#i know this is just epigenetics but that in itself is so pretty to me

[ohemaa-warrior]

Do you ever think parts of a past life or an ancestral trait shows up in the mundane?

[scripttorture]

I have a character who was a slave but was rescued and freed after about 2 years in slavery and eventually goes on to rescue other people in slavery. While in slavery, he was punished often with denial of food as well as being whipped and beaten when he refused to work. He also had his tongue partially cut out as a punishment. I already have a good idea about the psychological effects he is going to have, but I’m struggling with the physical effects and how long it would take to recover

Part of the answer here depends on this character’s age because while adults can generally make a good recovery from periods of starvation the effects on children (especially young children) are a lot more long lasting.

 The best places to start for the effects of starvation on adults are probably the Minnesota Starvation Experiment and the World Health Organisation (WHO, general link here, 1999 pamphlet on malnutrition in all ages here).

 Recovery is generally pretty quick unless someone’s at the point where they’re near death.

 Refeeding syndrome can be an issue in some cases (especially famine or forced labour camps) but it doesn’t have to be one here. If the character is eating normally (as opposed to being fed by IV for instance) then refeeding syndrome is less likely. My understanding is that this is because the body suppresses appetite during starvation so that it only takes in what it can manage (appetite recovers quickly as the patient regains weight.)

 There’s a detailed NHS guide to refeeding in adult here. It should give you an idea of how at risk your character is and how much food he’ll be able to handle in his first few days of recovery.

 A physical recovery period of around 1-3 months depending on the degree of starvation is reasonable. In this case by ‘recovery’ I mean being able to do normal physical activity, a return to previous healthy weight, or higher weight, return to normal appetite and nutrient levels.

 Recovery can be delayed by additional illness: it’s easier for starving people to contract diseases or infections and it takes longer for them to fight them off.

 There’s also a difference depending on whether you’re talking about a character who is consistently under fed and forced to work versus a character who is usually provided with enough food but sometimes denied food completely/on very reduced rations for periods of a few days. Consistent starvation and malnutrition is much more usual in slavery and… much more likely to be fatal.

 A character that has short periods where food is denied them (no more then two days) and is then allowed to eat as much as they want is probably not going to need hospital supervision/treatment for starvation. If that doesn’t sound like your character then the procedure is usually just to let the person eat as much as they want of whatever they want. The difficulty for people at this sort of stage is more about organising giving out food then it is about keeping doctors on hand to monitor them.

 Now I know less about this but I think there is some evidence that this sort of pattern of intermittent starvation (ie periods where the character is starved, then allowed to eat and this is repeated) can cause some pretty serious health effects. It can also make disordered eating behaviour more likely.

 On a cosmetic level it’s also linked to weight gain.

 Which ever option you’re picturing the following effects are all likely:

loss of muscle mass

lack of coordination

weaker bones

higher chance of hypothermia or heat exhaustion

fainting

poor circulation

higher chances of disease and infections

longer recovery time and more difficult recovery from disease and infections

 A survivor can get to a point where they’re no longer at immediate risk before they’re back to full health. It takes time to recover bone and muscle mass. It takes time for the internal organs to get back to normal. It takes time for enough fat to build up so a person’s body can regulate heat properly.

 There’s also a difference between someone being at peak physical fitness and getting back to average. My understanding is that if someone’s survived significant periods of starvation they’re… unlikely to reach peak physical fitness. If this character was an athlete or a super hero or otherwise had a physically demanding profession, they’re likely to notice a difference even when they’re ‘better’.

 They could improve with time and practice but they may never get back to their prior ability level.

 There’s evidence of epigenetic effects; the children of people who recover from starvation are likely to be shorter then the children of people who have never starved.

 The Minnesota Starvation experiment theorised that after a successful recovery there were few long term effects of starvation. There’s some evidence now that this was an optimistic conclusion but it’s difficult to get a clear picture because of the ethics around studying starvation.

 For young children starvation results in an adult who is:

physically weaker

less intelligent

more prone to illness

less able to fight off illness

has a shorter life expectancy

is physically smaller

 Starvation of children represents a blunting of potential: they will never reach their full strength or intelligence even if they may be stronger/smarter then some individuals. And there is really nothing that can be done to treat that. They needed food over a crucial period and did not receive it. The damage is done and can not currently be treated or healed.

 Beatings over a long period of time and forced labour both have a tendency to cause chronic pain in the joints. Shoulders and knees seem particularly common.

 There are a lot of possible causes for this sort of chronic pain. Ligament and muscle damage s possible. Beatings with objects can cause bone fragments to uh break away and lodge in soft tissues. Soft tissues around joints can be damaged.

 And there are also psychological causes or combinations of both physical damage and psychological causes.

 For instance this is something I saw in an account from a survivor of child abuse. The survivor had been punished using standing stress positions and he found as an adult that he got shooting pains in the backs of his legs while stressed at work. With the help of his doctors he found that when he was stressed he leaned forward on to his toes, mimicking part of the stress position he’d been subjected to as a child. This put more strain on his legs and caused the pain.

 These kinds of responses can be very difficult to stop.

 What I’m trying to illustrate here is that disabling pain is really common in survivors and you don’t necessarily need to know a specific cause for it.

 Chronic pain can cause long term problems to do with mobility and performing everyday activities. Most often it means that survivors need to rest more often, they may have less stamina and they might need to do things in ‘odd’/unusual ways in order to comfortably perform the activity.

 For instance someone with chronic pain in their shoulders might struggle to hang wet clothes on a line that’s above their heads. So they might get in the habit of lowering the clothes line, attaching the clothes and then raising it by pulling on the cord at waist height. They might have trouble moving their shoulder to put on jackets, so they could use their body weight to ‘flip’ the arm joint to the correct position without involving the muscles of the shoulder.

 Someone with knee pain would probably be more particular about the height of chairs in their house. They may stop keeping things in low drawers or shelves.

 Consider where your character might have pain, what activities might make it worse and life style adaptions you can work in to your story.

 These can actually be a great world building/character detail. Especially because healthy people have a tendency to assume these adaptions are eccentricities rather then necessity, prompting conversation between characters.

 There is one part of this scenario that worries me: mutilating the tongue.

 Cutting out tongues is one of those things that comes up a lot in fiction and is generally… less survivable then people assume. Tongues are not just for verbal communication: they’re a pretty essential part of how we swallow food and water, not to mention detecting whether said food/water is edible and they contain a lot of blood vessels. There’s a reason things like tongue splitting and tongue piercing don’t tend to show up as traditional body modification practices.

 The process of partially removing a tongue is life threatening in and of itself. Victims can drown in their own blood. Inflammation can block the airways causing suffocation. Infection can make breathing, eating or drinking impossible (increasing the chance of death from infection.)

 If the victim survives (some definitely did) they’d have trouble eating and drinking for the rest of their lives. This means malnutrition is likely, leading to shorter life expectancies and higher chances of disease (apart from the conditions malnutrition itself causes.)

 It also means recovery from starvation would be significantly longer. Which means a longer period when the character’s more at risk from infection and disease as well as the general uh ‘problems’ starvation causes.

 I’m not saying you’ve created an unsurvivable scenario. We know from history that some people have gone through stuff like this and survived.

 What I’m saying is the survival rate is low. Those survivors (and your character) got lucky.

 Keep that in mind when you write this scenario.

 In terms of long term recovery I honestly have no idea how a removed tongue is treated, I’m not a medic. I can guess at some lifestyle adaptions though.

 Because it makes eating more difficult I think it’s likely a survivors would have smaller meals and more frequent meals rather then large portions that might be cold/unpleasant by the time they’ve finished eating. They’d probably learn to cut their food into smaller pieces and might avoid tougher foods that require more chewing. Their sense of the taste and texture of food would be impaired which might effect their enjoyment of food which could in turn effect their motivation to eat and their recovery.

 Overall I think the take away message here is that while most of the physical long term effects of slavery are not immediately life threatening they have a massive effect on long term quality of life.

 A lot of survivors of modern slavery come out of similar time frames to this disabled by a combination of chronic pain, joint problems and untreated injury or disease.

 One of the recurring themes in Kara’s interviews with slaves is that slavery physically ages people. The combination of extreme distress, physical abuse, overwork, sleep deprivation and malnutrition makes survivors appear much older then they are.

 But the reasons why, the injuries and marks of abuse are often not immediately obvious.

 I hope that helps :)

Available on Wordpress.

Disclaimer

[uncloseted]

So I've had a conversation with a friend, and he was telling me that gay people are not Born gay but become gay because of social experiences and I called that homophobic he got really offended and said he was not that he didn't care if someone is gay or not but it's a fact and a point made by many psychologists that people become gay because of their environment, I said what I found homophobic was the implication it's like a mental disease he said he didn't believe it was a disease but that if you say it's inherent it's like saying it's genetic which it's not and that the same person has different chances of becoming gay according to their family and socio cultural experiences. It did got me thinking, are you aware of such studies and their revelance?

The answer to the question “what makes people gay” is really nuanced and I think probably more complicated than you might have expected.  I’ll get into explaining those nuances the best that I can in a second, but I think the best answer to your friend’s argument is just that he has the correlation and causation backwards.  

People who are raised in environments where being LGBT+ is permissible aren’t more likely to be gay; they’re just more likely to come out of the closet because they know they’ll be accepted and that they won’t be in any danger.  In places where homophobia is rampant, of course there appear to be fewer LGBT+ people- the LGBT+ people who are out in those places are disowned, harassed, bullied, attacked, and sometimes killed.  It makes sense that more LGBT+ people would opt to stay in the closet in a situation where violence is a possibility.  This comes out in the data; although it appears that more gay men live in costal cities in the US, the percentage of internet porn searches for gay male porn are the same across all states, around 5%.

Moving on to the “causes” of homosexuality, it’s likely a lot of different things in combination, and there’s not exactly a scientific consensus just yet.  Male homosexuality may have different causes than female sexuality and bisexuality, and trans identities are also a separate set of factors.  For the purposes of this conversation, let’s focus on male homosexuality, as it’s the most studied.

First, a couple of things that it’s not: per the Royal College of Psychiatrists, there’s no evidence that parenting or early childhood experiences play a role in sexual orientation.  Per the American Academy of Pediatrics, “there is no scientific evidence that abnormal parenting, sexual abuse, or other adverse life events influence sexual orientation. Current knowledge suggests that sexual orientation is usually established during early childhood.”  Children who grow up to be non-heterosexual are, on average, substantially more gender non-conforming in childhood (even if they’re bullied for it), supporting the idea that sexuality is established early in life.  Sexual orientation is not a choice (here, here, and here).  In (old, unethical) studies where newborn and infant boys were surgically reassigned into girls and raised as girls, they did not become more feminine or male-attracted than their AMAB counterparts.  Socialization does not induce feminine behaviors in men or make them attracted to men. “Nurture” is a lot stronger than “nature” in this case.  There are no scientifically rigorous studies that support the idea that sexuality can be changed after birth, whether through surgical treatments, lobotomies, hormone treatments, electric chock treatments, aversion therapy, hypnosis, psychoanalysis, or any other type of conversion treatment.  I would love to see his sources on all of these psychologists who supposedly believe people are gay due to their social environment.

Sexual orientation appears to be a complex interplay of biological and environmental (but not social) factors. Nonsocial, biological factors have more evidence to support them than environmental factors, particularly in homosexual men.  So your friend isn’t entirely wrong, although he’s right for the wrong reasons.  Environment is a factor, and so is family (since that’s where you get your genes and epigenetics from) but homosexuality is inherent.

Let’s start with strictly biological factors that go into sexual orientation.

One of the biggest hypotheses for the cause of homosexuality is the impact of hormones on a developing fetus. I’m going to skip over a lot of biology here, but basically the core of this theory is that gay men’s brains may have been exposed to less testosterone in the womb than their heterosexual counterparts, had less receptivity to the masculinizing effects of the testosterone, or experienced fluctuations in hormones at key times in their development.  In women, it’s hypothesized that the opposite is true- lesbians may have been exposed to higher levels of testosterone.  This is supported by right hand finger digit ratios (the length of the index finger divided by the length of the ring finger), which are a marker of prenatal testosterone exposure- lesbians have a lower digit ratio than heterosexual women, while gay men have a higher digit ratio than straight men.  Gay men may have been exposed to more testosterone than their straight counterparts for a number of different reasons, including maternal immune response and fraternal birth order, genes, epigenetics, and prenatal environmental chemical exposure.  We’ll go over each of those below:

Maternal immune responses during fetal development are demonstrated as being a cause of male homosexuality.  During pregnancy of a male child, male cells enter a mother’s bloodstream.  These cells are foreign to the mother, and so her body develops antibodies to neutralize them.  Again, skipping over a lot of nitty-gritty biology here, but basically, the more pregnancies a woman has, the better her body gets at neutralizing male cells (particularly, Y-linked antigens) and the more antibodies she has against those Y-linked antigens.  

In turn, this creates what’s known as the “fraternal birth order effect”- basically, the more male sons a woman has, the more likely it is that her next son will be gay.  One study found that each additional older brother increases the odds of a man being gay by 33%.  Researchers have found that mothers with a gay son have heightened levels of antibodies to the NLGN4Y Y-protein than mothers with heterosexual sons.  The fraternal birth order effect is estimated to account for between 15 and 29% of male homosexuality.  Some studies have identified structural differences in the brains of homosexual men as opposed to heterosexual men that are due to prenatal hormonal exposure.  For example, straight men typically have right hemispheres that are 2% larger than their left, while in gay men the two hemispheres are typically the same size. 

