Chapter 12. Psychopathology: The Biology of Behavioral Disorders
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Jon Hamilton A mind-altering drug called ketamine is changing the way some doctors treat depression. Encouraged by research showing that ketamine can relieve even the worst depression in a matter of hours, these doctors are giving the drug to some of their toughest patients. And they're doing this even though ketamine lacks approval from the Food and Drug Administration for treating depression. "It became clear to me that the future of psychiatry was going to include ketamine or derivatives of ketamine," says David Feifel, a professor of psychiatry at the University of California, San Diego, who began administering the drug to patients in 2010. Ketamine was developed as an anesthetic and received FDA approval for this use in 1970. Decades later, it became popular as a psychedelic club drug. And in 2006, a team from the National Institute of Mental Health published a landmark study showing that a single intravenous dose of ketamine produced "robust and rapid antidepressant effects" within a couple of hours. Since then, thousands of depressed patients have received "off-label" treatment with ketamine. One of those patients is Paul, 36, who lives in San Diego and is a patient of Dr. Feifel. We're not using his last name to protect his medical privacy. © 2015 NPR
By Karen Weintraub Depression makes people more vulnerable to alcoholism and vice versa, said Dr. Shelly Greenfield, a professor of psychiatry at Harvard Medical School and director of McLean Hospital’s Alcohol and Drug Abuse Clinical and Health Services Research Program. About a third of depressed people also have a problem with alcohol, she said, adding that the depression usually comes first. Genetics makes some people more vulnerable to each — and perhaps the combination, Dr. Greenfield said, “but it’s not the whole story.” Social environment, particularly in childhood, also plays a key role. People who are the victims of physical or sexual abuse, for example, are at higher risk for both alcoholism and depression later in life, she said. Depressed people who drink will most likely see their depression worsen, because alcohol is a depressant, tamping down the nervous system, said Dr. Kathleen Brady, a distinguished university professor at the Medical University of South Carolina. Abstinence will be harder for alcoholics who are depressed, because of the hopelessness that comes with depression. Getting help promptly may make recovery from alcoholism easier, Dr. Greenfield said. Needing help to quit drinking or to resolve depression is not a sign of weakness or personal failure, she noted. In families with a history of either depression or alcoholism, it is important to be vigilant about drinking, particularly in adolescence. © 2015 The New York Times Company
By BENEDICT CAREY Fourteen years ago, a leading drug maker published a study showing that the antidepressant Paxil was safe and effective for teenagers. On Wednesday, a major medical journal posted a new analysis of the same data concluding that the opposite is true. That study — featured prominently by the journal BMJ — is a clear break from scientific custom and reflects a new era in scientific publishing, some experts said, opening the way for journals to post multiple interpretations of the same experiment. It comes at a time of self-examination across science — retractions are at an all-time high; recent cases of fraud have shaken fields as diverse as anesthesia and political science; and earlier this month researchers reported that less than half of a sample of psychology papers held up. “This paper is alarming, but its existence is a good thing,” said Brian Nosek, a professor of psychology at the University of Virginia, who was not involved in either the original study or the reanalysis. “It signals that the community is waking up, checking its work and doing what science is supposed to do — self-correct.” The authors of the reanalysis said that many clinical studies had some of the same issues as the original Paxil study, and that data should be made freely available across clinical medicine, so that multiple parties could analyze them. The dispute itself is a long-running one: Questions surrounding the 2001 study played a central role in the so-called antidepressant wars of the early 2000s, which led to strong warnings on the labels of Paxil and similar drugs citing the potential suicide risk for children, adolescents and young adults. The drugs are considered beneficial and less risky for many adults over 25 with depression. © 2015 The New York Times Company
Neel V. Patel The concept of the insanity defense dates back to ancient Greece and the Roman Empire. The idea has always been the same: Protect individuals from being held accountable for behavior they couldn’t control. Yet there have been more than a few historical and recent instances of a judge or jury issuing a controversial “by reason of…” verdict. What was intended as a human rights effort has become a last-ditch way to save killers (though it didn’t work for James Holmes). The question that hangs in the air at these sort of proceedings has always been the same: Is there a way to make determinations more scientific and less traditionally judicial? Adam Shniderman, a criminal justice researcher at Texas Christian University, has been studying the role of neuroscience in the court system for several years now. He explains that neurological data and explanations don’t easily translate into the world of lawyers and legal text. Inverse spoke with Shniderman to learn more about how neuroscience is used in today’s insanity defenses, and whether this is likely to change as the technology used to observe the brain gets better and better. Can you give me a quick overview of how the role of neuroscience in the courts, has changed over the years? Especially in the last few decades with new advances in technology. Obviously, [neuroscientific evidence] has become more widely used as brain-scanning technology has gotten better. Some of the scanning technology we use now, like functional MRI that measures blood oxygenation as a proxy for neurological activity, is relatively new within the last 20 years or so. The nature of brain scanning has changed, but the knowledge that the brain influences someone’s actions is not new.
