by S. C.

It is estimated that about 10 to 15 percent of children and teens are depressed at any given time. Research indicates that one of four adolescents will have an episode of major depression during high school. According to a report of the surgeon general, suicide is the leading cause of death for ages 10 to 24 in America. And, preschoolers are the fastest-growing market for antidepressant medications.1 while pundits theorize about possible causes of this alarming trend, one root factor has been overlooked. According to a recent study published in the March 2012 issue of Public Health Nutrition consumption of fast foods such as hamburgers, hot dogs, sausages, and pizza as well as processed pastries including muffins, croissants, and doughnuts is linked to an increase in depression symptoms.2 The results reveal that consumers of fast food, compared to those who eat little or none, are 51% more likely to develop depression. furthermore, a dose-response relationship was observed, which means when more fast food is consumed, the risk of developing depression symptoms increases. Standard Antidepressant Treatments are Inadequate The use of Paroxetine (Paxil) and other standard SSRI (selective serotonin reuptake inhibitors) antidepressant medications (Prozac, Zoloft) continues to grow by about 10% annually among children and adolescents.3 However, antidepressants have been revealed to have serious risks ? especially for children- and are linked to violence, psychosis, abnormal bleeding and brain tumors.4 but the most alarming finding is the association of antidepressant drug usage in youth with increased risk of suicides.5 even the Food and Drug Administration (FDA) has published reports saying “these drugs are associated with a risk of suicidal behavior in children”.6 An Alternative Approach for Depression Symptoms clearly alternative solutions must be sought out and used by parents whose children or teenagers suffer from depression symptoms. Can diet changes alone make enough of a difference? Most integrative physicians work with parents to add both diet changes and some specific mood boosting nutrients. Natural Health Advisory Institute, a leader in validated natural health education for the public has detailed five key actions parents can take to help their children overcome their depression symptoms without the use of pharmaceutical drugs. These practical and effective steps can be found in the free report, Natural Remedies for Depression. The report describes how to increase serotonin ? the ?happy? neurotransmitter ? levels naturally, how to increase dopamine ? the focus and motivation neurotransmitter ? levels naturally and more. To receive the free digital report, Natural Remedies for Depression, visit link esterno Natural Health Advisory Institute continually strives to provide the proactive health consumer with actionable information on natural health remedies which have received clinical research validation or have been recommended by leading integrative medicine physicians.

[1] Mental Health: A Report of the Surgeon General. [2] Almudena S?nchez-Villegas, Estefan?a Toledo, Jokin de Irala, Miguel Ruiz-Canela, Jorge Pla-Vidal and Miguel A Mart?nez-Gonz?lez. “Fast-food and commercial baked goods consumption and the risk of depression.” Public Health Nutrition: page 1 of 9 doi:10.1017/S1368980011001856. [3] Psychiatric Services, April 2004. [4] W. Meijer, et al. ?Association of Risk of Abnormal Bleeding with Degree of Serotonin Reuptake Inhibition by Antidepressants.? Archives of Internal Medicine 2004, 164:2367-2370. [5] Olfson M, Marcus SC, Shaffer D (2006). ?Antidepressant drug therapy and suicide in severely depressed children and adults.? Arch Gen Psychiatry 63:865-872. [6] S. Vedantam. ?FDA Links Antidepressants, Youth Suicide Risk.? Washington Post, 23 February, 2004, page A01.

by S. C. 09 may 2012 Teatro Naturale International n. 5 Year 4 © REPRODUCTION RESERVED

Scientists say they have developed the first blood test to diagnose major depression in teenagers.  the test is also able to differentiate between at least two subtypes of depression: major depression and major depression combined with anxiety disorder.

Currently, doctors and psychiatrists diagnose depression solely by relying on the patient to recount his or her own symptoms.  Then, the doctor must interpret the patient’s descriptions to decide whether or not the patient is depressed.

However, Northwestern University researchers say a new blood test is able to identify certain ‘gene expression markers’ that can objectively diagnose the depression in teenagers.

“For someone who is depressed, basically every aspect of his or her cognition, perception, mood and ability to interact socially is somewhat impaired,” lead researcher Dr. Eva Redei, a professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine, told FoxNews.com.  “At the moment, diagnosis relies on a structured interview between the doctor and patient – which is not necessarily an objective description of what’s happening.”

Redei said she doesn’t expect the test will eliminate the doctor/patient interviews, but rather, act as a supplement to them.

“[This test] is not to replace psychiatrists’ interviews or their knowledge in that regard, just like a blood glucose test to diagnose diabetes doesn’t replace an endocrinologist,” Redei added.  “It merely helps to inform.  the idea is to give the same chance to depressed patients – of which there are many – which we are giving to other patients for hypertension, diabetes, etc.”

The test, developed over a period of more than 10 years, first identified 26 potential markers (called messenger RNA) for depression based on animal studies of severely depressed and anxious rats.   

Further research in humans found that 11 of those markers could be used to distinguish between depressed and non-depressed patients.  the levels of the 11 markers were typically below average range in the depressed patients.

In addition, another set of 12 markers, combined with six of the depression markers, identified the patients who suffered from anxiety as well as depression.

In the most recent study, Redei and her colleagues tested the blood analysis on 28 participants, 14 of whom had been previously diagnosed with major depression and 14 who were not depressed.  

Redei’s co-author Dr. Brian Andrus, who was blind to the participants’ diagnoses, was able to use the blood test by itself to accurately determine which participants had depression and which did not.  Furthermore, in the pool of depressed patients, Andrus was also able to make the distinction between those who also suffered from anxiety and those who did not.

The next steps are to extend the study to wider patient populations and determine if the test can accurately diagnose depression in adults as well, Redei said. However, she emphasized the long-term goal is not only to provide doctors with a tool to objectively diagnose patients, but also to remove the stigma of depression and better personalize treatment.

Currently, Redei said, there is some shame associated with being diagnosed with depression because patients can feel as if their inability to improve their mood is their own fault.  However, she hopes with a blood test proving that depression is in part rooted in genetics, outside of a patient’s own control, the stigma of the disease can be lifted.  

“One of the major goals of identifying biomarkers for depression is once you can measure it in a similar way as you would diabetes, you are at least partially removing the stigma, because it’s very difficult to say something like, ‘Get yourself together and control your liver function,” Redei said.  “It’s something you can objectively detect and follow and bring into the realm of medicine.”

