Natural therapy: Chronic

Showing posts with label Chronic. Show all posts

Thursday, June 20, 2013

Exposure to particulate matter and chronic alcohol intake can decrease lung function

by Dr.Enozia Vakil on? June 15, 2013 at 4:40 PM Lifestyle News Alveolar macrophage may play a huge role in protecting the lungs by removing partiulates.
Chronic drinking causes persistent oxidative stress in the lungs, leading to impaired AM function.
A new rodent study shows that chronic drinking appears to intensify lung damage caused by particulate matter. Exposure to Particulate Matter and Chronic Drinking may Decrease Lung Function
Alveolar macrophage (AM) function plays a critical role in protecting the lungs from particulate matter inhalation by removing particulates from the airway and secreting elements that facilitate airway repair. Chronic drinking causes persistent oxidative stress in the lungs, leading to impaired AM function as well as immune responses. A rodent study has found that chronic drinking, when coupled with particulate matter (PM) exposure, dramatically increases lung dysfunction compared to alcohol intake or PM exposure alone.

Results will be published in the November 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

"Macrophages are derived from monocytes, a subset of the white blood cells present in the body," explained Stephania A. Cormier, associate professor of pediatrics - currently at the University of Tennessee Health Science Center - as well as corresponding author for the study. "Under normal conditions, monocytes travel into the tissues of the body and mature into macrophages. In the tissues, they perform activities necessary to maintain normal functions and, along with other tissue resident immune cells, provide an initial layer of protection against invading pathogens. AMs, present throughout the large and small airways of the lungs, secrete factors that assist normal airway function while also serving a janitorial role by engulfing and removing inhaled debris and dead cells from the airways."

"The lung has 100s of millions of macrophages," added George Leikauf, professor of environmental and occupational Health at the University of Pittsburgh. "The term derives from macro = big + phage = cell that eats. Their main job is to 'eat' or phagocytize bacteria and particles that land on the alveolar surface. Once bacteria are engulfed, the macrophages kill the bacteria. When particles are engulfed that cannot be digested, macrophages retain the particles and then move up the airways to clear the particle from the lung. In humans, the alveolar surface is about the size of a tennis core, so these cells have a massive responsibility. Normally, macrophage are very efficient and kill all the bacteria, thus the alveolar region is sterile. However, when compromised the macrophage cannot keep up with this duty, and bacteria grow. This can result in a lower respiratory tract infection such as pneumonia, which is the third leading cause of death in the US."

"While research has yet to define the precise mechanisms of how alcohol consumption increases the levels of reactive oxygen species in the lungs, we do know that alcohol alters numerous processes on the cellular level," said Cormier. "Specifically, a portion of alcohol ingested is metabolized in the lungs by a detoxification pathway which is less efficient than the primary metabolism pathway used in the liver. This less efficient pathway produces reactive products which must be further metabolized within the cell, using up antioxidants available within the cell. Alcohol also reduces the ability of the cells to replenish these antioxidants. As a result, reactive oxygen species increase within the cell, where they react with cellular components, altering or completely destroying their function. This cycle continues with daily alcohol consumption, directly increasing oxidative stress while also impairing the ability of our cells to maintain and increase antioxidant defenses."

Cormier and her colleagues fed age- and gender-matched C57BL6 mice a liquid diet that contained either alcohol or an iso-caloric substitution for eight weeks. During the final two weeks, mice from both groups were exposed to combustion-derived PM. Study authors then assessed AM number, maturation, and polarization status; in addition, both invasive and noninvasive methods were used to assess pulmonary function and correlate it with histomorphological assessments of airway structure and matrix deposition.

"We already knew that PM derived from automotive, industrial, hazardous waste processes, and other combustion processes aggravates existing lung disease and can predispose children and other susceptible individuals to pulmonary diseases such as asthma," said Cormier. "Here we found that chronic drinking, when coupled with PM exposure, dramatically decreases antioxidant defenses in the lungs compared to alcohol intake or PM exposure alone. This was accompanied by a decrease in the number of AMs present in the lungs immediately following PM exposure. Furthermore, the AMs that were present in the airways after exposure to both alcohol and PM [had] dramatically altered function. Collectively, chronic drinking amplifies the effects of PM exposure and accelerates declines in lung function due to PM exposure."

