Scottish man has twins through IVF using 27-year-old sperm – The i … – iNews

A Scottish man has earned a world record after becoming the father of twins through IVF using sperm that he froze almost 27 years ago.

The man, who lives in Glasgow but has requested anonymity, was diagnosed with cancer at the age of 21 and was advised to freeze his sperm in case the chemotherapy he needed left him infertile.

When we finally saw on a scan we were having twins I was in shock

World record holder

After surviving cancer, his sperm remained frozen for 26 years and 243 days until he and his partner decided to use it to have children through IVF in 2010.

His partner became pregnant with twins at the age of 37 and the boy and girl were born the following year, landing him a Guinness World Record for the oldest sperm ever successfully used in IVF.

Although he has known about the record for years, the man did not have it verified because he did not want to be named in public. However, he has now had it accepted on the basis of anonymity.

Read more: Male fertility alert after sperm count dives by more than half

The man said he hoped his record would show other cancer patients that they can still have children years after finishing their treatment.

People going through chemotherapy should keep hope, he added. When we finally saw on a scan we were having twins I was in shock.

I kept looking for a third heartbeat, thinking we might even be having triplets.

The mans sperm was stored at an NHS lab in Edinburgh before his chemotherapy, before being transferred to the private GCRM fertility clinic in Glasgow for use in the couples IVF.

The clinics medical director Dr Marco Gaudoin said the mans case showed that sperm could theoretically be stored indefinitely and still be used to father children.

According to the Human Fertilisation and Embryology Authority regulator, the standard storage period for sperm is normally ten years. In some circumstances it can be kept for up to 55 years.

Women are also able to freeze their eggs while they are young for use in later IVF treatment, while couples hoping to conceive are also able to freeze fertilised embryos before they are implanted in the womb.

Last week it emerged that two men are set to become the first same-sex couple in Scotland to have twins through IVF, after using a donor egg and a surrogate mother.

Ryan Walker and Chris Watson, from Falkirk, are expecting a boy and a girl in the next few weeks. The pregnancy came against the odds.

Like the man from Glasgow, Mr Walker had to have his sperm frozen after being diagnosed with cancer five years ago.

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Grey’s Anatomy Season 13’s Gag Reel Is Here to Help You Start … – E! Online

The struggle is real, Grey's Anatomy fans.

We've still got over a month before we can check back in with the good doctors of Grey Sloan Memorial Hospital to see how they're recovering after last season's (literally) explosive finale.Our impatience over waiting for the two-hour season 14 premiere may be growing stronger, but we've got a new way to distract ourselves from our Grey's hunger pangs: The season 13 gag reel.

Exclusive to E! News, and available as a bonus feature on the season 13 DVD set (in stores August 29), this year's reel has all of your faves cutting loose and cracking up. There's Ellen Pompeo continually referring to Dr. Webber as the "Director of Admissions" despite knowing full-well that's not his title, and Justin Chambers stumbling over the usually easily pronounceable phrase "surgical consult." Not to be outdone, Jesse Williams begins saying lines that aren't even his, while an extra full-on breaks a table in one scene.

"We still doing the TV show?" Chandra Wilson asks hysterically.

When the show returns for season 14, some of the laughter from the gag reel just might be making its way into the final cut, Jessica Capshaw recently admitted to E! News. When asked how the hospital was handling the events of the finale, she had this to offer:"I think it's in a recovery and I think it's not only in a recovery, but it's in sort of like a moment where you find your placeand you gain a little traction and then you move positively and forward-ly on. We did a table read for both the firstand second episodes, and they are righteously hysterical. They're so much fun and very sort of going back to firstand second season Grey's. It's very funny. It's very irreverent and funny and sort of on its side. I think it'swhat you remember and love about the beginning of the original group."

Whose flub has you cracking up the most? Sound off in the comments below!

Grey's Anatomy: The Complete 13th Season hits shelveson Tuesday, Aug. 29, while Season 14 premieres Thursday, Sept. 28 at 8 p.m. on ABC.

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Grey's Anatomy Season 13's Gag Reel Is Here to Help You Start ... - E! Online

Popular to Contrary Opinion: The anatomy of a bar – Colorado Daily

Freeman

Bars are wonderful places, and they're staffed by more than just a Sam Malone from "Cheers" or whoever worked the taps at the Mos Eisley Cantina in "Star Wars."

I put myself through school working in a bar, and I'm still working in a few. It's a lot more than just pouring beers, flirting or cracking skulls. Today, we're talking about service industry workers that don't survive on tips. Certain employees make more money, work more and meet more, um, partners.

First off, owners foot the bills and in my experiences may be the most worthless person in the bar. Their opinion of what may or may not work usually doesn't. Owners change the dcor to from the dingy old music posters and Magic Markered dollar bills that everybody loved to clean-cut Jimmy Buffet-looking crap that looks like it was designed by your cat lady aunt who's trying really hard to impress her imaginary knitting club. Owners sometimes raise drink prices by a quarter which means a lot more math for bartenders, which means bartenders spend more time doing something besides making money.

Managers, duh, manage the bar. They do just about everything: order booze, run social media, fix computers, hire, fire, re-hire, make schedules and try to figure out how to keep the place afloat. There are "fun managers" that might let you drink on the job, and there are "dickhead managers" that treat the staff like personal slaves and may charge you for the half a Red Bull you chugged because you worked a double.

Owners and managers will tell you when to close or how late to stay open, even if there's nobody coming in for drinks or their leechlike friends aren't leaving after closing time.

Depending on your bar's size or style, you might have a chef, who's generally everybody's favorite. He's the dude that will add extra everything to your employee meal. Most important, the chef will probably be your drug connection.

Next are most people's least favorite workers: security. Bouncers are the smashed bugs underneath the totem pole. Movies make this job seem a lot cooler than it actually is. Nearly 99 percent is doing absolutely nothing, unless you're allowed to get drunk and screw off with your bouncer friends then the job can be really fun.

As a bouncer, you're standing, stopping fights, preventing fights, hoping that fights happen, getting into fights, talking to girls, checking IDs, charging covers (even when there isn't one) and other types of manual labor such as taking out garbage. Mostly just standing. Sitting if you're lucky.

Like I said, I've done most jobs, but there's one I never have and never will do: deejay. A deejay basically has the best job in the place. They don't deal with customers except for taking requests. (Here's a hint: If you want your song to get played, be a hot chick.) As long as the laptop, spinny things and electricity is working, deejays make their money because they don't work for tips. Pretty awesome. Even better, nobody gets hit on more than a deejay.

