Daily Archives: September 9, 2023

Richetto J, Meyer U. Epigenetic modifications in schizophrenia and related disorders: molecular scars of environmental exposures and source of phenotypic variability. Biol Psychiatry. 2021;89:21526.

Article CAS PubMed Google Scholar

Penner-Goeke S, Binder EB. Epigenetics and depression. Dialogues Clin Neurosci. 2019;21:397405.

Article PubMed PubMed Central Google Scholar

Levine A, Cantoni GL, Razin A. Inhibition of promoter activity by methylation: possible involvement of protein mediators. Proc Natl Acad Sci USA. 1991;88:65158.

Article CAS PubMed PubMed Central Google Scholar

Boyes J, Bird A. Repression of genes by DNA methylation depends on CpG density and promoter strength: evidence for involvement of a methyl-CpG binding protein. Embo J. 1992;11:32733.

Article CAS PubMed PubMed Central Google Scholar

Hwu WL, Lee YM, Lee SC, Wang TR. In vitro DNA methylation inhibits FMR-1 promoter. Biochem Biophys Res Commun. 1993;193:3249.

Article CAS PubMed Google Scholar

Aran D, Toperoff G, Rosenberg M, Hellman A. Replication timing-related and gene body-specific methylation of active human genes. Hum Mol Genet. 2011;20:67080.

Article CAS PubMed Google Scholar

Ball MP, Li JB, Gao Y, Lee JH, LeProust EM, Park IH, et al. Targeted and genome-scale strategies reveal gene-body methylation signatures in human cells. Nat Biotechnol. 2009;27:3618.

Article CAS PubMed PubMed Central Google Scholar

Hellman A, Chess A. Gene body-specific methylation on the active X chromosome. Science. 2007;315:11413.

Article CAS PubMed Google Scholar

Rauch TA, Wu X, Zhong X, Riggs AD, Pfeifer GP. A human B cell methylome at 100-base pair resolution. Proc Natl Acad Sci USA. 2009;106:6718.

Article CAS PubMed PubMed Central Google Scholar

Nakazawa K, Sapkota K. The origin of NMDA receptor hypofunction in schizophrenia. Pharm Ther. 2020;205:107426.

Article CAS Google Scholar

Chan SY, Matthews E, Burnet PW. ON or OFF? Modulating the N-Methyl-D-aspartate receptor in major depression. Front Mol Neurosci. 2016;9:169.

CAS PubMed Google Scholar

Zanos P, Moaddel R, Morris PJ, Georgiou P, Fischell J, Elmer GI, et al. NMDAR inhibition-independent antidepressant actions of ketamine metabolites. Nature. 2016;533:4816.

Article CAS PubMed PubMed Central Google Scholar

Krystal JH, Abdallah CG, Sanacora G, Charney DS, Duman RS. Ketamine: a paradigm shift for depression research and treatment. Neuron. 2019;101:7748.

Article CAS PubMed PubMed Central Google Scholar

Krystal JH, Kavalali ET, Monteggia LM. Ketamine and rapid antidepressant action: new treatments and novel synaptic signaling mechanisms. Neuropsychopharmacology. 2023. https://doi.org/10.1038/s41386-023-01629-w. Online ahead of print.

Vollenweider FX, Preller KH. Psychedelic drugs: neurobiology and potential for treatment of psychiatric disorders. Nat Rev Neurosci. 2020;21:61124.

Article CAS PubMed Google Scholar

Aleksandrova LR, Phillips AG. Neuroplasticity as a convergent mechanism of ketamine and classical psychedelics. Trends Pharm Sci. 2021;42:92942.

Article CAS PubMed Google Scholar

Deichmann U. Epigenetics: the origins and evolution of a fashionable topic. Dev Biol. 2016;416:24954.

Article CAS PubMed Google Scholar

Kumar S, Cheng X, Klimasauskas S, Mi S, Posfai J, Roberts RJ, et al. The DNA (cytosine-5) methyltransferases. Nucleic Acids Res. 1994;22:110.

