#epigenetic reversal

[sunset-peril]

I actually tend to hc that all the Links are descended from another at some point.

However, what do you think about epigenetics being a viable reason for such?

You mean epigenetics being the reason they all are similar? Or that epigenetics is the reason they're all descendants of each other? I'm not sure I understand the question.

However, considering that epigenetics regards the condensed-ness (that's not a word but oh well) of the histones and the DNA wrapped around them and that most epigenetic changes are extremely reversible due to being caused by environmental stimuli (the only epigenetic changes that are permanent being CpG methylations in gene promoters, because those control cell differentiation.), I don't think epigenetics would leave a permanent mark on all Links as a whole. If Twilight Princess was Ocarina of Time's grandson or great-grandson, then that would be the only time I could see epigenetics playing a role in more than one Link. However, I think the rest of them are too far apart in the bloodline to have any real epigenetic effect on each other. Generally, epigenetic changes have been reversed after two or three generations, unless whatever stimuli that caused the original modification was persistent. (We used diabetic rats and poor/proper dieting for this study, and research on psychological epigenetics is still very new)

Although now that you mention this, I am curious to see how epigenetics would play a role in BotW/TotK's children.

I hope that answers the question!

For me I definitely hc that Skyward, Ocarina, Twilight Princess and BotW/TotK being all relatives (BotW being descended from TP literally being a foundational piece in my lore). I just don't know enough about the rest of them to decide for the rest of them.

[peachesanmemes]

I'm obsessed with expectency effects and epigenetics. A brief summary for you using examples.

Researchers were given two sets of random rats from the same breeder and told one group was smarter and better at mazes. The researchers, after conducting studies, PROVED that that group was smarter. This is expectancy effects. We look for evidence of a thing we believe to be true and prove it somehow.

There are a couple thoughts on why this works. False or inflated reporting of evidence in support of the belief and/or subconcious influence on the part of the researchers leading to legitimately better results. I think both play a part, but I am mainly in the latter camp. I genuinely think that if you believe someone or something to be a certain way, then you will influence them subconsciously to meet that expectation.

For instance, if you believe kids are hard to deal with, kids are going to pick up on that and not be easy to deal with with you. You're going to find lots of evidence to support that they're hard to deal with.

Epigenetics is a whole field studying non visible genetically inherited traits. Epigenetic studies in mice found that it took FIVE generations for mice to stop responding negatively to a stimulus that only the first generation actually experienced. One very, very important thing to realize about epigenetics, though, is on the literal google search page for the word. "Unlike genetic changes, epigenetic changes are reversible."

So not only is your body/brain likely responding to stimulus from like 1870 to now subconciously (because of the way it reads it's own DNA,) but ALSO everything you believe to be true is more likely to be due to expectancy effects! And when you learn and believe that whatever negative triggers and responses come up for you are reversible, you will prove it.

Isn't that beautiful? The mutability of the mind and body?

Isn't it beautiful to believe that we are not stuck in one way of thinking and reacting to the world no matter how ingrained by time?

You're going to do great.

I believe in you!

[mleprae]

Epigenetics is one of my fav fields there and it's so cool... you know why some diseases are almost impossible to treat? Well, every cell has your entire DNA in it, every cell has access to the instructions to produce every single protein your body makes.. but they don't do it, gene expression is extremely regulated

And it may be frustrating to hear that well, technically, your muscle cells can become neurons on paper, but they don't ! This is where stem cells come in, the medical holy grail... think of every cell in the body as eevelutions, they all evolved from eevee but they can't evolve back nor into other types, stem cells would be that eevee, they can turn into other types of cells, the unfortunate part is that stem cells are usually only found in embryos and in ovules making them difficult to harvest

And if you know me, and you know where I'm going with this. In 2013, while scientists where trying to discover how leprosy, an inmobile bacteria, they stumbled upon (and I quote from them) "biological alchemy" for it turns out, leprosy can reverse cells states in other words, leprosy can turn cells into stem cells, which in turn it manipulates to become muscle/bone cells, these new cells then move to their respective tissues, carrying leprosy with them

Which is like, insane? We discovered that other bacteria such as H. pylori can also do something similar, but how cool is that?? It's been 11 years though, researchers have been trying to understand how it can convert them to further be able to cure neurological diseases soon like Alzheimer and Parkinson

[thesilliestrovingalive]

Updated: January 1, 2025

Reworked Character #13: Allen O'Neil

POTENTIAL TRIGGER WARNING: Viewer discretion is advised due to references to death, drug addiction, crime, and torture.

Real name: Alister Titus O’Neil Sr.

Esper title: Avatar of Peak Physicality, Cheating Death, and Assimilation

Aliases: Conqueror of the Staircase of Dead Bodies, Iron Cavalryman from Hell, Immortal Cacodemon, and Ghost Sergeant

Occupation: Sergeant of the Rebel Army, right-hand man of General Morden, Lance Corporal of the Marine Corps (formerly), and a high-ranking peacekeeping troop of the Regular Army (formerly)

Retirement plans: Open up an animal shelter and live the rest of his days in the countryside

Special skills: Armed and close quarters combat, crisis management, defensive tactics, and brainwashing

Esper abilities: He possesses superhuman strength, endurance, and stamina, demonstrated by his ability to effortlessly lift the main combat vehicles of the Rebel Army, withstand extreme physical stress, and carry the Jupiter King without its tracks without displaying any visible signs of exhaustion. His body is physically resilient to shotgun blasts and a single grenade or pipe bomb explosion. His body contains a silver-hued regenerative agent that rapidly repairs damaged cells and tissues, giving his blood a metallic grey sheen. When wrath consumes him, his skin erupts into a fiery crimson, radiating intense heat and morphing into a semi-scaly texture.

He possesses two unique, blubber-coated, kidney-shaped organs in his thighs, which are a pale pink streaked with bronze. These organs are connected to his esophagus by two trachea-like purplish-grey tubes. The kidney-shaped organs secrete a blood-streaked, sticky substance similar to intravascular and seminal fluids that gives birth to earwig-like pale brown creatures, approximately the length of a human arm. Each creature features bronze and crimson streaks, forest green antennae, and black centipede-like legs and forceps. The trachea-like tubes are lined with resilient, mucus-coated hair follicles, providing the creatures with a moderate layer of protection against blades and enhancing their ability to adhere to hosts.

These creatures serve as vectors for mental assimilation, allowing him to recruit individuals to General Morden’s cause. To achieve this, they inject neuroactive agents into a host's bloodstream by biting into a major vein and tightly latching onto their skin. Once established, the creatures transmit electrical signals to the brain, inducing brainwashing and instilling an unwavering sense of loyalty. This can only be reserved once the parasitic creature has been surgically removed, allowing the effects of these neuroactive agents to degrade slowly over a five-day period.

He's virtually immortal due to a biological self-resurrection process, which allows him to fully restore his psyche and physical body to optimal health. Upon death, his regenerative agents kick into overdrive, rapidly repairing minor and major wounds, replenishing energy in his blood, and revitalising his white blood cells to sustain their viability. His brain remains active, sending electrical impulses that stimulate cellular regeneration, tissue reorganisation, maintain blood circulation, reverse organ failure, and induce wakefulness. It can even correct genetic damage, reactivate dormant cellular functions through epigenetic reprogramming, reboot the immune system to eliminate pathogens and cancer cells, and restore cognitive function and memory. After each resurrection, his memories of his previous death are foggy, and his once-healed injuries leave lingering stiffness for a few days.

Hobbies: Whittling, extreme off-roading, frequenting pet shops, and hanging out with his family whenever he has the time to do so

Likes: Social justice, blowing stuff up, insulting his adversaries, and messing around with the Rebel Gigant

Dislikes: Ridicule directed at him, his family, General Morden, and the Armitage twins, being viewed as weak, the Regular Army, and insubordination

Favourite food: Pompano en papillote and bread pudding with vanilla whiskey sauce

Favourite drink: Cognac

Sexuality: Heterosexual

Gender: Male

Age: 38 (in 2022), 44 (in 2028), 46 (in 2030), 48 (in 2032), 50 (in 2034), 57 (in 2041), 59 (in 2043), 60 (in 2044), and 63 (in 2047)

Blood type: B+

Weight: 254 lbs. (115 kg)

Design: He’s a 6’ 7” (200.66 cm) American mesomorph of Creole and Scottish descent with an inverted triangle build, rippling muscles, and sloping shoulders. He has honey-hued skin and striking asymmetrical eyes—amber on the right with a luxor gold pupil and mahogany on the left with a foggy white glaze. His face features subtle wrinkles, including forehead lines, frown lines, and nasolabial folds. Allen has pointed ears that droop slightly, razor-sharp canines, a shaved head, and a full dark chocolate beard.

