Behavioral epigenetics

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Behavioral_epigenetics 

Behavioral epigenetics is the field of study examining the role of epigenetics in shaping animal (including human) behaviour. It seeks to explain how nurture shapes nature, where nature refers to biological heredity and nurture refers to virtually everything that occurs during the life-span (e.g., social-experience, diet and nutrition, and exposure to toxins). Behavioral epigenetics attempts to provide a framework for understanding how the expression of genes is influenced by experiences and the environment to produce individual differences in behaviour, cognition, personality, and mental health.

Epigenetic gene regulation involves changes other than to the sequence of DNA and includes changes to histones (proteins around which DNA is wrapped) and DNA methylation. These epigenetic changes can influence the growth of neurons in the developing brain as well as modify the activity of neurons in the adult brain. Together, these epigenetic changes in neuron structure and function can have a marked influence on an organism's behavior.

Background

In biology, and specifically genetics, epigenetics is the study of heritable changes in gene activity which are not caused by changes in the DNA sequence; the term can also be used to describe the study of stable, long-term alterations in the transcriptional potential of a cell that are not necessarily heritable.

Examples of mechanisms that produce such changes are DNA methylation and histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA.

Modifications of the epigenome do not alter DNA.

DNA methylation turns a gene "off" – it results in the inability of genetic information to be read from DNA; removing the methyl tag can turn the gene back "on".

Epigenetics has a strong influence on the development of an organism and can alter the expression of individual traits. Epigenetic changes occur not only in the developing fetus, but also in individuals throughout the human life-span. Because some epigenetic modifications can be passed from one generation to the next, subsequent generations may be affected by the epigenetic changes that took place in the parents.

Discovery

The first documented example of epigenetics affecting behavior was provided by Michael Meaney and Moshe Szyf. While working at McGill University in Montréal in 2004, they discovered that the type and amount of nurturing a mother rat provides in the early weeks of the rat's infancy determines how that rat responds to stress later in life. This stress sensitivity was linked to a down-regulation in the expression of the glucocorticoid receptor in the brain. In turn, this down-regulation was found to be a consequence of the extent of methylation in the promoter region of the glucocorticoid receptor gene. Immediately after birth, Meaney and Szyf found that methyl groups repress the glucocorticoid receptor gene in all rat pups, making the gene unable to unwind from the histone in order to be transcribed, causing a decreased stress response. Nurturing behaviours from the mother rat were found to stimulate activation of stress signalling pathways that remove methyl groups from DNA. This releases the tightly wound gene, exposing it for transcription. The glucocorticoid gene is activated, resulting in lowered stress response. Rat pups that receive a less nurturing upbringing are more sensitive to stress throughout their life-span.

This pioneering work in rodents has been difficult to replicate in humans because of a general lack of availability human brain tissue for measurement of epigenetic changes.

Research into epigenetics in psychology

Anxiety and risk-taking

Monozygotic twins are identical twins. Twin studies help to reveal epigenetic differences related to various aspects of psychology.

In a small clinical study in humans published in 2008, epigenetic differences were linked to differences in risk-taking and reactions to stress in monozygotic twins. The study identified twins with different life paths, wherein one twin displayed risk-taking behaviours, and the other displayed risk-averse behaviours. Epigenetic differences in DNA methylation of the CpG islands proximal to the DLX1 gene correlated with the differing behavior. The authors of the twin study noted that despite the associations between epigenetic markers and differences personality traits, epigenetics cannot predict complex decision-making processes like career selection.

Stress

The hypothalamic pituitary adrenal axis is involved in the human stress response.

Animal and human studies have found correlations between poor care during infancy and epigenetic changes that correlate with long-term impairments that result from neglect.

Studies in rats have shown correlations between maternal care in terms of the parental licking of offspring and epigenetic changes. A high level of licking results in a long-term reduction in stress response as measured behaviorally and biochemically in elements of the hypothalamic-pituitary-adrenal axis (HPA). Further, decreased DNA methylation of the glucocorticoid receptor gene were found in offspring that experienced a high level of licking; the glucorticoid receptor plays a key role in regulating the HPA. The opposite is found in offspring that experienced low levels of licking, and when pups are switched, the epigenetic changes are reversed. This research provides evidence for an underlying epigenetic mechanism. Further support comes from experiments with the same setup, using drugs that can increase or decrease methylation. Finally, epigenetic variations in parental care can be passed down from one generation to the next, from mother to female offspring. Female offspring who received increased parental care (i.e., high licking) became mothers who engaged in high licking and offspring who received less licking became mothers who engaged in less licking.