It's closing time for today. Tune in next week for bartenders, servers and a secret worker.

Read more Freeman: coloradodaily.com/columns. Stalk him: comfyconfines.wordpress.com

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Popular to Contrary Opinion: The anatomy of a bar - Colorado Daily

SPINELESS WONDERS: Happy itching when chiggers feast on human flesh – pharostribune.com

Dear Dr. Tim,

Every time I go out to pick raspberries I come home with chiggers. They itch like the blazes and especially so in very sensitive places. What are chiggers and why am I plagued by them?

Thanks, Itchy

Dear Itchy,

Americans should not have to tolerate rude behavior, especially from something as small as a chigger! And yet, that is just what we are exposed to every summer from May through September throughout the country. Chiggers are adolescent mites, so tiny that they are seldom seen. Several can actually fit on the period at the end of this sentence.

Most self-respecting mites feed on plants. It is only the teenage mites that bite people. Apparently, once they mature to adulthood, they grow out of their immature and obnoxious behavior of biting people, and live the rest of their lives feeding peacefully on plants.

Gangs of juvenile chiggers all have the following M.O. (modus operandi). They hang out on the tips of tall grasses, shrubs and weeds and wait to drop off onto any larger animal that happens to brush by. Usually these animals are birds, amphibians or small mammals but the mites are just as happy with the odd human that passes by. When chigger mites fall onto shoes or pant legs, they begin climbing in search of tender, moist skin to bite. They seem to concentrate in areas where clothing fits tightly against the body, such as around the ankles, groin, waist or armpits. This is exactly the rude behavior that I am talking about. A bite on an arm or back of the neck can be scratched in public. But public scratching of the groin, armpits or under the bra strap is an entirely different matter. It is socially unacceptable, politically incorrect and may even be illegal in some countries.

But, scratch you must. Once chiggers bite, there is no alternative. Chiggers do not burrow into the skin but rather pierce skin cells with their mouthparts and inject their special chigger saliva. This saliva contains enzymes that break down cell walls and causes the skin cells to liquefy. Meanwhile, human immune systems quickly react to this foreign enzyme resulting in, not only infuriatingly and intense itching, but also in the formation of a hard, red wall at the location of the bite. Chiggers capitalize on this body reaction by using the round wall, called a stylostome, as a straw to suck up their meals of dissolved body tissues, and then they promptly drop off. They are gone. They seem to never think twice about the trouble they have caused others. Meanwhile, the itching intensifies over the next 20 to 30 hours even though the mite is no longer present. Depending on the persons individual sensitivity and body reaction, itching may continue for days or even weeks.

So, what can be done? And probably most important, how does one stop chigger bites from itching?

Well, aside from amputation, physicians can sometimes prescribe an antiseptic/hydrocortisone ointment. This may help ease the itch and reduce chances of secondary infections caused by the itching and scratching, but it is not a perfect answer.

The best solution is prevention. Avoid getting into chiggers in the first place. Stay away from tall grasses and shrubs where chiggers are known to live. Chiggers love to live in brambles, as most people who pick black raspberries know or quickly learn. They also inhabit taller grasses close to the ponds and streams where bank fishermen stand. (Both raspberry pickers and fishermen can easily be spotted due to their obsessive scratching).

If you must go in those areas, tuck your pant legs into your socks and apply insect repellant containing DEET to the shoe and ankle area. This will stop many of the mites from gaining access to the skin and beginning their climb to areas where clothing fits tightly. (Theoretically, avoiding tight-fitting clothes or even going naked might help. If nothing else, it will certainly confuse the little biters not to mention friends and neighbors.)

I have found that if you know or suspect that you have been in chigger-infested habitats, take a hot, soapy shower as soon as possible. The mites are so small that it may take them several hours to crawl from shoes to where they want to bite, so you have plenty of time to wash them away. This is an effective prevention. Change your clothes and put the clothes you were wearing into the washer and dryer.

These methods are for the prevention of bites, but since you have already been bitten, happy itching.

Tim Gibb is a professor of entomology at Purdue University. He can be reached at gibb@purdue.edu

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Part II Beauty, Cooperation, and the Hadza Hunter-Gatherers – HuffPost

In The Evolution of Beauty, Yale ornithologist Richard Prum elaborates on Darwins theory of the effect of sexual selection on evolution. Beyond survival of the fittest, the sexes have asymmetric interests. Males, with their cheap sperm, seek to sire as many offspring as possible. Females with their expensive eggs and limited lifetime reproductive opportunity, seek to pick the best mates. Males compete with one another for control of females. Females seek to avoid male control and to choose their mates freely. In many species, male competition results in bigger, stronger, and more weaponized males, as in huge sea lion males with long tusks. Prum focuses on female choice.

Female choice, given free rein, can lead to arbitrary standards of beauty and behavior in a species. Among neotropical manakins, females do all the work of raising chicks while males contribute only sperm. Males dance, sing, and flash their colors on communal display grounds known as leks; the females arrive, watch, pick a male for a quickie, and leave. The females favor only a few of the males; the rest may never get to mate. Blue manakins have even evolved a cooperative dance among a group of five or six males; females choose between groups of dancers, mating with the alpha male.

Prum moves from birds to humans. Humans, he points out, are far more cooperative than our African ape relatives, gorillas, chimpanzees and bonobos. Men and women dont differ as dramatically in size as male and female apes. Unlike apes, humans tend to monogamy, he says, because females need help raising the kids. Prum also cites surveys showing that women do not prefer big, square-jawed macho males; rather, they go for men with moderate physiques and gentle behavior. Prum goes on from here to many interesting observations on possible effects of female choice, such as why do men, unlike apes, have long, dangling penises?

Yet in offering a generalized account of human behavior, Prum misses a human society that supports the female choice theory especially well. That society is the Hadza, as described in Nicholas Blurton-Jones new book: Demography and Evolutionary Ecology of Hadza Hunter-Gatherers (2016).

The Hadza are an ancient hunter-gatherer tribe living in northern Tanzania near Lake Eyasi. Traces of their culture in the area date back at least 130,000 years. The area is too dry for agriculture and the tsetse fly makes it unsuitable for livestock. But theres an abundance of seeds, nuts, berries, honey, and especially, underground tubers. The Hadza live in small groups, moving every few weeks depending on seasonal availability of foods. While all other group-living animals, including apes, consist of close kin, Hadza groups are quite fluid, with unrelated individuals continually coming and going. Like all hunter-gatherers, the Hadza are extremely egalitarian and cooperative.

