Dear glexia,
Thank you very much for sharing this story with us. My advise to you would be to make a list of all of the supplements/drugs you may take, and write them down. Then write down your diet and exercise program, and bring these into a doctor that is aware of your medical history as well.
I recall before these studies came out:
o Antioxidant Supplementation Increases the Risk of Skin Cancers in Women but Not in Men
o JAMA: Vitamin E, A, beta-caro increases mortality
o Archives of Internal Medicine: Vitamins C and E and Beta Carotene: No benefit, in the Secondary Prevention of Cardiovascular Events in Women
A lot of folks seemed to believe that there was some guaranteed benefit from multivitamins and other misc. antioxidants (NAC is an antioxidant).
Not to mention, if you check out Testing finds lead in vitamins, other problems, it seems about fifty percent (or 1/2) of multivitamins may be contaminated with lead or it appears may otherwise be unable to match their label claims.
So it's important to keep up to date on all of the latest research findings and to watch out for sales "hype" -- and most importantly, you should work with a licensed health care professional that is aware of your entire medical history before changing anything in your diet or exercise program.
I guess since no one seems to have provided us with the study abstract or its background information, I guess I will.
Here's some general background information regarding
The Journal of Clinical Investigation, copied from Wikipedia September 17, 2007; which seems to be accurate:
The Journal of Clinical Investigation (JCI or J Clin Invest) is a leading biomedical journal, which is radically different from many of its peers in having a high impact factor (in 2005, 15.053) and offering all its contents entirely free. It is also one of those rare journals whose entire archives, from 1924, are available online.
The website of the journal describes it as "a premier venue for critical advances in biomedical research, authoritative reviews, and commentaries that place research articles in context." The first issue of the journal appeared in 1924, and within a few decades, it had established itself as a reputed journal for primary clinical research.
The JCI's Editorial Board is unique in that its members are located chiefly at a singular academic medical center and are predominantly members of the American Society for Clinical Investigation. The leadership of the Editorial Board changes every five years: As of March 2007, the Editorial Board is located at the University of Pennsylvania under the leadership of Laurence A. Turka, M.D. From March 2002 to March 2007, the Editorial Board was located at Columbia University under the leadership of Andrew Marks, M.D. Ushma S. Neill, formerly with Nature Medicine, is the journal's Executive Editor.
This monthly journal publishes much original research, and one review article per issue, often ranked in par with the sophisticated and widely-cited reviews found in Physiological Reviews. A series of review articles (under the term "Review Series") focussing on an important biomedical topic is also regularly published, which has proved to be a positive addition to the journal's reputation.
Here is the study abstract that is referenced in the news report that glexia posted for us:
J. Clin. Invest. 117:2592-2601 (2007). doi:10.1172/JCI29444.
Copyright ©2007 by the American Society for Clinical Investigation
--------------------------------------------------------------------------------
Research Article
S-Nitrosothiols signal hypoxia-mimetic vascular pathology
Lisa A. Palmer1, Allan Doctor1, Preeti Chhabra1, Mary Lynn Sheram1, Victor E. Laubach2, Molly Z. Karlinsey3, Michael S. Forbes1, Timothy Macdonald3 and Benjamin Gaston1
1Department of Pediatrics and 2Department of Surgery, University of Virginia School of Medicine, and 3Department of Chemistry, University of Virginia, Charlottesville, Virginia, USA.
Address correspondence to: Benjamin Gaston, Pediatric Respiratory Medicine University of Virginia Health System, Box 800386, Charlottesville, Virginia 22908, USA. Phone: (434) 924-1820; Fax: (434) 924-8388; E-mail: bmg3g@virginia.edu.
Received for publication June 20, 2006, and accepted in revised form May 24, 2007.
NO transfer reactions between protein and peptide cysteines have been proposed to represent regulated signaling processes. We used the pharmaceutical antioxidant N-acetylcysteine (NAC) as a bait reactant to measure NO transfer reactions in blood and to study the vascular effects of these reactions in vivo. NAC was converted to S-nitroso-N-acetylcysteine (SNOAC), decreasing erythrocytic S-nitrosothiol content, both during whole-blood deoxygenation ex vivo and during a 3-week protocol in which mice received high-dose NAC in vivo. Strikingly, the NAC-treated mice developed pulmonary arterial hypertension (PAH) that mimicked the effects of chronic hypoxia. Moreover, systemic SNOAC administration recapitulated effects of both NAC and hypoxia. eNOS-deficient mice were protected from the effects of NAC but not SNOAC, suggesting that conversion of NAC to SNOAC was necessary for the development of PAH. These data reveal an unanticipated adverse effect of chronic NAC administration and introduce a new animal model of PAH. Moreover, evidence that conversion of NAC to SNOAC during blood deoxygenation is necessary for the development of PAH in this model challenges conventional views of oxygen sensing and of NO signaling.
Copyright © 2007 by the American Society for Clinical Investigation.
The issue of interest that seems to have prompted concern that might bring into question the issue of safety seems to be that:
"the NAC-treated mice developed pulmonary arterial hypertension (PAH) that mimicked the effects of chronic hypoxia." So it may seem clear if these effects manifest in humans taking NAC as a supplement, humans may manifest pulmonary arterial hypertension (PAH).
