9 Ways to Get Your Energy Back

You’re only as old as you feel, the saying goes. But what if you feel old, tired, and rundown?

Fatigue is a common complaint, especially after people hit middle age. Fortunately, there are plenty of simple ways to boost energy. Some even slow the aging process.

Here’s how to refill your tank when your energy levels sputter.

1. Rule out health problems.

Fatigue is a common symptom of many illnesses, including diabetes, heart disease, arthritis, anemia, thyroid disease, and sleep apnea. Talk to your doctor if you feel unusually tired.

Many medications can contribute to fatigue. These include some blood pressure medicines, antihistamines, diuretics, and other drugs. If you begin to experience fatigue after starting a new medication, tell your doctor.

2. Get moving.

The last thing you may feel like doing when you’re tired is exercising. But many studies show that physical activity boosts energy levels.

“Exercise has consistently been linked to improved vigor and overall quality of life,” says Kerry J. Stewart, professor of medicine and director of clinical and research exercise physiology at Johns Hopkins University School of Medicine. “People who become active have a greater sense of self-confidence. But exercise also improves the working efficiency of your heart, lungs, and muscles,” Stewart says. “That’s the equivalent of improving the fuel efficiency of a car. It gives you more energy for any kind of activity.”

3. Strike a pose.

Although almost any exercise is good, yoga may be especially effective for boosting energy. After six weeks of once-a-week yoga classes, volunteers in a British study reported improvements in clear-mindedness, energy, and confidence. 

It’s never too late to try, either. University of Oregon researchers offered yoga instruction to 135 men and women ages 65 to 85. At the end of six months, participants reported an increased sense of well-being and a boost in overall energy.

 

4. Drink plenty of water.

Dehydration zaps energy and impairs physical performance. “Our research shows that dehydration makes it harder for athletes to complete a weight lifting workout,” says Dan Judelson, PhD, assistant professor of kinesiology at California State University at Fullerton. "It’s reasonable to think that dehydration causes fatigue even for people who are just doing chores."

Dehydration has also been shown to decrease alertness and concentration.

How to know if you’re drinking enough water?“Urine should be pale yellow or straw colored,” Judelson says. “If it’s darker than that, you need to drink water.”

5. Get to bed early.

Lack of sleep increases the risk of accidents and is one of the leading causes of daytime fatigue. The solution: Get to bed early enough for a full night’s sleep.

When people enrolled in a 2004 Stanford University study were allowed to sleep as long as they wanted, they reported more vigor and less fatigue. Good sleep habits may also have important health benefits. Centenarians report better than average sleep.

If you do fall short on shut-eye, take a brief afternoon nap. Napping restores wakefulness and promotes performance and learning. A 10-minute nap is usually enough to boost energy. Don’t nap longer than 30 minutes, though, or you may have trouble sleeping that night. A nap followed by a cup of coffee may provide an even bigger energy boost, according to the American Academy of Sleep Medicine.

6. Go fish.

Good for your heart, omega-3 oils may also boost alertness. According to a 2009 study by scientists at Italy’s University of Siena, volunteers who took a fish oil capsule for 21 days demonstrated faster mental reaction times. They also reported feeling more vigorous.

7. Keep time with your body clock.

Some people get a burst of energy first thing in the morning. They're often called morning larks. Night owls are people who are at their best at the end of the day. 

These individual differences in daily energy patterns are determined by brain structure and genetics, so they can be tough to change. Instead, become aware of your own circadian rhythms. Then schedule demanding activities when your energy levels are typically at their peak.

8. Shed extra weight.

Losing extra weight can provide a powerful energy boost, says Stewart, of Johns Hopkins University. Even small reductions in body fat improve mood, vigor, and quality of life.

Most weight loss experts recommend cutting back on portion sizes, eating balanced meals, and increasing physical activity.

9. Eat more often.

Some people may benefit by eating smaller meals more frequently during the day. This may help to steady your blood sugar level.

Favor whole grains and other complex carbohydrates. These take longer than refined carbohydrates to digest, preventing fluctuations of blood sugar.

If you start eating more often, watch your portion sizes to avoid weight gain.

Source:  http://www.webmd.com/balance/features/get-energy-back

Acute psychological stress reduces ability to withstand physical pain

Traffic slows to a crawl, then a stop. You are trapped in a bottleneck nightmare, and late for a meeting. The stress takes a toll on you psychologically -- but your body is at risk as well, according to a Tel Aviv University researcher.

