How did accents first develop? Was it climate dependent? or was it a social behavioural issue?
Is there any biological reason for the development of accents?
No. Accent is purely environmental. The ability to pick up the unique sounds of a language or variation of a language ceases around puberty: http://en.wikipedia.org/wiki/Language_acquisition
This is why adults learning a second language have trouble distinguishing the unique sounds of the second language. For learners of English, the "th" sounds and the difference between "l" and "r" can be difficult. For languages based on Sanskrit, there are a variety of aspirated/unaspirated consonants somewhere between "b" and "v" that English-speakers have a hard time distinguishing, much less imitating.
'Gay genes': science is on the right track, we're born this way. Let’s deal with it.
I n a recent Guardian article , Simon Copland argued that it is very unlikely people are born gay (or presumably any other sexual orientation). Scientific evidence says otherwise. It points strongly to a biological origin for our sexualities. Finding evidence for a biological basis should not scare us or undermine gay, lesbian and bisexual (LGB) rights (the studies I refer to do not include transgendered individuals, so I’ll confine my comments to lesbian, gay and bisexual people). I would argue that understanding our fundamental biological nature should make us more vigorous in promoting LGB rights.
Let’s get some facts and perspective on the issue. Evidence from independent research groups who studied twins shows that genetic factors explain about 25-30% of the differences between people in sexual orientation (heterosexual, gay, lesbian, and bisexual). Twin studies are a first look into the genetics of a trait and tell us that there are such things as “genes for sexual orientation” (I hate the phrase “gay gene”). Three gene finding studies showed that gay brothers share genetic markers on the X chromosome the most recent study also found shared markers on chromosome 8. This latest research overcomes the problems of three prior studies which did not find the same results.
Gene finding efforts have issues, as Copland argues, but these are technical and not catastrophic errors in the science. For example, complex psychological traits have many causal genes (not simply “a gay gene”). But each of these genes has a small effect on the trait so do not reach traditional levels of statistical significance. In other words, lots of genes which do influence sexual orientation may fall under the radar. But scientific techniques will eventually catch up. In fact there are more pressing problems that I would like to see addressed, such as the inadequate research on female sexuality. Perhaps this is due to the stereotype that female sexuality is “too complex” or that lesbians are rarer than gay men.
Genes are far from the whole story. Sex hormones in prenatal life play a role. For example, girls born with congenital adrenal hyperplasia (CAH), which results in naturally increased levels of male sex hormones, show relatively high rates of same-sex attractions as adults. Further evidence comes from genetic males who, through accidents, or being born without penises, were subjected to sex change and raised as girls. As adults these men are typically attracted to women. The fact that you cannot make a genetic male sexually attracted to another male by raising him as a girl makes any social theory of sexuality very weak. Genes could themselves nudge one towards a particular sexual orientation or genes may simply interact with other environmental factors (such as sex hormones in the womb environment) to influence later sexual orientation.
The brains of gay and heterosexual people also appear to be organised differently. For example patterns of brain organisation appear similar between gay men and heterosexual women and between lesbian women and heterosexual men. Gay men appear, on average, more “female typical” in brain pattern responses and lesbian women are somewhat more “male typical”. Differences in brain organisation mean differences in psychology and study after study show differences in cognition between heterosexual and gay people. Thus gay differences are not just about who you fancy. They are reflected in our psychology and the ways we relate to others. The influence of biology runs throughout our sexual and gendered lives and those differences, that diversity, is surely to be celebrated.
Some writers tend to wave off the scientific evidence by urging us to look to the history of sexuality or claim that homosexuality is a social construction (cue Michel Foucault and the like). But these accounts are mere descriptions at best and not scientific theories. Social constructionist accounts generate no hypotheses about sexual orientation and are not subject to systematic testing. So why should we take their claims seriously? Social constructionism and postmodernist theory question the very validity of empirical science in the first place. That makes it no better than climate science denial.
Some will argue that our common sense experiences are full of people who are “fluid” in their sexual orientations or change their sexualities. This won’t do either because our experience fools us all the time. Change is widely used to argue against biological explanations. Critics will say that if behaviour changes, or is “fluid”, then surely it can’t have a biological basis? This is false because it is our biology that allows us to learn, respond to socialisation, and helps generate our culture. So showing evidence of change is not an argument against biology. There is indeed some fluidity in sexuality over time, predominantly among women. But there is no “bell shaped curve” to sexual orientation. People may change the identity labels they use and who they have sex with but sexual attractions seem stable over time.
Remember, sexual orientation is a pattern of desire, not of behaviour or sexual acts per se. It is not a simple act of will or a performance. We fall in love with men or women because we have gay, straight, or bisexual orientations and not because of choice. So let’s stop pretending there is choice in sexual orientation. Who truly “chooses” anything of substance anyway? Surely our choices are the result of things we didn’t choose (our genes, personalities, upbringing, and culture).
People worry that scientific research will lead to “cures” for homosexuality (which is an odd worry to have if you don’t believe in the “born this way” argument). They worry more about this than the consequences of choice or environmental explanations, which are not without risk either. But clearly none of the direst predictions have materialised. Sexual minority identities have not been medicalised nor has there been any genetic testing. Genetic tests would never result in 100% accurate identification of LGB individuals because, as I said, genes are less than one-third of the story. On the social policy and legal front we’ve gone in the direction of more rights and more freedoms for LGB people (at least in the West) and not less.
So should the causes of sexuality influence how we view sexual minority identities? No. The causes of a trait should not influence how we see it. But the science shows us that sexuality has a biological basis: that is simply how the science turned out. It’s no use denying it. So let’s use it to supplement, but not replace, a discussion about LGB rights and social policy. The biology of sexuality diversity tells the world to deal with it. We are who we are, and our sexualities are part of human nature.
My worry about the claims of social construction, choice and such like is that it plays into the hands of homophobic ideology, into the hands of the “aversion therapists”, and into the hands of a growing culture which seeks to minimise gay differences. It reminds me of something Noam Chomsky alluded to : if humans were entirely unstructured creatures we would be subject to the totalitarian whims of outside forces.
Dr Qazi Rahman is an academic at the Institute of Psychiatry, King’s College London. He studies the biology of sexual orientation and the implications for mental health and is the co-author of Born Gay? The Psychobiology of Sex Orientation
Transgender Prejudice And The Belief In A Biological Basis For Gender
As June comes to an end, so do many events associated with Pride Month, a month-long celebration of sexual diversity and gender variance — often geared towards increasing the visibility of the LGBTQIA community, as well as combatting stigma and advocating for equal rights.
But the battle to eliminate stigma and achieve these rights will certainly continue, as recent debates about which bathrooms transgender men and women should use illustrate all too well.
For years here at 13.7, Barbara J. King has been writing about what she calls the spectrum of gender expression, and "the fact that gender identity isn't only — or even mostly — about biology and that it's most certainly not reducible to the sex one is assigned at birth." That's an especially important lesson in light of new research that identifies one of the sources of prejudice against transgender individuals: the (mostly mistaken) belief that men's and women's stereotypical characteristics do, in fact, come down to some immutable feature of one's biology.
