Review the listed citation. If you are unsure where they are located, review the format of an APA format.
Some of the research does indicate that for some people there may be a biological basis for feeling more akin to the opposite sex due to atypical hormone exposure in utero. However the issue is there is no way to test for this in living people — the bstc size can only be observed post mortem. What this means is that many people who identify as trans may not have any biological condition at all. For many it may be psychological or caused by social contagion. The huge rise of young people suddenly developing a trans identity after a stint on the internet or lots of their friends coming out as non binary indicates this may well be an aetiology.
This then leaves the problem of young people being unecessary medicated. For example multiple personality disorder and repressed memory syndrome, both of which were subsequently shown to be incredibly rare. Re the article I picked out one reference which was inaccurately discribing. It is quoted that 1.
This is completely untrue. The figure is more like 0. These are women who in middle age develop an adrenal condition where they produce too much testosterone and start to grow a beard. Thus they were NOT born with ambiguous gentialia. They were born with entirely typical female genitalia. The internet and social media have merely provided a means of more broadly disseminating information, and thus those with gender dysphoria are able to find a name for their issue, talk to others with it, and find ways to treat it usually hormone replacement therapy, sometimes surgery.
Is this your real reasoning for your request or is it simply to drive home your political beliefs so that way you can belittle those with opposing views? Then that makes it bias nitpicking and not true research. The article is written under the umbrella of Harvard University and yet I see no in-text citations! Instead of classifying brains as male or female, why not embrace the diversity of brains in a particular sex and accept that whatever brain that inhabits a body, be it a male or female body, is the brain of that corresponding sex.
It would also be interesting to see a study of the brains of ultra-femme men and butch women to see if they are similar to the majority of brains of the opposite sex. In addition to that, compare them to the brains of transgender individuals of their corresponding biological sex. Cheryl Li, I like your ideas about the comparative studies. Links and Article Heads would be great. At best there is greater diversity in male brains and female brains than previously supposed and gender roles are too rigid. Both could be true. Brain studies show that whilst overall in populations there are some differences in male and female brains across the population, most people are in the middle.
Think of height — men are overall taller than women but there are many taller women and shorter men. Even if there is a biological spectrum of masculine and feminine it is certain that gender roles are very much socialised as well. The idea that we are a blank slate and socialisation is everything is I think untrue. However socialisation can also play a large role as does culture in general. Alas, it does not work that way.
Transsexual suffer from dysphoria which can be compared to having a throbbing psychic toothache, or if you have the good fortune of never having had a toothache, then maybe a persistent itch you cannot scratch. There is psychological damage that transsexuals go through. We have some of the highest rates of suicide of any group and suffer a high rate of homicide. This stems from societal rejection sometimes from nuclear families and from the persistent feeling that our bodies and social roles are plain wrong. However, with treatment, we can get relief. My sincere hope is that another generation does not have to go through an irreversible and disfiguring puberty before getting medical help.
Norman Spack, MD, now in retirement it seems, over at Boston Child Hospital and affiliated with Harvard Medical School has been instrumental in bringing what is often called the Dutch Protocol to help trans youth. In short, we do not need to study these children and leave them in bodies they loath. We need to help them.
Children are unreliable, and the younger they are the more unreliable they are. I was assigned boy at birth. I did not grow out of it. I was deeply harmed by having to go through an irreversible and disfiguring male puberty. I was reliable in my assertions. I insisted I was a girl for 20 years and your 30 days playing with an easy bake oven testimony a hollow testimony to the real pain than real transsexuals dealt with for decades. Stop forcing your false narratives down the throats of real transsexuals.
Can you explain why you did and what it felt like? You have to be kidding me… Deeply harmed… disfiguring male puberty…. You act as if your parents could have stopped that. Lucky for you there is in-depth science now and you can live as you please. Shame on you for hating your parents for doing what they thought to be right.
The fact is that some kids who experience symptoms of dysphoria when they are young will grow out of it, while others will develop into full-blown dysphoria. The solution this study proposes is to administer hormone therapy at age 14, but not everyone is mature enough to make such a huge decision at that age. Life altering decisions are made. Putting a child through a puberty of a sex they do not affirm creates problems for the person for the rest of their life. You are right that many patients will decide not to transition, but that shows up at puberty.
The kid will decide to go with the assigned birth. The bone density issue is speculative and seems not to be a factor. The alternative is to start cross sex hormones in middle school and some places are doing that where insurance is not covering blockers. I thought I was a girl for 20 years starting at age 6. However this was not widely available a the time.
I cried when I started puberty and felt misgendered when straight women were attracted to me because I saw myself as a woman and presented very femme. I was an effeminate bisexual man not a woman. But in childhood I had absorbed the idea I could not be a boy and have the interests and proclivities I had. Thank goodness I was not brought up now. I understand for you it may have been an underlying and permanent confidition but the problem is children are easily influenced and do not know their own minds- or at least can not be sure until they are grown up. For every child saved from natural puberty we risk putting children through unecessary treatment.
Here lies the issue. The idea of sterilising children on the basis of an untestable self diagnosis strikes me as incredibly dubious. Many children who would grow up to be gay may misdiag nose themselves as trans before they realise their sexuality. I like your thinking. I have an opinion, I have no evidence, but simply an intuition, that gender as an expression is commonly different in every individual.
Long story short, I claimed that men and women are actually just large social group in society that almost everyone belongs to. At the same time as society is forcing us to conform to this other social group. If you were at risk for biological disorders that impacted your health opposed to tour esteem, these standards might be relevant. We need objective standards of measurement, not subjective fluff. There is a huge difference between a Study of Genes and an Observational Study. The first one is objective knowledge, the second it is just a subjective interpretation that tends to be biased, or in the best scenario, not conclusive.
Observational studies are typically compared with randomized controlled experiments. In fact, most of the studies of human behavior, nutrition, and longevity among many other fields are observational studies. ANY kind of study can be flawed, but we take care to only cite articles that have been peer-reviewed and use appropriate statistical tests and methods.
Also, importantly, many studies of human genes rely on observational studies. Many of the aforementioned traits or aspects of identity may have roots in certain genes that affect many parts of a person, and environment can certainly interact with genes. Thanks for your response. However in rare cases mutations and abnormalities may alter the number of sex chromosomes, or cause the opposite genitalia to develop in xx or xy humans.
If so, it would appear that biological sex is binary, regardless of the genetic code behind the outcome. Or are you stating that these chromosomal abnormalities represent different sexes? Biological sex in mammals is very binary. The only two gamete options are ova or spermatozoa. Sexual development may be a sloppy er process but there is no inbetween gamete that is produced.
I am not talking about out of the ordinary examples of this condition or that condition possibly having effects on how those genes develop in a minute number of people. I mean on a regular without mitigating factors basis. Because if there is, then your argument of there being no genes for logic, republicans, and so forth is just a way to insult the intelligence of others while in some half ass way trying to avoid answering the question properly because the answer to that question does not suit your personal beliefs.
And that is what you are doing with such an answer — mocking others to coverup your desire to not have an honest discussion on this topic where you properly answer questions even if their answers do not suit your purposes. You know the correct answer to that question. There are some hypothesis on it, but nothing that can be proven at this time. And as your own answer say, such a gene is likely to never be found. With that we can finally break through to the reality of the situation. There is no gene for transgender. There are things that can happen that play a role in gender identity.
BUT those things are more rare exceptions than anything else. The reality of it all is that we are born with genetic make ups that can be tested and verified as either male or female. This is scientific fact. Any other identity or other such goobedlygook is something completely different. There is nothing to debate there. Transgenderism has been shown to have genetic influence as described in the article.
But if you asked a farmer centuries ago about inheritance, they would be able to tell you that certain traits are inherited generation to generation. I agree the genes have not been found but when they are that would make transgender treatable inutero making it possibly non existent.
Lack of existence makes fighting for permanent rights kinda moot point. It would be like putting the dodo on the endangered species list. Same for a gay gene or series of genes. Australians did a study that found issues with the SRY gene in male to female transsexuals. Sadly large amounts of the brain and genetic research into the causes of transsexualism have been conducted outside the U. S because of prejudice both inside and outside the academic world. I believe the use of the word transgender relates to that prejudice.
I know of no brain or chromosome research that has been conducted on those who identify as other than male or female. Here is a Popular Science article about the sry gene link to transsexualism. Add to that objections by the transgender leadership about studying transsexuals by sexual orientation. Those who know the research well know transvestites as well as other forms of pseudo at ran asexual a have been allowed to transition. The word transgender comes from that and a hatred towards transsexuals by lesbian feminist. Other than humans, has it been observed in nature?