Article CAS PubMed PubMed Central Google Scholar

Yen RW, Vertino PM, Nelkin BD, Yu JJ, el-Deiry W, Cumaraswamy A, et al. Isolation and characterization of the cDNA encoding human DNA methyltransferase. Nucleic Acids Res. 1992;20:228791.

Article CAS PubMed PubMed Central Google Scholar

Xie S, Wang Z, Okano M, Nogami M, Li Y, He WW, et al. Cloning, expression and chromosome locations of the human DNMT3 gene family. Gene. 1999;236:8795.

Article CAS PubMed Google Scholar

Suetake I, Shinozaki F, Miyagawa J, Takeshima H, Tajima S. DNMT3L stimulates the DNA methylation activity of Dnmt3a and Dnmt3b through a direct interaction. J Biol Chem. 2004;279:2781623.

Article CAS PubMed Google Scholar

Grippo P, Iaccarino M, Parisi E, Scarano E. Methylation of DNA in developing sea urchin embryos. J Mol Biol. 1968;36:195208.

Article CAS PubMed Google Scholar

Bianchi NO, Vidal-Rioja L, Cleaver JE. Direct visualization of the sites of DNA methylation in human, and mosquito chromosomes. Chromosoma. 1986;94:3626.

Article CAS PubMed Google Scholar

Edwards JR, ODonnell AH, Rollins RA, Peckham HE, Lee C, Milekic MH, et al. Chromatin and sequence features that define the fine and gross structure of genomic methylation patterns. Genome Res. 2010;20:97280.

Article CAS PubMed PubMed Central Google Scholar

Ehrlich M, Gama-Sosa MA, Huang LH, Midgett RM, Kuo KC, McCune RA, et al. Amount and distribution of 5-methylcytosine in human DNA from different types of tissues of cells. Nucleic Acids Res. 1982;10:270921.

Article CAS PubMed PubMed Central Google Scholar

Bird A, Taggart M, Frommer M, Miller OJ, Macleod D. A fraction of the mouse genome that is derived from islands of nonmethylated, CpG-rich DNA. Cell. 1985;40:9199.

Article CAS PubMed Google Scholar

Bird AP. DNA methylation and the frequency of CpG in animal DNA. Nucleic Acids Res. 1980;8:1499504.

Article CAS PubMed PubMed Central Google Scholar

Ioshikhes IP, Zhang MQ. Large-scale human promoter mapping using CpG islands. Nat Genet. 2000;26:6163.

Article CAS PubMed Google Scholar

Maunakea AK, Nagarajan RP, Bilenky M, Ballinger TJ, DSouza C, Fouse SD, et al. Conserved role of intragenic DNA methylation in regulating alternative promoters. Nature. 2010;466:2537.

Article CAS PubMed PubMed Central Google Scholar

Meehan RR, Lewis JD, McKay S, Kleiner EL, Bird AP. Identification of a mammalian protein that binds specifically to DNA containing methylated CpGs. Cell. 1989;58:499507.

Article CAS PubMed Google Scholar

Kokura K, Kaul SC, Wadhwa R, Nomura T, Khan MM, Shinagawa T, et al. The Ski protein family is required for MeCP2-mediated transcriptional repression. J Biol Chem. 2001;276:3411521.

Article CAS PubMed Google Scholar

Jones PL, Veenstra GJ, Wade PA, Vermaak D, Kass SU, Landsberger N, et al. Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription. Nat Genet. 1998;19:18791.

Article CAS PubMed Google Scholar

Kyle SM, Vashi N, Justice MJ. Rett syndrome: a neurological disorder with metabolic components. Open Biol. 2018;8:170216.

Article PubMed PubMed Central Google Scholar

Mohn F, Weber M, Rebhan M, Roloff TC, Richter J, Stadler MB, et al. Lineage-specific polycomb targets and de novo DNA methylation define restriction and potential of neuronal progenitors. Mol Cell. 2008;30:75566.

