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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Heritability of IQ - Wikipedia

We all have about 24,000 genes. How those genes are structured and interact can determine our current health and our future health.

Modern medicine includes specialists in this field called Clinical Geneticists. In todays TPR Lifeline, Bioscience-Medicine reporter Wendy Rigby talks to Baylor College of Medicines Scott McLean, MD, about his work at the Childrens Hospital of San Antonio.

Rigby: Dr. McLean, what is clinical genetics?

McLean: Clinical genetics is the medical specialty that uses genetic information to improve your genetic health or to understand the basis for a variety of medical conditions.

Those of us who have had children in Texas know that while youre still in the hospital, you get some genetic testing done. What is that called and what are you looking for?

We have newborn screening which is actually a blood test that is given to all babies 24 and 48 hours of age. The blood test involves collecting that blood on a piece of paper, filter paper, and sending that to the Texas State Department of Health Services in Austin where they do a series of tests.

This is the foot prick?

This is where you prick the heel. It seem awfully cruel. Babies cry. Parents dont like it. But its actually a wonderful test because it allows us to screen for over 50 conditions.

Give us some examples. What are some of the genetic conditions we might have heard of?

Well, the initial condition that was screened for in newborn screening in the United States was PKU which stands for Phenylketonuria. This is a condition that results in intellectual disability and seizures. We can change that outcome if we are able to identify the condition early enough and change the diet.

Lets say a child comes in to Childrens Hospital of San Antonio. Doctors are having trouble figuring out whats going on. Are you called in to consult?

Most of our patients that we see in the outpatient clinic are sent to us by consultation from physicians in the community or from nurseries, neonatal intensive care units. They range from situations such as multiple birth defects, to autism, intellectual disability, seizures, encephalopathy, blindness, deafness. Theres a whole gamut of reasons that folks come to see us.

When these children become grownups, does that information that youve learned about them help them out if theyre planning to have their own children in the future?

So when pediatric patients make the transition from pediatric care to adult care, its very common for information and ideas to get lost. And we certainly would hope that people remember that. Sometimes when we have identified a situation in a little baby, I tell the parents that I want them to put a sticky note on the last page of their baby book so that when they are showing the baby book to their childs fiance and they get to the last page, it reminds them you need to go back to see the geneticist because theres this genetic situation that you need to have a nice long chat about so that you can plan your family as carefully as possible.

Right. So the work youre doing today could help someone 30 years in the future.

Well, genetics is a very unique specialty in that regard because when we see a patient were not thinking about their next year of life or their next two years of life or the next month. We do think about that. But this is a lifelong diagnosis and a lifelong situation. So I often joke with my patients that Im going to try to put them on the 90-year plan. What we figure out now about their genetics is going to be helpful for them throughout their entire lifespan, at least up until 90 years. And then after that theyre on their own. But well get them to 90.

So its an exciting time to be in the field.

Very exciting. I think the era of gene therapy which for many people we thought was never going to happen, its very promising because we have new technologies that I think are going to allow for advances in that area.

Dr. Scott McLean with Baylor College of Medicine and the Childrens Hospital of San Antonio, thanks for the information.

Youre quite welcome.

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TPR Lifeline: Clinical Genetics Is A Growing Field - Texas Public Radio

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.

Continue reading here:
Does genetics make me what I am? - Sunbury Daily Item

Warwickshire-based investor Mercia Technologies has injected 2m into a business that produces virus and protein-based biologics for therapeutic companies.

The direct follow-on investment into Oxford Genetics brings Mercia's equity stake in the business to 40.5 per cent.

The 2m from Mercia formed part of a 7.5m funding round, which included Invesco Asset Management.

Proceeds will be used to bolster Oxford Genetics' operation in the US with the opening of a new office in Boston. The company will also expand its research and development facility in the UK.

Chief executive Ryan Cawood said: "The next few years for Oxford Genetics will be exciting. The industry for complex biologics has taken such huge steps forward to delivering real patient benefit and we are pleased to be providing our technology to many of the companies tackling some of medicine's most important unmet needs."

Mercia has worked with Oxford Genetics since 2012 and has ploughed a total of 4.7m into its development.

Mark Payton, chief executive of Mercia and board director of Oxford Genetics, added: "This sector is growing rapidly, driven by pharma and biotech companies' relentless drive for new therapeutics.

"The commercial validity of the business has been recently supported by a string of technology licence agreements. This syndicated investment alongside Invesco reflects our confidence in Oxford Genetics' strong position and its ability to deliver shareholder value in the medium term."

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Mercia invests further in Oxford Genetics - Insider Media

This weeks headlines were filled with news from Charlottesville, Virginia, after a white supremacist drove his car into a crowd of people opposing a march of supremacists and noe-Nazis, killing one woman and injuring many others. Which leads one to ask: how white are American white supremacists?

