For your brain, romantic rejection is the same thing as being physically hurt
When your sweetheart dumps you, there’s a reason why it hurts so much. It turns out your brain registers the psychological hell in exactly the same way it registers physical pain.
A group of scientists used fMRI scans to study the brains of people dealing with being rejected, and compared them to the brains of people experiencing physical pain. They found that the exact same regions of the brain are involved in processing both experiences. For humans, social rejection is tantamount to literal injury.
they saw the same regions of the brain lighting up during both physical and mental tasks - specifically, “areas that support the sensory components of physical pain (secondary somatosensory cortex; dorsal posterior insula).”
Read the full scientific paper via PNAS
by Annalee Newitz via raifontherocks
Another reason I’m paranoid about what I eat….
This guy just took a bunch of children with ADHD, and restricted their diet…
The study found that in 64 percent of children with ADHD, the symptoms were caused by food.
I wonder how many other mental conditions are food related?
Stanford’s Sapolsky On Depression in U.S. (Full Lecture) (via StanfordUniversity)
Loved this lecture and took notes :
Depression
symptoms:
Anhedonia
grief,guilt - can be so extreme it borders on delusion
self-injury; risk of suicide
—
psychomotor retardation->everything is exhausting. it’s exhausting to do + think stuff, can’t do laundry because where is the basket - can’t find change - have to get detergent - it’s too much, everything is too much, fall paralyzed state; you don’t worry about suicide in this state - because they are too exhausted
—
vegetative symptoms ->
sleep - depressives wake up early ; phases of sleep are completely disordered in depressives
appetite - is decreased, which is bizarre because for most of us carbohydrates decrease stress hormones and make you feel better, so you eat more
stress hormones elevated; adrenalin elevated
——
neurotransmitters:
norepinephrine- first class of antidepressants increased synaptic norepinephrine and depression lifted
; for a normal person, reserpine gets rid of norepinephrine and it causes depression (resperine is a drug that lowers blood pressure)
—
other neurotransmitters help with depression; simplistic version:
—-
dopamine has something to do with anhedonia
serotonin-has something to do with grief/guilt, OCD
norepinephrine - has something to do with psychomotor retardation
substance P - has something to do with pain and perception
—-
any one of these can compound; eg some people substance P is off and so it causes other depression symptoms.
—-
hormones
hypothyroidism-associated with depression; 20% of depressions are undiagnosed thyroid disorders
—
women; get depressed around their period, after birth, after menopause
—
glucocorticoids-half of depressed people have elevated hormone there; 4th or 5th stress induced depression can mess up hormones and cause you to get depression on their own without a psychological stressor
cushing’s disease - glucocorticoids are elevated and they are prone to depression and missing dopamine
—-
psychology of depression:
freud says you have mixed feelings about everyone….love/hate
when you lose a loved one. in most people focus on love and sense of loss
in freud’s view, melancholia wallow in ambivalence of lost person..lost loved one and opportunity to ever make things better with them; guilt over inability to do that
depression is “aggression turned inward”
—-
psychological stresses are much worse if…
need outlets for the stressor
no control
need shoulder to cry on
—-
eventually, you learn to be helpless with so called “learned helplessness”
—-
depression is 50% genetic; identical twins 50% risk of sharing depression
one gene that regulates glucorticoids hugely ups risk for depression
——
Interesting to find out about psychomotor retardation - wasn’t so familiar with that
PET scans showed increased dopamine release when subjects listened to pleasurable music (as opposed to “neutral” music). The fMRI results showed the researchers that the increased dopamine activity occured both during periods of anticipation of hearing the favorite bits of music and during the listening experience itself — although different parts of the brain were involved.
Brain reacts to music like a drug - chicagotribune.com
Pretty cool demonstration that you actually get a sort of high simply from listening to music.
men who sniffed drops of women’s emotional tears became less sexually aroused than when they sniffed a neutral saline solution that had been dribbled down women’s cheeks. While the studies were not large, the findings showed up in a variety of ways, including testosterone levels, skin responses, brain imaging and the men’s descriptions of their arousal.
Night owls vs. morning people: Who's smarter? - Yahoo! News
I’m a night owl.
Oxytocin – the love hormone – could cure shyness - Telegraph
Oxytocin … dubbed “the hormone of love” is known to increase empathy and bonding
oxytocin did improve powers of empathy – but only among those who were less socially proficient in the first place.
So if shyness is caused by a lack of social proficiency, it helps… in other words if people are shy because for whatever reason they are trapped in their own world, and not sufficiently immersed in the worlds of others this can help.
