Tag Archives: Columbia University

How to stop being furiously angry

Isabel Clarke, a clinical psychologist who runs an anger-management clinic, explains why bad temper is a growing problem — and how to keep it in check.

CLICK & SEE

Imagine a pill you could take that instantly calms your temper when it’s about to burst into a Herculean mess. That’s what researchers might be on the brink of formulating after experiments helped them to identify the brain’s anger centre. Scientists at New York University found that chemical changes in the brain’s lateral septum made the mice attack other animals. It’s a discovery that could lead to a calming drug.

Meanwhile, we remain a nation of quiet seethers. Research by PruHealth found that nearly half of us admit to snapping at colleagues, 28 per cent to shouting at people at work and one in four to slamming down phones and banging fists on desks. On social media, it takes far less than a Katie Hopkins soundbite to enrage the digital British public into attack mode. But until the anger pill is a reality, our only option is self-management…

Why are we all so angry?
The more stress someone is under, the more likely they are to have an anger problem. Because we are working harder than ever, more chronically stressed people are presenting to their GPs and mental health clinics with anger issues.

Add to this, disinhibition — there is a greater level of acceptance of anger, swearing and even violent behaviour than there was 50 years ago — and the increased speed of our reactions, thanks to social media and email (as opposed to writing letters) and the root of our anger problem is clear.

Anger manifests itself in different ways. One person might turn their anger against themselves, which can manifest as depression, addiction or self-harm. Another might explode. But anger has a necessary function: to protect, by alerting us to threat and giving us the courage to meet challenges.

That “threat system” is part of our evolution and changes your body from a calm state into one that is ready to attack or run away. A shot of the stress hormone adrenaline is released, which leads to tense muscles, increased blood circulation, short breathing and alertness.

People who are under chronic stress exist in a constant state of attack mode, which can have a detrimental effect on their health. It is like driving in second gear on the motorway — you’re using the car’s resources to tackle a problem that isn’t there, which means that your car is likely to be damaged, burn out or even explode. The other problem is that the buzz from adrenaline can be addictive. Likewise, when a person gets what they want as a result of showing their anger, they can get caught in an anger trap, where outbursts seem like the only way to express their needs. So controlling excess anger is essential.

Look out for warning signs:….CLICK & SEE
Notice when your body is moving into threat mode — this might be during a conversation, while driving or when commuting — and pay attention to your early-warning signs of anger. Everyone’s signs will be different but they might include a tenseness across the shoulders or an uncomfortable feeling in the stomach. Ask yourself: What’s the matter? Then do something about it. This might be having a constructive conversation or using a simple breathing technique. For example, making your out breath longer than your in breath can be instantly relaxing. Paying attention to the physical reality around you and taking in the bigger picture, rather than the thoughts in your head, can also help. This allows you to instantly distance yourself from your own threat system and get the mental space to ask yourself whether you need to take some time out (see below).

Escape wind-up thinking:
The language we use in our thoughts and conversations can alert the body to a threat, priming it to react with anger. Characteristic wind-up thoughts include “shoulds”, “musts” or “oughts” as well as phrases beginning with “You never”, “You always” or “It’s not fair”. These are definite, accusatory and inflexible, and can keep you fixed in threat mode where you’re more likely to blow up. It can be hard to change your thought patterns. Instead, recognise wind-up thinking and acknowledge that it’s not in your best interest to continue it.

Object without losing it:
Angry people often try to project an attitude of “I’m cool, nothing gets to me”. As a result, they may allow resentments to build up until they eventually explode. Learning to communicate assertively is essential. The key is to state what you want firmly and calmly with words such as: “Excuse me, I can’t let this go.” It’s also important to put yourself in the other person’s shoes — this is something people with anger issues often have a hard time with, as they tend to be wound up in their own position.

Call time:
It can be difficult to have a constructive conversation if one or both parties have switched into attack mode. Take a couple having an argument. If one of them notices their own, or the other person’s, anger building up with physical signs, such as increased breathing and a raised voice, they might say they need to go out for a walk to clear their head. Often, this is the point where the other partner won’t let them, desperate to get one last point across. But it’s also the point where arguments can escalate to emotional or physical violence.

