I'm interested in prevention.  I saw a study several years ago, which
included the information that a population using coconut oil (in Asia)
had very low rates of lung cancer, regardless of whether they were
chains smokers or never smoked.

Mary Enig (fatty acid expert) has written about the importance of
certain saturated fatty acids for lung health and resistance to
"disease."  If your diet is high in unsaturated fatty acids, which it
almost certainly is, you are going to be much more susceptible to lung
cancer and other cancers.  Here's a recent report, for example, which
just reiterates what I've been saying here for years (because
scientists have been saying it for years, for example, Jay Whelan's
1997 study about polyunsaturated fatty acids being signaling agents for
cancer).  And don't think that fish oil will cancel out all the bad
effects of omega 6 PUFAs.  These fatty acids are just as bad, though in
somewhat different ways, depending upon the context.

8/2/2005
Omega-6 Fatty Acids Cause Prostate Tumor Cell Growth In Culture

A study conducted at the San Francisco VA Medical Center (SFVAMC) has
demonstrated that omega-6 fatty acids such as the fat found in corn oil
promote the growth of prostate tumor cells in the laboratory. The study
also identifies a potential new molecular target for anti-tumor drugs:
an enzyme known as cPLA2, which plays a key role in the chain leading
from omega-6 fatty acids to prostate tumor cell growth.

The study was led by Millie Hughes-Fulford, PhD, director of the
Laboratory of Cell Growth at SFVAMC and scientific advisor to the U.S.
Undersecretary of Health for the Department of Veterans Affairs. It is
being published in the September 2005 issue of Carcinogenesis, and is
currently available online.

Working with human prostate cancer cells in tissue culture,
Hughes-Fulford and her fellow researchers identified for the first time
a direct chain of causation: When introduced into prostate tumor cells
in culture, omega-6 fatty acid causes the production of cPLA2, which
then causes the production of the enzyme COX2. In turn, COX2 stimulates
the release of PGE2, a hormone-like molecule that promotes cell growth.

"What's important about this is that omega-6 fatty acids are found in
corn oil and most of the oils used in bakery goods," says
Hughes-Fulford, who is also an adjunct professor of medicine at the
University of California, San Francisco (UCSF). "Which means that if
you're eating a diet high in omega-6 fatty acids, it's possible that
you're turning on this cancer cascade, which has been shown to be a
common denominator in the growth of prostate, colorectal, and some
breast cancers."

The study points out that 60 years ago in the United States, the
dietary ratio of omega-6 to omega-3, a beneficial fatty acid, was 1 to
2. Today, the ratio is 25 to 1. Over that same 60 years, the incidence
of prostate cancer in the U.S. has increased steadily.

Hughes-Fulford also found that flurbiprofen, a non-steroidal
anti-inflammatory drug commonly prescribed for arthritis, blocked the
production of cPLA2 and broke the chain leading to cell growth. This
means, she says, that new drugs might be developed that could
specifically target cPLA2 and prevent COX2 from being released.

"COX2 has been implicated in the growth of many types of tumors," she
notes. "So if you can find a way to block that cascade in the tumor,
starting with cPLA2, you might have a new way of modifying or slowing
tumor growth."

Hughes-Fulford points out that cPLA2 inhibitors would avoid the
problems inherent in the class of drugs known as COX2 inhibitors. These
drugs have been shown to be effective against tumor growth as well as
in treating the pain associated with inflammatory conditions such as
arthritis, but have been implicated in increased risk of cardiovascular
problems in people who take them regularly. "COX2 inhibitors also
inhibit prostacyclins, which are enzymes that are beneficial to the
heart, and cPLA2 inhibitors would not affect those," she explains.

In future research, Hughes-Fulford will be looking at the overall
effect of different types of fatty acids on different tumor types in
cell lines as well as human biopsies. She plans a study that will
correlate type of fatty acid with tumor stage and grade in order to
obtain a clearer picture of specific effects of different fats on tumor
progression.

Co-authors of the study were Raymond R. Tjandrawinata, PhD, of UCSF,
Chai-Fei Li, BA, of SFVAMC, and Sina Sayyah, BA, of SFVAMC and UCSF.