Genes also play a role in sexual orientation.  Identical twins are more likely to share a sexual orientation than fraternal twins or adopted siblings (an estimated 80% of identical twins share a sexual orientation).  The largest study on the genetic basis of sexuality, published in Science, determined that there are at least five different genes that are correlated with homosexuality.  The genes identified do all sorts of different things, and some have functions that are yet to be determined.  An estimated 25% of sexual behavior is attributed to genetics.  Another study found that maternal female relatives of homosexual men tend to have more offspring, suggesting that genetic material that promotes fertility in women and homosexuality in men is being genetically passed down on the X chromosome.  Researchers estimated that this explains about 20% of genetic homosexuality (which is right in line with the estimate that there are four other genes involved).

Epigenetic factors also impact a person’s sexuality.  Epigenetic changes are changes in gene activity that are not caused by changes to the DNA sequence itself.  Epigenetic factors can “turn on” or “turn off” the expression of certain genes.  Per an article from The Guardian, “think of DNA as an orchestral score, the notes on the page unchanging. But the annotations on the manuscript will dictate how the music sounds, with crescendo and lento and adagio. The conductor and orchestra play their annotated manuscript, and each performance is unique, even when the original scores are identical.”  Epigenetic marks can be “turned on” or “turned off” during gestation as well as after birth.  Researchers hypothesize that epigenetic factors change how cells respond to androgen signaling, which is critical to sexual development.  Like we talked about above, fetal levels of exposure to the androgen, testosterone, seem to impact sexual orientation.  In gay men, the epigenetic marks responsible for managing the amount of testosterone the fetus is exposed to are thought to be too aggressive, blocking testosterone from reaching the fetus. This is pretty new research still, so the evidence to support it is limited, but one study found that the methylation pattern (the epigenetic change) in nine regions of the genome appeared to be linked to sexual orientation, and could use it to predict the sexual orientation of a group with 70% accuracy. 

There are a handful of statistical physiological differences between gay and straight man in addition to the difference in brain hemisphere size I mentioned above.  These are averages across populations, so they may not apply to each and every homosexual or heterosexual individual.  The suprachiasmatic nucleus of the hypothalamus is larger in gay men than in non-gay men.  The INAH 3 in the brains of gay men are the same size as the INAH 3 in women; both are smaller than in heterosexual men’s brains. Homosexual and heterosexual brains respond differently to two putative sex pheromones.  The amygdala is more active in gay men than straight men when exposed to sexual material.  Gay men are more likely to be left handed or ambidextrous than straight men.  Gay men are more likely to have a counterclockwise hair whorl than the general population, which is also correlated with left handedness.  Gay men have increased ridge density in the fingerprints on their left thumbs and little fingers compared to straight men.  These are all minor, but support the idea that there is a biological basis to homosexuality.

Now that we’ve gotten through the biological factors, let’s talk environmental.  When we say, “environmental” people usually think of the environment a child is raised in- who they parents are, how their parents act, who their friends are, what kind of activities they do, etc.  But in this case, that’s not what we mean.  The impact of a person’s environment after birth seems to have a weak effect on sexual orientation at best; there is no substantial evidence to suggest that early childhood experiences influence sexual orientation at all.  So in that case, what do we mean by “environmental”?  We’re really talking about the environment the mother was in during the pregnancy, and the prenatal environment that the fetus experienced (the hormonal influences that we talked about above).  These may include things like maternal exposure to anti-androgenic chemicals and endocrine disruptors while pregnant.  However, given that homosexual people have always been present, even pre-industrialization, these factors cannot be considered central to what causes homosexuality. 

[lemonysnidget]

Dead Wrong

Or “Who is Beatrice Snicket’s father?”

Reading The End when it first came out, I remember finishing the book and being somewhat bewildered, somewhat dissatisfied, thinking “okay how is that related to anything that came before????”, but also overall thinking “Wow, I’ve got more questions than when I started reading this book.” That’s not to say that I didn’t like the book, or that I didn’t feel like it wrapped up the overarching theme of the series is a really great way. I enjoyed The End, but it’s very different in tone from the rest of the series, and it doesn’t answer a lot of questions you go in with. And even before Chapter 14, you have so many more questions that also won’t be answered. That’s a bold move on Handler’s part, and it’s a rare thing in Children’s Lit (and a lot of fiction overall). 

One of the big questions that has stuck with me as a fan throughout the years - and sparked a few conversations during lunch block with my friends - is Just who is Beatrice’s father? It’s a question you don’t even realize that you could ask until 13.13, and then you’re just kind of stuck with it for the rest of your life. Are the Baudelaire orphans raising the daughter of their former enemy? It’s a great question for Handler to leave the audience with. 

Let’s dive into the significance of why wondering about Beatrice’s father is big, and what implications it has for the meaning of the book.

Reading the series the first time around, you might not even think to ask who is the father of Kit Snicket’s baby. Kit’s presence in TPP is so quick that you might not even have the chance to wonder - I certainly don’t remember even thinking about it, since there were so many other questions to be asked at the time. But, once you have Dewey whisper Kit dramatically before he drowns, the answer seems obvious. You do wonder why Kit didn’t mention Dewey’s existence to the Baudelaires, but you don’t linger on it. You realize that “my brother sends his regards” in Frank’s note is actually talking about Dewey and is kinda cute (or creepy depending on how you’re looking at it) and not a code. And if you didn’t get all of that because the book moves at such a breakneck speed, by the last couple pages of the book, you get this line: 

For another terrible moment, it felt like the boat was going to sink into the water, just as Dewey Denouement had sunk into the pond, guarding his underwater catalog and all its secrets, and leaving the woman he loved pregnant and distraught. (12.13)

Pregnant? Distraught? Sounds like Kit Snicket. So, we have confirmation that Dewey loved Kit (or that Lemony thinks that Dewey loved Kit). And it’s phrased in a way that really makes you inclined to think that there’s little ambiguity on the matter of who impregnated the Snicket lass. 

You get to The End, and everything seems to continue down that same train of thought. Kit asks the Baudelaires specifically about Dewey, and hopes that he will join them too. And then when she finds out Dewey is dead, she just gives up. She tells the Baudelaires: “I've lost too many people—my parents, my true love, and my brothers” and you immediately think she’s talking about Dewey (13.13). You don’t even question it. You just accept that she’s talking about Dewey and move on. But then... suddenly it changes.

"I've lost too much to go on— my parents, my true love, my henchfolk, an enormous amount of money I didn't earn, even the boat with my name on it." (13.13)

There are very few times I’ve actually mentally heard a record scratch in reaction to something, but this was one of them. I remember just stopping and staring at the page for a few seconds, thinking I had misread something. I then flipped back a couple pages to confirm that yep, the parallel structure between Kit’s and Olaf’s statements wasn’t in my head. And I knew that there was absolutely no way that it was an accident. (The in-universe record scratch for the Baudelaires happened with the kiss.)

Handler’s a skilled writer, and he knows enough to be extremely deliberate with his words and phrasing. He knows the importance of punctuation. Even if he might make fun of Aunt Josephine, he uses grammar so well that it’s clear he does care how sentences are structured and how punctuation or the splicing of sentences can provide nuance. No writer worth their salt would have these two sentences in the same chapter (let alone a flip of a page away) if they weren’t trying to say something. Not only do you have similar words and sentiments, there’s similar sentence structure and punctation! These two lines are supposed to go together. And this isn’t even the first time that Olaf and Kit have had very similar lines, in fact in TPP, both Kit and Olaf say "A taxi will pick up anyone who signals for one” matching each other word to word (12.1, 12.9). Perhaps while reading TPP, you didn’t notice it or you assumed it was some kind of code or aphorism of VFD, so you didn’t pay it much mind. But, in hindsight, it seems that Handler was already hinting at Kit and Olaf having a very deep connection. 

More than just parallel structure, Handler has a major, major departure from tone of the whole series and the characterization of both Kit and Count Olaf. ASOUE is not a series that focuses on romance, and it certainly does not advocate the notion of true love - maybe you’d find that in The Pony Party or The Littlest Elf. Love in ASOUE is not a permanent thing, and it is not a good thing. Beatrice 1 moved on from Lemony and was very happy in the life she chose. Charles’ love for Sir was not at all healthy. Esme and Jacques marriage is hardly a fairy tale (more a Russian novel). And even though Lemony seems to carry an ever enduring torch for Beatrice, he never refers to her as his true love. No one mentions true love. But, at the end of The End, pragmatic, Machiavellian Kit brings it up for the first time. It’s a little bit jarring. And then when Count Olaf says it, the reader is asked once again to step back and re-evaluate their understanding of the story’s villain, and the story itself. 

Continuing on that theme of forcing you to re-evaluate a man readers have spent 13 books seeing as a deplorable/disgusting/unloveable individual, Handler gives Olaf and Kit the most intimate moment in the whole series when Kit reaches out to touch Olaf’s tattoo and recite a love poem to him. Two dying individuals on the opposite side of a war, just connecting one last time, to recite poetry to each other. Taken out of context, it seems pretty damn romantic. 

And what does Olaf do in response to Kit’s love poem? He ruins the moment by abridging a poem about the cyclical nature of misery and pain, how children inherit their parents trauma’s, and the best way to avoid passing that burden on is to not have kids and die. Let Olaf say fuck, cowards. Charming thing to say to a pregnant woman in the process of giving birth, eh? Definitely a very Olaf thing to do. Is he just being an asshole? Or is there something else going on? 

At that point, there is no choice but to consider the possibility that Olaf is the father of Kit’s baby. Handler wants us to wonder if Beatrice’s birth is book ended by her parents deaths. 

No doubt, in the year that follows on the coast shelf, the Baudelaires asked themselves just that. Are they raising the child of the man who relentlessly pursued them and who they believe murdered their parents in revenge? They would have definitely done the math and realized that their series of unfortunate events took less than 40 weeks, safely allowing Olaf to have fathered Beatrice before becoming their guardian. 

You can almost see Violet, Klaus, and Sunny searching Beatrice’s face as she grows up, looking for any similarities or clues as to who her father is. Unfortunately, Beatrice “look[s] very much like her mother” so they might never have come to a conclusion (13.14). But, the fact that even with the ambiguity and doubts the Baudelaires still lovingly raised the possible child of the person who they believe made them an orphan is huge. It shows that VFD’s cycle just might be broken. Unlike Olaf, who wasn’t able to let go of the fact that his parents were murdered by at least one of the Baudelaire’s parents and who let it turn him into a twisted villain, the Baudelaires give Beatrice a family, and they don’t let any doubts get in the way of raising her and loving her. And that flies right in the face of everything that has come before.

Instead of the intergenerational passing down of trauma, abuse, and pain that is a part of VFD and the story as a whole, the Baudelaires stand up and stop the cycle. The Baudelaires did not become like Count Olaf, despite their unfortunate events. The Baudelaires rose above their trauma. 

They directly contradict Olaf’s dying words. Man doesn’t have to hand misery to man, and your parents don’t have to fuck you up. Trauma does not have to be something that’s passed on as an epigenetic trait. You can have a terrible childhood, and you can grow up and make sure that whatever you suffered doesn’t happen to the next generation. This is a major takeaway point from the series. 

The ambiguity over Beatrice’s paternity is essential to the overall arc of ASOUE. It completes the circle, and it is a powerful message. So powerful, in fact, that Handler actually decided he had to include it, even if originally, he hadn’t planned on it. 

Handler has talked about how he had to rework some of TPP because of one throw-away line in TBB. But, he hasn’t talked about how suddenly, between TGG and TPP, Kit became 9 months pregnant.

In the driver's seat was a woman the Baudelaires had never seen before, dressed in a long, black coat buttoned up all the way to her chin. On her hands were a pair of white cotton gloves, and in her lap were two slim books, probably to keep her company while she waited.(11.13)

The Baudelaires can see her lap in TGG - Kit was not in her third trimester when Handler originally penned TGG. But, “her belly had a slight but definite curve” as of TPP (12.1). This is a ret-con, folks. Handler can’t change the fact that he had the Baudelaires be able to look into the car and see that she had two books in her lap instead of resting on top of a very pregnant belly, so he tries to act like nothing happened and hopes the readers won’t notice the contradiction. A woman who is about to give birth would have more than a slight curve, I might add, but that’s not exactly important.

Obviously, Kit being pregnant was vitally important to Handler’s story. So important that he contradicted himself, something that he went to great lengths to avoid doing in the same book. If Beatrice’s father was supposed to be Dewey - a character who was only in one book, who supported the Baudelaires rather than challenged them - then Handler would not have done this. Beatrice wouldn’t have been written in if Dewey was meant to be the obvious father. The Baudelaires raising Dewey’s daughter doesn’t really add anything to the story, and it would present far too small of an arc (just the last two books) to be worth it. 

So why even have Dewey be romantically connected to Kit at all? Why not just not give a candidate for who the father of Kit’s baby is until we see her with Olaf? Well... to quote the show:

ASOUE is filled with mysteries. Handler loves weaving them. He loves giving you a few clues here and there, and sometimes giving you enough clues to solve the puzzle on your own, and other times, he deliberately withholds stuff just because it suits his narrative aesthetic. And a lot of the time, he deliberately misleads or misdirects you. 

When it comes to Dewey and Kit’s relationship, Handler gives us enough to connect the dots, but connecting them isn’t necessarily the right thing to do. While it is entirely possible that Dewey and Kit were sexually involved, it is very important to note that Handler does not actually give us any confirmation that Dewey’s feelings were returned or if he and Kit actually were intimate. Dewey loved Kit, yes, that is a fact, but loving someone is not enough to create a baby with them. That’s not actually how it works, even if a lot of sex talks might want you to think so. 