Once depression is brought into this objective realm of medicine, then it is also easier to distinguish between more subtypes of the disease and treat them accordingly.

“In the future, we could be able to define depression much more profoundly and clearly with a blood test,” Redei said.  “It could explain why some drugs work for some patients and not for others.  It’s also could help develop new types of antidepressants.  right now, we are guessing.  even the best psychiatrists can’t do anything but prescribe one to three different types of drugs or treatments based on prior experience and trial-and-error.”

Part of the complexity involved in treating depression is that it can manifest in many different ways, according to Redei.  Current criteria dictates a person can have a depressed mood in combination with nine different symptoms – but only four or five of the those symptoms need to be present, in any combination, for a patient to qualify as depressed.

“That immediately tells you there’s a large number of potential variations [of depression],” Redei said. “The future goal is to find out whether there are more subtypes of depression, whether we can diagnose them, and whether we can develop treatment paradigms that work better [for those subtypes].”

“The future is really personalized medicine for every disease, and depression is not an exception,” she added.  

Scottsdale, AZ (PRWEB) April 18, 2012

New research out of Scotland’s University of Sterling, published this month in the journal Mental Health and Physical Activity showed that walking had a “large effect” on reducing the symptoms of depression. The challenge, especially among those currently experiencing symptoms of depression, is motivating individuals to move more throughout the day. TrekDesk Treadmill Desks make walking automatic, requiring no extra motivation or time out of the day.

The researchers analyzed more than 14,672 articles focusing on eight trials involving 341 patients. Study results reported that walking posed a significant effect on depression symptoms but cautioned that individuals should undertake walking regimens under the supervision of physicians if their aim is to eradicate symptoms of depression.

A CDC report on the mental health of Americans showed an estimated 9% of U.S. adults meet the criteria for clinical depression. The state by state breakdown reported the lowest rate in North Dakota at 4.8% and the highest rate of depression in Mississippi at 14.8%. A regional breakdown showed the highest rates of adult depression in the Southeast.

Lela McKnight-Eily, a clinical psychologist and epidemiologist at the CDC related these higher concentrations may be due to higher rates of obesity, heart disease, stoke and sleep patterns all of which are caused in part by sedentary lifestyles. these conditions are mitigated by continual daily movement as offered by the TrekDesk Treadmill Desk.

This is not the first study to show the curative powers of walking and its effect on depression. A major study, published in the American Journal of Preventive Medicine, showed that adults aged 20 to 45 with mild to moderate depression who participated in 30-minute aerobic exercise sessions three to five times a week reduced their symptoms by almost 50 percent. Studies at Harvard University found similar results and found that symptoms were impacted in as little as three weeks and walking was more effective than the most commonly prescribed drugs to fight depression. all studies stressed the importance of physician care and oversight to monitor the patient.

“The list of health conditions exacerbated by lack of physical activity should not surprise us any longer,” stated TrekDesk CEO Steve Bordley. “We should be looking into the rates of depression that are a direct result of sedentary lifestyles, that would be an eye opener to say the least.”

About TrekDesk Treadmill Desks: Designed to fit any existing treadmill, TrekDesk treadmill desk is an affordable, full sized, height adjustable workstation that allows individuals the opportunity to gain the necessary amount of exercise daily to maintain health, prevent disease, strengthen muscles, boost mood and productivity, without requiring additional time during the day or extra motivation. Let TrekDesk show you how to workout at work.

TrekDesk is currently available for sale online at trekdesk.com.

Join the TrekDesk “Movement Revolution” to learn more, win a free TrekDesk or ask any health related questions anytime at facebook.com/trekdesk, or follow TrekDesk on twitter -twitter.com/trekdesk.

Read the full story at prweb.com/releases/2012/4/prweb9417522.htm

His defense attorney has described the crimes as violent, sadistic and disgusting — and this week we’ve heard testimony from several victims, including two elderly women from Leon County, who claim they were burglarized and sexually assaulted in 2009 by the Twilight Rapist — a man who is pleading not guilty by insanity because he says he suffers from multiple personality disorder. The Leon County District Attorney believes those claims — are a bluff.

Underneath his dark brown suit and button-up shirt, you’ll find a belt wrapped around Billy Joe Harris’ torso. It’s not just any old belt — in fact, Alan Cohen, Harris’ defense attorney says it’s a belt filled with electricity and at the push of a button can send a shock that would render anyone helpless. The ‘stun belt’ is required for his client after several outbursts and physical disruptions he caused during his first trial in Edna, Texas in 2010.

Since the start of what has become his second trial, of potentially many more to come, Billy Joe Harris’ demeanor has been far from disruptive. in fact, the only movement is demonstrated as his head occasionally twitches and trembles; or if the shackled and chained convicted felon is being personally escorted out of the courtroom by security during recess.

As each victim took an oath of honesty before testifying, Harris appeared alert and attentive while sitting in a wooden chair. but that changed at 2:15 Wednesday as witness number 46 took the stand – Harris lowered his head and didn’t raise it back up until her 47 minute testimony was over.

Witness number 46 is more than just a number. she is an 82-year-old woman from Yoakum, Texas who dropped out of school in 7th grade to help her family earn money on their chicken farm. “Me and my mom, we had a whole lot of eggs to clean, 2,000 eggs at that, and we had to clean them really thoroughly,” she said.

Her whole life she’s taken care of people; growing up she took care of 28 children at a local nursery and as an adult, till this very day, she works for home healthcare, caring for the elderly. she admits she’s never ridden or driven a car in her life – but that all changed after the events that allegedly took place on November 9, 2009.

“He walked right through my front door like he owned the place, and I was just sitting at the edge of my couch and I just said, ‘Who are you, what do you want?’ he was wearing all black, with black gloves and he pushed me on the ground and I could hardly breathe. he was pushing on my rib cage so hard I thought they were going to crack; his hand was trembling and he forced my clothes off,” she recalled. “I asked him, ‘Why are you doing this to me?’ and he said in a very menacing voice, ‘I like little old ladies.’ “

The woman moved several blocks away shortly after the alleged assault. but Harris allegedly found his way back to her new home two weeks later. “I woke up around 5 that morning to the sound of something rocking a chair, and he was in my room naked, and he said, ‘Remember me? did you miss me?’ And I told him that my son was on his way and he was going to get caught, and he said ‘No, you’re lying, you don’t have no kids.’”

