Your Brain Reveals Who Your Friends Are

Your Brain Reveals Who Your Friends Are

Summary: By looking at how the brain responds to video clips, researchers are able to determine who your friends may be, a new study reveals.

Source: Dartmouth College.

You may perceive the world the way your friends do, according to a Dartmouth study finding that friends have similar neural responses to real-world stimuli and these similarities can be used to predict who your friends are.

The researchers found that you can predict who people are friends with just by looking at how their brains respond to video clips. Friends had the most similar neural activity patterns, followed by friends-of-friends who, in turn, had more similar neural activity than people three degrees removed (friends-of-friends-of-friends).

Published in Nature Communications, the study is the first of its kind to examine the connections between the neural activity of people within a real-world social network, as they responded to real-world stimuli, which in this case was watching the same set of videos.

“Neural responses to dynamic, naturalistic stimuli, like videos, can give us a window into people’s unconstrained, spontaneous thought processes as they unfold. Our results suggest that friends process the world around them in exceptionally similar ways,” says lead author Carolyn Parkinson, who was a postdoctoral fellow in psychological and brain sciences at Dartmouth at the time of the study and is currently an assistant professor of psychology and director of the Computational Social Neuroscience Lab at the University of California, Los Angeles.

The study analyzed the friendships or social ties within a cohort of nearly 280 graduate students. The researchers estimated the social distance between pairs of individuals based on mutually reported social ties. Forty-two of the students were asked to watch a range of videos while their neural activity was recorded in a functional magnetic resonance imaging (fMRI) scanner. The videos spanned a range of topics and genres, including politics, science, comedy and music videos, for which a range of responses was expected. Each participant watched the same videos in the same order, with the same instructions. The researchers then compared the neural responses pairwise across the set of students to determine if pairs of students who were friends had more similar brain activity than pairs further removed from each other in their social network.

The findings revealed that neural response similarity was strongest among friends, and this pattern appeared to manifest across brain regions involved in emotional responding, directing one’s attention and high-level reasoning. Even when the researchers controlled for variables, including left-handed- or right-handedness, age, gender, ethnicity, and nationality, the similarity in neural activity among friends was still evident. The team also found that fMRI response similarities could be used to predict not only if a pair were friends but also the social distance between the two.

network

“We are a social species and live our lives connected to everybody else. If we want to understand how the human brain works, then we need to understand how brains work in combination– how minds shape each other,” explains senior author Thalia Wheatley, an associate professor of psychological and brain sciences at Dartmouth, and principal investigator of the Dartmouth Social Systems Laboratory.

For the study, the researchers were building on their earlier work, which found that as soon as you see someone you know, your brain immediately tells you how important or influential they are and the position they hold in your social network.

The research team plans to explore if we naturally gravitate toward people who see the world the same way we do, if we become more similar once we share experiences or if both dynamics reinforce each other.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Amy D. Olson – Dartmouth College
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Carolyn Parkinson.
Original Research: Open access research in Nature Communications.
doi:10.1038/s41467-017-02722-7

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Abstract

Similar neural responses predict friendship

Human social networks are overwhelmingly homophilous: individuals tend to befriend others who are similar to them in terms of a range of physical attributes (e.g., age, gender). Do similarities among friends reflect deeper similarities in how we perceive, interpret, and respond to the world? To test whether friendship, and more generally, social network proximity, is associated with increased similarity of real-time mental responding, we used functional magnetic resonance imaging to scan subjects’ brains during free viewing of naturalistic movies. Here we show evidence for neural homophily: neural responses when viewing audiovisual movies are exceptionally similar among friends, and that similarity decreases with increasing distance in a real-world social network. These results suggest that we are exceptionally similar to our friends in how we perceive and respond to the world around us, which has implications for interpersonal influence and attraction.

Beliefs About Suicide Acceptability in the United States: How Do They Affect Suicide Mortality?

Beliefs About Suicide Acceptability in the United States: How Do They Affect Suicide Mortality?

The Journals of Gerontology: Series B, gbx153,https://doi.org/10.1093/geronb/gbx153
Published:
25 January 2018
Article history

Abstract

Objectives

Societies develop cultural scripts to understand suicide and define conditions under which the act is acceptable. Prior empirical work suggests that such attitudes are important in understanding some forms of suicidal behavior among adolescents and high-risk populations. This study examines whether expressions of suicide acceptability under different circumstances are predictive of subsequent death by suicide in the general U.S. adult population and whether the effects differ over the life course.

 

Method

The study uses 1978–2010 General Social Survey data linked to the National Death Index through 2014 (n = 31,838). Cox survival models identify risk factors for suicide mortality, including attitudinal and cohort effects.

 

Results

Expressions of suicide acceptability are predictive of subsequent death by suicide—in some cases associated with a twofold increase in risk. Attitudes elevate the suicide hazard among older (>55 years) adults but not among younger (ages 33–54) adults. Fully-adjusted models reveal that the effects of attitudes toward suicide acceptability on suicide mortality are strongest for social circumstances (family dishonor; bankruptcy).

 

Discussion

Results point to the role of cultural factors and social attitudes in suicide. There may be utility in measuring attitudes in assessments of suicide risk.

Dopamine may have given humans our social edge over other apes

chimps

Male chimpanzees signal their aggression when they display their big canines, in contrast with humans, who show small canines when they smile.