He has a tattoo on his left upper arm of a pygmy rattlesnake coiled around the base of a human skull with sparkling rubies embedded in the eye sockets. He has a few battle scars: one that starts from the centre of his right cheek to the side of his forehead, resembling a fiery comet flying upwards; three healed bullet wounds on his left deltoid; half of his left ring finger is missing; and a large, blotchy patch of scarred flesh on the right side of his abdomen.

His outfit consists of gunmetal grey wristbands, a burnt sienna armband displaying the Rebel Army insignia, and mud- and blood-stained laurel green army cargo pants tucked into spike-soled silver-white combat boots. He carries an old, cherished photograph of himself, his wife, their two children, and their two chestnut-fronted macaws securely tucked away in the right pocket of his army cargo pants. Allen wears a gold-buckled rifle green belt, complemented by a sheath for his Bowie knife and a gunmetal grey waist pack secured at the back, containing pipe bombs and a sprig of heather for good luck. He wears three black bandoliers, two forming an X-shape across his chest and one draped above his belt, holding ammunition for his M240 Bravo Machine Gun. He wears a burgundy cord necklace, showcasing a shark tooth as its centrepiece. The shark tooth is flanked by two canine teeth with three circular blue garnet beads positioned between each canine tooth.

He owns a personal Di-Cokka, twice the size of the original, its greenish-brown coat bearing battle scars—dented and scratched from a few bullet impacts. Besides transportation, he also uses it for storage, keeping portable ammo boxes and two extra weapons on hand: a M202 FLASH and a Mossberg 500 shotgun.

Super Devil form: He’s a 21’ 3” (647.7 cm) humanoid with an exaggerated musculature and smooth, rock hard rifle green skin. His head, marked by a pronounced underbite, has a canine-like appearance, with the skin tightly stretched over his skull. A wet gunmetal grey nose, reminiscent of a bear's, protrudes prominently, while his beard has grown into an unruly goatee that cascades down to the centre of his chest. He has twitching muscles, gleaming golden claws and talons, and six arms covered in decaying flesh and bulging veins, each ending in heavily scarred hands with only three fingers. He has the same eyes, ears, razor-sharp canines, and scars as the original, but his armpits and back are covered in coarse dark chocolate hair.

Two rows of stalagmite-like ruby red spikes run along his back, while two lengthy, glistening tentacles—each spanning the height of two adult males—protrude from the back of his deltoids. These tentacles boast a blue garnet hue and are adorned with mucus-coated, laurel green feelers on their underside. Allen’s tail is that of a pygmy rattlesnake, while his waist is encircled by partially protruding yellow-stained, shark-toothed human skulls with an alternating pattern of ruby and blue garnet eyes. His legs are feathered in a plumage that transitions from reddish-brown to burnt sienna, culminating in powerful silver-white ostrich feet.

Character summary: Allen is a proud and charismatic leader, renowned for his persistence in battle and unshakeable loyalty to those he holds dear, including his family, closest comrades, and General Morden. He passionately advocates against political corruption and systemic injustices, fearlessly standing up for what's right and recognizing it as his social responsibility to create a better world. He’s capable of compassion, but only extends his support, kindness, and sympathy to those he considers trustworthy friends and admires for their bravery and integrity. He can be somewhat forgetful, particularly when recalling complex instructions or distinguishing between appropriate and inappropriate times to use bladed weapons, such as when preparing food.

He derives great satisfaction from catching his foes off guard or disrupting their plans, gaining a strategic upper hand on the battlefield. He's ruthless and pragmatic, revelling in the suffering he inflicts on those who work for corrupt organisations and/or oppose General Morden. He relishes battling his enemies, particularly his arch-rivals, the Peregrine Falcons Squad and the S.P.A.R.R.O.W.S. His passion for frontline combat is why he chooses to remain a Sergeant, the highest rank that allows him to engage in daily battles. He displays subtle admiration for individuals who demonstrate impressive tactical expertise and skillful combat abilities.

He often rushes into battle with reckless abandon, yet occasionally takes a more measured and calculated approach. He frequently taunts his enemies, using psychological warfare to erode their resolve and sow seeds of self-doubt. He skillfully cultivates loyalty among Morden's followers by subtly undermining their critical thinking and independence, making them receptive to indoctrination. Through this manipulation, Allen implants new thoughts, reshapes attitudes, and alters values and beliefs to align with Morden's ideology. Occasionally, he spares new recruits from brainwashing if he detects genuine sympathy for Morden's cause or notices that they don't see the point in questioning the ideology and practices of the Rebel Army.

He strongly dislikes it when people underestimate his intelligence and make jokes about him having "stupid genes". When mocked for his lack of sophistication, he's quick to retaliate, scolding those who underestimate him, and will even resort to violence or intimidation if he feels provoked. Despite being a belligerent and ignorant individual, he can be surprisingly calm and composed during the heat of battle or when he isn't on the battlefield. He never fears his enemies due to a fear of being seen as a coward, but he will show prudent caution if there's a genuine reason to be concerned. He has always had a fondness for winter and working in snowy conditions, drawn to the cleanness of fresh snow and the challenge of battling through bitter cold, which he sees as a worthy obstacle to overcome during intense combat.

His phenomenal physicality and combat skills are matched only by the size of his ego, as he frequently disparages those he doesn’t trust and makes crass, demoralising, and dehumanising remarks about his adversaries. While Allen’s superiority complex often gets the better of him, he’s an adept soldier who can endure more physical and mental punishment than his weaker comrades. However, he doesn’t view himself as superior to his family, close friends, most trusted comrades, General Morden, and the law. Besides his strength, stubbornness, and gusty courage, the only thing that keeps him alive is his devotion and unrelenting will to return home to his loving wife, Henrietta, and their children, Nancy and Allen Jr.

He deeply loves Henrietta and cherishes every moment with her, yet he can't help but find her intimidating due to her stern demeanour and piercing gaze. He loves Allen Jr. deeply, but their relationship is strained by his son's blunt criticism of his shortcomings and, more painfully, his alliance with the Rebel Army's sworn enemy. He recognizes that Allen Jr. views his actions as morally misguided, driven by an unwavering loyalty to General Morden. Additionally, he's aware that his son is troubled by his own superiority complex and impulsive decisions on the battlefield, which have repeatedly put his life at risk and led to past fatalities. Nevertheless, he does his best to support his son's military career and love life, while also respecting his capabilities as a fighter. He does notice that Allen Jr. doesn’t listen to him at times, which frustrates him. However, he chooses not to verbally address the issue, fearing it may further strain their already estranged relationship.

He shares a cordial relationship with General Morden, often bonding over drinks and swapping stories, especially after missions. Beneath Morden's tough exterior, he recognizes his struggles with alcoholism and the emotional toll of losing his family, and genuinely empathises with him. He looks up to him as a great leader due to his caring and respectful nature towards his soldiers, exceptional intelligence, and strong sense of justice. He vows to protect him at all costs, support the growth of his military strength, and ensure the success of his plans. He finds it amusing how General Morden skillfully exploited Madoka's vulnerabilities, leveraging her unwavering loyalty to her younger sister, Rumi, and the Regular Army, to recruit her as a double agent.

He’s a good friend of Sagan, admiring her independence, resilience, and exceptional leadership abilities, which rival General Morden's in terms of tactical expertise and charisma. He treats her with the same respect he has for Morden, acknowledging her superior military rank and significant contributions to the Rebel Army's tactical prowess. He often goes out drinking with Sagan, assists her with her plans, helps implement her rigorous training programs for Rebel Army cadets, and playfully engages with her joking attitude.

He views Logan as somewhat infuriating and intimidating at times, yet treats him with equal respect alongside Sagan and Morden, recognizing his senior rank and crucial role in the Rebel Army's strategic planning and financial management. He admires Logan's easy-going attitude and willingness to offer him valuable advice on navigating more difficult tactical situations.