In the new study, forthcoming in the journal Sex Roles, researchers Boby Ho-Hong Ching and Jason Teng Xu presented 132 university students in Hong Kong with one of three articles to read. One article was intended to reinforce the idea that gender differences have a biological basis, one was intended to question this view, and a third was entirely unrelated to gender differences and served as a baseline comparison.
The article advocating a biological basis for gender presented a study purporting to find that "the brains of men and women are wired up differently," which "could explain some of the differences in personality and behaviour between male and female." It went on to describe the study and quote fictional experts, including "Professor Schneider," who summarized: "There is a neurological cause of sex differences, which suggests that these differences are difficult to change."
The alternative article reported the same study, but also included some cautionary remarks. For instance, the researchers noted that men and women "still have many similarities in terms of the brain architecture" and that "the relations between brain and human behavior are complex." In this version, Prof. Schneider instead warned that the studies do not "offer insights into the socio-biological developmental processes that lead to observed male/female differences. The neurological associations with sex differences are not fixed, but amenable to change by environmental factors."
After reading one of the three articles and completing an unrelated task, participants then responded to various questions designed to evaluate their stereotypes about transgender individuals, as well as their attitudes towards them. For example, they indicated how much they agreed with statements including, "transgenderism endangers the institution of the family," and "I would feel comfortable if I learned that my neighbor was a transgendered individual." A final set of questions concerned civil rights, with items such as: "Post-operative transsexuals in Hong Kong should have the right to get married in their new sex," and "Transgender people in Hong Kong should have the right to change their birth certificates."
The researchers found that those participants who had read the article endorsing a biological basis for gender differences were significantly more likely than participants who read either of the other articles to report negative stereotypes about transgender individuals, to report prejudicial attitudes, and to reject equal rights. Responses for participants who read the alternative article or the control article did not differ from each other.
The authors suggest that the article endorsing a biological basis for gender differences reinforced what psychologists call an "essentialist" view of gender — the idea that men and women belong to fundamentally different categories that have some inherent basis (some "essence"), such that the categories have sharp and immutable boundaries, and such that members of the same category share many important similarities with each other. On a view like this, it's hard to make sense of a mismatch between a person's gender identity and their assigned sex, if it's the biological basis for their assigned sex that's taken to reflect their true "essence." This, in turn, could support a more prejudicial attitude towards people who identify with a gender other than the one assigned at birth.
Prior work supports several of these ideas: that a biological basis for gender differences plays into psychological essentialism and that psychological essentialism can foster prejudice. For example, one study found that after reading a fictional news article that explained a sex difference in biological terms, participants were more likely to report that people cannot easily change, and to associate men and women with their stereotypical attributes, such as being nurturing for women and competitive for men. Another study found that people who thought of a particular social category in more essentialist terms tended to regard the group as lower status. Finally, a survey study found that the belief that gender has a biological basis was correlated with opposition to transgender civil rights.
The new study by Ching and Xu goes beyond this prior work in showing a causal relationship between beliefs about the biological basis of gender and a host of beliefs about transgender individuals, with a particular role for the essentialist commitments that a biological basis is taken to entail. Among other things, the findings suggest that if people appreciate the non-dichotomous and diverse nature of gender identity, they're less likely to maintain negative views towards people who are transgender, and less likely to oppose their rights.
Tania Lombrozo is a psychology professor at the University of California, Berkeley. She writes about psychology, cognitive science and philosophy, with occasional forays into parenting and veganism. You can keep up with more of what she is thinking on Twitter: @TaniaLombrozo
Sexual differentiation of the fetus occurs within the womb, as a result of hormonal influences on the development process. These hormones not only affect differentiation of the sex organs, but also affect brain development. Scientists hypothesized that variation in fetal hormones might affect brain development in such a way as to influence subsequent sexual preferences. However, since it would be unethical to obtain fetal hormone levels (too dangerous to the fetus), proxies have been used in place of actual hormone levels. These proxies include differences in skeletal size and shape, including the ratio of the long bones of the arms and legs relative to arm span or stature and the hand bones of adults (the ratio of the lengths of various fingers). However, there are no differences in circulating sex hormones between heterosexual and homosexual men (Meyer-Bahlburg 1984).
Studies have shown that ratios of digit length are predictors of several hormones, including testosterone (an androgen), luteinizing hormone and estrogen (Manning, et al. 1998). In women, the index finger (2D, second digit) is almost the same length as the fourth digit (4D). However, in men, the index finger is usually shorter than the fourth and that this 2D:4D ratio in females is established in two-year-old children. It was hypothesized that the sex difference in the 2D:4D ratio reflects the prenatal influence of androgens on males. A subsequent study showed that the 2D:4D ratios of homosexual men vs. heterosexual men were not different (Williams, et al. 2000). However, homosexual women displayed significantly smaller 2D:4D ratios compared with heterosexual women, suggesting that women exposed to more androgens in the womb tend to exhibit SSA.
Other studies have found that the more older brothers a male child has, the more likely he is to develop a homosexual orientation (McConaghy, et al. 2006). This study also found that homosexual men had a greater than expected proportion of brothers among their older siblings (229 brothers: 163 sisters) compared with the general population (106 males: 100 females). Subsequent, larger studies found that older brothers did not affect male sexual orientation (Zietsch, et al. 2012 Bogaert 2010). Males who had two or more older brothers were found to have lower 2D:4D ratios (Williams, et al. 2000), suggesting that they had experienced increased androgens in the womb. The reason increased androgens would predispose both males and females to exhibit homosexual behavior was not explained in the study. A study examining 2D:4D ratios in twins concordant and discordant for sexual orientation found differences between discordant female twins, but not male twins, although the sample sizes were very small (Hall and Love 2003). However, a large (255,116 participants) cohort from the UK found no link between female SSA and 2D:4D ratios (Manning, Churchill, and Peters 2007).
Another study examined the length of long bones in the arms, legs and hands. Both homosexual males and heterosexual females had decreased long bone growth in the arms, legs and hands compared to heterosexual males or homosexual females (Martin and Nguyen 2004). Accordingly, the researchers hypothesized that male homosexuals experienced decreased androgen exposure during development than male heterosexuals, while female homosexuals had greater steroid exposure during development than their heterosexual counterparts. Needless to say, this study directly contradicted the results of the Williams study above, which showed that males with multiple older brothers (who tended to be homosexual) experienced increased androgen exposure.
Congenital adrenal hyperplasia
Studies involving a rare hormonal imbalance, congenital adrenal hyperplasia (CAH), caused by defective 21-hydroxylase enzyme, suggest that extreme hormonal abnormalities can influence sexual orientation to some extent. CAH increases production of male hormones during development. In female fetuses, increased androgens resulted in development of ambiguous external genitalia. A meta-analysis of 18 CAH studies shows that 91.5% of those women suffering from CAH end up with a heterosexual orientation (Meyer-Bahlburg, et al. 2008), despite having a severe imbalance of testosterone during fetal development. These studies show that hormonal influences in utero are not the major reason for female SSA.
