Motif, QIAGEN, Bio-Rad, PerkinElmer, New...