If so, perhaps genes can be identified by comparing genomes? I hope some people are still on this old article. I am a cis man. E in bioengineering and Ph. And that this is a serious question. If I understand correctly, this is separate from what sex and by sex I understand that means outward biology they are attracted to sexually. So my sincere question, because I want to understand but I do not currently, is how anyone can identify with a particular gender apart from with sex they are attracted to sexually.
I saw the whole social club argument, but I am not sure I am buying it. I have both male and female friends, but I have more women friends and in this comparison I am not including past or present lovers. Again please emphasize I am interested in logical and factual discussion. I am not attacking anyone, and I will not respond to any personal attacks. Without referring to your primary or secondary sexual characteristics how do you know that you are a boy? The answer to that question is the same answer that those of us that are transgender have.
In much the same way that some people are left-handed. Genes — there are XX and XY. These genes set up the potential in the womb for natal development e. The genes determine sex, but the environment in the womb nurture results in the expression of trans-gender. XX and XY are not genes, they are pairs of chromosomes. Multiple genes are found on each of the chromosomes. While there may be certain genes that determine a single trait, often there are traits that are determined by multiple genes. As this article asserts, it may be a combination of genes on these x and y chromosomes that determine gender.
Here is more information on that topic: Funny how all of his sources were debunked years ago. Johns Hopkins has in fact resumed performing transgender surgery as of this year. Paul McHugh also tried to convince the world that the pedophelia in the Catholic priesthood was actually gay sex with remorse. This article is highly subjective and makes false presumptions. What we do know is that biological gender is indeed binary as the article correctly states , and as far as we know, biology describes the totality of our gender experience.
The rest is entirely speculation, most of it politicized, based on scant, often dated or discredited studies with hypothetical conclusions that establish nothing close to a consensus. This article is written based on scientific studies. We seek to always represent the science fairly. As the author, it is YOUR responsibility to provide cites and resources to justify the position that you hold or the findings your deduce from the research.
You have that backwards. In the article it pointed out that other scientific studies were debunked and discredited, but why? You cannot prove your point without backing it up with a source, that source being one you used to disprove and prove your point.
We agree that sources are important! While gender dysphoria used to be classified as a mental illness, it is now widely accepted that this is not the case. It is also widely accepted among both doctors and scientists that neither biological sex i. I have to agree with Marshall. The Scientific Method is the process of eliminating possibilities through experiments, not designing experiments to support their hypothesis. This article has not considered many other hypothesis but cherry picked evidence to support the desired conclusion.
In Neurobiology you can take any group of individuals and discover similarities in their brain composition. While the science may be sound in this article the conclusions can be misleading. There are some studies almost all human studies for which it is not possible to design the types of empirical experiments one can do with animals.
The studies presented in this article are very standard scientific studies, designed using the scientific method within ethical confines. Twin studies are the gold standard in determining genetic contribution in human studies. If more identical twins who have identical genomes than fraternal twins have something in common, then it is very likely that there is a genetic contribution.
This is because it is unlikely that two identical twins are raised in more similar environments than fraternal twins. And this is exactly what was seen with the trait of being transgender! And science is definitively about consensus! With the genetic and brain structure evidence we have now and is explained in this article , there is scientific consensus that gender identity has biological underpinnings.
However even with consensus, evidence behind that consensus still is the strength behind the scientific claim. On the note of my own personal evidence, I am not the one making a scientific claim.
Affect Regulation and the Origin of the Self. The distancing theory of emotions developed in the theatre suggests that backlogged emotion can either be merely relived a bad grief, anger, shame, efatigue or fear or, at what is called "aesthetic distance," as a relief from pain. In China, excessive emotion was believed to cause damage to qi , which in turn, damages the vital organs. Thank you for this article, would like to read more on genetics, as I have prior. I think there is some scientific literature to back this observation that there are higher rates of ASD in the trans population, but the reason for it is still unknown.
This paper is the one that makes a scientific claim and attempting to use evidence to support the claim. Incomplete evidence provides incomplete conclusions. If all of those experiments fail to disprove the hypothesis, then logically it can be concluded that the hypothesis is correct. All that this article does is show ONE experiment that supports the hypothesis and then published the conclusions.
To try and catch those holes before publishing? Again great, insightful article but it is incomplete and does not answer all questions related to transgenderism. In fact it raises more questions than it answers and that in it of itself tells me it is an incomplete study with an incomplete conclusion. This article is not a study.
It is a summary of peer-reviewed, scientific-method-using literature on this topic. The author is not trying to make or test a hypothesis. She is just summarizing available studies. When I asked you for evidence, I was responding to the part of your comment that said you agreed with Marshall. Marshall said claimed that there was evidence that explained transgenderism as a mental illness. This article talks about multiple experiments she cites at least 8 studies , btw.
The point of peer review is to catch holes in a single study, not holes in an entire field of research. Gender is much too complicated to be understood in a single study. The studies here asked and answered specific questions e. And these studies, according to their peer-reviewers, were able to reliably answer these questions. No one is trying to explain all of the reasons contributing to gender identity in a single study. Every field has more work to do to understand ourselves and our world more completely.
As scientists, we are glad that there are always more questions to answer, for this is what keeps us employed! I believe the claim he was making referred to the high suicide rates that are comparable to those with Gender-dysphoria. Studies have even determined that gender re-assignment surgery does not help with the suicide rates.
The easy answer is to explain this away by saying the high suicide rate is due to high exposure to bullying. Yet even among other groups that experience intense bullying still come no where close to the same amount of suicide rates. I myself have spent two years in a situation where I was constantly rejected, spit on, robbed and even threatened at gun point.
I believe that is what Marshall is referring to in the above comment and is a major flaw in the above article. Also it would be important to take into account individuals who have gone through what some would call a transgender lifestyle and lived to regret it. Understanding what helped them to not commit suicide and to come at peace with themselves.
Many children who believe they are a different sex tend to grow out of it as their brain and body develops. So why should we encourage a behavior that is potentially self destructive? You would encourage a bulimic individual to continue throwing up would you? I would hope you would try and get them the best help possible. In fact similar neuroscience studies have found brain developmental causes for depression. Does that mean we encourage individuals with depression because it is natural?
No we help them cope with it in spite of how their body naturally developed. I see no difference in with transgenderism especially because there is no indication in studies that transgender individuals would stop killing themselves if the world just stopped bullying them. White men, as a group, also have higher suicide rates than the general population. Does that mean that identifying as a white man is a sign of mental illness? Third, can you cite the studies that show transgender people have higher suicide rates that is not due to bullying?
And fourth, from the APA: Also I would look at: Figures lie and liars figure. Hiding behind the studies you choose to cherry pick while ignoring many others that YOU KNOW exist and that say something completely different with real consensus than your make believe consensus presented in this hack job article is no better than propaganda.
There are many elements of truth presented, but when you can not even address a simple question on a transgender gene without mocking people and talking in circles when the answer is nothing but CONSENSUS? Please, save us your self serving condescension. You lose all credibility at that point. If you have studies to disprove this i.
We have no intention of cherry-picking. Please let us know what other information you think should be included here so as not to give that impression. The Guardian article mentions that many therapists interviewed believe that the vast majority of their clients who have undergone sexual reassignment surgery are happy with the change. The consensus from the article from both sides of the argument is actually that more research needs to be done, because so many follow-up studies have sampled the population poorly.
Such a dramatic change inevitably produces psychological trauma. If you have a good health care provider, they will likely offer counseling after a skin transplant following severe burns that might alter your physical appearance for instance. Furthermore, this cohort study was comparing individuals who had undergone sexual reassignment to the general population.
Perhaps a better comparison would be to transgender individuals who had not undergone reassingnment to see if suicide rates had gone down — which would ACTUALLY comment on the effectiveness of sex reassignment. Finally, a much more recent study has actually addressed some of your concerns. It shows that while suicide attempt rates are indeed higher among transgender individuals, these rates drop dramatically if psychological and social factors bullying, marginalization, etc. If the individuals themselves did not have negative views surrounding transgenderism, rates dropped.
This was for attempted suicide not actual. I am generally suspicious of the regret rate as so many are lost to follow up. Having had two friends transition fully and partially and regret it i am aware neither cases were captured as regret. In the full case the mtf continued to live as a woman as having divested herself of her genitalia she thought this the better option along with the ability to use the protected trans characteristic in law to her advantage in applying for jobs and housing etc.