An expart councelor has worked with couples on negotiating this space and ensuring the other person respects it. Having such an agreement is essential for dealing with anger, especially at home. Don’t continue the discussion if you observe in someone’s behaviour or speech — or your own — that the body has gone into action mode. Take time out. Go for a walk outside, write in a journal or call a friend — set aside some alone time…...CLICK & SEE

Let go:
When your body is in threat mode, anything — from being told you might lose your job to someone jumping in front of you in a queue — can feel equally outrageous and worthy of an outburst. By taking a step back with the simple breathing practices mentioned above, you can see the bigger picture and work out whether it really is outrageous and worth fighting for. Ask yourself if it will matter in five minutes. If the answer is no, let it go.

Source: The Telegraph (Kolkata, India)

Best way to get rid from sudden anger  is to practice Yoga  with  Medition & Pranayama.

Products from Amazon.com

Advertisements

Glandular fever

Definition:
Glandular fever is a viral infection associated with a high fever.It’s also known as infectious mononucleosis or kissing disease (long ago it was realised that the infection was passed on through saliva – for example, by kissing).

It is a viral infection caused by the Epstein-Barr virus. Glandular Fever is often spread through oral acts such as kissing, which is why it is sometimes called “The Kissing Disease“. However, Glandular Fever can also be spread by airborne saliva droplets.

click to see the pictures

Infectious Mononucleosis (IM) is an infectious, widespread viral disease caused by the Epstein-Barr virus (EBV), one type of herpes virus, to which more than 90% of adults have been exposed. Occasionally, the symptoms can reoccur at a later period. Most people are exposed to the virus as children, when the disease produces no noticeable symptoms or only flu-like symptoms. In developing countries, people are exposed to the virus in early childhood more often than in developed countries. As a result, the disease in its observable form is more common in developed countries. It is most common among adolescents and young adults.

Especially in adolescents and young adults, the disease is characterized by fever, sore throat and fatigue, along with several other possible signs and symptoms. It is primarily diagnosed by observation of symptoms, but suspicion can be confirmed by several diagnostic tests.

The syndrome was described as an infectious process by Nil Filatov in 1887 and independently by Emil Pfeiffer in 1889.
Symptoms:-
The following are mainly the symptoms of Glandular Fever:
*Headache
*Fever
*Sore throat/hard to swallow
*Tiredness, fatigue and malaise
*Enlarged lymph nodes
*Loss of appetite
*Muscle aches
*Tender enlargement of the glands (lymph glands or lymph nodes)
*Skin rash
*Sweating
*Stomach pain and enlarged spleen
*Enlarged liver
*Jaundice
*Depression
*Joint pain
*Swelling around eyes
*Orange urine (or discolored
*High blood pressure

Causes:
Glandular fever is caused by the Epstein-Barr virus. This can attack only two types of cell in the body: those in the salivary glands and white blood cells known as B lymphocytes (B-cells).

The most common way of spreading the virus is through the transmission of saliva from one person to another. Coughing, sneezing, and sharing drink bottles, eating utensils and other personal items can also spread the virus. In addition, the virus can also be spread through blood transfusion and organ transplantation.

Infection begins in the salivary glands, which release large amounts of the virus into the saliva. The infection spreads to the B lymphocytes, causing them to multiply, and causing the lymph glands to swell and become painful.

Once infected, the virus remains dormant in the body’s cells for the rest of a person’s life.

Diagnosis:
The diagnosis of glandular fever or infectious mononucleosis is based on your physical symptoms, and will include a blood test and a throat swab. Your doctor will perform a blood test to determine abnormalities in the white blood cells. A throat swab will help determine if you have glandular fever.

The most commonly used diagnostic criterion is the presence of 50% lymphocytes with at least 10% atypical lymphocytes (large, irregular nuclei), while the person also has fever, pharyngitis and adenopathy. Furthermore, it should be confirmed by a serological test.  The atypical lymphocytes resembled monocytes when they were first discovered, thus the moniker “mononucleosis” was coined. Diagnostic tests are used to confirm infectious mononucleosis but the disease should be suspected from symptoms prior to the results from hematology. These criteria are specific; however, they are not particularly sensitive and are more useful for research than for clinical use. Only half the patients presenting with the symptoms held by mononucleosis and a positive heterophile antibody test (monospot test) meet the entire criteria. One key procedure is to differentiate between infectious mononucleosis and mononucleosis-like symptoms.