Science. 2005 Jul 29;309(5735):774-7.

Recognition of host immune activation by Pseudomonas aeruginosa.

Wu L, Estrada O, Zaborina O, Bains M, Shen L, Kohler JE, Patel N, Musch
MW, Chang EB, Fu YX, Jacobs MA, Nishimura MI, Hancock RE, Turner JR,
Alverdy JC.

Department of Surgery, University of Chicago, Pritzker School of
Medicine, Chicago, IL 60637, USA.

It is generally reasoned that lethal infections caused by opportunistic
pathogens develop permissively by invading a host that is both
physiologically stressed and immunologically compromised. However, an
alternative hypothesis might be that opportunistic pathogens actively
sense alterations in host immune function and respond by enhancing
their virulence phenotype. We demonstrate that interferon-gamma binds
to an outer membrane protein in Pseudomonas aeruginosa, OprF, resulting
in the expression of a quorum-sensing dependent virulence determinant,
the PA-I lectin. These observations provide details of the mechanisms
by which prokaryotic organisms are directly signaled by immune
activation in their eukaryotic host.

7/30/2005
Immune System's Distress Signal Tells Bacteria When To Strike Back

The human opportunistic pathogen, Pseudomonas aeruginosa, has broken
the immune system's code, report researchers from the University of
Chicago, enabling the bacteria to recognize when its host is most
vulnerable and to launch an attack before the weakened host can muster
its defenses.

In the July 29, 2005 issue of Science, the researchers show how this
lethal organism detects interferon-gamma, a chemical messenger the
immune system uses to coordinate its efforts to get rid of bacteria.
When these bacteria intercept this message, they recognize it as a
threat, assess their own numbers, and if they have sufficient strength,
activate genes that quickly transform them from benign passengers in
the bowel into deadly blood-stream invaders.

"Most of the time these microbes are content to live and grow in our
intestines," said John Alverdy, MD, professor of surgery at the
University of Chicago and director of the study. "They don't feel the
need or even look for the opportunity to attack. But when they detect a
threat, they have a remarkably sophisticated defense plan, based,
unfortunately, on the notion that the best defense is an overwhelming
offense."

Pseudomonas aeruginosa is ubiquitous. It lives in all sorts of moist
places, including damp soil and on the surface of vegetables, as well
as in streams, faucets, and drinking fountains. It is often a long-term
bowel tenant, colonizing the intestines of about three percent of
healthy people.

In the bowel this germ is usually harmless, but it can turn deadly,
causing gut-derived sepsis. It is also a frequent cause of infections
after major surgery.

Physicians have theorized, said Alverdy, that germs such as Pseudomonas
are always "probing for a weakness in the host and are ready and
willing to strike whenever they find one." He and his colleagues,
however, are testing an alternative theory: that "bacteria are
perfectly content in their niche until signals from the host--usually
during stress, such as after major surgery--let them know there's a
problem."

For Pseudomonas, detecting interferon-gamma, "is like receiving a
demolition notice from your landlord," Alverdy said. "It lets them know
they need to find a new home. They don't take that news any better than
we would."

A vulnerable host, like a condemned home, is a liability, a threat to
its tenants' survival. Pseudomonas, however, has the tools to engineer
its own escape--by killing off the host.

This wily pathogen can evade a host's immune system. It can repel
antibiotics, secrete toxins similar to those used by anthrax, latch
onto the bowel wall, bore its way through, and flow into the blood
stream. As a consequence, patients with widespread Pseudomonas
infection often die within a few days.

Alverdy and colleagues were able to pinpoint key early steps of this
lethal process. The transformation starts when a weakened host tries to
boost its defenses against any possible invasion. The host's T cells
release chemical signals that activate the immune system. One of those
signals, interferon-gamma, is intercepted by a protein, called OprF,
found on the outer membrane surface of Pseudomonas. This serves an
early warning system.

Once Pseudomonas detects the first signs of a brewing immune response,
they also begin to prepare for battle, gathering information and
responding with their own counteroffensive.

Their first move is a process called quorum sensing, which bacteria use
to gauge their own numbers. When interferon-gamma binds with OprF on
the bacterial cell surface, it activates a gene called rhII. RhII
triggers synthesis and secretion of a bacterial signaling molecule
called C4-HSL. By measuring the amount of C4-SHL in their environment
these bacteria can estimate their own numbers and density.