However she was fully aware that the procedure was a mistake and she realised she was a cross dresser who had a mental breakdown and became convinced that she was trans and transition the answer to her problems. The case of my friend who partially transitioned was similar. He came to realise he was a cross dresser whose therapist had persuaded him was a sign he was actually trans gender. He know considers that this was delusional thinking encouraged by a mental health professional when he was suffering depression.
As the other two trans people i know who are happy with their transitional so have serious mental health issues i am inclined to think from this case study of 4 that whilst for some genetics may be at play that there is a large scope for other aetiologies. In fact it seems negligent to ignore this as allowing vulnerable people to modify their bodies so drastically in ways they may later regret even if not officially is unethical.
The biological basis this article promotes acts to encourage a lack of gatekeeping for treatment which i see as very important to ensure only those who would really benefit are permitted to be treated. That said, you really should read up on intersex and how that works — on a genetic level.
Gender, on the other hand, is socio-cultural. Bibliographies on both these works are a good resource for bringing yourself up to speed in the gender studies field. Transgender is not viewed as a pathology. Moods do not necessarily correlate to some sort of neuro-pathological state e. Gender presentation by and large is a socio-cultural function.
There are two windows in natal development for sex differentiation: The DSM was changed not by scientific pressure but by political pressure. This is no different than the EPA changing its criteria based on Exxon lobbying. I would dearly love you to cite the evidence that gender dysphoria responds to psychopharmacological treatment or talking therapies as the disorders you mentioned do. Trans people have a perfectly good idea as to what their bodies look like. There is no fussing over any minor or imagined defect. Just one more bit of data suggesting that gender dysphoria is not in the same realm as BDD and other disorders if they were, it would stand to reason that the same type of treatment would effect similar results.
Transgenderism is not at all like anorexia or other body dysmorphic illnesses because transgender patients were treated in the same exact way medically and psychologically as people with BIID, anorexia, etc and did not respond to the therapies or medication in anyway. However, people with anorexia, BIID, etc did and do respond to those therapies and medications. You should look into the history of how transgender people were treated by the medical community because they treated exactly like people suffering from body dysmorphic illnesses.
However, transgenderism did and does respond very well to the way that it is treated today, which is first to help the person come to terms with their transgender status, and then from there to help the person decide what the next course of action should be from transitioning socially, medically, or do nothing. As for the comorbidity rate much of that is due to the very negative way in which transgender people are treated, and perceived by society.
As the current treatment and standards of care for. However, after talking with a gender therapist, socially transitioning, and especially after being on cross sex hormone replacement therapy for a few months my gender dysphoria completely went away. Again if transgenderism were cognitive disorder like BDD, anorexia, BIID, etc then is should have responded to the treatments used to help people with those disorders, and they had no effect at all. And certain not for lack of.
The reason I believe for this is simple and that is that transgenderism in and of itself is not a mental disorder or illness. Down below is an excerpt from a paper that Dr. Milton Diamond wrote in as well as a link to the entire paper. Milton Diamond is please google him as he has contributed probably more than anyone else to our understanding of gender, transgenderism, and interseuxality. He has been studying and publishing papers on every gender related since , and is also one of the people who did a study with fraternal and identical twins looking to see if there is a genetic component to transgenderism.
He located a set of identical twins who were adopted away at birth, and who were raised in different countries, spoke different languages, and both transitioned at around the same time, and both talked about experiencing their transgenderism similarly. In fact, down below is a link to a youtube video with him discussing the results.
I believe that transsexuals are intersexed in their brains as others are or might be more obviously so in their gonads, genitals, hormonal character, receptors, enzymatic or chromosomal constitution. And it is this brain intersexuality that biases the person to assert his or her gender identity. As a retired RN, having researched this thoroughly, I stand with you Kristin. They do basically consider it normal to have gender fluidity. As mentioned, at least 6 genes have been identified for gender ID.
As mentioned, indigenous peoples identified and were comfortable with this, until the arrival of missionaries, who punished if not complied with male or female period. Due to their choice of beliefs. Society is changing thank goodness, one is either for humane treatment of humans, or not. I remember I went through a Tomboy stage for a while and wanted everyone to call me Bobby but I grew out of it.
HB2 in North Carolina was passed not long after I came out last year, and I was told by a man in a Facebook thread, as a broad, sweeping declaration, that he was coming for us all with a can of gasoline. Teh Children never seem to come under consideration when we are discussing the suicide rates of queer youth, or the fact that some queer people, such as myself, have actual real live children of our own. Martin Luther King Jr, and ignore all the rest. It is so backward, I might laugh, but it is a serious matter when society thinks as you do.
Some academics highlight a pattern where those who benefit from a type of privilege are unwilling to acknowledge it. American sociologist Michael S. These special rights protect the marginalized from the many micro and macro aggressions taken on them, in daily life. The reproductive organs form during the first weeks of pregnancy. As with any early pregnancy time, all organs are fragile to outside events, genetics triggered, receptors working or not, hormones. My mother was exposed to DDT, and it did cause a defect for me.
Legislation is necessary for all marginalized, due to the current wave of outright acted upon hatred toward those not privileged to be born white. About something that does not impact others lives with harm. The marginalized have fear every day. In the USA, our Constitution demands equality for all. Wonder why this is not true? You are being dramatic about not being able to criticize an article.
Free speech is in our Constitution also. IF you are still reading, I would suggest using the Google to research privilege, the lives daily of marginalized persons non-white, non-binary , medical research- use. I do wish you well on a journey of eye opening, and hopefully more empathy and compassion for all the humans who live on this earth. Thanks, hope you can have success; usually humility is earned via suffering. I will pray you learn humility. It is proven science that the X and Y chromosomes are not the determinant of sex assignment.
To believe they are is to make yourself into a relic of the past. This is very interesting to read as a trans girl myself. Twin studies are a common way to determine how much a trait is caused by your genetics or the environment. Identical twins have the same genes, so if gender identity were entirely due to genetics, you would expect that two identical twins would always have the same gender identity.
However, identical twins often though perhaps less so in your case have very similar environments, too siblings are often exposed to the same water growing up , so these studies use fraternal twins who have different genetics, but similar environments as a control. In the case of gender identity, more identical twins share gender identity than fraternal twins, meaning that there are some genetic causes. So since you and your brother are identical twins, it suggests that differences in your environments played a role in the differences in your gender identity. I hope that answers your question!
Marshall, you represent the multitude of ignorant people that harbor anger toward anyone that is different from them. You discount science because you are threatened by a group of persons that are not doing anything personally to you. Human beings are sexually dimorphic, end of discussion. The author fails epicly to disprove this, instead touts out the vague assertion that science tells us that gender, mind you gender is a social not biological construct, is not binary.
This assertion takes the discussion from a hard science such as biology or chemistry to the soft science of sociology, in other words an educated guess. So effectively the author is arguing, poorly, that there might be some some scientific evidence to support a basis for this deviant behavior. Keep in mind I am using the sociological definintion of deviant, which is defined and any behavior that is contrary to the dominant norms of a society.
That pretty much ends the discussion right there. Saying something has strong support in the social sciences is like finding someone in a mental institution that claims God told me to do it. Saying something is peer reviewed in a hard science carries far more weight than one from a soft science. I do not see an overwhelming amount of evidence here to support most of the assertions made in this paper, plain and simple. Whining about the limited amount of funding available for research puts the final two nails in the coffin, first it is not an accepted cultural norm worthy of further study, second as noted perhaps spend less time on pseudo science and more effort to design and test a valid hypothesis as it might yeild more funding.
Please come on back to earth. Most people still do not understand that gender and biological sex, are not the same things. Most people speak of gender when what they technically mean is biological sex. I understand exactly why trans people such as yourself would like for the world to focus on gender rather than biological sex. Many trans women are beaten and or killed each year because they made the foolish assumption that the straight guy they were out on a date with, cared more about gender than biological sex.
Gender is of the mind. A sense of self. It is who you are. Biological sex is what you are male or female. Again, the thing that matters the most, IS biological sex. Gender does not determine who can and can not give birth. Gender is not what we as human beings are sexually attracted to. You want the world to care more about gender because your biological sex is not what you want it to be. Sorry but a trans woman is not the same as a biological woman. That is why one is called trans and the other is not.