Childhood gender nonconformity
The behaviors of children have been hypothesized to be influenced by hormonal imbalances during development or early childhood. Such non-stereotypical childhood behaviors (e.g., boys playing with dolls or girls showing interest in rough play) have been associated with same-sex sexual orientation (Bailey and Zucker 1995). However, such studies have been done retrospectively based upon the memories of participants or family members, which could be tainted by post-childhood experiences. The association of childhood gender nonconformity with SSA has been disputed by other scientists (Gottschalk 2003) and has been shown to be a predictor of poor psychological health (Rieger and Savin-Williams 2012).
Hormonal influences conclusion
All of the studies reporting possible hormonal influence on SSA suffer from the lack of any concrete evidence that hormones actually play any role in sexual orientation. In fact, androgen gene variants do not play a role in male sexual orientation (Macke, et al. 1993). The fact that contradictory studies report increased vs. decreased androgens as a basis for SSA does not provoke confidence that the proxies are legitimate. Fairly, a study that documented actual hormone levels, as opposed to proxies, would plausibly provide more definitive data. The fact the extreme hormonal abnormality found in CAH only moderately affects SSA shows that it is unconvincing that subtle abnormal hormonal influences account for few, if any, instances of SSA.
Scientists Say Race Has No Biological Basis
Researchers adept at analyzing the genetic threads of human diversity said Sunday that the concept of race--the source of abiding cultural and political divisions in American society--simply has no basis in fundamental human biology.
Scientists should abandon it, they said.
Their controversial conclusion grows out of a more precise understanding of the underlying genetics of the human species and how surface distinctions of skin color, hair and facial features, which may loom large in daily life, have nothing to do with the basic biology of human differences.
“Biologically, we are saying in essence that race is no longer a valid scientific distinction,” said Solomon H. Katz, a University of Pennsylvania anthropologist.
Speaking before the American Assn. for the Advancement of Science, which is meeting this week in Atlanta, the researchers made their presentations in the heart of a region that for centuries has been alternatively transfixed and transfigured by racial divisions.
“Race is a social construct derived mainly from perceptions conditioned by events of recorded history, and it has no basic biological reality,” said C. Loring Brace, a biological anthropologist at the University of Michigan.
The researchers were acting, in part, to correct a legacy of misconceptions about the biology of race, in which earlier generations of researchers provided the raw material for spurious claims of racial superiority. “They liked to concoct a biological basis for mistreating people,” said Brown University anthropologist John Ladd.
The work discussed Sunday draws on a new ability to reconstruct the genetic evolution of humankind and a new appreciation for how humanity developed genetic diversity as it spread around the globe.
With the tools of molecular biology, scientists can peer past superficial characteristics to explore more powerful, underlying genetic commonalities and differences, which are making racial categories look increasingly arbitrary and irrelevant, the experts said.
“The old biological definitions of race were based on what people looked like,” said Joseph L. Graves Jr., an evolutionary biologist at Arizona State University West. “Now that we have better ways of looking at race . . . we could construct races based on what type of fingerprints people have, or on what kind of blood type they have, and that would be just as legitimate.”
Rarely have Americans been so concerned about their ethnic and racial distinctions--in the last U.S. census, people claimed membership in some 300 racial or ethnic groups--nor have so many anthropologists been so willing to reject race as a biological category.
One survey by Central Michigan University says more than half of all cultural and physical anthropologists no longer embrace race as a useful scientific definition.
The scientists on Sunday said they are not attempting to deny human diversity, nor suggesting that historians, sociologists or federal census-takers should abandon racial categories in their work. Rather, they want to ensure that the scientific study of human diversity is no longer handicapped by reliance on artificial categories.
“Social scientists are confronted with a dilemma in that they use racial categories in order to conduct their research studies, to compare and contrast life chances or social and economic progress at the same time there is an understanding that race has no biological reality,” said Michael Omi, an expert in ethnic studies at UC Berkeley.
“In fact, we can never have any really stable, coherent categories of race and ethnicity. Much of this is socially or historically shaped and politically determined,” he said.
Researchers are re-evaluating scientific ideas of race at a time when many researchers generally are suspicious of efforts to link race and complex social behavior.
While there may be no significant biological racial differences between groups of people, the researchers said that does not undermine ideas--such as affirmative action--which may be based on cultural differences stemming from how groups may have been treated historically.
“The fundamental gulf between the races in the United States is not so much culture or cash or color instead, it is (a difference in) an explanation of behavior,” said Rhett Jones, director of Brown University’s Center for the Study of Race.
“Most white people--not all--really do believe that you can tell something about somebody by his or her skin color,” he said. “Most black people really do believe that behavior is determined by choice.
“Very few black people, for example, think there is a white gene for racism,” he said.
Criminologist Believes Violent Behavior Is Biological
Twenty years ago, when brain imaging made it possible for researchers to study the minds of violent criminals and compare them to the brain imaging of "normal" people, a whole new field of research — neurocriminology — opened up.
Adrian Raine was the first person to conduct a brain imaging study on murderers and has since continued to study the brains of violent criminals and psychopaths. His research has convinced him that while there is a social and environmental element to violent behavior, there's another side of the coin, and that side is biology.
"Just as there's a biological basis for schizophrenia and anxiety disorders and depression, I'm saying here there's a biological basis also to recidivistic violent offending," Raine, a professor at the University of Pennsylvania and author of the book The Anatomy of Violence: The Biological Roots of Crime, tells Fresh Air's Terry Gross.
Raine says this re-visioning of violent criminals could potentially help direct how we approach crime prevention and rehabilitation.
"I think prisoners . [are] not motivated to change, really," he says, " . because they just think they're a bad, evil person. If we reconceptualized recidivistic crime as a criminal disorder, would we make them more amenable to treatment?"
The key question that preoccupies Raine, however, is that of punishment and the question of the death penalty.
"Simply put," he says, "if bad brains do cause bad behavior, if brain dysfunction raises the odds that somebody will become a criminal offender — a violent offender — and if the causes of the brain dysfunction come relatively early in life . should we fully hold that adult individual responsible?"
"I've got to be careful here. There's no destiny here. Biology is not destiny, and it's more than biology, and there's lots of factors that we're talking about there, and one factor like prefrontal dysfunction or low heart rate doesn't make you a criminal offender. But what if all the boxes were checked? What if you had birth complications and you were exposed to toxins and you had a low resting heart rate and you had the gene that raises the odds of violence, et cetera, et cetera, stuff happening early on in life. I mean, you're not responsible for that. Then how in the name of justice can we really hold that individual as responsible as we do . and punish them as much as we do — including death?"
On studying psychopaths
"The most striking thing I found working one-to-one with psychopaths is . how I really liked being with them, which is shocking and at the time surprising to me but, gosh, I loved dealing with the psychopaths because they were great storytellers. They were always fun. They were always interesting, and I was fascinated most of all with how they could con and manipulate me."
Adrian Raine has studied the brains of violent criminals, including that of serial killer Randy Kraft, aka the "Freeway Killer." University of Southern California hide caption
Adrian Raine has studied the brains of violent criminals, including that of serial killer Randy Kraft, aka the "Freeway Killer."