If they feel they are sufficiently numerous, they produce two virulence
factors, molecular weapons known as PA-I and Pyocyanin. PA-I causes the
barrier cells that line the host's bowel to become more permeable,
which renders them more susceptible to the microbe's toxins. Pyocyanin
enhances the germ's ability to pass through the weakened bowel wall,
enter the bloodstream and invade tissue.

"Our goal," Alverdy said, "is to understand the many steps in this
process and use that knowledge to find novel ways to intervene, to stop
the infection before it starts rather than trying to kill all the
germs."

Many harmful bacteria have already learned how to resist the drugs
developed to treat them. Scientists are now looking at alternatives,
such as ways to block or scramble the chemical messages that allow
microbes to eavesdrop on their hosts or to conspire together to mount
an attack.

"We chose to study this in Pseudomonas because it is one of the
deadliest infections for patients who undergo major surgery," said
Alverdy. "We suspect something very similar, however, occurs in all
sorts of infections."

Inflammatory bowel disease patients, for example, have elevated
cytokines--the chemical messengers that trigger an immune response--in
the bowel. "These could signal the bug," said Alverdy, "then the bug
strikes back and then the inflammation process snowballs." Because the
bacteria in this case are "normal flora," people with no real infection
develop a chronic disease.

The battles between pathogens and their hosts have been going on for
millions of years, Alverdy said, with each side constantly devising
novel measures, countermeasures, and counter-countermeasures, including
sophisticated mutual espionage.

The discovery of antibiotics gave human hosts a temporary advantage,
"but that seems to be waning a bit," he added. "We need to learn new
ways to understand our germs and think about how to placate rather than
annihilate them."

The National Institutes for Health and the Canadian Institutes of
Health research supported this research. Additional authors of the
paper include Licheng Wu, Oscar Estrada, Olga Zaborina, Le Shen,
Jonathan Kohler, Nachiket Patel, Mark Musch, Eugene Chang, Yang-Xin Fu,
Michael Nishimura, and Jerrold Turner of the University of Chicago;
Michael Jacobs of the University of Washington; and Robert Hancock of
the University of British Columbia.

Source: sciencedaily.com

COMMENT:

Not if they killed him with chemo, it isn't. He had a terminal
condition in any case, but there are some cancers probably best left
untreated (except with paliative radiotherapy) and many types of lung
cancer fall into this category, after they've spread beyond the point
of surgical removal. Chemo doesn't slow them down much, and it
certainly quite often kills patients (they lose weight and get
pneumonia much faster, and die). Alas, oncologists continue to "offer"
chemo "paliatively" even in cases where it hasn't been shown to affect
life span, and certainly where it can negatively affect life quality.
In these cases a lot of patients might be better off just saying no to
cytotoxic-type chemotherapy.

(Radiation, by contrast, is a relatively well-tolerated cancer
treatment, causing few problems with quality of life, and rarely
contributing to death).

Understand, I'm not against chemo per se. In some cancers at some
stages (and even a few solid cancers at ANY stage), chemotherapy can be
lifesaving, and you'd be a fool not to use it. In a few others,
cytotoxic chemo does work paliatively, cutting bone pain from
metastases, even when everyone knows it won't be curative. This is
particularly helpful in very low and painful cancers that metastasize
to bone, with breast cancer being a prime example.

But at the same time, chemotherapy is overused, in general, in
oncology. It's used when the patient isn't in pain from the tumor, and
when there's little reason to believe it's doing anything to extend
life. Oncologists earn most of their money by giving chemotherapy, and
that might be part of the reason. However, the unwillingness of
patients to just "give up" and do nothing without continuing to
"fight," is another. Wisdom is needed when you have something like
inoperable lung cancer. It is fine to grasp at straws when they're
inexpensive and reasonably harmless straws. Chemotherapy often isn't
that kind of thing.

SBH

Voice changes, couching, shortness of breath. Usually, by the time you have
other symptoms (loss of weight, pain from metatstic disease), it is time to
make an appointment with the coffin maker.

Jeff