Backstory: Alister Titus O’Neil Sr. was born on November 17, 1984 in New Orleans, Louisiana, United States. He doesn’t remember his parents very well, as he didn’t spend much time with them, but he can recall his father being an Scottish-American chef and his Creole mother working as a construction worker. His parents instilled in him the importance of loyalty to loved ones and friends as well as the confidence to embrace his unique capabilities without shame. Tragically, at just 7 years old, his world was shattered when his mother was killed during a devastating robbery at a local convenience store. The loss proved too much for his father, who abandoned him, leaving him alone and frightened in a neighbourhood plagued by crime and bad influences.

Luckily for him, he was taken in by his uncle who, despite struggling with a fentanyl addiction and deep-seated feelings about systemic injustices, selflessly took him in. His uncle went above and beyond to raise him like the son he never had, teaching him essential school subjects and instilling in him a strong sense of social responsibility and courage to stand up against injustices. After his uncle's tragic death from a fentanyl overdose when Allen was just 13, he faced a harsh new reality and this pivotal event awakened his esper abilities. With no support system, he turned to a local gang for protection and began carrying blades for self-defence. As he gained more experience on the streets and honed his fighting skills, he gradually moved to firearms, progressively handling smaller weapons before moving on to larger ones. Following his revelation dream at 15, he dedicated himself to mastering his esper abilities.

At 16, Allen faced legal consequences for aggravated assault and burglary, leading to time in a juvenile detention centre. The Regular Army, recognizing his esper status, quickly intervened and offered guidance, aiming to mould him into a skilled soldier. The Regular Army offered him a stable home in a secure area of Scotland, aiming to provide a safer environment that would steer him away from a life of crime. With their therapeutic and parental support, he made a decision to turn his life around. Allen volunteered for social justice initiatives and animal welfare organisations to improve himself and give back to the community.

At 19, while working at an animal shelter, he met his future wife, Henrietta. A brief conversation about their future aspirations sparked a romance between them. As they went on multiple dates, their connection grew stronger. A year later, Allen proposed, and to his delight, she accepted. Soon after getting married, they welcomed their son, Allen Jr. Upon discovering a recruitment poster for the Regular Army, he felt a surge of purpose and a strong desire to fight for justice. This newfound passion prompted him to quit his old job and enlist in the Regular Army as a peacekeeping troop at the age of 22. After serving five years, he transitioned to the Marine Corps. Two days before his 30th birthday, he and Henrietta celebrated the birth of their daughter, Nancy. Their family grew again four years later with the adoption of two chestnut-fronted macaws, Shirley and Kingsley.

Allen's life took a dramatic turn when Donald Morden rescued him from a near-fatal confrontation with a notorious gang of terrorists and high-risk criminals, who had collaborated with pirates, in a volatile region of South Africa. Grateful for Morden's heroism, he offered his support and loyalty, forming a strong bond as a trusted friend and ally. A year later, following a successful mission against a dangerous criminal organisation bent on destabilising government authorities, Morden introduced Allen to Sagan and Logan. He formed strong bonds with Sagan and Logan, but their demanding schedules rarely allowed for downtime together.

He rose through the ranks to become a high-ranking peacekeeping troop in the Regular Army under Donald Morden's command, while also serving as a Lance Corporal in the Marine Corps. Renowned for his exceptional combat skills, toughness, and devotion to family, he was once known for his cool attitude. As Morden's most trusted soldier and the only esper under his command, he frequently received the most complex missions, which he executed with great success and enthusiasm. He always enjoyed fighting for Morden, just as he enjoyed unwinding with Henrietta, Nancy, and Allen Jr. after a tough day.

He played a crucial role in the Arms Deal Barrage, fighting as a soldier against the remnants of the Serapion Fellowship. Alongside fellow combatants, including Morden, Sagan, and Logan, he discovered the harsh reality of corruption within the Regular Army, a truth carefully concealed from the public. A small part of him yearned to defy them for their corruption, but Morden and Tequila cautioned against it, warning he'd land on their hit list. He faced off against 1st Lieutenant Wired in a fierce battle, alone and unsupported, yet he developed a hint of mutual respect for his opponent's tactical prowess and proficiency in grenades and armed combat.

After Morden defected from the Regular Army, Allen followed him out of loyalty and disappeared from public view for several years. During this period, Allen played a crucial role in building the Rebel Army's forces by brainwashing and training new recruits alongside Morden. He also contributed to the development of tactical plans with Logan and Morden and collaborated with Sagan on clandestine missions to raid weapon facilities and acquire advanced Tuatha Dé Danann technology.

When General Morden reemerged as the founding leader of the Rebel Army and launched his coup d'état, he stood by him, playing a pivotal role in the insurgency. Tasked with defending the supply warehouse at the summit of Käthehirt Valley, Allen single-handedly annihilated the troops brave enough to tackle the treacherous mountain. However, when Marco, Tarma, Tequila, Gimlet, and Red Eye ascended the mountain, they encountered Allen and were forced to engage him in battle. Gimlet and Red Eye managed to press onward, choosing to confront the Rebel Infantry instead of fighting their former comrade. After being burned alive and shot in the head for good measure, Allen was presumed dead.

Nevertheless, he would later be revived through his biological self-resurrection process and participate in the ambush on the Regular Army, Peregrine Falcons Squad, and S.P.A.R.R.O.W.S. troops. Under Morden's command, he brutally tortured and executed many of Marco’s and Tarma's comrades and friends. He played a major role in Tarma's torture, verbally exploiting his emotional sensitivity and insecurities about his academic intelligence. He also carried out General Morden's order to sever Marco's left arm.

Allen resurfaced in a secret Rebel Army base hidden in the Siberian frozen tundra, where he once again aided Morden in his plans for global conquest, this time in alliance with the Pipovulaj. When Regular Army troops infiltrated the base, Allen attempted to eliminate them but was ultimately defeated by Marco, Eri, Tarma, and Fio. In the heat of combat, Allen unleashed a ferocious strike, brutally severing Tarma's right forearm. His lifeless body plummeted down a snowy cliff and was devoured by a giant orca. However, Pipovulaj troops recovered his newly resurrected remains after Marco's team departed to confront General Morden.

After the Extraterrestrial Alliance Clash, Allen, Sagan, Logan, and some Rebel Infantry and cadets, along with a few Morden sympathisers, hatched a plan for a revenge attack on the South Pacific training island owned by the Peregrine Falcons Squad. Their aim was to install and house the earthquake-causing weapon, the Cabracan, which was jointly built by the Rebel Army, Pipovulaj, and Amadeus Syndicate, in their new base. This was necessary as their previous bases had been raided.

To achieve this, Allen and Sagan disguised themselves as drill instructors and led a group of Regular Army and Peregrine Falcons Squad cadets to a remote island in the South Pacific. Unbeknownst to the cadets, Allen had secretly brainwashed them, implanting a false sense of security and focusing their minds solely on training. Their sinister intention was to use the cadets and any Intelligence Agency agents on the island as hostages and test subjects for the experimental simian and mantis transformation serums developed by Doctor Amadeus.

Once Division 6 and the uncaptured cadets infiltrated the main base, he and his platoon of land troops would engage in a fierce clash with Allen Jr., Walter, and Dilovar. He would discover that his son had joined the archenemy of the Rebel Army, a revelation that had been previously kept secret from him. He felt a deep sense of betrayal, but he knew it would be rash to turn on his son simply because of their differing allegiances. With a heavy heart, he accepted the fact that Allen Jr. had chosen to serve the Regular Army, and it seemed unlikely that he would ever switch sides. Before he could retreat with his surviving soldiers, Walter and Dilovar took his life in a furious act of retribution for their fallen comrades. Fortunately, Sagan was able to recover his body, which was undergoing a biological self-resurrection process.

[circumlocutive]

My Adderall is hitting and I just wanna shit this text post out before I start work.

I don't think there's a practical point to this kind of navel gazing at this stage in my life, and really it's more of a symptom of an issue in psychiatry with labeling phenotypic categories that don't have much correlation to biochemical mechanisms. But. I do still wonder about whether my avolition and related executive dysfunction/motivation crisis is " better " characterized as a CPTSD thing than an ADHD thing. And whether that should play a role in my expectations for functioning.

