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.