That may be a very hurtful fact within your mind and heart but is the truth. Again, just because you claim something, does not make it factual. Reality does not exist according to your desires. If it did, then you would not be trans, you would be a biological woman. Tell me, what is is exactly, that makes a person gay? Notice the word sexual, not gender?! Most people are attracted to people of the opposite biological sex as them.
That is how nature designed us for the very specific purpose of reproduction in order to keep the human race thriving. Tinder is a very popular dating app. They had to add a transgender option because users kept getting angry that they were not informed that some of their matches were trans. After finding out, users would flag the trans users: Many trans women are attacked and or killed each year, after a straight male they date, finds out that they are trans.
Harming a trans person or any person is always wrong but the reason that leads them to such anger is yet another indication as to how strongly many people feel about gender vs biological sex. Being a biological woman is about far more than what they look like. That means that MOST trans women have a penis. Most trans women do not pass very well.
Most trans people do not begin HRT before puberty though HRT would be most effective if it began before puberty begins its natural course on the body. As a trans woman, you can not give birth. That is yet another important factor to not all but most men. Again, having a penis is a deal breaker to most straight men. I know many males, all of whom feel the same as I do. The other one looked trans, a mile away.
When the time is right, I will get married and have children with a biological woman. Again, biological sex is what you are as in your physical body. Gender is who you are as in your sense of self within your mind. Do you really not understand the difference? A biological male can have a great personality. He can be within his mind, everything that I like.
But I would never even consider wanting to date him. You can focus on gender all you want, but you can NOT force anyone else to do the same. That will never happen. See yourself as whatever you want. That is your business and your right. What is not your right is to try and tell other people what should be most important to them and how they should feel about you and your transgender reality. Why are there dating sites where men seek out trans women to date? The visual representation of gender is what the man cis wants.
If she has fully transitioned, he may never know the difference. That report is very controversial and not peer reviewed: To make such a conclusion from the few words you have offered is an intended deception which cast a doubt on the veracity of everything you say. The sentence you quote links to one of the studies which is actually a meta-study that contains a nice list of all the studies it examined.
We could probably write a whole article just about twin studies, but here we were trying to cover more ground.
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Twin studies are actually an extremely common way to determine the relative contribution of genetic and environmental factors. Harvard has jumped on the lunacy bandwagon now? This is just fake science and biased garbage. What happened to reason?? Everyone rejects facts now. You have all lost your minds. It is a mental disorder, end of. Harvard has jumped on its usual scientific facts now. This is just well researched science and blessed oops misread lol truth. Only fundamentalists reject facts now.
I am glad majority of all humans do not reject hard scientific work now. It is biological and genetic, end of. The idea that gender is fluid because Judith Butler and articles like this say so, is ridiculous. I read lots of different articles. A most informative piece. I found it very helpful. I found my dysphoria completely vanished once my body matched that of my mind. My arms, my legs, my body, my mind… I have become My self. Science — this science has helped me to make sense of why I am. I liked the article, and chased up a couple of references, but was disappointed by what I found.
In the paragraph on estrogen receptor sensitivity, you cite two articles. Do you have any more solid data on this? Thanks so much — you actually caught a mistake! We meant to cite another article by Fernandez et al. These two papers actually came out the same year and covered a similar topic, hence the error, which has now been corrected. So, I want to make sure I address your comments. Still, studying ERbeta in mice, we do know that polymorphisms can have drastic effects on nervous system develop. With MtF, the polymorphism is different, and thus has different repercussions.
Another interesting piece of evidence with FtM — http: CYP17 is involved in hormone metabolism, and thus may be affecting estrogen production. This study supports the idea that FtM may not have sufficient estrogen production and thus are not sufficiently feminized. I also want to address the other Fernandez et al. However, the androgen receptor paper cited above was fully vetted by us and met our standards.
Briefly comparing what is available between the papers, the Hare et al. There is, however, medical and scientific consensus that transgender identity is NOT a mental illness: Part of my difficulty with this field is understanding what is meant by having a sense of gender.
I could compare them to stereotypes, but perhaps people are talking of a different, extra thing: Is that a thing? I want to know—what does it feel like to be male or female? While transgender people seem very sure of being of a gender other than their biological sex, I, as someone who does not identify as transgender, would not know what makes me a woman other than my body, the only body I have ever had form follows function?
I was just me. Later on, of course, as an adult woman I felt the impact of that social construct on me, whether I liked it or not. Culturally, I am a woman because I am seen as a woman. But I always understood it as a construct, something given to me already made rather than a way of being. What I am wondering is what is like to feel like a woman or a man when these are not fixed qualities anyone can refer to. We are all different. But do we need a name for everything? Even for things we cannot describe? We are all fluid, one way or another. We should respect all human beings.
It feels like you fit your body. It feels like you know what bathroom to go into. It feels like you know what clothes look good on you. Your mind, psyche, body, all match. The only one that made sense to me. I was one of them the boys , but looking from the outside. I was just me, wanting to feel complete and whole like a cisgendered person does.
You look in the mirror, you see a woman. Society sees a woman. You FEEL like a woman. Society gives people roadmaps or blueprints to follow if we fit the gender normative life. Those are the standard roles, and are constructed All boys like blue, all girls like pink. We all see it in our specific society, and other countries have their own versions.
She worries about gender norms, she hopes someone will love her and find her attractive, she wants to dance and cry and who gives a damn what colors she likes? All you can do is listen to what they tell you, now. The long abbreviations are very tongue-in-cheek at this point. No way that we can all have labels that box everyone up. But it does help for reference, and for recognizing diversity. Science is rapidly proving the biological nature of transgender, even fluid gender. Indigenous peoples often accepted a variety of perhaps genders, until christian missionaries arrived insisting on M or F only, or punished.
As an RN, I do know genitals are formed in the first weeks of pregnancy, when one is very susceptible to outside sources such as chemicals, also hormone levels and receptors being on or off properly, and viruses. Thus there are intersex persons, who know who they are in gender. Prior to repair, a surgeon now waits until age , when the child persistently, consistently, insistently states WHO they are. There is a book out, about repair done during infancy, female; the boy knew he was a boy, and had considerable distress.
It is caused by the constant draining requirement to be unable to be out, who they are, due to job, school, any discrimination. Liberty Councel, made up of attorneys. Does anyone remember the gonadal changes occurring after exposure by pregnant mom to DDT? I can tell you it affected mine. The brain forms gender structure in last half of pregnancy, and is irreversible. Children do say who they are now, age , persistently, insistently, consistently. Their eyes show their change- going from sad, shaded to alive, sparkling once transition achieved.
This is no choice. Why would one choose a life of taking hormone, having a surgery, having to HIDE, being discriminated in jobs, housing, bullied terribly, hated by the very religious. Some commenters appear a bit biased against any proof. A discovery of this sort is usually given press, celebrated. Yet, there remains too much ignorance and hate. You cannot imagine being in the wrong body? That is because you are in alignment with your brain.
Try to write with the opposite hand if not able to write well with both. What if you woke up tomorrow with the opposite body? Would it be illusionary? Would you have dysphoria, depression, sadness? In Salem, they used to burn epileptics at the stake. The disabled were kept in rooms in the attic. Or institutionalized, blaming the mother. Personally I do not understand why this is so difficult to comprehend. Methylation is often mentioned in this anomaly. Their bodies have difficulty in methylizing and ability to make use of some vitamins, meds, etc.
I would like to see that studied. Thank you for this article, would like to read more on genetics, as I have prior. There is genetic component to autism also. There are higher numbers of autism kids in transgender population- genetics triggered in that first weeks of pregnancy. I would like and be open to comments by the author. Thank you for replying. My question was a genuine one. You give a clear example of how I might understand better: Whether it be a different race, sex, or species. That would be upsetting and confusing, at least in part due to me being used to, and having memory of, a particular physical nature.
I believe I have heard some transgender people describe their condition in those terms: I think this would sometimes be a sort of body dysphoria. Like thin anorexic people believing they are overweight. This seems to be a different thing. So, the body perception thing is something I can grasp. Societal punishment for not maintaining gender norms, I get, and do what I can to challenge such prejudices.
As I said, it has been proven there is a gender ID structure in the brain. It is like white striae. In males it is larger than in females. Same with trans women. Activation likelihood maps of fear are shown from another meta-analysis of 30 recent neuroimaging studies [ 8 ]; here hotter colors represent greater spatial overlap consistency among significant activations across multiple studies in the meta-analysis. The amygdala is prominently activated across studies of fear.
