BETWEEN: (2) MCDONALD'S RESTAURANTS LTD.
- AND - (2) HELEN MARIE STEEL (4) DAVID MORRIS
PLAINTIFFS' CLOSING SUBMISSIONS VOLUME 1 NUTRITION
BARLOW LYDE & GILBERT |
I. J's meaning*, broken down into its constituent parts
*Ruling 20.11.95; 26 AD
1. McD's food is very unhealthy
(ii) with the very real risk that you will suffer cancer of the breast or bowel or heart disease as a result.
2. McD's know this*, but
*that their food is v. unhealthy, for both (all) the stated reasons.
II. J's ruling as to defamatory effect of these allegations*:
*26F 27A
III. These are obviously connected: the allegation of deceit flows from the knowledge that the food is v. unhealthy. Statements made innocently, in the honest (but mistaken) belief that they were true, could not constitute deceit.
IV. This analysis shows that the defamatory allegations are allegations of fact, not comments:
V. It follows that the allegations must be shown to be (substantially) true, ie, proved as facts: viz, it must be shown (by clear & convincing e., because the allegations are very serious):
VI. So the qq. of fact, in order, are:-
(2) Is it high in fat, etc low in fibre etc? (each element to be considered in turn.
(3) Is it true that eating the food may well make your diet high in fat, etc. and low in fibre, etc.?
(4) Does that create the 'very real risk' that you will get cancer or heart disease as a result?
(5) Do McD's know that (1)(4) are the true facts?
(6) Do they deceive their customers by concealing those facts and pretending that their food is a useful and nutritious part of any diet?
FOOD FAT
FAT 1. Is 'the food' high in fat?1.2 What food?
1.3 Some of it is obviously fatfree - eg coke, black coffee
1.4 Some of it is obviously nearly so - eg salad w/o dressing
1.5 Some has modest amounts: eg
*P VI/7 (1993) hashbrowns or hamburgers*
p.46(?) TF 7. 8g TF 8. 6g
SF 1. 5g SF 4 . 0g
1.6 Some has (comparatively) large amounts:
* (same ref.) eg ¼ lbr : 22g +10.3g*
or ¼~ lbr w.cheese : 27.7g + 13.9g
Choice of meal
1.7 Sensible thing is to look at a meal remembering always that by no means all
those who visit McD's eat meals, as such
e.g black coffee & donut on the way to
work each day*
*NB
P VI/A/45/
207: "Lighter
users spend Can't look at every possible meal combination
more than heavy
users"
and 204: 1.8 So what I've done is to take what McD's themselves see as a 'typical' meal
"breakfast
has strongest 2+/5 customers (1991): entrée, fries, beverage also popular with children. *
following of
heavy McD's
users"
*P VI A/45/298
+243
but I've also added a pudding, to make a 'worst case' scenario.
1.9 Thus:
- Cheeseburger
- FF(R)
- Apple pie
- Coca Cola (M)
1.10 This has been chosen by ref. to fat content, simply because, of all the ingredients of
*SF= saturated a McD's meal, fat, and particularly SF*, is the
fat one which, on the evidence, is mostly closely associated with illhealth,
in the form of CHD* .
*See Admission
(more later)
1.11 I haven't chosen the fattiest possible meal (eg ¼lbr, FF(L), Donut + milkshake); nor, on the other hand, the least fatty (eg hamburger, salad, black coffee no pudding)
but tried to pick something which would fairly represent an 'average' sort of meal for
a person of any age (though small children might struggle to finish it!).
1.12 I will start with fat, for the reason stated, then examine each of the other constituents
which that meal happens to have: only when that has been done is it possible to give
a factual answer to the umbrella q:-
Is the food high in fat, etc low in fibre, etc
1.13 I have taken different years, both in UK and US, to test the allegation over a period of
time; this has been partly dictated by the availability of appropriate info. in the evidence.
1.14 Thus:
*P VI/4 and 5 UK: 1989* P VI/6/368 McD's Food:
are from 1985: The Facts.
they don't
give fig.s 1 1993: P VI/7/?46: McD's Nutrition
for SF at all Information
and apple pie
wasn't on menu
so no pt. using them for
this comparison US: 1987: P VI/19/?: McD's Food:
The Facts
1988: P VI/20/?: McD's Food:
The Facts
1989: P VI/15/?: Nutritional
Analysis
(Hazelton Labs.)
[1990: P VI/22 gives the same figures as 1989]
1.15 Methodology:
* Total fat (1) See what the TF* and SF content is of each item, in grammes.
(2) Since the epithet 'high', as applied to a particular constituent/ingredient of a
food or a meal is necessarily a word of proportion, the q. is, as a proportion of what?
*Any other Ans: Energy supply/requirement
measurement in k/cal (which seems to be the universal approach). *
such as
proportion by
weight is
obviously useless.
(3) Since the fat content of a particular food item, expressed as a proportion of the
*eg, Prof Naismith's energy derived from thatitem, is a meaningless calculation*, I have ignored it.
olive.
(4) Equally, the fat content of a single meal, expressed as a % of the total energy
derived from that meal, is likely to be valueless in answering the q "Is the food
unhealthy?.
So I have ignored that, too. The correctness of this approach confirmed by:
* 259 : 30;1231:18 Crawford *
+ 14 : 62:2463:8 - supported by Wheelock +
x 253 : 20:3841 - and Naismith
(5) These expert opinions confirm that it is, of course, the effect on diet that matters.
However, on the way to answering that (eventual) question, it may be relevant
to ask the preliminary q:
- what contribution to the customer's total daily energy intake/requirement
does the fat content of this meal make?
(6) There is, on the evidence, no clear or final scientific agreement or conclusion
about the precise max. (actual) % of daily energy requirement/intake which fat
should contribute.
(7) However, there does seem to be agreement (VW, Cannon, Crawford+)
+269 that the recommendations of COMA (41 and 46) should be given weight.
42:3242
*Also Naismith,
Arnott.
( Crawford
started to
retreat a bit
later on!)
(8) Since there is nothing better, I propose
to use those, and thus to calculate the %
contribution which the fat content of the
chosen meal makes to the EAR for
energy per day (as expressed in COMA
*Not the 41 (1991)) for different age groups* and
whole range! to compare that with the DRVs for fat
See below. recommended by COMA (as % of EAR for
energy) .
(9) In this way, and probably only in this way,
can one begin to see how the meal fits, or may fit,
into its consumer's overall diet, in relation to his/her fat consumption.
(10) When I go on to consider such things as
sodium, vitamins, minerals and fibre,
which are also important I shall use a
similar approach, though some of the materials will,
nec., be different.
(11) In passing -
(a) I propose to ignore two elements
of the "high in" category of supposed
unhealthiness:
"animal products" and "sugar"
(b) Reasons:
(i) "animal products" is meaningless;
except in so far as they contain
fat, salt, vitamins and minerals,
all of which must be considered
*See, eg, Arnott: 254:61 (Ans. J) separately (proteins*, as such,
* See COMA 41: 5.5, iiv on p.73. have not made anything but a
fleeting appearance in the case),
"animal products" contribute
nothing to the debate.
(ii) "Sugar" is also irrelevant, but for
a different reason: its only direct
effect on health is cariogenesis,
which has nothing to do with
cancer or CHD. * Otherwise, it is
a benign source of energy.
