Posts Tagged ‘aging’


The above images are eigenfaces … which are statistically distilled basic components of human faces … from which ANY human face can be reconstructed as a combination of the above basic components.  It’s a great mathematical trick – particularly if you’re into the whole mass surveillance and electronic police state thing.

If you are more into the whole, helping people and medical care thing, check out the global consortia at ENIGMA who have been carrying out massive genetic and brain scanning studies – like this one involving 437,607 SNPs in 31,622 voxels in 731 subjects using their new method, vGeneWAS, to study Alzheimer’s Disease:

“We hypothesized that vGeneWAS would, in some situations, have greater power to detect associations than existing SNP-based methods. One such situation might be when a gene contains many loci with weak individual effects. In addition, we expected that vGeneWAS would have greater overall power than mass SNP-based methods, like vGWAS, because of the drastic reduction in the effective number of statistical tests performed.”

The vGeneWAS method relies on the calculation of “eigenSNPs” which are eigenvectors that describe a matrix of n subjects by m SNPs in an individual gene (an n-x-m matrix of 1’s,0’s,-1’s for aa, aA, AA genotypes).  EigenSNPs are sort of like eigenfaces insofar as eigenSNPs (which are not actual SNPs) capture the majority of variance, or the basic essence of an individual gene … but seriously, you should read the original article ’cause every stats test I ever took totally punched me in the face.

In any case, the eigenSNP-by-voxel method pulled out some legit results such as rs2373115 (where the G-allele confers risk) in the GAB2 gene  which has repeatedly been implicated in the risk of age-related late-onset Alzheimer’s Disease (in folks who carry ApoE4  rs429358(C) alleles).  The authors found that the genetic risk of AD conferred by GAB2 may arise by way of GAB2’s effect on brain structure in the periventricular areas, which have been known to be among the first brain regions to show AD-related changes (time-lapse movie of AD tissue loss in the brain).

Picture 2

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Mitochondrial damage is associated with premature aging in the body and related disorders such as Parkinson’s Disease in the brain.  If you want to grow old and healthy … be nice to your mitochondria … eat healthy foods and exercise.

When mitochondria are damaged, cells can use proteolysis to clean them out, but when this cleaning out process fails … trouble ensues.   PINK1 plays a role on the clearance of damaged mitochondria as revealed by Dr. Derek P. Narendra and colleagues: PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin

Since neurons in the Substantia Nigra are postmitotic, any mitochondrial damage they acquire could accumulate over an organism’s lifetime, leading to progressive mitochondrial dysfunction—including increased oxidative stress, decreased calcium buffering capacity, loss of ATP, and, eventually, cell death—unless quality control processes eliminate the damaged mitochondria.

The findings we report in this paper suggest a new model in which PINK1 and Parkin together sense mitochondria in distress and selectively target them for degradation. In this pathway, PINK1 acts as a flag that accumulates on dysfunctional mitochondria and then signals to Parkin, which tags these mitochondria for destruction. Since disease-causing mutations in PINK1 or Parkin disrupt this pathway, patients with these mutations may not be able to clean up their damaged mitochondria, leading to the neuronal damage typical of parkinsonism.

Dr. Terry Wahls has some very inspiring experiences to share on the topic of mitochondrial care.

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Wobble base pair guanine uracil (GU)

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Hands shake and wobble as the decades pass … moreso in some.

A recently evolved “T” allele (rs12720208) in the  3′ untranslated region (3′ UTR) of the FGF20 gene has been implicated in the risk of Parkinson’s Disease … namely by creating a wobbly G:U base-pair between microRNA-433 (miR-433) and the FGF20 transcript.  Since the normal function of microRNA-433 is to repress translation of proteins (such as FGF20), it is suspected that the PD risk “T” allele carriers make relatively more FGF20 … which, in turn … leads to the production of higher levels of alpha-synuclein (the main component of Lewy body fibrils, a pathological marker of diseases such as PD).  This newly evolved T-allele has also been associated with brain structural differences in healthy individuals.

My hands will shake and wobble as the decades pass … but not because I carry the G:U wobble pairing between miR-433:FGF20.  My 23andMe profile shows that I carry 2 C alleles and will produce the thermodynamically favorable G:C pairing.  Something to keep in mind as I lose my mind in the decades to come.