She didn’t have kids, nor was she ever married. but the victim admitted she would make up information during the alleged assault to distract him, but he would always correct her. “It was like he knew everything about me,” she said. “He knew where everything was in my house too, every single small detail.”

ThursdayQuestions surrounding the validity of Harris’ claims of schizophrenia and multiple personality disorder surfaced after being convicted to life in prison in 2010. according to a testimony from a state psychiatrist Thursday, Harris never sought treatment for these medical conditions he claimed to have since the death of his dog in the early 1990’s.

The Leon County District Attorney asked the psychiatrist if it was common for inmates to fake illnesses or mental disorders in prison. he responded, “Yes – absolutely. they do this as a secondary gain; to get medication to help them sleep, to go to sky-view for air-conditioning, to avoid field work.”

The psychiatrist said Harris showed symptoms of depression, not schizophrenia. “If you take psychosis medication and you do not mentally need the medication, then the affects would make that person very calm, and sleepy.”

He said schizophrenia symptoms are distorted thoughts and hallucinations and usually start at a young age, “Typically in your early 20’s,” he said.

“In my experience, although not impossible, it is uncommon for an adult, age 40, to show symptoms of schizophrenia,” he said.

Harris’ defense attorney has argued his client’s condition was brought on during childhood after being exposed to pornography, bestiality as a teen, and child abuse.

In the Edna courtroom in 2010, Harris’ defense attorney said his client has at least four different personalities: “David the dog” is the personality who commits the crime; and “Bobby” is the mastermind.

Earlier this week during testimony from an 80-year-old Marquez victim, she claimed while Harris was sexually assaulting her, “I said to him, ‘Why are you doing this to me, I’m an old woman,’ and he said, ‘I know all about you, I’m Bobby Dawn, I’m 70-years-old and I live right behind you,’ and I just started screaming and fighting back,” she said. “I don’t have a neighbor named Bobby, and this man that was doing this to me, wasn’t 70-years-old.”

Prosecutors Question Harris’ Motive

Harris’ motive for these alleged crimes has been a significant debate during the trial in Walker County. during each alleged sexual assault, each victim claims he broke into their home twice in a two week period. The first time, they say, he would steal money, personal belongings such as deer-mounts, clocks, keys, computers, firearms, and checkbooks.

Those items, Texas Rangers say, were found inside Harris’ vehicle and many inside his Missouri City home where his wife and step-son lived.

The stolen items were strategically placed inside his home; an FBI agent who testified Wednesday said “Being able to see these items inside the home would conceivably be a reminder of the sexual assault,” the FBI agent said. “They get to relive the memories over and over again, so, in some cases, it’s not economic gain, rather fulfilling pride each time they see the victims’ belongings . The items resemble ‘trophies’ or ‘souvenirs’ to this individual.”

Investigators say dozens of keys to the homes of many of the victims were located inside a wooden box inside Harris’ home.

A Yoakum victim who claims Harris sexually assaulted her twice — on two different occasions — testified Wednesday saying Harris stole her entire life savings of $11,000. during a testimony later that day, Harris’ former roommate claimed he asked her to deposit three increments of $4,000 inside his bank account. The Leon County District Attorney asked her if she ever questioned how he got the money, and she replied, “He would never tell me, so I just did what he told me.”

The Yoakum victim says she never got her money back.

Trial will resume Monday. News 3’s Nicole Morten will bring you the latest information from the Twilight Rapist Trial.

Many ?f the government student loan programs require n? credit check ?nd w?ll provide students w?th substantial financial aid. however th??e programs are n?ed based and norm?lly carry additional criteria that ma? make ?t hard t? qualify. Even when students do qualify, th? loans w?ll only cover a portion ?f the total education bill ?n the majority ?f cases. if students ?r? caught ?n th?s position then the? ?ould lo?k t? private alternative student loans t? meet th? shortfall.

Private alternative student loans t?o hav? th??r own difficulties. A credit check i? alm?st universally required and th?s i? not a problem a? long ?s ??u h?ve ? good credit history. the problem is th?t ‘good’ ?? v?ry mu?h a relative term ?nd if y?ur credit history is not good en?ugh then ?ou may find that y?u ar? paying m?re th?n th? normal rates of interest.

As w?ll ?s the stated interest rate there ar? further monetary implications of private alternative loans. Fees will oft?n be added ?n to nominal loan amounts ?nd ? r??sonabl? modest loan of $3,000 might easily h?ve fees of 4% added prior to distribution. that means $120 of th? total loan ?s n?ver seen by th? borrower but nev?rthel??s h?d got to be paid back. As a guide, ?v?r? 3% of fees ?s equal t? 1% on top of th? normal interest rate.

Private alternative loans do carry ?ne or tw? advantages.

The f?rst ?nd prob?bl? most obvious advantage i? th?t money i? readily available. Private lenders make a profit from the interest and fees that they charge ?nd s? h?ve an interest ?n making money ava?lable t? borrowers and w?ll work hard to ensure th?t ever? applicant qualifies. on the ?ther hand Federal lenders operate t? ? rigid set of criteria ?nd th?r? is usu?ll? no appeal if ??ur loan application ?? denied.

Not h?ving to deal w?th that cold ?nd frequently illogical bureaucracy ?? an?th?r benefit ?f private loans. Private lenders operate customer service departments th?t exist specifically to deal w?th questions ?o that customers ??n g?t the answers that th?? need. Federal loan programs u?uall? h?ve h?l? ?v??l?ble t?o but the answers ?ne g?t? ?r? hit ?r miss when ?t ??m?? to quality.

Other things which make private alternative loans part??ul?rly desirable include:

The fact th?t students and parents do not hav? t? fill ?ut FAFSA (Free Application for Student Aid) forms ?nd supply ? lot of additional documentation. Alternative loan applications tend t? be simpler and th? whole process ?? easier. But, fees and interest rates ?ould be higher or lower depending ?n th? specific loan program.

The mo?t sought ?fter private loans w?ll have z?r? fees ?nd rates of interest that ar? ?b?ut equal t? th? prime rate. the ‘prime rate’ is th? rate which banks charge e?ch ?th?r ?r th?ir largest and m?st favored customers. if ??u ?r? ?ble t? find a rate at prime then th?? ?? ? good deal and finding a rate at 1% b?low prime ?s a great deal.