Like functionally I'm still going to treat my symptoms the same either way (it doesn't respond to CBT, DBT, or a few diff antidepressants, but does respond adequately [if inconsistently] to stimulants), so from a pragmatic angle fussing over which label is better is not useful to me. It's mostly identity wanking - unless the labels can implicate something actionable, all they really seem to do is saddle you with their sociocultural baggage.

I'd say I have evidence suggesting a genetic predisposition to ADHD traits (which I generally conceptualize based on handling in the broader psych literature as an innate/biological/"nature" [as in nature vs nurture] based thing, like the impairments are there whether or not the environment is good or bad though of course environment influences the final result). My dad is very ADHD and was long before he was a combat veteran if you listen to stories from his family, my dad was adopted bc he had a teen mom so highly likely she had something up too, and my brother is so textbook autism (and autism and ADHD genes run around skipping hand in hand) (stimulant side note these are not definitive scientific correlations I'm making here, autism looking presentation could be related to my brother being abused too and having far less social support, could be related to my mother's psychotic lineage [autism and schizo/bipolar/psychotic spec genes also run around skipping hand in hand], could be a lot of shit).

On the other hand, it is so obvious I have CPTSD (which I conceptualize as a nurture based, acquired dysfunction that does also alter your "nature" in the sense it affects your genetic expression. But while trauma will change your innate biochemical settings, I see the biggest distinction from ADHD in that cptsd wouldn't manifest without external initiation). In the narrative of my life, my current difficulty with motivation makes more sense as. Well. Something to do with living in constant fear for my life in my developmental period. How can I find anything as compelling or salient as preserving my life against a direct, explicit, and omnipresent threat. How am I supposed to give a fuck about tasks if no one is breaking plates over my head about them or depriving me of food and shelter. My whole risk reward system calibration is fuuuucked.

Realistically, I have issues with emotional regulation/motivation/self care because of the combination. I probably do have congenital neurological differences inherited from my parents, and then the extreme circumstances of my youth made for maladaptive neurological conditioning (think in the firing/electrical circuitry) + hormonal release + epigenetic changes + downstream effects that further stunted my prefrontal cortex and amygdala and striatum and whatever structures associated with emotion and reward. Some of the conditioning may be reversible with therapy/safe life experiences but the baseline performance won't be adjusted without biochemical intervention. Maybe that should play a role in setting my expectations for my performance and "improvement" over time.

Idk I have more feelings about labels and the ways they change our perception of the bio phenomena underlying "mental illness" and the self, but I need to do work instead of wasting hours getting the words out and refining them

[didanawisgi]

Abstract

Therapeutic applications of synthetic mRNA were proposed more than 30 years ago, and are currently the basis of one of the vaccine platforms used at a massive scale as part of the public health strategy to get COVID-19 under control. To date, there are no published studies on the biodistribution, cellular uptake, endosomal escape, translation rates, functional half-life and inactivation kinetics of synthetic mRNA, rates and duration of vaccine-induced antigen expression in different cell types. Furthermore, despite the assumption that there is no possibility of genomic integration of therapeutic synthetic mRNA, only one recent study has examined interactions between vaccine mRNA and the genome of transfected cells, and reported that an endogenous retrotransposon, LINE-1 is unsilenced following mRNA entry to the cell, leading to reverse transcription of full length vaccine mRNA sequences, and nuclear entry. This finding should be a major safety concern, given the possibility of synthetic mRNA-driven epigenetic and genomic modifications arising. We propose that in susceptible individuals, cytosolic clearance of nucleotide modified synthetic (nms-mRNAs) is impeded. Sustained presence of nms-mRNA in the cytoplasm deregulates and activates endogenous transposable elements (TEs), causing some of the mRNA copies to be reverse transcribed. The cytosolic accumulation of the nms-mRNA and the reverse transcribed cDNA molecules activates RNA and DNA sensory pathways. Their concurrent activation initiates a synchronized innate response against non-self nucleic acids, prompting type-I interferon and pro-inflammatory cytokine production which, if unregulated, leads to autoinflammatory and autoimmune conditions, while activated TEs increase the risk of insertional mutagenesis of the reverse transcribed molecules, which can disrupt coding regions, enhance the risk of mutations in tumour suppressor genes, and lead to sustained DNA damage. Susceptible individuals would then expectedly have an increased risk of DNA damage, chronic autoinflammation, autoimmunity and cancer. In light of the current mass administration of nms-mRNA vaccines, it is essential and urgent to fully understand the intracellular cascades initiated by cellular uptake of synthetic mRNA and the consequences of these molecular events.

[jackoshadows]

Loss of epigenetic information as a cause of mammalian aging

Scientists have reached a key milestone in learning how to reverse aging

Highlights:

Cellular responses to double-stranded DNA breaks erode the epigenetic landscape

This loss of epigenetic information accelerates the hallmarks of aging

These changes are reversible by epigenetic reprogramming

By manipulating the epigenome, aging can be driven forward and backward.

Study:

All living things experience an increase in entropy, manifested as a loss of genetic and epigenetic information. In yeast, epigenetic information is lost over time due to the relocalization of chromatin-modifying proteins to DNA breaks, causing cells to lose their identity, a hallmark of yeast aging. Using a system called "ICE" (inducible changes to the epigenome), we find that the act of faithful DNA repair advances aging at physiological, cognitive, and molecular levels, including erosion of the epigenetic landscape, cellular exdifferentiation, senescence, and advancement of the DNA methylation clock, which can be reversed by OSK-mediated rejuvenation. These data are consistent with the information theory of aging, which states that a loss of epigenetic information is a reversible cause of aging.

Summary:

In the Cell paper, Sinclair and his team report that not only can they age mice on an accelerated timeline, but they can also reverse the effects of that aging and restore some of the biological signs of youthfulness to the animals. That reversibility makes a strong case for the fact that the main drivers of aging aren't mutations to the DNA, but miscues in the epigenetic instructions that somehow go awry." ...

In the mice, he and his team developed a way to reboot cells to restart the backup copy of epigenetic instructions, essentially erasing the corrupted signals that put the cells on the path toward aging. They mimicked the effects of aging on the epigenome by introducing breaks in the DNA of young mice." ... "The rebooting came in the form of a gene therapy involving three genes that instruct cells to reprogram themselves—in the case of the mice, the instructions guided the cells to restart the epigenetic changes that defined their identity as, for example, kidney and skin cells, two cell types that are prone to the effects of aging." ... "That could mean that a host of diseases—including chronic conditions such as heart disease and even neurodegenerative disorders like Alzheimer's—could be treated in large part by reversing the aging process that leads to them." ... "We haven't found a cell type yet that we can't age forward and backward...Now, when I see an older person, I don't look at them as old, I just look at them as someone whose system needs to be rebooted."

[hyperadvancedbiotechnology]

Introducing Creative Society: A Glimpse into Hyper Advanced Body Regeneration Biotechnology

Creative Society is a global project that aims to develop a society where the potential and creativity of every individual is paramount. The group has supporters in more than 100 countries and organizes online events to discuss the concept and model of the creative society in all spheres of human life.

Creative Society has unveiled a video that exhibits a prospective sophisticated biotechnology, which would enable individuals to customize their physical traits.

This biotechnology technology would offer users many options and autonomy over their body, such as eliminating fat, enhancing muscle mass, and optimizing bones and ligaments. The video illustrates how the technology could significantly prolong life span and preserve the user’s body in a robust and youthful state. You can view a comprehensive demonstration of this technology by following the link provided below.

Creative Society vision is to develop a holistic care system that would enable users worldwide to personalize their preferences and access them from anywhere in the world. Additionally, the technology could abolish diseases, without any detrimental impacts while also significantly extending lifespan.

One of the most promising applications of biotechnology in general is on the subject of anti-aging, which aims to stop or reverse the aging process by targeting its underlying molecular mechanisms. Aging is associated with various epigenetic changes that alter gene expression and cellular function over time. By using techniques such as partial reprogramming with Yamanaka factors, researchers hope to reset the epigenetic clock and rejuvenate cells and tissues . Other approaches include using CRISPR gene editing to correct mutations that accumulate with age, or using senolytics to eliminate senescent cells that contribute to inflammation and tissue damage. These anti-aging therapies could potentially and significantly extend human lifespan.