In humans, a small clinical research study showed the relationship between prenatal exposure to maternal mood and genetic expression resulting in increased reactivity to stress in offspring. Three groups of infants were examined: those born to mothers medicated for depression with serotonin reuptake inhibitors; those born to depressed mothers not being treated for depression; and those born to non-depressed mothers. Prenatal exposure to depressed/anxious mood was associated with increased DNA methylation at the glucocorticoid receptor gene and to increased HPA axis stress reactivity. The findings were independent of whether the mothers were being pharmaceutically treated for depression.

Recent research has also shown the relationship of methylation of the maternal glucocorticoid receptor and maternal neural activity in response to mother-infant interactions on video. Longitudinal follow-up of those infants will be important to understand the impact of early caregiving in this high-risk population on child epigenetics and behavior.

Cognition

Learning and memory

A 2010 review discusses the role of DNA methylation in memory formation and storage, but the precise mechanisms involving neuronal function, memory, and methylation reversal remain unclear.

Studies in rodents have found that the environment exerts an influence on epigenetic changes related to cognition, in terms of learning and memory; environmental enrichment correlated with increased histone acetylation, and verification by administering histone deacetylase inhibitors induced sprouting of dendrites, an increased number of synapses, and reinstated learning behaviour and access to long-term memories. Research has also linked learning and long-term memory formation to reversible epigenetic changes in the hippocampus and cortex in animals with normal-functioning, non-damaged brains. In human studies, post-mortem brains from Alzheimer's patients show increased histone de-acetylase levels.

Psychopathology and mental health

Drug addiction

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction Note: colored text contains article links. Nuclear pore Nuclear membrane Plasma membrane Cav1.2 NMDAR AMPAR DRD1 DRD5 DRD2 DRD3 DRD4 Gs Gi/o AC cAMP cAMP PKA CaM CaMKII DARPP-32 PP1 PP2B CREB ΔFosB JunD c-Fos SIRT1 HDAC1 [Color legend 1] This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamate co-release by such psychostimulants, postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation. Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-Fos gene with the help of corepressors; c-Fos repression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron. A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-dose exposure to stimulants through this process. ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.

Environmental and epigenetic influences seem to work together to increase the risk of addiction. For example, environmental stress has been shown to increase the risk of substance abuse. In an attempt to cope with stress, alcohol and drugs can be used as an escape. Once substance abuse commences, however, epigenetic alterations may further exacerbate the biological and behavioural changes associated with addiction.

Even short-term substance abuse can produce long-lasting epigenetic changes in the brain of rodents, via DNA methylation and histone modification. Epigenetic modifications have been observed in studies on rodents involving ethanol, nicotine, cocaine, amphetamine, methamphetamine and opiates. Specifically, these epigenetic changes modify gene expression, which in turn increases the vulnerability of an individual to engage in repeated substance overdose in the future. In turn, increased substance abuse results in even greater epigenetic changes in various components of a rodent's reward system (e.g., in the nucleus accumbens). Hence, a cycle emerges whereby changes in areas of the reward system contribute to the long-lasting neural and behavioural changes associated with the increased likelihood of addiction, the maintenance of addiction and relapse. In humans, alcohol consumption has been shown to produce epigenetic changes that contribute to the increased craving of alcohol. As such, epigenetic modifications may play a part in the progression from the controlled intake to the loss of control of alcohol consumption. These alterations may be long-term, as is evidenced in smokers who still possess nicotine-related epigenetic changes ten years after cessation. Therefore, epigenetic modifications may account for some of the behavioural changes generally associated with addiction. These include: repetitive habits that increase the risk of disease, and personal and social problems; need for immediate gratification; high rates of relapse following treatment; and, the feeling of loss of control.

Evidence for related epigenetic changes has come from human studies involving alcohol, nicotine, and opiate abuse. Evidence for epigenetic changes stemming from amphetamine and cocaine abuse derives from animal studies. In animals, drug-related epigenetic changes in fathers have also been shown to negatively affect offspring in terms of poorer spatial working memory, decreased attention and decreased cerebral volume.

Eating disorders and obesity

Epigenetic changes may help to facilitate the development and maintenance of eating disorders via influences in the early environment and throughout the life-span. Pre-natal epigenetic changes due to maternal stress, behaviour and diet may later predispose offspring to persistent, increased anxiety and anxiety disorders. These anxiety issues can precipitate the onset of eating disorders and obesity, and persist even after recovery from the eating disorders.