Sergey Uryadnikov/shutterstock.com

Dopamine may have given humans our social edge over other apes

Humans are the ultimate social animals, with the ability to bond with mates, communicate through language, and make small talk with strangers on a packed bus. (Put chimpanzees in the same situation and most wouldn’t make it off the bus alive.) A new study suggests that the evolution of our unique social intelligence may have initially begun as a simple matter of brain chemistry.

Neuroanatomists have been trying for decades to find major differences between the brains of humans and other primates, aside from the obvious brain size. The human brain must have reorganized its chemistry and wiring as early human ancestors began to walk upright, use tools, and develop more complex social networks 6 million to 2 million years ago—well before the brain began to enlarge 1.8 million years ago, according to a hypothesis proposed in the 1960s by physical anthropologist Ralph Holloway of Columbia University. But neurotransmitters aren’t preserved in ancient skulls, so how to spot those changes?

One way is to search for key differences in neurochemistry between humans and other primates living today. Mary Ann Raghanti, a biological anthropologist at Kent State University in Ohio, and colleagues got tissue samples from brain banks and zoos of 38 individuals from six species who had died of natural causes: humans, tufted capuchins, pig-tailed macaques, olive baboons, gorillas, and chimpanzees. They sliced sections of basal ganglia—clusters of nerve cells and fibers in a region at the base of the brain known as the striatum, which is a sort of clearinghouse that relays signals from different parts of the brain for movement, learning, and social behavior. They stained these slices with chemicals that react to different types of neurotransmitters, including dopamine, serotonin, and neuropeptide Y—which are associated with sensitivity to social cues and cooperative behavior. Then, they analyzed the slices to measure different levels of neurotransmitters that had been released when the primates were alive.

Compared with other primates, both humans and great apes had elevated levels of serotonin and neuropeptide Y, in the basal ganglia. However, in line with another recent study on gene expression, humans had dramatically more dopamine in their striatum than apes, they report today in the Proceedings of the National Academy of Sciences. Humans also had less acetylcholine, a neurochemical linked to dominant and territorial behavior, than gorillas or chimpanzees. The combination “is a key difference that sets apart humans from all other species,” Raghanti says.

Those differences in neurochemistry may have set in motion other evolutionary changes, such as the development of monogamy and language in humans, theorizes Kent State paleoanthropologist Owen Lovejoy, a co-author. He proposes a new “neurochemical hypothesis for the origin of hominids,” in which females mated more with males who were outgoing, but not too aggressive. And males who cooperated well with other males may have been more successful hunters and scavengers. As human ancestors got better at cooperating, they shared the know-how for making tools and eventually developed language—all in a feedback loop fueled by surging levels of dopamine. “Cooperation is addictive,” Raghanti says.

Lovejoy thinks these neurochemical changes were already in place more than 4.4 million years ago, when Ardipithecus ramidus, an early member of the human family, lived in Ethiopia. Compared with chimpanzees, which display large canines when they bare their teeth in aggressive displays, A. ramidus males had reduced canines. That meant that when they smiled—like male humans today—they were likely signaling cooperation, Lovejoy says.

However, it’s a big leap to prove that higher levels of dopamine changed the evolution of human social behavior. The neurochemistry of the brain is so complex, and dopamine is involved in so many functions that it’s hard to know precisely why natural selection favored higher dopamine levels—or even whether it was a side effect of some other adaptation, says evolutionary geneticist Wolfgang Enard at Ludwig Maximilian University of Munich in Germany. But he says this painstaking research to quantify differences in neurochemistry among primates is important, especially as researchers study differences in gene expression in the brain. Raghanti agrees and is now writing a grant to study the brain tissue of bonobos.

Oxytocin Helps the Brain Modulate Social Signals

Oxytocin Helps the Brain Modulate Social Signals

Summary: A new study reports oxytocin plays a crucial role in processing numerous social signals.

Source: Harvard.

Between sights, sounds, smells and other senses, the brain is flooded with stimuli on a moment-to-moment basis. How can it sort through the flood of information to decide what is important and what can be relegated to the background?

Part of the answer, says Catherine Dulac, the Higgins Professor of Molecular and Cellular Biology, may lie with oxytocin.

Though popularly known as the “love hormone,” Dulac and a team of researchers found evidence that oxytocin actually plays a crucial role in helping the brain process a wide array of social signals. The study is described in a December 12 paper published in eLife.

The study, Dulac said, suggests that oxytocin acts like a modulator in the brain, turning up the volume of certain stimuli while turning others down, helping the brain to make sense of the barrage for information it receives from one moment to the next.

In investigating the role of oxytocin in processing social signals, Dulac and colleagues began with an oft-observed behavior – the preference for male mice to interact with females.

Studies have shown that this behavior isn’t just social – it’s actually hard-wired in the brains of male mice.

When male mice are exposed to pheromone signals of females, Dulac and colleagues found, neurons in their medial amygdala showed increased levels of activation. When the same mice were exposed to pheromones of other males, those same neurons showed relatively little stimulation.

Armed with that data, Dulac and colleagues targeted the gene responsible for producing oxytocin – which was known to be involved in social interactions ranging from infant/parent bonding to monogamy in certain rodents.

Using genetic tools, researchers switched the gene off, and were surprised to find that both males’ preference for interacting with females and the neural signal in the amygdala disappeared.

“This is a molecule that’s involved in the processing of social signals,” Dulac said. “We also showed, using pharmacology and genetics, that the effect happens on a moment-to-moment basis.