All of this would have seemed rather bizarre to Charles Darwin [ 17 ], were he alive to witness these debates. Aside from utilizing mostly data from fMRI, the debate has also mostly used data from humans. Yet one of the key points Darwin made regarding emotions was their phylogenetic continuity: Of course, there are aspects of all emotions that are likely unique to humans e.
But it would seem that a logical starting point would be to pick an emotion for which there is good reason to believe in a strong phylogenetic continuity, understand its neurobiological basis in animal models, and then build on that core emotion scaffold the elaborations that the human brain provides [ 18 ]. There would be no better place to start such an endeavor than the emotion of fear. Some psychological theories propose that fear is a biologically basic emotion of all humans and many other animals [ 3 ], a view in line with most lay opinions as well.
A variety of evidence supports a view also in line with common usage: The most common distinction is between fear and anxiety. Whereas fear is usually conceptualized as an adaptive but phasic transient state elicited through confrontation with a threatening stimulus, anxiety is a more tonic state related to prediction and preparedness-- the distinction is similar to the one between emotions versus moods. Some schemes have related fear and anxiety to dissociable neural structures for mediating their behavioral effects, for instance the central nucleus of the amygdala for fear , and the nearby bed nucleus of the striaterminalis for anxiety [ 19 ].
However, the dense interconnectivity of these two structures makes it difficult to uniquely assign either of them to participation in only one of these processes. A yet finer-grained classification makes distinctions between anxiety, fear, and panic, three varieties of fear that each are associated with particular packages of adaptive responses yet can all be mapped also onto a continuum of threat imminence respectively, from more distal to more proximal [ 20 ].
There is also evidence for multiple fear circuits in relation to the content of the threat. For instance, it has been argued that there are separate neural systems for fear of pain, predators, and aggressive conspecifics [ 21 ]. Each of these can be processed through a distinct sensory channel e. Some of these distinctions among putative fear-subsystems are also supported by distinct molecular markers. For example, the predator-related subsystem is marked by the expression of steroidogenic factor 1 across several species, and corticotropin releasing factor is expressed across a wide range of species and serves as a marker of the central amygdala in rodents see Box 1 in [ 21 ].
A recent comparison between humans and mice revealed that copy number variations at specific genetic loci can influence remarkably specific types of fear: Of course, partly different sets of individual neurons will no doubt be involved in processing different fear stimuli, or for that matter even the identical fear stimulus but on different occasions.
This no more shows that there are distinct fear systems than does the fact that different visual images evoke somewhat different patterns of neural response in visual parts of the brain: To demonstrate distinct fear systems, we would need to be able reliably to trace processing streams, and we would need to decide on the level of grain at which such processing streams are implemented in the brain. If we do find more than one such parallel processing stream for fear, then this could show that there are neurobiologically distinct types of fear that all share a common ecological theme they are about threat, but different types of threat.
But unless the number of such parallel systems gets very large, this would seem like progress in understanding the microstructure of fear, rather than an obstacle to using the term. A functional definition of fear motivates three recommendations that form recurring themes throughout this review. One is that an investigation, and ultimate functional and neurobiological understanding, of fear requires a comparative approach: A second, complementary, idea is that understanding fear requires careful ecological work by biologists observing particular species in their natural environment in order to describe its functional role.
This in turn suggests a need for close collaboration between psychologists and neuroscientists working in the lab, on the one hand, and biologists in the field, on the other. A third, more speculative, idea is that a fruitful purchase on understanding fear may be to investigate how it is experienced felt across species. A benefit of including animals with simpler brains in this range is that it forces us towards a concept of a fear state that is more abstract and functional, rather than one tied to any particular neurobiological implementation or type of conscious experience.
Another reason it is advantageous to investigate fear in nonhuman animals is of course that many experiments are simply much easier, or only feasible, carried out this way-- ranging from optogenetic manipulation of precisely defined cell populations, to mapping of gene loci that contribute to fearfulness. Inducing fear in the laboratory in ecologically valid ways also is much simpler in animals other than humans who typically know they are part of an experiment. The third recommendation opens the door for a particularly exciting set of future studies.
It not only investigates what the layperson might consider the most important and salient aspect of fear how it feels , but also may provide a clever experimental approach for how to classify the multi-dimensional behavioral and cognitive accompaniments of fear. The basic idea is that the brains of higher mammals and perhaps other animals already do a lot of the work for us: In humans, their joint representation provides an important part of the information on the basis of which people can verbally report that they feel afraid.
Of course, there are well-known difficulties with using verbal report as the sole source of data; the recommendation here is not to rely on verbal report per se, but to push it back one level to measurement of the neural representation on which verbal reports are in part based a measurement that is of course also available in nonverbal animals, once we know where to look. This third theme goes hand in hand with current developments in the neurobiology of consciousness, and it may bring back to the scientific study of emotions a topic that, ever since Behaviorism, has been excluded despite the fact that many modern neurobiological views on emotion now mention it [ 12 , 13 , 15 , 24 , 25 ].
Many cortical regions together with midbrain and brainstem nuclei participate in fear responses, but how they all interact still remains relatively unclear see [ 12 , 26 , 27 ] and Figure 5 for some partial schemes. I do not attempt any kind of comprehensive review of the neurobiological literature here, but outline some of the best studied circuits.
It is important to reiterate that the neurobiology of fear is still in its infancy; there are many structures that likely play key roles, but about which we know very little. For instance, subdivisions of the habenula likely contribute to signaling fear-related information to brainstem nuclei, and provide signals about punishment or absence of reward to reward-learning systems [ 28 ]; parts of this pathway are highly conserved across vertebrates [ 29 ].
Stress and anxiety have also been reported to activate the lateral septum [ 30 ], although the precise and causal role of this structure remains rather unclear. None of these structures is commonly encountered in neurobiological studies of fear in humans. The schematic outlines some of the processing that contributes to fear, including sensory inputs, central structures, and effectors. From [ 31 ]. Of course, the functional role of the participating brain structures depends on specific neurotransmitters and their receptors. This level of explanation has been informed by the actions of specific drugs, such as the anxiolytic effects of benzodiazepines.
Of some interest have been drugs acting on serotonin reuptake transporters, a very widely prescribed class of agents for treating mood and anxiety disorders such as the drug Prozac. There is some support for a classic theory of the differential actions of serotonin in facilitating anxiety but inhibiting panic [ 31 ]. Similar attention has also been devoted to another neuromodulator controlled by specific brainstem neurons: A distinguishing feature of both the serotonergic and noradrenergic systems is that a relatively discrete population of neurons in the dorsal raphe, and the locus ceruleus, respectively innervates a wide swath of distal targets, making possible precisely the kind of global and coordinated effects on information processing that an emotional state like fear requires.
At the cortical end, the most prominent of these is the orbital and medial prefrontal cortex, including cingulate cortex. At the other end are the hypothalamus, periaqueductal gray PAG , and many brainstem nuclei as well as the intermediolateral cell column of the spinal cord and peripheral components of the autonomic nervous system. It is tempting to view the function of this assembly of structures in terms of the lower levels implementing emotional responses, and the cortical levels exerting modulatory control and regulation see below. While such a view is not entirely inaccurate, it fails to capture the complexity of how these different structures implement fear -- in good part due to massive reciprocal interactions between all the components.
For instance, the amygdala projects to the PAG and conversely. The amygdala is also reciprocally connected with prefrontal cortex, and concurrent recordings in both structures clearly show that there is no simple serial processing but a much more complex iterative flow of information [ 32 ]. Two other sets of structures that need to be incorporated into the scheme are parts of the basal ganglia involved in reward processing and instrumental behavior, and the insula, involved in interoception. A Some of the main amygdala nuclei and their inputs and outputs, emphasizing the complex internal architecture of this structure.
B Amygdala connectivity with other brain structures, emphasizing its participation in multiple networks that process fear, and its central location in mediating between parts of the prefrontal cortex and nuclei in the hypothalamus and brainstem. Modified from [ 69 ] and [ ]. The basolateral amygdala receives most of the sensory inputs that specify fear associations with the exception of olfactory input, which comes into the medial nucleus and selective optogenetic activation of neurons within this nucleus is sufficient to associate the incoming sensory information with unconditioned fear responses [ 33 ] Figure 2.
The central nucleus of the amygdala is widely considered the main output regulator for mediating fear responses, and these are in turn mediated by distinct subdivisions of the central nucleus. Whereas some of these neurons can inhibit cholinergic targets mediating cortical arousal in the substantiainnominata, diagonal band of Broca, nucleus basalis , they can at the same time promote freezing through projections to the periaqueductal gray [ 34 ]. The flexible modulation of different downstream fear components by the central amygdala depends on an intricate inhibitory control balance internal to the amygdala [ 35 , 36 ].
