Depression Thwarts Attempts to Quit Smoking

By RICK NAUERT PHD Senior News Editor
Reviewed by John M. Grohol, Psy.D. on January 3, 2011

New research suggests diagnosed or undiagnosed depression can hinder an individual’s efforts to stop smoking.

In the study, published in the January 2011 edition of the American Journal of Preventive Medicine. scientists determined approximately 24 percent of surveyed callers to the California Smokers’ Helpline currently suffered from major depression and 17 percent of callers had mild depression.

Over half the surveyed callers, depressed or not, made at least one attempt to quit after calling the helpline.

At the two-month mark, however, the success rate of those with major depression was much lower than that of mildly depressed or non-depressed callers. Nearly one in five callers with major depression reported success, but of others, nearly one in three was able to remain smoke-free.

Most quit-lines do not assess smokers for depression, even though mild depression already is known to reduce the success of quitting. This study suggests that major depression reduces the success rate even farther.

That is important because the California quit-line receives a high number of calls from heavy smokers and smokers on Medicaid – two circumstances associated with depression. Since more than 400,000 smokers call U.S. quit-lines every year, the authors believe that up to 100,000 depressed smokers nationally are not getting the targeted treatment they need.

“Assessing for depression can predict if a smoker will quit successfully, but the assessment would be more valuable if it were linked to services,” said lead study author Kiandra Hebert, Ph.D., of the University of California at San Diego.

Hebert said an integrated health care model is a potential solution. Depressed smokers could have better quitting success if they receive services that address both issues. Quit-lines, which are extremely popular, are in a good position to offer such services to a large number of depressed smokers and to pass on the services they develop to quit-lines across the country.

Treatment programs, including quit-lines, report that a growing number of callers have other disorders, such as depression, said Wendy Bjornson, co-director of the Oregon Health & Science University Smoking Cessation Center, who was not involved in the study.

“The results of this study are important. They show the scope of the problem and point to the need for protocols that can lead to better outcomes.”

Source: Health Behavior News Service

Risk for Alcoholism Linked to Risk for Obesity


The researchers noted that the association between a family history of alcoholism and obesity risk has become more pronounced in recent years. Both men and women with such a family history were more likely to be obese in 2002 than members of that same high-risk group had been in 1992.

“In addiction research, we often look at what we call cross-heritability, which addresses the question of whether the predisposition to one condition also might contribute to other conditions,” says first author Richard A. Grucza, PhD. “For example, alcoholism and drug abuse are cross-heritable. This new study demonstrates a cross-heritability between alcoholism and obesity, but it also says — and this is very important — that some of the risks must be a function of the environment. The environment is what changed between the 1990s and the 2000s. It wasn’t people’s genes.”

Obesity in the United States has doubled in recent decades from 15 percent of the population in the late 1970s to 33 percent in 2004. Obese people — those with a body mass index (BMI) of 30 or more — have an elevated risk for high blood pressure, diabetes, heart disease, stroke and certain cancers.

Reporting in the Archives of General Psychiatry, Grucza and his team say individuals with a family history of alcoholism, particularly women, have an elevated obesity risk. In addition, that risk seems to be growing. He speculates that may result from changes in the food we eat and the availability of more foods that interact with the same brain areas as addictive drugs.

“Much of what we eat nowadays contains more calories than the food we ate in the 1970s and 1980s, but it also contains the sorts of calories — particularly a combination of sugar, salt and fat — that appeal to what are commonly called the reward centers in the brain,” says Grucza, an assistant professor of psychiatry. “Alcohol and drugs affect those same parts of the brain, and our thinking was that because the same brain structures are being stimulated, overconsumption of those foods might be greater in people with a predisposition to addiction.”

Grucza hypothesized that as Americans consumed more high-calorie, hyper-palatable foods, those with a genetic risk for addiction would face an elevated risk from because of the effects of those foods on the reward centers in the brain. His team analyzed data from two large alcoholism surveys from the last two decades.

The National Longitudinal Alcohol Epidemiologic Survey was conducted in 1991 and 1992. The National Epidemiologic Survey on Alcohol and Related Conditions was conducted in 2001 and 2002. Almost 80,000 people took part in the two surveys.

“We looked particularly at family history of alcoholism as a marker of risk,” Grucza explains. “And we found that in 2001 and 2002, women with that history were 49 percent more likely to be obese than those without a family history of alcoholism. We also noticed a relationship in men, but it was not as striking in men as in women.”