To g?t th?s sort ?f loan ?t is usu?lly n??e???r? f?r ?ou to hav? ?n excellent credit history or h?v? ? co-signer wh? h?s an excellent credit history.

Finally, th? b??t way t? discover wheth?r an alternative loan w?ll suit ??ur purposes i? to go ?ut into th? marketplace ?nd se? ju?t wh?t ?s ?n offer.

When Lewis Carroll sent Alice down the rabbit hole, she encountered a strange and twisted land with distortions of size and time. Some headache experts see something else — the possible ghosts of the author’s migraines, which can leave victims temporarily blinded, nauseated, hallucinatory, numb, unable to concentrate or seeking shelter from painful stings of light and sound.

People with migraines travel between two worlds: one in which they are having a migraine and one in which they are not. “I’m very brave generally,” Tweedledum tells Alice, “only today I happen to have a headache.” But even after the headache is gone, migraine sufferers live with the dread of its return.

For more than a century, researchers have been trying to step through the looking glass to find clues to the mystery of migraines, with little success. Treatments that can prevent or end migraine attacks exist only because drugs for something else were found, often by accident, to quiet the migraine’s neurological storm.

“All of the major things we use were not designed for migraine at all,” says Peter Goadsby, a neurologist at the University of California, San Francisco. “It’s not good enough that one of the commonest of medical problems has treatment developed by serendipity.”

A major barrier to relief, it turns out, has been that migraines, which affect 36 million people in the United States, have no known cause. But researchers now think that they are, at least, looking for the culprits in the right places.

“For almost 100 years, people believed it was a vascular disease,” says Rami Burstein, academic director of the Comprehensive Headache Center at Beth Israel Deaconess Medical Center in Boston. Blood vessels, it is now thought, are probably just aiding and abetting the crime. instead, the perpetrators are nerves inside the brain itself, which misfire and set off a disastrous sequence of events. Making things more complicated, migraine sufferers may differ in their thresholds of susceptibility and sets of triggers. “Migraine is for the most part a genetic disease,” Burstein says, “a problem with genes that regulate excitability of neurons in the cortex.”

Study results announced last year point to three genes that may be linked to migraines. along with other “migraine genes,” the findings seem to paint a picture of brain cells that remain too jumpy when they are supposed to be settled down. With each new discovery, migraine sufferers are brought closer to the day when they might finally be able to escape the hell in their heads.

Stemming the tide

Migraine researchers spent a long time focusing on blood vessels, partly because the notion seemed to make sense: The pain of a migraine throbs in sync with a person’s heartbeat, and triptans — the first class of drugs approved specifically for migraines — constrict blood vessels in the brain. Research suggested that vessels in the head set off a domino of neurological reactions after abnormally contracting, then dilating. Ironically, some of the shift away from the blood vessel theory arose from the study of triptans themselves.

Sumatriptan, the first of the triptans, was introduced for clinical use in the early 1990s. “It was a real milestone in the headache world,” Goadsby says. “But as people looked at sumatriptan, it became clear that it did more than just constrict blood vessels.” The drug also affected nerves, raising the possibility of a different explanation for its effectiveness. more recent evidence has poked holes directly in the blood vessel theory: a study in 2008 in the journal Brain found that blood vessel size during much of the headache is normal (though a more recent study with better resolution is more supportive of at least some vascular role in a migraine attack).

Goadsby was drawn to study migraines largely because one part of the vascular theory never made sense to him. The pain often strikes only one side of the head, and it isn’t necessarily the same side from episode to episode. “I never understood how something originating from the bloodstream would just affect one side of the head,” he said.

So Goadsby decided to use medical imaging as a window into the brains of people having a migraine attack. His curiosity had mostly to do with the brain stem, which controls many basic body functions, such as digestion and circulation — some of the same systems known to go haywire during a migraine attack. It seemed logical to him that a migraine had to originate in some central area since, other than the headache itself, the symptoms don’t tend to be lopsided.

“The brain stem has, in a small area, the ability to affect a large part of the brain,” Goadsby says. in experiments he began publishing in 2005, he used PET scans to identify three locations in the brain stem (corresponding to three distinct structures) that show greater than normal activity during a migraine attack. These parts of the brain usually act as a damper on nerve signals, he says. But when the structures allow too much input to pass through, nerve signals pour into the rest of the brain without control, Goadsby hypothesizes. That’s why normal sensations such as light, sound and even the pulsing of blood through the head become painful. he also believes that the malfunctioning of these areas of the brain stem give rise to one of the most peculiar aspects of a migraine — the aura.

An aura is a sensory disturbance that occurs in about one in four people with migraines. It commonly begins as a flickering of bright lights, like the flashes of an ambulance, in the corner of the visual field and gradually intensifies as it works its way across the line of sight. Some patients experience tingling, nausea and slurred speech during the aura, as well as blind spots once it subsides. An aura vanishes within an hour, and is replaced by a detonation of pain in the head.

Unbearable lightness

The origin of the aura has long been a topic of research fascination. An explanation now gaining consensus emerged in the 1940s from Brazilian biologist Aristides Leão while he worked on his dissertation at Harvard Medical School. after performing experiments in rabbits, Leão noted a marked change in electrical activity that started in one group of cells and rippled across the cortex, the outer layer of the brain. The hyper-excited nerves fire, and then appear to recalibrate, going temporarily silent. Leão called the phenomenon “cortical spreading depression.” Later researchers connected the phenomenon to a migraine aura, reasoning that the flickering light that patients see could occur as the cortical spreading depression crosses the visual center at the back of the brain.

The theory of cortical spreading depression was mostly confined to animal data, remaining at the margins of medical research for decades, until researchers could obtain brain scans of patients experiencing a migraine. One of the first of these images, published in 1994 in the New England Journal of Medicine, came about by chance. a young woman was in a scanner at UCLA for a study of cerebral blood flow when suddenly her migraine began. For about 15 minutes, researchers were able to document a wave of low blood flow (which they believe corresponded to nerve cells going temporarily inactive) spreading across the woman’s brain. a second study was led by Michael Moskowitz of Harvard Medical School. Moskowitz says that in the late 1990s he learned of an engineer who could induce his migraine auras with intense exercise. So Moskowitz and his team invited the man to campus, had him play basketball for 80 minutes and then whisked him off for an MRI.

