brain circuitry

Spot a Sociopath

10 signs for spotting a sociopath

#1) Sociopaths are charming. Sociopaths have high charisma and tend to attract a following just because people want to be around them. They have a “glow” about them that attracts people who typically seek guidance or direction. They often appear to be sexy or have a strong sexual attraction. Not all sexy people are sociopaths, obviously, but watch out for over-the-top sexual appetites and weird fetishes.

#2) Sociopaths are more spontaneous and intense than other people. They tend to do bizarre, sometimes erratic things that most regular people wouldn’t do. They are unbound by normal social contracts. Their behavior often seems irrational or extremely risky.

#3) Sociopaths are incapable of feeling shame, guilt or remorse. Their brains simply lack the circuitry to process such emotions. This allows them to betray people, threaten people or harm people without giving it a second thought. They pursue any action that serves their own self interest even if it seriously harms others. This is why you will find many very “successful” sociopaths in high levels of government, in any nation.

#4) Sociopaths invent outrageous lies about their experiences. They wildly exaggerate things to the point of absurdity, but when they describe it to you in a storytelling format, for some reason it sounds believable at the time.

#5) Sociopaths seek to dominate others and “win” at all costs. They hate to lose any argument or fight and will viciously defend their web of lies, even to the point of logical absurdity.

#6) Sociopaths tend to be highly intelligent, but they use their brainpower to deceive others rather than empower them. Their high IQs often makes them dangerous. This is why many of the best-known serial killers who successfully evaded law enforcement were sociopaths.

#7) Sociopaths are incapable of love and are entirely self-serving. They may feign love or compassion in order to get what they want, but they don’t actually FEEL love in the way that you or I do.

#8) Sociopaths speak poetically. They are master wordsmiths, able to deliver a running “stream of consciousness” monologue that is both intriguing and hypnotic. They are expert storytellers and even poets. 

#9) Sociopaths never apologize. They are never wrong. They never feel guilt. They can never apologize. Even if shown proof that they were wrong, they will refuse to apologize and instead go on the attack.

#10) Sociopaths are delusional and literally believe that what they say becomes truth merely because they say it! Charles Manson, the sociopathic murderer, is famous for saying, “I’ve never killed anyone! I don’t need to kill anyone! I THINK it! I have it HERE! (Pointing to his temple.) I don’t need to live in this physical realm…”

I have OCD. 

It doesn’t rule my life, but it used to. Knowing that I have the capacity for that kind of thought is exactly why it doesn’t rule my life like it used to. I’m perfectly aware that I’m going to have that capacity forever, as studies have shown that Obsessive Compulsive Disorder is genetic (if you have a parent with OCD, as I do, you have a fifty-fifty chance) and is caused by abnormal brain circuitry, which means you’re stuck with it. And I am okay with that. I’ll survive. Recently, readers have asked me a lot how I learned to control it, so this is my story.*

*with the obvious warning that I am not a therapist and you are not me and I am not you and this is just my story your mileage may vary.

I was an anxious child. OCD and anxiety play very well together, and back then, I didn’t really know what was happening. I was a twitchy creature of secret rituals.

The first thing that helped me was when I realized that my obsessions weren’t normal. Not everyone felt this way. And not all thoughts had to feel this way, either. 

The second thing that helped me was realizing that OCD didn’t really look the way it looked on television. Obsession could be about germs or cracks in the sidewalk, but really, it turns out that I can obsess about all kinds of things.

The third thing that helped me was figuring out that my compulsions weren’t always straightforward. Sometimes they were directly related to the obsession:

Tags in shirts —–> change clothing eleven times a day

tweets —–> refresh the screen every twelve seconds

Others, not so much:

Dying before making a mark —-> replacing all other activities like eating and sleeping with research, acquisition, and practicing of a new musical instrument

Datsuns —-> i don’t even know how i ended up with a datsun but i resent that entire chapter of my life

When my OCD was in control of me, it changed the way I looked at the world. Example. Here is life:

Life is always full of both bad and good things. Also trees. There will always be disasters and miracles happening in tandem. Mental illness changes the way you see it, though. For instance, a depressed person:


A content person:

The good or bad things don’t go away. You just point your gaze in a different direction. You are able to minimize some things and expand on others. When I got obsessive thoughts, they shifted my gaze onto something and held it there. It didn’t have to be something huge. It could have been about if my hair was dirty, or if I had said a prayer correctly, or if I had the precise same amount of air in each of my car’s tires.


In my head, the thought, whatever it was, became all encompassing. 