Studies of the amygdala in humans have implicated this structure in the recognition [ 37 ], expression [ 38 ], and experience [ 39 ] of fear. The enormous range of stimulus properties that have been reported to activate the amygdala has given way to views that try to provide a more unified picture. Such accounts typically acknowledge that the amygdala plays an important role in fear, but stop short of endorsing the claim that this is a basic function.
Instead, they propose that it is merely one example of a broader and more abstract function, such as processing arousal, value, preference, relevance, impact, vigilance, surprise, unsigned prediction error, associability, ambiguity or unpredictability. The extent to which any of these functions are domain-specific notably, in regard to processing social stimuli remains an open question [ 46 ]. Somewhat relatedly, there has been a shift towards more network-based views of fear processing, in which structures such as the amygdala are nodes in an anatomically much more extended collection of structures [ 52 ].
This shift emphasizes the fact that the initial question was simply ill-posed: This also points us towards a different view on the search for neuroimaging activation patterns specific to certain emotions: As important as moving from the amygdala outwards to include it in larger networks is moving inwards to consider its internal components. Earlier work in rodents began to show that different amygdala nuclei are involved in different types of fear-related behaviors, such as innate responses to conditioned stimuli or actions to avoid them e.
However, whereas the earlier studies investigated these issues using bulk lesions of tissue and generated some conflicting findings , it is now clear that the level of resolution required is at the level of specific neuronal subpopulations, often intermingled even within a single nucleus. Such subpopulations are distinguishable by a number of criteria, including the set of genes they express, their morphology, and most importantly their connectivity and electrophysiological properties whereby they subserve particular functions in processing fear.
Current investigations of this issue use optogenetics to address this issue. In this technique, light-activated ion channels are expressed in specific neuronal subpopulations through their coupling to a promotor specific to that subtype alternatively, one can also engineer ion channels gated by exogenous drugs that can then be administered experimentally. This is achieved best in transgenic mice, although it also possible to do it through focal injection of viruses, opening the door to such manipulations in monkeys as well. Optogenetic studies have demonstrated a tightly regulated network of inhibitory interneurons within the central nucleus that controls how sensory input coming into the basolateral amygdala can influence outputs to structures such as the hypothalamus and periaqueductal gray e.
This level of grain is impossible to investigate in humans so far, and poses a major challenge for how to interpret results from functional neuroimaging studies, which pool changes in blood-oxygenation-related activation over voxels several millimeters in size typically, 15—20 cubic millimeters over a timecourse of a few seconds.
Sorely needed are systematic comparative studies that focus on specific structures and networks, and that map out the similarities and differences in functional components. For instance, the role of the amygdala in associative learning of fear appears to be ubiquitous across species; the set of unconditioned stimuli that it processes vary to some extent; and its role in the conscious experience of fear has been investigated only in humans [ 39 ]. Fear is commonly thought to have adaptive functions in terms of both cognition and behavioral response.
Indeed, this flexibility is part of what distinguishes emotions: One feature that highlights this are the highly diverse yet integrated sets of psychophysiological, cognitive and behavioral changes that all serve as indices of a central state of fear Figure 3. Fear can be caused by a wide range of stimuli, from basic unconditioned stimuli to complex symbolic knowledge; and it can in turn trigger core biological responses as well as be modulated volitionally, at least in humans.
Very roughly, the components at the upper left are shared across a wider range of species, whereas the components at the bottom right may be unique to humans. B Schematic of some of the effects of a central state of fear on cognition and processing mode.
Fear interfaces with nearly all other aspects of cognition. Yet one of the most prominent behavioral aspects of fear in humans remains of debated functional significance: There is a vast literature regarding emotional facial expressions probably the single most commonly used class of stimulus in human studies of emotion , with strong claims regarding their cultural universality or relativity, their biological primacy or social construction.
But Darwin himself pointed out that emotional expressions could very well have evolved without having adaptive functions: This claim is only partly true, however: And even these aspects of fear behavior are certainly adaptive. Their main functions have simply changed, and now they play a primary role in social communication rather than direct protection and defense [ 62 — 64 ]. There also are still residual adaptive functions of many of these expressive behaviors, which give us some insight into how they likely evolved.
For instance, the wide eyes and flared nostrils typically associated with facial expressions of fear not only communicate fear to other viewers, but in fact alter sensory perception by increasing the eccentricity in the visual field of stimuli that can be detected, and increasing airflow through the nose so as to better detect olfactory cues [ 65 ]. A key current challenge is to assemble our knowledge at the level of individual structures, nuclei, and neuronal populations, to knowledge at the level of distributed large-scale networks a challenge that pervades all of emotional and social neuroscience [ 66 ].
An emerging theme from such network concepts is that there are structures more concerned with directly orchestrating fear-related responses e. Of particular interest for the latter have been prefrontal cortices, which some schemes have partitioned into orbital and medial networks, subserving processing of emotionally salient sensory stimuli and orchestrating of visceral emotional responses, respectively [ 67 ]; and into ventromedial and dorsolateral networks related to reward processing and cognitive control [ 68 ]. Moreover, such networks can be related to specific neurotransmitters and levels of action for pharmacological intervention [ 69 ].
The amygdala plays a key role in mediating between brainstem and cortical levels, with specific nuclei participating in distinct networks that may be similar across species [ 61 ]. Dissecting these networks and understanding their pharmacology, constitutes one of the main research components towards treating phobias and anxiety disorders [ 70 ]. The context-dependency of fear is seen in terms of the eliciting circumstances e. All of these have been described in some detail by ethologists working on fear in nonhuman animals [ 71 , 72 ], and emphasize the temporally extended and dynamic nature of a fear state that we noted earlier.
There are many examples that networks within the medial prefrontal cortex play a key role in the modulation of fear-related processing, by projecting to targets such as the amygdala, hypothalamus, and brainstem. For instance, prefrontal regions are implicated in the extinction of conditioned fear responses, and lesions to ventromedial sectors of the prefrontal cortex in humans may actually exert a protective role in the acquisition of disorders such as post-traumatic stress disorder [ 73 ].
Physical distance proximity is one of the most basic stimulus cues to trigger fear. A Different adaptive types of fear behaviors can be elicited as a function of distance, ranging from freezing to fleeing to defensive attack. Adapted from [ 74 ], see also [ 20 ] for a similar scheme. B Lesions of the human amygdala reduce interpersonal distance and the sense of invasion of personal space.
At the top are schematized the mean interpersonal distances from an experimenter for healthy controls left and a patient with bilateral amygdala lesions patient SM, right. At the bottom is a plot of the data showing mean distance that people felt comfortable standing from the experimenter at the origin , patient SM is the red bar and the rest are healthy controls. From [ 91 ]. C Approach or retreat of a threatening stimulus a tarantula in a human fMRI study showed differential activation of the amygdala and bed nucleus of the striaterminalis.
Participants lay inside the fMRI scanner while their foot was placed in compartments at varying distances from the tarantula, a procedure they observed through video left panel. Subtraction of approach minus retreat for the same distance, middle panel resulted in the activation shown on the right panel. From [ 96 ]. Another example implicating the prefrontal cortex comes from studies of threat imminence: These distinctions are mirrored in the neural structures that have been emphasized: This behavior depends in part on serotonergic modulation via the dorsal raphe nucleus, but also requires input to the dorsal raphe from the ventromedial prefrontal cortex to signal that a stressor is uncontrollable [ 76 ].
There are many behavioral fear responses that can be used by conspecific observers to infer fear, and several of them have been quantified as behavioral markers of fear by human investigators cf. Table 2 for a partial list. These include such laboratory measures as freezing immobility , increased startle, and increased heart rate. More species-specific are alarm calls signaling danger, which are observed in species from monkeys [ 77 ] to rats [ 78 ] to birds [ 79 ]. Humans are relatively unique in their repertoire of emotional facial expressions although chimpanzees, but not monkeys, can make such expressions as well, even though we generally do not know what they mean.
In addition to behavioral responses and autonomic changes, there are effects of fear on nearly all aspects of cognition, ranging from attention to memory to judgment and decision-making Figure 3b. Systematic effects of putative fear states on choice behavior have been claimed even in bees [ 81 ]. The table is only a partial listing of the many behavioral measures that can be used to index fear and anxiety. Whereas the rodent tests are all behavioral, probes in humans encompass a smaller set of psychophysiological measures and a large set of self-report questionnaires see [ 39 ] for details on these.