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A new study by Prof. Ruth Defrin of the Department of Physical Therapy at TAU's Sackler Faculty of Medicine published in the journal PAIN finds that acute psychosocial stress has a dramatically deleterious effect on the body's ability to modulate pain. Prof. Defrin, together with TAU doctoral student Nirit Geva and Prof. Jens Pruessner of McGill University, applied acute stress tests on a large group of healthy young male adults to evaluate the behavior of the body's pain modulation mechanisms prior to and after the induction of stress.
The researchers found that although pain thresholds and pain tolerance seemed unaffected by stress, there was a significant increase in pain intensification and a decrease in pain inhibition capabilities.
Doing the math
For the purpose of the study, 29 healthy men underwent several commonly accepted pain tests to measure their heat-pain thresholds and pain inhibition, among other factors. In one test, for example, subjects were asked to signal the moment a gradually increasing heat stimulus became painful to identify their respective pain thresholds. They underwent a series of pain tests before and immediately after exposure to the Montreal Imaging Stress Task (MIST), a computer program of timed arithmetic exercises, designed to induce acute psychosocial stress.
In a way, the stress test is a psychological trick. MIST provides live feedback on submitted responses, registering only 20-45% of the responses as correct, whether or not a submitted response is the right answer. Because the subject has been previously informed that the average participant tends to score 80%-90%, he is reminded of his "poor performance" but has no way of improving his score, despite his best efforts. This provides the "stress" element of the experiment.
"To further test the effect of stress on pain, we divided the group according to stress levels," said Prof. Defrin. "We found that not only does psychosocial stress reduce the ability to modulate pain, the changes were significantly more robust among subjects with stronger reaction to stress ('high responders'). The higher the perceived stress, the more dysfunctional the pain modulation capabilities became. In other words, the type of stress and magnitude of its appraisal determine its interaction with the pain system.
"We know from our previous studies and studies of others that chronic stress is far more damaging than acute stress, associated not only with dysfunctional pain modulation capabilities but also with chronic pain and systemic illnesses," said Prof. Defrin.
Defining stress
"Stress is defined as a sense of uncontrollability and unpredictability, precisely like being stuck in traffic where you are helpless and have no control over the situation," said Prof. Defrin. "Stress can have positive repercussions in a challenging work environment, for example, but overall it has primarily negative effects."
The results were also somewhat surprising. "We were sure we would see an increased ability to modulate pain, because you hear anecdotes about people who are injured during fighting or sports having greater pain modulation," said Prof. Defrin. "But we were surprised to find quite the opposite. While there was no visible effect of acute stress on the subject's pain threshold or tolerance, pain modulation decreased in a very dramatic way.
"Modern life exposes individuals to many, recurrent stressful situations," Prof. Defrin observes. "While there is no way to predict the type of stress we will feel under different circumstances, it is advisable to do everything in our power -- adopt relaxation and stress reduction techniques as well as therapy -- to reduce the amount of stress in our lives."
Source:  http://www.sciencedaily.com/releases/2015/02/150205111806.htm

Concordia University study has discovered a new link between chronic disease and social isolation

Difficult circumstances often bring people closer together. But a new Concordia study published in Health Psychology has found that the onset of chronic illness often results in sufferers feeling lonelier -- even for those who have had a steady partner for 50 years or more.
Researchers at the Personality, Aging, and Health Lab at Concordia took on the study because they found that, while plenty of research examined the effect of loneliness on illness, there was a lack of empirical evidence about whether or not illness contributes to loneliness.
"We were surprised by the amount of literature that examined whether people who are lonely are more likely to get sick," says Meaghan Barlow, the study's first author. "Yet none of them asked the opposite question: 'Do sick people get lonely?'"
The new study reveals that they often do when they advance in age, and that it happens regardless of being in a long-term relationship when faced with a bleak diagnosis. "The quality of our social ties plays a role when it comes to coping with the effects of serious disease in later life. And just having a partner around may not be enough," Barlow says.
Barlow and her co-author, Sarah Liu, measured changes in loneliness between 2004 and 2012 in a sample of 121 older adults who were mostly in their 70s. The study was supervised by Carsten Wrosch, who holds a research chair in aging and health at Concordia.
Looking at the numbers provided some insights into how self-protective strategies can reduce the stress associated with a serious health issue. In particular, positively reappraising a difficult health situation and not blaming oneself for the illness prevented feelings of loneliness, most likely because it helps maintain motivation for social involvement and prevents depressive symptoms. "Putting a halt to socializing only contributes to a downward spiral," Barlow says. "Dealing with a chronic illness shouldn't prevent you from still trying to get out there if you can."
Naturally, the challenge for society is to help an aging population find motivation to stay engaged, which means recognizing that the psychological side effects of disease can be offset with an increase in inspiring activity.
"The fact that loneliness can lead to further complications means that measures can be taken to prevent the effects from looping back around," Barlow says. "Finding different ways to connect with other people also means you are less likely to blame yourself for being sick, and you can't count on a partner to fill that gap."
Source:  http://www.medicalnewstoday.com/releases/289369.php

