Stress Relief - How 10 Minutes a Day Can Reduce Stress

Being overwhelmed with chores around the house and can be added to the total daily and weekly stress. You can reduce this voltage to 10 minutes a day.
Consumer confusion adds to the mental and emotional stress as well. Because of confusion stimulates your brain.
You can reduce a lot of stress, a little planning and with ten minutes a day to clean up, neaten up, and put in order.
Here's how it works:
Supplementing your regular cleaning, spending some time each day cleaning your home you will reduce stress and overwhelm.
For example:
• to use these few minutes to clean the surface clutter• neat baby room• while you're on the phone, clear the box and throw away useless or two points• Dust the long-forgotten places• put something, or something far obvious needs looking into your eyes
Do not spend too much time and effort on these tasks, the point here is to make a quick once over and do a big project task.
How do you work in this short task, you release some nervous energy, and so something very productive. Your crush and stress is reduced because of the small mess now been resolved. You also know that the rest of the mess will be implemented over the next few days.
You'll be amazed how this little attention to neatness can do for a long time, and how organized, productive, and stress is reduced you will become.
Now, when you get around a planned, more intense cleaning projects like spring cleaning or winter, which can be extremely depression and can take several weeks to finish this sentence and the action will be doubled, so your projects are much nicer.
You can also use this offer if you or a friend move. Concentrated effort in decluttering this stressful time can make navigation frustrating. Doing ten minutes a day, cleaning, as you prepare to pass orders and packaging process eliminates the buy Valium. You will find this task will be that much easier and less time consuming.
You will find the extra hours that you should not continue to spend ten minutes a day cleaning, because you are fully resolved disorder, and possibly other family members were taught to help in the cleanup process.
So, take ten minutes a day, pick it up, put in order and reduce stress.

High Levels of Leptin Associated With Lower Depression

Leptin is a hormone released by adipocytes (fat cells) that signals excess, or fullness, after a meal. Studies in chubby people have found that there is a coupling between weight gain and an ineptitude to produce adequate amounts of leptin. A group study looks at a new role excessive levels of the hormone may also demote symptoms of depression.

Leptin Levels Influence a Variety of Body Processes

Elizabeth Lawson MD of Massachusetts Blended Hospital and Harvard Medical Credo and colleagues studied the relationship between leptin levels and symptoms of foreboding and depression in 64 women of odd weights. Fifteen of the women had anorexia nervosa, an eating brouhaha characterized by abnormally low force and body fat.
Twelve were of ordinary weight but had hypothalamic amenorrhea, or the cessation of menstruation. Leptin is also known to flatter a role in regulation of reproductive go. Twenty of the remaining women were of orthodox weight and 17 were overweight or pot-bellied, but all in good health.
 The on participants were asked questions to assess symptoms of downheartedness and anxiety with higher scores indicating more symptoms. Blood leptin levels were regulated and BMI was assessed. The researchers establish that higher leptin levels were linked to decreased symptoms of anxiety and depression, a relationship that was neutral of BMI.
The finding, also seen in subhuman studies, indicates that leptin may mediate symptoms of impression and that this really is not a function of weight stature, Dr. Lawson said. Leptin injections are already being tested in gross models as an obesity treatment and supplementary research in humans “commitment be important in understanding whether this hormone has a potency role in the treatment of sadness,” concluded the authors.
It is provocative to note that a aforesaid study conducted at the University of Florida initiate that exercise can suffer with a positive effect on leptin levels, allowing the hormone to incite properly in the body. Worry has long been associated with a contract in depression symptoms, the buy generic Valium online, a find that could be relative in future studies as satisfactory.