Grucza says a possible explanation for obesity in those with a family history of alcoholism is that some individuals may substitute one addiction for another. After seeing a close relative deal with alcohol problems, a person may shy away from drinking, but high-calorie, hyper-palatable foods also can stimulate the reward centers in their brains and give them effects similar to what they might experience from alcohol.

“Ironically, people with alcoholism tend not to be obese,” Grucza says. “They tend to be malnourished, or at least under-nourished because many replace their food intake with alcohol. One might think that the excess calories associated with alcohol consumption could, in theory, contribute to obesity, but that’s not what we saw in these individuals.”

Grucza says other variables, from smoking, to alcohol intake, to demographic factors like age and education levels don’t seem to explain the association between alcoholism risk and obesity.

“It really does appear to be a change in the environment,” he says. “I would speculate, although I can’t really prove this, that a change in the food environment brought this association about. There is a whole slew of literature out there suggesting these hyper-palatable foods appeal to people with addictive tendencies, and I would guess that’s what we’re seeing in our study.”

The results, he says, suggest there should be more cross-talk between alcohol and addiction researchers and those who study obesity. He says there may be some people for whom treating one of those disorders also might aid the other.

This work was supported by grants from the National Institute on Alcohol Abuse and Alcoholism and the National Institute on Drug Abuse of the National Institutes of Health.

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Washington University School of Medicine.

A National Institute of Depression?

by Jonathan Rottenberg, Ph.D

I am reading Siddharta Murkherjee’s, wonderful, Emperor of All Maladies: A Biography of Cancer. One of the stories it tells is about the formation of the National Cancer Insitute in 1937. Here is the current mission statement of the NCI:

* Supports and coordinates research projects conducted by universities, hospitals, research foundations, and businesses throughout this country and abroad through research grants and cooperative agreements.
* Conducts research in its own laboratories and clinics.
* Supports education and training in fundamental sciences and clinical disciplines for participation in basic and clinical research programs and treatment programs relating to cancer through career awards, training grants, and fellowships.
* Supports research projects in cancer control.
* Supports a national network of cancer centers.
* Collaborates with voluntary organizations and other national and foreign institutions engaged in cancer research and training activities.
* Encourages and coordinates cancer research by industrial concerns where such concerns evidence a particular capability for programmatic research.
* Collects and disseminates information on cancer.
* Supports construction of laboratories, clinics, and related facilities necessary for cancer research through the award of construction grants.
which over time became a major institute within the National Institutes of Health.

In other words, the NCI is a national coordinating body for research and training to reduce the menace of cancer.

If we look across the National Insitutes of Health we see that many conditions have an institute. Alcohol has an institute. Drug Abuse does. Diabetes is covered. Stroke. Allergies. Check, check.

But not depression.

Depression is soon to become the emperor of all maladies. Serious depression affects nearly a fifth of the population and it is booming, especially in the young. If you need a call to action, look at the graph below from the National Comorbidity Study Replication, a comprehensive national survey of mental health in the United States. It shows that young people aged 18 to 29 have already experienced as much depression as people aged 60+, even though they have lived for less than half as long on planet earth.

Although it is hard to quantify the suffering caused by depression, it is straightforward to make sound estimates of its overall burden — for example the financial costs of lost work time and increased use of health care dollars. When you do the math, depression already ranks up there with the most burdensome disorders. The World Health Organization projects that in less than 10 years, depression will be the 2nd most burdensome condition. That’s greater, by the way, than cancer.

A National Institute on Depression makes sense not only because there is an urgent public health need but because there is so much about depression that we still don’t know. In my last post, I pointed out one striking example:  A recent search revealed only one well-designed  prospective study of the depressive prodrome (i.e., warning symptoms that herald depression). And much of our knowledge about depression isn’t well coordinated. We don’t do a good job of even knowing what we already know.

Poor integration of existing knowledge is one of the major limitations of the current national approach to depression. Thus, in addition to giving a new NID the broad mission along the lines of the NCI, it would be important for the NID to allow room for many approaches, not only the exclusive focus on genes and brains that has yielded relatively modest results so far but cognitive, sociological, and anthropological perspectives as well.

In our times of fiscal retrenchment, it’s easy to shoot down any new initiatives. But at the same time, wouldn’t keeping our current approach to depression be far riskier to the public health? and more costly in the long run? The time is right to make a modest investment to expand federal research on depression and bring together the work that’s currently done in several NIH insitutes (Mental Health, Aging, Child Health and Development) into a stand-alone National Insitute of Depression. If not now, when?