Choice of consumers
UK 1.16 (1) As will be seen in due course, overall
the most important category of McD's
customers in the UK is the age group
1634: not only do they constitute c.56%
of all those who visit McD's 1 x pa or
more often, they also constitute c.81% of
OMNIMAS those who visit McD's 1 x pw or more
[AF new often,(1624s = 60% in this cat.)
tables, 1995]
US (2) In the US the 1434s are 46% of
P VI A/45/212 (1991) he total, whilst the 1834s are
39%. Thus, though the spread is
1444s = 65% somewhat greater in the US*, the
* teenager young adult group is
2044s = 54% probably the single most important
2544s = 42% group (013s = 18%, 3555s = 36%).
1634's (3) Therefore, to represent this group, I
have taken a 17 year old male and a 25
year old female (who has a lower EAR
than a 17 yr old girl).
Children (4) Since children are also an important
group (partic. on a/c of the allegations
made about McD's advertising), I have
also taken a boy and a girl, each 8 yrs old.
(5) I have given each of these agegroups
the EAR for energy set out on xix of
COMA 41 in Table 1.1.
(6) These are, in fact, minima:
see pp 247 of COMA 41.
eg If you give a 20 yearold male a
'moderately active' PAL (1.7: see Table
2.3 on p.24), and you weigh him in at
75kg (11st 11lb), then you find that his
* 1 MJ EAR is actually 13 MJ/d (=3087.5 Kcal/d*
= 273.5 Kcal Table 2.7 on p.27. Whereas, according
to Table 1.1 on p . xix, his EAR is only
10.6 MJ/d (or 2550 Kcal). Looking back
at Table 2.7, one can then see that that
is (approx.) the EAR for a 75kg 20 yr
old male with a PAL of 1.4, ie,
active neither at work nor in his
* See Table 2.3 leisuretime* which is a v. unusual 20 yr old male!
on p. 24
(7) In the result, by giving the 4 consumers
minimum EARs, and by adding in a
pudding, I have produced a much gloomier
picture than reality suggests is likely to be
true or fair. No matter.
1.17 The calculations: see the tables which follow.
The Food
FAT
Table 1
UK: 1989 : P VI/6136
Cheeseburger 13.6 6.7 295 FF (R) 14.5 7.9 236 Apple pie 15.4 4.3 259 Cola (R) - - 105 Total 43.5 18.9 895
1 g Fat = 9 Kcal
Therefore: 43.5g. TF= 391.5 Kcal (1)
18.9g. SF = 170.1 Kcal (2)
17 yr. old male: EAR: 2755 Kcal/d DRVs:
(1) = 14.2% EAR TF: 33%
(2) = 6.2% EAR SF: 10%
(COMA 41: 3.8.vi)
25 yr. old female: EAR: 1940 Kcal/d
(1) = 20.2% EAR
(2) = 8.8% EAR
*based on 8 yr.old boy* EAR:1970Kcal/d* DRVs
table 2.2,
p.21) (1) = 19.9% EAR TF: 35% (no alc)
(2) = 8.6% EAR SF: 11% (no alc)
(COMA p. xx)
8 yr. old girl EAR: 1740 kcal/d
(1) = 22.5% EAR
(2) 9.8% EAR
Table 1A
The total Kcals derived from the meal in Table 1: 895
As a % of EAR:
17 yr old male (2755)= 32.5% (1/3)
25 yr old female (1940)= 46.1%
8 yr old boy (1970)= 45.4%
8 yr old girl (1740)= 51.4%
Table 1B
Recalculation of Table 1, excluding apple pie from the meal
for the two 8 yr olds, on grounds of common sense/experience and
also because the 'typical' children's meal ref. to in P VI
A/45/208 does not inc. a pudding: 'entree, fries, beverage').
(1) TF: 28.1g = 252.9 Kcal
(2) SF: 14.6g = 131.4 Kcal
Boy (1970)
(1) = 12.8%
(2) = 6.7%
Girl (1740)
(1) = 14.5%
(2) = 7.5%
A B
And if you do the same for the 17 yr old male and the 25 yr old female,
so as to produce the 'typical' McD's meal, you naturally get similar
reductions:-
A: (1) = 9.2%
(2) = 4.8%
B: (1) = 13%
(2) = 6.8%
Table 2
UK: 1993 : P VI/7/6 th p. (?46)
TF(g) SF(g) Cheeseburger 13.3 7.0 FF(M)* 20.3 4.4+ Apple pie 13.8 4.5 Coca Cola (R) - - Total 47.4(1) 15.9(2)
* New since 1989
+ After replacement of beef tallow with vegetable oil as frying medium.
(1) 47.4g = 426.6 Kcal
(2) 15.9g = 143.1 Kcal
17 yr old male (2755)
(1) = 15.5% EAR
(2) = 5.2% EAR
25 yr old female (1940)
(1) = 21.9% EAR
(2) = 7.4% EAR
8 yr old boy (1970)
Exc. apple pie
(1) = 21.7% EAR Totals: (TF: 33.6g) (1) = 15.4% (302.4 ÷ 19.7)
(2) = 7.3% EAR (SF: 11.4g) (2) = 5.2% (802.6 ÷ " )
8 yr old girl (1740)
Exc. apple Me
(1) = 24.5% EAR Totals: (TF: 33.6g) (1) = 17.4% (302.4 ÷ 17.4)
(2)=8.2% EAR (SF: 11.4g) (2) = 5.9% (102.6 ÷ 17.4)
- Also, of course, if you replace FF(M) with FF(R): TF: 14.3g} giving residual totals
SF: 3.1g} of: TF: 41.4g = 372.6 Kcal
SF: 14.6g = 131.4 Kcal
you get corresponding reductions in the % obtained from fat as proportion of EARS.
Table 3
US : 1987 : P IV/19/40, 42, 45 (internal)
TF SF Kcal Cheeseburger 16 6.66 318 FF 11.5 4.61 220 Apple pie 14 4.73 253 Coca Cola - - 129 Total 41.5 16.00 920
(1) (2)
Note: Since there are no US EARs for Kcal/d or agreed DRVs for % of energy from
TF/SF, COMA values are used below:
(1) = 373.5 Kcal
(2) = 144 Kcal
17 year old male (2755)
(1) = 13.6%
(2) = 5.2%
25 year old female (1940)
(1) = 19.2%
(2) = 7.4%
8 year old boy (1970)
Exc. apple pie
(1) = 18.9% (TF 27.5g) (1) = 12.6% (247.5 ÷ 19.7)
(2) = 7.3% Totals: (SF 11.27g) (2) = 5.1% (101.43 ÷ 19.7)
8 year old girl (1740)
(1) = 21.5% (1) = 14.2% (247.5 ÷ 17.4)
(2)=8.3% (2) = 5.8% (101.43 ÷ 17.4)
Table 3A
US: 1988 : P VI/20
TF SF Kcal Cheeseburger 13.8 5.17 308 FF* 11.5 4.61 220 Apple Pie 14.8 4.83 262 Coca Cola - - 144 Total 40.1 14.61 934
(1) (2)
+ Significantly less than l987
* = 1987
x Slight increase on 1987
Note: See Table 3 (1) = 360.9 Kcal
(2) = 126.9 Kcal
17 year old male (2755)
(1) = 13%
(2) = 4.6%
25 Year old female (1940)
(1) = 18.6%
(2) = 6.5%
8 year old boy (1970)
(1) = 18.3% exc. apple pie
(2) = 6.4%
Totals: (TF25.3g) (1) = 11.6% (227.7 Kcal)
(SF 9.78g) (2) = 4.5% ( 88.02 Kcal)
8 year old girl (1740)
(1) = 20.7% (1)= 13%
(2) = 7.3% (2) = 5%
TABLE 4
US: 1989: P VI/15/pp 3. 4 & 6 (NB: The figs for 1990 VI/22 are identical)
CHEESEBURGER 13.8 5.17 310 (=1988) FF(R)* 12.0 5.05 220 APPLE PIE 14.8 4.83 260 (=1988) COCACOLA(S) - - 140 TOTAL 40.6 15.05 930
(1) (2)
* Slight increase on 1988 and 1987: ? more fries/portion (or different analysis)
Note: See Table 3 (1) = 365.4 Kcal
(2) = 135.5 Kcal
17 year old male (2755)
(1) = 13.3%
(2) = 4.9%
25 year old female (1940)
(1) = 18.8%
(2) = 6.9%
8 year old boy (1970) exc. apple pie
(1) = 18.5% Totals: (TF25.8) (1)= 11.8% (232.2 ÷ 19.7)
(2) = 6.9% (SF 10.22) (2) = 4.7% (91.98 ÷ 19.7)
8 year old girl (1740)
(1) = 21% (1)= 13.3% (232.2 ÷ 17.4)
(2)=7.8% (2) = 5.3% (91.98 ÷ 17.4)
FAT
TABLE 5
Recalculation of effect of Meal in Table 1 using PAL to give EAR
via Table 2.7 on p. 27 of COMA 41.