Alison Abbott Only a decade ago, the idea that Alzheimer’s disease might be transmissible between people would have been laughed off the stage. But scientists have since shown that tissues can transmit symptoms of the disease between animals — and new results imply that humans, at least in one unusual circumstance, may not be an exception. The findings, published in this issue of Nature, emerged during autopsy studies of the brains of eight people who had died of the rare but deadly Creutzfeldt–Jakob disease (CJD; Z. Jaunmuktane et al. Nature 525, 247–250; 2015). They contracted it decades after treatment with contaminated batches of growth hormone that had been extracted from the pituitary glands of human cadavers. Six of the brains, in addition to the damage caused by CJD, harboured the tell-tale amyloid pathology that is associated with Alzheimer’s disease. “This is the first evidence of real-world transmission of amyloid pathology,” says molecular neuroscientist John Hardy of University College London (UCL). “It is potentially concerning.” If confirmed, the findings raise the spectre that tens of thousands of other people treated with the human growth-hormone (hGH) extracts might be at risk of Alzheimer’s. And although there is no suggestion that Alzheimer’s could be contracted through normal contact with patients, some scientists worry that the findings may have broader implications: that Alzheimer’s could be passed on by other routes through which CJD can be transmitted, such as blood transfusions or contaminated surgical instruments. © 2015 Nature Publishing Group
Sara Reardon Antipsychotic drugs are widely used to blunt aggressive behaviour in people with intellectual disabilities who have no history of mental illness, a UK survey of medical records finds, even though the medicines may not have a calming effect. The finding is worrisome because antipsychotic drugs can cause severe side effects such as obesity or diabetes. Psychiatry researcher Rory Sheehan and colleagues1 at University College London studied data from 33,016 people with intellectual disabilities from general-care practices in the United Kingdom over a period of up to 15 years. The researchers found that 71% of 9,135 people who were treated with antipsychotics had never been diagnosed with a severe mental illness, and that the drugs were more likely to be prescribed to those who displayed problematic behaviours. “We suspected that this would be the case, but we didn’t know the true extent,” Sheehan says. “We should be worried because the rates are high,” says James Harris, a psychiatrist at Johns Hopkins University in Baltimore, Maryland. But he adds that it is hard to determine whether treatment with antipsychotics is appropriate without knowing what other forms of treatment were available to people in the study. It is possible that medication was the only option available or that it was used to dampen a person's behaviour enough that they could participate in therapy or other types of treatment. Evidence suggests that the drugs are not effective at treating aggressive and disruptive behaviour, says psychiatrist Peter Tyrer of Imperial College London. I © 2015 Nature Publishing Group
By Simon Makin Scientists claim to have discovered the first new human prion in almost 50 years. Prions are misfolded proteins that make copies of themselves by inducing others to misfold. By so doing, they multiply and cause disease. The resulting illness in this case is multiple system atrophy (MSA), a neurodegenerative disease similar to Parkinson's. The study, published August 31 in Proceedings of the National Academy of Sciences, adds weight to the idea that many neurodegenerative diseases are caused by prions. In the 1960s researchers led by Carleton Gajdusek at the National Institutes of Health transmitted kuru, a rare neurodegenerative disease found in Papua New Guinea, and Creutzfeldt–Jakob disease (CJD), a rare human dementia, to chimpanzees by injecting samples from victims' brains directly into those of chimps. It wasn't until 1982, however, that Stanley Prusiner coined the term prion (for “proteinaceous infectious particle”) to describe the self-propagating protein responsible. Prusiner and colleagues at the University of California, San Francisco, showed this process caused a whole class of diseases, called spongiform encephalopathies (for the spongelike appearance of affected brains), including the bovine form known as “mad cow” disease. The same protein, PrP, is also responsible for kuru, which was spread by cannibalism; variant-CJD, which over 200 people developed after eating beef infected with the bovine variety; and others. The idea that a protein could transmit disease was radical at the time but the work eventually earned Prusiner the 1997 Nobel Prize in Physiology or Medicine. He has long argued prions may underlie other neurodegenerative diseases but the idea has been slow to gain acceptance. © 2015 Scientific American