Hadza men spend their days hunting with poison arrows. But they dont hunt the small game they learned to capture as boys. Rather, they hunt for big game, like baboons, antelope, zebra, or buffalowhich they very rarely catch. Some men never catch anything. But when a man does nail a big animal, the meat is equally shared among the whole group, gaining him prestige. One anthropologist has called this a show-off strategy.

Hadza women do almost all the work, including caring for children and gathering and preparing food. They get little contribution from their husbandsmaybe an occasional piece of honeycomb or a small bird, which the men expect their wives to prepare. In compensation, however, its the women who chose their husbands (often for only a few years). What sort of men do Hadza women prefer? Successful huntersnot good providers!

When the men are not hunting, they sit around in the mens place chatting, smoking, eating tubers prepared by their wives, and fiddling with their bows and arrows. Theres almost no violence among the men. Disputes are resolved by long discussions, or at the worst, one of the men will leave and join another group. If you look at pictures of Hadza, both sexes are small, thin and wiryno great differences in size or appearance. Both sexes go for bead necklaces.

Like the blue manakins, the Hadza seem to fit Prums model of extreme female choice. The women dont depend on their husbands for much besides sperm. Theyre free to choose the show-off hunters, who sire more children, but may actually contribute less to their childrens nutrition. Judging by the peacefulness of the men, female choice seems to have tamed male-male competition.

While all hunter-gatherer societies are highly egalitarian, not all allow as much freedom to women. In the Amazon rain forest, Ache men supply some 80% of the food by hunting. These men may ritually sacrifice children over womens objections, and engage in lethal quarrels. Hadza women seem to derive their independence from the terrain, where it takes no more than a sharp digging stick and knife, a leather sling and water gourd, plus long hours working in the hot sun, for women to fully provision themselves and their childrenand grandchildren. Another unrelated African hunter-gatherer society, the !Kung, lead a very similar life.

The latest evidence from Africa shows hominids manufactured flint tools as long as 3.3 million years ago. Once there were stone knives, female hominids must have used slings to carry themalong with food and infants. A Hadza life style could date back millions of years. Anthropologist Sarah Blaffer Hrdy, in Mothers and Others: The Evolutionary Origins of Mutual Understanding (2009), attributes human cooperativeness to womens shared mothering of childrena trait quite absent in apes. She draws examples from the Hadza. Blaffer Hrdys female cooperativeness together with Prums female preference for cooperative males might explain the evolution of the most cooperative species on earth: humans.

In Aristophanes comedy, Lysistrata (411 BCE), Lysistrata persuades all the women of Athens and Sparta to withhold sex until their men agree to end the long-running Peloponnesian war. Was Aristophanes onto something?

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Part II Beauty, Cooperation, and the Hadza Hunter-Gatherers - HuffPost

Can Stem Cells Finally Solve Hair Loss? – Wall Street Pit

56 million men and women in the US experience varying degrees of hair loss or baldness. Despite available medications and procedures, scientists are still striving to put an end to balding and the frustrations associated with it. Researchers from UCLAs Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research offered a new angle to solving hair loss problems: altering metabolic pathways of hair follicle stem cells. The study was published in Nature Cell Biology.

To understand how hair is lost, we must take a look on its growth cycle which has three components: the growth phase (anagen), a regression phase (catagen) and a resting phase (telogen). All hairs in our body undergo this cycle but the duration for each phase varies depending on the hairs location. For instance, the hair growing from our scalps will have 2-3 years of anagen, 2-3 weeks of catagen and about 3 months of telogen. Hairs from other body parts typically have shorter anagens but longer telogen phases.

Hair follicle stem cells (HFSC) are unspecialized skin cells that live inside hair-producing sacs called hair follicles. HFSCs are quiescent (meaning they are normally dormant) but they quickly activate during an anagen phase. Many factors regulate their quiescence but whenever they fail to activate as required, the rate of hair loss would exceed the rate of new hair growth. We lose an average of 100 scalp hairs daily and unnecessary disruptions in the hairs cycle lead to hair loss, hair thinning and other hair problems.

HFSCs have another important quality: they have a unique metabolic process. They metabolize glucose into a compound called pyruvate. Two things can happen to pyruvate: be sent to the mitochondria (the cells powerplant) to harvest energy or be converted to another compound called lactate.

The teams interest is to limit the entry of pyruvate into the mitochondria and see if this act will increase conversion to lactate, trigger activation of HFSCs and promote hair growth. To achieve that, they genetically altered two groups of mice differently. Subjects in the first group had their capacity for producing lactate erased; the mices HFSCs remained dormant. On the other hand, members of the second group were given the ability for higher-than-normal lactate production; the mice showed signs of activated stem cells and, eventually, they grew more hair! The study proved that there is a direct correlation between lactate production and hair growth.

The team then applied two drugs on mices skins to push the stem cells towards the lactate pathway. First was RCGD423 which increased lactate production and put the stem cells into an active state, thereby promoting hair growth. To do this, the drug utilizes a signaling pathway between the cells exterior and nucleus. Second drug was UK5099 which acts in a different way. It blocks pyruvates entry into the mitochondria thus forcing the stem cells to convert all their pyruvate into lactate, which also promotes hair growth. The provisional patents for these drugs are filed and covered by the UCLA Technical Development Group.

This isnt the first time a stem-cell-based treatment has been made for treating hair loss. While this discovery of stem cells relationship with hair growth (at least in mice) has big potential to be the cure for baldness weve been waiting for, the drugs are yet to be tested on humans.

Hair loss issues aside, one aspect that makes this research groundbreaking is the new information it added in the study of stem cells, particularly the link stem cells have with human metabolism. Aimee Flores, one of the author of the study, stated, The idea of using drugs to stimulate hair growth through hair follicle stem cells is very promising given how many millions of people, both men and women, deal with hair loss. I think weve only just begun to understand the critical role metabolism plays in hair growth and stem cells in general; Im looking forward to the potential application of these new findings for hair loss and beyond.

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More Droplets of Tau – Alzforum

18 Aug 2017

When it rains, sometimes it pours. In the second paper describing taus ability to undergo liquid-liquid phase separation in the past month, researchers led by Markus Zweckstetter of the German Center for Neurodegenerative Diseases in Gttingen report that phosphorylation of tau dramatically enhances droplet formation, and that taus repeat domains play a key role in the process. In their August 17 paper in Nature Communications, the researchers made the case that droplets are an essential precursor in the formation of toxic tau tangles, though experiments were all conducted in cell-freeconditions.

