Day 014 - 20 Jul 94 - Page 33
1 hormone levels and sex hormone binding globulin. Other
suggested mechanisms include modulation of immune function
2 and prostanoid synthetic pathways, and membrane lipid
peroxidation. In bowel cancer, it has been proposed that
3 the concentration of faecal bile acids is increased by
high fat diets and that secondary bile acids act as tumour
4 promoters. However, individuals living in areas with a
high risk of colon cancer do not have a higher faecal bile
5 acid concentration or total faecal bile acid output
compared with those living in areas with a low risk,
6 neither do cases of large bowel cancer have higher faecal
bile acid outputs or concentrations compared with
7 controls. Other factors modulating the solubility of free
bile acids may be involved."
8
Pausing there, Professor Wheelock, have you studied the
9 literature on these questions?
A. I would not claim to have studied all of the
10 literature thoroughly, quite honestly. It is voluminous.
11 Q. One notices that the panel gives references running from
41 to 66, which is either 25 or 26 references?
12 A. It will be clear that the relationships and the
mechanisms are very, very complicated. I think it is
13 going to take a long time to sort it out, quite frankly.
14 Q. One sees the panel's conclusion 3.5.6. on page 52: "The
Panel concluded that there is currently insufficient
15 evidence on which to base a recommendation for a decrease
in fat intakes to prevent cancer, although an increase in
16 consumption of any fatty acid should not be encouraged.
The Panel agreed that the DRVs based on other
17 considerations and presented in para 3.8 were consistent
with a prudent view of the current data relating dietary
18 fat and the occurrence of cancer".
19 Professor Wheelock, from your point of view as a
specialist, one might say academic nutritionist, is there
20 anything in that paragraph with which you disagree?
A. Not in the slightest; I think it is an excellent
21 summing up of the current position.
22 Q. Then we see obesity. This is canvassed in the next
following section 3.6. Again I draw your attention only
23 to the conclusion on page 53 at 3.6.5: "Conclusions: The
Panel concluded that there was insufficient evidence
24 either to establish or to exclude a special role for
dietary fat in the development of obesity. Nevertheless
25 fat increases the energy density of diets and is
palatable. This may be conducive to increased food energy
26 intake in some individuals with a genetic or behavioural
predisposition."
27
Leaving aside people with a genetic disposition, can we
28 say in plain English that what the panel is telling us is
that greedy people may get fatter than others?
29 A. Yes, especially the many foods that are high in fat.
30 Q. "Dietary fat restriction is a valuable contribution to the
management of established obesity". Next comes diabetes