University of Southern California
On the possible correlation between lead exposure and violence
"In the '70s, '80s and '90s, violence went up in America. What was causing that? Well, one hypothesis: It was the increase in environmental lead in the '50s, '60s and '70s. You know, lead in gas, for example. So, in the 1950s, little toddlers were playing outside, putting their fingers in dirt, putting their fingers in their mouths and absorbing the lead. Twenty years later, they became the next generation of violent criminal offenders because violence peaks at about 19 or 20. Then what happens is in the 1990s violence begins to come down, as it's been doing. What's partly explaining that? The reduction in lead in the environment. In fact, if you map environmental lead levels over time like that and map it onto the change in violence over time, lead can explain 91 percent of those changes. And to me, it's the only single cause that can both explain the precipitous rise in violence from the '70s, '80s and '90s and also the drop that we've been experiencing."
On what the fact that he has a brain scan similar to that of serial killer Randy Kraft means to him
"It makes you wonder, you know, what put me on one side of the bars in those four years in top-security prison when I was interviewing someone, when maybe with a different life course and other factors in my life, it could have flipped just the other way around? I've got a low resting heart rate. I'm a bit of a stimulation seeker, and, yes, I've got a brain scan like a serial killer. I had poor nutrition as a kid. . What stopped me [from] becoming a killer, for example, or becoming a violent offender? I was anti-social from the age of 9 to 11. I was in a gang, smoking cigarettes, setting fire to mail, letting car tires down. . But I've been intrigued: Why didn't I stay on that pathway? And it's an area that we need to do so much more on: protective factors. What protects some people who have some of the risk factors from actually becoming an offender? I think in my life, for example, I had parents who sort of loved me. I always felt loved. There was always a roof over my head. There was always a secure environment. And I got on with my brothers and sisters. You know, and maybe that's the critical ingredient: some love."
On changing his mind about the death penalty after being the victim of a violent crime
"At that point in time, I'd always been against the death penalty. I mean, I'm from England. We don't have the death penalty there, you know. You just think, 'That's crazy, having the death penalty.' After being that victim, I changed my mind about that because it made me feel more about victims' experience and how maybe — maybe in some cases — it could give them a sense of closure. Now I would not be ruled out of the jury on a death penalty case, but I'm not proud of that."
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'Less Than Human': The Psychology Of Cruelty
On reconciling the victim part of him with the criminologist part of him
"I'm a Jekyll and Hyde. So there's a Dr. Jekyll inside of me that's done the research, seen these risk factors, done longitudinal studies, documented these early risk factors beyond the individual's control that moves them into a criminal way of life, and that Dr. Jekyll is saying, 'You know, you can't ignore this. You can't turn a blind eye to the biology of violence and the social factors, too.' But there's a Mr. Hyde inside of me ranting and raving and saying, 'Look, I don't want sob stories. I don't want excuses. There's a cause for all behavior. We can always find a cause for behavior. . It comes from the brain: So what? We found the cause. OK, great.'
"You know, what about the victim? What about how they feel and what about that sense of retribution, you know? What about deterrence? So, I mean, I go backwards and forwards on this, and I bet I'll change my mind again at some point in time. . The scientist inside of me says, 'You know, that deterrence aspect — especially to capital punishment — that's not working,' and I don't think the science really shows it, too, but . there's a part of me that says, 'It's an eye for an eye and a tooth for a tooth and a pound of flesh: My throat was slit, his throat should be slit.' I mean, that's just how you feel as a victim. . Kids need to be socialized and punished for bad behavior, and doesn't that also apply as adults? If you buy into the argument, that Dr. Jekyll inside of me says then all bets are off: Nobody's responsible. You can't have that. That's what Mr. Hyde says."
Is there a biological basis for different accents? - Biology
Professor Declan Murphy and colleagues Dr. Michael Craig and Dr. Marco Catani from the Institute of Psychiatry at King's College London say they have found differences in the brain which may provide a biological explanation for psychopathy.
Psychopathy is strongly associated with serious criminal behavior (rape, murder, etc.) and repeat offending but despite its heinous aspects the biological basis of psychopathy has remained poorly understood. Some investigators also attribute social causes in explaining antisocial behaviours. To date, nobody has investigated the 'connectivity' between the specific brain regions implicated in psychopathy.
The new research investigated the brain biology of psychopaths with convictions that included attempted murder, manslaughter, multiple rape with strangulation and false imprisonment. Using the Diffusion Tensor Imaging technique (DT-MRI) the researchers say they have highlighted biological differences in the brain which may underpin these types of behavior and provide a more comprehensive understanding of criminal psychopathy.
Dr Michael Craig said, "If replicated by larger studies the significance of these findings cannot be underestimated. The suggestion of a clear structural deficit in the brains of psychopaths has profound implications for clinicians, research scientists and the criminal justice system."
Earlier studies had suggested that dysfunction of specific brain regions might underpin psychopathy. Such areas of the brain were identified as the amygdale, ie the area associated with emotions, fear and aggression, and the orbitofrontal cortex (OFC), the region which deals with decision making. There is a white matter tract that connects the amygdala and OFC, which is called the uncinate fasciculus (UF). However, nobody had ever studied the UF in psychopaths. The team from King's used an imaging method called in vivo diffusion tensor magnetic resonance imaging (DT-MRI) tractography to analyse the UF in psychopaths.
They found a significant reduction in the integrity of the small particles that make up the structure of the UF of psychopaths, compared to control groups of people with the same age and IQ. Also, the degree of abnormality was significantly related to the degree of psychopathy. These results suggest that psychopaths have biological differences in the brain which may help to explain their offending behaviours.
Craig added: 'This study is part of an ongoing programme of research into the biological basis of criminal psychopathy. It highlights that exciting developments in brain imaging such as DT-MRI now offer neuroscientists the potential to move towards a more coherent understanding of the possible brain networks that underlie psychopathy, and potentially towards treatments for this mental disorder.'
The results of their study are outlined in the paper 'Altered connections on the road to psychopathy', published in Molecular Psychiatry.
Is there a biological basis for the whole "gender debate"?
Iɽ like to ask you a question which really bugs me for a long time and sorry if this was discussed here earlier (I didn't find anything though). But Iɽ like to go more into detail.
Surely most of you - especially if you are from the US (I am not, so I could err here) - may have encountered the whole gender debate. That is, if you identify yourself as x-gender (where "x" may be an arbitrary name). On the internet, I've only encountered jokes about this (for example, identifiying as "attack helicopter" is one of those mocking jokes) or people who seriously claim that there exist that many genders, which especially occurs on platforms as tumblr.
But I really can't find any scientific work/paper (psychological, neurobiological, biological . ) on this case. Why is that so? Or did I simply have searched wrong? How sharp is the boundary between 'sex' and 'gender'? Wouldn't it be more precise to speak about 'gender roles' rather than 'gender'?
However, what I know is that there exist differences, especially in the brain, which could lead to more masculine or feminine behaviour and/or traits. And of course, there is the state of intersex where an individual exhibits both male and female attributes or genitals.
But - as my opinion is currently - this doesn't justify some arbitrary names which you then can call your 'gender'. For me, this looks like people invent some things in order to protect themselves from other inner problems or to feel somehow special. Anyway, all this above currently works only as my hypothesis, but Iɽ like to know. I live in order to find truth and knowledge and I am not interested in ideological wars because science should be objective enough to give evidence or refute such claims.