“What we are trying to do is understand the logic of social interactions in one particular species,” she said. “What this study says is, for this particular type of social interaction, oxytocin plays a role, and that role is both at the level of the brain and the behavior.”

mice

Understanding oxytocin – and molecules like it – might shed light on a number of brain disorders.

With an understanding of how various neurotransmitters work to amplify or quiet certain stimuli, Dulac said, researchers may gain new insight into how to treat everything from depression, which is often characterized by a lack of interest in social interactions, to autism, which is thought to be connected to an inability to sort through social and sensory stimuli.

Ultimately, Dulac said, the study offers a small glimpse into what could be a larger system of molecules which act like modulators in the brain, turning certain stimuli up or down depending on the situation.

“There may be many different regulators,” Dulac said. “Oxytocin might be one of a whole realm of modulators, each of which are important in a particular circumstance. That therefore gives the animal a great deal of plasticity in terms of engaging in a particular behavior, so it’s not the case that each time the animal encounters a particular stimulus it will react in exactly the same way. Depending on the state of the brain and the release of these neurotransmitters, the animal can boost its behavior toward the stimulus or ignore it.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Harvard
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Dulac et al./eLife.
Original Research: Full open access research for “Oxytocin signaling in the medial amygdala is required for sex discrimination of social cues” by Shenqin Yao, Joseph Bergan, Anne Lanjuin, and Catherine Dulac in eLife. Published online December 12 2017 doi:10.7554/eLife.31373

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Abstract

Oxytocin signaling in the medial amygdala is required for sex discrimination of social cues

The neural control of social behaviors in rodents requires the encoding of pheromonal cues by the vomeronasal system. Here we show that the typical preference of male mice for females is eliminated in mutants lacking oxytocin, a neuropeptide modulating social behaviors in many species. Ablation of the oxytocin receptor in aromatase-expressing neurons of the medial amygdala (MeA) fully recapitulates the elimination of female preference in males. Further, single-unit recording in the MeA uncovered significant changes in the sensory representation of conspecific cues in the absence of oxytocin signaling. Finally, acute manipulation of oxytocin signaling in adults is sufficient to alter social interaction preferences in males as well as responses of MeA neurons to chemosensory cues. These results uncover the critical role of oxytocin signaling in a molecularly defined neuronal population in order to modulate the behavioral and physiological responses of male mice to females on a moment-to-moment basis.

“Oxytocin signaling in the medial amygdala is required for sex discrimination of social cues” by Shenqin Yao, Joseph Bergan, Anne Lanjuin, and Catherine Dulac in eLife. Published online December 12 2017 doi:10.7554/eLife.31373

Marriage May Help Stave Off Dementia

Marriage May Help Stave Off Dementia

Summary: Widowers and life-long single people are at higher risk of developing dementia, a new study reports.

Source: BMJ.

Marriage may lower the risk of developing dementia, concludes a synthesis of the available evidence published online in the Journal of Neurology Neurosurgery & Psychiatry.

Lifelong singletons and widowers are at heightened risk of developing the disease, the findings indicate, although single status may no longer be quite the health hazard it once seemed to be, the researchers acknowledge.

They base their findings on data from 15 relevant studies published up to the end of 2016. These looked at the potential role of marital status on dementia risk, and involved more than 800,000 participants from Europe, North and South America, and Asia.

Married people accounted for between 28 and 80 per cent of people in the included studies; the widowed made up between around 8 and 48 per cent; the divorced between 0 and 16 per cent; and lifelong singletons between 0 and 32.5 per cent.

Pooled analysis of the data showed that compared with those who were married, lifelong singletons were 42 per cent more likely to develop dementia, after taking account of age and sex.

Part of this risk might be explained by poorer physical health among lifelong single people, suggest the researchers.

However, the most recent studies, which included people born after 1927, indicated a risk of 24 per cent, which suggests that this may have lessened over time, although it is not clear why, say the researchers.

The widowed were 20 per cent more likely to develop dementia than married people, although the strength of this association was somewhat weakened when educational attainment was factored in.

But bereavement is likely to boost stress levels, which have been associated with impaired nerve signalling and cognitive abilities, the researchers note.

No such associations were found for those who had divorced their partners, although this may partly be down to the smaller numbers of people of this status included in the studies, the researchers point out.

But the lower risk among married people persisted even after further more detailed analysis, which, the researchers suggest, reflects “the robustness of the findings.”

These findings are based on observational studies so no firm conclusions about cause and effect can be drawn, and the researchers point to several caveats, including the design of some of the included studies, and the lack of information on the duration of widowhood or divorce.

Nevertheless, they proffer several explanations for the associations they found. Marriage may help both partners to have healthier lifestyles, including exercising more, eating a healthy diet, and smoking and drinking less, all of which have been associated with lower risk of dementia.

Image shows people getting married.

Couples may also have more opportunities for social engagement than single people–a factor that has been linked to better health and lower dementia risk, they suggest.

In a linked editorial, Christopher Chen and Vincent Mok, of, respectively, the National University of Singapore and the Chinese University of Hong Kong, suggest that should marital status be added to the list of modifiable risk factors for dementia, “the challenge remains as to how these observations can be translated into effective means of dementia prevention.”

The discovery of potentially modifiable risk factors doesn’t mean that dementia can easily be prevented, they emphasise.