Kit and Dewey were not living together. If Kit and Dewey were planning to co-parent together as a couple, Kit would not be solely responsible for “[choosing] wallpaper for the baby's room” - they would be choosing it together, but instead, Dewey is still living with his brothers at at the Hotel at all hours (12.2) Further support for this is that were Dewey and Kit together, Frank wouldn’t have to act as a go-between for Kit and Dewey by telling her “my brother sends his regards” (12.2). Dewey would have been able to give Kit his regards himself... and he probably wouldn’t be giving regards. For a couple that’s romantically involved, that sounds incredibly formal! In fact, Kit actually describes Dewey as “a wonderful gentleman” (12.2). A similarly stiff way to refer to someone... not to mention the fact that referring to someone as a gentleman is frequently used in the context of a guy not being to forward or taking advantage of a situation sexually where he could have ignored the woman’s boundaries. It really does sound like Dewey, despite loving Kit after years of working with her, wasn’t actually physically intimate with Kit. Dewey’s love, therefore, seems to have a lot more in common with the courtly love of Dante and Beatrice rather than an erotic love.

That doesn’t mean they weren’t mutually emotionally intimate, creating a very strong bond. Kit was obviously extremely distressed by his death and they did work together for years. But, it’s hard to know if Kit was upset to find out about the death of her child’s father or if she was upset because her friend and everything that they had worked for was gone. Or both. Either one is pretty devastating. 

Olaf in book canon is more likely than not Beatrice’s father, for meta reasons and “in universe” reasons. Olaf being Beatrice’s father is consistent with the textual evidence, whereas the textual evidence does not support Dewey and Kit having a serious or even sexual relationship. The Baudelaires considering the possibility that Olaf is Beatrice’s father is absolutely essential for the meaning of the series. The Baudelaires, who unlike us cannot go back and pick apart the text, have to have their doubts, but they treat Beatrice in a way that the prior generations of VFD could not comprehend. 

So you might wonder, Does Olaf know? Does he consider the possibility for Beatrice being his daughter? For him, the matter might be pretty unambiguous, since he has knowledge that the Baudelaires, Lemony, and us the readers don’t have. Perhaps he knows that she isn’t, perhaps he knows she is, perhaps he doesn’t know one way or the other. Regardless, Olaf doesn’t care. Olaf was more than willing to claim he’d kill Kit and her unborn child at the start of The End, but when it comes down to it, Olaf chooses to suffer a lot of pain, prolonging his death, to help the both of them. Darwin might argue that Olaf being Beatrice’s father takes away the selflessness of the act. But, Darwin would be ignoring Count Olaf’s dying words: “Don’t have kids yourself.” Count Olaf did not want to become a father, but he suffers greatly to ensure that Kit’s child is born. 

That is a noble act. 

You could say it would be more noble if it were Dewey’s daughter, but I disagree. Why would Olaf care whether Dewey’s daughter lived or died? He wouldn’t. Olaf’s act is selfless because Beatrice isn’t Dewey’s daughter. 

On the topic of Netflix, and speculation for the third season: 

Do I think the show is going to go this route... possibly. Though the casting of a younger woman to play Kit and a younger man to play the Denouements makes it seem a little bit less likely that they would go for it. But, I do find it interesting that Netflix deliberately added the cake tasting scene in TBB.

Perhaps it might have just been to foreshadow to complicated relationship between Lemony and Olaf, but, it’s interesting that it’s cake when we know that cake is what Beatrice Snicket wants to bring along with her on the boat to escape the island - "Cake!" shrieked the baby, and her guardians laughed (13.14). 

“Cake” is the only non-babytalk line that Beatrice says, and the fact that Handler chose to have Beatrice love cake of all things not to long after he has Lemony inform of us of the fact that Dewey was able to document twenty-seven cakes “that Olaf has stolen” (12.13). Handler wanted to remind us of just how much Olaf loves cakes just before The End. Sure, he’s not the only character who likes cakes, but it is an interesting choice on Handler’s part, and an interesting choice for Netflix to include that scene.

In about a week, we’ll know what route they decided to take with the Netflix adaptation, but I do believe that they have set up the potential for Beatrice being Olaf’s daughter should they choose to keep Beatrice’s line about cake. 

And there you have it, the meta I have had in my ‘drafts’ for six months because I kept on writing it and scrapping it. 

[awildpoliticalnerd]

Book Review: The Moral Animal: Why We Are the Way We Are: The New Science of Evolutionary Psychology. By Robert Wright. (1994).

Robert Wright’s The Moral Animal is a look through the field of evolutionary psychology--at least as it stood at the book's writing in 1994. It's a promising work with a lot of insight. However, it can best be analogized to the peacock: If it survives, it does so despite the massive disadvantage of some obvious maladaptions. In the case of the peacock, the adaption is its oversized tail (or "train" as it's often referred to). In the case of The Moral Animal, it's Wright’s own unexamined moral and ideological biases presented as fact that lowered its potential. 

The big sell of the book is actually a rather interesting premise: Take the most famous proponent of the theory of evolution (Charles “the Chuck” Darwin) and use his life to demonstrate the principles of evolutionary psychology. Want to illustrate the theory that men are less biologically inclined towards lifelong monogamy thanks to our disproportionately small part in the baby-making process? Highlight the fact that Darwin literally sketched out a cost/benefit analysis of getting married in his notebook. Want to argue that young siblings should be both predisposed towards rivalry and cooperation thanks to kin selection? Give some (admittedly adorable) examples of Darwin’s many, many children. Because of this, the book was part popular-science exploration of a then-burgeoning topic and accessible biography on one of the most important scientific minds to ever emerge from the primordial ooze. When done well, this was the book at its best. It was discursive, informative, and enjoyable. It kept me engaged over much of the book’s nearly 400-pages.

(Lest someone use the opening example as evidence that I have no idea what the hell I’m talking about later in the review, let it be known that I know that the mystery of the peacock’s train was solved with the insights of sexual selection--that peahens select males with large trains because possessing one shows that the males have got to be pretty dang "fit" to survive with such a glaringly obvious disadvantage. Writing thematically consistent introductions is hard; I claim some artistic liberties here).

There are two core ways that this plays out throughout the book. The first is the odd insistence that every possible point that Wright could conceive of making in this vast subject was exemplified by good ol’ Chuck. And there were times that this was very clearly a stretch. The way he pursued his eventual wife, Emma, is described through a very genetic lens instead of primarily cultural terms (part of a supposed genetic predisposition towards the “Madonna-Whore” dichotomy for those of us with that infernal y chromosome). His differential patterns of grief for the loss of two of his children (he reportedly mourned the death of his ten year old daughter far longer, and far more intensely, then that of his infant son) are couched as being primarily due to their proximity to prime fertility age. His intense anxiety about publishing what would be his scientific legacy (you know, apart from being the 19th century’s foremost barnacle expert)? It’s the genes! It’s genes, genes, genes all the way down. 

I’d like to say that the book was always like this. Or, apparently, my desire to want to say this, my inability to do so, and the considerable amount of sarcasm required to pen these last two sentences are because of my genes. At least that’s the culprit if we were to take Wright literally. At times, he is positively (and ironically) evangelical about the power of our genetics in dictating our behavior. And it is to the rest of the work’s detriment. 

I’m not some biological denialist. I believe whole-heartedly in evolutionary theory. And, of course, the potential for any and all physical actions have to ultimately originate in the code that facilitates every biological process we undertake. But, first off, since natural selection works probabilistically, what do you think the odds are that, of the billions of humans to walk the Earth, the theory’s first popular progenitor is an acceptable exemplar of all of these processes? It’s laughably small. Literally smaller than the first common ancestor of all life on this planet compared to the sun. I don’t think that this means that Wright had to abandon the mission of using Darwin as an illustration--again, that’s part of what made this book so interesting--but it would be far better served if, instead, Wright said something to the effect of “we can see an imperfect analogy to these processes in Darwin’s life.” A small change but, as Wright knows, small changes can have a large impact.

I suspect that Wright’s self-admitted zealousy on the subject was partially spurred on by the fact that this book was written before epigenetics (the process through which different parts of the genome are activated/deactivated in response to environmental changes, changing the genes’ expression) was more rigorously demonstrated. I recall him adamantly insisting, once or twice, that genes “can’t be changed” once we’ve been conceived. At the time, that was the belief commensurate with the best available evidence. Although epigenetics do not disprove this, the truth is that our genes are far more flexible than originally thought. If genetic fixedness is what you’re arguing, it’s pretty tough to say anything other than “everything Darwin did ever is totally explainable through evolutionary psychology.” Even if it's not true. So I’ve decided to chalk this up to scientific progress and its inevitable, unenviable ability to reveal certain pronouncements as utterly wrong. It’ll undoubtedly happen to me; it happens to any practicing scientist. 

The second theme, though, is less able to be chalked up to the inexorable march of progress. That is the distinct, but related, assertion interwoven throughout the text that literally everything can be explained by evolutionary psychology. Moral codes? Evolutionary psychology. Selective memory of our own moral failings? Evolutionary psychology. Western social structures and the necessity of political and economic inequality? Survey says: Evolutionary psychology. 

These assertions are often manifest through what I call “cover your ass” language. We all know it; we all, regrettably, deploy it. It comes when the authors use absolute terms for the vast preponderance of the work and then say “now, do I really think that this explains everything? Of course not! But…” and then proceeds to make the exact same points, just with a couple of words interjected to signal intellectual humility. A few careful words do not erase the other 98% and the frames they collectively construct. Wright is arguing that evolutionary psychology alone can explain just about every social phenomenon, from the simple to profound. But the fact of the matter is that evolutionary psychology would be hard-pressed to understand why people on vacation with their families would bother to leave tips at restaurants despite the fact that they do, more often than not. (Seriously. Reciprocal altruism’s out since you’ll never see that server again. Odds are they weren’t related, so kin selection’s out too. Peacocking wealth contrasts with women’s supposed preference for mates who don’t needlessly divert resources away from her children. Tipping is a tough nut to crack for rational-choice-esque theoried like evolutionary psych). If it can’t explain something so banal as this, I have strong doubts of the deterministic account Wright explicates here. He will, almost begrudgingly, admit that social and environmental forces play a part in genetic expression. But he does not seem prepared to admit that it plays as big of a role as even the available evidence at the time did.

The more I read it, the more I felt that this book was symbolic of a lot of evolutionary science at the time: It contains real, interesting insight on genetic processes and their role (however expansive or limited) in complex interpersonal phenomena. These shouldn’t be undersold or ignored; I learned a great deal reading this book. The problem is that these insights come paired with uninterrogated moralizing, steeped in contemporaneous social events, passed off as timeless, objective Truth. The most obvious example (because of how often Wright returns to it) comes in the aforementioned asymmetry in male parental investment. Or, rather, the seemingly inevitable end-result: Divorce. This was often curiously paired with hand-wavey discussions of the Madonna-Whore dichotomy. Apparently, men who manage to have sex with women earlier in the relationship feel less inclined to see her as a viable marriage partner. Should a quickly-pairing couple (referring to the speed in which they decide to do the act and not, hopefully, the duration of the act itself) wind-up married, men are more likely to ditch the women--and ditch them for similar "kinds" of women. This discussion would often lead to Wright lamenting how women are engaging in sex earlier and earlier in romantic relationships. Things were better decades before this promiscuity was socially acceptable. Like back in Victorian England when Charles wed his beloved Emma. And the evidentiary linchpin, at times explicitly mentioned while only obliquely inferred at others, is the sky-high divorce rates that, Wright argues, came as a consequence of social structures being poorly designed considering our inherent genetic predispositions. 

Of course, we now know that the high divorce rates of the 90s were a temporary thing. First-marriages are lasting far longer than they did (on average) in the 80’s, 90’s, and early 00’s but divorces are just as easy (if not easier) than ever before. If it was entirely because of early sex and our baser nature, the pattern should continue. The fact that it doesn’t is both evidence that evolutionary psychology is more limited than Wright suggests and that the urgency imbued in his analysis was shaped by his own moral sensibilities rather than those seen in society as a whole, inculcated by natural selection.

This wasn’t all of the social critique Wright was inclined to wade in. All fields and theories have their critics. Good authors often anticipate common objections and address them in the text. He saw his most likely critics as less scientifically driven as ideologically so. Lofty prose to the contrary, he was on the attack far more than on the defense; Darwin found himself a new bull dog. His target: Those dastardly post-modernists. He often panned “post-modernism” for their critiques of evolutionary psychology, often claiming (without much evidence) that it stemmed from the post-modernists’ universal and fundamental ignorance about biology. Honestly, the way Wright so derisively talked about them, I was surprised that he didn’t bust out a couple of verbose “yo mamma” jokes. 

What makes his vituperative swipes so ironic 25 years later is that the post-structuralists were right. Many evolutionary scientists were predisposed towards advancing biologically deterministic theories of human behavior. Any practicing geneticist worth their salt today would tell you that human behavior is so dependent on genes' interactions with the social and physical environment that even things we take for granted as “hard-wired” (such as one’s sexual preference) has been persuasively shown to not be the consequence of singular genes--or even wholly the consequence of complex genetic interactions. This is a far, far cry from Wright’s portrayal in the book; I honestly think he would be aghast at this suggestion, as if it surrenders precious ground to heretical forces in the battle for all of science’s soul. And the post-modernists are consequently vindicated in questioning what kind of power is made manifest, and towards whom is it ultimately directed, when these assertions are given the pop-science stamp of total veracity. (Actually, despite it being basically their entire deal, I can’t recall a moment when Wright discussed power when issuing his disses of post-modernism. Instead, he discussed them in the same kind of shifting, ephemeral manner that paints them as boogeymen with accusations that were often equally grounded in reality. I think he would find his own intellectual horizons broadened if he allotted the same serious attention to their intellectual contributions as he demands for his subject). 