Newer Antidepressants Not Always Better

New antidepressants might be no more effective than the best existing drugs, according to two new systematic reviews that compared 12 commonly used medications.
“Patients are usually encouraged to take the newest medication,” said lead author Andrea Cipriani, M.D., of the University of Verona, in Italy. “But it’s better to have an old depression treatment that has been proved with many patients and many years in the market.”
The reviews suggest that sertraline — sold under the brand name Zoloft since 1991— could be the best initial choice of antidepressant in people with acute major depression. The generic formulation produced the best balance of effectiveness, tolerability and purchase price, the authors say.
Patients also did well on one of the newest antidepressants, escitalopram (Lexapro), but it is not yet available in lower-cost generic form. The authors note that comprehensive economic studies are necessary to evaluate overall cost-effectiveness of various treatments.
Cipriani said that the review recommendations are for new episodes of depression. “If a patient is taking another drug and doing well, we are not saying he has to change.”
The reviews appear in the most recent issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.
Depression is the fourth-leading cause of disease burden worldwide and antidepressant drugs are now the mainstay of treatment for moderate to severe cases.
The aim of the two reviews was to compare the benefits and side effects of sertraline and escitalopram, respectively, with those of other antidepressants during the first six to 12 weeks of treatment.
Cipriani noted that all of the included studies compared one depression drug against another — not to a placebo — so the results reveal not the absolute effect, but rather the relative advantages and disadvantages of various medications.
In addition, these reviews rely on summary data from each study, rather than individual patient data. Future studies that go into greater detail can help identify the best depression medications for various subgroups of patients such as men vs. women, teens vs. adults and so on.
For sertraline, the reviewers included 59 randomized controlled trials totaling about 10,000 participants. Sertraline proved more effective than fluoxetine (Prozac), but less effective than mirtazapine (Remeron). In terms of side effects, bupropion (Wellbutrin) was easier to tolerate than sertraline, while the latter outscored amitriptyline (Elavil), imipramine (Tofranil), paroxetine (Paxil) and mirtazapine (Remeron).
For escitalopram, the reviewers included 22 randomized controlled trials totaling about 4,000 participants. Few statistically significant differences appeared in this review, although escitalopram was more effective than citalopram (Celexa) and fluoxetine (Prozac) and had fewer side effects than duloxetine (Cymbalta). The drug manufacturer sponsored most of the studies in this review, so there may be biases in favor of escitalopram.
Rather than seeking genuine advances in treatment, the review authors say, some pharmaceutical companies seem to be introducing close chemical cousins of generic medications. By gaining patent protection for the “new” drug, a company can market it as a higher-priced brand name product.
Sponsorship bias is a recurring concern in trials of virtually all new medications. In the Cochrane reviews themselves, one of the co-authors has received research funds and speaking fees from the companies Asahi Kasei, Astellas, Dai-Nippon Sumitomo, Eisai, Eli Lilly, GlaxoSmithKline, Janssen, Kyowa Hakko, Meiji, Nikken Kagaku, Organon, Otsuka, Pfizer and Yoshitomi. The Japanese Ministry of Education, Science and Technology, and the Japanese Ministry of Health, Labour and Welfare have also funded some of his research.
However, the co-authors of these Cochrane reviews also published a recent study in The Lancet that was free of any potential funding bias. The study also used a more complex statistical method to analyze data from 117 randomized controlled trials involving 25,928 participants.

Scientists May Have Found Long-Pursued Binding Site For Antidepressants

Antidepressants
Sscientists have a major new clue as to where the long-pursued binding site for commonly used antidepressants ” potentially the site that triggers the medications ,, effects ” may be on brain cells. The finding could lead to better medications for depression, but also has important implications for other mental illnesses because it addresses a biological flaw that a number of them share.
The flaw involves a molecular mechanism that maintains the balance of key brain chemicals called neurotransmitters. The mechanism acts as a pump by transporting neurotransmitters into brain cells when needed, a process in which correct amount and timing are essential for parts of the brain to communicate with each other. However, the pumps are dysfunctional in depression and some other mental illnesses, including autism and obsessive-compulsive disorder.
Medications called tricyclic antidepressants help offset an imbalance in the neurotransmitters serotonin and norepinephrine by shutting the pumps. This stops the neurotransmitters from flooding back into the brain cells that emit them, making more available to other cells ” thus helping to relieve depression. However, it was not known how the medications shut the pumps at the molecular level.
The new study is the first to pinpoint a molecular mechanism that could provide an explanation. Results were published by Satinder Singh, PhD, Atsuko Yamashita, PhD, and Eric Gouaux, PhD, in the August 23 issue of Nature.
Rather than looking at the pump for these neurotransmitters, the researchers used a model in their experiments: a similar pump found in bacteria. Both are in a family of pumps called sodium-coupled transporters. The bacterial pump operates virtually identically to the one in brain cells, but changes in its molecular structure are easier to analyze.
Experiments showed that tricyclic antidepressants latch onto the bacterial pump, changing its molecular structure in a way that effectively plugs it. Could the medications be affecting similar pumps for serotonin and norepinephrine on human brain cells in the same way? The researchers are cautious about drawing a direct comparison; the two kinds of pumps are related, but somewhat different.
But now that scientists know that plugging these kinds of pumps is one way to reduce their activity, researchers may be able to develop medications that target them more directly and efficiently. This could result in more effective antidepressants with fewer side effects. The findings may also extend to development of medications for other mental illnesses in which pump dysfunction plays a role.