Epigenetic differences accumulating over the life-span may account for the incongruent differences in eating disorders observed in monozygotic twins. At puberty, sex hormones may exert epigenetic changes (via DNA methylation) on gene expression, thus accounting for higher rates of eating disorders in men as compared to women. Overall, epigenetics contribute to persistent, unregulated self-control behaviours related to the urge to binge.

Schizophrenia

Epigenetic changes including hypomethylation of glutamatergic genes (i.e., NMDA-receptor-subunit gene NR3B and the promoter of the AMPA-receptor-subunit gene GRIA2) in the post-mortem human brains of schizophrenics are associated with increased levels of the neurotransmitter glutamate. Since glutamate is the most prevalent, fast, excitatory neurotransmitter, increased levels may result in the psychotic episodes related to schizophrenia. Epigenetic changes affecting a greater number of genes have been detected in men with schizophrenia as compared to women with the illness.

Population studies have established a strong association linking schizophrenia in children born to older fathers. Specifically, children born to fathers over the age of 35 years are up to three times more likely to develop schizophrenia. Epigenetic dysfunction in human male sperm cells, affecting numerous genes, have been shown to increase with age. This provides a possible explanation for increased rates of the disease in men. To this end, toxins (e.g., air pollutants) have been shown to increase epigenetic differentiation. Animals exposed to ambient air from steel mills and highways show drastic epigenetic changes that persist after removal from the exposure. Therefore, similar epigenetic changes in older human fathers are likely. Schizophrenia studies provide evidence that the nature versus nurture debate in the field of psychopathology should be re-evaluated to accommodate the concept that genes and the environment work in tandem. As such, many other environmental factors (e.g., nutritional deficiencies and cannabis use) have been proposed to increase the susceptibility of psychotic disorders like schizophrenia via epigenetics.

Bipolar disorder

Evidence for epigenetic modifications for bipolar disorder is unclear. One study found hypomethylation of a gene promoter of a prefrontal lobe enzyme (i.e., membrane-bound catechol-O-methyl transferase, or COMT) in post-mortem brain samples from individuals with bipolar disorder. COMT is an enzyme that metabolizes dopamine in the synapse. These findings suggest that the hypomethylation of the promoter results in over-expression of the enzyme. In turn, this results in increased degradation of dopamine levels in the brain. These findings provide evidence that epigenetic modification in the prefrontal lobe is a risk factor for bipolar disorder. However, a second study found no epigenetic differences in post-mortem brains from bipolar individuals.

Major depressive disorder

The causes of major depressive disorder (MDD) are poorly understood from a neuroscience perspective. The epigenetic changes leading to changes in glucocorticoid receptor expression and its effect on the HPA stress system discussed above, have also been applied to attempts to understand MDD.

Much of the work in animal models has focused on the indirect downregulation of brain derived neurotrophic factor (BDNF) by over-activation of the stress axis. Studies in various rodent models of depression, often involving induction of stress, have found direct epigenetic modulation of BDNF as well.

Psychopathy

Epigenetics may be relevant to aspects of psychopathic behaviour through methylation and histone modification. These processes are heritable but can also be influenced by environmental factors such as smoking and abuse. Epigenetics may be one of the mechanisms through which the environment can impact the expression of the genome. Studies have also linked methylation of genes associated with nicotine and alcohol dependence in women, ADHD, and drug abuse. It is probable that epigenetic regulation as well as methylation profiling will play an increasingly important role in the study of the play between the environment and genetics of psychopaths.

Suicide

A study of the brains of 24 suicide completers, 12 of whom had a history of child abuse and 12 who did not, found decreased levels of glucocorticoid receptor in victims of child abuse and associated epigenetic changes.

Social insects

Several studies have indicated DNA cytosine methylation linked to the social behavior of insects, such as honeybees and ants. In honeybees, when nurse bee switched from her in-hive tasks to out foraging, cytosine methylation marks are changing. When a forager bee was reversed to do nurse duties, the cytosine methylation marks were also reversed. Knocking down the DNMT3 in the larvae changed the worker to queen-like phenotype. Queen and worker are two distinguish castes with different morphology, behavior, and physiology. Studies in DNMT3 silencing also indicated DNA methylation may regulate gene alternative splicing and pre-mRNA maturation.

Limitations and future direction

Many researchers contribute information to the Human Epigenome Consortium. The aim of future research is to reprogram epigenetic changes to help with addiction, mental illness, age related changes, memory decline, and other issues. However, the sheer volume of consortium-based data makes analysis difficult. Most studies also focus on one gene. In actuality, many genes and interactions between them likely contribute to individual differences in personality, behaviour and health. As social scientists often work with many variables, determining the number of affected genes also poses methodological challenges. More collaboration between medical researchers, geneticists and social scientists has been advocated to increase knowledge in this field of study.