“Therefore, ways of destigmatising dementia and producing dementia-friendly communities more accepting and embracing of the kinds of disruptions that dementia can produce should progress alongside biomedical and public health programmes,” they conclude.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Caroline White – BMJ
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Marriage and risk of dementia: systematic review and meta-analysis of observational studies” by Andrew Sommerlad, Joshua Ruegger, Archana Singh-Manoux, Glyn Lewis, and Gill Livingston in Journal of Neurology Neurosurgery & Psychiatry. Published online November 27 2017 doi:10/30/jnnp-2017-316274

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Abstract

Marriage and risk of dementia: systematic review and meta-analysis of observational studies

Background Being married is associated with healthier lifestyle behaviours and lower mortality and may reduce risk for dementia due to life-course factors. We conducted a systematic review and meta-analysis of studies of the association between marital status and the risk of developing dementia.

Methods We searched medical databases and contacted experts in the field for relevant studies reporting the relationship, adjusted for age and sex, between marital status and dementia. We rated methodological quality and conducted random-effects meta-analyses to summarise relative risks of being widowed, divorced or lifelong single, compared with being married. Secondary stratified analyses with meta-regression examined the impact of clinical and social context and study methodology on findings.

Results We included 15 studies with 812 047 participants. Compared with those who are married, lifelong single (relative risk=1.42 (95% CI 1.07 to 1.90)) and widowed (1.20 (1.02 to 1.41)) people have elevated risk of dementia. We did not find an association in divorced people.

Further analyses showed that less education partially confounds the risk in widowhood and worse physical health the elevated risk in lifelong single people. Compared with studies that used clinical registers for ascertaining dementia diagnoses, those which clinically examined all participants found higher risk for being unmarried.

Conclusions Being married is associated with reduced risk of dementia than widowed and lifelong single people, who are also underdiagnosed in routine clinical practice. Dementia prevention in unmarried people should focus on education and physical health and should consider the possible effect of social engagement as a modifiable risk factor.

“Marriage and risk of dementia: systematic review and meta-analysis of observational studies” by Andrew Sommerlad, Joshua Ruegger, Archana Singh-Manoux, Glyn Lewis, and Gill Livingston in Journal of Neurology Neurosurgery & Psychiatry. Published online November 27 2017 doi:10/30/jnnp-2017-316274

Grow your nerves to prevent depression – medications – drugs causes it

What causes depression?

Onset of depression more complex than a brain chemical imbalance

what causes depression

It’s often said that depression results from a chemical imbalance, but that figure of speech doesn’t capture how complex the disease is. Research suggests that depression doesn’t spring from simply having too much or too little of certain brain chemicals. Rather, there are many possible causes of depression, including faulty mood regulation by the brain, genetic vulnerability, stressful life events, medications, and medical problems. It’s believed that several of these forces interact to bring on depression.

To be sure, chemicals are involved in this process, but it is not a simple matter of one chemical being too low and another too high. Rather, many chemicals are involved, working both inside and outside nerve cells. There are millions, even billions, of chemical reactions that make up the dynamic system that is responsible for your mood, perceptions, and how you experience life.

With this level of complexity, you can see how two people might have similar symptoms of depression, but the problem on the inside, and therefore what treatments will work best, may be entirely different.

Researchers have learned much about the biology of depression. They’ve identified genes that make individuals more vulnerable to low moods and influence how an individual responds to drug therapy. One day, these discoveries should lead to better, more individualized treatment (see “From the lab to your medicine cabinet”), but that is likely to be years away. And while researchers know more now than ever before about how the brain regulates mood, their understanding of the biology of depression is far from complete.

What follows is an overview of the current understanding of the major factors believed to play a role in depression.

The brain’s impact on depression

Popular lore has it that emotions reside in the heart. Science, though, tracks the seat of your emotions to the brain. Certain areas of the brain help regulate mood. Researchers believe that — more important than levels of specific brain chemicals — nerve cell connections, nerve cell growth, and the functioning of nerve circuits have a major impact on depression. Still, their understanding of the neurological underpinnings of mood is incomplete.

Regions that affect mood

Increasingly sophisticated forms of brain imaging — such as positron emission tomography (PET), single-photon emission computed tomography (SPECT), and functional magnetic resonance imaging (fMRI) — permit a much closer look at the working brain than was possible in the past. An fMRI scan, for example, can track changes that take place when a region of the brain responds during various tasks. A PET or SPECT scan can map the brain by measuring the distribution and density of neurotransmitter receptors in certain areas.

Use of this technology has led to a better understanding of which brain regions regulate mood and how other functions, such as memory, may be affected by depression. Areas that play a significant role in depression are the amygdala, the thalamus, and the hippocampus (see Figure 1).

Research shows that the hippocampus is smaller in some depressed people. For example, in one fMRI study published in The Journal of Neuroscience, investigators studied 24 women who had a history of depression. On average, the hippocampus was 9% to 13% smaller in depressed women compared with those who were not depressed. The more bouts of depression a woman had, the smaller the hippocampus. Stress, which plays a role in depression, may be a key factor here, since experts believe stress can suppress the production of new neurons (nerve cells) in the hippocampus.

Researchers are exploring possible links between sluggish production of new neurons in the hippocampus and low moods. An interesting fact about antidepressants supports this theory. These medications immediately boost the concentration of chemical messengers in the brain (neurotransmitters). Yet people typically don’t begin to feel better for several weeks or longer. Experts have long wondered why, if depression were primarily the result of low levels of neurotransmitters, people don’t feel better as soon as levels of neurotransmitters increase.