So the goal of this thread shall be to find scientific evidence in order to finally shatter this debate (if it ever was one). We shall only acceppt peer-reviewed, solid papers or studies. And please restrain yourselves from jokes or other things that may be ideological in favor of one side. The whole internet is full enough of this.
EDIT: Thank you all for your responses, didn't expect THAT much resonance! Although I don't have the time to equally answer and participate to all your responses, I'll make sure to at least read them all!
Biological explanations of criminal behavior
There is a growing literature on biological explanations of antisocial and criminal behavior. This paper provides a selective review of three specific biological factors – psychophysiology (with the focus on blunted heart rate and skin conductance), brain mechanisms (with a focus on structural and functional aberrations of the prefrontal cortex, amygdala, and striatum), and genetics (with an emphasis on gene-environment and gene-gene interactions). Overall, understanding the role of biology in antisocial and criminal behavior may help increase the explanatory power of current research and theories, as well as inform policy and treatment options.
A growing body of literature has indicated the importance of considering neurobiological factors in the etiology of antisocial and criminal behavior. Behaviors, including criminality, are the result of complex, reciprocally influential interactions between an individual’s biology, psychology, and the social environment (Focquaert, 2018). As research progresses, the misconception that biology can predetermine criminality is being rectified. Elucidating the biological underpinnings of criminal behavior and broader, related outcomes such as antisocial behavior can provide insights into relevant etiological mechanisms. This selective review discusses three biological factors that have been examined in relation to antisocial and criminal behavior: psychophysiology, brain, and genetics.
Psychophysiology, or the levels of arousal within individuals, has become an important biological explanation for antisocial and criminal behavior. Two common psychophysiological measures are heart rate and skin conductance (i.e. sweat rate). Both capture autonomic nervous system functioning skin conductance reflects sympathetic nervous system functioning while heart rate reflects both sympathetic and parasympathetic nervous system activity. Blunted autonomic functioning has been associated with increased antisocial behavior, including violence (Baker et al., 2009 Choy, Farrington, & Raine, 2015 Gao, Raine, Venables, Dawson, & Mednick, 2010 Portnoy & Farrington, 2015). Longitudinal studies have found low resting heart rate in adolescence to be associated with increased risk for criminality in adulthood (Latvala, Kuja-Halkola, Almqvist, Larsson, & Lichtenstein, 2015 Raine, Venables, & Williams, 1990). However, there is likely a positive feedback loop whereby blunted autonomic functioning may lead to increased antisocial/criminal behavior, which in turn may reinforce disrupted physiological activity. For example, males and females who exhibited high rates of proactive aggression (an instrumental, predatory form of aggression elicited to obtain a goal or reward) in early adolescence were found to have poorer skin conductance fear conditioning in late adolescence (Gao, Tuvblad, Schell, Baker, & Raine, 2015 Vitiello & Stoff, 1997).
Theories have been proposed to explain how blunted autonomic functioning could increase antisociality. The fearlessness hypothesis suggests that antisocial individuals, due to their blunted autonomic functioning, are not deterred from criminal behavior because they do not experience appropriate physiological responses to risky or stressful situations nor potential aversive consequences (Portnoy et al., 2014 Raine, 2002). Alternatively, the sensation-seeking hypothesis suggests that blunted psychophysiology is an uncomfortable state of being, and in order to achieve homeostasis, individuals engage in antisocial behavior to raise their arousal levels (Portnoy et al., 2014 Raine, 2002).
Another mechanism that could connect disrupted autonomic functioning to antisocial behavior is the failure to cognitively associate physiology responses with emotional states. Appropriately linking autonomic conditions to emotional states is important in socialization processes such as fear conditioning, which is thought to contribute to the development of a conscience. The somatic marker hypothesis (Bechara & Damasio, 2005) suggests that ‘somatic markers’ (e.g. sweaty palms) may reflect emotional states (e.g. anxiety) that can inform decision-making processes. Impairments in autonomic functioning could lead to risky or inappropriate behavior if individuals are unable to experience or label somatic changes and connect them to relevant emotional experiences. Indeed, psychopathic individuals exhibit somatic aphasia (i.e. the inaccurate identification and recognition of one’s bodily state Gao, Raine, & Schug, 2012). Moreover, blunted autonomic functioning impairs emotional intelligence, subsequently increasing psychopathic traits (Ling, Raine, Gao, & Schug, 2018a). Impaired autonomic functioning and reduced emotional intelligence may impede the treatment of psychopathy (Polaschek & Skeem, 2018) and disrupt development of moral emotions such as shame, guilt, and empathy (Eisenberg, 2000). Such moral dysfunction, a strong characteristic of psychopaths, may contribute to their disproportionate impact on the criminal justice system (Kiehl & Hoffman, 2011).
While there is evidence that antisocial/criminal individuals typically exhibit abnormal psychophysiological functioning, it is important to acknowledge that there are different antisocial/criminal subtypes, and they may not share the same deficits. Whereas individuals who are high on proactive aggression may be more likely to exhibit blunted autonomic functioning, individuals who are high on reactive aggression (an affective form of aggression that is elicited as a response to perceived provocation) may be more likely to exhibit hyperactive autonomic functioning (Hubbard, McAuliffe, Morrow, & Romano, 2010 Vitiello & Stoff, 1997). This may have implications for different types of offenders, with elevated autonomic functioning presenting in reactively aggressive individuals who engage in impulsive crimes and blunted autonomic functioning presenting in proactively aggressive offenders engaging in more premediated crimes. Similarly, psychopaths who are ‘unsuccessful’ (i.e. convicted criminal psychopaths) exhibit reduced heart rate during stress while those who are ‘successful’ (i.e. non-convicted criminal psychopaths) exhibit autonomic functioning similar to non-psychopathic controls (Ishikawa, Raine, Lencz, Bihrle, & LaCasse, 2001). Despite differences among subgroups, dysfunctional autonomic functioning generally remains a reasonably well-replicated and robust correlate of antisocial and criminal behavior.
There has been increasing interest in the role of the brain in antisocial/criminal behavior. In general, research suggests that antisocial/criminal individuals tend to exhibit reduced brain volumes as well as impaired functioning and connectivity in key areas related to executive functions (Alvarez & Emory, 2006 Meijers, Harte, Meynen, & Cuijpers, 2017 Morgan & Lilienfeld, 2000), emotion regulation (Banks, Eddy, Angstadt, Nathan, & Phan, 2007 Eisenberg, 2000), decision-making (Coutlee & Huettel, 2012 Yechiam et al., 2008), and morality (Raine & Yang, 2006) while also exhibiting increased volumes and functional abnormalities in reward regions of the brain (Glenn & Yang, 2012 Korponay et al., 2017). These prefrontal and subcortical regions that have been implicated in antisocial/criminal behavior are the selective focus of this review.
Conventional criminal behavior has typically been associated with prefrontal cortex (PFC) structural aberrations and functional impairments (Brower & Price, 2001 Yang & Raine, 2009). The PFC is considered the seat of higher-level cognitive processes such as decision-making, attention, emotion regulation, impulse control, and moral reasoning (Sapolsky, 2004). In healthy adults, larger prefrontal structures have been associated with better executive functioning (Yuan & Raz, 2014). However, structural deficits and functional impairments of the PFC have been observed in antisocial and criminal individuals, suggesting that PFC aberrations may underlie some of the observed behaviors.