1. 20 year old male* weighing 75 kg (11st 11lb) with a PAL of 1.7 (moderate):
EAR is 13.0 MJ/d = 3087.5 Kcal
Therefore: (1) (391.5 Kcal) = 12.7% EAR
(2) (170.1 Kcal) = 5.5% EAR
2. 25 year old female weighing 55 Kg (8st 9lb) with a PAL of 1.6 (moderate):
EAR is 8.7 MJ/d = 2066.25 Kcal
Therefore: (1) = 18.9% EAR
(2) = 8.2% EAR
* No figs. given for younger male adults. But 1618s would be higher
see Table 1.1 on xix.
TABLE 6
Calculation by ref to Prof. Crawford's tables
McD's meal (1): McChicken S/wich, FF (M) Coke (M)
TF: 37.0g = 333 Kcal ÷ by say, 19.40 (25 year old female: EAR 1940) = 17.2% EAR
SF: 5.58g = 50.2Kcal ÷ by say, 19.40 (25 year old female: EAR 1940) = 2.6% EAR
McD's meal (2): Hamburger, FF (M), Coke (M)
TF: 32g = 288 Kcal = 8% for same woman
SF: 6.32g = 56.8 Kcal = 2.9% for same woman
And if that same woman ate both these meals on the same day ...?!
she'd still only be getting 32% of her EAR from the TF of those
2 meals taken together and 5.5 % of her EAR from the total SF
See xx of Crawford: 269: 647; which demonstrated that for a 20 year old male who ate meal
(2) once in a week, the meal would be making a 1/32 (3.2%) contribution
to his recommended SF intake for that week and a 1/19 (or 5.4%)
contribution to his TF intake. So, as Prof. Crawfordsaid, the meal
makes a contribution to the fat load in the diet; but it is a minute
contribution. *
* See further, under
Diet/Frequency,
post
1.18 What these calculations show.
(1) They do not demonstrate precise conclusions, rather a general picture.
(2) They do show that the consumption of a 'typical' McD's meal entrée,
fries, beverage provides a fat intake, both of TF and SF, which for all
ages, falls below the recommended maxima/d.
- And except in the case of the 8yrold girl unsurprisingly
that remains so even when you add an apple
pie to a cheeseburger, fries and coke.
(3) This is not to say that there won't be people for whom that particular
meal will push their intake for the day (if that is a meaningful measure,
which it may not be) over the limit simply because they have had
bacon and eggs for breakfast or sausage and mash for supper.
(4) But that is not the q. at this stage. The q. at this stage is:
Is the food itself high in fat?
Ans., by ref. to the contribution which that meal makes
to that day's fat intake,
NO
SODIUM
2. Is the food high in sodium?
2.1 I shall try to ans. this by ref. to the same meal used for FAT:
Cheeseburger
FF (R)
Apple pie
Coke (R)
- Remembering always
(1) that Na intakes do not, for most people, present the same 'risk factor'
as SF: see, eg, COMA: 46, 6.6.8.
(2) Naismith (253:31) as to the (comparatively) small effect of reducing dietary Na.
UK 2.2 I shall use COMA (41, but, in particular 46)
as the guide to appropriate intakes of Na.
2.3 Reason: COMA 41, 25.3.4 and Table 25.1 on p. 154, gives only RNI's
*As to RNI, (and LRNIs for Na. (1600 meld for adults)* .
see p.v
COMA 46, however, gives, in effect, a DRV:
R.2.9 on p.2
S.2.9.1 on p.12
6.6.10 on p.138
* COMA 41, The DRV is + 6g. NaC1/d
p. 154 at ** 1g. NaCl = 17.1 mmol Na *
1 mmol= 23 mg Na
Therefore 17.1 mmol = 393 mg Na
Therefore 1 g NaCl contains 393 mg Na
Therefore 6 g NaCl contain 2358 mg Na
Therefore DRV = 2358 m~ Na/d
US 2.4 No equiv. of COMA reports.
Nor, If you look at, eg, P VI/15&19 ff (198790) does there
appear to be a USRDA for Na (unlike other constituents).
Therefore, as with FAT, I shall use COMA DRVs.
2.5 The calculations: see Tables, post.
The Food Sodium
Table 7: UK: 1989: P VI/6/36-7
mg Na
Cheeseburger 600
FF(R) 200
Apple pie 200
Coke (R) Tr.
Total 1000
(Tr. = trace)
DRV for adults: 2358 mg Na/d. (None for children: COMA 46,
R2.9, p.2 and S.2.9.1, p.l2)
Therefore, for the 17 year old male and 25 year old female, this meal gives c.42% of DRV.
For the two 8 year olds, this % would be higher.
And, once again, the amount is reduced by 20% if you leave out the apple pie (leaving c.34% of DRV).
Table 8: U.K: 1993: P VI/7
mg Na
Cheeseburger 700
FF(M) 200
Apple pie 200
Cola (R) Tr.
Total 1100 = 46.7% DRV
Again, a reduction of 100 mg if you replace FF(M) with FF(R),
giving the same results as 1989. And if you leave out the AP as well,
you get down to 800 mg = 34% DRV (as for 1989).
Table 9: U.S: 1987: P VI/19
mg Na
Cheeseburger 740
FF 110
Apple pie 400*
Coke 5
Total 1255 = 53% UK DRV
(1994)
Table 10: U.S: 1988 : P VI/20
mg Na
Cheeseburger 750
FF(R) 110
Apple pie 240*
Coke (S) 15
Total 1115 = 47%
[Figs for US 1989: VI/15: are identical
and for US 1990: VI/22: are identical]
* Less AP, = 855 mg = 36%
Less AP = 875 mg = 37%
Maybe, if you are o/wt and/or hypertensive, you'd be better to leave out the AP!
2.6 Conclusion
The food not "high" in sodium.
FIBRE
3. Is the food low in fibre?
3.1 Same meal.
3.2 Remembering always that the role of 'fibre' in the diet is uncertain:
- COMA 41,Ch.4:p.61
4.5.1, 4.7.4:pp 65 and 67
- Also specific papers ref. to later.
and that 'dietary fibre' is an imprecise term: if anything is important, it must be
*whatever that the NSP fraction of fibre* :
may be. COMA 41:4.1:p.61
3.3 It shouldn't therefore be assumed that low
fibre content, in itself, is directly related
to health. It may simply be a 'marker' for
other dietary characteristics, positive and/or
negative. In other words, we are in the area
now of speculation/hypothesisgeneration. But
more of that anon.