Brain Magnetic Stimulation Effective for Severe Depression, Approved by FDA

Medical University of South Carolina physician Dr. Mark S. George has answered the question of whether a technique involving brain stimulation will work for resistant, severe depression. "The answer is 'yes’,” he says.
Transcranial magnetic stimulation (TMS) is a technique that uses magnetic coils to deliver a daily dose of an electrical current that passes through the skill to reach a specific part of the brain called the left prefrontal cortex that plays a role in emotion and mood regulation. It has been approved by the US Food and Drug Administration for depression resistant to other treatments.
Using electric current to resolve depression was first performed in the 1940’s and 1950’s. One more familiar technique, called electroconvulsive or electroshock therapy can induce seizures and may cause memory loss and brain damage. TMS is a less invasive form of ECT.
* New and safer brain stimulation treats depression
Issues with proving the technique’s effectiveness included the ability to compare TMS to a fake or placebo without either the participant or the researcher knowing which was which, called a “double blind study”. Dr. George solved the problem by developing a “dummy device” that clicks and causes the eye muscles to twitch, just like the real TMS device.
Dr. George and colleagues randomly assigned 190 patients to two groups, one receiving 37.5 minutes of TMS while the other spent the same amount of time on the dummy. The patients had been depressed at least three months, but not longer than five years, and had taken multiple medications that did not resolve the depression.
The treatments occurred once a day for three weeks. After the study period, 14% of the real TMS group recovered from their depression compared to 5% of the group receiving the placebo, making them four times as likely to recover.
In the second phase of the study, all patients were given the real TMS treatment, and 30% recovered from depression. Side effects reported by the study participants included headache, discomfort at the TMS site, and eye twitching.
Patients who had their depression resolve were then given the antidepressant Effexor (venlafaxine) and a small dose of lithium, a combination shown to help people stay well after treatment. Most participants remained depression-free for several months after the study.
Further studies of TMS will include learning how long a treatment is needed to be optimally effective. "It's very muddy now exactly how long we need to treat patients," George said. "It looks as if from this trial you at least need to try three weeks and maybe even six weeks before you would give up." Dr. George would also like to try intermittent TMS treatments in an effort to avoid giving the medications once symptoms resolved. "I'm optimistic that it's pointing us in a path of understanding how to interact with the brain in a non-invasive way to get people well."

Mechanism For Postpartum Depression Found In Mice

Researchers have pinpointed a mechanism in the brains of mice that could explain why some human mothers become depressed following childbirth. The discovery could lead to improved treatment for postpartum depression.Supported in part by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, the study used genetically engineered mice lacking a protein critical for adapting to the sex hormone fluctuations of pregnancy and the postpartum period.
“For the first time, we may have a highly useful model of postpartum depression,” said NIMH Director Thomas R. Insel, M.D. “The new research also points to a specific potential new target in the brain for medications to treat this disorder that affects 15 percent of women after they give birth.”
“After giving birth, female mice deficient in the suspect protein showed depression-like behaviors and neglected their newborn pups,” explained Istvan Mody, Ph.D., of the University of California at Los Angeles (UCLA), who led the research. “Giving a drug that restored the protein’s function improved maternal behavior and reduced pup mortality.”
Researchers had suspected that postpartum depression stemmed from the marked fluctuations in the reproductive hormones estrogen and progesterone that accompany pregnancy and childbirth. Yet manipulating the hormones experimentally triggers depression only in women with a history of the disorder. The roots of their vulnerability remain a mystery.
Evidence suggested that the hormones exert their effects on mood through the brain’s major inhibitory chemical messenger system, called GABA, which dampens neural activity, helping to regulate when a neuron fires.
Mody and Maguire discovered that a GABA receptor component, called the delta subunit, fluctuated conspicuously during pregnancy and postpartum in the brains of female mice, hinting that it might have pivotal behavioral effects. To find out, they used mice lacking the gene for this subunit and studied them in situations that can elicit responses similar to human depression and anxiety.
Much like human mothers suffering from postpartum depression, the genetically altered mouse mothers were more lethargic and less pleasure-seeking than normal mice. They also shunned their pups and failed to make proper nests for them.
This abnormal maternal behavior was reversed and pup survival increased after the researchers gave the animals a drug called THIP that acts on the receptor in a way that specifically restores its function in spite of the reduced number of subunits.
“Improper functioning of the delta subunit could impair the GABA system’s ability to adapt to hormone fluctuations during the highly vulnerable post partum period,” explained Maguire. “Targeting this subunit might be a promising strategy in developing new treatments for postpartum depression.”