While many studies on brain differences related to criminal behavior have consisted of correlational analyses, lesion studies have provided some insight into causal neural mechanisms of antisocial/criminal behavior. The most well-known example of the effects of prefrontal lobe lesions is the case of Phineas Gage, who was reported to have a dramatic personality change after an iron rod was shot through his skull and damaged his left and right prefrontal cortices (Damasio, Grabowski, Frank, Galaburda, & Damasio, 1994 Harlow, 1848, 1868). Empirical studies suggest that prefrontal lesions acquired earlier in life disrupt moral and social development (Anderson, Bechara, Damasio, Tranel, & Damasio, 1999 Taber-Thomas et al., 2014). A study of 17 patients who developed criminal behavior following a brain lesion documented that while these lesions were in different locations, they were all connected functionally to regions activated by moral decisionmaking (Darby, Horn, Cushman, & Fox, 2018), suggesting that disruption of a neuromoral network is associated with criminality. Nevertheless, while lesion studies have implicated specific brain regions in various psychological processes such as moral development, generalizability is limited because of the heterogeneity of lesion characteristics, as well as subjects’ characteristics that may moderate the behavioral effects of the lesion.
In recent years, non-invasive neural interventions such as transcranial magnetic stimulation and transcranial electric stimulation have been used to manipulate activity within the brain to provide more direct causal evidence of the functions of specific brain regions with regard to behavior. These techniques involve subthreshold modulation of neuronal resting membrane potential (Nitsche & Paulus, 2000 Woods et al., 2016). Using transcranial electric stimulation, upregulation of the PFC has been found to decrease criminal intentions and increase perceptions of moral wrongfulness of aggressive acts (Choy, Raine, & Hamilton, 2018), providing support for the causal influence of the PFC on criminal behavior.
Importantly, there is evidence of heterogeneity within criminal subgroups. Successful psychopaths and white-collar offenders do not seem to display these prefrontal deficits (Raine et al., 2012 Yang et al., 2005). While unsuccessful psychopaths exhibit reduced PFC gray matter volume compared to successful psychopaths and non-offender controls, there are no prefrontal gray matter volume differences between successful psychopaths and non-offender controls (Yang et al., 2005). Similarly, while prefrontal volume deficits have been found in conventional criminals (i.e. blue-collar offenders), white-collar offenders do not exhibit frontal lobe reductions (Brower & Price, 2001 Ling et al., 2018b Raine et al., 2012) and in fact may exhibit increased executive functioning compared to blue-collar controls (Raine et al., 2012). Lastly, antisocial offenders with psychopathy exhibited reduced gray matter volumes in the prefrontal and temporal poles compared to antisocial offenders without psychopathy and non-offenders (Gregory et al., 2012). It is therefore important to acknowledge that there are various types of antisocial and criminal behavior that may have different neurobiological etiologies.
The amygdala is an important brain region that has been implicated in emotional processes such as recognition of facial and auditory expressions of emotion, especially for negative emotions such as fear (Fine & Blair, 2000 Murphy, Nimmo-Smith, & Lawrence, 2003 Sergerie, Chochol, & Armony, 2008). Normative amygdala functioning has been thought to be key in the development of fear conditioning (Knight, Smith, Cheng, Stein, & Helmstetter, 2004 LaBar, Gatenby, Gore, LeDoux, & Phelps, 1998 Maren, 2001), and appropriate integration of the amygdala and PFC has been argued to underlie the development of morality (Blair, 2007). The amygdala is thought to be involved in stimulus-reinforcement learning that associates actions that harm others with the aversive reinforcement of the victims’ distress and in recognizing threat cues that typically deter individuals from risky behavior. However, amygdala maldevelopment can lead to a diminished ability to recognize distress or threat cues disrupting the stimulus-reinforcement learning that discourages antisocial/criminal behavior (Blair, 2007 Sterzer, 2010). Indeed, while reduced amygdala volume in adulthood has been associated with increased aggressive and psychopathic characteristics from childhood to early adulthood, it is also associated with increased risk for future antisocial and psychopathic behavior (Pardini, Raine, Erickson, & Loeber, 2014).
Although the amygdala has been implicated in criminal behavior, there may be important differences between subtypes of offenders. Whereas psychopathic antisocial individuals may be more likely to exhibit cold, calculating forms of aggression, non-psychopathic antisocial individuals may be more likely to engage in impulsive, emotionally-reactive aggression (Glenn & Raine, 2014). Research suggests the former may exhibit amygdala hypoactivity and the latter, amygdala hyperactivity (Raine, 2018a). Indeed, violent offenders have been found to exhibit increased amygdala reactivity in response to provocations (da Cunha-Bang et al., 2017). Spousal abusers have also been found to exhibit increased amygdala activation when responding to aggressive words compared to nonabusers (Lee, Chan, & Raine, 2008). In a community sample of healthy adults, psychopathy scores were negatively related to amygdala reactivity while antisocial personality disorder scores were positively associated with amygdala reactivity after adjusting for overlapping variance between psychopathy and antisocial personality disorder (Hyde, Byrd, Votruba-Brzal, Hariri, & Manuck, 2014). Nevertheless, more research is needed to determine whether the presence of callous-unemotional traits (e.g. lack of guilt Lozier, Cardinale, VanMeter, & Marsh, 2014 Viding et al., 2012) or severity of antisocial behavioral traits (Dotterer, Hyde, Swartz, Hariri, & Williamson, 2017 Hyde et al., 2016) are most relevant to the observed amygdala hypo-reactivity.
The striatum has recently garnered more attention as a region that could be implicated in the etiology of criminal behavior because of its involvement in reward and emotional processing (Davidson & Irwin, 1999 Glenn & Yang, 2012). Dysfunction in the striatum has been hypothesized to be a neural mechanism that underlies the impulsive/antisocial behavior of criminals. Indeed, individuals with higher impulsive/antisocial personality traits have been found to exhibit increased activity in the striatum (Bjork, Chen, & Hommer, 2012 Buckholtz et al., 2010 Geurts et al., 2016). Psychopathic individuals, compared to non-psychopathic individuals, demonstrate a 9.6% increase in striatal volumes (Glenn, Raine, Yaralian, & Yang, 2010). Moreover, striatal enlargement and abnormal functional connectivity of the striatum has specifically been associated with the impulsive/antisocial dimension of psychopathy (Korponay et al., 2017), suggesting this dimension of psychopathy is related to reward processes (Hare, 2017).
While much of the literature on striatal abnormalities in antisocial individuals has focused on psychopathic individuals, there is some evidence that offenders in general exhibit striatal abnormalities. Increased volume (Schiffer et al., 2011) and increased reactivity to provocations (da Cunha-Bang et al., 2017) have both been found in violent offenders as compared to non-offendersMoreover, weak cortico-striatal connectivity has been associated with increased frequency of criminal convictions (Hosking et al., 2017). In contrast, one study found reduced striatal activity to be associated with antisocial behavior (Murray, Shaw, Forbes, & Hyde, 2017). While more research is needed, current literature suggests that striatal deviations are linked to criminal behavior. One important consideration for future studies is to determine a consistent operationalization for the striatum, as some studies examine the dorsal striatum (i.e. putamen and caudate Yang et al., 2015), others assess the corpus striatum (i.e. putamen, caudate, and globus pallidus Glenn et al., 2010), and still others analyze the role of the ventral striatum (i.e. nucleus accumbens and olfactory tubercle Glenn & Yang, 2012) in relation to antisocial/criminal behavior.