3.4 For the present
A cautious DRV is to be found at COMA 41:4.9 1 on p.68
- But this is for NSP, not fibre as such.
- And there is no DRV for children, save that their intakes
of NSP should be proportionately less.
The DRV for NSP is 18g/d for adults.
3.5 McD's nutrition docs do contain figs. for
'fibre', so that, bearing in mind the need for
caution, a rough calculation of McD's food's
r/ship with DRV can be made for the UK.
3.6 The calculations: see Tables, post.
3. 6A No calculations can be made for the US
because the US docs. do not contain amounts
of fibre.
TABLE 11: UK: 1989: P W61367
g. fibre Cheeseburger 0.8 FF(R) 2.3 Apple pie 1.8 Total 4.9
27% of DRV for NSP for adults; higher % for children.
TABLE 12: UK: 1993: P VI/7
Significant increases over 1989
g. fibre Cheeseburger 4.0 FF(R) 8.2 Apple pie 4.3 Total 16.5
92% of DRV for NSP for adults; higher % for children in fact, the two 8 year olds might be overdosing!
Notes: 1. Coke excluded because no fibre.
2. If you exclude an AP for the 8 year olds, then fibre content will go down, with fat & Na.
3. Ditto if you reduce FF(M) of this meal to FF(R): fibre content 5.8g: diff 2.4g:
leaving 4.1g 78%DRVforNSP
3.7 Conclusion
Whichever way you look at it, the food not low in fibre.
VITAMINS & MINERALS
4. Is the food low in vitamins and minerals (V&M) ?
4 .1 I shall deal with these together because, like
Na, they are essential nutrients. This is
important, because it means that the V and M
content of the meals is relevant not only to
the q. whether the meals are "unhealthy",
but also to the q:
"Are McD's deceiving their customers
when they say that their food is a useful
and nutritious part of any diet?
4 . 2 The calculations are complicated by the
following difficulties
(1) McD's UK does. for 1989 and 1993 do not
gives values for V and M (other than
Na) .
(2) The most recent doe. to give values for
Be, B12 and K is P VI/2, which is UK,
1985.
(3) The US does. give values for the other important
V and M and for the %s of USRDAs which those
values represent.
(4) COMA 41 gives EARs for most of the V
and Ms (except K; and B6 in a comprehensible
form) and RNIs for all.
(5) The values given by the US
McD's docs for vits. C, B1, B2, Niacin,
Ca and Fe and by P VI/2 for B6, B12
and K can then be set against the EARs
and RNIs in COMA 41.
(6) The assumption can then reasonably be
made that the amounts of V and M found in
the US meals for 198790 are likely to
be approx. the same as those which would be
found in UK meals for the same period: eg, Na content:
Table 7: UK 1989 : 1000mg (P VI/6)
Table 10: US 1989 : 1115mg (P VI/15)
(7) By this route, it is poss. to make a fair stab at judging
how, eg the UK 1989 meal (Table 1) might have
matched up to COMA's EARs and RNIs for the
V and Ms given by the US docs.'
(8) Greater disparity may be present between 1989
values and the values for B6, B12 and K given
by P VI/2, because these date from 1985: eg Na content:
Table 7 :UK 1989:1000 ma. Table 10: US 1989: 1115 mg; but,
P VI/2 :UK 1985:1357 ma.
(9) All this means is that the figs. for B6,
B12 and K which I have calculated by
ref. to P VI/2 and COMA 41, must be
treated with some caution or, at least, more caution.
(10) The 'rogue' is Vit A. Although the US
does. and P VI/2 give amounts for A,
they do so in units of measurement (IU)
which are different from those used by
COMA (micro g/d. ) Since I have not
been able to discover how to transpose
/convert one into the other, I've had to
ignore A. This is a pity, because A is an
important vitamin and is available in
significant quantities (as retinal) in dairy
products (COMA 41:8.2 on p.85).
[See also PVI/4/p.18 and p.10.]
4.3 The tables which follow must therefore be read
with all these qualifications in mind.
4.4 Not but what, the burden is on the Ds to
prove that the food is low in V & Ms: these
calculations, however broadly they must be
viewed, suggest quite the reverse; and the Ds
have offered no e to contradict that suggn.
TABLE 13 US : 1987 P VI/19
CHEESEBURGER FF APPLE PIE TOTALS
EAR mg % US mg % US mg % US mg % US % EAR
mg/d RDA RDA RDA RDA
1. Vitamin C 25 2.05 4 12.53 20 >0.85 - 15.43 24 61.7
2. Thiamin B1 0.83 0.30 20 0.12 8 0.02 - 0.44 28 53
3. Riboflavin 1 0.24 15 0.02 - 0.02 - 0.28 15 28
B2
4. Niacin 15.2 4.33 20 2.26 10 0.19 - 6.78 30 44
5. Calcium 750 169.0 15 9 - 14 - 192 15 25.6
6. Iron 8.8 2.84 15 0.61 4 0.62 4 4.07 23 46.8
NOTES: . .
Vit. C 1. EARs in Table 17.1 on p 120 of COMA 41. The EAR given here is for the whole population
over 15. The EAR for 8 year olds is 20 mg/d, so that this meal would yield 77% of his/her
EAR of Vit. C (73% of the AP is removed).
B1 2. Table 9.1 on p.91; EARs expressed in mg/1000 Kcal. For the whole population 150+,
EAR is 0.3 mg/1000 Kcal. The EAR for B' which is given here is that of the 17 year
old male (EAR for energy: 2755 KcaVd. 0.3 x 2.755 = 0.83 mg/d). The EAR for a
25 year old female (1940) would therefore be 0.48 mg/d, so the meal would yield
75.9% of her EAR . The EARs for the 2 8 year olds must also be adjusted accordingly
(0.59 (M) and 0.52(F), so that 0.44 = 74.% and 84.6% respectively).
(Removal of AP virtually insignificant.)
B2 3. Table 1.1 on p. 96. The EAR given is for males 1150+. Those for females and young children
are lower, so that the contribution from this meal to their EARs for B: would be
correspondingly higher:
25 year old F: EAR 0.9 mg/d: Therefore 0.28 mg = 31%
8 year old M/F: EAR 0.8 mg/d: Therefore 0.28 mg = 35%
(Removal of AP virtually insignificant).
Niacin. 4. Table 11. 1 on p. 100. EAR's expressed as mg/1000 Kcal. It is 5.5 mg/1000 Kcal for the
whole population. The EAR given here is for a 17 year old male (5.5 x 2.755 = 15.2).
For 25 year old female (i940) it would be 10.7 mg/d: 6.78 mg = 62.7%
For 8 year old boy (1970) it would be 10.8 mg/d: 6.78 mg= 62.7%
For 8 year old girl (1740) it would be 9.6 mg/d: 6.78 mg = 70.6%
(Removal of AP is virtually insignificant).
.
Ca 5. Table 22.3 on p. 141. EAR given is for 17 year old male.
25 year old F: 524: 192 = 36.5% EAR
8 year old M/F: 425: 192 = 45% EAR (without AP = 41.9%)
Fe. 6. Table 28.2 on p. 163; EAR given is for 17 year old male.
25 year old F: 11.4*: 4.07 = 35.7% EAR
8 year old M/F: 6.7: 4.07 = 60.7% EAR (without AP = 51.5%).