To shoehorn in a personal complaint that I had, the book was heavy in evolutionary theory but very, very sparse in social-psychological insight. Spare a chapter where Wright tried to rehabilitate Freud’s reputation (as successful attempt as one’s going to have considering how uphill that battle is), most of the psychology was relegated to sexual pairing preferences and over-general suggestions on morality and social bonding. The former was interesting and insightful; the rest woefully underdeveloped. I may be spoiled by books like Behave and How Emotions Are Made (part of these phenomenal works both touched on how evolution may bring around specific cognitive processes), but I think Wright could have comfortably fit interesting, more specific insights if he shed the weird moralism and extensive post-modernist vendetta.

I hate closing reviews with negatives, no matter how well deserved. Presumably that’s in my genes as well. So I’d actually like to conclude by saying that I well and truly learned a lot from this book. Some of it was less novel so much as it was a refresher (I have read a number of prominent books on evolutionary theory, including the oft-referenced Selfish Gene by Richard Dawkins), but some insights were well and truly new to me and illuminating. The one that stands out the most at the moment is the game theoretic accounts claiming that monogamy ultimately serves men (while institutional polygyny would be better for women) and the argument that people are more rude in spaces with fewer permanent interpersonal ties. I also thought the point that adherence to cultural values are an expedient for environmentally contingent reproductive success was well argued. I don’t buy these arguments entirely, but I think they and other points are worth mulling over to extract the useful bits. But in order to get to these bits, you have to be attentive and willing to parse through a lot of things that, in the rat-race of ideas, deserve to be thoroughly out-competed. 

[heroesarelife]

Replying and debate

@luzonmfjel asked:

Hey! About your quirk genetics post, it was a really interesting read on a topic I've been thinking a lot about too. Now all of my genetics qualifications come down to 9th grade biology so this probably doesn't make much sense, but I was wondering if it was possible that quirks were passed on like blood types, with multiple different alleles existing? Not about if you have/don't have a quirk, but more about what that quirk would be. For example, Todoroki. Say his dad’s genotype was Aa, and his mom’s was Bb. With A being fire and B being ice, of course. So put on a punnett square, the possible outcomes would be Ab, Ba, and AB. Ab would mean either a partial or full dominance of fire, Ba of ice. That would result either in someone having a quirk that’s entirely one, or mostly one, like Shouto’s siblings, and AB would be the half and half codominance that we see with him. Those are just the genotypes though, and the way that those genes would present themselves in phenotype could just vary. I'm sorry if that was less than coherent, just thought I'd offer my two cents. ^^ 

Hell yeah, debate debate. I love so much <3

Don’t fret at all, mate. Let’s see if I understood you right. Like as I see it, you said pretty much the same thing I did (?). It’s just that you chose to use different letters instead of only A’s. Using A’s was just a personal choice, not an avoidance of distinction between quirks. When I described Todoroki’s case... well here, let me just reiterate:

One way it could go is that if a child ends up being dominant homozygous (AA), then they should probably inherit “both” the quirks - and how those genes would express themselves is another point entirely. It could also happen (perhaps more rarely) with the child being heterozygous (Aa), in which one of the parent’s quirk is recessive homozygous (aa). So here are the options:

Mother: Aa

Father: Aa

Possibilities: AA (25%), Aa (50%), aa (25%)

Or:

Mother/father (vice versa): Aa, aa

Possibilities: Aa (50%), aa (50%)

In that description, for Todo’s case, the father “A” would mean Fire, and the mother “A” would mean Ice (or their aa would mean Fire/Ice on the second choice). The possibilities are the punnett square results of that. Besides that I fail to see what the argument here is, as it seems like a pretty good sum up of what I described on that meta. Like, what you said is exactly what I meant in it, so I do apologize if it wasn’t clear and made it sound like I was talking again about quirk vs no-quirk (the intention was to had moved on from the quirkless argument by this point of the meta). I tried not to say which was Todoroki’s genotype, because I wanted to leave it more open, and give more freedom for the whole thing (it had inferences and, in the end, it’s a fiction thing).

However, if you do want to get very realistic I reckon that the correct answer for Todoroki would be that he is an heterozygous (Aa). And the second option is the correct one for the parents. That’s because, as far as I know, Codominance is usually a trait observed on heterozygous. Whereas Partial Dominance is a trait usually observed in homozygous (AA/aa).

About the multiple alleles point (ABO blood type)... That’s not the direction I chose on my Meta, because I thought would make it a bit overcomplicated, and also because I didn’t think it likely that quirks have multiple alleles (which doesn’t mean is not the case). But determining factors for quirk inheritance can involve maybe more than one pair of chromosomes, as well.

I hope this helps, I mean, assuming that’s what you wanted to know. Let me know if you meant something else /o/

@masterlazywriter reblogged your post and added:

Hi! I want to say that I am a biology major and your genetics analyses are on point! I’m very surprise your include epigenetic at the end! :o cause I was thinking about epigenetic for a while while I read it. 

THANK YOU! Epigenetic has logic for this situation, doesn’t it? <3 so interesting.

@roquelg replied toy our post “Quirks and Genetics”:

Oh, I love your analysis. It is very well structured. Only one question, aizawa is able to neutralize the alpha factor (the ability to use a quirk) the bullets are the same or do they work also eliminating the quirk? ... Thanks for sharing your ideas 

Oh thank you, mate! I’m that glad you liked it! <3 took some time and effort, so this feedback makes me quite happy actually :3

I do need to disclaim that the logic I used for the meta regarding the quirk factor is the hugest leap I did, the largest inference, and it may very well be wrong (regarding the relationship between quirk, quirk factor, plus alpha. I mean, the explanation was confusing and it may be that these 3 terms are interchangeably talking about the same thing, for example. There are other hypothesis as well, but I needed to settle for one to move on with the rest of what I wanted to say).

So, Aizawa says that Erasure “doesn’t attack the quirk itself”, then proceeds to say that Plus Alpha is a mechanism added to a normal human body, and that the collection of these are called Quirk Factor. And then he says that Erasure halts the Quirk Factor. I took that to mean that he affected the response between the Plus Alpha and the Quirk. A friend interpreted it as a neurotransmitter inhibitor and I think that’s a pretty accurate metaphor to how Erasure seems to work. If my hypothesis is correct, that is.

The bullets are a whole other problem. So, in the beginning we are led to believe that they cause damage to the Quirk Factor. In Mirio’s case, a permanent one. However, we now know that Eri’s quirk is that of Rewind, not really the same thing as a quirk that erases quirks. It seems that the bullet formula is using Eri’s blood/quirk to attack specifically the Quirk Factor and Rewind only that part of the body. In theory, the same aspect can be rewinded back to before the person took the bullet. So I wouldn’t say that it’s the same as eliminating the quirk per se.

Applying my theory, it would seem that the bullets rewind the Plus Alpha mechanism to either a time in a person’s life before they developed enough to be able to use their quirks (4 years old in canon), OR to a time in evolution where the Plus Alpha did not exist yet (?). This is all highly hypothetical though, so have that in mind. I hope this answered your question XD let me know if it didn’t.

@sarahhaley101  replied to your post “Quirks and Genetics”:

This analysis is super good and thorough!! However I’m not sure that Todoroki’s quirks is the perfect example of typical codominance. It is not just his quirk that has two expressions — his hair color and eye color do as well, and these multiple alleles at different foci are split right down his center. He could be a chimera! So, he has two completely different sets of chromosomes, not just two alleles at one foci. Chimerism has never been recorded in humans to this degree, but this is anime so! 

Thank you so much, mate! <3 This means a lot, I’m very happy with the positive response *was lowkey expecting to receive hate* /o/

Well yeah, but codominance is an expression on different cromossomes and in fact hair colour can have a codominance expression (and todo hair seems to be that). All in all he’s all a codominance isn’t he? I would like to point out that  heterochromia is not a result of codominance though. So have that in mind. All in all it might as well be chimerism, so I can’t say you are wrong. I mean, this is an anime afterall. I just tried to bring real world genetics to the whole thing so talking about that didn’t even cross my mind, to be perfectly honest. It is a thing to consider, of course. Thanks for introducing the idea, mate :3

@bakushima-ima replied to your post “Quirks and Genetics”:

Wait Bakugou was born out of a quirk marriage??? Did I miss this in the manga????? 

Awesome analysis though, I love seeing people analyse the scientific side of bnha because it's so well thought out and planned 👍

Why, thank you <3 I’m really glad you enjoyed it, thank you kindly for letting me know! o/

It’s not stated anywhere in canon that Bakugou was born out of a Quirk Marriage. Like, I use the term quirk marriage just to mean the same as quirk fusion. In canon the term “quirk marriage” means a social behaviour in which people marry just so their offspring would have their quirk combined. The fandom has been using that word to also mean a “fused quirk”, so the quirk itself is married, say. It’s just a collective choice, really. So Bakugou’s quirk is a “marriage” between his parent’s quirks, but his parent’s marriage was not a result of a quirk marriage objective (as far as we know). Two different things, then, yeah?

I hope this was your question XD let me know if that was not the case and I misunderstood :3

[grimark]

some thoughts i just had about cloning in the radch:

it’s pretty clear that anaander mianaai has at least some degree of contact with radchaai citizens- having audiences, performing religious duties, sometimes mingling with the populace. obviously this would mainly be pretty prestigious and respectable radchaai, i doubt your average citizen could just waltz up and, say, steal a hair or take a cheek swab or whatever. But given the time the radch has been established, the number of anaanders there are around, and the fact that she doesn’t seem to go to any specific effort to keep her bodies segregated from people, it’s not out of the question that someone could get their hands on a DNA sample. Now, actually doing something with that DNA sample would be difficult, given the scrutiny all radchaai are subject to. But as we see from the series itself, illegal activities can and often do slip by the notice of whichever AI may be watching, or they’re not brought to the attention of authorities. So if you were very careful and lucky, i don’t see any reason why you couldn’t grow your own bootleg anaander clone.

Now obviously this would develop differently to the official anaanders, and wouldn’t be linked up to the anaander hive mind. But even without actually being anaander, without having all the knowledge and memories and accesses that comes along with that, having a person who is genetically identical to anaander around could be useful. After all, wouldn’t most radchaai be used to deferring to a person who looks like anaander, no questions asked? You might not even have to go to all the effort of growing a clone if you wanted to con people into believing you were anaander, i’m sure radchaai cosmetic surgery would be up to the task.

anyway all this brings me to the point that i’d be very surprised if anaander’s genome is the same as that of the original or template anaander, assuming there was one. aside from other kinds of genetic modifications and enhancements she might have introduced, it’s interesting to speculate about the sorts of safeguards she might have added to prevent ‘unauthorised’ clones being made. Maybe some kind of classified epigenetic switch only she knows about, without which the clone embryo might not be able to develop, or might turn out not looking like anaander at all. I bet all the scientists and technicians in charge of growing the bodies and hooking them up are anaander clones themselves. 

[makingscipub]

“It’s just like epigenetics” – scientific metaphors for non-scientific concepts

This is a guest post by Cath Ennis. Cath is a Knowledge Translation Specialist with the University of British Columbia’s Human Early Learning Partnership and the Kobor Lab at BC Children’s Hospital Research Institute.

***

In our new paper, Brigitte Nerlich, Aleksandra Stelmach and I examined the metaphors used by academic social scientists and alternative health marketers to describe and discuss epigenetics. We found some overlap between the metaphors used by these two very different publics, as well as some shared misunderstandings and over-interpretations of the science of epigenetics.

I’ve been intrigued for years by the diversity of the metaphors that people use to explain epigenetics, and by how such metaphors can highlight some of the common misperceptions of the field. In my 2017 book “Introducing Epigenetics: A Graphic Guide” I referred to the DNA sequence as the text of an instruction manual, and epigenetic marks as highlighting and crossing-out that helps each type of cell to identify which parts to use and which to ignore. My colleague Dr. Michael Kobor refers to genes as lightbulbs and epigenetic marks as dimmer switches, and I’ve seen others use everything from hardware/software to musical scores/artistic interpretation to describe the same phenomena. (Aviad Raz, Gaëlle Pontarotti, and Jonathan Weitzman published a fantastic paper earlier this year about how different epigenetic metaphors are perceived by technical and non-technical audiences, which I highly recommend reading if you’re interested in this topic).

While working with Brigitte and Aleksandra on our paper, I also stumbled across various examples of the opposite case: of people using epigenetics as a metaphor or analogy to explain non-biological concepts. This seems to be a recent trend (quite possibly a premature one, given that even biologists can’t agree on the precise definition of epigenetics), and one deserving of a more systematic analysis than is possible in a short blog post. Hopefully, though, the four diverse examples presented here can provide a good starting point for whoever wishes to pick up this baton!

Mapping aspects of molecular epigenetics onto sacred texts

The first example is a comparison between different cells using different parts of the genome, and different Christian denominations using different parts of the bible in their sermons. I encourage you to read the entire article by David Sloan Wilson, SUNY Distinguished Professor of Biology and Anthropology at Binghamton University, but here are the most relevant parts:

“sacred texts bear an intriguing resemblance [to] genomes. Both are replicated with a high fidelity and even have a hierarchical and segmented structure. The Protestant Christian Bible, for example, is segmented into 66 books, which in turn are divided into chapters and verses. […] 

Just as differences in gene expression are often visualized in the form of “heat maps” (the brighter the color, the more the gene is being expressed), we can create a heat map for the expression of books in the bible [this refers to the use of different parts of the bible in sermons] by the six churches. […]

Thus, when differences in Biblical citations are combined with differences in interpretation, the concept of a sacred text as a cultural epigenetic inheritance system, capable of adapting a religious community to a wide range of environmental circumstances, has much to recommend it. […]

Formalized sacred texts such as the Bible or Quran are the cultural equivalent of an epigenetic system because only the expression of the passages, and not the passages themselves, are allowed to change. However, the cultural equivalent of genetic evolution (the addition and subtraction of the passages) took place at an earlier stage of their history and to some extent still, to the extent that religions accumulate supplemental texts in addition to their core text. During the Protestant Reformation, even the core text of the Catholic and Orthodox Christian Bibles was reduced”

Here we have a metaphor that I think would work well in either direction, and that’s pretty similar to my own preferred epigenetic metaphor of text and highlighting. The author seems to have a solid grasp of the science of epigenetics, and applies it to a concept that does indeed have a number of parallels to genetic regulation.