Tau is one of many proteins involved in neurodegenerative disease that have been spotted mingling in liquid droplets (Oct 2015 webinar, Oct 2016 news). Inside the cell, the process of liquid-liquid phase separation (LLPS) leads to membrane-less organelles, including stress granules and the nucleolus. Interactions between proteinsespecially those donning low complexity domainsand nucleic acids trigger the process, and researchers have proposed the close quarters in the droplets could breed toxic aggregates, or derail essential cellular functions (May 2016 news). A recent study led by Kenneth Kosik and Songi Han of the University of California, Santa Barbara reported that tau coalesced into liquid droplets in a dish, and that interactions between positively charged tau and negatively charged RNA made the magic happen (Jul 2017 news). Researchers led by Anthony Hyman of Germanys Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, along with Bradley Hyman and Suzanne Wegmann of Massachusetts General Hospital in Charlestown, have also reported that tau forms droplets in vitro and in neurons (May 2017 news).

Fluorescently labeled tau (green) forms droplets at body temperature (bottom), but not at 5C (top). [Image courtesy of Ambadipudi et al., Nature Communications,2017]

In the current study, first author Susmitha Ambadipudi and colleagues investigated if, and under what conditions, tau undergoes LLPS, and how that relates to its propensity to aggregate into fibrils. They started by analyzing various regions of the tau protein with catGranule, a program that predicts propensity of a given protein region to undergo phase separation. While much of taus N-terminus scored low, its repeat domains scored high. The researchers therefore conducted most of their experiments using the K18 fragment of tau, which contains only the four repeatdomains.

They reported that under reducing conditions similar to those inside a cell, K18 formed a turbid solution. Bright field and confocal microscopy revealed K18 formed droplets under Goldilocks conditionsnot too cold (5C), not too hot (above 65C), but just right (37C). Under these conditions, K18 did not appear to form outright fibrils, although CD and NMR spectroscopy suggested the protein started exhibiting signs of b-sheet structure and that droplet-resident tau proteins formed tight molecular interactions, akin to amesh.

Could this mesh facilitate fibril formation under certain conditions? To get closer to answering this question, the researchers toggled multiple parameters, including temperature and pH, and added the polyanion heparin into the mix. They found that heparin triggered fibril formation most efficiently and under the very same conditions that facilitate LLPS, suggesting the two processes are linked. Polyanions have long been used to promote formation of tau fibrils (Goedert et al., 1996).

In the cell, tau occurs in six isoforms due to alterative splicing, and can be further processed by proteolytic fragmentation and a variety of post-translation modifications. How might these permutations affect LLPS? They found that droplet formation correlated with the number of repeats, and did not occur at all in an N-terminal fragment that lacked repeats. They also found that phosphorylation of repeat domains by the MARK2 kinase promoted LLPS. Notably, phosphorylated tau underwent LLPS at just 2 mM, a concentration similar to that inside of neurons. Interestingly, another recent study found that phosphorylation had the opposite effect on phase separation of the FUS protein, which plays a role in amyotrophic lateral sclerosis (Aug 2017 news).

In this proposed model of tangle formation, phosphorylation of tau promotes the formation of liquid droplets, which crowds tau, recruits polyanions, and triggers aggregation. [Courtesy of Ambadipudi et al., Nature Communications,2017]

The in vitro findings mesh with Kosik and Hans recent study, which found that tau formed droplets in the presence of RNA. Though Zweckstetter used heparin as a polyanion instead of RNA, both studies point to the importance of electrostatic interactions between tau and negatively charged molecules in promoting LLPS and aggregation. As a post-translational modification bearing a negative charge, phosphorylation may play a similar role, Zweckstetter pointed out. Zweckstetter added that phase separation of full-length, unphosphorylated tau did not occur in their hands. Mostly likely phosphorylation or interactions with RNA would be needed to facilitate that, he toldAlzforum.

The latter finding contradicts the findings of Wegmann and colleagues who did detect phase separation of full-length tau, and even of N-terminal tau completely devoid of repeat domains, she told Alzforum (May 2017 conference news). Wegmann was fascinated by this difference, adding that it underscores the complex process of phase separation, pointing to varying contributions of different regions of the tau protein in the process. For her part, Wegmann is working on pinning down the presence of liquid droplets of tau in cultured neurons, and in AD braintissue.

In a joint commentary to Alzforum, Kosik and Han agreed that understanding the physiological significance of these droplets was crucial: The in vitro studies lay the groundwork for the next big step: how might these phenomena operate in vivo where life is not only many-fold more complicated but rife with emergent properties.JessicaShugart

No Available Further Reading

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More Droplets of Tau - Alzforum

Heritability of IQ – Wikipedia

Research on heritability of IQ infers, from the similarity of IQ in closely related persons, the proportion of variance of IQ among individuals in a study population that is associated with genetic variation within that population. This provides a maximum estimate of genetic versus environmental influence for phenotypic variation in IQ in that population. "Heritability", in this sense, "refers to the genetic contribution to variance within a population and in a specific environment".[1] In other words, heritability is a mathematical estimate that indicates how much of a traits variation can be attributed to genes. There has been significant controversy in the academic community about the heritability of IQ since research on the issue began in the late nineteenth century.[2]Intelligence in the normal range is a polygenic trait, meaning it's influenced by more than one gene.[3][4]

The general figure for the heritability of IQ, according to an authoritative American Psychological Association report, is 0.45 for children, and rises to around 0.75 for late teens and adults.[5][6] In simpler terms, IQ goes from being weakly correlated with genetics, for children, to being strongly correlated with genetics for late teens and adults. The heritability of IQ increases with age and reaches an asymptote at 1820 years of age and continues at that level well into adulthood.[7] Recent studies suggest that family and parenting characteristics are not significant contributors to variation in IQ scores;[8] however, poor prenatal environment, malnutrition and disease can have deleterious effects.[9][10]

"Heritability" is defined as the proportion of variance in a trait which is attributable to genetic variation within a defined population in a specific environment.[1] Heritability takes a value ranging from 0 to 1; a heritability of 1 indicates that all variation in the trait in question is genetic in origin and a heritability of 0 indicates that none of the variation is genetic. The determination of many traits can be considered primarily genetic under similar environmental backgrounds. For example, a 2006 study found that adult height has a heritability estimated at 0.80 when looking only at the height variation within families where the environment should be very similar.[11] Other traits have lower heritabilities, which indicate a relatively larger environmental influence. For example, a twin study on the heritability of depression in men calculated it as 0.29, while it was 0.42 for women in the same study.[12] Contrary to popular[citation needed] belief, two parents of higher IQ will not necessarily produce offspring of equal or higher intelligence. In fact, according to the concept of regression toward the mean, parents whose IQ is at either extreme are more likely to produce offspring with IQ closer to the mean (or average).[13][14]