In 2001 in the Proceedings of the Na-tional Academy of Sciences, Moskowitz’s team published the first MRIs of an aura from start to finish. in addition to the engineer, the researchers also took brain images of two campus employees who entered the scanner shortly after their auras had begun. as predicted, the images showed a wave of overactive (then underactive) neurons creeping across the cortex. “It’s not unlike what would happen if a stone were dropped in quiet pond,” Moskowitz says. The data suggest that the blood flow changes in the brain — the ones that led researchers in the wrong direction for decades — are more likely caused by the aura, and not vice versa. Active neurons grow hungry for fuel.

There is little debate about whether cortical spreading depression is a component of a migraine, but one central question is where it comes from, as well as its exact relationship with the pain. Goadsby believes the aura and pain arise from the brain stem, but others, like Moskowitz, say the activity changes observed in the brain stem are a result of a migraine, not the cause.

“The evidence that this kind of an event is triggered in any precise region of the brain is overstated,” Moskowitz says. instead of having origins in the brain stem, he suggests, the cortical spreading depression can arise in any part of the brain, an idea consistent with animal studies.

Moskowitz also does not agree that the changes that occur in the brain stem during a migraine open the floodgates on nerve signals, allowing normal sensations to become painful. instead, he points to laboratory experiments supporting the idea that the cortical spreading depression itself is responsible for the pain. Most of the brain does not have the capacity to feel pain; only the nerve endings in the dura mater, the organ’s tough outer covering, and related tissue are pain-sensitive. a headache happens because of the stimulation of these nerves, which fire as the wave of excitability makes its way across the cortex, Moskowitz believes. “Cortical spreading depression releases in a drastic way a group of chemicals that are normally sequestered in cells of the brain,” he says. when those chemicals — such as potassium, hydrogen ions and the neurotransmitter glutamate — get dumped, they may activate the pain fibers on the brain’s surface through a process that is still being worked out.

Skeptics of this idea point out that most people get migraines without an aura. Moskowitz’s belief is that cortical spreading depression occurs but does not affect the brain’s visual processing and thus remains undetected — a kind of hidden aura.

In truth, much about migraines is still unknown, says Burstein of Beth Israel. “Migraine is a complex disorder,” he says, involving abnormalities in both the cortex and the brain stem. where the pain comes from is still unclear, and perhaps the mechanisms behind chronic migraines (which occur more than 15 days a month) are different from those for less frequent ones. Migraines that strike regularly could originate from the cortex but over time could damage the cells of the brain stem. “This damage may reduce the ability of the brain stem to mitigate incoming signals,” he says.

And none of the research so far has clearly answered the biggest question: What’s the first thing that goes wrong? The list of potential migraine triggers reads like a catalog of daily life experiences: hunger, flashing lights, alcohol, strong smells, chocolate, cheese, too little sleep, too much sleep, stress, relaxation after stress, menstrual cycle changes, weather changes, and on and on. (And there may be no triggers at all; the changes in the brain that lead to an attack could cause someone to crave chocolate or feel stressed, or undergo other physiological shifts.)

“We don’t know why someone gets a migraine when they are exposed to a perfume in the elevator, when 10 other days they smelled the perfume and didn’t get it,” Burstein says. “Once it starts, we know a lot about it. what we don’t know is why and how.”

Tinderbox of nerves

While scientists debate the why and how of the trigger, genetic studies are getting at a separate question — who. Most researchers believe that genes contribute to a person’s susceptibility to the triggers. The headaches seem to run in families, and the risk is higher if you have an immediate family member with migraines.

Most migraine sufferers probably possess a constellation of genes, each one of which contributes a little to the susceptibility. But there is one kind of migraine, called familial hemiplegic migraine, that appears to have an even stronger genetic component.

An international team of researchers studying this kind of migraine described the first “migraine gene” in the journal Cell in 1996. The discovery came after neurologist Michel Ferrari of Leiden University Medical Center in the Netherlands happened to see two patients on the same day with familial hemiplegic migraine. (They turned out to be both from the same region of the country and were obliquely related.)

Since then, researchers have discovered a handful of genes that may contribute. By understanding the role of these genes, scientists could gain clues to the mechanism behind a migraine. So far, all signs point to nerve activation.

“They confirm that migraine is a disease of hyperexcitability in the brain,” says Ferrari.

Nerve cells work by transmitting electrical impulses. normally, the inside of a nerve cell is negatively charged (thanks to a lot of negatively charged chlorine ions) and the outside is positive (from positively charged sodium, calcium and potassium ions). when a nerve cell releases a signaling molecule called a neurotransmitter, channels on the cell next door open up and allow positive ions to rush in. The cell briefly depolarizes — the inside loses its negative charge — and then returns back to its normal state.

Genes that have been linked to migraine all have some role in the firing of nerve cells and this positive-negative ion swap. The gene mutation described in 1996 affected the calcium ion channel. Another DNA variation, described in 2010 in Nature Genetics, inhibits a cell’s ability to clear away the neurotransmitter glutamate after the nerve has fired, allowing it to accumulate. in June 2011, Ferrari and an international team of researchers described signs of three more rogue genes in Nature Genetics. These, too, are involved in the transmission of signals from cell to cell.

“The story seems to go in the same direction,” Ferrari says. in a migraine-susceptible brain “it’s easier to trigger neuronal activity.”

The idea is also supported by a study published last January in the journal Neurology. Researchers exposed patients suffering a migraine attack to light — a normal stimulus that becomes excruciating during the headache. PET scans of the patients revealed that the light caused the nerves in the occipital cortex of the brain to fire. But when the patients were not experiencing an attack, the light did not have an effect on that part of the brain. like a drought-stricken forest, the nerves may be easy to ignite, and easy to fuel once they do.

“The fact of the matter is there is plenty of evidence now that the brain of a migraine sufferer is never normal,” says David Dodick, a neurologist at the Mayo Clinic in Scottsdale, Ariz., and president of the American Headache Society. It now appears that a migraine brain exists on edge, quick to set off a headache when the right combination of circumstances comes along. “Networks are active when normally they shouldn’t be,” Dodick says. “The threshold for generating an attack is always just below the surface.” The rabbit hole is always near.

But maybe not forever. soon migraine sufferers may, like Alice, be able to wake up from the nightmare inside their heads — something Alice’s creator could never do.

