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Celebration Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Aug-31-06 04:32 PM
Original message
Anger Tough on the Lungs
http://www.forbes.com/forbeslife/health/feeds/hscout/2006/08/31/hscout534679.html

"Our psychological colleagues have worked out quite well in the lab that psychological stress and distress and negative emotional states like hostility can disrupt immune function and trigger inflammatory processes, much like allergens in the environment," noted senior study author Dr. Rosalind Wright, an assistant professor of medicine at Harvard Medical School in Boston.

"Psychological stress seems to trigger similar types of biological disruptions," she said. "When you have something throwing the system out of balance, that might put you in a state of chronic inflammation."

To see if there was any link between anger and hostility and the way the lungs work, Wright and her colleagues examined at 670 men aged 45 to 86.

Levels of hostility, measured at the beginning of the study in 1986, averaged 18.5 points on a standard scale, with values ranging from seven to 37 points. Lung function appeared to decline as anger numbers rose, and vice-versa.


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serryjw Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Aug-31-06 04:54 PM
Response to Original message
1. That's what triggers
asthma. The inflammation constricts the bronchial tubes and lungs
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Celebration Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Aug-31-06 05:19 PM
Response to Reply #1
2. I was thinking the same thing
Asthma, asthma, asthma. Also, so anger influences the lungs like this. What about other emotions? Could they be causing a different sort of inflammation or immune response? Sadness, for example, or isolation, disappointment, inhibition, helplessness, repression, shame, grief, etc.? What about joy, delight, and love? Are they antidotes?

These are rather rhetorical questions.
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serryjw Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Aug-31-06 07:27 PM
Response to Reply #2
3. I learned the hard way
part of an email I sent a friend that I had not written for several months after 11/04

quote.......
Sorry, I haven't written to explain. It has been a wild ride the
>last several months. I took a job in market research that started 11/2. I
>have not worked full time for a long while. We then lost the election(??)
>and I never expected that.


>November/December were bitter cold in Denver. Quit unusual. I got one of
>the worst cases of bronchitis that turned into pneumonia and a 2 month
>asthma attack that I could not get under control. My asthma is not brought
>on from smoking or environmental pollutants like most people. I have 'cold
>induced asthma' that is bought on by severe cold and emotion.
It was
>a'perfect storm' the weather, the loss of the election and a new full time job.
end quote.......

In your wildest nightmare I can't explain how bad it was. I couldn't walk 2 feet in the cold. Thank god for my gal at Wild Oats. She knew exactly how to fix me up.....I was crazy for not going in sooner. I am a smoker and never had a problem until that time. OHHHHHHH yes, emotion is worse than pollutants for asthma.NEVER want to go through that again..and haven't since fall of '04. I will be prepared if we lose '06!
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HysteryDiagnosis Donating Member (1000+ posts) Send PM | Profile | Ignore Sat Sep-02-06 12:24 PM
Response to Reply #2
4. Molecules of emotion.... and the importance of antioxidants
in asthma and COPD.

www.CandacePert.com

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16787173&query_hl=6&itool=pubmed_docsum
1: Curr Drug Targets. 2006 Jun;7(6):707-20.Click here to read Links
Antioxidant therapeutic targets in COPD.

* Rahman I,
* Kilty I.

Department of Environmental Medicine, Division of Lung Biology and Disease, University of Rochester Medical Center, 601 Elmwood Ave., Box 850, Rochester, NY 14642, USA. irfan_rahman@urmc.rochester.edu

Oxidative stress and chronic inflammation are important features in the pathogenesis of chronic obstructive pulmonary disease (COPD). Oxidative stress has important consequences for several elements of lung physiology and for the pathogenesis of COPD, including oxidative inactivation of antiproteases and surfactants, mucus hypersecretion, membrane lipid peroxidation, alveolar epithelial injury, remodeling of extracellular matrix, and apoptosis. Therefore, targeting oxidative stress with antioxidants or boosting the endogenous levels of antioxidants is likely to be beneficial in the treatment of COPD. Antioxidant and/or anti-inflammatory agents such as thiol molecules (glutathione and mucolytic drugs, such as N-acetyl-L-cysteine and N-acystelyn), dietary polyphenol (curcumin-diferuloylmethane, a principal component of turmeric), resveratrol (a flavanoid found in red wine), green tea (theophylline and epigallocatechin-3- gallate), ergothioneine (xanthine and peroxynitrite inhibitor), quercetin, erdosteine and carbocysteine lysine salt, have been reported to control NF-kappaB activation, regulation of glutathione biosynthesis genes, chromatin remodeling and hence inflammatory gene expression. Specific spin traps such as alpha-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), manganese (III) meso-tetrakis (N,N'-diethyl-1,3-imidazolium-2-yl) porphyrin (AEOL 10150 and AEOL 10113), and a SOD mimetic M40419 have also been reported to inhibit cigarette smoke-induced inflammatory responses in vivo. Since a variety of oxidants, free radicals and aldehydes are implicated in the pathogenesis of COPD it is possible that therapeutic administration of multiple antioxidants will be effective in the treatment of COPD. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in COPD are discussed.

PMID: 16787173
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