There are a number of points to consider when interpreting heritability:

Various studies have found the heritability of IQ to be between 0.7 and 0.8 in adults and 0.45 in childhood in the United States.[6][18][19] It may seem reasonable to expect that genetic influences on traits like IQ should become less important as one gains experiences with age. However, that the opposite occurs is well documented. Heritability measures in infancy are as low as 0.2, around 0.4 in middle childhood, and as high as 0.8 in adulthood.[7] One proposed explanation is that people with different genes tend to seek out different environments that reinforce the effects of those genes.[6] The brain undergoes morphological changes in development which suggests that age-related physical changes could also contribute to this effect.[20]

A 1994 article in Behavior Genetics based on a study of Swedish monozygotic and dizygotic twins found the heritability of the sample to be as high as 0.80 in general cognitive ability; however, it also varies by trait, with 0.60 for verbal tests, 0.50 for spatial and speed-of-processing tests, and 0.40 for memory tests. In contrast, studies of other populations estimate an average heritability of 0.50 for general cognitive ability.[18]

In 2006, The New York Times Magazine listed about three quarters as a figure held by the majority of studies.[21]

There are some family effects on the IQ of children, accounting for up to a quarter of the variance. However, adoption studies show that by adulthood adoptive siblings aren't more similar in IQ than strangers,[22] while adult full siblings show an IQ correlation of 0.24. However, some studies of twins reared apart (e.g. Bouchard, 1990) find a significant shared environmental influence, of at least 10% going into late adulthood.[19]Judith Rich Harris suggests that this might be due to biasing assumptions in the methodology of the classical twin and adoption studies.[23]

There are aspects of environments that family members have in common (for example, characteristics of the home). This shared family environment accounts for 0.25-0.35 of the variation in IQ in childhood. By late adolescence it is quite low (zero in some studies). There is a similar effect for several other psychological traits. These studies have not looked into the effects of extreme environments such as in abusive families.[6][22][24][25]

The American Psychological Association's report "Intelligence: Knowns and Unknowns" (1995) states that there is no doubt that normal child development requires a certain minimum level of responsible care. Severely deprived, neglectful, or abusive environments must have negative effects on a great many aspects of development, including intellectual aspects. Beyond that minimum, however, the role of family experience is in serious dispute. There is no doubt that such variables as resources of the home and parents' use of language are correlated with children's IQ scores, but such correlations may be mediated by genetic as well as (or instead of) environmental factors. But how much of that variance in IQ results from differences between families, as contrasted with the varying experiences of different children in the same family? Recent twin and adoption studies suggest that while the effect of the shared family environment is substantial in early childhood, it becomes quite small by late adolescence. These findings suggest that differences in the life styles of families whatever their importance may be for many aspects of children's lives make little long-term difference for the skills measured by intelligence tests.

Although parents treat their children differently, such differential treatment explains only a small amount of non-shared environmental influence. One suggestion is that children react differently to the same environment due to different genes. More likely influences may be the impact of peers and other experiences outside the family.[6][24] For example, siblings grown up in the same household may have different friends and teachers and even contract different illnesses. This factor may be one of the reasons why IQ score correlations between siblings decreases as they get older.[26]

Certain single-gene genetic disorders can severely affect intelligence. Phenylketonuria is an example,[27] with publications demonstrating the capacity of phenylketonuria to produce a reduction of 10 IQ points on average.[28] Meta-analyses have found that environmental factors, such as iodine deficiency, can result in large reductions in average IQ; iodine deficiency has been shown to produce a reduction of 12.5 IQ points on average.[29]

The APA report "Intelligence: Knowns and Unknowns" (1995) also stated that:

"We should note, however, that low-income and non-white families are poorly represented in existing adoption studies as well as in most twin samples. Thus it is not yet clear whether these studies apply to the population as a whole. It remains possible that, across the full range of income and ethnicity, between-family differences have more lasting consequences for psychometric intelligence."[6]

A study (1999) by Capron and Duyme of French children adopted between the ages of four and six examined the influence of socioeconomic status (SES). The children's IQs initially averaged 77, putting them near retardation. Most were abused or neglected as infants, then shunted from one foster home or institution to the next. Nine years later after adoption, when they were on average 14 years old, they retook the IQ tests, and all of them did better. The amount they improved was directly related to the adopting family's socioeconomic status. "Children adopted by farmers and laborers had average IQ scores of 85.5; those placed with middle-class families had average scores of 92. The average IQ scores of youngsters placed in well-to-do homes climbed more than 20 points, to 98."[21][30]

Stoolmiller (1999) argued that the range of environments in previous adoption studies were restricted. Adopting families tend to be more similar on, for example, socio-economic status than the general population, which suggests a possible underestimation of the role of the shared family environment in previous studies. Corrections for range restriction to adoption studies indicated that socio-economic status could account for as much as 50% of the variance in IQ.[31]

On the other hand, the effect of this was examined by Matt McGue and colleagues (2007), who wrote that "restriction in range in parent disinhibitory psychopathology and family socio-economic status had no effect on adoptive-sibling correlations [in] IQ"[32]

Turkheimer and colleagues (2003) argued that the proportions of IQ variance attributable to genes and environment vary with socioeconomic status. They found that in a study on seven-year-old twins, in impoverished families, 60% of the variance in early childhood IQ was accounted for by the shared family environment, and the contribution of genes is close to zero; in affluent families, the result is almost exactly the reverse.[33]

In contrast to Turkheimer (2003), a study by Nagoshi and Johnson (2005) concluded that the heritability of IQ did not vary as a function of parental socioeconomic status in the 949 families of Caucasian and 400 families of Japanese ancestry who took part in the Hawaii Family Study of Cognition.[34]

Asbury and colleagues (2005) studied the effect of environmental risk factors on verbal and non-verbal ability in a nationally representative sample of 4-year-old British twins. There was not any statistically significant interaction for non-verbal ability, but the heritability of verbal ability was found to be higher in low-SES and high-risk environments.[35]

Harden and colleagues (2007) investigated adolescents, most 17 years old, and found that, among higher income families, genetic influences accounted for approximately 55% of the variance in cognitive aptitude and shared environmental influences about 35%. Among lower income families, the proportions were in the reverse direction, 39% genetic and 45% shared environment."[36]

Rushton and Jensen (2010) criticized many of these studies for being done on children or adolescents. They argued that heritability increases during childhood and adolescence, and even increases greatly between 1620 years of age and adulthood, so one should be cautious drawing conclusions regarding the role of genetics from studies where the participants are not adults. Furthermore, the studies typically did not examine if IQ gains due to adoption were on the general intelligence factor (g). When the studies by Capron and Duyme were re-examined, IQ gains from being adopted into high SES homes were on non-g factors. By contrast, the adopted children's g mainly depended on their biological parents SES, which implied that g is more difficult to environmentally change.[17] The most cited adoption projects that sought to estimate the heritability of IQ were those of Texas,[37] Colorado[38] and Minnesota[39] that were started in the 1970s. These studies showed that while the adoptive parents' IQ does correlate with adoptees' IQ in early life, when the adoptees reach adolescence the correlation has faded and disappeared. The correlation with the biological parent seemed to explain most of the variation.