Mapping aspects of epigenesis onto understanding how robots learn

Our next example is drawn from the world of epigenetic robotics. I’ll freely admit that I don’t have anywhere near enough knowledge of robotics to truly understand the nuanced distinction between epigenetic and other forms of the discipline, but the primary allusions here seem to be to the role of epigenetics in human development, and the concept of epigenetic plasticity in response to changing environments.

Epigenetic robotics is concerned with “the study of cognitive development in natural and robotics systems”, and what it can tell us about “the typical and atypical development of children, and creating better robots” as well as “the appearance and modification of cognitive structures in a progression from the embryo to the adult form”. According to Jordan Zlatev and Christian Balkenius, “The term was used to refer to such development, determined primarily by the interaction between the organism and the environment, rather than by genes”.

The focus of this metaphor is on the plasticity afforded to organisms by epigenetic marks that change during development and in response to certain environmental exposures. If I’m understanding these texts correctly, what this means to a robot relates to how it learns from experience rather than from pre-programmed routines.

My perception of the robotics metaphor is that it’s built on a solid foundation, but might overstate the science to some extent. Epigenetic marks do change during human development (some of them so predictably that our group at BC Children’s Hospital in Vancouver has used them to develop an “epigenetic clock” to assess childhood development), but to what extent these epigenetic changes actually drive rather than merely reflect pre-programmed (genetic) and responsive biological changes is still a matter of active scientific debate. Perhaps this distinction isn’t critical to the use of the word epigenetics in the field of robotics, though – I’m hoping that a reader who knows more about robotics than I do can help to enlighten me on this point!

Using epigenetics as a free-floating signifier attached to ‘cultural DNA’

I also spotted a reference to epigenetics in an article written by anti-bullying activist Monica Lewinsky for Vanity Fair in 2018:

“something fundamental changed in our society in 1998 […] And ever since, the scandal has had an epigenetic quality, as if our cultural DNA has slowly been altered to ensure its longevity. If you can believe it, there has been at least one significant reference in the press to that unfortunate spell in our history every day for the past 20 years. Every. Single. Day.”

This is a bit of a puzzling one. At first glance, Lewinsky’s metaphor seems similar to the use of epigenetic concepts to describe how sacred texts and their interpretations change over time. However, the references to cultural “DNA” being altered slowly, and with long-term effects, seem to contradict the common perception of epigenetic changes as a faster and more transient alternative to the slower and more permanent evolution of the genetic sequence. My best guess here is that the author has heard of epigenetics as a new concept in evolution and/or phenotypic plasticity in response to environmental changes, and used the term in her article to draw attention to her theme of the lasting cultural impact of her unique experiences in 1998, despite these contradictions. As such, I would say that this comparison is based on an incomplete understanding of the science of epigenetics. (my apologies to Ms. Lewinsky if my assumption is incorrect!).

And finally: the metaphor of epigenetics detaches itself from all meaning

In his recent novel “Bob Honey Who Just Do Stuff”, the actor Sean Penn writes:

“While the privileged patronize this pickle as epithet to the epigenetic inequality of equals, Bob smells a cyber-assisted assault emboldened by right-brain Hollywood narcissists”

What does ‘epigenetic’ mean here, other than a technobabble word that’s fashionable and sounds sciencey? Something to do with subtle differences between superficially equal entities, such as the common trope in the public discussion of epigenetics of DNA methylation differences between genetically identical twins? Something else? All answers welcome!

Epigenetics as a (flawed) tool to think with

So there we have it: four examples of people using epigenetics as a metaphor to explain three very different concepts, plus one rather nihilist use of the word. As we also saw in our published analysis, these examples use different aspects of the popular understanding of epigenetics to drive their comparisons, with varying success in terms of scientific accuracy.

I think we’re going to see more examples of this phenomenon arise as discussions of epigenetics continue to migrate out of academic science and into more common usage. I also think that epigenetic metaphors are likely to add to the rather muddled nature of the public epigenetics discourse; some of the same misunderstandings that we highlighted in our paper are already apparent in these first few reversed comparisons that I stumbled across (and also in some of the uses of epigenetics that I’ve seen crop up in science fiction, which is a topic for another day). I believe that all scientists working in this field should be aware of common public perceptions and misperceptions of epigenetics as we endeavour to communicate our work to non-expert audiences; paying attention to the epigenetic metaphors people use – in either direction – is part of this awareness.

Image: Writing Robot (writing a biblical text), Wikimedia Commons

The post “It’s just like epigenetics” – scientific metaphors for non-scientific concepts appeared first on Making Science Public.

via Making Science Public https://ift.tt/2DsDo5m

[snakecolumn95]

Why You Can’t Afford Not To Meditate (& One Simple Mindfulness Exercise You Can Do Today)

The following is a guest post by Emily Fletcher, a leading expert in meditation for extraordinary performance and former podcast guest of mine on the episode, “Meditation For Mind-Blowing Sex, Meditation For Insomnia, Meditation For Energy & Much More.“

Emily is also the founder of Ziva Meditation. You can use code: BEN50 to save $50 off of The Ziva Technique, a powerful trifecta of mindfulness, meditation, and manifesting designed to unlock your full potential. Its benefits include decreased stress, deeper sleep, improved immune function, and extraordinary performance.

Her book, ​Stress Less, Accomplish More,​ debuted at #7 out of all books on Amazon. Basically, Emily is a meditation ninja, so I couldn’t think of a better person to fill my readers in on the health benefits on meditating. Enjoy!

How To Reverse The Damage Of Stress

It’s easy to fall into the illusion that once you become successful your stress will magically disappear. As a meditation teacher to some of the world’s top performers, I have learned that even people at the top of their game are often crippled with stress. Where this gets tricky is that many of them see this as a positive thing. Most of my CEO clients will say, “Stress gives me my competitive edge.” Many of my actor clients will say, “My stress is where my creativity comes from.” And my fitness friends will say, “Stress fuels me so I can kick a$$ during my workouts.”

The problem is, this isn’t true.

Don’t get me wrong. ​Some​ stress is great. The acute stress of a HIIT workout, a cold plunge, or even something as simple as eating wild plants is indeed good for you. It strengthens the strong mitochondria and kills off the weak ones. This is called hormesis—and it is wildly different than the low-grade chronic stress most of us have been living with for decades.

I’m talking about work deadlines, your passive aggressive mother-in-law, someone cutting you off in traffic. All of these things send us into a fight or flight stress reaction that was once reserved for fighting off predators. Today, our bodies are continuously preparing for battle—even when there’s no physical threat in sight. Add to that the fact that much of our food isn’t food anymore, the 24-hour fear-inducing news cycle, soaking in screen lights instead of sunlight, and we have a perfect recipe for overwhelm and fatigue.

Get The Low Carb Athlete - 100% Free!Eliminate fatigue and unlock the secrets of low-carb success. Sign up now for instant access to the book!<![CDATA[ #_form_64_ font-size:14px; line-height:1.6; font-family:arial, helvetica, sans-serif; margin:0; #_form_64_ * outline:0; ._form_hide display:none; visibility:hidden; ._form_show display:block; visibility:visible; #_form_64_._form-top top:0; #_form_64_._form-bottom bottom:0; #_form_64_._form-left left:0; #_form_64_._form-right right:0; #_form_64_ input[type="text"],#_form_64_ input[type="date"],#_form_64_ textarea padding:6px; height:auto; border:#979797 1px solid; border-radius:4px; color:#000 !important; font-size:13px; -webkit-box-sizing:border-box; -moz-box-sizing:border-box; box-sizing:border-box; #_form_64_ textarea resize:none; #_form_64_ ._submit -webkit-appearance:none; cursor:pointer; font-family:arial, sans-serif; font-size:14px; text-align:center; background:#eb7000 !important; border:0 !important; color:#fff !important; padding:10px !important; #_form_64_ ._close-icon cursor:pointer; background-image:url('https://d226aj4ao1t61q.cloudfront.net/esfkyjh1u_forms-close-dark.png'); background-repeat:no-repeat; background-size:14.2px 14.2px; position:absolute; display:block; top:11px; right:9px; overflow:hidden; width:16.2px; height:16.2px; #_form_64_ ._close-icon:before position:relative; #_form_64_ ._form-body margin-bottom:30px; #_form_64_ ._form-image-left width:150px; float:left; #_form_64_ ._form-content-right margin-left:164px; #_form_64_ ._form-branding color:#fff; font-size:10px; clear:both; text-align:left; margin-top:30px; font-weight:100; #_form_64_ ._form-branding ._logo display:block; width:130px; height:14px; margin-top:6px; background-image:url('https://d226aj4ao1t61q.cloudfront.net/hh9ujqgv5_aclogo_li.png'); background-size:130px auto; background-repeat:no-repeat; #_form_64_ ._form-label,#_form_64_ ._form_element ._form-label font-weight:bold; margin-bottom:5px; display:block; #_form_64_._dark ._form-branding color:#333; #_form_64_._dark ._form-branding ._logo background-image:url('https://d226aj4ao1t61q.cloudfront.net/jftq2c8s_aclogo_dk.png'); #_form_64_ ._form_element position:relative; margin-bottom:10px; font-size:0; max-width:100%; #_form_64_ ._form_element * font-size:14px; #_form_64_ ._form_element._clear clear:both; width:100%; float:none; #_form_64_ ._form_element._clear:after clear:left; #_form_64_ ._form_element input[type="text"],#_form_64_ ._form_element input[type="date"],#_form_64_ ._form_element select,#_form_64_ ._form_element textarea:not(.g-recaptcha-response) display:block; width:100%; -webkit-box-sizing:border-box; -moz-box-sizing:border-box; box-sizing:border-box; #_form_64_ ._field-wrapper position:relative; #_form_64_ ._inline-style float:left; #_form_64_ ._inline-style input[type="text"] width:150px; #_form_64_ ._inline-style:not(._clear) + ._inline-style:not(._clear) margin-left:20px; #_form_64_ ._form_element img._form-image max-width:100%; #_form_64_ ._clear-element clear:left; #_form_64_ ._full_width width:100%; #_form_64_ ._form_full_field display:block; width:100%; margin-bottom:10px; #_form_64_ input[type="text"]._has_error,#_form_64_ textarea._has_error border:#f37c7b 1px solid; #_form_64_ input[type="checkbox"]._has_error outline:#f37c7b 1px solid; #_form_64_ ._error display:block; position:absolute; font-size:13px; z-index:10000001; #_form_64_ ._error._above padding-bottom:4px; top:-41px; right:0; #_form_64_ ._error._below padding-top:4px; top:100%; right:0; #_form_64_ ._error._above ._error-arrow bottom:0; right:15px; border-left:5px solid transparent; border-right:5px solid transparent; border-top:5px solid #f37c7b; #_form_64_ ._error._below ._error-arrow top:0; right:15px; border-left:5px solid transparent; border-right:5px solid transparent; border-bottom:5px solid #f37c7b; #_form_64_ ._error-inner padding:8px 12px; background-color:#f37c7b; font-size:13px; font-family:arial, sans-serif; color:#fff; text-align:center; text-decoration:none; -webkit-border-radius:4px; -moz-border-radius:4px; border-radius:4px; #_form_64_ ._error-inner._form_error margin-bottom:5px; text-align:left; #_form_64_ ._button-wrapper ._error-inner._form_error position:static; #_form_64_ ._error-inner._no_arrow margin-bottom:10px; #_form_64_ ._error-arrow position:absolute; width:0; height:0; #_form_64_ ._error-html margin-bottom:10px; .pika-single z-index:10000001 !important; @media all and (min-width:320px) and (max-width:667px) ::-webkit-scrollbar display:none; #_form_64_ margin:0; width:100%; min-width:100%; max-width:100%; box-sizing:border-box; #_form_64_ * -webkit-box-sizing:border-box; -moz-box-sizing:border-box; box-sizing:border-box; font-size:1em; #_form_64_ ._form-content margin:0; width:100%; #_form_64_ ._form-inner display:block; min-width:100%; #_form_64_ ._form-title,#_form_64_ ._inline-style margin-top:0; margin-right:0; margin-left:0; #_form_64_ ._form-title font-size:1.2em; #_form_64_ ._form_element margin:0 0 20px; padding:0; width:100%; #_form_64_ ._form-element,#_form_64_ ._inline-style,#_form_64_ input[type="text"],#_form_64_ label,#_form_64_ p,#_form_64_ textarea:not(.g-recaptcha-response) float:none; display:block; width:100%; #_form_64_ ._row._checkbox-radio label display:inline; #_form_64_ ._row,#_form_64_ p,#_form_64_ label margin-bottom:0.7em; width:100%; #_form_64_ ._row input[type="checkbox"],#_form_64_ ._row input[type="radio"] margin:0 !important; vertical-align:middle !important; #_form_64_ ._row input[type="checkbox"] + span label display:inline; #_form_64_ ._row span label margin:0 !important; width:initial !important; vertical-align:middle !important; #_form_64_ ._form-image max-width:100%; height:auto !important; #_form_64_ input[type="text"] padding-left:10px; padding-right:10px; font-size:16px; line-height:1.3em; -webkit-appearance:none; #_form_64_ input[type="radio"],#_form_64_ input[type="checkbox"] display:inline-block; width:1.3em; height:1.3em; font-size:1em; margin:0 0.3em 0 0; vertical-align:baseline; #_form_64_ button[type="submit"] padding:20px; font-size:1.5em; #_form_64_ ._inline-style margin:20px 0 0 !important; #_form_64_ position:relative; text-align:left; margin:0px 0px; padding:20px; -webkit-box-sizing:border-box; -moz-box-sizing:border-box; box-sizing:border-box; *zoom:1; background:transparent !important; border:0px solid #b0b0b0 !important; width:300px; -moz-border-radius:0px !important; -webkit-border-radius:0px !important; border-radius:0px !important; color:#000 !important; #_form_64_ ._form-title font-size:22px; line-height:22px; font-weight:600; margin-bottom:0; #_form_64_:before,#_form_64_:after content:" "; display:table; #_form_64_:after clear:both; #_form_64_._inline-style width:auto; display:inline-block; #_form_64_._inline-style input[type="text"],#_form_64_._inline-style input[type="date"] padding:10px 12px; #_form_64_._inline-style button._inline-style position:relative; top:27px; #_form_64_._inline-style p margin:0; #_form_64_._inline-style ._button-wrapper position:relative; margin:27px 12.5px 0 20px; #_form_64_ ._form-thank-you position:relative; left:0; right:0; text-align:center; font-size:18px; @media all and (min-width:320px) and (max-width:667px) #_form_64_._inline-form._inline-style ._inline-style._button-wrapper margin-top:20px !important; margin-left:0 !important; #_form_64_ ._form_10 text-align:center !important; #_form_64_ ._x20518276 label,#_form_64_ ._field10 label text-align:left; #_form_64_ ._form_31 width:100% !important; ]]>

