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The full article cited below demonstrates that most negative attributes are
generally form the most promoted synthetic fats which contain trans fatty
acids by the virtue of how they are manufactured. This includes most
polysaturated, unsaturated and even monounsaturated fats. I have yet to
find a good study linking saturated fats to all the bad things on hears
about them! The more I study saturated fats the more good things I find
about them... Yet again it appears that one cannot go wrong in going back
to the most natural products which have been maligned in the search for
ever higher profits of the synthetics and modified foods.

Chris Gupta

"The issue of the trans fatty acids as a causative factor in cancer remains
underexplored, but recent reports have found a connection. Bakker and
colleagues (1997) studied the data for the association between breast
cancer incidence and linoleic acid status across European countries, since
animal and ecological studies had suggested a relationship. They found that
the mean fatty acid composition of adipose did not show an association with
omega-6 linoleic acid and breast, colon or prostate cancer. However,
cancers of the breast and colon were positively associated with the trans
fatty acids. Kohlmeier and colleagues (1997) also reported that data from
the EURAMIC study showed adipose tissue concentration of trans fatty acids
having a positive association with postmenopausal breast cancer in European

"Lowering the trans fatty acids in foods in the US can only be done by
returning to the use of the natural, unhydrogenated and more saturated fats
and oils."


One major concern expressed by the nutrition community is related to
whether or not people are getting enough elongated omega-3 fatty acids in
their diets. The elongated omega-3 fatty acids of concern are
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Some research
has shown that the basic omega-3 fatty acid, linolenic acid, is not readily
converted to the elongated forms in humans or animals, especially when
there is ingestion of the trans fatty acids and the consequent inhibition
of the delta-6-desaturase enzyme. One recent study (Gerster, 1998), which
used radioisotope-labelled linolenic acid to measure this conversion in
adult humans, showed that if the background fat in the diet was high in
saturated fat, the conversion was approximately 6% for EPA and 3.8% for
DHA; whereas, if the background fat in the diet was high in omega-6
polyunsaturated fatty acids (PUFA), the conversion was reduced 40-50%.
Nanji and colleagues (1995) reported that a diet enriched with saturated
but not unsaturated fatty acids reversed the alcoholic liver injury in their animals which was caused by dietary linoleic acid. These researchers concluded that this effect may be explained by the down-regulation of lipid peroxidation. This is another example of the need for adequate saturated fat in the diet.

Cha and Sachan (1994) studied the effects of saturated fatty acid and
unsaturated fatty acid diets on ethanol pharmacokinetics. The hepatic enzyme alcohol dehydrogenase and plasma carnitines were also evaluated. The
researchers concluded that dietary saturated fatty acids protect the liver
from alcohol injury by retarding ethanol metabolism, and that carnitine may be involved.

Hargrove and colleagues (1999) noted the work of Nanji et al. and
postulated that they would find that diets rich in linoleic acid would also
cause acute liver injury after acetaminophen injection. In the first
experiment, two levels of fat (15g/100g protein and 20g/100g protein),
using corn oil or beef tallow, were fed. Liver enzymes indicating damage
were significantly elevated in all the animals except for those animals fed
the higher level of beef tallow. These researchers concluded that "diets
with high [linoleic acid] may promote acetaminophen-induced liver injury
compared to diets with more saturated and mono-unsaturated fatty acids".

Extracted form:


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