Thursday, December 14, 2017

5 ways to reverse SAD (Seasonal Affective Disorder)

Seasonal Affective Disorder: What You Should Know

Woman sitting in front of a light box

The bright lights of the holiday season aren’t just for decoration; they can also help regulate your mood.

In late fall and winter, shorter daylight hours leave many people with little to no sun exposure, signaling the brain to create too much of the sleep-regulating hormone melatonin.
This overproduction of melatonin leads to seasonal affective disorder (SAD), a mood disorder that affects an estimated 10 to 20 percent of the population. 

SAD Differs from Depression

Major depression is a disease in which your brain’s pleasure responses are broken. You may have a loss of appetite, fatigue, trouble sleeping and feelings of hopelessness. Depressed people often have a harder time managing their symptoms in the winter. But when depressive symptoms are only affecting you in the winter, it’s considered seasonal affective disorder (SAD). 

SAD Affects Men and Women Equally

Historically, researchers have considered women to be more likely to experience seasonal depression. But psychiatrists are increasingly finding that’s not the case. “The classic crying and melancholic depression is more the norm of expression in women. But men express things differently, showing depression with more irritability, anger or frustration,” said Dr. Andrew Angelino, director of psychiatry at Howard County General Hospital.

Ways to Reverse SAD

If you can’t get outside during daylight hours, there are ways to help reverse your body’s creation of too much melatonin.
“If you find that you’re prone to getting the blahs in the winter months or you know you have depression and are taking your medicine, you can also get a light box,” says Dr. Angelino.
Absorbing natural, full-spectrum light regulates hormones in the brain, and helps keep your moods stabilize. In addition to obtaining a light box, Dr. Angelino recommends these five tips to help chase away the seasonal blues:
Drug abuse can follow addiction. Learn more.

    1. Keep your holiday expectations realistic. Don’t let your hopes for perfection spoil your holiday spirit. Learn how to embrace things as good enough, like food, company and gifts.
       
    2. Practice wellness. A daily routine of at least 7 hours of sleep, a 30-minute exercise routine and limiting your alcohol intake can go a long way in fighting the blues.
       
    3. Stand in the sun. Take a break from your desk. At least 15-30 minutes of sunlight, especially in the early morning, helps to regulate your internal clock.
       
    4. Cultivate some winter hobbies. The chilly weather may freeze your weekend gardening plans but it may be the best time to catch up on your reading list or tackle a new project in the house. Adjust your leisure activities to fit the seasons.
       
    5. See a doctor if natural interventions are not successful. If your symptoms are regularly interfering with your everyday life, make an appointment with your doctor. ---Source: Johns Hopkins Medicine

Tuesday, December 12, 2017

Healthy cell structure could stop Alzheimer's


Alzheimer's disease is the most common form of dementia and neurodegeneration worldwide. A major hallmark of the disease is the accumulation of toxic plaques in the brain, formed by the abnormal aggregation of a protein called beta-amyloid inside neurons.
Still without cure, Alzheimer's poses a significant burden on public health systems. Most treatments focus on reducing the formation of amyloid plaques, but these approaches have been inconclusive. As a result, scientists are now searching for alternative treatment strategies, one of which is to consider Alzheimer's as a metabolic disease.