*But see nn at on p. 163
TABLE 14 US: 1989 P VI/15
CHEESEBURGER FF(R) AP TOTALS
EAR mg/d mg % mg % mg % mg % % EAR
USRDA USRDA USRDA USRDA
VITAMIN C 25 2.15 4 8.16 15 11.4 20 21.35 39 85.4
THIAMIN .83 0.29 20 0.14 10 0.06 4 0.49 34 59
B1
RIBOFLAVIN 1.00 0.21 15 0 - 002 - 0.23 15 23
B2
NIACIN 15 3.86 20 1.84 10 0.32 - 6.02 30 40
Ca 750 198.51 20 9.93 - 10.65 - 219.09 20 29
FE 8.7 2.3 15 0.52 2 0.71 4 3.53 21 40.6
Notes: 1. This meal gave 930 Kcal (Table 4);
The UK meal for the same year (Table 1) gave 895 Kcal.
It is therefore likely that the UK meal would yield similar values for V or M.
2. The 1993 UK meal (Table 2) would yield higher values for most of these nutrients
because FF (M) was used instead of FP (R).
3. The EARs given are as for Table 13 (see the on. thereto).
Recalculation of the figures given in this table for the 25 year old female and the two
8 year olds gives the following results (EARs in mg/d).
Vitamin C: 25/F (25): 85.4%
*boy and girl 8/b and g* (20): 106%
B1: 25/F (0.58): 84.5%
8/b (0.59): 83%
8/g (0.52): 94%
B2: 25/F (0.9): 25.5%
8b/g (0.8): 28.8%
Niacin: 25/F (10.7): 56%
8/b (10.8): 55.7%
8/g ( 9 6): 62.7%
Ca: 25/F (525): 41.7%
8b/g (425): 51.6%
Fe: 25/F (11.4): 30.9%
8b/g( 6.7): 52.7%
4. % of EARs are > % of RNIs because RNIs > EARs.
4.1 Recalculation of Vitamin C values using RNIs instead of EARs.
Table 1.4 of COMA 41 (p.xxii) gives the following RNIs:
17 year old male }
} : 40mg/d
25 year old female }
8 year old boy and girl : 30 mg/d
Thus Table (14! gives the following results in % RNI:
17M/25F: 53%
8/b & g: 71%
Table 13 (1987) gives:
17M/25F: 38.6%
8/b & g: 51.4%
4.2 B1: Table 9.1 on p.91 of COMA41 gives RNIs in mg/1000 Kcal.
Using the same formula as in n.2 to table 13, ante, Tables
13 and 14 give the following %s of RNI (mg/d):
Table 13
17/M (1.1): 40%
25/F (0.78): 56.4%
8/b (0.79): 55~7%
8/g (0.69): 63.8%
Table 14
17/M: 44.5%
25/F: 62.8%
8/b: 62%
8/g: 71%
4.3 B2: Table 10.l on p.96 gives RNIs in mg/d. Therefore:
Table 13
17/M (1.3): 21.5%
25/F (1.1): 25.5%
8/b&g (1.0): 28%
Table 14
17/M: 17.7%
25/F: 20.9%
8/b&g: 23%
4.4 Niacin: COMA 41 Table 11.1 on p.l00: RNIs in mg/1000 Kcal.
Same formula as in note 4 to Table 13, ante, to give RNIs in (mg/d):
Table 13
17/M (18.2): 37.25%
25/F (12.8): 52.9%
8/b: (13.0): 52%
8/g: (11.5): 58.9%
Table 14
17/M: 33%
25/F: 47%
8/b: 46%
8/g: 52%
4.5 Calcium: COMA41 Table 22.3 on p.141: RNIs in mg/d. Therefore:
Table 13
17/M (1000): 19.2%
25/F ( 700): 27%
81b&g: ( 550): 34.9%
Table 14
17/M: 21.9%
25/F: 31.3%
8/b&g: 39.8%
4.6 Iron COMA 41 Table 28.2 on p. 163. RNIs in (mg/d), Therefore:
Table 13
17/M (1 1.3): 36%
25/F (14.8): 27.5%
81b&g (8.7): 46.8%
Table 14
17/M: 31%
25/F: 23.9%
8/b&g: 40.6%
4.5 Comment .
(1) The USRDAs are obviously significantly higher then the COMA EARs.
This may be because they are closer to RNIs (which, in COMA 41, are
consistently higher than the EARs)*.
*see note 4 to Table 14, ante.
(2) EARs, however, may be the better criterion, because they are an average,
rather than an umbrella: it would not be right to answer the q: Is McD's
food low in V and M?, by reference to the maximum and minimum
requirements within a group. The right q. is:
Is the nutrient content of the meal sufficient to constitute a valuable
proportion of the average person's daily requirements for those nutrients?
In the result,
however, this
probably does not
matter see pare.
4.6, post.
*
ie missing from
the McD's Charts
198793 (3) The 'missing' vitamins:
A : already explained
( B6: readily available from protein,
( inc. meat, fish and egg sources
Both in ( (COMA 41: 12.2 and P W4/11)
As to ) McD's (
these, { food: { B12: readily available from protein,
see (4),) see eg ( inc. meat, fish and egg sources
post. ) P VI/2/9 IJ ( etc
(also potassium)( (COMA 13.1.2: P W4/11)
( (but not plants)
D : Not readily available from many
dietary sources: main
requirement is sunlight
(COMA 18.2.2)
E : PUFA intakes determine E
requirements. Therefore not
poss. to set DRVs RNIs or
EARs, etc. (COMA 19.4.1).
Therefore figs wd. be meaningless.
(4) As to B6 and B12:
(i) B6.
Table 12.1 on p.103 of COMA 41
gives EARs (and RNIs) expressed
as mg/g protein which, to me at
least, is unhelpful!
Table 1.4 on p.xxii give RNIs
expressed as mg/d related to protein
providing 14.7% of EAR for energy
which is not much better!
However, the relevant RNIs are as follows:
17 yr old male: 1.5 mg/d
25 yr old female: 1.2 mg/d
8 yr old boy/girl: 1.0 mg/d
P VI/2/9 Id (1985) gives the following
values for B6 in mg/serving:
Cheeseburger: 0.04
FF(R) 0.33
AP: 0.02 (Coke:0)
Total: 0. 39
If those values can legitimately be compared with the RNIs given in
Table 1 .4 of COMA 41, then the results are:
17 yr old male: 26% RNI
25 yr old female: 32.5%
8 yr old b/g : 39%
(ii) B12
Table 13.1 on p.107 of COMA 41 gives EARs as mg/d:
17 yr old male }
:}1.25 micro g/d
25 yr old female }
8 yr old big : 0.8 micro g/d
P VI/2/9 I gives, for a Cheeseburger (FF,AP and coke
irrelevant: no B12 in plants):
0.8 mg
This gives, as % of EARs:
17/M (1.5)} 17 yr old m. }
25/F (1.5)} = 53% 25 yr old f. }: 64%
8/b&g(1.0) = 80% 8 yr old big: 100%
(5) The only 'missing' mineral of any importance is potassium.
COMA 41 does not five any EARs for K.
But Table 26.1 on p.157 gives RNIs in mg/d:
17 yr old m : 3500
25 yr old f :
8 yr old b/g: 2000
Pink VI/2/I,J and L give the following values (in mg)
Cheeseburger : 153
FF(R) : 602
AP : 52
Coke : 3
Total : 810 mg
This gives, as % of RNIs:
17 yr old m. )
25 yr old f. ) 23%
8 yr old b/g: 40.5%
4.6 Conclusion
On these figures, the 'food' could not conceivably be said to be 'low' in any of the more important vitamins or minerals (in so far as they are obtainable from food at all). On the contrary, for some of them (in particular, vit.C, which may have a special significance in relation to cancer & CHD), it is conspicuously high. And this is so whether the food's contribution of each nutrient is measured as a % of EAR or of RNI: see the Summary Tables, post.