A 2011 study by Tucker-Drob and colleagues reported that at age 2, genes accounted for approximately 50% of the variation in mental ability for children being raised in high socioeconomic status families, but genes accounted for negligible variation in mental ability for children being raised in low socioeconomic status families. This gene-environment interaction was not apparent at age 10 months, suggesting that the effect emerges over the course of early development.[40]

A 2012 study based on a representative sample of twins from the United Kingdom, with longitudinal data on IQ from age two to age fourteen, did not find evidence for lower heritability in low-SES families. However, the study indicated that the effects of shared family environment on IQ were generally greater in low-SES families than in high-SES families, resulting in greater variance in IQ in low-SES families. The authors noted that previous research had produced inconsistent results on whether or not SES moderates the heritability of IQ. They suggested three explanations for the inconsistency. First, some studies may have lacked statistical power to detect interactions. Second, the age range investigated has varied between studies. Third, the effect of SES may vary in different demographics and different countries.[41]

A 2017 King's College London study suggests that genes account for nearly 50 per cent of the differences between whether children are socially mobile or not.[42]

A meta-analysis by Devlin and colleagues (1997) of 212 previous studies evaluated an alternative model for environmental influence and found that it fits the data better than the 'family-environments' model commonly used. The shared maternal (fetal) environment effects, often assumed to be negligible, account for 20% of covariance between twins and 5% between siblings, and the effects of genes are correspondingly reduced, with two measures of heritability being less than 50%. They argue that the shared maternal environment may explain the striking correlation between the IQs of twins, especially those of adult twins that were reared apart.[2] IQ heritability increases during early childhood, but whether it stabilizes thereafter remains unclear.[2][old info] These results have two implications: a new model may be required regarding the influence of genes and environment on cognitive function; and interventions aimed at improving the prenatal environment could lead to a significant boost in the population's IQ.[2]

Bouchard and McGue reviewed the literature in 2003, arguing that Devlin's conclusions about the magnitude of heritability is not substantially different from previous reports and that their conclusions regarding prenatal effects stands in contradiction to many previous reports.[43] They write that:

Chipuer et al. and Loehlin conclude that the postnatal rather than the prenatal environment is most important. The Devlin et al. (1997a) conclusion that the prenatal environment contributes to twin IQ similarity is especially remarkable given the existence of an extensive empirical literature on prenatal effects. Price (1950), in a comprehensive review published over 50 years ago, argued that almost all MZ twin prenatal effects produced differences rather than similarities. As of 1950 the literature on the topic was so large that the entire bibliography was not published. It was finally published in 1978 with an additional 260 references. At that time Price reiterated his earlier conclusion (Price, 1978). Research subsequent to the 1978 review largely reinforces Prices hypothesis (Bryan, 1993; Macdonald et al., 1993; Hall and Lopez-Rangel, 1996; see also Martin et al., 1997, box 2; Machin, 1996).[43]

Dickens and Flynn (2001) argued that the "heritability" figure includes both a direct effect of the genotype on IQ and also indirect effects where the genotype changes the environment, in turn affecting IQ. That is, those with a higher IQ tend to seek out stimulating environments that further increase IQ. The direct effect can initially have been very small but feedback loops can create large differences in IQ. In their model an environmental stimulus can have a very large effect on IQ, even in adults, but this effect also decays over time unless the stimulus continues. This model could be adapted to include possible factors, like nutrition in early childhood, that may cause permanent effects.

The Flynn effect is the increase in average intelligence test scores by about 0.3% annually, resulting in the average person today scoring 15 points higher in IQ compared to the generation 50 years ago.[44] This effect can be explained by a generally more stimulating environment for all people. The authors suggest that programs aiming to increase IQ would be most likely to produce long-term IQ gains if they taught children how to replicate outside the program the kinds of cognitively demanding experiences that produce IQ gains while they are in the program and motivate them to persist in that replication long after they have left the program.[45][46] Most of the improvements have allowed for better abstract reasoning, spatial relations, and comprehension. Some scientists have suggested that such enhancements are due to better nutrition, better parenting and schooling, as well as exclusion of the least intelligent, genetically inferior, people from reproduction. However, Flynn and a group of other scientists share the viewpoint that modern life implies solving many abstract problems which leads to a rise in their IQ scores.[44]

More recent research has illuminated genetic factors underlying IQ stability and change. Genome-wide association studies have demonstrated that the genes involved in intelligence remain fairly stable over time.[47] Specifically, in terms of IQ stability, "genetic factors mediated phenotypic stability throughout this entire period [age 0 to 16], whereas most age-to-age instability appeared to be due to non-shared environmental influences".[48][49] These findings have been replicated extensively and observed in the United Kingdom,[50] the United States,[48][51] and the Netherlands.[52][53][54][55] Additionally, researchers have shown that naturalistic changes in IQ occur in individuals at variable times.[56]

Spatial ability has been shown to be unifactorial (a single score accounts well for all spatial abilities), and is 69% heritable in a sample of 1,367 twins from the ages 19 through 21.[57] Further only 8% of spatial ability can be accounted for by a shared environmental factors like school and family.[58] Of the genetically determined portion of spacial ability, 24% is shared with verbal ability (general intelligence) and 43% was specific to spatial ability alone.[59]

A 2009 review article identified over 50 genetic polymorphisms that have been reported to be associated with cognitive ability in various studies, but noted that the discovery of small effect sizes and lack of replication have characterized this research so far.[60] Another study attempted to replicate 12 reported associations between specific genetic variants and general cognitive ability in three large datasets, but found that only one of the genotypes was significantly associated with general intelligence in one of the samples, a result expected by chance alone. The authors concluded that most reported genetic associations with general intelligence are probably false positives brought about by inadequate sample sizes. Arguing that common genetic variants explain much of the variation in general intelligence, they suggested that the effects of individual variants are so small that very large samples are required to reliably detect them.[61] Genetic diversity within individuals is heavily correlated with IQ.[62]