Limited access to human brain tissue poses a challenge to conducting human research. Not yet knowing if epigenetic changes in the blood and (non-brain) tissues parallel modifications in the brain, places even greater reliance on brain research. Although some epigenetic studies have translated findings from animals to humans, some researchers caution about the extrapolation of animal studies to humans. One view notes that when animal studies do not consider how the subcellular and cellular components, organs and the entire individual interact with the influences of the environment, results are too reductive to explain behaviour.

Some researchers note that epigenetic perspectives will likely be incorporated into pharmacological treatments. Others caution that more research is necessary as drugs are known to modify the activity of multiple genes and may, therefore, cause serious side effects. However, the ultimate goal is to find patterns of epigenetic changes that can be targeted to treat mental illness, and reverse the effects of childhood stressors, for example. If such treatable patterns eventually become well-established, the inability to access brains in living humans to identify them poses an obstacle to pharmacological treatment. Future research may also focus on epigenetic changes that mediate the impact of psychotherapy on personality and behaviour.

Most epigenetic research is correlational; it merely establishes associations. More experimental research is necessary to help establish causation. Lack of resources has also limited the number of intergenerational studies. Therefore, advancing longitudinal and multigenerational, experience-dependent studies will be critical to further understanding the role of epigenetics in psychology.

Dominion theology

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Dominion_theology 

Dominion theology (also known as dominionism) is a group of Christian political ideologies that seek to institute a nation governed by Christians based on their understandings of biblical law. Extents of rule and ways of achieving governing authority are varied. For example, dominion theology can include theonomy, but does not necessarily involve advocating Mosaic law as the basis of government. The label is applied primarily toward groups of Christians in the United States.

Prominent adherents of these ideologies are Calvinist Christian reconstructionism, Charismatic and Pentecostal Kingdom Now theology, New Apostolic Reformation, and perhaps others not identified. Most of the contemporary movements labeled dominion theology arose in the 1970s from religious movements asserting aspects of Christian nationalism.

Some have applied the term dominionist more broadly to the whole Christian right. This usage is controversial. Some members of these communities are concerned that this is a label being used to marginalize Christians from public discourse.

Etymology

Dominion theology is a reference to the King James Bible's rendering of Genesis 1:28, the passage in which God grants humanity "dominion" over the Earth.

And God blessed them, and God said unto them, "Be fruitful, and multiply, and replenish the earth, and subdue it: and have dominion over the fish of the sea, and over the fowl of the air, and over every living thing that moveth upon the earth."

In the late 1980s, several prominent evangelical authors used the phrase dominion theology (and other terms such as dominionism) to label a loose grouping of theological movements that made direct appeals to this passage in Genesis. Christians typically interpret this passage as meaning that God gave mankind responsibility over the Earth, but one of the distinctive aspects of dominion theology is that it is interpreted as a mandate for Christian stewardship in civil affairs, no less than in other human matters.

Types

Christian reconstructionism

An example of dominionism in reformed theology is Christian reconstructionism, which originated with the teachings of R. J. Rushdoony in the 1960s and 1970s. Rushdoony's theology focuses on theonomy (the rule of the Law of God), a belief that all of society should be ordered according to the laws that governed the Israelites in the Old Testament. His system is strongly Calvinistic, emphasizing the sovereignty of God over human freedom and action, and denying the operation of charismatic gifts in the present day (cessationism); both of these aspects are in direct opposition to Kingdom Now Theology.

Full adherents to reconstructionism are few and marginalized among most Christians. Dave Hunt, Albert James Dager, Hal Lindsey, and Thomas Ice specifically criticize Christian reconstructionism from a Christian viewpoint, disagreeing on theological grounds with its theocratic elements as well as its Calvinism and postmillennialism. J. Ligon Duncan, Sherman Isbell, Vern Poythress, Robert Godfrey, and Sinclair Ferguson analyze reconstructionism as conservative Calvinists, primarily giving a theological critique of its theocratic elements. Michael J. McVicar has noted that many leading Christian reconstructionists are also leading writers in paleolibertarian circles.

Some social scientists have used the word dominionism to refer to adherence to Christian reconstructionism.

Kingdom Now theology

Kingdom Now theology is a branch of dominion theology which has had a following within Pentecostalism. It attracted attention in the late 1980s.