SUMMARY TABLES FOR V&M
TABLE 15
C B1 B2 B6 B12 Niacin Ca Fe K %* EAR RNI EAR RNI EAR RNI EAR RNI EAR RNI EAR RNI EAR RNI EAR RNI EAR RNI 17/M 62 39 53 40 28 22 - 26 64 53 44 37 26 19 47 36 - 23 25/F 62 39 76 56 31 26 - 33 64 53 63 53 37 27 36 28 - 23 8/b 77 51 75 56 35 28 - 30 100 80 63 52 45 35 61 47 - 41 8/g 77 51 85 64 35 28 - 39 100 80 71 59 45 35 61 47 - 41
* %s rounded up/down
Summary Table I: Results from Table 13 (1987); with those for B6, Bl2 and K based on P VI/2 (1985)
Notes: 1 EARs for B6 and K not given by COMA.
2 % RNI uncertain n because of mode of expression of RNI by COMA
TABLE 16
C B1 B2 Niacin Ca Fe %* EAR RNI EAR RNI EAR RNI EAR RNI EAR RNI EAR RNI 17/M 86 53 59 45 23 18 40 33 29 22 41 31 25/F 86 53 85 63 26 21 56 47 42 31 31 24 8/b 106 71 83 62 29 23 56 46 52 40 53 41 8/g 106 71 94 71 29 23 63 52 52 40 53 41
* %s rounded up/down
Summary Table II: Results from Table 14 (1989); Without B., Bl2, and K (because no data more recent than
for Table 15; i.e. treated as constant).
OVERALL CONCLUSION
VIII 1. The first q was:
Is the food (very unhealthy because it is) high in fat, sugar animal products and salt (sodium) and low in fibre, vitamins and minerals?
2. That q. has now been examined in detail. The answer to it must be:
NO
3. This applies both to the UK and the US . And, because of the broad
uniformity of McD's food throughout the world, the same
conclusion can safely be drawn for the whole world. In fact, for most
people, the meal is remarkably wellbalanced from a nutritional p.o.v.
4. Nevertheless, it might be said,
"Ah yes; but for some people at some ages, the content of, eg, saturated fat is so high that, if the same or a similar meal is eaten repeatedly over a period of time, such people will be endangering their health."
5. There are two ways of approaching that question:
(1) Take Table 1, with the 8 yr old as its consumer; and assume
she eats (or is made to eat) the AP along with all the rest:
(i) Her DRVs (ex COMA) for FAT are:
*We assume she TF: 35% of her EAR for energy/d
doesn't drink SF: 11% of her EAR for " *
alcohol:
COMA 41, xx, (ii) The meal gives her:
Table 1.2
TF: 22.5%, leaving (only) 12.5% for the rest of the day.
SF : 9.8%, leaving (only) 1.2% for the rest of the day.
(iii) But the same meal gives her:
(a) plenty of fibre: Table 11: and
(b) very substantial proportions of her average
daily requirements for Vs and Ms, in particular:
C, B1, B12, Niacin, Ca and Fe. :
Summary Tables I and II
% EARs % RNIs
C : 106% (II) 71%
B1 : 94% (II) 71%
Bee : 100% (I) 80%
Niacin: 63% (II) 52%
Ca : 52% (II) 40%
Fe: 53% (II) 41%
(iv) Approaching the q. in this way, the answer may still be
'NO', because, as will be seen later on, the quantities
of beneficial nutrients in p'lar C, which are
consumed at the same time as the SF may well mean
that the malign effects (if any) of the SF are neutralised.
(v) Another important consequence of this approach is that
it bears very powerfully on the further q:
"Do McD's know that their food is very unhealthy?"
(2) But there is another approach: this is to try to answer the
further qq. which this q. begs:
(i) How often must one eat such a meal in order to give
rise to any significant health risk?
(ii) How often, in practice/reality do people eat such meals?
(3) That approach foreshadows consideration of the next part
of J's meaning: see following.
DIET/FREQUENCY (page 52)
J. Mng. part (2) (i)
IX 1. The q. is:
"Is McD's food very unhealthy because eating it may well make your diet high in fat, sugar, animal products and salt (sodium) and low in fibre, vitamins and minerals"?
2. Some preliminary observations:-
V&M (1) It is clear from the analysis which
I have done of the constituents of
a 'typical' McD's meal that,
however often you eat it, it will
not make your diet low in Vs or MS
*the only - even if you eat little else*.
relative
'deficiency Fibre (2) The only effect that repeated
would be Be consumption might have on the
@ 35% and 29% fibre content of your diet is that,
EAR: this if you ate the meal, say, twice in
increases a day, you might feel disinclined
dramatically to eat anything else; thus
(to 98% and depriving yourself of your full
74%) if you intake of fibre for that day. But
substitute a that is a reductio ad absurdum: in
vanilla the real world, the meal makes a
milkshake for perfectly satisfactory contribution
the coke: but to daily fibre intake.
then you also
raise TF & SF!)
(ditto Ca. )
Sodium (3) The sodium content of the meal is
never more than about ½ the DRV
- (for adults) for a day.
Tables 7-10 (COMA 46, R.2.9 etc.)
So, again, looked at as a matter of
reality, the food is not going to
make your diet high in sodium.
TF (4) Roughly the same is true of the
TF content, except where the 25
yr old female is concerned, who
gets, variously, c.55-60% of her
Tables 1-5 DRV (33% of EAR) from the meal;
and the two 8 yr olds who, if they
eat the AP, are getting about the
same proportion (if they don't eat
the AP, then the proportions come
down significantly, to a range
between 33% (8/b, Table 3A) and
49. 7% (8/g, Table 2) ) . So again,
you are going to find it difficult
to make your diet high in TF by
eating McD's food-unless you have
an appetite for it that exceeds the
bounds of imagination.
SF (5) The SF content of the meal generally
constitutes a higher proportion of the
DRVs (10% for adults, 11% for children)
than the TF content: from just under ½
(17/M: Tables 3A and 4) to nearly 90%
(8/g: Table 1, with AP) .
It follows that, if there is a danger to
* because health* in exceeding the DRVs for SF
of the link over a period of time regardless of the
with CHD. other constituents of the diet during
that time (which is by no means 100%
clear, on the evidence), then all but
the 17 yr old male should probably
refrain from eating such a meal more than
one a day for any period of time which is
long enough to allow the food to become
"a substantial or dominant part of
the diet"
Crawford: 269: 31: 12-15
(6) In reality, that is, of course, another
reductio ad absurdum: more of this later,
under actual frequency.
(7) Finally, by way of introduction to the
related qq. of diet and the frequency of
consumption of McD's food,
(i) In the context of a libel action,
where McD's are accused of selling
food which they know to be very
unhealthy, I am unwilling to
concede the relevance of the
consumer's choices of food from
other sources: that is the
consumer's responsibility (or
his/her parents'), not McD's.
(ii) Thus,
"Do not eat too much of the kind of
food that McD's sells; you may well
make your diet high in fat, etc, if you
do (with adverse consequences for
your health)."
is not defamatory of McD's.
(iii) Whereas,
"Do not eat McD's food; it may
well make your diet [etc, as
above] . "
plainly is.