The answer may be that mood only improves as nerves grow and form new connections, a process that takes weeks. In fact, animal studies have shown that antidepressants do spur the growth and enhanced branching of nerve cells in the hippocampus. So, the theory holds, the real value of these medications may be in generating new neurons (a process called neurogenesis), strengthening nerve cell connections, and improving the exchange of information between nerve circuits. If that’s the case, medications could be developed that specifically promote neurogenesis, with the hope that patients would see quicker results than with current treatments.

Figure 1: Areas of the brain affected by depression

Areas of the brain affected by depression

Amygdala: The amygdala is part of the limbic system, a group of structures deep in the brain that’s associated with emotions such as anger, pleasure, sorrow, fear, and sexual arousal. The amygdala is activated when a person recalls emotionally charged memories, such as a frightening situation. Activity in the amygdala is higher when a person is sad or clinically depressed. This increased activity continues even after recovery from depression.

Thalamus: The thalamus receives most sensory information and relays it to the appropriate part of the cerebral cortex, which directs high-level functions such as speech, behavioral reactions, movement, thinking, and learning. Some research suggests that bipolar disorder may result from problems in the thalamus, which helps link sensory input to pleasant and unpleasant feelings.

Hippocampus: The hippocampus is part of the limbic system and has a central role in processing long-term memory and recollection. Interplay between the hippocampus and the amygdala might account for the adage “once bitten, twice shy.” It is this part of the brain that registers fear when you are confronted by a barking, aggressive dog, and the memory of such an experience may make you wary of dogs you come across later in life. The hippocampus is smaller in some depressed people, and research suggests that ongoing exposure to stress hormone impairs the growth of nerve cells in this part of the brain.

Nerve cell communication

The ultimate goal in treating the biology of depression is to improve the brain’s ability to regulate mood. We now know that neurotransmitters are not the only important part of the machinery. But let’s not diminish their importance either. They are deeply involved in how nerve cells communicate with one another. And they are a component of brain function that we can often influence to good ends.

Neurotransmitters are chemicals that relay messages from neuron to neuron. An antidepressant medication tends to increase the concentration of these substances in the spaces between neurons (the synapses). In many cases, this shift appears to give the system enough of a nudge so that the brain can do its job better.

How the system works. If you trained a high-powered microscope on a slice of brain tissue, you might be able to see a loosely braided network of neurons that send and receive messages. While every cell in the body has the capacity to send and receive signals, neurons are specially designed for this function. Each neuron has a cell body containing the structures that any cell needs to thrive. Stretching out from the cell body are short, branchlike fibers called dendrites and one longer, more prominent fiber called the axon.

A combination of electrical and chemical signals allows communication within and between neurons. When a neuron becomes activated, it passes an electrical signal from the cell body down the axon to its end (known as the axon terminal), where chemical messengers called neurotransmitters are stored. The signal releases certain neurotransmitters into the space between that neuron and the dendrite of a neighboring neuron. That space is called a synapse. As the concentration of a neurotransmitter rises in the synapse, neurotransmitter molecules begin to bind with receptors embedded in the membranes of the two neurons (see Figure 2).

The release of a neurotransmitter from one neuron can activate or inhibit a second neuron. If the signal is activating, or excitatory, the message continues to pass farther along that particular neural pathway. If it is inhibitory, the signal will be suppressed. The neurotransmitter also affects the neuron that released it. Once the first neuron has released a certain amount of the chemical, a feedback mechanism (controlled by that neuron’s receptors) instructs the neuron to stop pumping out the neurotransmitter and start bringing it back into the cell. This process is called reabsorption or reuptake. Enzymes break down the remaining neurotransmitter molecules into smaller particles.

When the system falters. Brain cells usually produce levels of neurotransmitters that keep senses, learning, movements, and moods perking along. But in some people who are severely depressed or manic, the complex systems that accomplish this go awry. For example, receptors may be oversensitive or insensitive to a specific neurotransmitter, causing their response to its release to be excessive or inadequate. Or a message might be weakened if the originating cell pumps out too little of a neurotransmitter or if an overly efficient reuptake mops up too much before the molecules have the chance to bind to the receptors on other neurons. Any of these system faults could significantly affect mood.

Kinds of neurotransmitters. Scientists have identified many different neurotransmitters. Here is a description of a few believed to play a role in depression:

  • Acetylcholine enhances memory and is involved in learning and recall.
  • Serotonin helps regulate sleep, appetite, and mood and inhibits pain. Research supports the idea that some depressed people have reduced serotonin transmission. Low levels of a serotonin byproduct have been linked to a higher risk for suicide.
  • Norepinephrine constricts blood vessels, raising blood pressure. It may trigger anxiety and be involved in some types of depression. It also seems to help determine motivation and reward.
  • Dopamine is essential to movement. It also influences motivation and plays a role in how a person perceives reality. Problems in dopamine transmission have been associated with psychosis, a severe form of distorted thinking characterized by hallucinations or delusions. It’s also involved in the brain’s reward system, so it is thought to play a role in substance abuse.
  • Glutamate is a small molecule believed to act as an excitatory neurotransmitter and to play a role in bipolar disorder and schizophrenia. Lithium carbonate, a well-known mood stabilizer used to treat bipolar disorder, helps prevent damage to neurons in the brains of rats exposed to high levels of glutamate. Other animal research suggests that lithium might stabilize glutamate reuptake, a mechanism that may explain how the drug smooths out the highs of mania and the lows of depression in the long term.
  • Gamma-aminobutyric acid (GABA) is an amino acid that researchers believe acts as an inhibitory neurotransmitter. It is thought to help quell anxiety.