Article CAS PubMed Google Scholar

Rajarajan P, Jiang Y, Kassim BS, Akbarian S. Chromosomal conformations and epigenomic regulation in schizophrenia. Prog Mol Biol Transl Sci. 2018;157:2140.

Article CAS PubMed PubMed Central Google Scholar

Laurent L, Wong E, Li G, Huynh T, Tsirigos A, Ong CT, et al. Dynamic changes in the human methylome during differentiation. Genome Res. 2010;20:32031.

Article CAS PubMed PubMed Central Google Scholar

Roussos P, Mitchell AC, Voloudakis G, Fullard JF, Pothula VM, Tsang J, et al. A role for noncoding variation in schizophrenia. Cell Rep. 2014;9:141729.

Article CAS PubMed PubMed Central Google Scholar

Wray NR, Ripke S, Mattheisen M, Trzaskowski M, Byrne EM, Abdellaoui A, et al. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression. Nat Genet. 2018;50:66881.

Article CAS PubMed PubMed Central Google Scholar

Zhubi A, Veldic M, Puri NV, Kadriu B, Caruncho H, Loza I, et al. An upregulation of DNA-methyltransferase 1 and 3a expressed in telencephalic GABAergic neurons of schizophrenia patients is also detected in peripheral blood lymphocytes. Schizophr Res. 2009;111:11522.

Article CAS PubMed PubMed Central Google Scholar

Dong E, Ruzicka WB, Grayson DR, Guidotti A. DNA-methyltransferase1 (DNMT1) binding to CpG rich GABAergic and BDNF promoters is increased in the brain of schizophrenia and bipolar disorder patients. Schizophr Res. 2015;167:3541.

Article CAS PubMed Google Scholar

Veldic M, Caruncho HJ, Liu WS, Davis J, Satta R, Grayson DR, et al. DNA-methyltransferase 1 mRNA is selectively overexpressed in telencephalic GABAergic interneurons of schizophrenia brains. Proc Natl Acad Sci USA. 2004;101:34853.

Article CAS PubMed Google Scholar

Veldic M, Guidotti A, Maloku E, Davis JM, Costa E. In psychosis, cortical interneurons overexpress DNA-methyltransferase 1. Proc Natl Acad Sci USA. 2005;102:21527.

Article CAS PubMed PubMed Central Google Scholar

Ruzicka WB, Zhubi A, Veldic M, Grayson DR, Costa E, Guidotti A. Selective epigenetic alteration of layer I GABAergic neurons isolated from prefrontal cortex of schizophrenia patients using laser-assisted microdissection. Mol Psychiatry. 2007;12:38597.

Article CAS PubMed Google Scholar

Veldic M, Kadriu B, Maloku E, Agis-Balboa RC, Guidotti A, Davis JM, et al. Epigenetic mechanisms expressed in basal ganglia GABAergic neurons differentiate schizophrenia from bipolar disorder. Schizophr Res. 2007;91:5161.

Article PubMed PubMed Central Google Scholar

Antun FT, Burnett GB, Cooper AJ, Daly RJ, Smythies JR, Zealley AK. The effects of L-methionine (without MAOI) in schizophrenia. J Psychiatr Res. 1971;8:6371.

Article CAS PubMed Google Scholar

Noh JS, Sharma RP, Veldic M, Salvacion AA, Jia X, Chen Y, et al. DNA methyltransferase 1 regulates reelin mRNA expression in mouse primary cortical cultures. Proc Natl Acad Sci USA. 2005;102:174954.

Article CAS PubMed PubMed Central Google Scholar

Jaffe AE, Gao Y, Deep-Soboslay A, Tao R, Hyde TM, Weinberger DR, et al. Mapping DNA methylation across development, genotype and schizophrenia in the human frontal cortex. Nat Neurosci. 2016;19:4047.