There have been few studies on infectious mononucleosis in a primary care environment, the best of which studied 700 patients, of which 15 were found to have mononucleosis upon a heterophile antibody test. More useful in a diagnostic sense are the signs and symptoms themselves. The presence of splenomegaly, posterior cervical adenopathy, axillary adenopathy, and inguinal adenopathy are the most useful to suspect a diagnosis of infectious mononucleosis. On the other hand, the absence of cervical adenopathy and fatigue are the most useful to dismiss the idea of infectious mononucleosis as the correct diagnosis. The insensitivity of the physical examination in detecting splenomegaly means that it should not be used as evidence against infectious mononucleosis.

In the past the most common test for diagnosing infectious mononucleosis was the heterophile antibody test which involves testing heterophile antibodies by agglutination of guinea pig, sheep and horse red blood cells. As with the aforementioned criteria, this test is specific but not particularly sensitive (with a false-negative rate of as high as 25% in the first week, 5–10% in the second and 5% in the third). 90% of patients have heterophile antibodies by week 3, disappearing in under a year. The antibodies involved in the test do not interact with the Epstein-Barr virus or any of its antigens. More recently, tests that are more sensitive have been developed such as the Immunoglobulin G (IgG) and Immunoglobulin M (IgM) tests. IgG, when positive, reflects a past infection, whereas IgM reflects a current infection. When negative, these tests are more accurate in ruling out infectious mononucleosis. However, when positive, they feature similar sensitivities to the heterophile antibody test. Therefore, these tests are useful for diagnosing infectious mononucleosis in people with highly suggestive symptoms and a negative heterophile antibody test. Another test searches for the Epstein-Barr nuclear antigen, while it is not normally recognizable until several weeks into the disease, and is useful for distinguishing between a recent-onset of infectious mononucleosis and symptoms caused by a previous infection. Elevated hepatic transaminase levels is highly suggestive of infectious mononucleosis, occurring in up to 50% of patients.

A fibrin ring granuloma may be present.

Diagnosis of acute infectious mononucleosis should also take into consideration acute cytomegalovirus infection and Toxoplasma gondii infections. These diseases are clinically very similar by their signs and symptoms. Because their management is much the same it is not always helpful, or possible, to distinguish between EBV mononucleosis and cytomegalovirus infection. However, in pregnant women, differentiation of mononucleosis from toxoplasmosis is associated with significant consequences for the fetus.

Acute HIV infection can mimic signs similar to those of infectious mononucleosis and tests should be performed for pregnant women for the same reason as toxoplasmosis.

Other conditions from which to distinguish infectious mononucleosis include leukemia, tonsillitis, diphtheria, common cold and influenza

Treatment:
Self care:
Infectious mononucleosis is generally self-limiting and only symptomatic and/or supportive treatments are used.  Rest is recommended during the acute phase of the infection, but activity should be resumed once acute symptoms have resolved. Nevertheless heavy physical activity and contact sports should be avoided to mitigate the risk of splenic rupture, for at least one month following initial infection or splenomegaly has resolved, as determined by a treating physician.

MedicationsIn terms of pharmacotherapies, non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen may be used to reduce fever and pain. Prednisone, a corticosteroid, is commonly used as an anti-inflammatory to reduce symptoms of pharyngeal pain, odynophagia, or enlarged tonsils, although its use remains controversial due to the rather limited benefit and the potential of side effects. Intravenous corticosteroids, usually hydrocortisone or dexamethasone, are not recommended for routine use but may be useful if there is a risk of airway obstruction, severe thrombocytopenia, or hemolytic anemia. There is little evidence to support the use of aciclovir, although it may reduce initial viral shedding. However, the antiviral drug valacyclovir has recently been shown to lower or eliminate the presence of the Epstein-Barr virus in subjects afflicted with acute mononucleosis, leading to a significant decrease in the severity of symptoms. Although antivirals are not recommended for patients presenting with simple infectious mononuscleosis, they may be useful (in conjunction with steroids) in the management of patients with severe EBV manifestations, such as EBV meningitis, peripheral neuritis, hepatitis, or hematologic complications. Antibiotics are not used as they are ineffective against viral infections. The antibiotics ampicillin and later the related amoxicillin   are relatively contraindicated in the case of any coinciding bacterial infections during mononucleosis because their use precipitates a non-allergic rash close to 99% of the time.