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… from The Big Picture

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Have you ever suddenly realized, “OMG, I’m just like my dad (or mom)!”  Oh, the horror .. the horror.  Here’s John Updike from A Month of Sundays:

Also my father, who in space-time occupied a stark room of a rest home an hour distant, which he furnished with a vigorous and Protean suite of senility’s phantoms, was in a genetic dimension unfolding within me, as time advanced, and occupying my body like, as Colette had written to illustrate another phenomenon, a hand being forced into a tight glove.

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Telomere caps he:תמונה:Telomere caps.gif
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A startling article that appears today in the science journal Nature, shows that reactivation and restoration of DNA telomeres was sufficient to reverse the aging process! From the article:

Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.

Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease risk1, 3 and the marked reversal of systemic degenerative phenotypes in adult mice observed here support the development of regenerative strategies designed to restore telomere integrity.

Love yourself, love your DNA – especially the telomeres ! For more on this topic, see a few weeks back, when I covered a research article by Nobel Prize winning scientist Elizabeth Blackburn on meditation, telomeres and longevity.

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Stick model of NAD + , based on x-ray diffract...
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Yogis are by far the healthiest eaters I have ever met.  If you’re reading this blog, you’re probably one of them – faithful in the observance of your Yamas and Niyamas – leaving me  reluctant to confess my own (pre-yoga) pizza-scarfing, soda-swilling ways.  Please don’t hold it against me.  I’ve changed, really.

Here – as plain as I can make it – is the scientific reason why eating a low-calorie vegetarian diet is a good thing.  Good, as in living longer and cancer-free.

All you need to know is that when you eat less, your levels of Nicotinamide adenine dinucleotide (NAD – the contorted, yogic-looking molecule shown at left) are HIGH – and this increases the activity of the “longevity gene” SIR2. The amazing life-extending effects of the NAD-dependent SIR2 genes are described in detail on Leonard Guarente’s website at M.I.T.:

The discovery that Sir2p requires NAD for its activity immediately suggested a link between SIR2 activity and caloric restriction. This link was strengthened by the observation that life span extension by caloric restriction requires Sir2 protein. Caloric restriction is likely to reduce the carbon flow through glycolysis and result in more free cytoplasmic NAD. SIR2 could act as a sensor of NAD levels within the nucleus. Under conditions of caloric restriction, NAD levels are high, SIR2 is activated, and the rate of aging is decreased.

The hard science link between cancer and NAD is more recent – this week in fact – with the release of a study entitled, “Transcriptional regulation of BRCA1 expression by a metabolic switch” [doi:10.1038/nsmb.1941].  Here the researchers found that NAD/NADH levels via binding to CTBP1 can regulate the anti-tumor properties of BRCA1.  In a nutshell, a high-calorie diet leads to LOW levels of NAD which has the net effect (via CTBP1) of turning OFF the anti-tumor gene BRCA1 (a bad thing).  From the article:

The elevated expression of estrogen in the context of higher levels of NADH or lower NAD+/NADH ratios due to high caloric intake and/or obesity could establish a state in which the pro-proliferative effects of estrogen are not completely balanced by the protective functions of BRCA1 that would normally restrain estrogen-induced proliferation and heighten genome surveillance.

I realize that most yoga folks need no such hard science to convince them of the merits of a low-calorie, healthy diet.  In the science-world however, empirical evidence can take decades to gather, so its an important milestone to now have established causal links between caloric intake, longevity and cancer risk.

For (former) junk food junkies like myself, there is no room to debate or side-step the issue.  Eat less, eat healthy – live longer and cancer-free.  More on yoga and aging (here, here, here).  Now, off to the shala for NADasana pose!

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This is a cross post from my other “science & self-exploration” blog about mindfulness and the mind-body connection (yoga).

In 2009, Elizabeth Blackburn received the Nobel Prize in Physiology or Medicine for her work on the biology of so-called telomeres – the DNA sequences found at the end of our chromosomes (actually just a repeating sequence of TTAGGG). The very cool thing about telomeres is that the overall length of these sequences (number of repeating units of TTAGGG) correlates with life-span. This is because as cells in your body are born, they go through a number of cell divisions (each time the cell divides, the telomeres shorten) until they go kaput (replicative senescence). Amazingly, regular cells like these (that normally die after several cell divisions) can be induced to live far longer by simply – lengthening their telomeres (increasing the amount of a telomere lengthening enzyme known as telomerase) – which is why some think of telomeres as the key to cellular immortality.