The neuromoral theory of antisocial behavior
Abnormalities in brain regions other than the PFC, amygdala, and striatum are also associated with antisocial behavior. The neuromoral theory of antisocial behavior, first proposed by Raine and Yang (2006), argued that the diverse brain regions impaired in offenders overlap significantly with brain regions involved in moral decision-making. A recent update of this theory (Raine, 2018b) argues that key areas implicated in both moral decision-making and the spectrum of antisocial behaviors include frontopolar, medial, and ventral PFC regions, and the anterior cingulate, amygdala, insula, superior temporal gyrus, and angular gyrus/temporoparietal junction. It was further hypothesized that different manifestations of antisocial behavior exist on a spectrum of neuromoral dysfunction, with primary psychopathy, proactive aggression, and life-course persistent offending being more affected, and secondary psychopathy, reactive aggression, and crimes involving drugs relatively less affected. Whether the striatum is part of the neural circuit involved in moral decision-making is currently unclear, making its inclusion in the neuromoral model debatable. Despite limitations, the neuromoral model provides a way of understanding how impairments to different brain regions can converge on one concept – impaired morality – that is a common core to many different forms of antisocial behaviors.
One implication of the model is that significant impairment to the neuromoral circuit could constitute diminished criminal responsibility. Given the importance of a fully developed emotional moral capacity for lawful behavior, moral responsibility would appear to require intactness of neuromoral circuity. To argue that the brain basis to moral thinking and feeling are compromised in an offender comes dangerously close to challenging moral responsibility, a concept which in itself may be just a short step removed from criminal responsibility.
There is increasing evidence fora genetic basis of antisocial/criminal behavior. Behavioral genetic studies of twins and adoptees have been advantageous because such designs can differentiate the effects of genetics and environment within the context of explaining variance within a population (Glenn & Raine, 2014). Additionally, a variety of psychological and psychiatric constructs associated with antisociality/criminality, such as intelligence, personality, and mental health disorders, have been found to be heritable (Baker, Bezdjian, & Raine, 2006). While individual study estimates vary, meta-analyses have suggested the level of heritability of antisocial behavior is approximately 40% (Raine, 2013). Shared environmental factors have been estimated to explain approximately 11% of the variance in antisocial/criminal behavior and non-shared environmental influences approximately 31% (Ferguson, 2010 Gard, Dotterer, & Hyde, 2019). However, the heritability of antisocial/criminal behaviors vary in part based upon the specific behaviors examined (Burt, 2009 Gard et al., 2019).
Inspired by prominent theories of the neurobiology of aggression, there have been several candidate genes implicated in the serotonergic and catecholaminergic neurobiological systems that have been examined in relation to antisocial/criminal behavior (Tiihonen et al., 2015). However, a meta-analysis of genetic variants related to antisocial/criminal behavior yielded null results at the 5% significance level (Vassos, Collier, & Fazel, 2014). Nevertheless, genes do not operate in isolation, thus it is important to consider the context in which genes are activated.
Gene-environment (G x E) interactions have garnered increasing attention over the years, as these can increase risk for antisocial behavior and/or produce epigenetic changes within individuals. Longitudinal studies and meta-analyses have documented the moderating effect of the monoamine oxidase A (MAOA) gene on the relationship between maltreatment and antisocial behaviors, with the maltreatment-antisocial behavior relationship being stronger for individuals with low MAOA than high MAOA (Byrd & Manuck, 2014 Caspi et al., 2002 Fergusson, Boden, & Horwood, 2011 Kim-Cohen et al.,2006). Similarly, in a large study of African-American females, having the A1 allele of the DRD2 gene or a criminal father did not individually predict antisocial outcomes, but having both factors increased risk for serious delinquency, violent delinquency, and police contacts (Delisi, Beaver, Vaughn, & Wright, 2009). This type of G x E interaction reflects how genotypes can influence individuals’ sensitivity to environmental stressors. However, there may be important subgroup differences to consider when examining genetic risk for criminal behavior. For example, low-MAOA has been associated with higher risk for violent crime in incarcerated Caucasian offenders but not incarcerated non-Caucasian offenders (Stetler et al., 2014). Additionally, high-MAOA may protect abused and neglected Caucasians from increased risk of becoming violent or antisocial, but this buffering effect was not found for abused and neglected non-Caucasians (Widom & Brzustowicz, 2006). Thus, while the MAOA gene has been associated with antisocial/criminal behavior, there are still nuances of this relationship that should be considered (Goldman & Rosser, 2014).
Another way in which G x E interactions manifest themselves is when environmental stressors result in epigenetic changes, thus becoming embedded in biology that result in long-term symptomatic consequences. For example, females exposed to childhood sex abuse have exhibited alterations in the methylation of the 5HTT promoter region, which in turn has been linked to subsequent antisocial personality disorder symptoms (Beach, Brody, Todorov, Gunter, & Philibert, 2011). There has been a growing body of work on such epigenetic mechanisms involved in the biological embedding of early life stressors and transgenerational trauma (Kellermann, 2013 Provencal & Binder, 2015). Thus, just as biological mechanisms can influence environmental responses, environmental stressors can affect biological expressions.
While genes may interact with the environment to produce antisocial/criminal outcomes, they can also interact with other genes. There is evidence that dopamine genes DRD2 and DRD4 may interact to increase criminogenic risk (Beaver et al., 2007 Boutwell et al., 2014). The effect of the 7-repeat allele DRD4 is strengthened in the presence of the A1 allele of DRD2, and has been associated with increased odds of committing major theft, burglary, gang fighting, and conduct disorder (Beaver et al., 2007 Boutwell et al., 2014). However, there is some evidence that DRD2 and DRD4 do not significantly affect delinquency abstention for females (Boutwell & Beaver, 2008). Thus there may be demographic differences that moderate the effect of genetic interactions on various antisocial outcomes (Dick, Adkins, & Kuo, 2016 Ficks & Waldman, 2014 Rhee & Waldman, 2002 Salvatore & Dick, 2018), and such differences warrant further research.
Interactions between biological factors
Importantly, biological correlates of antisocial and criminal behavior are inextricably linked in dynamical systems, in which certain processes influence others through feedback loops. While a detailed summary is beyond the scope of this review, some interactions between biological mechanisms are briefly illustrated here. Within the brain, the PFC and amygdala have reciprocal connections, with the PFC often conceptualized as monitoring and regulating amygdala activity (Gillespie, Brzozowski, & Mitchell, 2018). Disruption of PFC-amygdala connectivity has been linked to increased antisocial/criminal behavior, typically thought to be due to the impaired top-down regulation of amygdala functioning by the PFC. Similarly, the brain and autonomic functioning are linked (Critchley, 2005 Wager et al., 2009) output from the brain can generate changes in autonomic functioning by affecting the hypothalamic-pituitary-adrenal axis, but autonomic functions also provide input to the brain that is essential for influencing behavioral judgments and maintaining coordinated regulation of bodily functions (Critchley, 2005). While not comprehensive, these examples illustrate that biological systems work together to produce behavior.