Depressed people who display "risky behaviour", agitation and impulsivity are at least 50% more likely to attempt suicide, a study has found. Research by the European College of Neuropsychopharmacology (ECNP) concluded that the behaviour patterns "precede many suicide attempts". The study said effective prevention measures were "urgently needed". The World Health Organisation estimates that there were more than 800,000 suicides worldwide in 2012. The ECNP study evaluated 2,811 patients suffering from depression, of whom 628 had previously attempted suicide. Researchers "looked especially at the characteristics and behaviours of those who had attempted suicide", and found that "certain patterns recur" before attempts. They said the risk of an attempt was "at least 50% higher" if a depressed patient displayed: "risky behaviour" such as reckless driving or promiscuous behaviour "psychomotor agitation" such as pacing around rooms or wringing their hands impulsivity - defined by the researchers as acting with "little or no forethought, reflection, or consideration of the consequences" Dr Dina Popovic, one of the report's authors, added: "We found that 'depressive mixed states' often preceded suicide attempts. "A depressive mixed state is where a patient is depressed, but also has symptoms of 'excitation', or mania." © 2015 BBC.
Link ID: 21364 - Posted: 08.31.2015
By Roni Caryn Rabin Q: Is it harmful to go on and off antidepressants a few times a year? I seem to respond quickly and quite well to S.S.R.I.'s. I don't desire to be on them long-term, but would like to use them occasionally, to get through a rough patch like a stressful quarter at work. Is it harmful to go on and off of S.S.R.I.'s a few times a year? Yes, it may be harmful. You should always start and stop medication “under a physician’s supervision. Don’t do it on your own,” said Dr. Renee Binder, president of the American Psychiatric Association. It usually takes at least four weeks for an antidepressant to take effect, and patients should give themselves several weeks to taper off a drug when ending treatment. Starting and quitting abruptly expose you to the risks of initiation and withdrawal. Also, you may not get sustained relief from your depression. Antidepressants “don’t work right away,” Dr. Binder said. “It’s the kind of medication that you have to take every single day, and it takes awhile to build up in your body before it starts working.” When starting antidepressants, patients may experience anxiety and agitation and develop other transient side effects like headaches and nausea. Teenagers need close monitoring because they may be at a higher risk of suicide when starting treatment, some studies suggest. It also may take time for your doctor to find the antidepressant and dose that’s right for you. Withdrawal can trigger troubling symptoms like nausea, dizziness and “brain zaps,” a sensation that feels like electric shocks to the head. It can also trigger psychological problems like anxiety, irritability, moodiness and changes in appetite and sleep that mimic depression or may signal a recurrence. Some patients may become paranoid or suicidal. © 2015 The New York Times Company
Link ID: 21363 - Posted: 08.31.2015
By Lily Hay Newman Mental health issues manifest in a number of ways, and they're not all behavioral. Increasingly, scientists are using speech analysis software to detect subtle changes in voice acoustics and patterns to detect or even predict potentially problematic conditions. A study published Wednesday in NPG-Schizophrenia by researchers at Columbia University Medical Center, the New York State Psychiatric Institute, and IBM's T. J. Watson Research Center found that digital speech analysis correctly predicted whether 34 youths at risk for mental illness (11 female, 23 male) would develop psychosis within 2.5 years. The system, which evaluated the study participants quarterly, correctly predicted all of their outcomes; five became psychotic. The algorithm evaluated transcripts for predictive "semantic and syntactic features" like coherence and phrase length. "These speech features predicted later psychosis development with 100% accuracy, outperforming classification from clinical interviews," the researchers wrote. Clinicians are able to accurately categorize patients as "at-risk," but within that subpopulation it is difficult to determine who will actually experience psychosis and potentially develop schizophrenia. If voice recognition software can help identify these individuals, they may be able to receive more effective care. "Computerized analysis of complex human behaviors such as speech may present an opportunity to move psychiatry beyond reliance on self-report and clinical observation toward more objective measures of health and illness in the individual patient," the researchers wrote. © 2015 The Slate Group LLC.