Taking this line of thought, Johan Auwerx's lab at EPFL looked at mitochondria, which are the energy-producing powerhouses of cells, and thus central in metabolism. Using worms and mice as models, they discovered that boosting mitochondria defenses against a particular form of protein stress, enables them to not only protect themselves, but to also reduce the formation of amyloid plaques.
During normal aging and age-associated diseases such as Alzheimer's, cells face increasing damage and struggle to protect and replace dysfunctional mitochondria. Since mitochondria provide energy to brain cells, leaving them unprotected in Alzheimer's disease favors brain damage, giving rise to symptoms like memory loss over the years.
The scientists identified two mechanisms that control the quality of mitochondria: First, the "mitochondrial unfolded protein response" (UPRmt), which protects mitochondria from stress stimuli. Second, mitophagy, a process that recycles defective mitochondria. Both these mechanisms are the key to delaying or preventing excessive mitochondrial damage during disease.
While we have known for a while that mitochondria are dysfunctional in the brains of Alzheimer's patients, this is the first evidence that they actually try to fight the disease by boosting quality control pathways. "These defense and recycle pathways of the mitochondria are essential in organisms, from the worm C. elegans all the way to humans," says Vincenzo Sorrentino, first author of the paper. "So we decided to pharmacologically activate them."
The team started by testing well-established compounds, such as the antibiotic doxycycline and the vitamin nicotinamide riboside (NR), which can turn on the UPRmt and mitophagy defense systems in a worm model (C. elegans) of Alzheimer's disease. The health, performance and lifespan of worms exposed to the drugs increased remarkably compared with untreated worms. Plaque formation was also significantly reduced in the treated animals.
And most significantly, the scientists observed similar improvements when they turned on the same mitochondrial defense pathways in cultured human neuronal cells, using the same drugs.
The encouraging results led the researchers to test NR in a mouse model of Alzheimer's disease. Just like C. elegans, the mice saw a significant improvement of mitochondrial function and a reduction in the number of amyloid plaques. But most importantly, the scientists observed a striking normalization of the cognitive function in the mice. This has tremendous implications from a clinical perspective.
According to Johan Auwerx, tackling Alzheimer's through mitochondria could make all the difference. "So far, Alzheimer's disease has been considered to be mostly the consequence of the accumulation of amyloid plaques in the brain," he says. "We have shown that restoring mitochondrial health reduces plaque formation -- but, above all, it also improves brain function, which is the ultimate objective of all Alzheimer's researchers and patients."
The strategy provides a novel therapeutic approach to slow down the progression of neurodegeneration in Alzheimer's disease, and possibly even in other disorders such as Parkinson's disease, which is also characterized by profound mitochondrial and metabolic defects.
The approach remains to be tested in human patients. "By targeting mitochondria, NR and other molecules that stimulate their 'defense and recycle' systems could perhaps succeed where so many drugs, most of which aim to decrease amyloid plaque formation, have failed," says Vincenzo Sorrentino.
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Sunday, December 10, 2017

Take the distracted driving quiz.

Learn about drugs and the brain.
Questions:
  1. Of the top five causes of death for teens in the U.S., where do motor vehicle crashes belong on the list?
  2. For high school seniors, what’s more common: driving after using drugs, or driving drunk?
  3. Fill in the blank: ____ percent of all drivers aged 15 to 19 who were involved in fatal crashes were distracted (not focusing on the main task of driving) at the time of the crashes.
  4. Are teens more likely to take risks when they’re driving alone or when they have passengers in the car?
  5. True or false: Marijuana impairs a person’s ability to drive.
  6. The average car’s weight is closest to that of a:
    1. Tyrannosaurus rex
    2. Black bear
    3. Beluga whale
    4. None of the above
  7. If you text while you’re driving, how long on average do you take your eyes off the road while texting?
Answers:
  1. Motor vehicle crashes are the leading cause of death for teens. Each year, enough teens die in car crashes to fill 50 school buses. 
  2. More high school seniors are now driving after using drugs than are driving after drinking. 
  3. Ten percent of all drivers aged 15 to 19 were distracted at the time they were involved in a fatal crash. 
  4. One study found that teens are more likely to take risks when driving with their friends in the car, even if their friends aren’t talking. (National Highway Traffic Safety Administration.
  5. True! Even a single marijuana cigarette can make it harder for a person to drive safely.
  6. The answer is c., a beluga whale. The average car or truck weighs about 4,000 pounds—even more than a beluga whale. Driving one is a big responsibility! 
  7. Almost five seconds is the average time your eyes are off the road while texting. When you’re driving at 55 miles per hour, that's enough time to cover the length of a football field blindfolded.
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Thursday, December 7, 2017

Is Trump suffering from dementia? You judge.


Definition of dementia  from the National Institute of Neurological Disorders and Stroke. (NINDS).

Dementia is the loss of cognitive functioning—the ability to think, remember, problem solve or reason—to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living. 

Learn about the brain in everyday language.

Functions affected include memory, language skills, visual perception, problem solving, self-management, and the ability to focus and pay attention. Some people with dementia cannot control their emotions, and their personalities may change. Signs and symptoms of dementia result when once-healthy neurons (nerve cells) in the brain stop working, lose connections with other brain cells, and die. 

While everyone loses some neurons as they age, people with dementia experience far greater loss. Unlike dementia, age-related memory loss isn’t disabling. While dementia is more common with advanced age (as many as half of all people age 85 or older may have some form of dementia), it is not normal part of aging. Many people live into their 90s and beyond without any signs of dementia. 