While biological processes can contribute to antisocial/criminal behavior, these do not guarantee negative outcomes. Considering that many of the aforementioned biological risk factors are significantly influenced by social environment, interventions in multiple spheres may help mitigate biological risks for antisocial behavior.
With regard to psychophysiological correlates of antisocial behavior, research suggests differential profiles of arousal impairment depending on the type of antisocial behavior (Hubbard et al., 2010 Vitiello & Stoff, 1997). Treatments designed to address the issues associated with psychophysiological differences are typically behavioral in nature, targeted at associated symptoms. Studies of mindfulness have suggested its utility in improving autonomic functioning (Delgado-Pastor, Perakakis, Subramanya, Telles, & Vila, 2013) and emotion regulation (Umbach, Raine, & Leonard, 2018), which may better help individuals with reactive aggression and hyperarousal. Hypo-arousal has been associated with impaired emotional intelligence (Ling et al., 2018a), but emotional intelligence training programs have shown some promise in reducing aggression and increasing empathy among adolescents and increasing emotional intelligence among adults (Castillo, Salguero, Fernandez-Berrocal, & Balluerka, 2013 Hodzic, Scharfen, Ropoll, Holling, & Zenasni, 2018), and in reducing recidivism (Megreya, 2015 Sharma, Prakash, Sengar, Chaudhury, & Singh, 2015).
Regarding healthy neurodevelopment, research has supported a number of areas to target. Poor nutrition, both in utero and in early childhood, have been associated with negative and criminal outcomes (Neugebauer, Hoek, & Susser, 1999). Deficits of omega-3 fatty acids have been linked with impaired neurocognition and externalizing behavior (Liu & Raine, 2006 McNamara & Carlson, 2006). The opposite relationship is also supported increased intake of omega-3 fatty acids has been associated with a variety of positive physical and mental health outcomes (Ruxton, Reed, Simpson, & Millington, 2004), increased brain volume in regions related to memory and emotion regulation (Conklin et al.,2007), and reduction in behavioral problems in children (Raine, Portnoy, Liu, Mahoomed, & Hibbeln, 2015). Studies examining the effect of nutritional supplements have suggested that reducing the amount of sugar consumed by offenders can significantly reduce offending during incarceration (Gesch, Hammond, Hampson, Eves, & Crowder, 2002 Schoenthaler, 1983). Thus, nutritional programs show some promise in reducing antisocial and criminal behavior.
A healthy social environment is also crucial for normative brain development and function. Early adversity and childhood maltreatment have been identified as significant risk factors for both neurobiological and behavioral problems (Mehta et al., 2009 Teicher et al., 2003 Tottenham et al., 2011). A review of maltreatment prevention programs supports the efficacy of nurse-family partnerships and programs that integrate early preschool with parent resources in reducing childhood maltreatment (Reynolds, Mathieson, & Topitzes, 2009). Promoting healthy brain development in utero and in crucial neurodevelopmental periods is likely to reduce externalizing behaviors, as well as other psychopathology.
Knowing that the social context could help to buffer biological risks is promising because it suggests that changing an individual’s environment could mitigate biological criminogenic risk. Rather than providing a reductionist and deterministic perspective of the etiology of criminal behavior, incorporating biological factors in explanations of antisocial/criminal behaviors can highlight the plasticity of the human genome (Walsh & Yun, 2014). They can also provide a more holistic understanding of the etiologies of such behavior. For example, sex differences in heart rate have been found to partially explain the gender gap in crime (Choy, Raine, Venables, & Farrington, 2017). Social interventions that aim to provide an enriched environment can be beneficial for all, but may be particularly important for individuals at higher biological risk for antisocial behavior. While biological explanations of antisocial and criminal behavior are growing, they are best thought of as complementary to current research and theories, and a potential new avenue to target with treatment options.
For some clades covered by the International Code of Zoological Nomenclature, several additional classifications are sometimes used, although not all of these are officially recognized.
|Name||Latin prefix||Example 1||Example 2|
|Magnorder||magnus, 'large, great, important'||Boreoeutheria|
|Mirorder||mirus, 'wonderful, strange'||Primatomorpha|
|Parvorder||parvus, 'small, unimportant'||Catarrhini|
In their 1997 classification of mammals, McKenna and Bell used two extra levels between superorder and order: grandorder and mirorder.  Michael Novacek (1986) inserted them at the same position. Michael Benton (2005) inserted them between superorder and magnorder instead.  This position was adopted by Systema Naturae 2000 and others.
In botany, the ranks of subclass and suborder are secondary ranks pre-defined as respectively above and below the rank of order.  Any number of further ranks can be used as long as they are clearly defined. 
The superorder rank is commonly used, with the ending -anae that was initiated by Armen Takhtajan's publications from 1966 onwards. 
The order as a distinct rank of biological classification having its own distinctive name (and not just called a higher genus (genus summum)) was first introduced by the German botanist Augustus Quirinus Rivinus in his classification of plants that appeared in a series of treatises in the 1690s. Carl Linnaeus was the first to apply it consistently to the division of all three kingdoms of nature (then [mineral]]s, plants, and animals) in his Systema Naturae (1735, 1st. Ed.).
For plants, Linnaeus' orders in the Systema Naturae and the Species Plantarum were strictly artificial, introduced to subdivide the artificial classes into more comprehensible smaller groups. When the word ordo was first consistently used for natural units of plants, in 19th century works such as the Prodromus of de Candolle and the Genera Plantarum of Bentham & Hooker, it indicated taxa that are now given the rank of family. (See ordo naturalis, 'natural order'.)
In French botanical publications, from Michel Adanson's Familles naturelles des plantes (1763) and until the end of the 19th century, the word famille (plural: familles) was used as a French equivalent for this Latin ordo. This equivalence was explicitly stated in the Alphonse De Candolle 's Lois de la nomenclature botanique (1868), the precursor of the currently used International Code of Nomenclature for algae, fungi, and plants.
In the first international Rules of botanical nomenclature from the International Botanical Congress of 1905, the word family (familia) was assigned to the rank indicated by the French famille, while order (ordo) was reserved for a higher rank, for what in the 19th century had often been named a cohors  (plural cohortes).
Some of the plant families still retain the names of Linnaean "natural orders" or even the names of pre-Linnaean natural groups recognised by Linnaeus as orders in his natural classification (e.g. Palmae or Labiatae). Such names are known as descriptive family names.
In zoology, the Linnaean orders were used more consistently. That is, the orders in the zoology part of the Systema Naturae refer to natural groups. Some of his ordinal names are still in use (e.g. Lepidoptera for the order of moths and butterflies Diptera for the order of flies, mosquitoes, midges, and gnats). [ citation needed ]
In virology, the International Committee on Taxonomy of Viruses's virus classification includes fifteen taxa to be applied for viruses, viroids and satellite nucleic acids: realm, subrealm, kingdom, subkingdom, phylum, subphylum, class, subclass, order, suborder, family, subfamily, genus, subgenus, and species.  There are currently fourteen viral orders, each ending in the suffix -virales.