The Magic Drug for Depression and Anxiety? Exercise

Two new studies released recently have highlighted the positive influence that exercise can have in lifting depression and quelling anxiety. Researchers encourage mental health providers to begin prescribing exercise in addition to other standard therapies of medication and therapy.
The first study, published in the Archives of Internal Medicine in February, found that in physically inactive patients with chronic health conditions such as heart disease or arthritis, exercise training may significantly reduce anxiety. The research, from the University of Georgia in Athens, found that sessions of at least 30 minutes a day had lasting effects on the participants.
In the second study, Jasper Smits, director of the Anxiety Research and Treatment Program at Southern Methodist University in Dallas and Michael Otto, psychology professor at Boston University, analyzed dozens of studies and meta-analytic reviews related to exercise and mental health. Individuals who exercise reported fewer symptoms of anxiety and depression and lower levels of stress and anger.
Exercise affects certain neurotransmitters systems in the brain and can re-establish positive behaviors which may have been put aside. It can also reduce the fear and physical symptoms of anxiety.
Because the standard treatments of cognitive behavioral therapy and pharmacotherapy (medications such as anti-depressants), do not reach everyone who needs them, all physicians should encourage those who can to perform daily exercise to help ease the symptoms of depression and/or anxiety.
"Exercise can fill the gap for people who can't receive traditional therapies because of cost or lack of access, or who don't want to because of the perceived social stigma associated with these treatments," says Smits. "Exercise also can supplement traditional treatments, helping patients become more focused and engaged." The research suggests that patients work up to 150 minutes of moderate-intensity exercise a week for mental health benefits.
Smits emphasizes that the benefits are seen immediately for those who suffer from depression and anxiety. "After just 25 minutes, your mood improves, you are less stressed, you have more energy - and you'll be motivated to exercise again tomorrow. A bad mood is no longer a barrier to exercise; it is the very reason to exercise."
Depression and anxiety can either occur together or separately. Depression is a serious medical condition that can potentially affect every part of a person’s life, such as the physical body, mood, thoughts, and eating and sleeping patterns. It is not a “case of the blues” and it does not relate to a specific situation, such as grief or sadness. Anxiety in itself is not harmful – it is a normal reaction to stress. However, when anxiety becomes and “excessive, irrational dread of everyday situations”, it can be disabling.
There are five major types of anxiety. Generalized Anxiety (GAD) is characterized by chronic anxiety, exaggerated worry and tension, even when there is nothing to provoke it. Obsessive Compulsive Disorder (OCD) is characterized by recurrent and unwanted thoughts and/or repetitive behaviors. Panic disorder is the unexpected and repeated episode of intense fear that is accompanied by physical symptoms, such as chest pain, heart palpitations, shortness of breath or abdominal distress. Post-Traumatic Stress Disorder (PTSD) is an anxiety that can develop after a terrifying event in which grave physical harm occurred or was threatened, such as disasters, accidents, or military combat. Social Anxiety Disorder is the overwhelming feeling of anxiety and excessive self-consciousness in everyday social situations.
The researchers presented their findings March 6 in Baltimore at the annual conference of the Anxiety Disorder Association of America. Their workshop was based on their therapist guide "Exercise for Mood and Anxiety Disorders," with accompanying patient workbook (Oxford University Press, September 2009).