Link ID: 21362 - Posted: 08.31.2015
We all have days when we feel like our brain is going at a snail’s pace, when our neurons forgot to get out of bed. And psychologists have shown that IQ can fluctuate day to day. So if we’re in good health and don’t have a sleep deficit from last night’s shenanigans to blame, what’s the explanation? Sophie von Stumm, a psychologist at Goldsmiths University, London, set about finding out. In particular, she wanted to know whether mood might explain the brain’s dimmer switch. Although it seems intuitively obvious that feeling low could compromise intellectual performance, von Stumm says research to date has been inconclusive, with some studies finding an effect and others not. “On bad mood days, we tend to feel that our brains are lame and work or study is particularly challenging. But scientists still don’t really know if our brains work better when we are happy compared to when we are sad.” To see if she could pin down mood’s effect on IQ more convincingly, von Stumm recruited 98 participants. Over five consecutive days they completed questionnaires to assess their mood, as well as tests to measure cognitive functions, such as short-term memory, working memory and processing speed. Surprisingly, being in a bad mood didn’t translate into worse cognitive performance. However, when people reported feeling positive, von Stumm saw a modest boost in their processing speed. © Copyright Reed Business Information Ltd.
By Amy Ellis Nutt Magnetic pulses from a device applied to the head appear to "reset" the brains of depressed patients, according to a new study from the United Kingdom. The circuitry in a part of the right prefrontal cortex is known to be too active in depressed patients, causing excessive rumination and self absorption and impaired attention. When the TMS was applied to healthy subjects in this study, the activity in that region slowed. "We found that one session of TMS modifies the connectivity of large-scale brain networks, particularly the right anterior insula, which is a key area in depression," lead scientist Sarina Iwabuchi, told the European College of Neuropsychology at a conference in Amsterdam this week. This was the first time an MRI was used to guide the TMS impulses and, at the same, time measure subtle changes in brain circuit activity. In addition, the researchers used magnetic resonance spectroscopy to analyze subjects' brain chemistry. "We also found that TMS alters concentrations of neurotransmitters. Iwabuchi said, "which are considered important for the development of depression," and which are the targets of most current antidepressant medications. Transcranial Magnetic Stimulation is the use of an electromagnetic coil to deliver small, powerful bursts of energy to targeted areas known to be involved in mood regulation. It is a painless, non-invasive treatment than involves no drugs, no IVs, or any other kind of sedation, and whose chief possible side effect is a headache. (The Food and Drug Administration approved limited use of TMS in 2008 for the treatment of depression.)
Link ID: 21352 - Posted: 08.28.2015
By Felicity Muth You might have heard of serotonin as one of the ‘happy’ hormones in humans. Indeed, mood disorders like anxiety and depression are associated with low levels of serotonin. However, this neurotransmitter also has other functions. One of the more interesting ones in humans is its role in cooperation. Lowering the serotonin levels of people increases peoples’ reactions to unfairness and makes them less cooperative. On the other hand, increasing the level of serotonin in people makes people less argumentative and more communicative and cooperative. Serotonin also plays a role in peoples’ intimate relationships, for example men and women who were fed tryptophan (necessary for serotonin production) were more likely to judge photos of couples as intimate and romantic than people who had not been fed tryptophan. Humans are of course not the only animals that form intimate relationships or cooperate with each other. One of the best examples of unrelated animals cooperating comes from cleaner fish, who form relationships with ‘clients’ (visiting reef fish) where they clean their bodies, gills and even mouths. This relationship is very cooperative: the cleaner fish would rather eat the mucus from the skin of their clients than the ectoparasites (it’s yummier, apparently), but they usually keep this particular urge under control. In return, the clients don’t eat the cleaner fish, even when they are cleaning the inside of their mouths and one might think that it would be pretty tempting just to swallow one. Of course, cleaner fish do ‘cheat’ occasionally, taking a bite from the skin of a client, making the client jolt away and probably choose not to return to that particular cleaner again. © 2015 Scientific American