A novel molecular genetic method for estimating heritability calculates the overall genetic similarity (as indexed by the cumulative effects of all genotyped single nucleotide polymorphisms) between all pairs of individuals in a sample of unrelated individuals and then correlates this genetic similarity with phenotypic similarity across all the pairs. A study using this method estimated that the lower bounds for the narrow-sense heritability of crystallized and fluid intelligence are 40% and 51%, respectively. A replication study in an independent sample confirmed these results, reporting a heritability estimate of 47%.[63] These findings are compatible with the view that a large number of genes, each with only a small effect, contribute to differences in intelligence.[61]

The relative influence of genetics and environment for a trait can be calculated by measuring how strongly traits covary in people of a given genetic (unrelated, siblings, fraternal twins, or identical twins) and environmental (reared in the same family or not) relationship. One method is to consider identical twins reared apart, with any similarities which exists between such twin pairs attributed to genotype. In terms of correlation statistics, this means that theoretically the correlation of tests scores between monozygotic twins would be 1.00 if genetics alone accounted for variation in IQ scores; likewise, siblings and dizygotic twins share on average half of their alleles and the correlation of their scores would be 0.50 if IQ were affected by genes alone (or greater if, as is undoubtedly the case, there is a positive correlation between the IQs of spouses in the parental generation). Practically, however, the upper bound of these correlations are given by the reliability of the test, which is 0.90 to 0.95 for typical IQ tests[64]

If there is biological inheritance of IQ, then the relatives of a person with a high IQ should exhibit a comparably high IQ with a much higher probability than the general population. In 1982, Bouchard and McGue reviewed such correlations reported in 111 original studies in the United States. The mean correlation of IQ scores between monozygotic twins was 0.86, between siblings, 0.47, between half-siblings, 0.31, and between cousins, 0.15.[65]

The 2006 edition of Assessing adolescent and adult intelligence by Alan S. Kaufman and Elizabeth O. Lichtenberger reports correlations of 0.86 for identical twins raised together compared to 0.76 for those raised apart and 0.47 for siblings.[66] These number are not necessarily static. When comparing pre-1963 to late 1970s data, researches DeFries and Plomin found that the IQ correlation between parent and child living together fell significantly, from 0.50 to 0.35. The opposite occurred for fraternal twins.[67]

Another summary:

Although IQ differences between individuals are shown to have a large hereditary component, it does not follow that mean group-level disparities (between-group differences) in IQ necessarily have a genetic basis. The Flynn effect is one example where there is a large difference between groups(past and present) with little or no genetic difference. An analogy, attributed to Richard Lewontin,[70] illustrates this point:

Suppose two handfuls are taken from a sack containing a genetically diverse variety of corn, and each grown under carefully controlled and standardized conditions, except that one batch is lacking in certain nutrients that are supplied to the other. After several weeks, the plants are measured. There is variability of growth within each batch, due to the genetic variability of the corn. Given that the growing conditions are closely controlled, nearly all the variation in the height of the plants within a batch will be due to differences in their genes. Thus, within populations, heritabilities will be very high. Nevertheless, the difference between the two groups is due entirely to an environmental factordifferential nutrition. Lewontin didn't go so far as to have the one set of pots painted white and the other set black, but you get the idea. The point of the example, in any case, is that the causes of between-group differences may in principle be quite different from the causes of within-group variation.[71]

Arthur Jensen has written in agreement that this is technically correct, but he has also stated that a high heritability increases the probability that genetics play a role in average group differences.[72][73]

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Genesis and Genetics | We look at Genetics in Genesis

One lingering mystery concerning Noahs ark is: How many animals were on board? Since DNA has a very good reputation for solving mysteries in the courtroom, now its time to unleash its powers and reveal Noahs passenger list.

As we look about the earth we see a multitude of animals reproducing after their kind, each retaining their distinction as a kind/specie. How does this happen? Two things are required for kinds/species to remain distinct:

(1) They must have the desire (instincts coded in their DNA) to mate with their own kind/species and

(2) They must have the ability (compatible DNA) to produce viable offspring like themselves.

These two requirements are the basis for both the Biblical and secular scientific definition of species/kinds. The words species and kinds are synonyms, but usually species is used by the secular scientific community and kinds is used by the Biblical community. Nonetheless, both words should define the same creatures, and our conclusion is that they do. Our position is as follows:

Fundamentally, all of the species currently defined by modern science were on the Ark

Consider humans, we have the desire and ability to produce more humans like ourselves. We know that we cannot produce a pig or a chimpanzee because we do not have the genetic ability in our DNAto do so.

Next, consider the great horned owls, they desire to mate with other great horned owls and they have the ability to produce other great horned owls. However, their DNA does not produce the desire or the ability to create a bluebird, a barn owl, or even an eagle owl which is the same genus as the great horned owl.

We wrote a technical paper, The Genetics of Kinds Ravens, Owls, and Doves, and found that not one of the owl kinds/species we examined could possibly produce any other owl kinds/species. That is also true for the ravens and doves. They differ from one another by too much genetic information. We also wrote a technical paper, A Study of Biblical Kinds Using 62 Species of Mice; which showed the various species/kinds of mouse DNA differed from one another by significant amounts with distinct DNA gaps between the kinds/species. It would be impossible to bridge these gaps by means of any natural process.

Our study of the mouse was very interesting in that we found that there are more than one hundredmouse kinds/species and they all remain distinct. How do they do it? They have been magnificently designed with the desire and ability to reproduce after their kinds. Here are a few facts: They can read each others genetics like a barcode (Ref 1). They mate only with their own species (Ref 2). They dont breed with close relatives (Ref 3) and the males do not mate with under aged females (Ref 4). All of this is coded in the DNA and not only does it preserve their distinctiveness, but also maintains good genetic health. You may read all about it, get all of the references, and gain access to all of the DNA sequences at: A Study of Biblical Kinds Using 62 Species of Mice.

If only a few kinds would have been on the Ark, there would only be a few kinds now. The scriptures are clear: every kind was created (Genesis 1); every kind was loaded on the Ark (Genesis 6:19-20); and every kind disembarked from the Ark (Genesis 8:17-20). The kinds were distinct and remain distinct.