Operating day in and day out with that low-grade, chronic stress is basically like dumping acid—adrenaline and cortisol—into our brains and bodies all day every day. And it’s not doing us any favors in the performance or beauty department. The effects include insomnia, inflammation, premature aging, erectile dysfunction, infertility, irritable bowel syndrome, and anxiety.

So, while it’s not bad for you to ​get​ stressed, it’s terrible for you to stay​ stressed. According to research from Harvard Medical School, stress is responsible for ​90%​ of all doctors visits. Yup, you read that right—90%. And that stress and inflammation may be keeping you from getting the most out of your life and performing at the top of your game.

Ready for some good news? This is all reversible—and the method used to reverse it has been used successfully for over 6,000 years. I’m talking about ​meditation.

Why You’re Not Too Busy to Meditate

Right now, it seems everyone is talking about meditation. And at this point, you probably know you ​should​ be doing it. You’ve heard the seemingly endless amounts of neuroscience behind it; you’ve read the articles about the countless benefits. Maybe you’ve even dabbled with free mindfulness apps or a drop-in studio.

But now that we know for sure it’s so good for us, ​why do so many of us still think we’re too busy to meditate?​ Especially since many of the world’s top performers have outed themselves as meditators, including Bill Gates, Ray Dalio, Tim Ferriss, Oprah, and Jack Dorsey (Check out Ben’s podcast, “Advanced Stress Mitigation Tactics, Extreme Time-Saving Workouts, DIY Cold Tubs, Hormesis, One-Meal-A-Day & More.” for more on how Dorsey uses mediation to handle the tremendous amount of stress he deals with in his life and work.)

People come to me every day and say that they simply don’t have time to meditate. When I ask them what style they are doing they usually say they listen to a YouTube video or do 10 minutes of a guided app here and there. While there is nothing wrong with these styles, they may not be giving you the kind of return on time investment you are looking for. And if you don’t do it everyday you simply aren’t getting the same amount of benefit available if you get your buns in the chair on the reg.

None of us have time to waste. So if you aren’t noticing you have more time, better decision-making capabilities, a stronger sex drive, and more flow state you may want to explore other styles; perhaps even one that you look forward to instead of feeling like it is yet another chore on your to-do list (yes, they do exist).

Right now, meditation is undergoing the same facelift exercise did in the 70s. The evidence is pretty stacked—meditation will indeed make your life better.

Why?

Because it eliminates stress from your brain and body. And eliminating that stress helps you to ​sleep better, have sharper focus, better decision-making skills, a stronger immune system, increased productivity, and even better sex.

Before you roll your eyes, I want you to take all preconceived notions you have about meditation and throw them out the window. If the first thing you think about when you hear “the M word” is monks, incense, fancy fingers, gongs, or hippies, then you’re in luck. You don’t need to be or have any of those things to meditate. Here’s what you ​do​ need to start your meditation career: training.

The reason why so many of us feel like meditation failures is that we assume we should already magically know how to do it. But like anything else, we need to ​learn​ how to do it in order to get the highest return on our time investment. You wouldn’t decide, “I’m going to do a Japanese challenge” and then try to speak Japanese for 20 minutes a day without investing in some sort of training first. That would be unproductive, frustrating and likely lead to you quitting. Similarly, in order to get the most benefit from your meditation practice, you have to learn how to do it. Don’t confuse simplicity for weakness or ease.

But first, let’s get clear on the difference between mindfulness (what most people are practicing) and meditation (what I teach).

Mindfulness vs. Meditation

Recently, the ​New York Times​ reported that out of the 38 million people who downloaded the Headspace app, only 1 million people have paid for a continuing membership.

What that suggests to me is that there are 37 million people out there looking for a mental tool that will make them want to continue on.

This makes sense; because most of the “meditation” apps out there are teaching shades of mindfulness—which is very good at relieving your stress in the right now. Mindfulness is beautiful (it’s even a part of the technique that I teach at Ziva), ​but if you want to get rid of the stress you’ve built up in your cellular and epigenetic memory then we need to give the body the deep healing rest of meditation.​

Research has shown that we are ​storing several generations of stress in our nervous systems​, meaning that your stress isn’t just YOUR stress—it will also affect future generations after you if you don’t take care of it now. To really dive deep and clear out the stress you’ve been storing in your nervous system, it’s time for a hardware upgrade on your brain machine.

So how do you do that?

By practicing a technique that was made for people with busy minds and busy lives. A practice that’s specifically designed to go in and de-excite the nervous system, giving your body rest that is deeper than sleep to help you perform at the top of your game.

I teach a powerful trifecta of mindfulness, meditation, and manifesting called The Ziva Technique. The mindfulness portion is a lovely runway from your 100mph day into the deep, healing rest that is meditation. If mindfulness is the appetizer of The Ziva Technique, meditation really is the main course. I teach a way of meditating that lets you access a verifiable fourth state of consciousness—different that waking, sleeping or dreaming. And this state is what allows your body to access a type of rest allows your body to heal itself—mainly from stress.

You’ll be amazed to find that when you chip away at the backlog of stress stored in your nervous system, you become more productive, more clear, more creative, more patient. Your sleep gets more restful, your anxiety abates, and your sex even gets better! All things that save you time and energy (and help you enjoy your life a lot more).

A perfect example of why you don’t have time NOT to meditate is this: in a case study for meditation and the workplace, Aetna participated in a meditation program to see how it affected general work performance. ​The CEO found that the employees who meditated gained over an hour of productivity each week (translating to a savings of $3,000 per employee per year!). ​This means they were able to work through their to-do lists in less time while also reducing stress.

In addition to increased productivity, meditation also helps you:

Mindfulness and meditation are both important to becoming the most amazing version of yourself and used in tandem will help wipe out stress right now while digging up the trauma that’s been stored in your cells.

Come To Your Senses – One Simple Mindfulness Exercise You Can Do Right Now

If you’re interested in dipping a toe into the type of technique that I teach, here’s a mindfulness exercise that we use to prepare for a sitting of the full Ziva Technique.

This is great for slowing down the momentum of your day so that you can allow everything happening around you to be part of the experience instead of trying to block things out or pretend you can’t hear.

Have a seat with your back supported and your head free. Close your eyes and move through each of your five senses. Notice what you hear, what you feel, what you see, what you taste and what you smell—one at a time. For each one, notice the most prevalent and the most subtle sensations. Then, begin to stack all of your senses on top of one another, holding all of them in your awareness at one time. I would recommend starting with five minutes and building up to eight.

Using your five senses is a great way to ground yourself in your body and in the present moment which is where your fulfillment lives, inside of you and in this moment.

Summary

Meditation is a proven, powerful tool that the world’s top performers rely on to minimize stress. It’s been proven to help with symptoms of depression, enhance longevity, and minimize the cognitive decline that comes with aging.

If you haven’t already, check out my podcast with Emily to learn more about meditation, how you can use it to get the equivalent of taking a power nap, the best form of meditation for sleep or insomnia, and much more.

If you’re ready to give meditation a try for yourself, my company Kion will be leading a FREE 5-day meditation challenge starting next week. Whether you’re new to meditation, want to learn more about it and its benefits, or are a seasoned veteran looking to take part in a worldwide meditation challenge with thousands of other like-minded people from across the globe (Kion’s fasting challenge had over 10,000 participants!), you won’t want to miss this.

With guided meditations led by yours truly, along with Emily Fletcher, Paul Chek and Kion COO, Angelo Keely, you’ll learn how to make meditation practical, the most effective techniques, as well as how to customize your own practice with a comprehensive eBook.

Sign up here to get in on all of the upcoming meditation goodness.

What about you? What are your experiences with meditation, or what questions do you have for Emily or me? Please leave your questions, comments, and feedback in the comments section below, and one of us will reply!

Ask Ben a Podcast Question

Source: https://bengreenfieldfitness.com/article/brain-articles/health-benefits-of-meditation/

[type2diabetestreatments-blog]

What Twins Can Tell Us About the Causes of Diabetes

New Post has been published on http://type2diabetestreatment.net/diabetes-mellitus/what-twins-can-tell-us-about-the-causes-of-diabetes/

What Twins Can Tell Us About the Causes of Diabetes

Stacey Divone sees double every time she looks in the mirror. She’s the slightly older of a pair of identical twins born on Christmas Eve 1976, and when she was just 5 years old, Stacey -- just like her father -- was diagnosed with type 1 diabetes.

The Divone twins

Thirty-five years later, her genetic double is still diabetes-free.

“It fascinates me that we share 100% of the same genes, developed in the exact same womb and grew up in the exact same environment, eating the exact same things, having the same father who had type 1 -- yet one of us has (T1D) and the other doesn’t," Stacey says. "The human body is a mysterious thing sometimes.”

So how common is it for one identical twin to have diabetes, and the other not to? The first line of the first study I dug into to answer that question read, “Monozygotic twins are usually discordant for type 1 diabetes.”

Let me translate that into English for you: When it comes to identical twins, usually only one gets diabetes.

How many sets of twins both have diabetes? About a third, according to the literature.

If your identical twin (should you have one) has type 1 diabetes, your risk for developing type 1 yourself is “only” 35%. That's still a pretty high risk -- and there plenty of stories about twins sharing diabetes, like Amylia Grace Yeaman and her sister in Iowa, Ashley and Emily in Pennsylvania, and the Tale of Two Twins in Massachusetts -- but it’s by no means a slam-dunk, and two-thirds of sets of identical twins have a D-sibling and a sugar-normal sibling.

Despite the scientific knowledge that type 1 is basically genetic, diabetes researchers have long known that identical twins don’t have the identical risk of developing type 1 diabetes; and this fact has long fueled theories of environmental causes as the root source of type 1 diabetes.

But not so fast. It turns out that identical twins are not so identical after all. We have cancer researchers to thank for this insight, not diabetes researchers.

You Look the Same

Monozygotic twins, commonly called identical twins (like Stacey and her sister) are a pair of babies that came from one egg and one sperm cell. In the womb a pair of such embryos have always been viewed as carbon copies of each other, sharing an identical genetic blueprint. And they do.

At least in the beginning.

But in recent decades, genetic research has shown that the DNA of identical twins diverges over time. These so-called epigenetic changes are powered by environmental factors, and drive the twins farther apart genetically as they explore the world on their separate paths.

But wait, that’s not all.

Once published, each of our individual "books of DNA" mutates all on its own, independently of the epigenetic changes, via so-called somatic mutations, a.k.a. copy errors. Something goes wrong during cell division and the DNA changes.

So the older the twins get, the less identical they become, due to these two types of genetic changes. This is why younger identical twins look more the same than older sets—because the younger pairs actually are more identical.

But it’s more than just looks. Somatic changes have a larger impact on the DNA blueprint than epigenetic changes do, and while most somatic changes seem harmless, it’s now believed that most cancers can be traced to somatic mutations.

Thus the interest in somatic mutations on the part of cancer researchers.

So when do somatic changes start happening? Apparently long before birth. One recent study found that the average pair of identical twins actually has more than 300 genetic differences at birth.

Not so identical after all. Yeah, twins can still pull the wool over elementary school teachers’ eyes with the old switch-a-roo in math class, but apparently diabetes isn’t so easy to fool.

Back to the Drawing Board?

So where does that leave us? Does the fact that identical twins aren’t fully identical make twin research worthless in the diabetes arena? Quite the contrary. Identical twins are still very similar. Consider that a human being has something in the neighborhood of 24,000 genes, and typically around 30% of those differ between any two people. That’s 7,200 differences between you and me, while our “identical” twins might only vary by 300 genes or so, at least at birth. In short: There are a lot fewer differences to sort out between twins. If type 1 diabetes turns out to be purely genetic, looking at the differences between not-quite-identical twins may be the fastest way to find the genes causing type 1 diabetes.