The causes of dementia can vary. Many people with dementia have both Alzheimer’s disease and one or more closely related disorders that share brain scanning or clinical (and sometimes both) features with Alzheimer’s disease. When a person is affected by more than one dementia disorder, the dementia can be referred to as a mixed dementia. 

Some people may have mixed dementia caused by Alzheimer’s-related neurodegenerative processes, vascular disease-related processes, or another neurodegenerative condition. Many other conditions such as Creutzfeldt-Jakob disease, Huntington’s Disease, and chronic traumatic encephalopathy can cause dementia or dementia-like symptoms. 

Risk factors for dementia include advancing age, stroke, high blood pressure, poorly controlled diabetes, and a thickening of blood vessel walls (atherosclerosis). Other dementias include frontotemporal disorders, vascular dementia, and Lewy body dementia.

Chronic pain: An unwanted memory


The brain, in easy-to-read language.
Dr. Allan Basbaum, pain specialist, called chronic pain a memory...one we don't want. Yet pretreatment of pain in the 1990s with drugs such as oxycontin has, many say, led to our current addiction crisis with opioids, including heroin and fentanyl.

Pain Management

YESTERDAY

  • Early Greeks and Romans advanced the idea that the brain played a role in producing the perception of pain.
  • In the 19th century, physician-scientists discovered that opiates such as morphine could relieve pain and chemist Felix Hoffmann developed aspirin from a substance in willow bark. Aspirin remains the most commonly used pain reliever.
  • The French physician, Dr. Albert Schweitzer, proclaimed in 1931 that, “Pain is a more terrible lord of mankind than even death itself.”
  • In 1994, the International Association for the Study of Pain (IASP) (http://www.iasp-pain.org/) defined pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage.”

TODAY

  • Pain affects more Americans than diabetes, heart disease and cancer combined.
  • Pain is cited as the most common reason Americans access the health care system. It is a leading cause of disability and it is a major contributor to health care costs.
  • According to the National Center for Health Statistics (2006), approximately 76.2 million, one in every four Americans, have suffered from pain that lasts longer than 24 hours and millions more suffer from acute pain.
  • Chronic pain is the most common cause of long-term disability.
  • The diversity of pain conditions requires a diversity of research and treatment approaches.
  • Pain can be a chronic disease, a barrier to cancer treatment, and can occur alongside other diseases and conditions (e.g. depression, post-traumatic stress disorder, traumatic brain injury).
  • For infants and children, pain requires special attention, particularly because they are not always able to describe the type, degree, or location of pain they are experiencing.
  • Discoveries of differences in pain perceptions and responses to treatment by gender has have led to new directions for research on the experience and relief of pain. For example, medications called kappa-opioids provide good relief from acute pain in women, yet increase pain in men.
  • NIH-supported scientists identified a gene variant of an enzyme that reduces sensitivity to acute pain and decreases the risk of chronic pain.
  • COX-2 (cyclooxygenase-2) is a major contributor to pain associated with inflammation. A study of genes affected by COX-2 led to the discovery of its role in connection to multiple cellular pathways that contribute to pain relief and adverse side-effects.
  • Behavioral interventions for pain also demonstrate promise for providing pain relief either in conjunction with or in lieu of drug interventions. For example, NIH-supported research has demonstrated that individualized pain management programs may reduce cancer pain for some patients.

TOMORROW

The NIH is poised to make major discoveries that will improve health outcomes for individuals experiencing acute or chronic pain by applying opportunities in genomics and other technologies to improve our understanding of the fundamental causes of pain. This will be accomplished through translating basic laboratory science to new, improved pain treatments and by providing strategic support for the research community to discover more effective pain treatment strategies.

Applying genomics and other technologies to understand pain. Advances in basic and clinical genetics are making it possible to both characterize genetic factors related to pain sensitivity and develop novel therapeutic approaches.

  • In ongoing pain studies, scientists are using technologies such as microarray-based assays (complex genetic and molecular tests) to better understand the mechanisms of pain and analgesia, identify new targets for analgesic drugs, and test the efficacy and adverse reactions of newly developed or currently used drugs to treat pain. Researchers are currently using these technologies to discover the mechanisms by which drugs such as COX-inhibitors and neurotropins may relieve pain.
Translating basic science to improved pain treatments. Researchers will continue to focus on advancing both biological and behavioral pain management strategies from the research sphere to clinical applications.