Article CAS PubMed Google Scholar

Hannon E, Dempster EL, Mansell G, Burrage J, Bass N, Bohlken MM, et al. DNA methylation meta-analysis reveals cellular alterations in psychosis and markers of treatment-resistant schizophrenia. Elife. 2021;10:e58430.

Article CAS PubMed PubMed Central Google Scholar

Aberg KA, McClay JL, Nerella S, Clark S, Kumar G, Chen W, et al. Methylome-wide association study of schizophrenia: identifying blood biomarker signatures of environmental insults. JAMA Psychiatry. 2014;71:25564.

Article CAS PubMed PubMed Central Google Scholar

Wang W, Li W, Wu Y, Tian X, Duan H, Li S, et al. Genome-wide DNA methylation and gene expression analyses in monozygotic twins identify potential biomarkers of depression. Transl Psychiatry. 2021;11:416.

Article CAS PubMed PubMed Central Google Scholar

Grayson DR, Jia X, Chen Y, Sharma RP, Mitchell CP, Guidotti A, et al. Reelin promoter hypermethylation in schizophrenia. Proc Natl Acad Sci USA. 2005;102:93416.

Visit link:
DNA methylation and the opposing NMDAR dysfunction in ... - Nature.com

'I don't think it's in her DNA': Man who co-authored Murdaugh book with Colleton Co. Clerk of Court discusses allegations  ABC NEWS 4

Here is the original post:
'I don't think it's in her DNA': Man who co-authored Murdaugh book with Colleton Co. Clerk of Court discusses allegations - ABC NEWS 4

For many years, nobody in the Daly family knew what had become of their long lost relative who had simply upped and vanished one day. His mother, as well as his brothers and sisters, had all died without getting any answers.

Frances Daly (50), originally from Carrickmacross, Co Monaghan, but now living in Dublin, describes using her DNA to solve this family mystery of her fathers uncle, who was named John Daly, as one of her proudest moments.

He used to get remembered at various family events, recalls Daly. He would regularly get a decade of the rosary said for him. Everybody thought he just went off and made his fortune, but unfortunately that didnt happen.

It was only when Daly took an interest in tracing her family tree that she came up with answers.

I saw him in the Census, and then I found him two years later, dead in Australia at 23 from typhoid, she says. I found a guy coming in from London on a boat to Perth, and I think its him. His name is too common to be absolutely sure.

But if it is him, he got the whole way across Australia and then got bitten by something. He was in the sugar cane territory so there would have been regular outbreaks of diseases.

Daly managed to find his grave in Brisbane, and also found a small article in a newspaper marking his death. The big question left for Daly and her family was why this man had travelled all the way to the other side of the world without a word to anybody.

It was only when she sent her DNA to a genealogy company, which operates by building a database and cross-referencing peoples genetic codes, that she finally closed the circle and got what is at least plausible explanation for what happened.

He had two maternal aunts in New Zealand, and it seems he was going out to them, she says. Well never know for sure, but I didnt know about the New Zealand people until I did the DNA so that kind of closed a circle for me.

It brought great comfort to some of the older relatives to know he was buried properly and there was a priest and everything there with him. My father had a cousin who was a priest so to be able to tell him everything was done right was special.

Daly, whose family are spread over counties Louth, Monaghan and Kildare, also unearthed relatives from Melbourne, Montana, Canada, and New Zealand through the DNA testing.

I call them my new relatives, she says. Its great to be able to show them photographs of the homestead, or the graves weve some very old graves in the family and share stories. To be able to show them, this is your auntie Mary, or whatever the case may be.

Ive gone off and taken photographs of fields and old houses and farmyards and sent them away to people. You can see family resemblances and traits in photographs of people going back generations too.

A number of these people even made the long journeys back to Ireland to meet Daly and see these familial landmarks for themselves. Sometimes the biggest connection is to be able to go and put some flowers on a grave and acknowledge somebody, she says.