So twin studies continue. In fact, the prestigious Barbara Davis Center for Diabetes at the University of Colorado is currently recruiting D-twins and their “unaffected” co-twins for a study. And beyond trying to sort out the root causes of diabetes itself, researchers at the Barbara Davis Center are also studying other autoimmune diseases that appear in conjunction with diabetes. They are investigating how genes might affect an individual’s response to “preventive agents or treatment aimed at preserving insulin-producing cells.”

Exciting stuff.

Fraternal Twins, Unite!

Just to be clear here, the genetic research to date has not focused on fraternal twins, because they are actually two different individuals who came from two separate eggs, but just happened to be in the womb together. As separate individuals, their risk of sharing diabetes would be the same as any (non-twin) siblings.

The Singer twins

But of course being born and growing up in lockstep, fraternal twins still have a very special bond with each other.

We know many of these pairings in the Diabetes Community, including the famous Singer Twins, Mollie and Jackie, who happen to have a mom and aunt by the same names who are also twins and happen to all be part of a country band, MJ2. Mollie is the T1 peep diagnosed at age 4 and has a blog called Cure Moll, while her sister Jackie is a sugar-normal. For the record, they're fraternal twins.

In response our query about her twin relationship, Mollie shares the following:

"I think this is an important topic to write on. Even though we're fraternal and not identical twins, Jackie has gone through extensive testing over the years to see if she carried the R Protein. She's also always been one of my strongest advocates, which is why we started the Diabetic Angels community together, and have always been a team, even though she doesn't have diabetes. But maybe because we're twins, Jackie is very knowledgeable about diabetes and stays informed regarding new management techniques and research. She always says if she were ever diagnosed, she wouldn't be overly concerned because she knows exactly what to do and how to do it... meaning she would be right on a CGM and pump. The other thing Jackie has said since she was a child is that if she could, she 'would take my diabetes for me.' That really is very much a 'twin thing.'"

Twin Type 2s

Meanwhile, diabetes twin research isn’t limited just to those of us with type 1. Swedish researchers recently published the results of a study that followed over 4,000 pairs of twins over a six-year period starting in 1998. They selected identical twins with different BMIs to try to understand the effect of increased weight on health. At the study’s end they announced that they had confirmed one long-held belief about weight and health, and made one confounding discovery.

Not too surprisingly, they say, the heavier twins had increased risk of type 2 diabetes, but the lighter twin actually had a higher risk of heart attack, overturning the long-held belief that weight is an independent heart attack risk.

But is type 2 really as simple as the right genes plus weight? Maybe not.

A smaller study (also from Sweden) suggests that T2D isn't that simple after all. The study looked at 14 sets of twins, in which one in each pair had type 2 diabetes and the other did not, focused on the genes. It found there were differences in the genes that control fat and glucose metabolism between the twin with type 2 diabetes and the sugar-normal twin.

Not Clones, After All

It may turn out that the subtle differences between “identical” twins will be more valuable to our understanding of both types of diabetes than if identical twins were truly identical. While the early differences between “identical” twins may prove over time to weaken the environmental origins theories behind the cause of diabetes, modern twin studies looking at subtle differences between the genetic blueprints of similar people might allow us to determine the role that genes play in the development of diabetes.

For example, take the diabetes research that the Divone Sisters have been a part of.

In 2012, Stacey and her twin signed up for the groundbreaking diabetes genetic project Trialnet to get a better understanding of their "identical," yet not identical DNA.

The Divone sisters with their dad

“The test results confirmed what we already knew: my sister and I are identical twins," Stacey shares. "We were also tested for a number of auto-antibodies for things like type 1 diabetes, celiac disease and Addison’s disease. My m1AA auto antibody level was way elevated, obviously since I have type 1. Everything else for me was at normal levels, thankfully. My sister showed normal levels for everything, including type 1.”

Like the majority of “identical” twins, Stacey’s sister was just different enough from Stacey, genetically, to duck the diabetes bullet. Even though their dad had lived with type 1, only one of the sisters have followed in those pancreatically-challenged footsteps.

“This was such a relief, I’m sure to both of us, but for me especially,” says Stacey, who blogs over at The Girl With The Portable Pancreas. “Even though I’ve lived with it for 35 years, I never would want to see her have to live with it, too.”

I guess twins don’t really share everything after all. Which is heartening, in some ways...

Disclaimer: Content created by the Diabetes Mine team. For more details click here.

Disclaimer

This content is created for Diabetes Mine, a consumer health blog focused on the diabetes community. The content is not medically reviewed and doesn't adhere to Healthline's editorial guidelines. For more information about Healthline's partnership with Diabetes Mine, please click here.

Type 2 Diabetes Treatment Type 2 Diabetes Diet Diabetes Destroyer Reviews Original Article

[mthrynn]

For more than a decade the swelling output from life sciences experimental instruments has been overwhelming research computing infrastructures intended to support them. DNA sequencers were the first – instrument capacities seemed to jump monthly. Today it’s the cryo electron microscope – some of them 13TB a day beasts – causing consternation. Even a well-planned brand new HPC environment can find itself underpowered by the time it is switched on.

A good example of the challenge and nimbleness required to cope is Van Andel Research Institute’s (VARI) initiative to build a new HPC environment to support its work on epigenetic, genetic, molecular and cellular origins of cancer – all of which require substantial computational resources. VARI (Grand Rapids, MI) is part of Van Andel Institute.

With the HPC building project largely finished, Zack Ramjan, research computing architect for VARI, recalled wryly, “About 10 months ago, we decided we were going to get into the business of cryo-EM. That was news to me and maybe news to many of us here. That suite of three instruments has huge data needs. So we went back and luckily the design that we had was rock solid that’s where we kind of started adding.” He’d been recruited from USC in late 2014 specifically to lead the effort to create an HPC environment for scientific computing.

Titan Krios

The response was to re-examine the storage system, which would absorb the bulk of the new workload strain, and deploy expanded DDN storage – GS7K appliances and WOS – to cope with demand expected from three new cryo-EMs (FEI Titan Krios, FEI Arctica, and smaller instrument for QC). Taken together, the original HPC building effort and changes made later on the fly showcase the rapidly changing choices often confronted by “smaller” research institutions mounting HPC overhauls.

Working with DDN, Silicon Mechanics, and Bright Computing, VARI developed a modest-size hybrid cluster-cloud environment with roughly 2000 cores, 2.2 petabytes of storage, and 40Gb Ethernet throughout. Major components include private-cloud hosting with OpenStack, Big Data analytics, petabyte-scale distributed/parallel storage, and cluster/grid computing. The work required close collaboration with VARI researcher – roughly 32 groups of varying size – to design and support computing workloads in genomics, epigenetics, next-gen sequencing, molecular-dynamics, bioinformatics and biostatistics

As for many similar-sized institutions, bringing order to storage architecture was major challenge. Without centralized HPC resources in-house, individual investigators (and groups) tend to go it alone creating a chaotic disconnected storage landscape.

“These pools of storage were scattered and independent. They were small, not scalable, and intended for specific use cases,” he recalled. “I wanted to replace all that with a single solution that could support HPC because it’s not just about the storage capacity; we also need to support access to that data in a high performance way, [for] moving data very fast, in parallel, to many machines at once.”

A wide range of instruments – sequencers and cry-EM are just two – required access to storage. Workflows were mixed. Data from external collaborators and other consortia were often brought in-house and had a way of “multiplying after being worked on.” Ramjan’s plan was to centralize and simplify. Data would stream directly from instruments to storage. Investigator created data would likewise be captured in one place.

“There’s no analysis storage and instrument storage, it’s all one storage. The data goes straight to a DDN device. My design was to remove copy and duplications. It comes in one time and users are working on it. It’s a tiered approach. So data goes straight into the highest performing tier, from there, there is no more movement.” DDN GS7K devices comprise this higher performing tier.

As the data ‘cools’ and investigators move to new projects, “We may have to retain the data due to obligations or the user wants to keep it around; then we don’t want to keep ‘cold’ data on our highest performing device. Behind the scenes this data is automatically moved to a slower and more economical tier,” said Ramjan. This is the WOS controlled tier. It’s also where much of the cryo-EM data ends up after initial processing.

DDN GRIDScaler-GS7K

Physically there are actually four places the data can be although the user only sees one, emphasized Ramjan. “It’s either on our mirrored pool – we have two GS7Ks, one either side of the building for disaster recovery in terms of a flood or tornado something like that. If the data doesn’t need to have that level of protection it will be on one of the GSK7s or it will be replicated on WOS. There are two WOS devices also spread out in the same way so the data could be sitting mirrored, replicated, on either side. The lowest level of protection would be a single WOS device.”

“Primary data being – data we’re making here, it came of a machine, or there’s no recreating it because the sample is destroyed – we consider that worthy of full replication sitting in two places on the two GS7Ks. If the user lets it cool down and it will go to the two WOS devices and inside those devices is also a RAID so you can say the replication factor is 2-plus. We maintain that for our instrument data.”

Data movement is widely control by policy capabilities in the file system. Automating data flow from instruments in this way, for example, greatly reduces steps and admin requirements. Choosing an effective parallel file system is a key component in such a scheme and reduces the need for additional tools.

“There are really only three” options for a very high performance file systems,” said Ramjan, “GPFS (now Spectrum Scale from IBM), Lustre, and OneFS (Dell DMC/Isilon).” OneFS, said Ramjan, which VARI had earlier experience with, was cost-prohibitive compared to the other choices. He also thinks Lustre is more difficult to work than GPFS and lacked key features.

“We had Isilon before. I won’t say anything bad about it but pricewise it was pretty painful. I spent a lot of time exploring both of the others. Lustre is by no means a bad option but for us the right fit was GPFS. I needed something that was more appliance based? You know we’re not the size of the university of Michigan or USC or a massive institute with 100 guys in the IT department ready to work on this. We wanted to bring something in quick that would be well supported.

“I felt Lustre would require more labor and time than I was willing to spend and it didn’t have some of the things GPFS does like tiering and rule-based tiering and easier expansion. DDN could equally have sold us a Lustre GSK too if we wanted,” he said.

Zack Ramjan-VARI

On balance, “Deploying DDN’s end-to-end storage solution has allowed us to elevate the standard of protection, increase compliance and push boundaries on a single, highly scalable storage platform,” said Ramjan. “We’ve also saved hundreds of thousands of dollars by centralizing the storage of our data-intensive research and a dozen data-hungry scientific instruments on DDN.”

Interesting side note: “The funny things was the vendors of the microscopes didn’t know anything about IT so they couldn’t actually tell us concretely what we’d need. For example, would 10Gig network be sufficient? They couldn’t answer of those questions and they still can’t unfortunately. It put me in quite a bind. I ended up talking with George Vacek at DDN and he pointed me towards three other cryo-EM users also using DDN, which turned out to be a great source of support.”

Storage, of course is only part of the HPC puzzle. Ramjan was replacing a systems that had more in common with traditional corporate enterprise systems than with scientific computing platforms. Starting from scratch, he had a fair degree of freedom in selecting the architecture and choosing components. He says going with a hybrid cluster/cloud architecture was the correct choice.

Silicon Mechanics handled the heavy lifting with regard to hardware and integration. The Bright Computing provisioning and management platform was used. There are also heterogeneous computing elements although accelerators were not an early priority.

“The genomics stuff – sequencing, genotyping, etc. – that we’ve been doing doesn’t benefit much from GPUs, but the imaging analysis we are getting into does. So we do have a mix of nodes, some with accelerators, although they are all very similar at the main processer. The nodes all have Intel Xeons with a lot of memory, fast SSD, and fast network connections. We have some [NVIDIA] K80s and are bringing in some of the new GTX 1080s. I’m pretty excited about the 1080s because they are a quarter of the cost and in our use case seem to be performing just as well if not a little but better,” Ramjan.

“I had the option of using InfiniBand, but said listen we know Ethernet, we can do Ethernet in a high performance way, let’s just stick with it at this time. Now there’s up to a 100 Gig Ethernet.”

In going with the hybrid HPC cluster/cloud route, Ramjan evaluated public cloud options. “I wanted to be sure it made sense to do it in-house (OpenStack) when I could just put it Google’s cloud or Amazon or Microsoft. We ran the numbers and I think cloud computing is great for someone doing a little bit of computing a few times year, but not for us.” It’s not the cost of cycles; they are cheap enough. It’s data movement and storage charges.

Cloud bursting to the public cloud is an open question for Ramjan. He is already working with Bright Computing on a system environment update, expected to go live in March, that will have cloud bursting capability. He wonders how much it will be used.

“It’s good for rare cases. Still you have to balance that against just acquiring more nodes. The data movement in and out of the cloud is where they get you on price. With a small batch I could see it being economical but I have an instrument here that can produce 13 TB a day – moving that is going to be very expensive. We have people doing molecular dynamics, low data volume, low storage volume, but high CPU requirements. But even then latency is a factor.”

System adoption has been faster than expected. “I thought utilization would ramp up slowly, but [already] we’re sitting at 80 percent utilization on a constant basis often at 100 percent. It surprised me how fast and how hungry our investigators were for these resources. If you would have asked them beforehand ‘do you need this’ they probably would have said no.”

The post Van Andel Research Optimizes HPC Pipeline with DDN appeared first on HPCwire.

via Government – HPCwire

[the-fire-genome-blog]

Chapter Two - Fire

Tristan was aware that something was not normal, but he didn’t know what. This “Illness” as he describes it, is a biological mutation on a microscopic level. Even before he was born, a part of his epigenetic code had undergone an alteration. This change meant that some cells in his body would stop inhibiting a certain part of his genetic code, his DNA, fundamentally changing how his body functions.