Countering ‘Memory Loss’ In The Immune System

On December 26, 2010, in Immunology, by Christopher Fisher, PhD

After recovering from a cold or other infection, your body’s immune system is primed to react quickly if the same agent tries to infect you. White blood cells called memory T cells specifically remember the virus or bacterium and patrol the body looking for it. Vaccines work on the same principle: Harmless fragments of a virus or bacterium provoke the immune system to generate memory T cells that can attack the real thing later on.

As time passes, however, this specific immunity can wear off. That is because not all memory T cells live long enough to foster long-term immunity.

MIT biologists have now demonstrated the conditions that favor development of long-term memory T cells over short-term memory T cells, which can respond quickly but do not stick around for very long after the initial infection. That discovery could help vaccine designers better tailor their formulas to elicit long-term memory immunity, says Jianzhu Chen, MIT professor of biology and member of the David H. Koch Institute for Integrative Cancer Research.

Chen and Herman Eisen, emeritus professor of biology, are senior authors of a paper on the work that appeared in the Proceedings of the National Academy of Sciences the week of Dec. 13.

In the PNAS study, the MIT team looked at mice infected with influenza. In mice, as in humans, influenza virus stimulates T cells, whose job is to kill infected cells. Every T cell is programmed to recognize different foreign proteins (also called antigens) located on the surfaces of infected cells. When a T cell binds to the antigen, the T cell becomes activated and starts rapidly reproducing, creating an army of cells that can identify and destroy the invader.

Once the infection is eliminated, most of the activated T cells die off, but a few of them stick around, in case the virus comes back. These are short-term memory T cells. Because they have already battled the virus and reproduced many times, they survive only weeks or months after the initial infection. (T cells can only divide a certain number of times before they die.)

A set of long-term memory T cells also develops during infection. These cells are programmed differently, so they can persist for decades. Recipients of the smallpox vaccine, for example, have been shown to still have T cells against the virus up to 70 years later, says Eisen.

Until now, it has been unclear how these different cell types develop. In their new study, Eisen and Chen investigated the role three factors: T-cell location, the amount of antigen exposure, and length of exposure.

Scientists already knew that T cell contact with a large amount of virus provokes development of short-term memory T cells, says Eisen. Chen and colleagues discovered that large amounts of antigen also suppress development of long-term memory T cells. Those cells only develop when exposed to a small amount of the antigen for a short period of time.

For example, if you have an infection in the respiratory tract, nearby T cells will be exposed to many viruses and become short-term memory cells. Those cells hang around the respiratory tract, ready to pounce quickly if the same virus re-infects you, but they eventually die off.

In more distant parts of the body, T cells are exposed to only small amounts of the virus, and some of those cells become long-term memory T cells specific to that virus. These maintain a low level of constant vigilance in case the virus ever returns.

Ulrich von Andrian, professor of immunopathology at Harvard, says the new study’s major contribution is its experimental support of existing theories. “It builds on ideas that have been around for a while, that were not rigorously tested by experiments, for the most part,” says von Andrian, who was not part of the research team.

When developing vaccines, the goal is usually to generate a stable population of long-term memory T cells. This study suggests that the best way to do that is to give a small amount of antigen, and, for vaccines that require multiple injections, not to give them too frequently.

“The general rule of thumb is that you don’t want to give a large amount of antigen on a short-term basis,” says Chen. He adds that the amount of antigen for inducing a long-term memory T cells likely varies depending on the route of immunization and the form of antigen, and so the dosage for each vaccine will have to be determined through experiments.

He says the findings will likely not impact flu-vaccine design because existing dosages have already been optimized over many decades. However, the findings should be applicable to vaccines now under development for other diseases, such as HIV, tuberculosis and dengue fever, says Chen.

Material adapted from MIT.

Four ways to avoid getting sick during the holiday season

By Madison Park, CNN

(CNN) — The Badger family holidays are filled with medical catastrophes.

One year, Melissa Badger’s niece stopped breathing at the Thanksgiving table because of a strep infection. In 2003, Badger’s son came down with a severe fever and ended up in the emergency room on Christmas. On Christmas Eve 2005, Badger tripped on ice while delivering presents to needy families and sprained her ankle.

