That's what these scientists are saying, though they don't seem to understand that smoking is an
"irritant" due to the free radical damage, so I also included a study after the first that discusses
this. Omega 6 PUFA are very pro-inflammatory, but oxidative stress is also very unhealthy, and omega
3 PUFAs are about 5 times more susceptible to free radical degradation than omega 6s, so it's best
to stay away from PUFAs as much as possible. Also, damaged protein and oxidized cholesterol should
be avoided as well (along with the obvious things to avoid - smoking, asbestos, etc.).
"ASPIRIN FOUNDATION
MEDIA RELEASE 25 September 2000 ASPIRIN CAN PREVENT CANCER
The recent information from Imperial College Medical School London concerning the possible use of
aspirin in the prevention of prostate cancer confirms early data. Work by Professor Angus Dalgleish
and Dr Ken O'Byrne has postulated a theory as to the mechanisms involved. Professor Angus Dalgleish
of St George's Hospital, London concluded from reports published on patients taking aspirin over
many years, that they had a lower rate of cancer, including colorectal, lung cancer and oesophageal
cancer. To this might now be added prostate cancer. One in three people develop cancer at some in
their life so that treatment or prevention has been a primary target of medical research for
decades. In theory, the body's own immune system should seek out and destroy cancerous cells which
are constantly produced as the result of genetic damage. This self-protective system does not always
happen. The new theory which ties the spread of cancer to the failure of the immune system to stop
the spread of the disease, was first proposed in a lecture which Professor Angus Dalgleish gave in
1999. He showed that studies of the immune systems of colon cancer patients highlighted unusually
low levels of so called Th1-type immunity normally associated with the destruction of bacteria. He
believed that this permitted the cancer to thrive and believed that Th1 (thymus-derived helper cell
type 1) was present in low levels as a result of inflammatory disease being tackled by the body's
immune system. Professor Dalgleish's lecture was given at Leicester Royal Infirmary and Dr Ken
O'Byrne, who was working at Leicester on how tumours spread, saw how this permitted a lot of
questions to be answered. Cancer starts when healthy cells are attacked over a long period by
irritants such as chemicals from smoking. Long-term inflammation occurs and the body's immune system
attempts to eliminate this. The Th1 level is lowered. Th1, apart from its work on cancer cells is
needed by the body to deal with viruses and bacteria. When Th1 levels are low, normal cells that
have become cancerous can multiply because the immune system is compromised. In addition Dr O'Byrne
believes inflammation triggers the wound healing process which increases the so-called Th2 response.
This is involved in the creation of new blood vessels around damaged tissue in normal healthy
conditions. If however the tissue is cancerous, the blood vessels make it easier for the cancer to
grow and spread. In effect, long-term tissue inflammation not only lowers Th1 levels allowing cancer
cells to develop undetected but increases the Th2 level encouraging growth and spread. Inflammatory
conditions such as ulcerative colitis and chronic hepatitis are linked to cancer in later life. It
is the immune system's involvement with the inflammatory process which allows cancer cells to
thrive. Drugs that fight inflammation therefore raise Th1 levels so that cancer can be targeted or
even prevented. "Aspirin is an obvious case in point", said Dr O'Byrne. The linking of cancer with
inflammation could lead to the development of drugs which reduce inflammation in order to frustrate
the development of cancer. The theory has attracted interest from many leading experts in cancer
control including Professor Adrian Harris of the Imperial Cancer Research Fund who said that, "To
spread, tumours have got to get a blood supply and escape immune surveillance. This new approach
gives two routes for dealing with that." Professor Dalgleish believes that a big clinical trial is
needed to test this new approach involving thousands of patients over several years. All the same,
he himself is so convinced of the link between inflammation and cancer that he is taking 300mg of
soluble aspirin daily but emphasises that such a course should only be undertaken with medical
supervision."