Part of the appeal of all this, Daly adds, is putting the pieces of the jigsaw together without having the picture on the box to help you along. For her, it isnt just about what happened, but why.

They were farmers from the country so they left for economic reasons a chance of a better life, she says. Back in the day, if there was a small farmer and the eldest son got the land and there were three other sons, the others had no choice but to go.

I have relatives who went out to mining towns in Montana. A lot of people from Carrickmacross went there for some reason. I dont know why because there isnt much of a mining tradition in Carrickmacross.

Claire Bradley, a professional genealogist specialising in Irish family history, says there are huge leaps that can be made in tracing family trees through the use of DNA, but stresses it must be used as a compliment to paper records.

In Ireland, we are really hampered by the fire in the Four Courts in 1922 when a lot of records were destroyed, largely Census records, but also wills and things like that, she says. I have gone from about 1,000 in my family tree when I started using DNA to about 4,000 now.

Claire Bradley, a professional genealogist specialising in Irish family history

All that being said, many people have raised concerns around the idea of handing their DNA over to private companies and what the implications of that could be down the road. Unsurprisingly, perhaps, Bradley dismisses much of this as scaremongering.

Youre agreeing to give it over, she says. You can have it removed from the database if you change your mind. I think there is a lot of scaremongering in it. I think people give away a lot more information on Facebook than they do with a DNA swab.

[Centuries of documents burned in the Four Courts in 1922. Now theyre being recreated]

[Irish DNA atlas maps genes of the people of Ireland]

Bradley says the DNA aspect of genealogy is more adept at widening family trees than it is at tracing backwards. This was the case for Gina Dooley (46) from Limerick who describes herself as a newcomer to all this.

About a month before the Covid-19 pandemic hit Irish shores, her grandmother died. During the grieving process, a lot of old photographs were taken out and pored over as the family took stock.

It was when she looked at a photograph of her great-grandmother that she was stopped in her tracks. I was struck by how I knew nothing about this woman, yet she looked so much like me and my mother, she says. So, she started digging, and later did the DNA test.

She didnt uncover any terrible secrets and describes her family history as a normal one regular peasant farmers but remarks that building a picture of the time they lived in and the town they came from makes them feel more real and me feel more grounded.

One particular story of a second cousin she discovered in Australia stands out. After they made contact, the man told her about an uncle of his with whom he had lived as a child. She then went to the Military Archives to find out more about him.

I dont know how to describe the feeling of sitting in the Military Archive holding pages that he wrote, she says. I never met this man he was my grandmothers uncle but it was like a piece of him was still alive.

I could share that with James in Australia, and he could relay to me things he remembered of this man, and how he used to go off on a rant about Ian Paisley. James was five years old, and he didnt know who Ian Paisley was, but that is all he remembers of this man.

Continued here:
Using DNA to solve a family mystery: 'It brought great comfort to ... - The Irish Times

Epigenetic factors regulate the genes youre born with and can cause them to malfunction, from the impact of stress, adversity and pollution to diet, exercise and whether or not you drink and/or smoke. Illustration / Getty Images

Halfway through a challenge to lower her cellular age before a significant birthday, Joanna Wane looks at how a biological clock based on data from the world-famous Dunedin Study can show whether youre speeding up or slowing down time

When Terrie Moffitt first came out from the United States to work on the Dunedin Study as a PhD graduate, the 1000-plus people whove been involved in the project since birth were in their early teens. Next year, when the latest round of exhaustive tests and interviews begins, theyll be turning 52.

Back then, in the mid-80s, a few of them were already causing minor havoc. Shoplifting at Woolworths. Converting cars. Sniffing glue in the Octagon. Drugs, alcohol, risky sex. Moffitts research over the following years into why some kids grow out of juvenile delinquency (or goofing around, as she calls it) and others grow up to be career criminals is still widely cited by criminologists worldwide.