(iv) Here, the allegation is of the second
(defamatory) type:
"Eating McD's food may well
make your diet high in fat, etc"
(v) Suppose, then, a person who eats the
'typical' McD's meal (Table 1 ff.) for
lunch twice a week: in itself, harmless
(indeed, probably beneficial) .
(vi) But then suppose that that person
also eats, on most days of the week,
- bacon and eggs for breakfast
- fish and chips, sausage and mash,
steak sad kidney pie (etc) for
supper.
(vii) Or suppose that he/she eats
- the McD's meal twice a week
- a similar BK meal twice a week
- a KFC meal twice a week
- fish and chips twice a week
- pub sandwiches twice a week
- pizzas twice a week
- Berni Inn steaks twice a week
(= 14 meals out of 21).
(viii) Such a person would, almost certainly,
be overloading on TF, SF and (probably)
Na during that week.
(ix) And if that were the pattern of his diet
(as to the meaning of which,
see later) then it might fairly be
said that his diet was 'unhealthy'.
(x) But what is it in that diet which has
made it unhealthy? Is there a 'prime
suspect'?
(xi) Is it
- the McD's meals?
- the BK meals?
- the fish and chips?
- the pub sandwiches?
- the bacon and eggs?
- and so on.
(xii) The obvious answer is:
individually, none of them;
- in combination, all of them.
(xiii) This means that no single food source
can make a diet 'unhealthy', however
regularly it is eaten; unless it is, on its
own, a very substantial - probably
dominant (see later) - element of the diet.
(xiv) Absent such 'dominance', no single
food source - be it McD's, BK, fish and
chips, pub sandwiches or bacon and
eggs - can logically, for fairly,
be inculpated as the prime because
('maker') of an 'unhealthy' diet.
(xv) To complete the circle: consumption
of McD's food does not make its consumer
eat fish and chips, BKs, pork pies, etc; nor
is the reverse true.
(xvi) Each makes a contribution, and the extent
to which each makes that contribution is
the whole extent of its responsibility for
the overall diet. * (<10% 51%! )
*see, eg,
Dr. Lobstein:
32:74:24-55
(and Prof.
Crawford;
see later)
3. There are 4 qq:
(1) What is 'diet'?
(2) With what frequency must a person
eat particular categories of food
for them to become "a [substantial
* In fact, on or]* dominant part of the diet"?
the evidence,
"substantial" (3) With what frequency do people eat
should be McD's food?
omitted because
it doesn't matter (4) Is there any significant number of
(and anyway is people for whom McD's food is a
imprecise). substantial or] dominant part of
their diet"?
4. There is, of course, a fifth q. flowing from
(4) above: -
If there is, does it matter?
- But that is the 3rd and last limb
of this enquiry.
Q.(1) 5. What is diet?
(1) No wholly satisfactory definition: but
it is, perhaps, clear what it isn't:
"These arguments (against fast food)
use lack of balance to dramatise a point
that would be seen instantly to be
ludicrous if presented reasonably. No
one in their right mind would live
exclusively on sausages or hamburgers
or meat pies (or sweets or crisps) but the
arguments are presented as if they would. "
Comment BNF May 1987. Professor David
Conning, Director General, British
Nutrition Foundation, (attrib. ) .
P VI/6/13.
(2) If diet has any relevance to this case,
- it is only in relation to the effect which
it may (or may not) have on the incidence
of 3 degenerative diseases: CHD and cancer
of the breast and colon.
(3) Those diseases are called degenerative
because they develop over time. In all 3
cases, they are generally diseases of
later life, often old age, because they
take many years to develop to a stage
where their symptoms show and they
have a discernible effect on health:
thus a cancer may be initiated many
before promotion to tumour starts (if it
does) and symptoms finally appear (if
they do).
(4) No clear relationship has been shown in
this case between the time for which a
particular diet is eaten and the time
when symptoms of disease first appear:
the nearest one gets is some of the
longer prospective cancer studies;
but even then it is impossible to know what
the starting point of the relationship
might have been - if, indeed, there ever
was one.
(5) Notwithstanding these difficulties, it is
obviously not sensible to look at diet,
in the context of degenerative disease,
in terms of weeks or months, or probably
*See Naismith even sever years*. The most that a
252:22:42-8 'snapshot' of that kind might be capable
of telling one is what sort of diet the
person is likely to have been eating in
the past and is likely to continue to eat
over a much longer period of time -
though obviously such inferences require
a good deal of caution.
(6) This is an important consideration,
because (leaving aside all other qq. s)
what the actual figures for frequency of
consumption of McD's food tend to show
is that frequency is at a peak between
the ages of about 16-24 (slightly longer
in the US), whereafter it declines
rapidly.
(7) The final word on this q: what is diet?,
might be left to Prof. Naismith:
253:20:12-41.
Q (2) 6. How often do you have to eat a particular food
for it to become a [substantial or]
dominant part at your diet?
Not easy, but the best answer is probably:
When that kind of food is providing
the majority [or a substantial part]
of your energy requirement for each
day over a long period of time.
6.1 If that is a reasonable approach, then it is
worth looking back at Table 1A: the four
age-categories are getting between 1/3 and 1/2
(respectively) of their EARs for daily energy
(at the lowest levels of EAR) from that meal.
So If they were eating that meal every day
over a substantial period of time, you could,
no doubt, reasonably say that the food
constituted a substantial or dominant part of
their diets.
So-
Q(3) 7. How often do people eat McD's food?
7.1 The ans. to this q. appears to be a bit
different according to whether you look at the
UK or the US figures, at any rate so far as
*1 x pw or the most frequent customers (HUs*) are
more often concerned:
*inc. SHUs: in the US, HUs = 22% of customers*
P. VIA/45/216
and 218
in the UK, HUs = 12% of customers*
*OMNIMAS
(See later)
7.2 P VIA/45 does not, alas, allow one to
calculate precisely how many McD's customers
there were in the USA in 1991.
US 7.3 It is, however, possible to make an educated
guess.
7 .4 (1) Assume that the proportion of the US
pop. that visits McD's at least once in
the course of year is significantly
higher that it is in the UK.
(2) This is a reasonable assumption because:
(a) Fast-food, and, in p'lar
hamburgers, have been part of the
American way of life for a long
*Green 46:54-55 time:* and McD's have been in
business in the US since 1955.
(b) McD's are the market leader in both
the QSR sector and the hamburger
*Green: 43:21 group within that sector. * They
have 4096 of the 33% -which
hamburgers have of the QSR
*Green: 43:20 sector sector = 13.2% of QSR*
*AFT, pp 6-7. (UK:11.2%)*.
Y Vl3
(c) The 'density' of McD's rests. per
1000s of pop. is much greater in
the US than it is in the UK:
*P VI A/45/212 US. In 1991, the US pop. was 251.4m*.
In that year, McD's had 8764
*P III/5/135 rests. in the US*.
This means that in 1991,
there was 1 McD's rest. for every
28,686 people in the US, (say
29,000) .
UK. In 1995, the UK pop. was 56.6m.
In that year, McD's had 680 rests.
So 'density' was 1 McD's rest. for
every 83,235 people in the UK
( say, 83,000) .
C. Therefore US density was nearly 3
times UK density.
D. Therefore accessibility to McD's/nos.
of people is very significantly
greater in US than in UK.
(d) Green (who ought to know) said
that he thought the figure was
*46:7 likely to be between 85% and 95%*.
(In the UK, the fig. in 1995 was
about 40% (39.8) : see later.)