Mouse study finds that serotonin deficiency does increase depression risk

A new study from researchers at Duke University in Durham, NC, finds that mice deficient in serotonin are more vulnerable to social stressors than a group of healthy control mice.

Although the normal mice saw reduced depression symptoms following treatment with Prozac, the low-serotonin mice did not.

Low serotonin levels have traditionally been suspected as playing a role in depression, but there has been little solid evidence to support this hypothesis. Consequently, scientists have been increasingly moving away from the low-serotonin theory and looking instead at other possible causes of depression, such as the relationship between stress and inflammation and other environmental factors.
Last September, Medical News Today reported on a study published in ACS Chemical Neuroscience that found no difference in behaviors between mice that lacked serotonin and a normal group of control mice.
From this finding, the researchers behind that study - from Dingell VA Medical Center and Wayne State University School of Medicine, both in Detroit, MI - concluded that serotonin may not be a dominant factor in depression. Instead, they suggested that risk for the condition may instead be comprised of a range of different factors.
However, the Duke paper - which is published in the Proceedings of the National Academy of Sciences - reports opposite findings to that study.
Senior author Marc Caron, the James B. Duke professor of cell biology at the Duke University School of Medicine and a member of the Duke Institute for Brain Sciences, explains:

"Our results are very exciting because they establish in a genetically defined animal model of serotonin deficiency, that low serotonin could be a contributing factor to the development of depression in response to psychosocial stress - and can lead to the failure of [selective serotonin reuptake inhibitors] to alleviate symptoms of depression."

In their study, the Duke researchers used a transgenic mouse strain - Tph2KI - bred to have only 20-40% of normal serotonin levels.
The team exposed the mice to stress by briefly housing them with an aggressive stranger mouse every day for 7-10 days. To test for depression-like behaviors, the researchers then examined whether the test mice would avoid interacting with the stranger mouse.
The control mice did not exhibit these depression symptoms after a week of social stress, but the serotonin-deficient mice did. Both groups eventually displayed depression-like symptoms following longer periods of stress exposure.
The mice with depression-like symptoms were then treated with Prozac for 3 weeks. Although the normal mice saw reduced depression symptoms following treatment, the Tph2KI mice did not.
Because Prozac is a selective serotonin reuptake inhibitor (SSRI) and works by blocking cells' ability to "recapture" serotonin, Prof. Caron says it makes sense that the antidepressant would be less effective in animals that have low levels of serotonin.
The researchers think this might explain why some depressed people are unresponsive to treatment with SSRIs.

The lateral habenula as drug target for treatment-resistant depression

A brain region called the lateral habenula has been investigated by some studies as a potential drug target for treatment-resistant depression. The lateral habenula is also known as the "punishment" region of the brain, and scientists think that an overactive lateral habenula may trigger depression.
To investigate this, Prof. Caron's team targeted the lateral habenulae of the mice with "designer receptors exclusively activated by designer drugs." (DREADDs) - designer drugs that control the activity of specific neurons.
The scientists found that by inhibiting neurons in the lateral habenulae of the Tph2KI mice using the DREADDs, they were able to reverse the social avoidance behavior of these mice.
Although this is a promising first step in identifying targets for treatment-resistant depression, the researchers say that DREADDs are not appropriate for use in humans.
"The next step is to figure out how we can turn off this brain region in a relatively non-invasive way that would have better therapeutic potential," says lead author Benjamin Sachs, a postdoctoral researcher in Prof. Caron's group.
An additional finding from the research was that the serotonin-deficient mice produced a signaling molecule - β-catenin - in different areas of the brain to the normal mice when they were exposed to social stress.
According to Sachs, this suggests that serotonin deficiency may block a protective pathway that includes β-catenin: "If we can identify what's both upstream and downstream of β-catenin, we might be able to come up with attractive drug targets to activate this pathway and promote resilience."
Written by David McNamee
Source:  http://www.medicalnewstoday.com/articles/289230.php