In the months after checking out of Walter Reed Army Medical Center, he found himself easily frustrated and, his wife said, perpetually angry. Envisioning threats in grocery stores and shopping malls, he stopped leaving his house and started drinking heavily. His marriage was near collapse when, in a fit of alcohol-fueled despair, he drove his car into a brick wall, emerging so dazed that he thought he was back in Iraq.

“with a physical injury — three months, six months, whatever — your cuts will heal,” he said. but post-traumatic stress “is more difficult because people don’t see it.”

Like Mr. Pennington, many veterans injured in combat are finding that their invisible psychological and neurological wounds are proving more debilitating than their obvious physical ones.

About 1,700 American service members have lost limbs in Iraq and Afghanistan, most in roadside bombings that seared skin, shattered bones and damaged internal organs as well. Most of those troops also came home with traumatic brain injuries and post-traumatic stress disorder, which in many cases were not recognized for months.

While advances in prosthetics have made it possible for many lower-limb amputees to regain full mobility, the track record for overcoming brain injuries and chronic P.T.S.D. — both capable of altering personality and hampering mental functioning — is more spotty, experts acknowledge.

“I think the limiting factor for these people going back to their lives is not having lost a limb,” said Dr. Douglas Cooper, a neuropsychologist at Brooke Army Medical Center in San Antonio. “The P.T.S.D. symptoms and post-concussive symptoms are the ones that seem to get in the way.”

For Mr. Pennington, medications seemed to worsen his depression and therapy did not ease his anxiety. He seemed headed for divorce, isolation and perhaps alcoholism. And there his story might have ended, a case study on the intransigence of war’s psychological scars. but it did not end there.

In 2009, an unexpected opportunity landed in his e-mail inbox: a casting call, forwarded by a friend in Nashville, from an undergraduate filmmaker looking for someone to play a combat veteran who had lost a leg, had post-traumatic stress disorder and lived in Maine.

This is my life, Mr. Pennington thought.

So on a lark, Mr. Pennington — whose last appearance on stage was in middle school and who had become nervous in crowds and, indeed, avoided most human contact — decided that fixing his life depended on performing before a camera.

“I thought acting would be so out of the normal that it would force me to deal with things,” he recalled. “I wanted my life back.”

The struggle by wounded veterans like Mr. Pennington to reclaim their lives is the unfolding next chapter in America’s wars in Iraq and Afghanistan. Since 2001, 46,000 American service members have been injured in combat, perhaps a third or more seriously. Those veterans now face years of rehabilitation at a cost of billions of dollars annually.

In the coming weeks, The New York Times will profile a few of those veterans. Their cases say much about the critical importance of high-quality health care and loving families. but as with Mr. Pennington, they also underscore the individuality of recovery, where the most effective therapies are often discovered by the veterans themselves.

Mr. Pennington, 28, grew up in central Maine and Fort Worth, Tex., toggling across the continent between divorced parents. He was a talkative boy who loved the outdoors and was good in school, but bad at keeping the jobs that helped support him after he said he had problems with his alcoholic father. When he turned 17, he joined the Army.

He fell in love with the life immediately. His first deployment to Afghanistan in 2002 with the XVIII Airborne Corps was uneventful, so he volunteered to go to Iraq almost as soon as he returned home. He lost a dear friend during that tour, but it did little to sour him on the adventure of war. He raised his hand a third time.

On that third deployment, to Iraq in 2006, he was driving the lead Humvee in a convoy through the insurgent-friendly city of Samarra when a powerful bomb exploded beneath the engine. Through fire and thick smoke, he managed to maneuver the vehicle out of danger with a push from a truck behind.

But when he went to slam on the brakes, he realized his left foot was gone, taken off by shrapnel that had penetrated the bottom of the truck.

His rehabilitation at Walter Reed Army Medical Center in Washington went relatively smoothly, fueled by his hatred of wheelchairs. He was discharged from the Army and returned to Maine in just a year. And there his problems really began.

Perhaps it was leaving the secure cocoon of Walter Reed. perhaps it was living in a rural town, far from Army buddies. perhaps it was his battles with the Veterans Affairs bureaucracy over benefits. perhaps it was the long menu of medications his doctors prescribed: narcotics to ease his pain, antipsychotics to control his moods, sleep aids to tame his nightmares.

Whatever the cause, he grew more irritable, anxious and depressed, symptoms of post-traumatic stress disorder. After he crashed his car into the wall, he told his wife, Marjorie, “I can’t do it anymore.”

With the help of a nonprofit group, the couple moved to Houston in 2008, where he found the care at the veterans health center more to his liking. Doctors there got him off most of his medications, started treating him for traumatic brain injury for the first time and expanded his P.T.S.D. therapy. He felt he was getting better.

But in 2009, Ms. Pennington’s brother committed suicide and the couple returned to Maine to help care for her nephew. Mr. Pennington again fell into a deep funk. He imagined people everywhere judging him, for having killed Iraqis, for being a “crazy veteran.” He spent more of each day in front of the television, afraid to leave home.

Around that time, Nicholas Brennan was looking for actors for his senior project at New York University, a film about a wounded veteran struggling with the transition to civilian life. a casting call sent across a veterans’ e-mail network got about a dozen responses, mainly from soldiers who had lost legs or from out-of-work actors. but the last one, from Mr. Pennington, seemed the most poignant.

“I was injured in 2006,” Mr. Pennington wrote. “it resulted in a personality change for the far worse.”

Mr. Brennan, who was also from Maine, visited Mr. Pennington and was struck by the similarities between the real soldier and his lead character, a Marine named Connor. both had worked in boat repair shops, both loved to fish, both struggled with life in small-town Maine.

“it was pretty clear from the first few minutes I met him,” Mr. Brennan recalled, “that he would be a perfect partner on this project.”

At first, Mr. Pennington simply hoped that acting would force him out of his shell. but as he inhabited the role, he found himself not just identifying with Connor, but also realizing things about his P.T.S.D.

In the final scene of the 15-minute film, titled “a Marine’s Guide to Fishing,” Connor sits on a pier at sunset, his prosthetic by his side, decompressing after a violent flashback in front of his co-workers. His boss, a Vietnam veteran, counsels him to take his time, but leaves with a gentle warning: “You stay out here too long, you’ll never get back.”

“that rang right home to me,” Mr. Pennington said in his Texas twang. “I said, ‘well, dang, that’s what I’m doing.’ ”

After the film was finished last spring, Mr. Brennan and Mr. Pennington showed it publicly for the first time in Portland. Mr. Pennington says he was terrified about speaking before an audience, but afterward people came up looking for advice about relatives struggling with P.T.S.D. His ability to help them was deeply satisfying.