The following five scientific studies exemplify the feasibility and actuality of reversing human aging through various interventions.

(1) Biological age of humans reversed by years in groundbreaking study .... https://www.independent.co.uk/news/science/biological-clock-ageing-turn-back-reverse-study-new-a9094261.html. (2) The ‘Benjamin Button’ effect: Scientists can reverse aging in ... - CNN. https://www.cnn.com/2022/06/02/health/reverse-aging-life-itself-scn-wellness/index.html. (3) Scientist Discovers Aging Clock to Speed and Reverse Aging | Time. https://time.com/6246864/reverse-aging-scientists-discover-milestone/. (4) Anti-Ageing Research: Ageing in Human Cells Reversed 30 Years in New .... https://www.bloomberg.com/news/articles/2022-04-07/researchers-reverse-ageing-in-human-cells-by-30-years-study. (5) Reverse Aging: Study Finds Hyperbaric Oxygen Chamber Slows Aging. https://www.popularmechanics.com/science/health/a34730692/study-reverse-aging-in-humans/.

Furthermore there is abundant scientific evidence that validates the idea that biotechnology can facilitate fat reduction, muscle augmentation, and bone and ligament reinforcement. However, these interventions are not as efficacious or convenient as the ones Creative Society has envisioned for the future. You can access the links to some of the research papers that substantiate this idea below:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6279907/

2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016236/

3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804956/

4. https://www.mdpi.com/2304-8158/12/6/1218

If you're keen on delving deeper into Creative Society and their mission to bring about a better future, you can visit their official website at https://creativesociety.com/, where you can also participate in their online events and contribute your own ideas. By joining forces, we can use biotechnology and creativity to mold the future according to our aspirations.

I trust that you found this article insightful and gained fresh knowledge about the vast potential of biotechnology. To acquire further information about the potential of biotechnology, I recommend watching the video that presents Creative Society's vision for future biotechnology at

Article by Michael Wichkoski

#regenerationcapsule #creativesociety #biotechnology #michaelwichkoski

[xtruss]

Scientists Have Reached a Key Milestone in Learning How to Reverse Aging

— Time Magazine | January 12, 2023 | By Alice Park

Tim Flach Photography ltd—Getty Images

It’s been 13 years in the making, but Dr. David Sinclair and his colleagues have finally answered the question of what drives aging. In a study published Jan. 12 in Cell, Sinclair, a professor of genetics and co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School, describes a groundbreaking aging clock that can speed up or reverse the aging of cells.

Scientists studying aging have debated what drives the process of senescence in cells—and primarily focused on mutations in DNA that can, over time, mess up a cell’s normal operations and trigger the process of cell death. But that theory wasn’t supported by the fact that older people’s cells often were not riddled with mutations, and that animals or people harboring a higher burden of mutated cells don’t seem to age prematurely.

Sinclair therefore focused on another part of the genome, called the epigenome. Since all cells have the same DNA blueprint, the epigenome is what makes skin cells turn into skin cells and brain cells into brain cells. It does this by providing different instructions to different cells for which genes to turn on, and which to keep silent. Epigenetics is similar to the instructions dressmakers rely on from patterns to create shirts, pants, or jackets. The starting fabric is the same, but the pattern determines what shape and function the final article of clothing takes. With cells, the epigenetic instructions lead to cells with different physical structures and functions in a process called differentiation.

In the Cell paper, Sinclair and his team report that not only can they age mice on an accelerated timeline, but they can also reverse the effects of that aging and restore some of the biological signs of youthfulness to the animals. That reversibility makes a strong case for the fact that the main drivers of aging aren’t mutations to the DNA, but miscues in the epigenetic instructions that somehow go awry. Sinclair has long proposed that aging is the result of losing critical instructions that cells need to continue functioning, in what he calls the Information Theory of Aging. “Underlying aging is information that is lost in cells, not just the accumulation of damage,” he says. “That’s a paradigm shift in how to think about aging. “

His latest results seem to support that theory. It’s similar to the way software programs operate off hardware, but sometimes become corrupt and need a reboot, says Sinclair. “If the cause of aging was because a cell became full of mutations, then age reversal would not be possible,” he says. “But by showing that we can reverse the aging process, that shows that the system is intact, that there is a backup copy and the software needs to be rebooted.”

In the mice, he and his team developed a way to reboot cells to restart the backup copy of epigenetic instructions, essentially erasing the corrupted signals that put the cells on the path toward aging. They mimicked the effects of aging on the epigenome by introducing breaks in the DNA of young mice. (Outside of the lab, epigenetic changes can be driven by a number of things, including smoking, exposure to pollution and chemicals.) Once “aged” in this way, within a matter of weeks Sinclair saw that the mice began to show signs of older age—including grey fur, lower body weight despite unaltered diet, reduced activity, and increased frailty.

The rebooting came in the form of a gene therapy involving three genes that instruct cells to reprogram themselves—in the case of the mice, the instructions guided the cells to restart the epigenetic changes that defined their identity as, for example, kidney and skin cells, two cell types that are prone to the effects of aging. These genes came from the suite of so-called Yamanaka stem cells factors—a set of four genes that Nobel scientist Shinya Yamanaka in 2006 discovered can turn back the clock on adult cells to their embryonic, stem cell state so they can start their development, or differentiation process, all over again. Sinclair didn’t want to completely erase the cells’ epigenetic history, just reboot it enough to reset the epigenetic instructions. Using three of the four factors turned back the clock about 57%, enough to make the mice youthful again.

“We’re not making stem cells, but turning back the clock so they can regain their identity,” says Sinclair. “I’ve been really surprised by how universally it works. We haven’t found a cell type yet that we can’t age forward and backward.”

Rejuvenating cells in mice is one thing, but will the process work in humans? That’s Sinclair’s next step, and his team is already testing the system in non-human primates. The researchers are attaching a biological switch that would allow them to turn the clock on and off by tying the activation of the reprogramming genes to an antibiotic, doxycycline. Giving the animals doxycycline would start reversing the clock, and stopping the drug would halt the process. Sinclair is currently lab-testing the system with human neurons, skin, and fibroblast cells, which contribute to connective tissue.

In 2020, Sinclair reported that in mice, the process restored vision in older animals; the current results show that the system can apply to not just one tissue or organ, but the entire animal. He anticipates eye diseases will be the first condition used to test this aging reversal in people, since the gene therapy can be injected directly into the eye area.

“We think of the processes behind aging, and diseases related to aging, as irreversible,” says Sinclair. “In the case of the eye, there is the misconception that you need to regrow new nerves. But in some cases the existing cells are just not functioning, so if you reboot them, they are fine. It’s a new way to think about medicine.”

That could mean that a host of diseases—including chronic conditions such as heart disease and even neurodegenerative disorders like Alzheimer’s—could be treated in large part by reversing the aging process that leads to them. Even before that happens, the process could be an important new tool for researchers studying these diseases. In most cases, scientists rely on young animals or tissues to model diseases of aging, which doesn’t always faithfully reproduce the condition of aging. The new system “makes the mice very old rapidly, so we can, for example, make human brain tissue the equivalent off what you would find in a 70 year old and use those in the mouse model to study Alzheimer’s disease that way,” Sinclair says.

Beyond that, the implications of being able to age and rejuvenate tissues, organs, or even entire animals or people are mind-bending. Sinclair has rejuvenated the eye nerves multiple times, which raises the more existential question for bioethicists and society of considering what it would mean to continually rewind the clock on aging.

This study is just the first step in redefining what it means to age, and Sinclair is the first to acknowledge that it raises more questions than answers. “We don’t understand how rejuvenation really works, but we know it works,” he says. “We can use it to rejuvenate parts of the body and hopefully make medicines that will be revolutionary. Now, when I see an older person, I don’t look at them as old, I just look at them as someone whose system needs to be rebooted. It’s no longer a question of if rejuvenation is possible, but a question of when.”

[a-typical]

Scientists Have Reached a Key Milestone in Learning How to Reverse Aging

Loss of epigenetic information as a cause of mammalian aging

Scientists Have Reached a Key Milestone in Learning How to Reverse Aging

Highlights from the Study

Cellular responses to double-stranded DNA breaks erode the epigenetic landscape

This loss of epigenetic information accelerates the hallmarks of aging

These changes are reversible by epigenetic reprogramming

By manipulating the epigenome, aging can be driven forward and backward

“Underlying aging is information that is lost in cells, not just the accumulation of damage,” says Dr. David Sinclair, a professor of genetics and co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School. His latest results seem to support that theory.