This year, Badger’s husband complains of cold-like symptoms — fatigue, coughing and a sore throat. Badger struggled with a bug going around her office that was giving everyone stuffy noses and cold symptoms.

“Now, we get to worry about that lingering cold all of us have, since we’re hosting family this Christmas Eve,” said Badger. Hosting family means more than 30 people at their Beloit, Wisconsin, home.

Illness for many of us seems to knock at the most inopportune moments — after finishing a year-end project, before a holiday or after taking exams.

It had Shannon Duffy, who spent this Thanksgiving in bed with the flu, asking: “Is too much excitement and anticipation of the holiday season a bad thing? Or is it that my immune system just gets so overloaded with life stresses that when I step back and take a break, it is like an open invitation for the flu bug to intervene?”

With Mom sick in bed, Duffy’s sons had to microwave their TV dinners for Thanksgiving.

“I’ve been sick a lot during the holidays,” said the Palm Springs, California, resident. “If it’s not Thanksgiving, it’s Christmas.”

There are a few theories why sickness comes at the worst time.

“The holidays are a virus-distribution system,” said Dr. William Schaffner, chair of the department of preventive medicine at Vanderbilt University. “They help us distribute the viruses, influenza and other common cold virus from person-to-person because of close contact.”

1) Achoo to you, and you, and you

Flu season reaches its height in late fall and early winter. This is because viruses circulate better in the colder weather, said Dr. Philip Tierno, director of microbiology and immunology at New York University’s Langone Medical Center.

It’s not only cold and flu bugs that become active during colder seasons. CDC: Seasonal FluView

Other viruses, such as the norovirus and rotavirus, become more active during winter. Norovirus, known as the stomach flu, easily spreads through contamination in food, drink and surface contact. The virus is found in the stool and vomit of infected people. Rotavirus also causes diarrhea, vomiting, fever, and abdominal pain.

Advice: If you’re sick, cough into the crook of your arm.

If someone is coughing or wiping his or her nose, don’t hug or kiss the person. Use common sense, Tierno said.

5 Immunity boosting tips for moms

2) The sea of humanity … at the mall

Think of the holiday traditions: catching a show, shopping at a crowded mall, attending holiday parties.

All this means you’re indoors in crowds and exposed to everyone’s germs. As people cluster indoors, they use the same doorknobs, banisters and surfaces after wiping their noses or sneezing.

“During the winter season, we’re more subject to crowding, touching something that’s not hygienic and crowding,” Tierno said.

People get less fresh air, too.

“They don’t open up windows to get fresh air. They don’t go outside as much during cold weather. They decide to stay in, so any virus that may be present would be more easily spread,” he said.

Advice: Practice frequent hand-washing (at least 20 seconds wiping both the top, bottom of hands and between the fingers prior to eating and drinking) or use hand sanitizers.

Occasionally open the window to let fresh air circulate.

Must-know winter health & safety tips

3) Germs fly free

Air travel means if there’s a small flu outbreak on the West Coast, that virus could be in New York in less than five hours.

“Human travel is synonymous with virus travel,” said Shaffner, an infectious disease expert.

When family members travel across the country, they’re bringing along pathogens that have been in their communities and exposing them to new places.

It’s not only the act of being in an enclosed cabin of a car, bus, train or plane, Shaffner said.

“Remember we’re talking about being on an airplane, getting to the airplane, making your way through the crowds and other crowds in the other end,” he said. “It is just as important as the airplane.”

Advice: The Centers for Disease Control and Prevention recommends everyone older than 6 months old be vaccinated for influenza. Get your flu vaccine to reduce chances of getting sick.

Dr. Sanjay Gupta talks to Sebelius about flu shots

4) You’re super-stressed before vacation

End-of-the-year projects, reports, final exams — it could be all that work before break that spikes a stress hormone in your body.

“The increased cortisol level induces likelihood of infection during the holidays,” said Dr. Robert Hasty, assistant professor of internal medicine at Nova Southeastern University’s medical school.

Cortisol is a natural hormone that responds to stress, lowering immunity and making you more susceptible to infections.

The interval between acquiring a virus and becoming sick takes about 48 to 72 hours. You may have become infected when you were stressed and the symptoms may start to show right when you go on holiday break.

Advice: Stress might be unavoidable, but try getting enough sleep and hydrating.

Prevent the stress hormones from wreaking havoc by better planning, avoiding traffic, buying presents earlier.

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