Figure 2: How neurons communicate

How neurons communicate

  1. An electrical signal travels down the axon.
  2. Chemical neurotransmitter molecules are released.
  3. The neurotransmitter molecules bind to receptor sites.
  4. The signal is picked up by the second neuron and is either passed along or halted.
  5. The signal is also picked up by the first neuron, causing reuptake, the process by which the cell that released the neurotransmitter takes back some of the remaining molecules.

Genes’ effect on mood

Every part of your body, including your brain, is controlled by genes. Genes make proteins that are involved in biological processes. Throughout life, different genes turn on and off, so that — in the best case — they make the right proteins at the right time. But if the genes get it wrong, they can alter your biology in a way that results in your mood becoming unstable. In a genetically vulnerable person, any stress (a missed deadline at work or a medical illness, for example) can then push this system off balance.

Mood is affected by dozens of genes, and as our genetic endowments differ, so do our depressions. The hope is that as researchers pinpoint the genes involved in mood disorders and better understand their functions, treatment can become more individualized and more successful. Patients would receive the best medication for their type of depression.

Another goal of gene research, of course, is to understand how, exactly, biology makes certain people vulnerable to depression. For example, several genes influence the stress response, leaving us more or less likely to become depressed in response to trouble.

Perhaps the easiest way to grasp the power of genetics is to look at families. It is well known that depression and bipolar disorder run in families. The strongest evidence for this comes from the research on bipolar disorder. Half of those with bipolar disorder have a relative with a similar pattern of mood fluctuations. Studies of identical twins, who share a genetic blueprint, show that if one twin has bipolar disorder, the other has a 60% to 80% chance of developing it, too. These numbers don’t apply to fraternal twins, who — like other biological siblings — share only about half of their genes. If one fraternal twin has bipolar disorder, the other has a 20% chance of developing it.

The evidence for other types of depression is more subtle, but it is real. A person who has a first-degree relative who suffered major depression has an increase in risk for the condition of 1.5% to 3% over normal.

One important goal of genetics research — and this is true throughout medicine — is to learn the specific function of each gene. This kind of information will help us figure out how the interaction of biology and environment leads to depression in some people but not others.

Temperament shapes behavior

Genetics provides one perspective on how resilient you are in the face of difficult life events. But you don’t need to be a geneticist to understand yourself. Perhaps a more intuitive way to look at resilience is by understanding your temperament. Temperament — for example, how excitable you are or whether you tend to withdraw from or engage in social situations — is determined by your genetic inheritance and by the experiences you’ve had during the course of your life. Some people are able to make better choices in life once they appreciate their habitual reactions to people and to life events.

Cognitive psychologists point out that your view of the world and, in particular, your unacknowledged assumptions about how the world works also influence how you feel. You develop your viewpoint early on and learn to automatically fall back on it when loss, disappointment, or rejection occurs. For example, you may come to see yourself as unworthy of love, so you avoid getting involved with people rather than risk losing a relationship. Or you may be so self-critical that you can’t bear the slightest criticism from others, which can slow or block your career progress.

Yet while temperament or world view may have a hand in depression, neither is unchangeable. Therapy and medications can shift thoughts and attitudes that have developed over time.

Stressful life events

At some point, nearly everyone encounters stressful life events: the death of a loved one, the loss of a job, an illness, or a relationship spiraling downward. Some must cope with the early loss of a parent, violence, or sexual abuse. While not everyone who faces these stresses develops a mood disorder — in fact, most do not — stress plays an important role in depression.

As the previous section explained, your genetic makeup influences how sensitive you are to stressful life events. When genetics, biology, and stressful life situations come together, depression can result.

Stress has its own physiological consequences. It triggers a chain of chemical reactions and responses in the body. If the stress is short-lived, the body usually returns to normal. But when stress is chronic or the system gets stuck in overdrive, changes in the body and brain can be long-lasting.

How stress affects the body

Stress can be defined as an automatic physical response to any stimulus that requires you to adjust to change. Every real or perceived threat to your body triggers a cascade of stress hormones that produces physiological changes. We all know the sensations: your heart pounds, muscles tense, breathing quickens, and beads of sweat appear. This is known as the stress response.

The stress response starts with a signal from the part of your brain known as the hypothalamus. The hypothalamus joins the pituitary gland and the adrenal glands to form a trio known as the hypothalamic-pituitary-adrenal (HPA) axis, which governs a multitude of hormonal activities in the body and may play a role in depression as well.

When a physical or emotional threat looms, the hypothalamus secretes corticotropin-releasing hormone (CRH), which has the job of rousing your body. Hormones are complex chemicals that carry messages to organs or groups of cells throughout the body and trigger certain responses. CRH follows a pathway to your pituitary gland, where it stimulates the secretion of adrenocorticotropic hormone (ACTH), which pulses into your bloodstream. When ACTH reaches your adrenal glands, it prompts the release of cortisol.

The boost in cortisol readies your body to fight or flee. Your heart beats faster — up to five times as quickly as normal — and your blood pressure rises. Your breath quickens as your body takes in extra oxygen. Sharpened senses, such as sight and hearing, make you more alert.