For most of them, the most convincing way to prove their whiteness is DNA tests from companies like 23andMe.com and Ancestry.com. To their consternation, the results are often not what they expected. White supremacist Craig Cobb was outed on daytime TV in 2013 as 86 percent European, and 14 percent Sub-Saharan African.

Whats interesting is how the white supremacists respond to these disconcerting test results. Aaron Panofsky and Joan Donovan, sociologists at UCLA, studied online discussions of genetic ancestry test results on the white nationalist website Stormfront. They found that the participants used fairly sophisticated reasoning to challenge the results and regain their whiteness.

Cobb, for instance, denounced his test as statistical noise and described it as a Jewish conspiracy to spread junk science whose intent is to defame, confuse and deracinate young whites on a mass levelespecially males. Using a test from another company he was able to claim that he was European, apart from a 3% Iberian thing.

Panofsky and Donovan conclude that genetics cannot refute racist views. Even though mankind probably came from Africa and even though the notion of racial purity is absurd, racists can manipulate and interpret data for their own purposes. They conclude:

clear communication, simple forms of education, and collective denunciations of scientific misuses, scientists preferred forms of anti-racist action, are insufficient for the task. Challenging racists public understanding of science is not simply a matter of more education or nuance, but may require scientists to rethink their research paradigms and reflexively interrogate their own knowledge production.

More here:
Can genetics refute white supremacist theories? - BioEdge

August 17, 2017

Photo credit: Dreamstime

What makes humans different from chimpanzees? Evolutionary biologists from Howard University and the Yale School of Public Health have developed a unique genetic analysis technique that may provide important answers.

Michael C. Campbell, Ph.D., the papers first author and assistant professor in the Howard University Department of Biology, and co-author Jeffrey Townsend, Ph.D., the Elihu Associate Professor in Biostatistics at Yale, published their findings in the journal Molecular Biology and Evolution.

Their methodModel Averaged Site Selection via Poisson Random Field (MASS-PRF)looks at protein-coding genes to identify genetic signatures of positive selection. These signatures are actually DNA changes that contribute to the development of beneficial traits, or human adaptations, that emerged during human evolutionary history and that are shared across the human species.

It's a quantum leap in our statistical power to detect selection in recently diverged species.

Other approaches have examined this question but analyses have focused on whole genes, typically missing focused evolution that often occurs in small regions of genes. The method Campbell and Townsend created identifies selection within genes, pinpointing sets of mutations that have undergone positive selection.

Our method is a new way of looking for beneficial mutations that have become fixed or occur at 100 percent frequency in the human species, Campbell said. What we are concerned with are mutations within genes and traits that are specific to humans compared to closely related species, such as the chimpanzee. Essentially, we want to know is what are the mutations and traits that make us human and that unite us as a biological species.

Townsend said the technique has far-reaching implications. It helped the research team discover several genes whose evolution appears to have been critical to the divergence of humans from their common ancestor with chimpanzees. The genes play roles in neurological processing, immunity, and reproduction, and the method could eventually help scientists identify many more. It's a quantum leap in our statistical power to detect selection in recently diverged species, Townsend said.

Campbell began the research project with Drs. Zhao and Townsend while they were associate research scientists in the Department of Biostatistics at the Yale School of Public Health, before he arrived at Howard University in 2015. Dr. Zhao, currently a research scientist at The Jackson Laboratory for Genomic Medicine, co-authored the paper.

This article was submitted by Elisabeth Ann Reitman on August 17, 2017.

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Evolutionary Biologists Probe Long-standing Genetics Mystery - Yale News

Deutsche Bank upgraded Myriad Genetics, Inc. (NASDAQ: MYGN), as it believes the risk/reward is now balanced following the company below-consensus sales and earnings per share guidance for 2018.

The firm upgraded the rating from Sell to Hold, with the price target at $28.

At time of writing, shares of Myriad Genetics were rallying 3.19 percent to $28.75.

Analyst Dan Leonard said he was earlier concerned that the Street numbers were too high and didn't sufficiently reflect downside in the company's Hereditary Cancer Testing, or HTC, business, which accounts for 74 percent of the total sales. The company's sales guidance for 2018 was 4 percent below the Street estimates at the midpoint, the analyst noted.

See also: August PDUFA Dates: Biotech Investors Stay Tuned To A Month Of Plenty

Deutsche Bank believes the price erosion in the core hereditary cancer testing business is likely to be metered post 2019, given that cost of HCT isn't a large portion of spend at any given payer.

Additionally, the firm noted that payers have historically used prior authorization as the primary lever to limit genetic testing spend, rather than price. The firm said payers may not prefer discriminating between providers, given the challenge posed by getting acquainted with the evolving medical practice, the firm said.

Meanwhile, Deutsche Bank also indicated Myriad Genetics is able to convince payers that the other HCT options aren't perfect substitutes for its tests due to its variant database and the FDA approved status of its BRCAnalysis test.

The firm also sees opportunity for volume gains to continue.

Deutsche Bank believes the Street estimates through 2020 now appear more appropriate, while opining that its estimates are largely in line save some timing differences.