Similarly, we can think of several broad classes of prototypical fear-inducing stimuli [ 82 ]. There are those stimuli whose detection parameters have been set by evolution, for instance visual presentation of snakes or spiders in humans [ 83 ], or the odor of a fox for a ground squirrel. The bed nucleus of the striaterminalis has been implicated in unconditioned fear responses freezing behavior to a specific odor component of fox feces, trimethylthiazoline [ 84 ].
Then there are those stimuli that an organism has learned are dangerous through experience or, in some species, social observation , as well as those stimuli that are not themselves dangerous but have been associated with the above two classes of stimuli and can thus serve as conditioned warning cues. However, most stimuli of which humans are afraid are probably learned socially [ 85 ], a mechanism also ubiquitous in other animals [ 86 ].
Learning about a harmful stimulus from another animal involves the amygdala, in both rats [ 87 ] and humans [ 88 ]. An interesting aspect of fear-associated behaviors are those actions taken not proactively but in order to terminate the state of fear itself: Cues associated with the cessation of fear can reinforce certain behaviors [ 89 ], suggesting a broader perspective in how fear behaviors unfold in time. Rather than thinking of a fear state as a static functional state, or as a fixed sequence triggered by a fear-inducing stimulus, we should conceive of it as a dynamic process.
While this makes things more complicated, it also imposes bounds, since specific structures come into play at certain points in time. One of the most prototypical of threat stimuli is an approaching predator Figure 4. This is a good example for the functionally specific organization of fear behaviors: These range from freezing to avoid being detected to vocalization to warn others or recruit help , to defensive attack. Such behaviors also show substantial differences between individuals and species: A related stimulus attribute is intensity.
Sudden-onset, or high intensity physical properties of stimuli in many cases elicit fear. To some extent, this can simply reflect the graded quality of fear cues, and of course intensity is often correlated with distance. Shrinking interpersonal distance and increasing sound intensity are two examples; in these cases both are known to activate the amygdala [ 91 , 92 ].
It has been known for some time that the different packages of fear behaviors that can be engaged at different distances or intensities e. Columnar arrangements of neurons within the periaqueductal gray play an important role in these different components of fear responses, with more dorsal regions controlling active escape behaviors, and more ventral regions controlling inhibition e.
However, as we noted earlier, there are substantial ascending projections from the PAG as well, making the functional role of this brain region considerably more complex than a mere orchestration of emotion-related output. Switches from passive to active fear responses freezing to fleeing are tightly dependent on distance from a predator [ 20 , 27 ], since different behaviors would be adaptive at different distances e.
Neural correlates of such shifts have been observed in relation to several structures in addition to the PAG. The central nucleus of the amygdala can orchestrate switches between forebrain arousal and freezing in mice [ 34 ], and shifts from activation in the prefrontal cortex distal threat to PAG proximal threat have even been observed in human neuroimaging studies [ 95 ]. A related finding showed that activation in the bed nucleus of the striaterminalis correlated not with the sheer physical distance of threat in that study, a tarantula , but with whether it was approaching or receding [ 96 ] Figure 4.
Flexibility and learning in the elicitation of fear depends on plasticity and inhibitory control within the amygdala [ 35 ] as well as both ascending e. Exactly how an organism integrates sensory information together with its own coping ability in order to make the choice to switch from freezing to fleeing is a very rich question in the ecology of decision-making that deserves more study across species. A major contextual factor in the evaluation of fear-inducing stimuli is whether or not escape might be possible, or whether the threat seems inescapable, a distinction related to the modulatory factor of control that we noted earlier.
The former is typically associated with flight, whereas the latter is typically associated with freezing and defense Figure 4a. This dimension can require substantial evaluation and amounts to ongoing monitoring and decision-making. The availability or unavailability of a place for concealment or escape has also been found to modulate the scenario-elicited fear behaviors of humans, in general quite in line with what would be predicted based on observations in rodents [ 2 ] cf.
Another quite broad stimulus attribute that elicits fear is unpredictability. This can be a computationally more complex cue to detect, since it depends on comparisons of stimuli, or patterns of stimuli, over time. Several commonly used laboratory assays for fear, such as open-field tests, neophobia, and measures of latency to emerge from a secure nest, likely tap this category as well cf. Table 2 ; the fear-related behaviors elicited are the complement of exploration.
These fear-inducing attributes are found from mammals through zebrafish [ 98 ]. There are various types of unpredictability: One can identify at least two ways in which the occurrence of a stimulus is uncertain: An important category of fear-inducing stimuli are social. Animals can show strong fear behaviors in response to aggressive or dominant conspecifics. One common model of mood disorders in rodents is social defeat, a set of long-lasting submission-related behaviors induced by the inability to defend cage territory against the intrusion of an aggressive and dominant male.
This social stimulus reliably elicits neuronal, endocrine, and immune changes indicative of anxiety, although longer-term effects are more akin to phenomena such as learned helplessness and depression [ ]. Similar types of responses are found in other species ranging from zebrafish to humans. In humans, social aspects of fear can be elicited by cues such as untrustworthy faces or invasion of personal space, all stimuli that reliably involve the amygdala [ 91 , , ].
Despite the high inter-individual variability in fear responses, there are consistent patterns across time within an individual. That is, many aspects of fear and anxiety can usefully be characterized as traits, in humans as well as other animals [ 82 , ]. As with moods in general, there is substantial heritability for trait anxiety, and for anxiety disorders, although it seems clear that most of the genetic variance is accounted for by complex polygenic interactions with environmental stressors, rather than by any single gene [ ].
The decoupling between an immediate stimulus trigger and a fear state also makes trait anxiety prone to dysregulation: There are clinical distinctions between dysfunctions of fear processing that have some evidence for involvement of specific brain structures and neurotransmitter systems, making them candidates for functional subtypes of fear that will be reflected in the brain. Generalized anxiety disorder features chronic worry about a range of events, typically focused on the future.
Panic disorder, on the other hand, results from a severe and acute fear response-- often in the absence of an ability to cope, such as the sensation of suffocation that can be experimentally induced by inhaling carbon dioxide other experimental inducers of panic are intravenous administration of lactate or cholecystokinin.
Phobias are characterized both by predictive anxiety as well as acute flight responses, often to specific classes of stimuli e. Ever since Freud, anxiety disorders have been viewed as resulting from pathological suppression, repression or avoidance of fear-eliciting situations, thoughts, and stimuli [ ]. The reasonable hypothesis based on such views is that treatment should emphasize exposure to fear-inducing stimuli, and access to fear-related thoughts and memories [ , ], essentially updating emotional information [ ]. The psychological concepts related to anxiety and its treatment have been mapped onto behavioral processes such as adaptation and extinction, and onto their neural correlates [ ], a thriving corpus of research in modern neuroscience.
There are alternative possibilities for how pathology might emerge from fear, not mutually exclusive with the above: Phobias would be an example. One plausible point in processing for such exaggeration to exert its effect would be at the earliest stage a component that itself may involve learning: Thus, increased expectation of, and rumination about fear, can be associated with increased vigilance and attention to potentially dangerous stimuli [ , ].
The consequence is a generally heightened state of arousal, accompanied by many fear-like responses that can be thought of as false positives from a signal detection perspective. The threshold for detecting fear has simply been set too low and too many stimuli that have a very low probability of being dangerous are misinterpreted as dangerous [ ]. One might wonder why pathological anxiety should be so prevalent at all. Is it so hard to set the right threshold? The solution is to realize the asymmetry between false negatives which can result in death and false positives which, in isolation, often have few consequences.
It is only when false positives cumulatively begin to impair daily functioning, or when their number increases as environmental circumstances change, that pathology becomes evident. An example illustrates the point [ ]: You are a hunter-gatherer at a watering hole and hear a noise, which could be a lion. Suppose the cost of fleeing in panic is calories, and the cost of engaging a lion is , calories. There is yet another view regarding pathological states of fear: All these features could render such a module not only difficult to override, but also responsive to stimuli in a way that would have been adaptive in our ancestral environment but may no longer be so.
Another distinguishing feature of such fear modules typically is the proposal that they can operate, to some extent, outside conscious awareness of the eliciting stimuli cf. Animals can also show fear in response to subtle cues picked up from the fear induced in another conspecific; these can be innate e. Somewhat the flip side of increasing sound intensity that we noted above, sudden cessation of background sounds can be a social signal of fear in rodents as well [ ].