Imagine your own longevity if all your cells lived twice as long.

With this in mind, it was awesome to read a paper by Dr. Blackburn and colleagues entitled, “Can Meditation Slow Rate of Cellular Aging? Cognitive Stress, Mindfulness, and Telomeres” [doi: 10.1111/j.1749-6632.2009.04414.x]. The authors carefully ponder – but do not definitively assert – a connection between meditative practices and telomere length (and therefore, lifespan). The main thrust of the article is that there are causal links between cellular stress and telomere length AND causal links between physiological stress and meditative practices. Might there, then, be a connection between meditative practices and telomere length?

Above we have reviewed data linking stress arousal and oxidative stress to telomere shortness. Meditative practices appear to improve the endocrine balance toward positive arousal (high DHEA, lower cortisol) and decrease oxidative stress. Thus, meditation practices may promote mitotic cell longevity both through decreasing stress hormones and oxidative stress and increasing hormones that may protect the telomere.

Given that eastern meditative practices are thousands of years old, its strange to say, but these are early days in beginning to understand HOW – in terms of molecular processes – these practices might influence health.

Still, I think I’ll send some thoughts to my telomeres next meditation session!

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The human brain has some 100 billion neurons.  That sounds like a lot, but I’m still keen on keeping ALL of mine healthy and in good working order.  One way that cells protect themselves from damage and untimely death is by protecting their DNA – by wrapping it up and coiling it tightly – using chromatin proteins – which keeps it away from chemical and viral damage.  This is especially important in the brain, since – unlike the skin or gut – we can’t really re-grow brain tissue once its damaged.  We have to protect the neurons we have!

Here’s the problem. In order to USE the BRAIN (to learn and remember stuff) we have to also USE the GENOME (to encode the proteins that synapses use in the process of memory formation).  When we’re thinking, we have to take our precious DNA out of its protective supercoiled, proteinaceous shell and allow the double helix to melt into single strands and expose their naked A’s, G’s, T’s and C’s to the chemical milieu (to the start the transcription process).  This is risky business damage to DNA can lead to cell death!

One might imaging that its best to carry out this precarious act quickly and in proximity to DNA repair enzymes (I’d think).  A very important job that includes: uncoiling chromatin superstructures, transcribing DNA (that encodes proteinaceous building blocks that synapses use to strengthen and weaken themselves) – and then – making sure there was no damage incurred along the way.  A BIG job that MUST get done each and every time my cells engage in learning.  Wow!  I didn’t realize that learning new stuff means I’m exposing my DNA to damage?  Hmm … I wonder if that PhD was worth it?

To perform this important job, it seems there is an amazing handyman of a molecule named poly(ADP-ribose) polymerase-1 (PARP-1).  Amazing, because it – itself – can function in many of the steps involved in uncoiling chromatin structures, transcription initiation and DNA repair.  The protein that can “do it all” … get the job done quickly and even fix any errors made along the way! It is known to function in the so-called base excision repair (BER) pathway and is also known have a role in transcription through remodeling of chromatin by ADP-ribosylating histones and relaxing chromatin structure, thus allowing transcription to occur (click here for a great open review of PARP-1).  Nice!

According to OMIM, earlier studies by Cohen-Armon et al. (2004) found that poly(ADP-ribose) polymerase-1 is activated in neurons that mediate several forms of long-term memory in Aplysia. Because poly(ADP-ribosyl)ation of nuclear proteins is a response to DNA damage in virtually all eukaryotic cells (indeed, PARP-1 knock-out mice are more sensitive to DNA damage), it was surprising that activation of the polymerase occurred during learning and was required for long-term memory. Cohen-Armon et al. (2004) suggested that the fast and transient decondensation of chromatin structure by poly(ADP-ribosyl)ation enables the transcription needed to form long-term memory without strand breaks in DNA.

A recent article in Journal of Neuroscience seems to confirm this function –  now in the mouse brain.  Histone H1 Poly[ADP]-Ribosylation Regulates the Chromatin Alterations Required for Learning Consolidation [doi:10.1523/JNEUROSCI.3010-10.2010] by Fontán-Lozano et al., examined cells in the hippocampus at different times during the learning of an object recognition paradigm.  They confirm (using a PARP-1 antagonist) that PARP-1 is needed to establish object memory and also that PARP-1 seems to contribute during the paradigm and up to 2 hours after the training session.  They suggest that the poly(ADP-ribosyl)ation of histone H1 influences whether H1 is bound or unbound and thus helps regulate the opening and closing of the chromatin so that transcription can take place. 