"This study is unique in that - by examining the combined insults of excessive alcohol and inhaled particles together - the study comes closer to the human experience in that we are often exposed to more than one adverse life style or environmental risk factor," added Leikauf. "Results suggest these two events can initiate damage to lung tissue and decrease the mice's capacity to breathe. While the effects are small and the study was only conducted over a short period of time, these risk factors can persist in humans over a lifetime. As with any animal study, caution needs to be paid to species' differences in susceptibility, but this study supports additional evaluation of the combined effects of such risk factors in a large human population."

"The relationships between alcoholism and PM exposure are particularly concerning given an estimated 18 million people in the US with alcohol use disorders and the high percentage of individuals who heavily consume alcohol and smoke cigarettes, which is a source of combustion-derived PM," added Cormier. "Therefore, our model of chronic alcohol intake and exposure to PM mimics a very real-world scenario."

Source-Eurekalert

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Wednesday, June 5, 2013

Research Links Depression to Telomere Enzyme, Aging, Chronic Disease

by Rukmani Krishna on? May 25, 2013 at 11:42 PM Mental Health News The first symptoms of major depression may be behavioral. Despite this, the common mental illness is based in biology ? and not limited to the brain. In recent years some studies have linked major, long-term depression with life-threatening chronic disease and with earlier death, even after lifestyle risk factors have been taken into account. Research Links Depression to Telomere Enzyme, Aging, Chronic Disease
Now a research team led by Owen Wolkowitz, MD, professor of psychiatry at UC San Francisco, has found that within cells of the immune system, activity of an enzyme called telomerase is greater, on average, in untreated individuals with major depression. The preliminary findings from his latest, ongoing study will be reported today at the annual meeting of the American Psychiatric Association in San Francisco.

Telomerase is an enzyme that lengthens protective end caps on the chromosomes' DNA, called telomeres. Shortened telomeres have been associated with earlier death and with chronic diseases in population studies.

The heightened telomerase activity in untreated major depression might represent the body's attempt to fight back against the progression of disease, in order to prevent biological damage in long-depressed individuals, Wolkowitz said.

The researchers made another discovery that may suggest a protective role for telomerase. Using magnetic resonance imaging (MRI), they found that, in untreated, depressed study participants, the size of the hippocampus, a brain structure that is critical for learning and memory, was associated with the amount of telomerase activity measured in the white blood cells. Such an association at a single point in time cannot be used to conclude that there is a cause-and-effect relationship with telomerase helping to protect the hippocampus, but it is plausible, Wolkowitz said.

Remarkably, the researchers also found that the enzyme's activity went up when some patients began taking an antidepressant. In fact, depressed participants with lower telomerase activity at baseline ? as well as those in whom enzyme activity increased the most with treatment ? were the most likely to become less depressed with treatment.

"Our results are consistent with the beneficial effect of telomerase when it is boosted in animal studies, where it has been associated with the growth of new nerve cells in the hippocampus and with antidepressant-like effects, evidenced by increased exploratory behavior," Wolkowitz said. Wolkowitz cautions that his new findings are preliminary due to the small size of the study and must be confirmed through further research.

The researchers also measured telomere length in the same immune cells. Only very chronically depressed individuals showed telomere shortening, Wolkowitz said.

"The longer people had been depressed, the shorter their telomeres were," he said. "Shortened telomere length has been previously demonstrated in major depression in most, but not all, studies that have examined it. The duration of depression may be a critical factor."

The 20 depressed participants enrolled in the study had been untreated for at least six weeks and had an average lifetime duration of depression of about 13 years. After baseline evaluation and laboratory measures, 16 of the depressed participants were treated with sertraline, a member of the most popular class of anti-depressants, the serotonin-selective-reuptake-inhibitors (SSRIs), and then evaluated again after eight weeks. There were 20 healthy participants who served as controls.

The ongoing study still is accepting depressed participants who are not now taking antidepressants. Wolkowitz's team also studies chronic inflammation and the biochemical phenomenon of oxidative stress, which he said have often been reported in major depression. Wolkowitz is exploring the hypothesis that inflammation and oxidative stress play a role in telomere shortening and accelerated aging in depression.

"New insights into the mechanisms of these processes may well lead to new treatments ? both pharmacological and behavioral ? that will be distinctly different from the current generation of drugs prescribed to treat depression," he said. "Additional studies might lead to simple blood tests that can measure accelerated immune-cell aging."