Kingdom Now theology states that although Satan has been in control of the world since the Fall, God is looking for people who will help him take back dominion. Those who yield themselves to the authority of God's apostles and prophets will take control of the kingdoms of this world, being defined as all social institutions, the "kingdom" of education, the "kingdom" of science, the "kingdom" of the arts, etc. C. Peter Wagner, the founder of the New Apostolic Reformation, writes: "The practical theology that best builds a foundation under social transformation is dominion theology, sometimes called 'Kingdom Now'. Its history can be traced back through R. J. Rushdoony and Abraham Kuyper to John Calvin."

Kingdom Now theology is influenced by the Latter Rain movement, and critics have connected it to the New Apostolic Reformation, "Spiritual Warfare Christianity," and Fivefold ministry thinking.

Kingdom Now theology should not be confused with Kingdom theology, which is related to inaugurated eschatology.

Dominionism and the Christian right

In the late 1980s sociologist Sara Diamond began writing about the intersection of dominion theology with the political activists of the Christian right. Diamond argued that "the primary importance of the [Christian reconstructionist] ideology is its role as a catalyst for what is loosely called 'dominion theology'". According to Diamond, "Largely through the impact of Rushdoony's and North's writings, the concept that Christians are Biblically mandated to 'occupy' all secular institutions has become the central unifying ideology for the Christian Right" in the United States.

While acknowledging the small number of actual adherents, authors such as Diamond and Frederick Clarkson have argued that postmillennial Christian reconstructionism played a major role in pushing the primarily premillennial Christian right to adopt a more aggressive dominionist stance.

Misztal and Shupe concur that "Reconstructionists have many more sympathizers who fall somewhere within the dominionist framework, but who are not card-carrying members". According to Diamond, "Reconstructionism is the most intellectually grounded, though esoteric, brand of dominion theology".

Journalist Frederick Clarkson defined dominionism as a movement that, while including dominion theology and reconstructionism as subsets, is much broader in scope, extending to much of the Christian right in the United States.

In his 1992 study of dominion theology and its influence on the Christian right, Bruce Barron writes,

In the context of American evangelical efforts to penetrate and transform public life, the distinguishing mark of a dominionist is a commitment to defining and carrying out an approach to building society that is self-consciously defined as exclusively Christian, and dependent specifically on the work of Christians, rather than based on a broader consensus.

In 1995, Diamond called the influence of dominion theology "prevalent on the Christian Right".

Journalist Chip Berlet added in 1998 that, although they represent different theological and political ideas, dominionists assert a Christian duty to take "control of a sinful secular society".

In 2005, Clarkson enumerated the following characteristics shared by all forms of dominionism:

1. Dominionists celebrate Christian nationalism, in that they believe that the United States once was, and should once again be, a Christian nation. In this way, they deny the Enlightenment roots of American democracy.
2. Dominionists promote religious supremacy, insofar as they generally do not respect the equality of other religions, or even other versions of Christianity.
3. Dominionists endorse theocratic visions, insofar as they believe that the Ten Commandments, or "biblical law," should be the foundation of American law, and that the U.S. Constitution should be seen as a vehicle for implementing Biblical principles.

Essayist Katherine Yurica began using the term dominionism in her articles in 2004, beginning with "The Despoiling of America" (February 11, 2004), Authors who also use the term dominionism in the broader sense include journalist Chris Hedges  Marion Maddox, James Rudin, Michelle Goldberg, Kevin Phillips, Sam Harris, Ryan Lizza, Frank Schaeffer, and the group TheocracyWatch. Some authors have applied the term to a broader spectrum of people than have Diamond, Clarkson, and Berlet.

Sarah Posner in Salon argues that there are various "iterations of dominionism that call on Christians to enter ... government, law, media and so forth ... so that they are controlled by Christians". According to Posner, "Christian right figures promoted dominionism ... and the GOP courted ... religious leaders for the votes of their followers". She added: "If people really understood dominionism, they’d worry about it between election cycles."

Michelle Goldberg notes that George Grant wrote in his 1987 book The Changing of the Guard: Biblical Principles for Political Action:

Christians have an obligation, a mandate, a commission, a holy responsibility to reclaim the land for Jesus Christ—to have dominion in civil structures, just as in every other aspect of life and godliness. ... But it is dominion we are after. Not just a voice. ... Christian politics has as its primary intent the conquest of the land—of men, families, institutions, bureaucracies, courts, and governments for the Kingdom of Christ.

A spectrum of dominionism

Writers including Chip Berlet and Frederick Clarkson distinguish between what they term "hard" and "soft" dominionism. Such commentators define "soft" dominionism as the belief that "America is a Christian nation" and opposition to separation of church and state, while "hard" dominionism refers to dominion theology and Christian reconstructionism.