Nice to know that PARP-1 is on the job!  Still am wondering if the PhD was worth all the learning.  Are there trade-offs at play here?  MORE learning vs. LESS something?   Perhaps. Check out the paper by Grube and Bürkle (1992) – Poly(ADP-ribose) polymerase activity in mononuclear leukocytes of 13 mammalian species correlates with species-specific life span. This gene may influence life span!

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Last night I was watching a TV show on the story of The Buddha.   There was a part in the story where, “Siddhartha saw a man lying on the ground and moaning. Out of compassion, he rushed over to the man. Channa warned him that the man was sick and that everyone, even noble people like Siddhartha or the king could get sick.” Later, “Siddhartha lost all interest in watching the dancing girls and other such pleasures.  He kept on thinking instead about how to free himself and others from sickness, ageing and death.”

When Siddhartha looked at the beautiful young dancers, he saw them as old, dying women and felt empathy for the suffering they would endure in their lives.

This part of the story reminded me of the way mass marketeers often use sexuality to market yoga, and the backlash it creates.   I thought that this moment in Siddhartha’s life really captured the “true” spirit of yoga/Buddhism – in stark contrast to so many slick, sexy advertisements.  Yoga and meditation – while enjoyed by many young and beautiful people – provides something deeper – a path to cope with the painful, frightening and inexorable loss one’s health, (outer) beauty, memory and breath.

I’d be a hypocrite to say I’m averse to the “sex sells” media, but Siddhartha’s insight is one to keep in mind – and heart.

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Cinematicode wall
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As far as science movies go, the new movie, “To Age or Not To Age” seems like a lot of fun.  The interview with Dr. Leonard Guarente suggests that the sirtuin genes play a starring role in the film.  Certainly,  an NAD+ dependent histone deacetylase – makes for a sexy movie star – especially when it is able to sense diet and metabolism and establish the overall lifespan of an organism.

One comment in the movie trailer, by Aubrey de Grey, suggests that humans may someday be able to push the physiology of aging to extreme ends.  That studies of transgenic mice over-expressing SIRT1 showed physiological properties of calorie-restricted (long lived) mice – even when fed ad libitum – suggests that something similar might be possible in humans.

Pop a pill and live it up at your local Denny’s for the next 100 years?  Sounds nice (& a lot like grad school).

Just a few twists to the plot here.  It turns out that – in the brain – SIRT1 may not function as it does in the body.  Here’s a quote from a research article “Neuronal SIRT1 regulates endocrine and behavioral responses to calorie restriction” that inactivated SIRT1 just in the brain:

Our findings suggest that CR triggers a reduction in Sirt1 activity in hypothalamic neurons governing somatotropic signaling to lower this axis, in contrast with the activation of Sirt1 by CR in many other tissues. Sirt1 may have evolved to positively regulate the somatotropic axis, as it does insulin production in β cells, to control mammalian health span and life span in an overarching way. However, the fact that Sirt1 is a positive regulator of the somatotropic axis may complicate attempts to increase murine life span by whole-body activation of this sirtuin.

To a limited extent, it seems that – in the brain – SIRT1 has the normal function of promoting aging.  Therefore, developing “pills” that are activators of SIRT1 would be good for the body, but somehow might be counteracted by what the brain would do.  Who’s in charge anyway?  Mother Nature will not make it easy to cheat her! Another paper published recently also examined the role of SIRT1 in the brain and found that – normally – SIRT1 enhances neuronal plasticity (by blocking the expression of a  micro-RNA miR-134 that binds to the mRNA of, and inhibits the translation of, synaptic plasticity proteins such as CREB).

So, I won’t be first to line up for SIRT1 “activator” pills (such as Resveratrol), but I might pop a few if I’m trying to learn something new.