It didn’t matter what else I tried to do, my mind would return to it. It became everything, my whole world, looped again and again and again.

I don’t even know if those are what lady bugs look like. I guess that’s okay. It’s a metaphor. They are only what I imagine ladybugs to look like, and my obsessive thoughts are not real thoughts, either. They aren’t really me. They are something my brain does to process stress and uncertainty and decision-making.***

***this took me a long time to figure out. More in a bit.

My personal breakthrough came when I decided that I would give myself rules. I was a champion with rules. I was a champion with rituals. I was a champion with things that involved numbers and counting and generally being compulsive. So my rule was that if I caught myself thinking about something obsessively, the timer began.

I would tell myself I could obsess for a certain number of minutes, and then I had to do something else until a designated time when I was allowed to obsess over it again. I could obsess for ten minutes. Then I had to put it down completely for thirty minutes. Then I could have another ten minutes. Then I had to put it down for two hours. Then I could have another ten minutes. I wasn’t allowed to act on any of the thoughts, either. 

I told myself a rule was a rule. I couldn’t cheat on the time. And when I put it down, I had to really mean that I was putting it down. Did I want to be free or not? 

And it began to work. I began to be able to reward myself with less and less obsessing time.

And then the really amazing thing happened, the thing that changed my life. Once I had spent enough time disciplining my obsessive thoughts, I realized … they weren’t really my thoughts. They were markedly different in character from my ordinary thoughts. The further I got from them, the more I realized that they were mental illness, not me, and moreover, that I could be free of them if I wanted to be. All I had to do was identify a thought as obsessive when it first appeared:

And then give it the time it deserved:

And I got better and better at it. I still sometimes have to give myself three minutes, especially when under stress. I still have to sometimes remove myself from a physical location to give myself those three minutes. And sometimes I still end up with a Datsun. But mostly, I just live my life, and it’s invisible.

So much of it is knowing that it’s the place your brain goes to under stress. Knowing that you can be out from under it. Knowing that ladybugs don’t really look like that. I just googled them and it turns out they have an entire additional segment in front of that black bit where the head goes which means I just drew an entire flock of headless ladybugs. 

Well, all the better reason to avoid them.

Humans are not isolated entities. You are cells in a universal whole—intelligence cells, now dormant, but with mind/brain circuitry designed to reflect the thoughts of the creative spirit at the source of your life. As you release the fictitious beliefs that stand in your way, memory of these things will return. You will recognize eternity’s thoughts as your own, and activate historically latent features of human design. You will see that creature and environment are inseparable, and that environment does not stop with an ecosystem but extends to include your star-system, and every galaxy resting in the universal sea.
—  Ken Carey

THE POWER OF TECH NOSTALGIA

why blackberry is still betting on the keyboard

Some memories are written more strongly into the brain’s circuitry, like memories tied to emotions and memories for things that we hold every day for years — including gadgets. 

In the tech world, only a handful of companies have been around long enough to gin up nostalgic responses to their aged products. And that nostalgia can spur fans of these products to demand their return.

— Katie Boehret for The Verge

telegraph.co.uk
Men and women do not have different brains, claims neuroscientist

“Neuroscientist Prof Gina Rippon, of Aston University, Birmingham, says gender differences emerge only through environmental factors and are not innate… Any differences in brain circuitry only come about through the ‘drip, drip, drip’ of gender stereotyping.”

*gives middle finger to all of my neurosexist Psychology professors*

This is your brain on fried eggs

High-fat feeding can cause impairments in the functioning of the mesolimbic dopamine system, says Stephanie Fulton of the University of Montreal and the CHUM Research Centre (CRCHUM.) This system is a critical brain pathway controlling motivation. Fulton’s findings, published in Neuropsychopharmacology, may have great health implications.

“Our research shows that independent of weight gain and obesity, high-fat feeding can cause impairments in the functioning of the brain circuitry profoundly implicated in mood disorders, drug addiction, and overeating – several states and pathologies that impinge on motivation and hedonia,” Fulton explained. Hedonia relates to a mental state of wellbeing. “Another key finding is that the effects of prolonged high-fat feeding to dampen the sensitivity of this brain reward system are specific to saturated fats – palm oil used in this study – but not monounsaturated fat such as the olive oil used in this study.”