Moffitt is now associate director of the Dunedin Study and the clear link she identified between serious adult offending and childhood trauma bears revisiting amid the current political rhetoric over getting tough on youth crime. Once they got out the other side [from their teens], we began to see those two groups diverge, she tells Canvas, from her home in North Carolina. Then you could look back and see that the ones who continued with crime into their 20s and 30s were the ones who had a lot of difficulties as very young children and grew up in very adverse homes.

The major contribution [of the research] was pointing out to governments and the justice system that the vast majority of teenagers who break the law are not going to develop into hardcore criminals, so you should really help them not get a prison record. Give them a chance to grow out of it and reform themselves and they will naturally.

What the Dunedin Study has shown over more than five decades now is that childhood exposure to poverty, trauma or victimisation leaves a lasting cellular imprint on the body, too. A tough start in life means youre likely to age faster and die earlier, you increase the risk of developing chronic age-related conditions such as cardiovascular disease, dementia, hypertension, type 2 diabetes and cancer.

Of course, the reverse is also true if youve been dealt a better hand and make the most of it, increasing your chances of an extended healthspan, defined as the number of quality years where youre generally healthy, active and free from disease.

The impact, for better or worse, of both the environment you live in and the way you behave in it holds more power over your life than you might think. Epigenetic factors regulate the genes youre born with and can cause them to malfunction, from the impact of stress, adversity and pollution to diet, exercise and whether or not you drink and/or smoke. This process of DNA methylation is the most significant influence on how well people age; some estimates put it as high as 70 to 80 per cent.

Moffitt, a professor of psychology and neuroscience at Duke University in North Carolina and a professor of social behaviour and development at Kings College, London, has remained closely involved with the Dunedin Study. Having followed the cohort from adolescence to midlife, shell be back in New Zealand next year for the latest phase of research, which will look at how well theyre preparing for old age.

Since the study members turned 26, data has been collected every five or six years on a series of key biomarkers widely used as an indicator of risk for disease, including cholesterol levels, blood pressure, gum recession, lung function, heart health and blood glucose (a potential red flag for pre-diabetes). Physical functions have been added: how long they can stand on one leg, how many times they can get up out of a chair in 30 seconds without using their hands. Brain scans, first done at age 45, will also be repeated next year.

The first epigenetic clock was invented a decade or so ago, using DNA methylation levels as a way to measure biological ageing. However, what makes the Dunedin Study so unique is its access to waves of progressive data on the same group of people. We figured out, hey, I bet we could do the same thing [as the other epigenetic clocks] but using our biomarkers, says Moffitt. So thats what we did. And we determined there were 173 of those methylation marks on top of genes that differentiated between those who were falling apart swiftly over the past 20 years, those who were holding steady and those who were staying young.

The DunedinPACE algorithm, developed in collaboration with Duke University and Columbia University in New York, analyses those epigenetic marks via a pin-prick blood test. Its now considered the most precise measure of how fast or slowly a person is ageing and the best predictor of future health outcomes. Unlike other epigenetic clocks that have been named after the scientists who invented them (Horvath, Hannum, Levine), DunedinPACE acknowledges the members of the study whove made it possible.

Likened to a speedometer, the test captures a specific moment in time and is a fluid measure that can show significant change in as little as eight weeks reflecting a lifestyle change, perhaps, or the efficacy of a new medication. The fastest rate of ageing recorded so far is 1.4, which means that a person is ageing biologically by almost five extra months for every chronological year. The slowest rate of ageing thats been measured is 0.6.

Moffitt hasnt been surprised to find such a huge variation between fast and slow agers. There are people [in the Dunedin Study] who are Olympic athletes and there are people who lead a really down-and-out life, in and out of prison, on and off addictive drugs. So I knew some were taking care of themselves and some were really not, she says. When study members came to the unit for assessment day, some would look so young while others really showed their age. Seeing that reflected in the [rate of ageing] numbers was quite amazing.