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Hindus believe in reincarnation, the process w...
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The concept of “immortality” lies deep in the core of Indian spirituality and the religious traditions of many other cultures.  Its probably not a coincidence that one of the first and, still, most influential books on the history of yoga is entitled, Yoga: Immortality and Freedom by Mircea Eliade (you can read the book online here)

Most of the time, this refers to some part of a person – the soul, spirit or otherwise – that lives on forever after the physical body decays.  That we are able to recognize and ponder our mortality and the suffering of the physical body, is an integral part of why, in the first place, we seek to practice religion  (covered here).

I mean, no one ever took the concept of immortality LITERALLY, did they?  Perhaps not.  Until now.  Check out the trailer for a new movie that opens tonight in New York City on the science of Aging:  To Age or Not To Age – a film by Robert Kane Pappas. At the center of this film is likely the so-called longevity gene known as SIRT1 (covered earlier here).

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Oxygen is the key to life.  This is because it loves electrons.  In the mitochondria of every cell in your body, oxygen (in is atmospheric O2 state) serves as the ultimate electron acceptor and provides the chemical energy that drives the formation of ATP (a form of chemical energy storage that our body uses for all its cellular functions).

Oxygen is the key to death.  This is because it loves electrons.  When so-called reactive oxygen species (small molecules that contain oxygen in an ionized form) are permitted to roam free in cell and the body, they can indiscriminately pull electrons from other molecules (oxidation) and cause undesirable protein damage and premature cell death.

There is no escaping this chemical reality.  The very substance that giveth life, doth take it away and our longevity teeters on the quantum mechanical balance of electrons whizzing around the nucleus of the oxygen atom.  (I’ll think about this and the chemical symbol for oxygen (O), next time I chant “Om” in yoga class).

So it is with this humbling knowledge that many search for ways to optimize this balance (several populations have already figured out how to routinely live to 100+ years!) or at least improve the quality of our naturally limited life-span.  Light exercise, vegetables, friends and not too much alcohol.

Consider the recent paper, by Srivastava et al., “Association of SOD2, a Mitochondrial Antioxidant Enzyme, with Gray Matter Volume Shrinkage in Alcoholics” [doi: 10.1038/npp.2009.217].  The authors report that shrinkage of the neocortex (gray matter) of the brain is associated  chronic high levels of alcohol consumption.  That’s right, too much alcohol shrinks your brain.  Yikes!  How does alcohol exert its effect on brain shrinkage?  Well,  the authors measured many aspects of liver function (various enzyme levels), but these did not correlate with gray matter shrinkage.  Rather, the authors traced the effect to an enzyme that normally keeps harmful reactive oxygen species at bay – the so-called superoxide dismutase (SOD) enzyme.  We all have this enzyme, but in some of us, those who carry the rs4880 “G” allele of our SOD2 gene produce an enzyme that has an alanine at position 16 (Ala16) and is less active than the rs4880 “A” allele which encodes a more active enzyme with a Valine at position 16 (Val16).  The authors report that the rs10370 “TT”, rs4880 “GG” diplo-genotype (diplotype) was associated with more gray matter shrinkage in 76 individuals who report chronic high levels of alcohol consumption.  Here, the less active form of SOD2 is seemingly less able to metabolize all the harmful superoxide radicals that are generated during chronic exposure to alcohol.  Apparently their neurons are in retreat.

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In his undergraduate writings while a student at Harvard in the early 1900’s E. E. Cummings quipped that, “Japanese poetry is different from Western poetry in the same way as silence is different from a voice”.  Isabelle Alfandary explores this theme in Cummings’ poetry in her essay, “Voice and Silence in E. E. Cummings’ Poetry“,  giving some context to how the poet explored the meanings and consequences of voice and silence.  Take for example, his poem “silence”




ing;edge, of

(inquiry before snow

e.e. cummings

Lately, it seems that the brain imaging community is similarly beginning to explore the meanings and consequences of the brain when it speaks (activations whilst performing certain tasks) and when it rests quietly.  As Cummings beautifully intuits the profoundness of silence and rest,  I suppose he might have been intrigued by just how very much the human brain is doing when we are not speaking, reading, or engaged in a task. Indeed, a community of brain imagers seem to be finding that the brain at rest has quite a lot to say – moreso in people who carry certain forms of genetic variation (related posts here & here).