Michelle Goldberg uses the terms Christian nationalism and dominionism for the former view. According to Goldberg:

In many ways, Dominionism is more a political phenomenon than a theological one. It cuts across Christian denominations, from stern, austere sects to the signs-and-wonders culture of modern megachurches. Think of it like political Islamism, which shapes the activism of a number of antagonistic fundamentalist movements, from Sunni Wahabis in the Arab world to Shiite fundamentalists in Iran.

Berlet and Clarkson have agreed that "[s]oft Dominionists are Christian nationalists". Unlike "dominionism", the phrase "Christian nation" occurs commonly in the writings of leaders of the Christian right. Proponents of this idea (such as David Barton and D. James Kennedy) argue that the Founding Fathers of the United States were overwhelmingly Christian, that founding documents such as the Declaration of Independence and the Constitution are based on Christian principles, and that a Christian character is fundamental to American culture. They cite, for example, the U.S. Supreme Court's comment in 1892 that "this [the United States] is a Christian nation", after citing numerous historical and legal arguments in support of that statement.

Kennedy characterized his perspective on Christian political involvement as more akin to participatory democracy than to dominionism. In an interview with NPR's Terry Gross, Kennedy was asked whether he wanted all public office holders to be Christians. Kennedy answered, "We have people who are secular and humanist and unbelievers who are constantly supporting in every way possible other people who share those views. And I don't object to that. That's their privilege. And I think that Christians should be allowed the same privilege to vote for people whom they believe share their views about life and government. And that's all I'm talking about."

Criticism of the usage of the term dominionism

Those labelled dominionists rarely use the terms dominionist and dominionism for self-description, and some people have attacked the use of such words. Journalist and conservative comentator Anthony Williams, writing for Frontpage Magazine, charged that such usage aims "to smear the Republican Party as the party of domestic Theocracy, facts be damned". Journalist and conservative commentator Stanley Kurtz, writing for the National Review, labeled it "conspiratorial nonsense", "political paranoia", and "guilt by association", and decried Hedges' "vague characterizations" that allow him to "paint a highly questionable picture of a virtually faceless and nameless 'Dominionist' Christian mass". Kurtz also complained about a perceived link between average Christian evangelicals and extremism such as Christian reconstructionism:

The notion that conservative Christians want to reinstitute slavery and rule by genocide is not just crazy, it's downright dangerous. The most disturbing part of the Harper's cover story (the one by Chris Hedges) was the attempt to link Christian conservatives with Hitler and fascism. Once we acknowledge the similarity between conservative Christians and fascists, Hedges appears to suggest, we can confront Christian evil by setting aside 'the old polite rules of democracy.' So wild conspiracy theories and visions of genocide are really excuses for the Left to disregard the rules of democracy and defeat conservative Christians—by any means necessary.

Joe Carter of First Things writes:

[T]here is no "school of thought" known as "dominionism." The term was coined in the 1980s by Diamond and is never used outside liberal blogs and websites. No reputable scholars use the term for it is a meaningless neologism that Diamond concocted for her dissertation.

Diamond has denied that she coined the broader sense of the term dominionism, which appears in her dissertation and in Roads to Dominion solely to describe dominion theology. Nevertheless, Diamond did originate the idea that dominion theology is the "central unifying ideology for the Christian Right".

Jeremy Pierce of First Things coined the word dominionismist to describe those who promote the idea that there is a dominionist conspiracy, writing:

It strikes me as irresponsible to lump [Rushdoony] together with Francis Schaeffer and those influenced by him, especially given Schaeffer's many recorded instances of resisting exactly the kinds of views Rushdoony developed. Indeed, it strikes me as an error of the magnitude of some of Rushdoony's own historical nonsense to consider there to be such a view called Dominionism [sic] that Rushdoony, Schaeffer, James Dobson, and all the other people in the list somehow share and that it seeks to get Christians and only Christians into all the influential positions in secular society.

Lisa Miller of Newsweek writes that "'dominionism' is the paranoid mot du jour" and that "certain journalists use 'dominionist' the way some folks on Fox News use the word sharia. Its strangeness scares people. Without history or context, the word creates a siege mentality in which 'we' need to guard against 'them'." Ross Douthat of The New York Times noted that "many of the people that writers like Diamond and others describe as 'dominionists' would disavow the label, many definitions of dominionism conflate several very different Christian political theologies, and there's a lively debate about whether the term is even useful at all."