The Dunedin cohort is predominantly Pkeh but comparative studies internationally have applied the DunedinPACE algorithm successfully across ethnicities and among the elderly. Moffitt is also co-director of a longitudinal study following twins born into 1100 British families in the mid-90s and has analysed blood samples from them that show the same trajectories. Its miraculous, she says. Born 20,000 miles and 20 years apart from the Dunedin Study and yet the DunedinPACE can still tell you something about them.

Ironically, no equivalent trials have yet been done on Mori and Pasifika in New Zealand.

On my 59th birthday last November, I took a DNA Age test through Auckland-based biotechnology company SRW and sent it off to TruDiagnostics in the US for analysis. A whole swag of results came back, including my extrinsic epigenetic age (a shade under 44) and my DunedinPACE value at 0.71. A follow-up test, done six months later, shows my rate of ageing holding steady. The other big news was that the length of my telomeres had extended markedly.

Protective caps on the tips of chromosome DNA strands, telomeres have been likened to the aglets that protect shoelaces from fraying. Each time a cell divides, our telomeres shorten and they shorten faster under oxidative stress. Once they reach a critical length, the cell dies. Research in adults has shown that telomere length is a predictor of lifespan and is causally linked to age-related diseases. According to the latest test results, mine have actually extended from 7.01 to 7.24 kilobases, longer than 97.94 per cent of people my age. On this measurement, my predicted biological age is 30.90.

Before I celebrate too hard, though, the full reveal of how my baseline data has shifted over a period of 12 months will come when I do a final test, on the day of my 60th birthday.

Over the past year, Ive made some lifestyle tweaks in an attempt to shift the dial in the right direction more alcohol-free days, a bit more exercise (hampered by a knee and shoulder injury), a daily dose of the blackcurrant-based brain drink repa, a monthly visit to my osteopath Glyn Flutey, and a regime of SRW supplements, Cel1, Cel2 and Cel3, developed in collaboration with leading scientists around the world to support nine key cellular functions that decline with age.

One of the molecules in Cel1 is astragaloside, a compound found in a plant root that stimulates telomere repair. Ill never know for sure but it seems likely the supplements have contributed to my positive result. An observational trial by the company in New Zealand showed a biological age reduction of two and a half years in people who took the full suite of Cel supplements for six months. An independent 12-month trial SRW hopes will verify those findings is now underway in the US.

Apart from a regular yoga class, and a hypnotherapy session to help break a lifetime habit of grinding my teeth, I havent specifically targeted stress reduction yet as a way to work on lowering my biological age. I did a transcendental meditation course once, in my early 30s, and I know my brain needs some time to slow down, but fitting in two 20-minute sessions a day just never seemed realistic to me.

Rachel Grunwell, a former investigative journalist-turned-wellness coach, teaches mindfulness meditation through her company Inspired Health to a whole range of clients, from people like me to corporate directors and high-performance athletes. The mother of three boys and a former Herald columnist, she interviewed 30 global experts for her recent book Balance: Food, Health + Happiness and found plenty of science to support the idea that lowering stress levels can help slow down ageing.

We live on a planet thats speeding up; everything is getting faster and faster, she says. I feel anxious just thinking about the idea of having to fit 20 minutes of meditation into my life! But even taking a minute can be incredibly powerful to slow down your breathing, be in the moment and reset a stressed nervous system.

ONE-MINUTE MEDITATIONS

Chronic stress hammers the body physically, increasing your risk of everything from heart disease (particularly for women post-menopause) and high cholesterol to depression and cognitive problems. It can actually shrink your brain. Here are three mindful minute tools wellness coach Rachel Grunwell recommends to help de-stress your nervous system:

Box breathing meditation: Breathe in for four counts, pause for four counts, breathe out for four counts, pause for four counts. Repeat. This forces you to slow down your breathing and focusing on the count is a good distraction.