"Parents' Smoke Injures Children's Blood Vessels CHICAGO, Nov. 18 - Children with one parent who
smoked in their presence had up to 50 percent higher levels of a biological marker of oxidative
stress in their blood, Austrian researchers reported today at American Heart Association's
Scientific Sessions 2002. In another study on the effects of second-hand smoke, Japanese researchers
sought to determine if short-term exposure to environmental tobacco smoke affected free-radical
production in young, healthy nonsmokers. Increasing evidence shows that second-hand smoke breaks
down the antioxidant defenses, which is associated with impairment of the endothelial-dependent
function of arterial walls. Endothelial dysfunction is an early feature of atherosclerosis, the
disease process that underlies heart disease and stroke, and is an important marker of vascular
damage. Free-radicals, which are unstable molecules produced during a process called oxidation, can
damage cells in the body. This damage is often called oxidative stress. It is significantly higher
in children exposed to second-hand smoke. To measure oxidation injury, the Austrian researchers
examined levels of a biological compound called 8-epi-PGF2alpha in the blood and urine of 158
children (71 boys, 87 girls) ages 3 to 15. The compound is formed when free radicals attack
arachidonic acid, a chemical whose normal function includes blood vessel dilation, blood clot
prevention and inflammation reaction. "It is a very potent blood vessel constrictor and may help
create blood vessel spasm and set the stage for blood clot formation," says senior researcher Helmut
F. Sinzinger, M.D., of the University of Vienna in Austria. Children were grouped according to the
smoking levels of their parents, whether both parents were smoking at home, and according to the
number of cigarettes smoked each day. Researchers compared results to those from a nonsmoking
control group. Blood and urinary 8-epi-PGF2alpha levels were elevated if children were exposed to
second-hand smoke by smoking parents. "Even if exposed to the second-hand smoke from less than 20
cigarettes a day by one smoking parent, levels were elevated in plasma by 35 to 50 percent and in
urine by 20 to 30 percent," Sinzinger says. Increasing the number of cigarettes smoked in the home
correlated to higher levels of 8-epi-PGF2alpha, regardless of the child's age or gender. Researchers
found that if parents were together smoking more than 40 cigarettes a day, blood 8-epi-PGF2alpha was
as much as 130 percent higher than that of the control group and urinary 8-epi-PGF2alpha was about
65 percent higher than in the control group. Further, smoking by the mother had a significantly more
pronounced influence. "We speculate that mothers may have closer contact with their children at
home," Sinzinger says. It's too early to speculate on measures other than recommending parents not
smoke when their children are present. "It is well known that atherosclerotic lesions on vascular
tissue are strongly correlated to risk factors that include cigarette smoking," Sinzinger says.
"Considering that in the United States and Western Europe nearly half of all children are exposed to
second-hand smoke in some way, these findings could be of great importance. Later vascular disease
might be triggered early in childhood by exposure to second-hand smoke." In the Japanese study,
researchers recruited 12 non-smoking men, average age 30, with no history of cardiovascular disease,
high blood pressure or diabetes. They tested their levels of 8-epi-PGF2alpha and used ultrasound to
measure endothelial function in subjects' brachial artery before and after a 30-minute exposure to
environmental tobacco smoke. Flow-mediated dilation (FMD) is an inexpensive and safe way to evaluate
endothelial function. It measures changes in the amount of blood flow through a particular blood
vessel. The endothelium is the inner lining of blood vessels. This thin layer of cells helps vessels
expand and contract in response to different amounts of blood flow. If these cells are damaged, the
blood vessels will be "stiff" and less able to handle the body's changing blood flow needs. After
exposure to tobacco smoke, the men's blood levels of 8-epi-PGF2alpha significantly increased from an
average of 20 picograms per milliliter (pg/mL) to 36 pg/mL. Their FMD decreased from 7.8 percent to
3.9 percent. "These findings may add relevance to the idea that everyone should be protected from
even short-term exposure to second-hand smoke," says lead researcher Toru Kato, M.D., Ph.D., of the
division of cardiology at Saitama Medical Center, Saitama Medical School in Japan. Co-authors of the
Japanese study are Shunichi Sato, M.D.; Toshihiko Nishioka; Mikio Yuhara; Yoshiro Inoue; Hiroyuki
Ito; Yoshiaki Maruyama; Shugo Tanaka; and Nobuo Yoshimoto, M.D., Ph.D. Co-authors of the Austrian
study are Anthony Oguogho, M.D., and Heidemarie Pilz, M.D."
From www.sciencedaily.com