Stress Hormones Could Predict Boxing Dominance | Playbook
researchers took saliva samples minutes before two monkeys engaged in a staged competition for a pile of food. When dominant males won, there was a clear increase in the stress hormone right before the competition. In these cases, the dominant male was ready. He had sized up his opponent and knew, no doubt, that he’d prevail. Conversely, when the dominant male lost, the hormone level decreased before the food game. Although these apes live in very well-defined social societies – and the dominant male had more than likely battled with this opponent before and won – something had psyched him out.
Serotonin cell discoveries mean rethink of depression (New Scientist)
If you thought depression was caused by low serotonin levels, think again. It looks as if the brain chemistry of a depressed person is much more complex, with mounting evidence suggesting that too much serotonin in some brain regions is to blame.
If correct, it might explain some of the negative side-effects associated with selective serotonin re-uptake inhibitors (SSRIs), antidepressants like Prozac which increase the amount of the neurotransmitter serotonin in some parts of the brain.
The traditional view of depression was largely based on the observation that SSRIs boost mood- although why they do so is unknown. “Because antidepressants increase serotonin in some parts of the brain, people assumed that depression must be the result of low serotonin levels,” says Christopher Lowry of the University of Boulder in Colorado. But the discovery of multiple types of serotonin-releasing neurons in the brain, along with high levels of serotonin recorded in people with depression, is prompting a rethink.
“What’s more likely is that there are subgroups of serotonin neurons that are overactive in depressed patients, rather than underactive as we have all been assuming,” says Lowry.
One of the first clues that something might be amiss with the traditional theory came three years ago, when Murray Esler at the Baker Heart Research Institute in Melbourne, Australia, and colleagues found that the level of serotonin in the brains of people with panic disorder was four times higher than in healthy volunteers (Stress, DOI: 10.1080/10253890701300904), and in depressed people who were not receiving treatment it was two times higher than in volunteers (Archives of General Psychiatry, vol 65, p 38). They also showed that long-term use of SSRIs in people with depression and panic disorder seemed to decrease serotonin levels through an as yet unidentified mechanism.
Now, in studies of rats and mice, Lowry has found that there are multiple types of serotonin neurons that can be independently regulated. He presented his results at the Forum of European Neuroscience in Amsterdam, the Netherlands, last week.
This fits well with findings from other groups that there are two types of serotonin receptor in the amygdala, a brain region linked to emotion and anxiety: 5-HT2A receptors that inhibit anxiety, and 5-HT2C receptors that promote it. The roles of the receptors were identified by injecting drugs that either stimulated or inhibited each receptor and observing the animals’ behavioural response.
Together, the findings might mean that while high levels of serotonin in some brain regions like the prefrontal cortex can lead to improved mood, high serotonin in other regions could have negative effects.
Evidence for this idea comes from Gina Forster at the University of South Dakota in Vermillion and colleagues, who injected a stress-related molecule into the brains of rats and found that it triggered two phases of serotonin release. An initial wave of serotonin appeared to increase fear-like behaviour in the rats, while a second wave decreased this behaviour, possibly because it activated a brain region called the medial prefrontal cortex, which is associated with calming of fears (Neuroscience, vol 141, p 1047).
The new findings have implications for how SSRI drugs work. In the long-term, SSRIs do tend to have a calming effect, although more research is needed to understand how they do this.
However, in the short-term some people taking SSRIs report feeling increased anxiety. This is “almost certainly due to the activation of one of these groups of serotonin neurons”, says Lowry. The suicidal thoughts some people taking SSRIs claim to experience may also be linked to boosting serotonin, as suicide is thought to be associated with increased impulsivity. “It may be that certain types of SSRI are affecting these impulsivity circuits in the brain,” says Lowry.
Learning more about these different groups of serotonin neurons could lead to better treatments for depression and anxiety disorders. “It might be possible to design very specific drugs that can turn on or off specific groups of neurons that are deregulated in anxiety or depression,” says Lowry.
powerfully important - for those who care about these sorts of things.
Ketamine is a Very Effective Anti-Depressant (CalorieLab Lab Notes)
An anti-depressant usually takes weeks to take effect if it works at all and people often have to try different ones, while ketamine was able to fight off depression in a matter of hours. In rats, connections between neurons injured by long term stress were restored by ketamine. A study done by the National Institute of Mental Health showed that 70 percent of people for whom other types of anti-depressants did not work improved within hours of receiving ketamine. Drawbacks to using it are intravenous administration and sometimes short-term psychotic behavior occurs.

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