In a small percentage of cases, mononucleosis infection is complicated by co-infection with streptococcal infection in the throat and tonsils (strep throat). Penicillin or other antibiotics (with the exception of the two mentioned above) should be administered to treat the strep throat. Opioid analgesics are also relatively contraindicated due to risk of respiratory depression.
Prognosis:
Serious complications are uncommon, occurring in less than 5% of cases:

*CNS: Meningitis, encephalitis, hemiplegia, Guillain-Barré syndrome, and transverse myelitis. EBV infection has also been proposed as a risk factor for the development of multiple sclerosis (MS), but this has not been confirmed.

*Hematologic: Hemolytic anemia (direct Coombs test is positive) and various cytopenias; Bleeding (caused by thrombocytopenia).[

*Mild jaundice

*Hepatitis (rare)

*Upper airway obstruction (tonsillar hypertrophy) (rare)

*Fulminant disease course (immunocompromised patients) (rare)

*Splenic rupture (rare)

*Myocarditis and pericarditis (rare)

Once the acute symptoms of an initial infection disappear, they often do not return. But once infected, the patient carries the virus for the rest of his or her life. The virus typically lives dormantly in B lymphocytes. Independent infections of mononucleosis may be contracted multiple times, regardless of whether the patient is already carrying the virus dormantly. Periodically, the virus can reactivate, during which time the patient is again infectious, but usually without any symptoms of illness.  Usually, a patient has few if any further symptoms or problems from the latent B lymphocyte infection. However, in susceptible hosts under the appropriate environmental stressors the virus can reactivate and cause vague physical complaints (or may be subclinical), and during this phase the virus can spread to others. Similar reactivation or chronic subclinical viral activity in susceptible hosts may trigger multiple host autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s syndrome, antiphospholipid antibody syndrome, and multiple sclerosis. Such chronic immunologic stimulation may also trigger multiple type of cancers, particularly lymphoma—strongest cancer associations with EBV are nasopharyngeal carcinomas, Burkitt’s lymphoma, and Hodgkin’s lymphoma. EBV’s potential to trigger such a wide range of autoimmune diseases and cancers probably relates to its primary infection of B lymphocytes (the primary antibody-producing cell of the immune system) and ability to alter both lymphocyte proliferation and lymphocyte antibody production.

Prevention:
A vaccine against the Epstein-Barr virus is under development. The infection is most contagious during the feverish stage, when contact with others should be avoided.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.nativeremedies.com/ailment/glandular-fever-symptoms-info.html
http://simple.wikipedia.org/wiki/Glandular_fever
http://simple.wikipedia.org/wiki/Glandular_fever
http://www.bbc.co.uk/health/physical_health/conditions/glandularfever2.shtml

http://www.treatfast.com/mononucleosis-xidc18255.html

Enhanced by Zemanta

Foe Turns Friend

A-beta, a protein implicated in Alzheimer’s, may be the brain’s shield against germs.
………………...CLICK & SEE THE PICTURES
For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of.

The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognising friends and family.

But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defences against invading bacteria and other microbes.

Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing.

The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.

To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.

That evening, Tanzi wandered into the office of a junior faculty member, Robert Moir, and mentioned what he had seen. As Tanzi recalled, Moir turned to him and said, “Yeah, well, look at this.”

He handed Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny. Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.

In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.

The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill — listeria, staphylococcus, pseudomonas. It killed eight out of 12. “We did the assays exactly as they have been done for years,” Tanzi said. “And A-beta was as potent or, in some cases, more potent than LL-37.”

Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer’s and from people of the same age who did not have dementia when they died.

Brain samples from Alzheimer’s patients were 24 per cent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from non-demented people in killing the yeast.

The innate immune system is also set in motion by traumatic brain injuries and strokes and by atherosclerosis that causes reduced blood flow to the brain, Tanzi noted.

And the system is spurred by inflammation. It’s known that patients with Alzheimer’s have inflamed brains, but it hasn’t been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Tanzi said, A-beta levels rise as a result of the innate immune system’s response to inflammation; it may be a way the brain responds to a perceived infection. But does that mean Alzheimer’s disease is caused by an overly exuberant brain response to an infection?

That’s one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.

Dr Norman Relkin, director of the memory disorders programme at New York-Presbyterian / Weill Cornell hospital, said that although the idea was “unquestionably fascinating”, the evidence for it was “a bit tenuous”.

As for the link with infections, Dr Steven DeKosky, an Alzheimer’s researcher at the Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer’s and have come up mostly empty handed.

