And I demand a lollipop.
You: One brief research report basically proving just that "diet is responsible for bowel cancer". And "prevalent mostly in industrialised countries" does even support my original suggestion. Thank you. But it's quite off topic when it comes to food additives' responsibility for cancer.
Me: Several public resources referring to findings of institutes like The US Center for Science in the Public Interest, Canadian Cancer Society, The Food & Drug Administration or Joint FAO/WHO Expert Committee.
But since you're such a patient fellow, I provide you with one about Carrageenan (E407). As the table at (
) states "a fibre extracted from seaweed, it has recently been linked with cancer because it may become contaminated when ethylene oxide is added to an inferior product, this results in ethylene chlorohydrins forming, a highly carcinogenic compound; linked to toxic hazards, including ulcers and cancer; the most serious concerns relate to degraded carrageen, which is not a permitted additive; however, native carrageen an, which is used, may become degraded in the gut". But since I suppose it wouldn't be a credible source for you, make your conclusions from something else:
Quote:
Review of Harmful Gastrointestinal Effects of Carrageenan in Animal
Experiments
Joanne K. Tobacman
College of Medicine, University of Iowa, Iowa City, Iowa, USA, October 2001
(...)
Conclusion
Inflammatory bowel disease and colorectal
malignancy represent major sources of morbidity
and mortality in the United States. A
possible factor in the etiology of these
pathologies is exposure to carrageenan.
Several investigators have expressed their
concerns about the use of undegraded carrageenan
in food products (6-10), yet no
legislative protection to restrict incorporation
of low molecular weight fractions has
been enacted. In fact, there has been no substantive
review by the Food and Drug
Administration of carrageenan since the
studies undertaken more than two decades
ago. However, there has been increased evidence
regarding the cancer-promoting activity
of undegraded carrageenan and further
confirmation of the carcinogenic potential of
degraded carrageenan.
Evidence for the role in carcinogenesis of
carrageenan appears to support a nongenotoxic
model based on direct toxic effects,
for carrageenan has been nonmutagenic in
Salmonella mutagenicity testing and nongenotoxic
by DNA repair tests (60,102). A model
of cellular destruction—from disruption of
lysosomes by accumulation of carrageenan
by-products or by interference with normal
cellular oxidation-reduction processes from
sulfate metabolites—emerges from review of
the experimental studies. The impact of sulfatases,
of either bacterial or human origin, on
the metabolism of carrageenan requires further
investigation. By interference with the
normal intracellular feedback mechanisms
associated with arylsulfatase activity, including
steroid sulfatase, the highly sulfated carrageenan
may have an impact on the availability
of active, unsulfated hormones, such as
dehydroepiandrosterone, derived from dehydroepiandrosterone-
sulfate, and estrone-1,
derived from estrone-1 sulfate.
Genetic characteristics that affect sulfatase
and hydrolysis reactions as well as the
individual intestinal microflora may influence
how carrageenan is metabolized and
how its effects are manifested. These factors
may determine how carrageenan is metabolized
differently by different individuals, but
these characteristics may not be accessible to
manipulation. A basic factor that can be
controlled is the intake of carrageenan,
which is amenable to dietary modification or
food additive regulation.
Although carrageenan is widely used as a
food additive for its texture-enhancing
properties, other gums, some of which are
used in combination with carrageenan, such
as locust bean gum, gum arabic, alginate,
guar gum, or xanthan gum, potentially can
be used alone or in different combinations
as substitutes for carrageenan (41,46).
Alternatively, higher fat composition can
lead to changes in food properties that may
compensate for exclusion of carrageenan.
Other hydrocolloids that are used as stabilizers
and thickeners have not been associated
with harmful gastrointestinal effects,
and it is reasonable to expect that they could
replace carrageenan in many food products.
Although the dietary fibers pectin and psyllium
affect intestinal motility, ulcerations or
neoplasms have not been induced with
either these or the other water-soluble polymers
used as food additives. In contrast,
other highly sulfated polysaccharides, amylopectin
sulfate and dextran sulfate sodium,
have induced ulcerations and neoplasia, suggesting
that the degree of sulfation and polysaccharide
molecular weight may be critical
for induction of the observed effects (102).
End of demo version. Are you interested in more studies on carcinogenic effects of next E food additives as well? Exhaustive and detailed reports are scarce on the net, but I might stop by in Medical Faculty tomorrow and ask them for some. I'm still interested in that bargain.
Authorities do tend to contradict each other, because that's how it goes in scientific community. Results of any research can be potentially replaced by a newer, more precise research. Or not.