Our conclusion would necessitate that on the order of 6000 amphibian, 10,000 bird, 6,000 mammal, and 8,000 reptile kinds/species were aboard the Ark. Accounting for pairs, sevens of clean animals, and those that have gone extinct since the flood, the total number aboard the Ark would be on the order of 100,000. This would be no problem for the very large Ark with all of the animals in Biblical deep sleep (Ref 5)

As we look at this glorious creation, we see that the kinds are distinct. They are distinct because they have both the desire and ability to mate with their own kind and produce offspring of like kind. God always does things right, and in order to replenish the earth properly, He gave every kind a berth on the Ark. All of the passengers were peacefully asleep being transported to a new world filled with adventure and hope.

Key words:

Animals of the Ark, Species on the Ark, Kinds on the Ark, Noahs Ark, Noahs Ark, species vs. kinds, and DNA Noahs Ark

Additional Suggested Reading:

Noahs Ark A Fresh Look

Noahs Ark Hermetically Sealed and Safe

References:1. Beynon, R.J. and Hurst, J.L., 2003. Multiple roles of major urinary proteins in the house mouse, Mus domesticus., Biochem Soc Trans. 2003 Feb;31(Pt 1):142-6. PMID:12546672.

2. Lane, R.P., Young, J., Newman, T., and Trask, B.J., 2004. Species specificity in rodent pheromone receptor repertoires. Genome Res. 14: 603-608. [PMC free article] [PubMed]

3. Sherborne, A.L., Michael D., Thom, M.D., Paterson, S., Jury, F., Ollier, W.E.R., Stockley, P., Beynon, R.J. and Hurst, J.L., 2007. The Genetic Basis of Inbreeding Avoidance in House Mice, Current Biology 17, 20612066, December 4, 2007.

4. Ferrero, D.M., Moeller, L.M., Osakada T., Horio, N., Li, Q., Dheeraj S.R., Cichy, A., Spehr, M. Touhara, K. Liberles, S.D., 2013. A juvenile mouse pheromone inhibits sexual behaviour through the vomeronasal system.Nature, 2013; DOI: 10.1038/nature12579

5. http://www.genesisandgenetics.org/2013/07/20/122/

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Genesis and Genetics | We look at Genetics in Genesis

Does genetics make me what I am? – Sunbury Daily Item

Two timely issues call into question our use of genetics, both in science and popular usage: CRISPR technology used in the pre-natal state to genetically edit-out/repair potentially fatal genes, and the Google controversy.

CRISPR Clustered Regularly Interspersed Short Palindromic Repeats technology, discovered by scientists at UC Berkeley and modified by those at MIT, will almost certainly result in a Nobel Prize. Berkeley scientists discovered that these repeats were used by bacteria to protect themselves against viral infections. Between the repeats, they found pieces of the viral DNA that had previously attacked the bacterium. If, and when, the same virus again attacked, the intruder viral DNA would be compared to the DNA stored between the repeats. If it is recognized as a repeat offender, the bacterium sends in proteins to destroy the viral DNA. They additionally noted that in non-virally infected bacteria, CRISPR could be used to delete some bacterial genes and replace them with others.

Our use of this technology in human cells allows injection of the DNA-modifying proteins into a human egg while it is being fertilized in a test-tube. Fatal genetic conditions identified in the mother or father in the recent report this was a cardiac abnormality, hypertrophic cardiomyopathy can potentially be corrected pre-natally and, after the correction, the fertilized egg implanted into the mother. An incredibly promising technology, it may allow, as with this cardiac abnormality, children at-risk for sudden death to grow old.

Of course, there are ethical concerns related to this technology. Will it be used to create perfect people, eliminating the diversity that makes us better and stronger? That is up to us. A head-in-the-sand refusal to engage with this is not the answer.

The scientific use of genetics and the concept of diversity, above, is tied to its non-scientific use in the Googles James Damore controversy.

Damore spent 3,400 words to say three things: Women and ethnic minorities are genetically different than (select) men; Those genetic differences are why there are more men than women (and minorities) in positions of power; Refusing to acknowledge this creates all sorts of difficulties and controversy, and is bad for business.

Google, he argues, doesnt allow ideas such as his from being discussed, as people are shamed into silence.

The differences between men and women in the workplace are due to inherent, genetic differences, he claims. What?

There are differences between men and women phenotypic (hair color, eye color) and genotypic (a slight variation in genes coding for gender) for which I am always pleased. Do these explain workplace differences? Pay differences? IQ? No. What we term Intelligence Quotient is heavily influenced by surroundings and upbringing, including social class. Not that inherent ability is meaningless, but environment matters. It is not nurture versus nature, it is nurture and nature.

There is a thoughtful part of Damores thesis, meriting consideration. Diversity is right because it makes us better and stronger; we should welcome diverse voices. He muddles this logical point by claiming women are paid less than men for the same job because they spend more money and, somehow, this is genetic; so much for diversity.

Genetics both does and does not make us who we are. Yes, there are genetic elements within us that make us phenotypically what we are: Brown eyes rather than green; black hair rather than blond. But brilliance? Thoughtfulness? Humanity? Empathy? The ability to work together to solve a problem? To work on a problem day after day until the solution appears?

If there is a genetics to this, it is the ability of multiple genes to be turned on by stimulation in a young person. These on-switches are flipped by parents and a society that loves and provides for the child, allows the child to explore and ask questions. A society that takes the child seriously. A society that does not think of the child, the sum of her phenotype, what she looks like.

The danger from CRISPR technology is it could be used to create the perfect human, eliminating the diversity that makes us better, and our world more beautiful. Damores paper, without using such technology, does just that. He turns women and ethnic minorities into caricatures of themselves, while asserting that it is he who is not appreciated or valued.

Peoples opinions vary, but facts suggest we are surrounded by conservative voices, of which I am a multi-faceted one.

CRISPR technology has downsides; we need international guardrails for its use. But the misuse of genetics to explain our societys flaws is an error of the highest magnitude. Much more dangerous than the CRISPR tool-set, we see it in action every day. In papers such as Mr. Damores, and in the way we think of, and treat, our children, boys and girls.

Our world view, ideology, is like the air we breathe: invisible, almost indescribable. It is this ideological view that allows Damore and sometimes us to simultaneously argue for diversity, while doing all in our power to eliminate it.

Follow Dr. A. Joseph Layon on Twitter @ajlayon or on his health blog, also titled Notes from the Southern Heartland (ajlayon.com). Letters may be sent to: LettersNFTSH@gmail.com.

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Does genetics make me what I am? - Sunbury Daily Item