But if Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.

“It means you don’t want to hit A-beta with a sledgehammer,” Tanzi said.

But other scientists not connected with the discovery said they were impressed by the new findings. “It changes our thinking about Alzheimer’s disease,” said Dr Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego.

Source : New York Times News Service

Reblog this post [with Zemanta]

Benefits of Sleeping ‘Early’

Products from Amazon.com

Adolescents who went to bed early were less likely to suffer from depression or contemplate suicide, a new study has found.
click to see
It shows that adolescents with parental-set bedtimes of midnight or later were 24 percent more likely to suffer from depression and 20 percent more likely to have suicidal thoughts than those with parental-set bedtimes set for 10 p.m. or earlier.

Those who reported sleeping five or fewer hours per night were 71 percent more likely to suffer from depression and 48 percent more likely to think about committing suicide than those who reported eight hours of sleep.

Also, participants who reported that they “usually get enough sleep” were significantly less likely to suffer from depression and suicidal ideation.

James E. Gangwisch, assistant professor at the Columbia University Medical Centre (CUMC), who led the study, said the results strengthen the argument that short sleep duration could play a role in a person’s history of depression.

“Our results are consistent with the theory that inadequate sleep is a risk factor for depression, working with other risk and protective factors through multiple possible causal pathways to the development of this mood disorder,” said Gangwisch.

“Adequate quality sleep could, therefore, be a preventive measure against depression and a treatment for the disease,” added Gangwisch, according to a CUMC release.

Data were collected from 15,659 adolescents and their parents who had participated in the National Longitudinal Study of Adolescent Health (Add Health), a school-based, nationally representative, probability-based sample of US students in grades seven to 12 in 1994 to 1996.

Source: The study was published in the Friday issue of Sleep. (Republished in the Times Of India)

Enhanced by Zemanta

Fearlessness Can be Taught

The brain can produce antidepressants with the right signal, a finding that suggests that meditating, or going to your “happy place,” tru ly works, scientists reported .

Mice, who were forced to swim endlessly until they surrendered and just floated, waiting to drown, could be conditioned to regain their will to live when a tone they associated with safety was played.

The experiment suggests that there are good ways to teach people this skill, and points to new routes for developing better antidepressants, said Dr Eric Kandel of the Howard Hughes Medical Institute and Columbia University in New York, who led the research.

“The happy place works. This is like going to the country,” Kandel said in a telephone interview.

Writing in the journal Neuron, Kandel’s team said they used classical conditioning to train mice. They had already conditioned some mice to fear a neutral tone by playing the sound when they shocked the animals’ paws. After a while, the tone itself creates fear. “It scares the hell out of the animal,” Kandel said.

They decided to reverse the study — they played the tone when they were not shocking the mice. “It learned that the only time it was really safe is when the tone comes on,” Kandel said.

To make a mouse depressed, they used a method favored by drug companies called learned helplessness. “You put an animal into a pool of water and it can’t get out. It gives up and it stops swimming and it just floats,” Kandel said. “When you give the animal an antidepressant, it starts swimming again. When we played the tone, it started to swim again just as it did with the antidepressant.”

Further experiments showed the tone and an antidepressant drug worked synergistically, he said. When they looked at the brains of their mice, they saw using the conditioned “safety” tone activated a different pathway than the drugs did.

It affected dopamine, while antidepressants work on serotonin. Both are message-carrying molecules called neurotransmitters. The conditioning also affected a compound called brain-derived neurotrophic factor or BDNF —which helps nourish and encourages the growth of brain cells. The learned safety did not affect serotonin.
Mice conditioned by the “safety” tone also had more newborn brain cells in the dentate gyrus, a part of the brain linked with learning and depression.

When Kandel’s team used radiation to slow the birth of new cells in the dentate gyrus, the effects of learned safety and of antidepressants were blunted.

Kandel noted that antidepressant drugs appear to work, in part, by encouraging the growth of new brain cells — as does psychotherapy.

“Learning involves alterations in the brain and gene expression,” Kandel said. “Psychotherapy is only a form of learning.”

This shows how effective psychotherapy, meditation and other stress-reduction tools may be, and it could help in the design of new drugs, Kandel said. “This opens up new pathways that may profitable,” he said.

Sources: The Times Of India

Reblog this post [with Zemanta]