Here's a definition of Pulmonary Arterial Hypertension from
The National Heart Lung and Blood Institute (last updated August 2006):
What Is Pulmonary Arterial Hypertension?
Pulmonary (PULL-mun-ary) arterial hypertension (PAH) is continuous high blood pressure in the pulmonary artery. The average blood pressure in a normal pulmonary artery is about 14 mmHg when the person is resting. In PAH, the average is usually greater than 25 mmHg.
PAH is a serious condition for which there are treatments but no cure. Treatment benefits many patients.
The pulmonary arteries are the blood vessels that carry oxygen-poor blood from the right ventricle (VEN-trih-kul) in the heart to the small arteries in the lungs. In PAH, three types of changes may occur in the pulmonary arteries:
o The muscles within the walls of the arteries may tighten up. This makes the inside of the arteries narrower.
o The walls of the pulmonary arteries may thicken as the amount of muscle increases in some arteries. Scar tissue may form in the walls of arteries. As the walls thicken and scar, the arteries become increasingly narrow.
o Tiny blood clots may form within the smaller arteries, causing blockages.
o There is less room for the blood to flow through these narrower arteries. The arteries may also stiffen. Over time, some of the arteries may become completely blocked.
The narrowing of the pulmonary arteries causes the right side of heart to work harder to pump blood through the lungs. Over time, the heart muscle weakens and loses its ability to pump enough blood for the body's needs. This is called right heart failure. Heart failure is the most common cause of death in people with PAH.
There are two types of PAH:
o Primary pulmonary arterial hypertension (PPAH) is inherited or occurs for no known reason.
o Secondary pulmonary arterial hypertension (SPAH) either is caused by or occurs because of another condition. The conditions include chronic heart or lung disease, blood clots in the lungs, or a disease like scleroderma (skler-o-DER-ma).
About 300 new cases of PPAH are diagnosed in the United States each year. SPAH is much more common.
Doctors have learned a lot about PAH in recent years. More treatments are now available. Researchers are also studying several promising new treatments that may prolong lives as well as improve the quality of life for people living with PAH.
August 2006
It seems results from animal studies will translate to humans
approximately half the time, so does this imply everyone that has been taking NAC should stop taking it? What if the only basis for using a therapy is based on animal research (which is not the case for NAC)?
Regardless, that's not the reason I am posting here today.
I am reporting on a study instead originally published in the journal
Cancer Cell September 11, 2007:
Info on this journal:
Cancer Cell publishes reports of novel results in any area of cancer research, from molecular and cellular biology to clinical oncology. The work should be not only of exceptional significance within its field but also of interest to researchers outside the immediate area. In addition, Cancer Cell findings in cancer research, diagnosis and treatment. The goal of Cancer Cell is to promote the exchange of ideas and concepts across the entire cancer community, cultivating new areas of basic research and clinical investigation.
Cancer Cell will consider papers for publication in any aspect of cancer biology and clinical research, including (but not limited to): Genetics, epigenetics, genomic instability • Cell signaling and communication • Cell cycle, DNA repair • Diagnostics (molecular profiling, pharmacogenomics) • Telomerase and transformation • Apoptosis • Angiogenesis, metastasis • Animal models • Cancer therapy (rational drug design, small molecule therapeutics) • Epidemiology and prevention.
The abstract of potential interest:
Copyright © 2007 Cell Press. All rights reserved.
Cancer Cell, Vol 12, 230-238, 11 September 2007
Article
HIF-Dependent Antitumorigenic Effect of Antioxidants In Vivo
Ping Gao,1 Huafeng Zhang,2,6 Ramani Dinavahi,1 Feng Li,1 Yan Xiang,1 Venu Raman,4,5 Zaver M. Bhujwalla,4,5 Dean W. Felsher,8 Linzhao Cheng,6 Jonathan Pevsner,3 Linda A. Lee,1 Gregg L. Semenza,1,2,4,6,7 and Chi V. Dang1,4,7,
1 Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
2 Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
3 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
4 Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
5 Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
6 Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
7 McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
8 Departments of Medicine and Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
Corresponding author
Chi V. Dang
cvdang@jhmi.edu
Summary
The antitumorigenic activity of antioxidants has been presumed to arise from their ability to squelch DNA damage and genomic instability mediated by reactive oxygen species (ROS). Here, we report that antioxidants inhibited three tumorigenic models in vivo. Inhibition of a MYC-dependent human B lymphoma model was unassociated with genomic instability but was linked to diminished hypoxia-inducible factor (HIF)-1 levels in a prolyl hydroxylase 2 and von Hippel-Lindau protein-dependent manner. Ectopic expression of an oxygen-independent, stabilized HIF-1 mutant rescued lymphoma xenografts from inhibition by two antioxidants: N-acetylcysteine and vitamin C. These findings challenge the paradigm that antioxidants diminish tumorigenesis primarily through decreasing DNA damage and mutations and provide significant support for a key antitumorigenic effect of diminishing HIF levels.
Copyright 2007 Elsevier Inc.
So while subjects that may report taking NAC as a supplement may be at increased risk for PAH, alternatively they may be at reduced risk of cancer -- or so this
in-vivo evidence might suggest.
Thoughts, comments, or suggestions?
Take care.