Other criticism has focused on the proper use of the term. Berlet wrote that "just because some critics of the Christian Right have stretched the term dominionism past its breaking point does not mean we should abandon the term", and argued that, rather than labeling conservatives as extremists, it would be better to "talk to these people" and "engage them". Sara Diamond wrote that "[l]iberals' writing about the Christian Right's take-over plans has generally taken the form of conspiracy theory", and argued that instead one should "analyze the subtle ways" that ideas like Dominionism "take hold within movements and why". Authors Robert Gagnon and Edith Humphrey argued strongly against the use of the term in reference to US presidential candidate Ted Cruz in a 2016 op-ed for Christianity Today.

Heritability of IQ

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Heritability_of_IQ 

Research on the heritability of IQ inquires into the proportion of variance in IQ that is attributable to genetic variation within a population. "Heritability", in this sense, is a mathematical estimate that indicates an upper bound on how much of a trait's variation within a population 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. Intelligence in the normal range is a polygenic trait, meaning that it is influenced by more than one gene, and in the case of intelligence at least 500 genes. Further, explaining the similarity in IQ of closely related persons requires careful study because environmental factors may be correlated with genetic factors.

Twin studies of adult individuals have found a heritability of IQ between 57% and 73% with the most recent studies showing heritability for IQ as high as 80% 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 18–20 years of age and continues at that level well into adulthood. This phenomenon is known as the Wilson Effect. However, poor prenatal environment, malnutrition and disease are known to have lifelong deleterious effects.

Although IQ differences between individuals have been 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 current scientific consensus is that there is no evidence for a genetic component behind IQ differences between racial groups.

Heritability and caveats

"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. 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. 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.

Caveats

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

• Heritability measures the proportion of variation in a trait that can be attributed to genes, and not the proportion of a trait caused by genes. Thus, if the environment relevant to a given trait changes in a way that affects all members of the population equally, the mean value of the trait will change without any change in its heritability (because the variation or differences among individuals in the population will stay the same). This has evidently happened for height: the heritability of stature is high, but average heights continue to increase. Thus, even in developed nations, a high heritability of a trait does not necessarily mean that average group differences are due to genes. Some have gone further, and used height as an example in order to argue that "even highly heritable traits can be strongly manipulated by the environment, so heritability has little if anything to do with controllability."
• A common error is to assume that a heritability figure is necessarily unchangeable. The value of heritability can change if the impact of environment (or of genes) in the population is substantially altered. If the environmental variation encountered by different individuals increases, then the heritability figure would decrease. On the other hand, if everyone had the same environment, then heritability would be 100%. The population in developing nations often has more diverse environments than in developed nations. This would mean that heritability figures would be lower in developing nations. Another example is phenylketonuria which previously caused mental retardation for everyone who had this genetic disorder and thus had a heritability of 100%. Today, this can be prevented by following a modified diet, resulting in a lowered heritability.
• A high heritability of a trait does not mean that environmental effects such as learning are not involved. Vocabulary size, for example, is very substantially heritable (and highly correlated with general intelligence) although every word in an individual's vocabulary is learned. In a society in which plenty of words are available in everyone's environment, especially for individuals who are motivated to seek them out, the number of words that individuals actually learn depends to a considerable extent on their genetic predispositions and thus heritability is high.
• Since heritability increases during childhood and adolescence, and even increases greatly between 16–20 years of age and adulthood, one should be cautious drawing conclusions regarding the role of genetics and environment from studies where the participants are not followed until they are adults. Furthermore, there may be differences regarding the effects on the g-factor and on non-g factors, with g possibly being harder to affect and environmental interventions disproportionately affecting non-g factors.
• Polygenic traits often appear less heritable at the extremes. A heritable trait is definitionally more likely to appear in the offspring of two parents high in that trait than in the offspring of two randomly selected parents. However, the more extreme the expression of the trait in the parents, the less likely the child is to display the same extreme as the parents. At the same time, the more extreme the expression of the trait in the parents, the more likely the child is to express the trait at all. For example, the child of two extremely tall parents is likely to be taller than the average person (displaying the trait), but unlikely to be taller than the two parents (displaying the trait at the same extreme).

Estimates

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. 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. One proposed explanation is that people with different genes tend to seek out different environments that reinforce the effects of those genes. The brain undergoes morphological changes in development which suggests that age-related physical changes could also contribute to this effect.

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.

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

Shared family environment

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, 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. Judith Rich Harris suggests that this might be due to biasing assumptions in the methodology of the classical twin and adoption studies.

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.

The American Psychological Association's report "Intelligence: Knowns and Unknowns" (1996) 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.

Non-shared family environment and environment outside the family

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. 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.

