Day 256 - 04 Jun 96 - Page 62


     
     1        with a much more complete analysis of the data that has not
     2        yet been published, and I guess I am not really at liberty
     3        to discuss that.  It is the report that I am the co-chair
     4        of, and I prefer not to.  But, in any case, the dietary fat
     5        hypothesis, I can assure you, has not gone away.
     6
     7   MR. JUSTICE BELL:   No.  That is not what Mr. Rampton is on at
     8        the moment.  He is challenging your general consensus
     9        statement, as I understand it, at the moment.
    10
    11   MR. RAMPTON:  I understood you to say -- and I may be quite
    12        mistaken -- I understood you to say that there is a general
    13        consensus amongst the scientific community who know
    14        anything about this topic that dietary fat is a direct
    15        causal agent in the onset of breast cancer, by one route or
    16        another.
    17        A.  Right.
    18
    19   Q.   I am challenging that statement, if I have not
    20        misrepresented it.
    21        A.  OK.  Your question actually leads us to the question of
    22        how do we study the effects of these individual nutrients,
    23        if you will.  In the case of humans, it is very difficult,
    24        trying to tease away the facts by statistical methods.
    25        What one has to do is either one of two things:  they
    26        either have to intervene in the case of humans by giving
    27        them high or low intakes of fat, on the one hand, over some
    28        period of time, making observations; or, on the other hand,
    29        going to experimental animal studies and actually there
    30        controlling everything except for fat intake, to see what
    31        happens.  I mean, I cannot think of anything else other
    32        than those two sort of operations.  We have not done that
    33        in the case of humans by basically giving fat all by
    34        itself, following people, to see what happens.  The best we
    35        can do is to look at all the various kinds of data, draw
    36        them together, see what we have at the end of the day, and
    37        then go to the question concerning: is this plausible?  The
    38        only way we can really get a hand on plausibility at this
    39        point in time, or the best way, is to go to experimental
    40        animal studies, give them fat and see the kind of effect
    41        that actually is produced in the animals that leads to
    42        causality conclusions, to see whether these kinds of effect
    43        we see there are consistent with what we see in the case of
    44        humans.  Indeed, we find this is true.
    45
    46        So, in the case of animal studies, there is a paper that
    47        was published in 1991 which actually collected together all
    48        this studies that have been done on animals over the years
    49         -- about 512, as I recall, really an enormous number of
    50        studies -- where they found that increase in fat intake in 
    51        animals, given under various and sundry conditions, leads 
    52        to a highly significant increase in the development of 
    53        mammary tumours; and all the things that occur in these
    54        animals, such as increase in levels, etcetera, etcetera, we
    55        turn around and see in humans.
    56
    57        So, I think any reasonable conclusion from that is that fat
    58        does make an independent contribution to breast cancer.
    59        I do not think there is really any serious dispute about
    60        that.

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