  • Innovative ways to categorize and measure pain are currently being studied. For example, scientists are using computer-assisted technology to develop a novel program that will capture and quantify pain experiences. Tools such as this will be combined with existing methods to more accurately and consistently measure pain over time and across groups, diseases, and conditions.
  • Research will continue identifying biomarkers and biological pathways associated with painful conditions resulting from the use of drugs to treat diseases such as cancer and HIV/AIDS (http://www.umgcc.org/research/et.htm).
Providing Strategic Support for Research into Pain Treatment Strategies.

  • The NIH Pain Consortium (http://painconsortium.nih.gov/), an effort involving over 21 NIH Institutes, Centers, and Offices, promotes collaboration among the various NIH programs that support pain research, and provides strategic direction for accelerating advances in pain prevention, and treatment.
  • The Patient Protection and Affordable Care Act has established an Interagency Pain Research Coordinating Committee, led by the Department of Health and Human Services, to assess and coordinate pain research efforts across the Federal government.
Contact: NINR Office of Science Policy and Public Liaison, info@ninr.nih.gov, 301-496-0207

National Institute of Nursing Research (NINR): 
http://www.ninr.nih.gov/


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Wednesday, December 6, 2017

Steeler's football injury: Protecting the miraculous, fragile spinal cord

Source: USA Today
As Ryan Shazier continues to undergo tests at the University of Cincinnati Medical Center for a spine injury, he tweeted a thank-you Tuesday evening. 
Shazier was injured during the Pittsburgh Steelers' win over the Cincinnati Bengals onMonday Night Football. He was taken by ambulance to the hospital after being removed from the field on a backboard.
"Thank you for the prayers. Your support is uplifting to me and my family. #SHALIEVE"

Earlier Tuesday, team general manager Kevin Colbert said Shazier is not expected to need surgery. Doctors released a statement that said he will remain hospitalized for more tests and evaluations during the next 24-48 hours.
Shazier underwent a CT scan and MRI after being injured in the first quarter of the Steelers' 23-20 win.
After he tackled receiver Josh Malone with the crown of his helmet, he slumped to the turf and his body went limp. He later grabbed his middle back and it appeared he was having trouble moving his legs.

Learn about the brain, the spinal cord and the central nervous system in easy-to-read form.


Source: National Institute of Neurological Disorders and Stroke:

How does the spinal cord work? To understand what can happen as the result of a spinal cord injury, it is important to understand the anatomy of the spinal cord and its normal functions. The spinal cord is a tight bundle of neural cells (neurons and glia) and nerve pathways (axons) that extend from the base of the brain to the lower back. It is the primary information highway that receives sensory information from the skin, joints, internal organs, and muscles of the trunk, arms, and legs, which is then relayed upward to the brain. It also carries messages downward from the brain to other body systems.

Millions of nerve cells situated in the spinal cord itself also coordinate complex patterns of movements such as rhythmic breathing and walking. Together, the spinal cord and brain make up the central nervous system (CNS), which controls most functions of the body. The spinal cord is made up of neurons, glia, and blood vessels. The neurons and their dendrites (branching projections that receive input from axons of other neurons) reside in an H-shaped or butterfly-shaped region called gray matter. The gray matter of the cord contains lower motor neurons, which branch out from the cord to muscles, internal organs, and tissue in other parts of the body and transmit information commands to start and stop muscle movement that is under voluntary control.

Upper motor neurons are located in the brain and send their long processes (axons) to the spinal cord neurons. Other types of nerve cells found in dense clumps of cells that sit just outside the spinal cord (called sensory ganglia) relay information such as temperature, touch, pain, vibration, and joint position back to the brain. The axons carry signals up and down the spinal cord and to the rest of the body. Thousands of axons are bundled into pairs of spinal nerves that link the spinal cord to the muscles and the rest of the body. The function of these nerves reflects their location along the spinal cord. 4 • Cervical spinal nerves (C1 to C8) emerge from the spinal cord in the neck and control signals to the back of the head, the neck and shoulders, the arms and hands, and the diaphragm. • Thoracic spinal nerves (T1 to T12) emerge from the spinal cord in the upper mid-back and control signals to the chest muscles, some muscles of the back, and many organ systems, including parts of the abdomen.

