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

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