The two men decided to create a Web site to distribute the film and offer their services as speakers. they have done about a dozen such engagements, including one at the Veterans Affairs Health Care Center in Augusta, where Mr. Pennington receives his care and has, at times, clashed with bureaucrats and doctors.

For Mr. Pennington, the public engagements have been a form of exposure therapy, pushing him to articulate bad memories and buried feelings that he had avoided before. The experience has also motivated him to return to therapy himself, making him realize, he said, that “this P.T.S.D. is really getting the best of me.”

Experts say that public speaking alone is not a solution for the symptoms of P.T.S.D. but it can be therapeutic, helping people articulate their emotions and give meaning to their experiences.

“it gives people some authority over what happened to them,” said Dr. Matthew J. Friedman, director of the Veterans Affairs National Center for P.T.S.D. in New Hampshire.

Recently, the Penningtons, who live with their five dogs in a bungalow on a grassy knoll overlooking Dexter, renewed their wedding vows. He spends his days chain-smoking Marlboros, riding a mountain bike for exercise and studying books on acting. He is considering joining a local theater group and doing stints as a regular guest on a radio station owned by the author Stephen King.

He still wakes each morning hating his carbon-fiber leg, which gives him cysts under the skin of his stump. but it is a part of him now. His relationship with P.T.S.D. is more complicated.

He is learning, he says, to talk about his darker memories of war, including the time he nearly killed an Iraqi family that had driven through a checkpoint. The family lived, he says, only because his gun jammed, and the event has haunted him since.

He is also learning how to talk about killing. it has not been easy, he says, because he still feels ashamed when acquaintances blithely ask how many Iraqis he killed. His solution has been to answer bluntly and without explanation: 18.

But the best thing, he says, is that he has become more confident about offering advice to other veterans.

During a recent trip to Augusta for a checkup, Mr. Pennington was approached by an older veteran, who pushed himself in a small cart. a former submariner with a bushy white beard, the man had diabetes, and doctors wanted to remove one of his legs. He nervously asked about what lay ahead.

Balancing gracefully on his good leg, Mr. Pennington removed his prosthetic and described the various annoyances the silicone sleeve could cause. then he put it back on and smiled.

“It’s not so bad,” he said. “if this was my only problem, I’d be doing great.”

“This is the time of the year when days are noticeably shorter, and that absence of light in the late-afternoon hours really seems to affect some people—they feel an acute lowering of their mood,” says Erik Nelson, MD, an associate professor of psychiatry and behavioral neuroscience who specializes in mood disorders and depression at UC Health Psychiatry in Clifton.

“Additionally, the holidays can play a role in depression. some people might have painful memories related to loss of loved ones or stressful childhoods. These are memories with a lot of emotional and psychological significance, and the holidays tend to bring that out.”

When assessing a patient for winter depression, Nelson says, it’s important to determine what triggers their feelings before prescribing a course of treatment.

Some people, for instance, might feel fine for most of the year but report feelings of depression as the days grow shorter. In such cases, known as winter-onset seasonal affective disorder (SAD), treatment with a light box, known as therapeutic light, can be affective.

Symptoms of winter-onset SAD include depressed mood, changes in appetite and weight, fatigue, difficulty concentrating, changes in sleep (often oversleeping) and loss of interest in formerly enjoyable activities.

As with any mood disorder, Nelson says, “If the condition is interfering with your normal life, it’s time to seek help.”

Therapeutic light involves a specially designed lamp giving off an intensity of light that mimics the full spectrum and intensity of sunlight. Such devices are generally used for about 15 to 30 minutes in the morning, with the light shining indirectly on the person’s face, and can be used while he or she is involved in another activity such as reading or exercising.

The antidepressant  bupropion (trade name Wellbutrin) has been approved by the FDA to treat seasonal major depressive episodes, but the proper medication for any individual case should be determined in consultation with a physician. another treatment option is cognitive behavioral therapy, a pragmatic interactive therapy that has the goal of changing specific thoughts and behaviors.

Moreover, some people who are already being treated for depression notice a worsening of their symptoms during the winter months. if this appears to be related to the decreased hours of daylight, adding light therapy to the person’s current treatments for depression is often helpful, Nelson says.

For worsening of depression that appears to be related to the emotions or stress associated with the holidays, Nelson says, a change in the person’s current regimen, which would typically include psychotherapy and/or antidepressant medication, would be the likely course of treatment.

“There are a lot of factors that can affect a person’s mood this time of year, and it is helpful to assess the likely cause to determine the best course of treatment such as therapeutic light, medications, psychotherapy or behavioral changes that can be made.”

If people have milder seasonal symptoms that do not reach the level of a major depressive episode, Nelson says, they should try exercise and getting outdoors more to see if that helps their symptoms.

Provided by University of Cincinnati (news : web)

TEL AVIV, Israel, Dec. 11 (UPI) — Children whose mothers were depressed throughout their first year of life have a higher risk of mental disorders themselves by age 6, researchers in Israel say.

Ruth Feldman, a professor at Bar-Ilan University in Israel, found 60 percent of children born to mothers who were consistently depressed across the first year of the children’s lives exhibited mental disorders when they were older. The children, similar to their mothers, also showed disordered functioning of the Oxytocin system.

Oxytocin, a mammalian hormone, is involved with sexual reproduction, childbirth, breastfeeding and pair bonding.

Researchers studied the mental health status, Oxytocin levels, genetic variation in Oxytocin receptors and interactions in 155 mother-child pairs during at-home visits. The mothers were surveyed for mental health symptoms at the birth of their child, and at 6 and 9 months after the birth of their child.

Of the pairs participating when the child reached 6 years of age, 30 percent of mothers were diagnosed with depression and had demonstrated symptoms of depression throughout the child’s first year of life. On average, these mothers had disordered Oxytocin functioning and produced less peripheral Oxytocin in their saliva.

Most children born to depressed mothers exhibited mental disorders, but 40 percent demonstrated more normal functioning of the Oxytocin system, no signs of mental illness, better social engagements and empathic behaviors.

“We found Oxytocin system functioning helps safeguard some children against the effects of chronic maternal depression,” Feldman said.

The findings were presented at the American College of Neuropsychopharmacology annual meeting.