Brain marker hints at depression, anxiety years later

A car accident, the loss of a loved one and financial trouble are just a few of the myriad stressors we may encounter in our lifetimes. Some of us take it in stride, while others go on to develop anxiety or depression. How well will we deal with the inevitable lows of life?

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A clue to this answer, according to a new Duke University study, is found in an almond-shaped structure deep within our brains: the amygdala. By measuring activity of this area, which is crucial for detecting and responding to danger, researchers say they can tell who will become depressed or anxious in response to stressful life events, as far as four years down the road.
Published Feb. 4, 2015, in Neuron, the results may eventually lead to new strategies to treat depression and anxiety and prevent them from occurring in the first place.
"Often, individuals only access treatment when depression and anxiety has become so chronic and difficult to live with that it forces them to go to a clinic," said the study's first author Johnna Swartz, a Duke postdoctoral researcher in the lab of senior author Ahmad Hariri. "With a brain marker, we could potentially guide people to seek treatment earlier on, before the disorders become so life altering and disruptive that the person can't go on."
Small studies of people at risk for post-traumatic stress disorder (PTSD), such as soldiers deployed to combat zones, have hinted at the link between individual differences in brain activity and the ability to handle stressors.
Those studies also focused on the amygdala -- for its established link to psychiatric disorders including PTSD, anxiety and depression -- but included participants who had endured highly traumatic events such as active combat. In contrast, most people in the general population experience less severe forms of stress, such as unemployment, divorce, or a death in the family.
In the new study, Hariri's team scanned the brains of healthy college students as they looked at angry or fearful faces, which signal danger in our environment. These threatening pictures normally trigger the amygdala, and the scientists measured the intensity of this activation using functional magnetic resonance imaging, a noninvasive, indirect measure of brain activity.
Every three months after the scan, participants completed an online survey documenting stressful life events and their impact, as well as a questionnaire that assessed symptoms of depression and anxiety.
From the initial 753 participants who were scanned, nearly 200 completed the online surveys an average of two years, and as long as four years, after the scan. In these individuals, the more reactive the amygdala was at the study's start, the more severe their symptoms of anxiety or depression in response to stressful events they encountered after scanning.
Importantly, the participants who had an overzealous amygdala but who had not experienced recent stress did not show these elevations in symptoms.
"To find that a single measure of the brain can tell us something important about a person's psychological vulnerability to stress up to four years later is really remarkable and novel," said Hariri, a professor of psychology and neuroscience and a member of the Duke Institute for Brain Sciences.
The ability for the brain marker to predict symptoms was surprising, Hariri said, given that the population was healthy and, for the most part, dealing with normal and relatively mild stressors for young adults, like an argument with a parent, or problems at work or school.
The new research is part of the Duke Neurogenetics Study, a long-term collection of data on genes, brain activity, environmental factors and symptoms related to psychiatric disorders. The ultimate goal is to understand why some people are more vulnerable to developing depression, anxiety and other mental health problems.
Hariri and his team are continuing to follow their study participants. "We want to know just how far in the future knowing something about an individual's brain helps us understand their risk," he said.
The group is also exploring other measures, such as a person's genes, to predict the differences in amygdala activity, and in turn, the relative risk for anxiety and depression.
Isolating a person's DNA from a saliva sample and looking for specific differences in its letter code is easier and less expensive than having them undergo a brain scan. Thus, a genetic screen that tells us about a person's amygdala reactivity is more likely to be available and useful for doctors working to prevent mental illness in their patients, Hariri said.
Source:  http://www.sciencedaily.com/releases/2015/02/150204125756.htm

Depression: New Causes, New Treatments

People who experience depression are usually more focused on treating the condition than finding its cause. But new research is beginning to shed light on both the triggers for depression and how to alleviate it.
Depression affects one in 10 Americans at some point in their lives, and the number of patients diagnosed with depression goes up by about 20 percent each year. The World Health Organization says it is the top cause of disability worldwide, and that five to seven percent of people on Earth experience a major depressive episode in a given year.
As science evolves and more people speak out about the issue, we’re finding that depression has more root causes than anyone suspected.
Read More: Meditation's Effects Similar to Pills for Depression »