In zebrafish, injured fish release a chemical that functions as an alarm signal: Social communication of fear is even seen in crickets in response to spiders [ ]. Another good example from invertebrates is the emission of carbon dioxide by Drosophila when flies encounter an innate fear-evoking stimulus such as electric shock. This odor can evoke avoidance behaviors in other flies, thus serving as a social signal, and is processed by a highly specific neural circuit [ ].
A class of social stimuli that commonly induces anxiety and is likely unique to humans is public evaluation, such as when one is forced to give a public speech; this potent scenario is in fact used experimentally to induce anxiety e. One intriguing class of stimuli that can trigger states of panic are interoceptive signals. In particular, signals related to suffocation and panting are known to be represented in the periaqueductal gray [ ] and the amygdala. There is a specific pH-sensitive ion channel expressed on neurons within the amygdala that may directly sense acidosis due to rising carbon dioxide levels [ ].
Other examples would include strong interoceptive signals of major homeostatic imbalance, or organ failure e. It remains relatively unclear to what extent direct interoceptive signals about such events can be used to trigger fear, and to what extent fear is instead triggered more derivatively by secondary consequences and background knowledge at least in humans.
Finally, it is worth emphasizing that humans stand out from other animals in having fear and anxiety triggered not by occurrent stimuli, but merely by thinking about such stimuli. The bulk of psychopathology arises from worrying about what could happen and what might be, often to the point of distorting what actually is. This aspect of fear induction in humans probably also contributes to the impression we have that fear depends very much on conscious experience. Clearly, different instances of fear and anxiety do all feel similar, and we categorize and verbally describe them as similar.
This fact must be reflected both in psychology and neurobiology. At the psychological level, two sets of theories have attempted to incorporate the diversity of stimuli, situations, and behaviors related to fear, on the one hand, with their apparent psychological and subjective unity, on the other. The first such theory is appraisal theory, a theory about the adaptive functional role which fear is thought to accomplish. Older theories that had lists of functional evaluations [ 97 ] have been advanced with more recent accounts that relate specific stimulus evaluation checks to specific points in a processing sequence [ ].
The second psychological theory is the conceptual act theory [ 6 , 14 , ]. According to this constructivist framework, our experience of fear, and certainly our reports of having fear and any other emotion , are a highly cognitive synthesis. Emotion categories such as fear are then seen as highly constructed, rather than as biological primitives cf. A major challenge for future work will be to elucidate the neural substrates of these psychological components, and to probe whether anything similar can be found perhaps in nonhuman primates or whether this aspect of fear is unique to humans.
While this review advocates a broadly comparative and functional approach to fear, there is no reason to exclude the conscious experience of fear. Instead, it seems timely to incorporate modern theories of consciousness into the study of emotion, including the study of fear in nonhuman and hence nonverbal animals [ 12 , ]. There are several advantages to doing so. First and foremost, it would seem compelling to try to incorporate what laypeople find the most salient component of a state of fear.
We already know that healthy humans feel fear, that such feelings are the main basis for complaint in psychiatric anxiety disorders, and that they are abolished by lesions of the amygdala [ 39 ]. It is a perfectly respectable scientific question now to ask whether monkeys, rats, reptiles or flies have feelings of fear, although it requires some dissection of components of feeling fear Box 2.
Of course, we could not approach this question in the same way that we typically do in humans by using language and asking. Instead, we would need to use other measures that all require some neurobiological theory of consciousness. But something like this has already been done for other types of conscious content: This allowed the authors of that study to infer that the patients were conscious, in the absence of any behavioral measure. Extending such an approach to nonhuman species requires a broader theory of consciousness, but the basic idea is no different in principle.
There are in fact several modern theories of consciousness that are functionally congenial to understanding the conscious experience of fear, and that offer testable neurobiological hypotheses. There is a large literature investigating the role of consciousness in fear, but it is heterogeneous in regard to the content of that conscious experience.
Some studies have shown that stimuli that communicate or trigger fear can do so even when perception of those stimuli is subliminal, at least to some degree, a mechanism that appears to involve the amygdala good evidence; [ , ]. Others have claimed that such nonconscious fear processing depends on a particular subcortical route of input to the amygdala that typically bypasses cortex debated; [ 75 , , ].
More controversial is the possibility of unawareness of the feeling of fear itself, rather than just of the eliciting stimuli. However, non-conscious emotions have been proposed as a possibility based on some psychological experiments [ ]. Regardless of the empirical status of these dissociations, they highlight the different components of an experience of fear: When people report that they feel afraid, they could be reporting on their awareness of any number of these components.
Three such theories are focused, respectively, on the information-conveying nature of conscious experiences [ , ] integrated information theory , on their ubiquitous functional consequences [ ] global workspace theory , and on their subjectivity [ 23 , 24 , ] theories of subjectivity and the self. The reader is referred to the original references for further description of these theories, but each of them makes neurobiological predictions. Briefly, these theories could relate to our investigation of fear as follows. The integrated information theory proposes that a specific conscious experience conveys a very high amount of information, since it is distinct from so many other experiences and yet typically integrates very many component attributes [ , ].
Thus, all the different shades of feeling fear should correspond to informationally distinct, yet richly integrated, brain states at the neuronal level. This would put an upper bound on the number of distinct fear experiences or emotion experiences more generally that any organism could experience, deriving from the complexity of the neural systems instantiating fear. Presumably, the addition of further cortical territory into the representation of fear in humans allows for much more nuanced and elaborate experiences of fear [ 14 ].
There are some efforts underway to estimate integrated information in the brain a very difficult problem from measures such as EEG. With respect to the second popular theory, global workspace theory, a conscious state of fear has access to a vast number of other cognitive and behavioral processes [ ], with the result that fear modulates attention, memory, perception, and decision-making. The theory often appeals to nuclei in the thalamus that have the requisite wide connectivity, but the connectivity of the amygdala could also support such a network in the case of fear [ 48 , ], and may explain why focal lesions to this structure can abolish the ability to feel fear, at least in humans [ 39 ].
The subjectivity of feeling afraid requires not only a subject to experience the fear, but also to a good extent specifies why fear feels the way that it does, at the same time providing the organism with information about its homeostatic state, its state of preparedness to cope with an environmental challenge, and motivating it to engage in instrumental behavior.
These components have been hypothesized to depend on regions of the brain that map interoceptive information, such as the insula and anterior cingulate cortex [ 23 , 25 ]. This view also makes the strong prediction that species without interoception cannot feel fear -- a conjecture that remains entirely unexplored.
One intriguing possibility is that a readout of the neuronal representation of fear in interoceptive structures such as the insula might in principle provide neuroscientists with the same information that it provides to the subject feeling fear. This could allow a direct link between psychological theories of emotion that place a premium on our experience of them, on the one hand, and neurobiological substrate, on the other.
There is no single brain structure for processing fear, and even a small set of necessary and sufficient structures has not emerged. One likely reason that it has been difficult to find clear evidence of a dedicated fear circuit from fMRI studies in humans [ 10 ] is that it is now apparent that rather different emotional behaviors, ranging from defense to aggression to mating, are controlled by specific populations of neurons that are spatially within the same structure and hence unresolvable using fMRI e.
Much the same is true of value encoding in general: Another reason is that fear evoked by different classes of stimuli unpredictability, social, predators, etc. There is better evidence, and more reason to believe a priori , that extended systems comprised of a network of structures could be identified.
Some fMRI studies have suggested this, and several models have been proposed [ 12 , 27 ]. Ultimately, we may need to redraw the boundaries of the component structures, however: How is it that I can tell my cat is afraid? Of course, there are also differences between species, differences between individuals, and things are vastly more complex in humans than in a mouse. But comparative as well as developmental observations suggest that a fruitful starting point is to begin with a primitive concept of fear that is shared across mammals or even more broadly than that , and then investigate the variations on this theme.
The neurobiological evidence is then one additional piece of evidence, supplementing the behavioral and situational clues, and allowing us to begin constructing causal links between these. In humans, there is of course another component of fear: A complete program for the scientific study of fear will need to go hand-in-hand with the development of neurobiological and functional theories of conscious experience. The questions are extremely challenging to answer, but they are questions that make sense and are interesting to try to answer.
At what level of phylogeny does the feeling of fear become incorporated into its neural representation? What components of fear constitute the contents of its conscious experience? Do we have any control over which components of fear we can become aware of?