All living things experience entropy manifested as a loss of genetic and epigenetic information. Genetic information is the hardware and the epigenome is the software. We think aging is due to corrupted software, that can be rebooted to restore youth.

It’s similar to the way software programs operate off hardware, but sometimes become corrupt and need a reboot. But by showing that we can reverse the aging process, that shows that the system is intact, that there is a backup copy and the software needs to be rebooted.”

In the mice, he and his team developed a way to reboot cells to restart the backup copy of epigenetic instructions, essentially erasing the corrupted signals that put the cells on the path toward aging. They mimicked the effects of aging on the epigenome by introducing breaks in the DNA of young mice. - Once “aged” in this way, within a matter of weeks Sinclair saw that the mice began to show signs of older age—including grey fur, lower body weight despite unaltered diet, reduced activity, and increased frailty.

The rebooting came in the form of a gene therapy involving three genes that instruct cells to reprogram themselves— These genes came from the suite of so-called Yamanaka stem cells factors—a set of four genes that Nobel scientist Shinya Yamanaka in 2006 discovered can turn back the clock on adult cells to their embryonic, stem cell state so they can start their development, or differentiation process, all over again. Sinclair didn’t want to completely erase the cells’ epigenetic history, just reboot it enough to reset the epigenetic instructions. Using three of the four factors turned back the clock about 57%, enough to make the mice youthful again.

Using a system called “ICE” (Inducible Changes to the Epigenome), we show the act of repairing DNA breaks accelerates aging at the physiological, cognitive, & molecular levels, including erosion of the epigenetic landscape, loss of cell identity, senescence & increased epi-age ... "We show these changes can be reversed by OSK-mediated rejuvenation. With an ability to drive aging in both the forward and reverse directions, we conclude that loss of epigenetic information is a cause of aging in mammals."

“We haven’t found a cell type yet that we can’t age forward and backward.”

In 2020, Sinclair reported that in mice, the process restored vision in older animals; the current results show that the system can apply to not just one tissue or organ, but the entire animal. He anticipates eye diseases will be the first condition used to test this aging reversal in people, since the gene therapy can be injected directly into the eye area.

"If correct, it means that cancer, diabetes and Alzheimer's might have the same underlying cause that can be reversed to treat or cure age-related conditions with a single treatment. Experiments in the lab are testing this."

Even before that happens, the process could be an important new tool for researchers studying these diseases.

"The age-reversal technology -- virally-delivered genes (Oct4, Sox2, Klf4, aka, Yamanaka factors), which turn on an embryonic program -- is being tested at @lifebiosciences in non-human primates. Results out in a few months from Bruce Ksander's lab & http://lifebiosciences.com"

[cashewcashew]

i was obsessed with the molecular bio / epigenetics approach to stopping/reversing aging for a bit and unfortunately it likely will not be a thing in any of our lifetimes due to just how much goes into it.

between telomeres and removing stress induced epigenetic stuff and a whole host of other factors, science just doesn’t move THAT quick to make reversing aging a possibility in the next 7-10 decades.

that dental regeneration stuff looks hype though i’m very excited to see that come to fruition since it’s far more feasible with current stem cell tech (assuming legal/ethical barriers don’t hold it back)

[metamediameltdown]

Optimized Neuropsychiatric Drug Development

I also had an insight of how model drug development. It is just modelling the effect of a drug one biological active potential and electric discharge patterns 1on one 4d neuron, then one neuron surrounded moderately abstracted glial cells, then on two neurons surrounded by glial cells, then two neurons surrounded by moderately abstracted glial cells and an abstracted vascular system, then model this progression on each type of neuron. Then model on combinations. Then reduce all of this modelling to black box modules. Then you can model networks of neurons (and ignore the glial cells and vascular flows as their impact on the later models would be accounted for in the black boxes). Similar to the MM SI units. You can then model neurons in a way where the actual distance between them is irrelevant apart from biochemical and electrical synapse based transmission speed.

Of course this doesn't factor in the complexity of epigenetics, mature mRNA, sensitization, tolerance responses, genomic responses, metabolomics, and secondary receptor modulation of medications like sertraline. But it doesn't need to, this data can be approximated from in silico, cortical organoid, or in vivo research and the general signal mathematics is developed enough from what I have pretended to understand.

Then you create models of each brain region and their rough connectivity. Later you can model function and train neural nets on them.

Back to the single neurons. In order to test drugs, you can get the structure of the drug in the case of neuropsychiatric or positive (augmentative) medicine. You can model the binding affinity and and pharmokinetics of extant well modelled drugs and then plug them into the single neurons. If all these models and axiomatic systems is integrated and iteratively synchronized, you can model changes on whole brain activity just based on changing the dose or parameters of drugs/medications. The reverse process is true, or should be. Given physical and energetic systems seem to have time reversible symmetry. You can plug in the desired functionality resulting from brain activity then get GAN or GN neural networks to run through permutations of specific drugs, concentration, dosages, etc to elicit that response. This approach also falls under the scope of a MM0000 system so it should be relatively simple to either target a specific brain region or network or add/remove brain regions for further discrimination.

Then in Clinical phase I trials, the drugs can be administered with regular PET scans of the subjects allowing for visualization of brain region activity to allow for faster iterations of product development and research via oxygenated areas showing elevated or decreased blood flow and by proxy, brain activity compared to a pre trial PET scan of each subject

[healthcaremarketanalysis]

Exploring the Epigenetics Market: Trends, Growth, and Future Prospects

The epigenetics market is gaining significant momentum in the life sciences and healthcare sectors. This field, which studies heritable changes in gene expression without altering the DNA sequence, is instrumental in understanding complex biological processes and diseases. From drug discovery to personalized medicine, epigenetics offers transformative potential, making it a crucial area of research and development.

In this blog, we’ll delve into the key trends, market dynamics, applications, and growth drivers shaping the epigenetics market.

Understanding Epigenetics

Epigenetics refers to modifications on DNA or associated proteins that regulate gene activity without changing the underlying sequence. These modifications include:

DNA Methylation – The addition of methyl groups to DNA, often silencing gene expression.

Histone Modification – Changes in proteins around which DNA is wrapped, affecting gene accessibility.

Non-Coding RNAs – Molecules that influence gene expression post-transcriptionally.

Epigenetic mechanisms are reversible, making them attractive therapeutic targets for diseases like cancer, neurodegenerative disorders, and autoimmune conditions.

Market Overview

Market Size and Growth

The global epigenetics market was valued at approximately $1.4 billion in 2023 and is projected to grow at a CAGR of 15-18% over the next decade. This growth is driven by increasing research in gene therapy, rising cancer prevalence, and advancements in epigenetic technologies.

Key Market Segments

The market can be categorized into the following:

Products:

Reagents

Kits

Instruments (e.g., sequencers, microarrays)

Software

Applications:

Oncology

Developmental Biology

Metabolic Disorders

Neurology

End Users:

Academic Research Institutions

Pharmaceutical and Biotechnology Companies

Contract Research Organizations (CROs)

Drivers of Market Growth

1. Rising Prevalence of Cancer

Cancer is a leading application area for epigenetic research. Abnormal epigenetic modifications are closely linked to tumorigenesis. Epigenetic therapies, such as DNA methylation inhibitors and histone deacetylase (HDAC) inhibitors, are showing promising results in cancer treatment.

2. Advances in Epigenomics Technologies

The development of high-throughput sequencing and microarray platforms has made it possible to study epigenetic changes on a genome-wide scale. Tools like CRISPR-based epigenome editing are expanding research possibilities.

3. Increasing Focus on Personalized Medicine

Epigenetics plays a critical role in tailoring therapies based on individual genetic and epigenetic profiles. This approach is gaining traction, especially in oncology and chronic disease management.

4. Government and Private Funding

Governments worldwide are investing heavily in genomics and epigenetics research. For instance, the National Institutes of Health (NIH) in the U.S. allocates substantial grants for epigenetics projects. Private investments and collaborations are also fueling market growth.

