Studies Show Genetic Variations in Multiple Chemical Sensitivity

Released on = March 21, 2007, 4:04 pm

Press Release Author = MCS America / Lourdes Salvador

Industry = Healthcare

Press Release Summary = Three recent studies show that a genetic variant makes
sufferers of multiple chemical sensitivity (MCS) more likely to develop the
condition.

Press Release Body = Salem, NY -- Three recent studies show that a genetic variant
makes sufferers of multiple chemical sensitivity (MCS) more likely to develop the
condition. In 2004, McKeown-Eyssen studied 203 MCS sufferers and 162 controls and
found that genetic differences relating to detoxification processes were present
more often in those with MCS than those without. The study concluded that \"a
genetic predisposition for MCS may involve altered biotransformation of
environmental chemicals. Haley found similar, confirmatory results in a 1999 study
with the PON1 gene in Gulf War syndrome veterans.

A new study by Schnakenberg et al (2006) confirmed the genetic variation previously
found by McKeown-Eyssen and Haley. A total of 521 unrelated individuals
participated in the study. Genetic variants of four genes were analyzed: NAT2,
GSTM1, GSTT1, and GSTP1. The researchers concluded that individuals who are NAT2
slow acetylators and those with homozygously deleted GSTM1 and GSTT1 genes are
significantly more likely to develop chemical sensitivity.

\"According to the study the glutathione S-transferases act to inactivate chemicals
so people without these GSTM1 and GSTT1 genes are less able to metabolize
environmental chemicals," said Lourdes Salvador, Founder and President of MCS
America. "If a person cannot metabolize chemicals they build up in the body and
cause disturbances in normal body function," added Salvador who is also the chief
editor of MCS America News. Schnakenberg and fellow researchers explain that
\"glutathione S-transferases play an important role in the detoxification of
chemicals... the deletion of this gene may be an important step in the early onset
of diseases\" which is a critical discovery that provides a biological basis behind
the etiology of multiple chemical sensitivity.

The researchers also noted that diseases such as non-Hodgkin\'s lymphoma,
hepatocellular and prostate carcinoma, and Alzheimer\'s disease have been associated
with the common chemicals metabolized by GSTP1. The deletion of the GSTP1 gene
leaves individuals more susceptible to developing these diseases, as lack of these
genes means a loss of protection from oxidative stress. "This discovery is crucial
to being able to diagnose and treat those who suffer from multiple chemical
sensitivity and other toxic injuries," said Salvador. "It is the first step toward
understanding and explaining the cause of chemical injury and resulting
sensitivities so that treatments can be developed."

For additional information e-mail MCS America, admin@mcs-america.org or visit
www.mcs-america.org.
To request a free subscription to the MCS America News, send an e-mail to
subscriptions@mcs-america.org

Cited References:

Haley, RW, Billecke, S, & La Du, BN (1999). Association of low PON1 type Q (type A)
arylesterase activity with neurologic symptom complexes in Gulf War veterans.
Toxicology and Applied Pharmacology 157(3):227-33.

McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R, Marshall, L, & Jazmaji,
V (2004). Case-control studies of genotypes in multiple chemical sensitivity: CYP2D,
NAT1, NAT2, PON1, PON2 and MTHFR. International Journal of Epidemiology 33, 1-8.

Schnakenberg, E, Karl-Rainer, F, Stanulla, M, Strobl, N, Lustig, M, Fabig, N, &
Schloot, W (2007). A cross-sectional study of self-reported chemical-related
sensitivity is associated with gene variants of drug-metabolizing enzymes. Environ
Health. 2007 Feb 10;6:6.
--- END --

Web Site = http://www.mcs-america.org

Contact Details = Contact: Lourdes Salvador
Address: 13 Vale Street, Salem, NY 12864
Phone: 213-985-3096
Email: admin@mcs-america.org
Website: www.mcs-america.org

  • Printer Friendly Format
  • Back to previous page...
  • Back to home page...
  • Submit your press releases...
  •