Lumbar spinal nerves (L1 to L5) emerge from the spinal cord in the low back and control signals to the lower parts of the abdomen and the back, the buttocks, some parts of the external genital organs, and parts of the leg. Between the vertebrae of the spinal column are discs that act as passages through which the spinal nerves travel. These places are particularly vulnerable to injury

Sunday, December 3, 2017

To learn better, take a nap (and don't forget to dream)

Source:
Beth Israel Deaconess Medical Center
Summary:
It is by now well established that sleep can be an important tool when it comes to enhancing memory and learning skills. And now, a new study sheds light on the role that dreams play in this important process.

     
FULL STORY

It is by now well established that sleep can be an important tool when it comes to enhancing memory and learning skills. And now, a new study sheds light on the role that dreams play in this important process.
Learn about your brain in easy-to-understand language.

"What's got us really excited, is that after nearly 100 years of debate about the function of dreams, this study tells us that dreams are the brain's way of processing, integrating and really understanding new information," explains senior author Robert Stickgold, PhD, Director of the Center for Sleep and Cognition at BIDMC and Associate Professor of Psychiatry at Harvard Medical School. "Dreams are a clear indication that the sleeping brain is working on memories at multiple levels, including ways that will directly improve performance."
At the outset, the authors hypothesized that dreaming about a learning experience during nonrapid eye movement (NREM) sleep would lead to improved performance on a hippocampus-dependent spatial memory task. (The hippocampus is a region of the brain responsible for storing spatial memory.)
To test this hypothesis, the investigators had 99 subjects spend an hour training on a "virtual maze task," a computer exercise in which they were asked to navigate through and learn the layout of a complex 3D maze with the goal of reaching an endpoint as quickly as possible. Following this initial training, participants were assigned to either take a 90-minute nap or to engage in quiet activities but remain awake. At various times, subjects were also asked to describe what was going through their minds, or in the case of the nappers, what they had been dreaming about. Five hours after the initial exercise, the subjects were retested on the maze task.

The results were striking.
The non-nappers showed no signs of improvement on the second test -- even if they had reported thinking about the maze during their rest period. Similarly, the subjects who napped, but who did not report experiencing any maze-related dreams or thoughts during their sleep period, showed little, if any, improvement. But, the nappers who described dreaming about the task showed dramatic improvement, 10 times more than that shown by those nappers who reported having no maze-related dreams.
"These dreamers described various scenarios -- seeing people at checkpoints in a maze, being lost in a bat cave, or even just hearing the background music from the computer game," explains first author Erin Wamsley, PhD, a postdoctoral fellow at BIDMC and Harvard Medical School. These interpretations suggest that not only was sleep necessary to "consolidate" the information, but that the dreams were an outward reflection that the brain had been busy at work
"The subjects who dreamed about the maze had done relatively poorly during training," explains Wamsley. "Our findings suggest that if something is difficult for you, it's more meaningful to you and the sleeping brain therefore focuses on that subject -- it 'knows' you need to work on it to get better, and this seems to be where dreaming can be of most benefit."
Furthermore, this memory processing was dependent on being in a sleeping state. Even when a waking subject "rehearsed and reviewed" the path of the maze in his mind, if he did not sleep, then he did not see any improvement, suggesting that there is something unique about the brain's physiology during sleep that permits this memory processing.
"In fact," says Stickgold, "this may be one of the main goals that led to the evolution of sleep. If you remain awake [following the test] you perform worse on the subsequent task. Your memory actually decays, no matter how much you might think about the maze.
"We're not saying that when you learn something it is dreaming that causes you to remember it," he adds. "Rather, it appears that when you have a new experience it sets in motion a series of parallel events that allow the brain to consolidate and process memories."
Ultimately, say the authors, the sleeping brain seems to be accomplishing two separate functions: While the hippocampus is processing information that is readily understandable (i.e. navigating the maze), at the same time, the brain's higher cortical areas are applying this information to an issue that is more complex and less concrete (i.e. how to navigate through a maze of job application forms).
"Our [nonconscious] brain works on the things that it deems are most important," adds Wamsley. "Every day, we are gathering and encountering tremendous amounts of information and new experiences," she adds. "It would seem that our dreams are asking the question, 'How do I use this information to inform my life?'"
Study coauthors include BIDMC investigators Matthew Tucker, Joseph Benavides and Jessica Payne (currently of the University of Notre Dame).
This study was supported by grants from the National Institutes of Health.

Story Source:
Materials provided by Beth Israel Deaconess Medical CenterNote: Content may be edited for style and length.