Did all of you see the new report, which contains the following
passage:

QUOTE:  ...The researchers couldn't explain why eating more animal fat
was associated with breast cancer risk. It may be that factors other
than fat are involved. For instance, grilling red meat can create
cancer-causing chemicals, and high-fat dairy products contain growth
factors that could affect breast cancer risk.

Earlier studies had suggested one reason for the increased cancer
risk, relating this to the heterocyclic amines (HCAs) that form when
red meat is cooked at high temperatures (like frying and grilling),
especially well-done. In laboratory studies, HCAs bond to estrogen
receptors and create estrogen-like effects. In earlier research with
women past menopause, those who consistently ate hamburger, beef steak
and bacon very well done thus getting high levels of HCAs -had more
than four times the breast cancer risk in comparism with women who
consumed these meats raw or medium done.

New research suggests that HCAs may pose more danger to some people
than others. Like many carcinogens, HCAs have to be activated to be
able to damage our DNA and pose cancer risk...  UNQUOTE.

I explained this on my site quite a while ago, and I also cited
evidence showing how important a role PUFAs play in this process.  The
evidence is so clear that the question that most intrigues me is how
people like Ron refuse to even consider it.

Source of the quoted passage:  http://www.tribune.com.ng/22032007/hlt2.html

Here is my point made in 2002.  As I've said before, these points I am
making are not orginal, and are not being made by "alternative"
types.  Instead, they reflect the molecular-level evidence, as opposed
to the "epidemiological."  As any epidemiologist will tell you, if the
underlying assumptions used for an epidemiological study are
incorrect, the results can not only be inaccurate, but also misleading
in the extreme, which is why they are not really science, in that they
only deal with correlations, not causation.

Mutat Res. 2002 Sep 30;506-507:9-20.
"Comments on the history and importance of aromatic and heterocyclic
amines in public health."
Weisburger JH.
The carcinogenic risk of aromatic amines in humans was first
discovered when a physician related the occurrence of urinary bladder
cancer to the occupation of his patients. They were employed in the
dyestuff industry, chronically exposed to large amounts of
intermediate arylamines. Laboratory investigations disclosed that rats
and mice administered specific azo dyes arylamines or derivatives
developed cancer, primarily in the liver. Also, at that time, a
possible pesticide, 2-aminofluorene, was tested for chronic toxicity,
revealing that it rapidly induced cancers in several organs of
rodents. This led to investigations on the mode of action of this
class of chemicals, including their metabolic conversion. Biochemical
activation to more reactive N-hydroxy compounds was found to occur,
mostly in the liver, through what is now known as the cytochrome p450
enzyme systems, and also through prostaglandin synthetases. There were
species differences. Guinea pigs were resistant to carcinogenesis
because of the low titer of the necessary activating enzymes. In
target tissues, a second essential reaction was necessary, namely
acylation or sulfate ester formation. The reactive compounds produced
display attributes of genotoxicity in appropriate test systems.
Interest in this class of compounds increased when of Sugimura and
colleagues discovered the formation of mutagens at the surface of
cooked meat or fish, that were identified as heterocyclic amines
(HCAs). These compounds undergo the same type of activation reactions,
as do other arylamines. Epidemiological data suggest that meat eaters
may have a higher risk of breast and colon cancer. HCAs induced cancer
in rats in these organs and also in the prostate and the pancreas. In
addition, there is some evidence that they affect the vascular system.
The formation of HCAs during cooking can be decreased by natural and
synthetic antioxidants, by tryptophan or proline, or by removing the
essential creatine through brief microwave cooking prior to frying or
broiling. The amounts of HCAs in cooked foods are small, but other
components in diet such as omega-6-polyunsaturated oils have powerful
promoting effects in target organs of HCAs. On the other hand, the
action of HCAs may be decreased by foods containing antioxidants, such
as vegetables, soy, and tea. Some constituents in foods also induce
phase II enzymes that detoxify reactive HCA metabolites. Additional
mechanisms involved decreased growth of neoplasms by intake of
protective foods. Possibly, the carcinogenic effect of HCAs is
accompanied by the presence of reactive oxygen species (ROS), which
are also inhibited by antioxidants. World-wide, there have been many
contributors to knowledge in this field. Adequate information may
permit now to adjust lifestyle and lower the risk of human disease
stemming from this entire class of aryl and HCA.