A paper by Perrson and colleagues “Altered deactivation in individuals with genetic risk for Alzheimer’s disease” [doi:10.1016/j.neuropsychologia.2008.01.026] asked individuals to do something rather ordinary – to pay attention to words – and later to then respond to the meaning of these words (a semantic categorization task). This simple endeavor, which, in many ways uses the very same thought processes as used when reading poetry, turns out to activate regions of the temporal lobe such as the hippocampus and other connected structures such as the posterior cingulate cortex.  These brain regions are known to lose function over the course of life in some individuals and underlie their age-related difficulties in remembering names and recalling words, etc.  Indeed, some have described Alzheimer’s disease as a tragic descent into a world of silence.

In their recordings of brain activity of subjects (60 healthy participants aged 49-79), the team noticed something extraordinary.  They found that there were differences not in how much the brain activates during the task – but rather in how much the brain de-activates – when participants simply stare into a blank screen at a small point of visual fixation.  The team reports that individuals who carry at least one copy of epsilon-4 alleles of the APOE gene showed less de-activation of their their brain (in at least 6 regions of the so-called default mode network) compared to individuals who do not carry genetic risk for Alzheimer’s disease.  Thus the ability of the brain to rest – or transition in and out of the so-called default mode network – seems impaired in individuals who carry higher genetic risk.

So, I shall embrace the poetic wisdom of E. E. Cummings and focus on the gaps, empty spaces, the vastness around me, the silences, and learn to bring my brain to rest.  And in so doing, perhaps avoid an elderly descent into silence.


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Last year I dug a bit into the area of epigenetics (indexed here) and learned that the methylation (CH3) and acetylation (OCCH3) of genomic DNA & histones, respectively, can have dramatic effects on the structure of DNA and its accessibility to transcription factors – and hence – gene expression.  Many of the papers I covered suggested that the environment can influence the degree to which these so-called “epigenetic marks” are covalently bonded onto the genome during early development.  Thus, the thinking goes, the early environment can modulate gene expression in ways that are long-lasting – even transgenerational.  The idea is a powerful one to be sure.  And a scary one as well, as parents who read this literature, may fret that their children (and grandchildren) can be epigenetically scarred by early nutritional, physical and/or psycho-social stress.  I must admit that, as a parent of young children myself, I began to wonder if I might be negatively influencing the epigenome of my children.

I’m wondering how much physical and/or social stress is enough to cause changes in the epigenome?  Does the concern about epigenetics only apply to exposure to severe stress?  or run of the mill forms of stress?  How much do we know about this?

This year, I hope to explore this line of inquiry further.  For starters, I came across a fantastic paper by Fraga et al., entitled, “Epigenetic differences arise during the lifetime of monozygotic twins” [doi:10.1073/pnas.0500398102].   The group carries out a remarkably straightforward and time honored approach – a twin study – to ask how much identical twins differ at the epigenetic level.  Since identical twins have the same genome sequence, any differences in their physiology, behavior etc. are, strictly speaking, due to the way in which the environment (from the uterus to adulthood) shapes their development.  Hence, the team of Fraga et al., can compare the amount and location of methyl (CH3) and acetyl (OCCH3) groups to see whether the environment has differentially shaped the epigenome.

An analysis of some 40 identical twin pairs from ages 3-74 years old showed that – YES – the environment, over time, does seem to shape the epigenome (in this case of lymphocytes).  The most compelling evidence for me was seen in Figure 4 where the team used a method known as Restriction Landmark Genomic Scanning (RLGS) to compare patterns of methylation in a genome-wide manner.  Using this analysis, the team found that older twin pairs had about 2.5 times as many differences as did the epigenomes of the youngest twin pairs.  These methylation differences also correlated with gene expression differences (older pairs also had more gene expression differences) and they found that the individual who showed the lowest levels of methylation also had the highest levels of gene expression.  Furthermore, the team finds that twin pairs who lived apart and had more differences in life history were more likely to have epigenetic differences.  Finally, measures of histone acetylation seemed consistent with the gradient of epigenetic change over time and life-history distance.

Thus it seems that, as everyday life progresses, the epigenome changes too.  So, perhaps, one does not need extreme forms of stress to leave long-lasting epigenetic marks on the genome?  Is this true during early life (where the team did not see many differences between pairs)?  and in the brain (the team focused mainly on lymphocytes)?  Are the differences between twins due to the creation of new environmentally-mediated marks or the faulty passage of existing marks from dividing cell-to-cell over time?  Will be fun to seek out information on this.

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