20-second hack: Practise belly breathing by imagining youre blowing up a balloon in your belly as you inhale. Then, as you breathe out, picture the balloon deflating. To check if youre doing it right, place one hand on your chest and the other on your stomach to see which one moves as you breathe.

Body scan meditation: You can do this sitting, lying down or with your legs up the wall. Taking deep belly breaths, scan yourself from the feet up, relaxing the different parts of your body on each exhalation. Especially good just before sleep.

10-second hack: Most of us carry tension in our shoulders. Grab a few seconds to take a deep breath, squeeze your shoulders up towards your ears as high as you can, hold for a beat or two, then release with a strong out-breath.

Senses meditation: When youre having a hot drink, at home or at a cafe, tune into all your senses to be present and aware in the moment. Savour the feeling of the warm cup in your hands, the patterns you see in the crema, the sounds you can hear around you, the aromas you can smell, the taste in your mouth.

10-minute hack: If youre in a virtual meeting where you need to listen but not participate, pop in your earbuds and go for a quick walk. You cant be entirely anxious when youre walking, says Grunwell. Part of your brain disengages. Or just be still and look for shapes in the clouds.

See the rest here:
How to live longer: DNA, wellbeing and ageing - New Zealand Herald

Summary

Terminators are some of the most formidable and deadly Sci-Fi villains in the history of the genre, but they didnt reach their peak until they merged with another science fiction monster, Aliens Xenomorph. The hybridization of the two creatures unlocked the Terminators' ultimate weapon, one that it could never have wielded without Xenomorph DNA.

Despite the fact that these respective franchises originally had nothing to do with each other upon their films initial releases, their crossover comic series Aliens vs Predator vs The Terminator asserts that Alien and The Terminator have been a part of the same continuity all along. Apparently, Alien takes place in the future after Skynets attack on Planet Earth and the AIs subsequent defeat to the Human Resistance led by John Connor. It seems Skynets reign was pretty short-lived, though remnants of the evil artificial intelligence remained scattered across the galaxy. As humanity rebuilt from the ashes of Skynets assault on the planet and became the space-faring race of humans introduced in 1979s Alien, a rogue squadron of surviving Terminators is plotting the return of Skynet. By the time of this crossover - which takes place after Alien Resurrection - those rogue Terminators finally figured out how they were going to pull it off.

In Aliens vs Predator vs The Terminator by Mark Schultz and Mel Rubi, the remaining Terminators are able to successfully create Terminator/Xenomorph hybrids. These creatures have the biological weapons inherent in every Xenomorph, along with the ferocity and hive-mind-like coordination of the perfect organism, but thats not all. This hybridization also gave the Terminators an entirely new ability, one that isnt derived from either the Xenomorph or the Terminators entirely, but is rather a unique result of their merging: the Absorption Matrix. This ability allows the hybrids to literally absorb their physical surroundings, which both makes themselves more durable in any given situation with the added benefit of absolutely demolishing their surroundings, which is an aspect to the ability that can be weaponized in and of itself given the right circumstances (like inside a spaceship or within a highly volatile laboratory, for instance).

This ability manifested through the sheer malleability of Xenomorph DNA, and the Terminators ability to manipulate it to suit their needs. It is well established in Alien canon that Xenomorphs adapt gradually to their surroundings with each generation, as their hosts allow them to evolve through genetic imprint, which naturally makes them better suited for their environment. The Terminators know this, but since they cant impart pieces of themselves with every new generation of Xenomorph in the more natural way (if one considers Facehugger impregnation natural), they opted to speed up that process through experimentation.

These experiments conducted by the Terminators to create the best versions of themselves for the resurgence of Skynet results in perhaps the most ferocious Terminator in the history of the franchise, one with an ultimate attack it could never have had without the DNA of Aliens Xenomorph.

Read this article:
Terminator's Ultimate Weapon Was Only Unlocked by Alien DNA - Screen Rant