Sara Reardon Some of the people who survived Hurricane Katrina lost loved ones, and many were made homeless by the storm. New Orleans still bears the scars of Hurricane Katrina, ten years later. More than 500,000 people fled when the storm hit, and many never returned. Large swathes of the city are sparsely populated, particularly in the poor neighbourhoods that suffered the most severe flood damage. Psychological scars linger, too. Many hurricane survivors continue to experience mental-health problems related to the storm, whether or not they returned to New Orleans, say researchers tracking Katrina’s psychological aftermath. Such work could ultimately aid people affected by future disasters, by identifying factors — such as lack of a social-support network and unstable environments for children — that seem to increase risk of mental-health trauma. “What’s unique about this disaster is the magnitude of it,” says Joy Osofsky, a clinical psychologist at Louisiana State University in New Orleans. Katrina, a category 3 hurricane when it made landfall on 29 August 2005, ultimately damaged an area the size of the United Kingdom. In New Orleans, it destroyed basic resources such as schools and health clinics to a degree unparalleled in recent US history. Osofsky saw the devastation and despair first hand. With their clinics flooded after the storm, she and other mental-health experts set up treatment centres for emergency responders on cruise ships docked nearby on the Mississippi River, and an emergency psychology unit at the city’s central command centre. Osofsky says that the centres treated thousands of displaced and traumatized people. © 2015 Nature Publishing Group
By Laura Sanders By tweaking a single gene, scientists have turned average mice into supersmart daredevils. The findings are preliminary but hint at therapies that may one day ease the symptoms of such disorders as Alzheimer’s disease and schizophrenia, scientists report August 14 in Neuropsychopharmacology. The altered gene provides instructions for a protein called phosphodiesterase-4B, or PDE4B, which has been implicated in schizophrenia. It’s too early to say whether PDE4B will turn out to be a useful target for drugs that treat these disorders, cautions pharmacologist Ernesto Fedele of the University of Genoa in Italy. Nonetheless, the protein certainly deserves further investigation, he says. The genetic change interfered with PDE4B’s ability to do its job breaking down a molecular messenger called cAMP. Mice designed to have this disabled form of PDE4B showed a suite of curious behaviors, including signs of smarts, says study coauthor Alexander McGirr of the University of British Columbia. Compared with normal mice, these mice more quickly learned which objects in a cage had been moved to a new location, for instance, and could better recognize a familiar mouse after 24 hours. “The system is primed and ready to learn, and it doesn’t require the same kind of input as a normal mouse,” McGirr says. These mice also spent more time than usual exploring brightly lit spaces, spots that normal mice avoid. But this devil-may-care attitude sometimes made the “smart” mice blind to risky situations. The mice were happy to spend time poking around an area that had been sprinkled with bobcat urine. “Not being afraid of cat urine is not a good thing for a mouse,” McGirr says. © Society for Science & the Public 2000 - 2015
Helen Thomson Serious mood disorders such as bipolar may be the price humans have had to pay for our intelligence and creativity. That’s according to new research which links high childhood IQ to an increased risk of experiencing manic bipolar traits in later life. Researchers examined data from a large birth cohort to identify the IQ of 1,881 individuals at age eight. These same individuals were then assessed for manic traits at the age of 22 or 23. The statements they provided were part of a checklist widely used to diagnose bipolar disorder. Each person was given a score out of 100 related to how many manic traits they had previously experienced. Individuals who scored in the top 10% of manic features had a childhood IQ almost 10 points higher than those who scored in the lowest 10%. This correlation appeared strongest for those with high verbal IQ. “Our study offers a possible explanation for how bipolar disorder may have been selected through generations,” said Daniel Smith of the University of Glasgow , who led the study. “There is something about the genetics underlying the disorder that are advantageous. One possibility is that serious disorders of mood - such as bipolar disorder - are the price that human beings have had to pay for more adaptive traits such as intelligence, creativity and verbal proficiency.” Smith emphasises that as things stand, having a high IQ is only an advantage: “A high IQ is not a clear-cut risk factor for bipolar, but perhaps the genes that confer intelligence can get expressed as illness in the context of other risk factors, such as exposure to maternal influenza in the womb or childhood sexual abuse.” © 2015 Guardian News and Media Limited
Dean Burnett Yesterday, an article in the Entrepreneurs section of the Guardian purported to reveal a “cloth cap that could help treat depression”. This claim has caused some alarm in the neuroscience and mental health fields, so it’s important to look a little more closely at what the manufacturers are actually claiming. The piece in question concerns a product from Neuroelectrics: a soft helmet containing electrodes and sensors. According to the company’s website, it can be used to monitor brain activity (electroencephalography, or EEG), or administer light electrical currents to different areas of the brain in order to treat certain neurological and psychiatric conditions (known as transcranial direct current stimulation or tDCS). While this would obviously be great news to the millions of people who deal with such conditions every day, such claims should be treated with a considerable amount of caution. The fields of science dedicated to researching and, hopefully, treating serious brain-based problems like depression, stroke, personality disorder etc. work hard to find new and inventive methods for doing so, or refining and improving existing ones. Sometimes they succeed, but probably not as often as they’d like. The problem is that when a new development occurs or a new approach is found, it doesn’t automatically mean it’s widely applicable or even effective for everyone. The brain is furiously complicated. There is no magic bullet for brain problems [Note: you shouldn’t use bullets, magic or otherwise, when dealing with the brain]. © 2015 Guardian News and Media Limited