Cause: Concussions

A new study in the Journal of Adolescent Health recommends that doctors screen teens with a history of concussion, as they are three times more likely to suffer from depression. Researchers evaluated data from 36,000 adolescents; of them, 2.7 percent had a concussion and 3.4 percent experienced depression.
According to the Centers for Disease Control and Prevention, 1.6 to 3.8 million sports- and recreation-related concussions occur each year in the U.S. Moreover, a mild brain injury occurs every 21 seconds, so screenings are crucial.

Cause: Chronic Stress

A research team at the Hebrew University of Jerusalem found that changes in one type of brain cell, called microglia, indicate depressive symptoms brought on by exposure to chronic stress. Microglia make up about 10 percent of brain cells and represent the immune system in the brain. They are also involved in physiological processes that have nothing to do with infection or injury—such as the body’s response to stress, research has shown.

The Israeli researchers were able to demonstrate in animals that compounds which alter the function of microglia make efficient drugs. The findings were published in Molecular Psychiatry.
Raz Yirmiya, a professor at the university, said the research shows that disturbances in microglia cells play a role in causing psychopathology in general and depression in particular.
“They may be able to help people get symptom relief faster,” said Amy Morin, a therapist from Maine, who said this could be great news for people who are experiencing a loss of day-to-day function due to depression.
“Waiting four to six weeks to see if an anti-depressant is working can be fatal for people who experience suicidal ideation as part of their depression,” she added.
See Why Emergency Rooms May Be the Wrong Solution for the Mentally Ill »

Cause: Immune Cells

Other research also indicates that immune cells outside of the brain can play a role in the development of depression.
Scientists at the Icahn School of Medicine at Mount Sinai found that rodents with high levels of the circulating pro-inflammatory immune chemical known as interleukin-6 were more vulnerable to symptoms of depression. This suggests that differences in the peripheral immune system can affect a person's mental state.
Learn More: Newly Discovered ‘Teen Gene’ May Help Doctors Combat Mental Illness »

Cause: Inactivity

The December issue of the Canadian Journal of Cardiology included a report showing that people who were inactive after cardiac surgery had as much as a 40 percent greater risk of depression.
The researchers recommend that doctors screen heart patients for depression and level of physical activity to minimize symptoms. Patients should also remain as active as possible after surgery.

Treatment: Psychobiotics

Research into depression treatments is also advancing rapidly.

In an article in Biological Psychiatry, Timothy Dinan and his colleagues at University College Cork in Ireland discuss the concept of psychobiotics. These are live organisms taken like probiotics to help treat psychiatric illnesses.

Dinan and his team examined a study on the benefits of B. infantis, a specific probiotic. They found that it normalized rats’ behavior and previously abnormal immune response. Some psychobiotics have anti-inflammatory effects, which is beneficial because depression and stress are exacerbated by inflammation in the body.
“We need to be careful not to reduce all depression to a purely biological level,” noted Eileen Kennedy-Moore, a psychologist and co-author of Smart Parenting for Smart Kids. “People can have marvelously healthy guts but still need to work on communicating better with their spouse, coping with their child's tantrums, making time for friends, managing office politics, or finding meaningful and satisfying work.”
Read More: Therapy Provides 'Critical Breakthrough' for Depressed Insomniacs »
Morin agreed that the development could be a game-changer.
“Although it sounds a little like a science fiction movie, the research on psychobiotics is showing some interesting results,” Morin said. “It could prove to open up a lot of new possible treatment options for people suffering from depression.”

Treatment: Pharmacogenomics

Mona Shattell, a registered nurse and professor at DePaul University specializing in mental health, said that new research on genetics and psychopharmacology—called pharmacogenomics—can help doctors determine which medication works best to treat an individual patient's depression. This would do away with the “trial and error” method currently used, which involves testing different medications that can take weeks to have an effect.
“It can't be overstated…providers who can better target—that is, choose the right drug the first time—will improve the quality of life for persons experiencing debilitating depression,” she said, adding that it could also have a positive impact on those experiencing despair and suicidal thoughts.
Source:http://www.healthline.com/health-news/mental-new-causes-of-and-treatments-for-depression-011314#3