(Medical Xpress) — the images of war often stay with those who have experienced it long after a conflict is over. While the physical wounds are apparent, we are learning more and more about the toll these conflicts take on a soldier’s mental health, particularly in terms of post-traumatic stress disorder, or PTSD, and depression.

While traumatic events such as a car accident, natural disaster or an assault may trigger PTSD in some people in the general population, the data collected from troops who have served in combat, such as during the Vietnam War and the conflicts in Iraq and Afghanistan, suggest that in many cases, soldiers exposed to deployment-related stressors have endured a more potent PTSD trigger that involves constant, ongoing stress.

“We’re seeing double the rate of PTSD in vets than in the general population,” said Ananda B. Amstadter, Ph.D., assistant professor of psychiatry at the Virginia Commonwealth University School of Medicine and the Virginia Institute for Psychiatric and Behavioral Genetics.

In the general American adult population, who are not in the military, approximately 8 percent of the population will meet criteria for PTSD at some point in their lives. for returning veterans, the scientific data suggest closer to 20 percent of veterans will have symptoms of PTSD or experience another comorbid psychiatry condition, such as depression or a substance use disorder.

According Amstadter, an active researcher in the area of traumatic stress, many of the troops returning home from service in Iraq and Afghanistan – Operation Iraqi Freedom and Operation Enduring Freedom – suffer from ongoing stress brought about by lengthy deployments and multiple tours. the PTSD symptoms endured by this population is not always just related to one isolated incident or event, and the more times they return to war, the more likely they will develop a stress-related psychiatric condition, such as PTSD, she said.

Further, research based on both troops from the Vietnam War era, and the conflicts in Iraq and Afghanistan, suggest that troops involved with direct combat-related exposure, such as a bombing or attack, are more likely to experience PTSD compared to a service member who has been involved with other aspects of deployment that do not involve direct exposure to combat – for example, those in military intelligence.

Amstadter said that individuals who experience PTSD generally have a cluster of symptoms including re-experiencing or reliving the event, avoiding anything or anyone that is related or reminds them of the event, numbing and increased arousal.

Amstadter said that when a person re-experiences or re-lives the event, he or she may have repeated memories or thoughts or repeated disturbing dreams of the trauma; may feel like the trauma was happening again; may feel upset when something triggers memories of the trauma; and may have physical reactions when something reminds them of the trauma. Numbing involves avoiding thinking or talking about the trauma, avoiding activities or situations that are related to the trauma, proving unable to recall parts of the event and showing a decreased interest in activities, a disconnection from others, a restricted range of emotions and a sense of a shortened future. Increased arousal includes sleeping difficulties, concentration difficulties and an exaggerated startle response.

PTSD and genomics

The focus of Amstadter’s work is to understand the post-trauma trajectory of symptoms by examining the environmental factors, as well as the biologic or neuroendocrine, and genetic factors of PTSD. through her research she hopes to help better predict the factors that differentiate individuals who either do not develop symptoms or who experience a naturalistic recovery, from those who develop long-lasting symptoms of a mental health disorder, such as PTSD.

“we know that PTSD is about 30 percent heritable,” Amstader said. “In other words, genes account for about one third of the variance in risk for PTSD. We’re trying to identify exactly which genes are involved, and how the environment might moderate these relationships.”

“If we can determine which genes are involved and understand the effects of a particular variant we may be able to identify people that may need help in the aftermath of a traumatic event,” she said.

For example, according to Amstadter, some theories suggest that there are a handful of sequence variants that you could be carrying around your entire life and if you’re never exposed to a traumatic event, your risk for PTSD is no higher than if you had the other form of the gene. But, if you are exposed to a traumatic event and you have that specific gene, you could be at an increased risk for developing PTSD than somebody with the alternate form of that gene.

To date, Amstadter said researchers have identified a host of different genes by conducting molecular genetic studies. However, replication of this work has not been consistent and further research is necessary.

Stress reactivity study

Through support from a National Institutes of Health grant, Amstadter and her team are examining the effects of combat history and PTSD status on stress reactivity in returning soldiers, and how their response to the stressor affects their drinking behavior, as well as the role of genetic variants that may play a role in stress-related drinking.

Amstadter and other mental health experts are seeing a lot of alcohol problems and other substance use issues in veterans returning from recent service. Some experts suggest that combat exposure and PTSD symptoms may lead some returning vets to feel like they are on edge all the time and they may be engaging in substance use to self-medicate.

“we are trying to identify the biological link between the effect of combat on somebody’s stress response and how that effects drinking in a controlled environment,” she said.

Combat exposure and fear conditioning

In other work, Erin Berenz, a post-doctoral fellow with Amstadter, is looking at how combat exposure and PTSD affect fear conditioning in veterans. the study is testing the hypothesis that people with PTSD acquire responses to trauma-related stimuli quicker than people without PTSD. Their theory is that if somebody has PTSD then his or her fear conditioning system is ramped up, so it is really easy for him or her to gain a stress reaction or a fear reaction to particular stimuli and then it’s really hard for that feeling to extinguish, or go away and return to a normal state.

Both the stress reactivity study and the fear conditioning study will pull from the same population sample of 240 veterans. Data from these participants will be gathered and analyzed in the coming months.

Collaboration with the Richmond VA

Through a project supported by the Mental Illness Research, Education, Clinical Center or MIRECC, VCU is working closely with mental health experts at the Hunter Holmes McGuire Veterans Affairs Medical Center in Richmond to understand post-deployment mental health issues.

The majority of VAs across the country are part of a network based on their geographic location and VCU is part of the multi-site center Mid-Atlantic MIRECC, which is led by Duke University. there are 22 different MIRECC groups across the country, each focused on a different aspect of mental health as it relates to helping veterans.

Amstadter and Vladimir Vladimirov, M.D., Ph.D., assistant professor in the VCU Department of Psychiatry, together with Richmond-based researchers Treven Pickett, Psy. D., associate chief and supervisory psychologist for Mental Health Service, and Scott McDonald, Ph.D., and MIRECC researchers Jeannie Beckman, Ph.D., and Mike Hauser, Ph.D., are collaborating on a study that will examine microRNA collected from veterans who are combat exposed with and without PTSD. further, their future work will examine genomics of PTSD – which includes the analysis of DNA and RNA – and not merely a genetic sequence.

Provided by Virginia Commonwealth University (news : web)