Link ID: 21305 - Posted: 08.18.2015
By NICHOLAS BAKALAR “Insanity Treated By Electric Shock” read the headline of an article published on July 6, 1940, in The New York Times. The article described “a new method, introduced in Italy, of treating certain types of mental disorders by sending an electric shock through the brain.” It was the first time that what is now called electroconvulsive therapy, or ECT, had been mentioned in The Times. The electric shock, the article said, “is produced by a small portable electric box which was invented in Italy by Professor Ugo Cerletti of the Rome University Clinic.” Dr. S. Eugene Barrera, the principal researcher on the project, “emphasized that hope for any ‘miracle cure’ must not be pinned on the new method.” On April 29, 1941, the subject came up again, this time in an article about a scientific meeting at which a professor of psychiatry at Northwestern reported “ ‘very promising instantaneous results’ in the recently developed electric shock method of relieving schizophrenic patients of their malady.” The treatment entered clinical practice fairly quickly. In October 1941, The Times reported on the opening of several new buildings at Hillside Hospital in Queens (today called Zucker Hillside Hospital). “The hospital has pioneered in the use of insulin and metrazol, and also in the electric shock treatment, which has proved useful in shortening the average stay of patients,” the article read. Over the years, ECT has had its ups and downs in the public imagination and in the pages of The Times. In an article on Nov. 25, 1980, the reporter Dava Sobel seemed to relegate it to another age. © 2015 The New York Times Company
Link ID: 21304 - Posted: 08.18.2015
There may finally be a way to stop people progressing beyond the first signs of schizophrenia – fish oil. When people with early-stage symptoms took omega-3 supplements for three months, they had much lower rates of progression than those who did not, according to one small-scale trial. People with schizophrenia are usually diagnosed in their teens or 20s, but may experience symptoms for years beforehand, such as minor delusions or paranoid thoughts. Only about a third of people with such symptoms do go on to develop psychosis, however, and antipsychotic drugs can cause nasty side effects, so these are rarely given as a preventative. Fish oil supplements, which contain polyunsaturated fatty acids like omega-3, may be a benign alternative. These fatty acids may normally help dampen inflammation in the brain and protect neurons from damage, and lower levels in the brain have been implicated in several mental illnesses. Tests have found that people with schizophrenia have lower levels of these fatty acids in their blood cells, suggesting the same could be true for their brain cells. Fish oil supplements have been investigated as a treatment for adults with schizophrenia, but so far results have been mixed – four trials found no benefit while another four found a small reduction in symptoms. But a study that gave omega-3 fish oil pills to younger people suggests that what matters is catching the condition in time. The trial followed 81 people aged 13 to 25 with early signs of schizophrenia. Roughly half took fish oil pills and half took placebo tablets for three months. A year later, those given fish oils were less likely to have developed psychosis. © Copyright Reed Business Information Ltd.
Link ID: 21288 - Posted: 08.12.2015
By Ariana Eunjung Cha Everyone knows that a diet full of white bread, pasta and rice is bad for your waistline. Now scientists say these types of refined carbs could also impact your mind — putting post-menopausal women at higher risk for depression. In a new study published in the the American Journal of Clinical Nutrition, researchers looked at data from more than 70,000 women who participated in the National Institutes of Health's women's health initiative between 1994 and 1998. They found that the more women consumed added sugars and refined grains and the higher their score on the glycemic index (GI) — a measure of the rate carbohydrates are broken down and absorbed by the body — the more they were at risk of new-onset depression. Those who had a different sort of diet — one with more dietary fiber, whole grains, vegetables and non-juice fruits — had a decreased risk. "This suggests that dietary interventions could serve as treatments and preventive measures for depression," wrote James Gangswisch, an assistant professor of psychiatry at Columbia University Medical Center, and his co-authors. The researchers explained that refined foods trigger a hormonal response in the body to reduce blood sugar levels. That is believed to lead to the "sugar high" and subsequent "crash" some people say they feel after eating such foods. This can lead to mood changes, fatigue and other symptoms of depression.