CRH also affects the cerebral cortex, part of the amygdala, and the brainstem. It is thought to play a major role in coordinating your thoughts and behaviors, emotional reactions, and involuntary responses. Working along a variety of neural pathways, it influences the concentration of neurotransmitters throughout the brain. Disturbances in hormonal systems, therefore, may well affect neurotransmitters, and vice versa.

Normally, a feedback loop allows the body to turn off “fight-or-flight” defenses when the threat passes. In some cases, though, the floodgates never close properly, and cortisol levels rise too often or simply stay high. This can contribute to problems such as high blood pressure, immune suppression, asthma, and possibly depression.

Studies have shown that people who are depressed or have dysthymia typically have increased levels of CRH. Antidepressants and electroconvulsive therapy are both known to reduce these high CRH levels. As CRH levels return to normal, depressive symptoms recede. Research also suggests that trauma during childhood can negatively affect the functioning of CRH and the HPA axis throughout life.

Early losses and trauma

Certain events can have lasting physical, as well as emotional, consequences. Researchers have found that early losses and emotional trauma may leave individuals more vulnerable to depression later in life.

Childhood losses. Profound early losses, such as the death of a parent or the withdrawal of a loved one’s affection, may resonate throughout life, eventually expressing themselves as depression. When an individual is unaware of the wellspring of his or her illness, he or she can’t easily move past the depression. Moreover, unless the person gains a conscious understanding of the source of the condition, later losses or disappointments may trigger its return.

The British psychiatrist John Bowlby focused on early losses in a number of landmark studies of monkeys. When he separated young monkeys from their mothers, the monkeys passed through predictable stages of a separation response. Their furious outbursts trailed off into despair, followed by apathetic detachment. Meanwhile, the levels of their stress hormones rose. Later investigators extended this research. One study found that the CRH system and HPA axis got stuck in overdrive in adult rodents that had been separated from their mothers too early in life. This held true whether or not the rats were purposely put under stress. Interestingly, antidepressants and electroconvulsive therapy relieve the symptoms of animals distressed by such separations.

The role of trauma. Traumas may also be indelibly etched on the psyche. A small but intriguing study in the Journal of the American Medical Association showed that women who were abused physically or sexually as children had more extreme stress responses than women who had not been abused. The women had higher levels of the stress hormones ACTH and cortisol, and their hearts beat faster when they performed stressful tasks, such as working out mathematical equations or speaking in front of an audience.

Many researchers believe that early trauma causes subtle changes in brain function that account for symptoms of depression and anxiety. The key brain regions involved in the stress response may be altered at the chemical or cellular level. Changes might include fluctuations in the concentration of neurotransmitters or damage to nerve cells. However, further investigation is needed to clarify the relationship between the brain, psychological trauma, and depression.

Seasonal affective disorder: When winter brings the blues

Many people feel sad when summer wanes, but some actually develop depression with the season’s change. Known as seasonal affective disorder (SAD), this form of depression affects about 1% to 2% of the population, particularly women and young people.

SAD seems to be triggered by more limited exposure to daylight; typically it comes on during the fall or winter months and subsides in the spring. Symptoms are similar to general depression and include lethargy, loss of interest in once-pleasurable activities, irritability, inability to concentrate, and a change in sleeping patterns, appetite, or both.

To combat SAD, doctors suggest exercise, particularly outdoor activities during daylight hours. Exposing yourself to bright artificial light may also help. Light therapy, also called phototherapy, usually involves sitting close to a special light source that is far more intense than normal indoor light for 30 minutes every morning. The light must enter through your eyes to be effective; skin exposure has not been proven to work. Some people feel better after only one light treatment, but most people require at least a few days of treatment, and some need several weeks. You can buy boxes that emit the proper light intensity (10,000 lux) with a minimal amount of ultraviolet light without a prescription, but it is best to work with a professional who can monitor your response.

There are few side effects to light therapy, but you should be aware of the following potential problems:

  • Mild anxiety, jitteriness, headaches, early awakening, or eyestrain can occur.
  • There is evidence that light therapy can trigger a manic episode in people who are vulnerable.
  • While there is no proof that light therapy can aggravate an eye problem, you should still discuss any eye disease with your doctor before starting light therapy. Likewise, since rashes can result, let your doctor know about any skin conditions.
  • Some drugs or herbs (for example, St. John’s wort) can make you sensitive to light.
  • If light therapy isn’t helpful, antidepressants may offer relief.

Medical problems

Certain medical problems are linked to lasting, significant mood disturbances. In fact, medical illnesses or medications may be at the root of up to 10% to 15% of all depressions.

Among the best-known culprits are two thyroid hormone imbalances. An excess of thyroid hormone (hyperthyroidism) can trigger manic symptoms. On the other hand, hypothyroidism, a condition in which your body produces too little thyroid hormone, often leads to exhaustion and depression.

Heart disease has also been linked to depression, with up to half of heart attack survivors reporting feeling blue and many having significant depression. Depression can spell trouble for heart patients: it’s been linked with slower recovery, future cardiovascular trouble, and a higher risk of dying within about six months. Although doctors have hesitated to give heart patients older depression medications called tricyclic antidepressants because of their impact on heart rhythms, selective serotonin reuptake inhibitors seem safe for people with heart conditions.