This mutation had laid dormant for 18 years, waiting for the ample time to activate. That time had come as he had grown enough, now able to produce enough energy to supply his cells with the needed nutrients. Over the last year and 4 months, his body had been working hard at multiplying this cell with a completely new function, into fully operational organelles, masses of cells with a similar purpose.

Tristan’s DNA had stretched out, revealing the PYL-145 gene for the first time in his life. This gene caused the cell to change functionality completely, transforming itself into the first Pyrocial cell that’s ever existed. This Cell multiplied so much, that it created a new layer of skin beneath the endodermal layer on his finger-tips. The Pyrodermal layer, a square centimeter of biological mass that siphons oxygen and iron from his body, had become a functional part of his body.

In addition to that, Tristan felt uncomfortable pain in the abdomen, the upper torso and the skull. PYL-145 was also affecting the function of the cells in his esophagus, stomach, brain and lungs. His lungs became better at absorbing larger quantities of Oxygen atoms from the air he breathes in. His stomach discarded a lot less of the Iron atoms found in his food. His brain also devoted a small section of the frontal lobe to creating neurons that control those new organelles. Tristan’s body was mutating at an alarming rate, and he had every right to be terrified.

WHAT’S GOING ON WITH ME? - cried Tristan, whilst running through the forest - HELP!

Who’s there? - a voice was heard in the distance.

Huh? … Is anyone there? IS ANYONE THERE? HELP!

I’m coming!

Tristan had stopped to judge where that sound was coming from. A nearby brush rattled, only to reveal the face of a concerned young girl, running towards the desperate call for help. Just as she locked eyes with the startled Tristan, the coat he was holding instantly caught on fire. He quickly let go of the coat and as it fell to the ground, the magnitude of the situation became apparent, but while Tristan was petrified, the girl instantly detached her cloak and threw it atop the flaming jacket.

Jump!

What? - mumbled Tristan while still trying to understand the situation.

Jump, Jump! On top of it! Put it out!

Tristan had suddenly snapped back to reality and involuntarily jumped face-first atop the cloak. He stood there for a split second while realizing how stupid he must look to this kind stranger. In one swift motion he got up and faced the girl, with a grin that begged this situation to be instantly forgotten.

I meant … with your shoes… - said the girl whilst motioning her head towards her own feet - see, I’m barefoot!

Yeah… yeah… uh, hi. I mean, thank you. Very much.

Hi - forced the girl through her giggle - No worries. Why were you holding a flaming coat, though?

Holding, I wasn’t holding …

Uh, i’m pretty sure I saw you holding it.

Yeah, but, no, I mean, uhm …

You ok?

Actually - Tristan sighed as he took a deep breath and regained his composure - no ....

No?

I’m a bit lost at the moment, sorry for dragging you into this. I best be going. - Tristan turned around and started to walk away calmly.

Wait… - the girl yelled out and Tristan instantly froze. - Wait, my name is Melina.

I’m Tristan. Nice to meet you.

I’m sure it was nice, since you forgot your coat …

Oh … I, uh. - Tristan hesitated and looked at his fingertips, they were neither warm nor glowing. - I think i’ll just leave it there. Sorry about your cloak.

My cloak? It should be fine, we put out the fire.

Yeah …

Speaking of … Why exactly were you holding a flaming coat.

It - Tristan stopped and began thinking of what to say.

C’mon you can tell me, we probably won’t ever meet again.

Are you not from around here?

No. My family and I are nomads, we never stay in the same forest twice.

Nomads? Like Murrio?

Who?

You know, Murrio. Altarian war hero, black hair, very famous.

I’m afraid I don’t know sorry. Look …

Ye?

I can see you’re all stressed and stuff … My mom’s finishing up a batch of mushroom stew.

I really shouldn’t …

It’s about a minute away. Really delicious too.

I …

I can’t make you come, y’know. You just said you weren’t ok … I thought I was being helpful…

You are! Really, thank you. You just … You should stay away from me.

What? … I’m confused. Why?

You … you just might get burned.

Tristan forced himself to turn around and sighed. He took a step forth and started running back home as if nothing had happened at all. As he got back into the rhythm of spriting, he noticed how empty his hand felt without the jacket in it and briefly turned around, only to realise that whatever he encountered in that forest, he had no choice but to forget.

[makingscipub]

A road called ‘gene drive’ and the road to ‘gene drive’: Trials and tribulations of media analysis

As people might know, I enjoy doing media analysis of emerging biotechnologies, from cloning to gene editing and beyond.

I have lately become fascinated with something called ‘gene drive’, a new genetic engineering technology that was brought to public attention around 2014/2015 at the confluence of two ‘events’: the outbreak of Zika and advances in CRISPR-Cas9 as a new tool to ‘edit’ genomes more or less at will (declared breakthrough of the year in 2015).

Zika is an emerging infectious disease caused by the Zika virus. Like malaria or dengue fever, it is transmitted by mosquitoes. The Zika outbreak around 2015 made people think more intensively about how to deal with the spread of such diseases and about finding new ways of dealing with the spreaders, namely the mosquitoes.

CRISPR-Cas9 is a new genome editing tool that makes it easier for scientists to modify genomes, of, for example, mosquitoes, in such a way that the change spreads exceedingly quickly through a population bypassing normal laws of inheritance. With the help of this new technology called ‘gene drive’, whole populations of mosquitoes can thus, in theory, be changed, eliminated, replaced and so on. This has so far not been tried anywhere in the wild and is, as you can imagine, rather controversial. The use of gene drive using genome editing for insect/disease control was put on the map in 2014 by Kevin Esvelt and others and has attracted some media attention ever since.

How is this controversy reported in the media, we wondered? By ‘we’ I mean Sarah Hartley, PI on a Wellcome Trust funded ‘Talking about gene drive’ project, Aleksandra Stelmach, research fellow on the project, and I, co-applicant.

Easy-peasy I thought. Put the phrase “gene drive” into Nexis, my favourite news database, and see what happens, i.e. see how it spreads, possibly exponentially, through the main English speaking news outlets. So we did. What happened was chaos.

Dead ends, new pathways and resurfaced roads

There were two problems. There is somewhere in the United States a road called “gene drive”. That’s the first problem. The second problem was that despite using quotation marks in order to search for the exact phrase ‘gene drive’, the machine picked out instances of, for example, ‘the cart that Gene drives’ or ‘genes drive the development of x’ and so on. Yet another problem was that Nexis was, unbeknown to us, in a process of transformation and quite a few things, like downloading, didn’t work.

In the end, we used another search engine, one I am not so familiar with, namely Factiva. We found it quite useful, as it also provides access to graphs and keywords etc. We searched for ‘gene drive’ in four regions: US, UK, Australia and Uganda. There were still some problems, but we got some interesting corpora and data.

Just when we had started to analyse these, Nexis changed. It became usable again (but the exact phrase search thing still doesn’t really work). It even has little graphs now and key word analyses.

As I have access to Nexis but not Factiva (only Aleksandra has access to Factiva in Exeter), I did a bit of searching once Nexis worked again – I couldn’t resist. I got some interesting results, once I had discarded the still lurking roads called ‘gene drive’ and some other anomalies.

The road to ‘gene drive’

For this little post I just wanted to know how and when conversations about gene drive started to emerge (but as I said above they only really got going around 2015). What I found confirmed what I had already dug out in my first blog post on gene drive. The first English language news article using the phrase ‘gene drive’ was published in 2007. The second in 2009. The topic exploded after 2015 (but not as much other topics, such as epigenetics and the microbiome, for example). I still haven’t met anybody out in the real world who knew what I was talking about when I mention ‘gene drive’….

The 2007 article refers to research carried out into this issue about 20 years earlier, that is, around 1996/97. As the phrase ‘gene drive’ wasn’t used before 2007 in English news, I searched for the larger category of ‘genetically modified mosquitoes’ (or GMM) and found an article from 1996.

I’ll now say a little bit about these early articles. First the 1996 one (i.e. the first one on GMM), then the 2007 and then the 2009 ones (i.e. the first two on gene drive proper). In between there were of course many others relating to various forms of GMM, including gene drive before the name started to be used. And it should be stressed that research into what one might call population GM was carried out in the sixties by Chris Curtis and George Craig, for example.

1996

The 1996 article, published on 15 June 1996 in The San Diego Union-Tribune, reports on research carried out at the University of California San Diego by Jane Burns and published in Proceedings of the National Academy of Sciences (PNAS). She talks about how one could in “a specific and controlled way… be genetically altering the mosquitoes so they can’t transmit diseases”. Her work dealt with Anopheles gambiae, which are mosquitoes that transmit malaria. They are also one the test organisms of choice used nowadays by gene drive researchers at Imperial College.

Burns compares what she does to ‘vaccinating’ the mosquitoes instead of vaccinating the people, a framing that is still being used today, for example by Austin Burt at Imperial College. In practice this means the GMM would have a trait conveyed by a “transferred gene” that “can be passed from generation to generation”.

How is this done? “Burns has succeeded in engineering the mosquito cells because she designed a virus that can penetrate the cells and deliver genes”. You have to read the whole article to understand exactly what’s going on! The title of the PNAS paper is: “Pantropic retroviral vectors integrate and express in cells of the malaria mosquito, Anopheles gambiae”. She basically succeeded in doing something that nowadays can be achieved more quickly by genome editing using CRISPR-Cas9 I think…

2007

The 2007 article, also based on a paper published in PNAS – the first using the phrase ‘gene drive’ in our corpus – appeared on 25 July in US States News and is in fact a press release by Virginia Tech and the University of California Irvine. It starts by saying: “A decade ago, scientists announced the ability to introduce foreign genes into the mosquito genome. A year ago, scientists announced the successful use of an artificial gene that prevented a virus from replicating within mosquitoes” (that 2006 paper also appeared in PNAS – it focused on genetically modifying Aedes aegypti which transmit dengue fever).

The 2007 paper, also focusing on Aedes aegypti, “demonstrated the ability to express a foreign gene exclusively in the female mosquito germline”. The main player here was Zach Adelman. The gene drive system they developed used “the nanos (nos) gene, which is essential for germline formation”.

To explain how their ‘gene drive system’ works, Adelman used a metaphor, namely that of key. “’Think of the nanos instructions as a key to a room,’ Adelman said.” Unfortunately, we don’t hear much more about that key! The metaphor is not elaborated and the rest of the press release is pretty impenetrable to lay people!

2009

The 2009 article, which appeared on 30 May 2009 in New Scientist, is quite long, well written, draws the reader in and focuses mainly on the use of Wolbachia in an Australian experiment. At the very end, the reporter Rachel Nowak also talks about various kinds of ‘gene drive’, but only briefly.

Back to a dead end – and the road ahead

Reading this New Scientist article, I remembered another one published in 2003 by Oliver Morton, entitled Splat!, and reporting on work relating to what one might call a proto-gene-drive carried out by Austin Burt and Andrea Crisanti at Imperial College. I searched Nexis high and low and I could not find the article. It should be there, but it wasn’t. This shows that one cannot rely on anything!

2003

Anyway, the article describes the work of Burt and Crisanti very nicely and in much needed detail. It turns out that they developed a ‘gene drive’ before CRISPR-Cas9 was even on the horizon, which is interesting, as, confusingly, some people, even scientists and commentators in Nature, define gene drive by reference to CRISPR-Cas9. In the 2003 case, researchers used a different genetic trick to do what CRISPR-Cas9 now does, namely ‘homing endonuclease genes’.

Morton homes in on the most important aspect of gene drives, namely the copying of a genetic change from one chromosome to the other in a cell – which was also used in this case. “In organisms that have paired chromosomes, a gene present on only one chromosome normally gets passed on to exactly half the organism’s offspring. Unless, that is, the gene is an HEG [homing endonuclease genes]. An HEG on one chromosome in a cell can use that cell’s repair mechanisms to get itself copied onto the chromosome’s partner. If the cell in question is a cell that makes eggs or sperm, this copying means that all the eggs or sperm will contain a copy of the HEG – and so all the offspring get a copy. In this way HEGs can spread through a population very quickly indeed.” That’s ‘gene drive’.

Homing endonuclease genes or HEGs were, some say, “the first engineered ‘gene drive’”, but the news, at least as recorded by Nexis, didn’t pick that up. For gene drives to become newsworthy we had to wait for them to go CRISPR.

Finding a road through the semantic jungle

Gene drive research seems to have started about two decades ago (with roots that reach into the 1960s), but it will still be long time before gene drives will be deployed, if at all, according to most experts involved. GMM, by contrast, are being field-tested already.

For me, it will take an even longer time still to get my head around all the types of gene drives that I have now read about (natural and synthetic, global and local, etc…. there is even a lovely sounding daisy drive)! So I was quite relieved when reading through our Nexis samples and found Burt saying in 2018: “there isn’t even agreement on what a gene drive is”!

‘Gene drive’ seems to be an extremely polysemous phrase, that is to say, it has many meanings, some old, some new, some used by some people, some by others, sometimes denoting an object (a ‘cassette’), sometimes a process (‘mutagenic chain reaction’), and so on. This makes it very difficult for non-experts to talk about ‘gene drive’ in any, at least vaguely knowledgeable, way. That’s at least my personal impression!

I’d appreciate any help I can get to find a road through this semantic jungle! Something like this perhaps, metaphorically entitled ‘Sculpting Evolution, but catering more for the lay person.

Image: Road in California, Pixabay

  The post A road called ‘gene drive’ and the road to ‘gene drive’: Trials and tribulations of media analysis appeared first on Making Science Public.

via Making Science Public https://ift.tt/2NeqqfU