"We would be more constructive on greater conviction in MYGN's efforts outside of hereditary cancer testing and/or greater volume growth in hereditary cancer testing," the firm concluded.

View More Analyst Ratings for MYGN View the Latest Analyst Ratings

Posted-In: Deutsche Bank - Dan LeonardAnalyst Color Upgrades Analyst Ratings Best of Benzinga

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Increased Confidence Earns Myriad Genetics An Upgrade - Benzinga

The white-nationalist forum Stormfront hosts discussions on a wide range of topics, from politics to guns to The Lord of the Rings. And of particular and enduring interest: genetic ancestry tests. For white nationalists, DNA tests are a way to prove their racial purity. Of course, their results dont always come back that way. And how white nationalists try to explain away non-European ancestry is rather illuminating of their beliefs.

Will the Alt-Right Promote a New Kind of Racist Genetics?

Two years agobefore Donald Trump was elected president, before white nationalism had become central to the political conversationAaron Panofsky and Joan Donovan, sociologists then at the University of California, Los Angeles, set out to study Stormfront forum posts about genetic ancestry tests. They presented their study at the American Sociological Association meeting this Monday. (A preprint of the paper is now online.)After the events in Charlottesville this week, their research struck a particular chord with the audience.

For academics, there was some uneasiness around hearing that science is being used in this way and that some of the critiques that white nationalists are making of genetics are the same critiques social scientists make of genetics, says Donovan, who recently took up a position at the Data and Society Research Institute. On Stormfront, the researchers did encounter conspiracy theories and racist rants, but some white-nationalist interpretations of genetic ancestry tests were in fact quite sophisticatedand their views cannot all be easily dismissed as ignorance.

If we believe their politics comes from lack of sophistication because theyre unintelligent or uneducated, says Panofsky, I think were liable to make a lot of mistakes in how we cope with them.

Panofsky, Donovan, and their team of researchers analyzed 3,070 Stormfront posts spanning more than a decadeall from forum threads in which at least one user revealed the results of a DNA test. Some of the results were 100 percent European, as users expected. But oftensurprisingly often, says Panofskyusers disclosed tests results showing non-European ancestry. And despite revealing non-European ancestry on a forum full of white nationalists, they were not run off the site.

While some commenters reacted with anger, many reacted by offering up arguments to explain away the test results. These arguments largely fell into two camps.

First, they could simply reject all genetic ancestry testing. Genealogy or the so-called mirror test (When you look in the mirror, do you see a Jew? If not, youre good) were better tests of racial purity, some suggested. Others offered up conspiracies about DNA testing companies led by Jews: I think 23andMe might be a covert operation to get DNA the Jews could then use to create bio-weapons for use against us.

The second category of explanation was a lot more nuancedand echoed in many ways legitimate critiques of the tests. When companies like 23andMe or AncestryDNA return a result like 23 percent Iberian, for example, theyre noting similarities between the customers DNA and people currently living in that region. But people migrate; populations change. It doesnt pinpoint where ones ancestors actually lived. One Stormfront user wrote:

See, THIS is why I dont recommend these tests to people. Did they bother to tell you that there were whites in what is now Senegal all that time ago? No? So they led you to believe that youre mixed even though in all probability, you are simply related to some white fool who left some of his DNA with the locals in what is now Senegal.

Panofsky notes that legitimate scientific critiques are often distorted by a white-nationalist interpretation of history. For example, the mixing of DNA in a region would be explained by the heroic conquest of Vikings. Or a white female ancestor was raped by an African man.

The team also identified a third group of reactions: acceptance of the genetic ancestry test results. Some users did start to rethink white nationalism. Not the basic ideologyStormfronts forums are not exactly the place you would do thatbut the criteria for whiteness. For example, one user suggested a white-nationalist confederation, where different nations would have slightly different criteria for inclusion:

So in one nation having Ghengis Khan as your ancestor wont disqualify you, while in others it might. Hypothetically, I might take a DNA test and find that I dont qualify for every nation and every nations standards, though I'm sure that at least one of those nations (and probably many of them) will have standards that would include me

Another user dug deep into the technical details of genetic ancestry testing. The tests can rely on three different lines of evidence: the Y chromosome that comes from your fathers fathers father and so on, the mitochondrial DNA that comes from your mothers mothers mother and so on, and autosomal DNA that can come from either side. One user suggested that a purity in the Y chromosome and mitochondrial DNA were more important than in the autosomal DNA. But others disagreed.

Sociologists have long pointed out the categories of race are socially constructed. The criteria for who gets to be whiteItalians? Arabs? Mexicans?are determined by social rather than biological forces. And DNA is the newest way for white nationalists to look for differences between the races.

In these years of posts on Stormfront, you can see users attempting to make sense of DNA, figuring out in real time how genetics can be used to circumscribe and preserve whiteness. The test results are always open to interpretation.

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When White Nationalists Get DNA Tests Revealing African Ancestry ... - The Atlantic