Malnutrition and diseases

Certain single-gene metabolic disorders can severely affect intelligence. Phenylketonuria is an example, with publications demonstrating the capacity of phenylketonuria to produce a reduction of 10 IQ points on average. 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.

Heritability and socioeconomic status

The APA report "Intelligence: Knowns and Unknowns" (1996) 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."

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."

Stoolmiller (1999) argued that the range of environments in previous adoption studies was 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.

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"

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.

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.

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.

Harden, Turkheimer, and Loehlin (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."

In the course of a substantial review, Rushton and Jensen (2010) criticized the study of Capron and Duyme, arguing their choice of IQ test and selection of child and adolescent subjects were a poor choice because this gives a relatively less hereditable measure. The argument here rests on a strong form of Spearman's hypothesis, that the hereditability of different kinds of IQ test can vary according to how closely they correlate to the general intelligence factor (g); both the empirical data and statistical methodology bearing on this question are matters of active controversy.

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.

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.

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.

Maternal (fetal) environment

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. IQ heritability increases during early childhood, but whether it stabilizes thereafter remains unclear. 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.

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. 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 Price’s hypothesis (Bryan, 1993; Macdonald et al., 1993; Hall and Lopez-Rangel, 1996; see also Martin et al., 1997, box 2; Machin, 1996).

Dickens and Flynn model

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. 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. 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 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.

Influence of genes on IQ stability

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. 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". These findings have been replicated extensively and observed in the United Kingdom, the United States, and the Netherlands. Additionally, researchers have shown that naturalistic changes in IQ occur in individuals at variable times.

Influence of parents genes that are not inherited

Kong reports that, "Nurture has a genetic component, i.e. alleles in the parents affect the parents' phenotypes and through that influence the outcomes of the child." These results were obtained through a meta-analysis of educational attainment and polygenic scores of non-transmitted alleles. Although the study deals with educational attainment and not IQ, these two are strongly linked.

Spatial ability component of IQ

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. Further only 8% of spatial ability can be accounted for by a shared environmental factors like school and family. Of the genetically determined portion of spatial ability, 24% is shared with verbal ability (general intelligence) and 43% was specific to spatial ability alone.

Molecular genetic investigations

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. 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, but see. 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. Genetic diversity within individuals is heavily correlated with IQ.

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%. These findings are compatible with the view that a large number of genes, each with only a small effect, contribute to differences in intelligence.

Correlations between IQ and degree of genetic relatedness

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 that exist 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 alleles and the correlation of their scores would be 0.50 if IQ were affected by genes alone (or greater if 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.

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.

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. 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.

Every one of these studies presented next contains estimates of only two of the three factors which are relevant. The three factors are G, E, and GxE. Since there is no possibility of studying equal environments in a manner comparable to using identical twins for equal genetics, the GxE factor can not be isolated. Thus the estimates are actually of G+GxE and E. Although this may seem like nonsense, it is justified by the unstated assumption that GxE=0. It is also the case that the values shown below are r correlations and not r(squared), proportions of variance. Numbers less than one are smaller when squared. The next to last number in the list below refers to less than 5% shared variance between a parent and child living apart.

Another summary:

• Same person (tested twice) .95 next to
• Identical twins—Reared together .86
• Identical twins—Reared apart .76
• Fraternal twins—Reared together .55
• Fraternal twins—Reared apart .35
• Biological siblings—Reared together .47
• Biological siblings—Reared apart .24
• Biological siblings—Reared together—Adults .24
• Unrelated children—Reared together—Children .28
• Unrelated children—Reared together—Adults .04
• Cousins .15
• Parent-child—Living together .42
• Parent-child—Living apart .22
• Adoptive parent–child—Living together .19

Between-group heritability

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, 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 factor—differential 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.

Psychologist Arthur Jensen has written that while this is technically correct, a high heritability among individuals suggests to him that genetics play a role in average group differences. However, in contrast to Jensen's view, geneticist and neuroscientist Kevin Mitchell explains why "systematic genetic differences in intelligence between large, ancient populations" are "inherently and deeply implausible":

Because most random mutations that affect intelligence will reduce it, evolution will tend to select against them. Inevitably, new mutations will always arise in the population, but ones with a large effect on intelligence – that cause frank intellectual disability, for example – will be swiftly removed by natural selection. Mutations with moderate effects may persist for a few generations, and ones with small effects may last even longer. But because many thousands of genes are involved in brain development, natural selection can’t keep them all free of mutations all the time. . . . The result is that any population at any time will carry a varied bunch of mutations that affect intelligence. These will differ between populations, clans, families, and individuals. This constant churn of genetic variation works against any long-term rise or fall in intelligence.