Challenges in the Epigenetics Market

1. High Costs of Research and Equipment

Epigenetic research requires advanced instruments and reagents, which can be cost-prohibitive for smaller organizations.

2. Complexity of Epigenetic Mechanisms

The dynamic and reversible nature of epigenetic changes makes it challenging to pinpoint causal relationships between modifications and diseases.

3. Regulatory and Ethical Issues

Using epigenetic data in personalized medicine raises concerns about data privacy and ethical implications.

Emerging Trends in the Epigenetics Market

1. Integration of AI and Big Data

Artificial Intelligence (AI) and machine learning algorithms are being used to analyze complex epigenomic datasets, accelerating discoveries.

2. Focus on Epitranscriptomics

This subfield studies modifications in RNA rather than DNA, opening new avenues for understanding gene regulation.

3. Development of Epigenetic Biomarkers

Biomarkers are being developed for early diagnosis, prognosis, and treatment monitoring in diseases like cancer, Alzheimer’s, and diabetes.

4. Expansion of Non-Oncology Applications

While oncology dominates the market, epigenetics is increasingly applied in neurodegenerative diseases, cardiovascular disorders, and metabolic syndromes.

Competitive Landscape

Key players in the epigenetics market include:

Illumina, Inc. – Leading in sequencing technologies.

Thermo Fisher Scientific, Inc. – Offering comprehensive epigenetics solutions.

Abcam plc – Specializing in antibodies and kits for epigenetic research.

Qiagen – Providing tools for epigenomic studies.

Merck KGaA – Known for its advanced reagents and inhibitors.

Collaborations, acquisitions, and product launches are common strategies adopted by these players to strengthen their market position.

Applications of Epigenetics

1. Cancer Research and Therapy

Epigenetic drugs are used to reprogram cancer cells, making them more susceptible to traditional therapies.

2. Developmental Biology

Epigenetics helps unravel how environmental factors influence gene expression during development.

3. Neurology

Research in conditions like Alzheimer’s and Parkinson’s diseases focuses on epigenetic mechanisms underlying neuronal dysfunction.

4. Agriculture and Veterinary Science

Epigenetic studies in plants and animals aim to enhance productivity and disease resistance.

Future Prospects

The future of the epigenetics market is promising, with continued advancements in technology and an expanding scope of applications. Personalized medicine and precision oncology are expected to be major growth areas. Moreover, the rise of epigenome editing tools and novel biomarkers will drive innovation in diagnostics and therapeutics.

Conclusion

The epigenetics market represents a dynamic and rapidly evolving field with immense potential to transform healthcare and research. As we continue to uncover the intricacies of the epigenome, the applications of this science will expand, offering solutions to some of the most challenging medical and scientific problems.

For stakeholders, the key to success lies in leveraging technological advancements, fostering collaborations, and addressing ethical challenges. With sustained investment and innovation, epigenetics is poised to become a cornerstone of modern medicine.

[ultrimio]

Persistent Spike Protein Production and Early Mortality: Exploring the Detrimental Impact of Frameshift Mutations in mRNA Vaccines

In the rapidly evolving landscape of mRNA vaccines, understanding the mechanisms underlying persistent spike protein production and potential adverse effects is paramount. Emerging scientific theories suggest that persistent spike protein production, frameshift mutations, and related mechanisms could lead to earlier mortality in some individuals. Here's a comprehensive exploration of these phenomena:

Persistent Spike Protein Production Mechanisms

Integration into the Genome Emerging evidence suggests that mRNA from vaccines could potentially undergo reverse transcription and integrate into the host genome. Although traditional understanding posits that mRNA remains in the cytoplasm, some studies indicate that under specific conditions, integration might occur. This could happen through:

Reverse Transcriptase Presence: Reverse transcriptase enzymes from other infections or cellular sources may facilitate the reverse transcription of vaccine mRNA, resulting in integration into the host DNA. Nuclear Entry: Under certain conditions, such as inflammation or cellular stress, mRNA might gain access to the nucleus.

Epigenetic Modifications mRNA vaccines could potentially induce long-lasting epigenetic changes that sustain spike protein production. This could be due to:

Immune Response-Induced Changes: Prolonged alterations in gene expression patterns could result from vaccine-induced immune responses. Cellular Stress: The stress induced by the vaccine formulation or immune response might lead to epigenetic modifications that continue to drive spike protein production. Histone Modifications and DNA Methylation: Changes in histone acetylation or DNA methylation could result in sustained activation of spike protein-encoding genes.

Viral Reservoirs A proposed mechanism involves the establishment of viral reservoirs in specific tissues, where spike protein production could persist:

Localized Immune Responses: The vaccine may provoke localized immune reactions that lead to sustained spike protein expression in certain tissues. Immune Privilege Sites: Some tissues, such as the central nervous system or reproductive organs, may serve as immune-privileged sites where spike protein production persists due to limited immune surveillance.

Circulating Spike Protein Research has revealed elevated levels of circulating spike protein in individuals experiencing adverse events post-vaccination, such as myocarditis. This phenomenon could be due to:

Inflammatory Responses: Inflammation might prolong the presence of spike protein in the bloodstream. Autoimmune Phenomena: Autoimmune reactions could also contribute to persistent spike protein production.

Potential Dysregulation There are indications that certain immune responses or conditions might lead to continued spike protein production even after mRNA degradation. This dysregulation could result from:

Lipid Nanoparticles: The lipid nanoparticles used in vaccine formulations might trigger inflammatory responses that interfere with the degradation of mRNA. Spike Protein-Host Cell Interactions: Interactions between the spike protein and host cellular machinery could lead to prolonged spike protein production.

Understanding Frameshift Mutations and Their Negative Effects Recent research has highlighted that modifications like 1-methyl-Ψ (1-methylpseudouridine) enhance mRNA stability and efficacy but may also increase the production of frameshifted proteins. Frameshift mutations are known for their detrimental effects, often leading to severe clinical outcomes:

Loss of Function: Frameshift mutations result in premature stop codons, leading to truncated and non-functional proteins. Such mutations can impair essential biological functions, particularly in critical proteins like enzymes or structural proteins. Gain of Toxic Function: In some cases, frameshift mutations produce elongated or misfolded proteins that gain aberrant, toxic functions, contributing to cellular dysfunction. Disease Association: Frameshift mutations are implicated in various genetic disorders and cancers. For instance, they can cause conditions like cystic fibrosis or muscular dystrophy, where normal protein function is disrupted. Cellular Stress and Apoptosis: The production of abnormal proteins can trigger the unfolded protein response (UPR) and endoplasmic reticulum (ER) stress, potentially leading to apoptosis (programmed cell death) or contributing to neurodegenerative diseases. Immune Response to Aberrant Proteins: Mice vaccinated with the BNT162b2 mRNA vaccine (Pfizer-BioNTech) exhibited heightened immune responses against frameshifted products compared to those vaccinated with viral vector vaccines. This immune response to aberrant proteins could have implications for both efficacy and adverse reactions.

Early Mortality Concerns Scientific theories suggest that persistent production of spike proteins, coupled with frameshift mutations, may contribute to increased early mortality among individuals who received doses of mRNA vaccines. This risk could vary depending on dosage and individual body response, particularly due to:

Frameshift Mutations Leading to Dysfunctional Proteins: The production of dysfunctional proteins due to frameshift mutations could result in chronic cellular stress and disease progression.