The following medical conditions have also been associated with mood disorders:

  • degenerative neurological conditions, such as multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease
  • stroke
  • some nutritional deficiencies, such as a lack of vitamin B12
  • other endocrine disorders, such as problems with the parathyroid or adrenal glands that cause them to produce too little or too much of particular hormones
  • certain immune system diseases, such as lupus
  • some viruses and other infections, such as mononucleosis, hepatitis, and HIV
  • cancer
  • erectile dysfunction in men.

When considering the connection between health problems and depression, an important question to address is which came first, the medical condition or the mood changes. There is no doubt that the stress of having certain illnesses can trigger depression. In other cases, depression precedes the medical illness and may even contribute to it. To find out whether the mood changes occurred on their own or as a result of the medical illness, a doctor carefully considers a person’s medical history and the results of a physical exam.

If depression or mania springs from an underlying medical problem, the mood changes should disappear after the medical condition is treated. If you have hypothyroidism, for example, lethargy and depression often lift once treatment regulates the level of thyroid hormone in your blood. In many cases, however, the depression is an independent problem, which means that in order to be successful, treatment must address depression directly.

An out-of-sync body clock may underlie SAD and other mood disorders

Research into one form of depression — seasonal affective disorder (SAD) — has uncovered another potential factor in mood disorders: an internal body clock that has gone awry.

Experts don’t fully understand the cause of SAD, but a leading theory has been that the hormone melatonin plays a role. The brain secretes melatonin at night, so longer periods of darkness in the winter months may spur greater production of this hormone. Some researchers believe light therapy has been helpful in treating SAD because exposure to light artificially lengthens daytime and decreases melatonin production.

But another theory has emerged: that SAD stems, at least partly, from an out-of-sync body clock. The researchers who propose this idea suggest that light therapy works because it resets the body’s internal clock.

Each of us has a biological clock that regulates the circadian (meaning “about a day”) rhythm of sleeping and waking. This internal clock — which is located in a small bundle of brain cells called the suprachiasmatic nucleus and gradually becomes established during the first months of life — controls the daily ups and downs of biological patterns, including body temperature, blood pressure, and the release of hormones. Although the clock is largely self-regulating, it responds to several cues to keep it set properly, including light and melatonin production.

When researchers expose people to light at intervals that are at odds with the outside world, this resets the subjects’ biological clocks to match the new light input. Likewise, melatonin affects the body clock. It’s produced in a predictable daily rhythm by the pineal gland, with levels climbing after dark and ebbing after dawn. Scientists believe this daily light-sensitive pattern helps keep the sleep/wake cycle on track.

Beyond SAD

A case is being made that circadian rhythms influence other mood disorders as well. Studies have uncovered out-of-sync circadian rhythms among people with bipolar disorder, schizophrenia, borderline personality disorder, or night eating disorder.

Figure 3: Getting back in sync

Getting back in sync

Medications

Sometimes, symptoms of depression or mania are a side effect of certain drugs, such as steroids or blood pressure medication. Be sure to tell your doctor or therapist what medications you take and when your symptoms began. A professional can help sort out whether a new medication, a change in dosage, or interactions with other drugs or substances might be affecting your mood.

Table 1 lists drugs that may affect mood. However, keep in mind the following:

  • Researchers disagree about whether a few of these drugs — such as birth control pills or propranolol — affect mood enough to be a significant factor.
  • Most people who take the medications listed will not experience mood changes, although having a family or personal history of depression may make you more vulnerable to such a change.
  • Some of the drugs cause symptoms like malaise (a general feeling of being ill or uncomfortable) or appetite loss that may be mistaken for depression.
  • Even if you are taking one of these drugs, your depression may spring from other sources.

Table 1: Medications that may cause depression

Antimicrobials, antibiotics, antifungals, and antivirals
acyclovir (Zovirax); alpha-interferons; cycloserine (Seromycin); ethambutol (Myambutol); levofloxacin (Levaquin); metronidazole (Flagyl); streptomycin; sulfonamides (AVC, Sultrin, Trysul); tetracycline
Heart and blood pressure drugs
beta blockers such as propranolol (Inderal), metoprolol (Lopressor, Toprol XL), atenolol (Tenormin); calcium-channel blockers such as verapamil (Calan, Isoptin, Verelan) and nifedipine (Adalat CC, Procardia XL); digoxin (Digitek, Lanoxicaps, Lanoxin); disopyramide (Norpace); methyldopa (Aldomet)
Hormones
anabolic steroids; danazol (Danocrine); glucocorticoids such as prednisone and adrenocorticotropic hormone; estrogens (e.g., Premarin, Prempro); oral contraceptives (birth control pills)
Tranquilizers, insomnia aids, and sedatives
barbiturates such as phenobarbital (Solfoton) and secobarbital (Seconal); benzodiazepines such as diazepam (Valium) and clonazepam (Klonopin)
Miscellaneous
acetazolamide (Diamox); antacids such as cimetidine (Tagamet) and ranitidine (Zantac); antiseizure drugs; baclofen (Lioresal); cancer drugs such as asparaginase (Elspar); cyclosporine (Neoral, Sandimmune); disulfiram (Antabuse); isotretinoin (Accutane); levodopa or L-dopa (Larodopa); metoclopramide (Octamide, Reglan); narcotic pain medications (e.g., codeine, Percodan, Demerol, morphine); withdrawal from cocaine or amphetamines
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