Ecological Study of the Role of Highly Processed Milk, Meat and Vegetable Oil in Prostate Cancer Causation
by Carl Hans Norgauer
View First 25 Pages:
(free download) Synopsis
The transition from locally-produced, whole foods to distant-produced, fractioned foods
marks food consumption patterns in the United States and other developed nations. Chief risk
factors for prostate cancer - milk, meat and vegetable oils – were examined to determine how
modern processing of these foods has impacted the incidence of prostate cancer. Food
consumption patterns in six nations with consistently low prostate cancer mortality were
compared with seven nations with consistently high cancer mortality. Several of the low prostate
cancer mortality nations included in this study have primitive food processing technology while
all the high prostate cancer mortality nations have advanced refining and food fractionating
technology. World Health Organization (WHO) mortality data for 1980-1995 were correlated
with Food and Agricultural Organization (FAO) food consumption data for 1995. Milk
consumption statistics are weakly supportive of the hypothesis that the effect of milk processing
is important in prostate cancer etiology (p < 0.06). Supportive of this hypothesis is the fact that
the low mortality nations, Turkmenistan and Uzbekistan, are big consumers of milk but their milk
processing technology is primitive. Consumption patterns of the unstable oils - soybean and
canola - strongly support the hypothesis that the formation of trans fats and oxidized fats by
modern processing raises the risk of prostate cancer (p < 0.05). The correlation of meat
consumption and prostate cancer mortality is consistent with the food processing hypothesis (p <
0.03) and potential mechanisms are suggested. The formation of reactive oxygen species (ROS)
resulting from milk homogenization is suggested as a source of toxic lipid peroxides and
aldehydes that form in the body causing antioxidant depletion. The formation of trans fats by vegetable oil hydrogenization is linked to the formation of abnormal spermatozoa. Defective
spermatozoa are proposed as a mechanism for prostate cancer initiation. The formation of ROS
by activated neutrophils and spermatozoa is a source of oxidative stress in prostatic tissue that
promotes tumor development. Future research is recommended into gut absorption of dietary
lipid peroxides and aldehydes, the role of iron as a catalyst for lipid peroxidation in prostate
cancer etiology and the possible correlation of prostate cancer and male infertility.