Persistent Spike Protein Production and Early Mortality Concerns

Persistent Spike Protein Production: Prolonged spike protein production, whether due to genomic integration, viral reservoirs, or epigenetic modifications, could lead to chronic inflammation or autoimmune reactions. This persistent antigenic presence may: Trigger Chronic Inflammation: Continuous immune activation can lead to tissue damage, fibrosis, and organ dysfunction. Induce Autoimmune Reactions: Persistent spike protein expression may break immune tolerance, leading to the development of autoimmune diseases. Frameshift Mutations and Immune Dysregulation: Aberrant Immune Responses: Frameshift mutations could produce neoantigens that the immune system recognizes as foreign, potentially leading to immune-mediated tissue damage. Cytokine Storms: The immune response to persistent spike proteins may result in hyperinflammatory states such as cytokine storms, further contributing to organ damage and earlier mortality. Amplifying Adverse Effects through Frameshift Mutations Increased Production of Aberrant Proteins: 1-Methyl-Ψ Modifications: While enhancing mRNA stability and efficacy, these modifications may also increase the likelihood of frameshift mutations, leading to a higher production of aberrant proteins. Ribosomal Slippage: Errors in reading frames due to ribosomal slippage can exacerbate the production of dysfunctional proteins. Impaired Protein Quality Control: Proteasomal Overload: A surge in aberrant proteins may overwhelm the proteasome, impairing its ability to degrade misfolded proteins. ER Stress and UPR Activation: Accumulation of misfolded proteins in the endoplasmic reticulum can trigger the unfolded protein response, leading to ER stress and apoptosis. Disease Progression and Early Death: Neurodegenerative Diseases: Persistent cellular stress and aberrant protein accumulation are known contributors to neurodegenerative diseases like Alzheimer's and Parkinson's. Cardiac Complications: Chronic inflammation and immune dysregulation can lead to myocarditis, pericarditis, and other cardiac conditions. Cancer Development: Frameshift mutations and immune dysregulation could increase the risk of oncogenesis by promoting genomic instability.

Conclusion While mRNA vaccines represent a remarkable scientific breakthrough, it is crucial to investigate the persistent spike protein production mechanisms and potential frameshift mutations that might contribute to earlier mortality among some individuals. Further research into these mechanisms will be essential for understanding the long-term safety profile of mRNA vaccines and ensuring their safe and effective use in the future.

Long-Term Manifestation of Harmful Effects Given the nature of frameshift mutations and their impact on essential biological functions, harmful effects could manifest or continue to manifest long after initial exposure to mRNA vaccines. Factors that could contribute to long-term adverse outcomes include:

Accumulation of Truncated or Abnormal Proteins: Continuous production of dysfunctional proteins due to frameshift mutations may lead to cumulative cellular damage over time. Persistent Spike Protein Production: Prolonged spike protein production, whether due to genomic integration, viral reservoirs, or epigenetic modifications, could lead to chronic inflammation or autoimmune reactions. This persistent antigenic presence may: Trigger Chronic Inflammation: Continuous immune activation can lead to tissue damage, fibrosis, and organ dysfunction. Induce Autoimmune Reactions: Persistent spike protein expression may break immune tolerance, leading to autoimmune diseases that could manifest years later. Frameshift Mutations Leading to Dysfunctional Proteins: Critical Proteins Affected: Frameshift mutations could impair essential biological functions in critical proteins like enzymes, structural proteins, and those involved in DNA repair and cell cycle regulation. Chronic Cellular Stress: The accumulation of abnormal proteins may cause prolonged ER stress, unfolded protein response (UPR) activation, and programmed cell death (apoptosis). This cellular stress could contribute to neurodegenerative diseases and other chronic conditions. Increased Risk of Neurodegenerative Diseases: Protein Misfolding and Aggregation: Frameshift mutations and persistent spike protein production could lead to the misfolding and aggregation of proteins, which is a hallmark of neurodegenerative diseases like Alzheimer's, Parkinson's, and Huntington's. Neuroinflammation: Sustained immune activation within the central nervous system could exacerbate neuroinflammation, accelerating neurodegeneration. Cardiac Complications: Myocarditis and Pericarditis: Persistent spike protein production may lead to chronic inflammation of the heart muscle (myocarditis) and outer lining (pericarditis), potentially resulting in long-term cardiac complications. Accelerated Atherosclerosis: Chronic inflammation could contribute to the development and progression of atherosclerosis, increasing the risk of cardiovascular events. Oncogenesis and Cancer Development: Genomic Instability: Frameshift mutations in genes involved in DNA repair and cell cycle regulation could lead to genomic instability and an increased risk of cancer. Chronic Inflammation and Cancer: Persistent spike protein production may result in chronic inflammation, which is a known promoter of tumorigenesis. Immune Dysregulation and Autoimmune Diseases: Autoimmune Phenomena: Frameshift mutations in genes regulating immune tolerance could increase susceptibility to autoimmune diseases. Cytokine Storms: Aberrant immune responses due to persistent spike protein production could lead to hyperinflammatory states like cytokine storms, which could have long-term health implications.

[opinionated-opinion]

The Role of Epigenetic Modifications in Gene Regulation: A Critical Review Cellular differentiation, development, and response to various environmental changes all are multistep biological processes that depend fundamentally on gene regulation. Epigenetic modifications allow the cell to respond interactively to environmental changes without altering the DNA sequence and have thus gained increased attention during the last few years. This blog will critically review some of the important epigenetic mechanisms-DNA methylation, histone modifications, and noncoding RNAs-and their involvement in health and disease.

What is Epigenetic? Epigenetics is defined as the study of heritable features concerning the role of gene regulation and not the underlying DNA sequence. These types of modification, usually reversible, have the ability to dynamically alter the expression of a gene by a cell. The epigenetic mechanisms allow cell differentiation in multicellular organisms beginning from the same DNA sequence genome.

Key Mechanisms of Epigenetic Regulation

DNA Methylation

DNA Methylation DNA methylation is one among the well-studied epigenetic mechanisms. It comprises the addition of a methyl group to the cytosine residue in the CpG dinucleotides, usually associated with the silencing of gene expression. Methylation patterns are important in normal development, while abnormal methylation is associated with diseases including cancer. For instance, the hypermethylation of tumor suppressor genes has been related to the inactivation of such genes in many kinds of cancers Esteller 2007.

Histone Modifications

DNA wraps around core histone proteins to form a nucleoprotein called chromatin, and changing the tail domains of the histones affects both the structure of chromatin and gene expression. Acetylation, methylation, phosphorylation, and sumoylation of histones affects the access of DNA to the transcriptional machinery. For example, in general, histone acetylation activates transcription whereas deacetylation causes silencing, Kouzarides 2007.

Non-coding RNAs: ncRNAs Non-coding RNAs, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), also play significant roles in gene regulation. miRNAs can degrade messenger RNA (mRNA) or inhibit translation, thus controlling gene expression post-transcriptionally. lncRNAs, on the other hand, regulate gene expression at various levels, including chromatin modification, transcription, and post-transcriptional processes (Rinn & Chang, 2012).

Critical Review: Epigenetic Changes Are of a Janus Nature Epigenetic modification is an indispensable component in physiological processes but turns out to be a double-edged sword since inappropriate epigenetic change gives rise to diseases like tumorigenesis, neurodegeneration, and autoimmune disease.

Epigenetic Therapies Epigenetic alterations, due to their reversible nature, represent very promising therapeutic targets. Therapeutic drugs like DNA methyltransferase inhibitors (for example, azacitidine) and histone deacetylase inhibitors (for example, vorinostat) are effective in the treatment of some cancers (Jones et al., 2016). However, the main challenges lie in guaranteeing specificity because broad epigenetic reprogramming leads to off-target effects.

Epigenetic and Environmental Influence The epigenome is very sensitive to nutrition, toxicants, and stresses. For example, prenatal exposure to malnutrition results in epigenetic modification, increasing the susceptibility to metabolic diseases later in life (Heijmans et al., 2008). Such sensitivities underline how understanding of epigenetic regulation involves lifestyle factors.

Conclusion:

Epigenetic modifications also play crucial roles in fine-tuning gene expression and the maintenance of cellular homeostasis. While allowing new possibilities of therapeutic intervention, especially in cancer, some problems remain to be investigated concerning specificity and also environmental impact. Further research will thus become necessary regarding the dynamic nature of the epigenome if specific and efficacious treatments are to be developed.

References

Esteller, M. (2007). Epigenetic gene silencing in cancer: The DNA hypermethylome. Human Molecular Genetics, 16(R1), R50–R59.

Heijmans, B. T., Tobi, E. W., Stein, A. D., Putter, H., Blauw, G. J., Susser, E. S., Slagboom, P. E., & Lumey, L. H. (2008). Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proceedings of the National Academy of Sciences, 105(44), 17046-17049.

Jones, P. A., Issa, J. P., & Baylin, S. (2016). Targeting the cancer epigenome for therapy. Nature Reviews Genetics, 17(10), 630–641.

Kouzarides, T. (2007). Chromatin modifications and their function. Cell, 128(4), 693-705.

Rinn, J. L., & Chang, H. Y. (2012). Genome regulation by long noncoding RNAs. Annual Review of Biochemistry, 81, 145-166.