The research team obtained these findings by working with three groups of rats. The first group of rats was the control group: they were given a low-fat diet containing roughly equal amounts of monounsaturated and saturated fatty acids. The second group was given a monounsaturated high fat diet, of which 50% of the calories were from fat derived from olive oil. The third group was given a saturated high fat diet – again, 50% of the calories were from fat, but this time derived from palm oil. The high-fat diets were all the same in terms of sugars, proteins, fat content and caloric density, and the animals were free to eat as much or as little as they liked. After eight weeks, all of the rats still had comparable body weights and levels of insulin, leptin (which are major metabolic hormones) and relative glycemia.

At this time, the rats underwent a series of behavioural and biochemical tests known to be indicative of the functioning of rats’ dopamine system. “We established that the rats on the palm diet had a significantly blunted dopamine function,” said Cecile Hryhorczuk, the first author of the study. “Our research group and others hypothesize that this leads the brain to try to compensate by heightening reward-seeking behaviour, much like the phenomenon of drug tolerance where one has to increase the drug dose over time to get the same high. So, a person consuming too much saturated fat may then compensate a reduced reward experience by seeking out and consuming more high-fat and high-sugar foods to get the same level of pleasure or reward.”

Fulton’s study is the first of its kind to show that, regardless of weight changes, unrestrained intake of saturated fats can have negative effects on the controls of motivation by the brain. “As we were able to control for changes in body weight, hormones and glucose levels, we think that the fats may be affecting the dopamine system by a direct action in the brain,” Fulton said. “We in fact have separate evidence that brain inflammation could be involved in this process, as it is evoked by saturated high-fat feeding, which will be presented in a future publication.”

The other day, @taymonbeal​ was telling me that most of the trans people he knows were cis kids once; and then puberty happened and turned them trans.

To which my response was basically: Huuuuuuh???

(But, like, a thousand times more incredulous.)

I mean, I was most definitely Born This Way. I couldn’t have been more born-this-way if I had literally been born in a frilly pink dress. I wanted to be the mummy in the “mummies and daddies” game when I was 2; I told my mother I wanted to be a girl at 3; I started tucking my penis at 4; I hated my (gendered) school uniform at 5; I nearly tried cutting off my penis at 6; etc.

I can’t prove I was a girl at a year old because, unlike for the aforementioned things, my parents don’t remember me doing queer stuff at that age. However, I’d be willing to bet that for as long as my brain had gendered circuitry, it was female.

To be honest, I actually became way more cisgender during puberty. I mean, I’m still a girl, but now it’s way less intense and urgent. My dysphoria is more like “I would be a lot happier if I were considered female” instead of “NO BAD WRONG PLEASE HELP NOW”.

So to hear that, for some people, puberty knocked them the other way is really weird. I don’t think I can convey the sheer amount of wft I felt. Mind = Blown

So, now I’m wondering: What are my trans followers like? Were you born-this-way? Were you turned-this-way? If you turned, when?

Huntington’s Disease Protein Helps Wire the Young Brain

The protein that is mutated in Huntington’s disease is critical for wiring the brain in early life, according to a new Duke University study.

(Image caption: The protein associated with Huntington’s disease, Htt, is critical in early brain development. Brains of 5-week-old mice whose Htt was deleted show signs of cellular stress – reactive astrocytes (green) and microglia (white and red) and faulty connections – in brain circuits that have already been linked to the disease. Credit: Spencer McKinstry)

Huntington’s disease is a progressive neurodegenerative disorder that causes a wide variety of symptoms, such as uncontrolled movements, inability to focus or remember, depression and aggression. By the time these symptoms appear, usually in middle age, the disease has already ravaged the brain.

The new findings, published July 9 in the Journal of Neuroscience, add to growing evidence that Huntington’s and other neurodegenerative disorders, such as Alzheimer’s disease, may take root during development, said lead author Cagla Eroglu, an assistant professor of cell biology in the Duke University Medical School, and member of the Duke Institute for Brain Sciences.

“The study is exciting because it means that, if we understand what these developmental errors are, we may be able to interfere with the first stage of the disease, before it shows itself,” Eroglu said.

Several years ago, Eroglu and her team were looking for molecular players involved in the formation of new connections, or synapses, in early brain development in mice when their studies unexpectedly hit on the huntingtin (Htt) protein, which is present throughout the body and which forms clumps in the brain cells of people with Huntington’s disease.

“(Htt) had been implicated in certain cellular functions and synaptic dysfunction in Huntington’s, but the possibility that Htt is playing a direct role in synapse formation was not explored,” Eroglu said.

To understand the protein’s role as synapses form, the scientists created mice in which Htt is deleted only in the cortex, a part of the brain that is implicated in the disease and that controls perception, memory and thought.

At three weeks of age (roughly similar to the first two years of human life), a time when a mouse begins to take in its surroundings through its eyes and ears, the synapses of the mutant mice formed more rapidly compared with those of healthy mice, the scientists found.

 But by five weeks, when some synapses typically strengthen while others weaken in a normal process called pruning, the synapses had completely deteriorated in the mutant mice. In collaboration with another Duke researcher, Henry Yin, an assistant professor in psychology & neuroscience, the team also investigated the changes in synaptic function in these mutant mice and found severe alterations of the synaptic physiology.

Not only did the researchers see faulty circuits in the mice missing cortical Htt, they also saw signs of cellular stress in the brain, in the exact spot within the cortex that projects to the striatum, another brain area targeted by Huntington’s disease in people. “There’s something about that particular circuit that is vulnerable to changes in Htt,” Eroglu said.

The researchers also examined what happens in early brain development in a mouse model of Huntington’s disease. Similar to people with the disease, these animals have one normal copy of the Htt gene, and one mutated copy, which produces a protein that is present in cells but in expanded form.

The researchers found the same pattern: the Huntington’s disease model animals have synapses that initially mature much faster than normal in the cortex and then die off.

The new results also suggest that missing Htt for a prolonged period may not only affect the development but also the maintenance of healthy synapses, Eroglu said.

That’s especially relevant to a current strategy for treating Huntington’s disease: dialing down Htt levels in the brain using gene therapy or small-molecule inhibitors. But it has been a challenge to target the mutated copy of the gene, not the normal copy. Interested in the implications of lowering overall Htt levels, the group plans to delete Htt in the mouse brain later in life and measure the number of its synapses.

Other mouse models of the disease are also likely to have these faulty circuits. “We think this is probably a common thing, but that’s something we’re working on: whether we can detect early signs of faulty connections, correct it before the disease starts, and make these mice better,” Eroglu said.

Final piece found in puzzle of brain circuitry controlling fertility

In a landmark discovery, the final piece in the puzzle of understanding how the brain circuitry vital to normal fertility in humans and other mammals operates has been put together by researchers at New Zealand’s University of Otago.

Their new findings, which appear in the leading international journal Nature Communications, will be critical to enabling the design of novel therapies for infertile couples as well as new forms of contraception.

The research team, led by Otago neuroscientist Professor Allan Herbison, have discovered the key cellular location of signalling between a small protein known as kisspeptin* and its receptor, called Gpr54. Kisspeptin had earlier been found to be crucial for fertility in humans, and in a subsequent major breakthrough Professor Herbison showed that this molecule was also vital for ovulation to occur.

In the latest research, Professor Herbison and colleagues at Otago and Heidelberg University, Germany, provide conclusive evidence that the kisspeptin-Gpr54 signalling occurs in a small population of nerve cells in the brain called gonadotropin-releasing hormone (GnRH) neurons.

Using state-of-the-art techniques, the researchers studied mice that lacked Gpr54 receptors in only their GnRH neurons and found that these did not undergo puberty and were infertile. They then showed that infertile mice could be rescued back to completely normal fertility by inserting the Gpr54 gene into just the GnRH neurons.

Professor Herbison says the findings represent a substantial step forward in enabling new treatments for infertility and new classes of contraceptives to be developed.

“Infertility is a major issue affecting millions of people worldwide. It’s currently estimated that up to 20 per cent of New Zealand couples are infertile, and it is thought that up to one-third of all cases of infertility in women involve disorders in the area of brain circuitry we are studying.

"Our new understanding of the exact mechanism by which kisspeptin acts as a master controller of reproduction is an exciting breakthrough which opens up avenues for tackling what is often a very heart-breaking health issue. Through detailing this mechanism we now have a key chemical switch to which drugs can be precisely targeted,” Professor Herbison says.

As well as the findings’ benefits for advancing new therapies for infertility and approaches to controlling fertility, they suggest that targeting kisspeptin may be valuable in treating diseases such as prostate cancer that are influenced by sex steroid hormone levels in the blood, he says.

Professor Herbison noted that the research findings represent a long-standing collaborative effort with the laboratory of Professor Gunther Schutz at Heidelberg University, Germany.

Professor Herbison is Director of the University’s Centre for Neuroendocrinology, which is the world-leading research centre investigating how the brain controls fertility.

“We are delighted to have published this work in one of the top scientific journals and also to be able to maintain the leading role of New Zealand researchers in understanding fertility control,” he says.