7.5 If one therefore makes the (reasonable)
assumption that the proportion of the US
pop. that visited McD's at least once in 1991
was about 90%, the number of people would
be about 226.26m.
7.6 Using that figure, and making the
(reasonable) assumption that the % in each age
- group in the pop. at large was (roughly)
reflected in the 'McD's visitors' population,
one can arrive at an estimate of the average
frequency with which each age-group visited
McD's in the US during 1991.
See Table 17, over, in which the figures
in cots. 1,2,3 and 5 are taken from
P VI A/45/212.
TABLE 17: Average frequency by age-group: US 1991
Customer base: 226.26m
1 2 3 4 5 6 7
AGE GROUP NUMBER IN % US POP NUMBER OF NO OF NO. OF FREQUENCY
US POP. McD's VISITS TO VISITS PER : 1x EVERY
(m.) CUSTOMERS McD'5 (m.) CAPUT pa .....DAYS
1 0- 7 29.6 11.8 26.7 520.9 19.5 18.7 (19)
2 8-13 21.4 8.5 19.2 ~352.1 18.3 19.9 (20)
3 14-17 13.5 5.4 12.2 323.1 26.5 13.8 (14)
4 18-19 7.7 3.0 6.8 217.0 31.9 11.4 (11)
5 20-24 18.9 7.5 16.9- 559.5 33.1 11.02 (11)
6 25-34 42.7 17.0 38.5 1114.1 28.9 12.6 (13)
7 35-44 38.3 15.2 34.4 911.5 26.5 13.8 (14)
8 45-54 26.4 10.5 23.8 410.0 17.2 21.2 (21)
9 55+ 52.8 21.0 47.5 414.8 8.7 41.9 (42)
NOTES:
1: The figs in Col.4 are the Col 3 %s of 226.26 m.
2. Col. 6 represents Col. 5 divided by Col. 4.
3. Col. 7 represents 365 divided by Col. 6
4. Col. 4 totals only 226 m because of rounding up/down.
5. The % of 0-13s visiting McD's in a year might be higher than shown in Col. 4, simply because of McD's popularity with families: if so, their average frequencies (Col. 7) would be lower.
7.7 To get an accurate picture of actual frequency
by age-group, you need to know how many
people within each age-group visited with what
frequency. This can be done for the UK
(see later), but not for the US.
7.8 One can go a little further, however, with the
HUs (inc. SHUs) in the US.
7.9 P VI A/45/216 and 218: HUs totalled 22% of
McD's customers in 1991.
7.10 If McD's customers totalled 226.26m., then HUs
numbered 49.8m.
7.11 P VI A/45/212: The total number of
visits was 4822.9m., of which 72%
*P VI A/45/216 were contributed by HUs* = 3472.5m visits.
7.12 Therefore, the average frequency for HUs
was 69.7 times in 1991 1.3 x pw or
1 x every 5.2 days.
7.13 Unfortunately, a split between HUs (1-3 x
pw) and SHUs (4+ x pw) is impossible to
achieve. The reason is that the final colt on
P VIA/45/216 must be wrong: if SHUs visit
more often than HUs, then, if the no. of SHUs
*11% in each and HUs is the same*, SHUs would be
case expected to generate substantially more visits
* 23% and 49% than the HUs, not < ½!*
7.13.1 Nor do the figures work if you assume that
the two 11%s are correct, but that the 23% and
the 49% are the wrong way round: if you
assume, for example, that SHUs average 5 x
pw,then each SHU would be averaging 260
visits pa.
- 49% of total visits = 2363.22, which would
need 9.08m SHUs at 260 visits each.
- 9.08m = 11% of only 82.6m total no.
of customers (<2 x the UK total!).
7.13.2 5 times a week is about once every
day-and-a-half (1.4) .
If one assume that SHUs were about 2% (not
11%) of 226.26m, they'd number 4.53m.
If they generated 23% of the visits
(1109.27m), then they'd be averaging about
245 visits each once every 1.5 days (which
seems reasonable).
7.13.3 If, therefore, the HUs are about 20% (not
*Assumed at 11%) of the customers* they'd number 42.25m.
226.26m Since they generate 49% of the visits
(2363.22m), their average annual frequency
would be about once every 6 ½ days, ie slightly
more often than once a week (which also
seems reasonable).
7.13.4 So if the total no. of HUs (inc. SHUs) was
about 47m., this means that the rest of the
customers (about 179m) were visiting less
often than once a week.
7.13.5 These 'calculations' are obviousb somewhat
speculative; but since the broad picture they
give is consistent with the much more precise
picture that can be drawn for the UK (see
later), they may be worth something.
7.14 The only other thing worth noting is that if
the figs. in colt 7 of Table 17 are even
broadly accurate, they tend to suggest that
most of the HUs (inc. SHUs) are likely to be
found amongst the 18-24s, with some in the
35-44s and some in the 14-17s.
7.15 This accords with the UK picture (next),
except that the graph of declining use with
age from 24 onwards is probably less steep in
the US than it is in the UK.
7.16 One can also notice from Table 17 that the
only age-group whose average frequency was
more than about once a fortnight were the
18-24s.
UK: 7.17 Here we have some (relatively) harder figs.:
OMNIMAS 1995 (exAF/TN) (explain how it works)
7.18 These figs. give the following results:
(1) Total who ate at McD's at least once in 1995:
22,511,000 (= 39.8% of UK pop. of 56.6m)
(2) Of those 22.5m:
Category 1 Every day 0 0
Category 2 Nearly every day 55,000 0.24}
2.34
}
Category 3 Several times per 477,000 2.1 }
week
Category 4 Once a week 2,139,000 9.5
Total 2,671,000 11.84 (say 12%)
These are the HUs of the UK (no HU/SHU split).
(3) Table 18, over, gives the above figs. split by age-group and
gender (for categories 2, 3 and 4).
TABLE 18: Frequency by age and sex: UK: 1995
Hus:
2. = Nearly every day
3. = Several times a week
4. = Once a week
Cate 16-18 19-2 M F 25-34 M F 35-4 M F 45-54 M F 55-6 M F Total
gory 4 16-24 16-2 4 5+ s
4
2 0 38 38 0 0 0 0 8 8 0 6 0 6 3 0 3 55
3 242 83 166 160 79 55 25 39 27 12 28 22 6 5 5 0 476
4 459 772 727 504 481 175 306 255 123 131 128 67 61 45 21 24 2140
Tota 701 893 931 664 560 230 331 302 158 143 162 89 73 53 26 27 2671
ls
(000 1594
's)
Notes: 1. All figures in OOOs.
2. 50% of all in category 3 were 16-18. -
3. The 38,000 19-24 males were 69% of the total in category 2.
4. 60% of all HUs were 16-24.
5. 81.% of all EllJs were 16-34.
6. 86% of the 25-34s were in category 4
7. 68% of all those in categories 2 and 3 were 16-24; of those, 56% were M and 44% were F.
8. See Table 19 (over) for graphic representation of usage by age: all HU's
and Table 20 (over) for graphic representation of usage by age: HUs in categories 2 and 3 ('SHU's?).
TABLE 19 Heavy usage by age: UK 1995 (categones 2, 3 and 4)
TABLE 20 'Super' heavy usage by age: UK 1995 (categories 2 & 3)
7.19 This analysis allows some important
conclusions to be drawn (remembering always
*market that the figs. are not precise* and are more
research: valuable as showing general trends and
sample of patterns than exact nos. ):
8204 people
(1) Total no. of customers who are 'heavy
users' is relatively small:
2.7m/22. Sm (c.12%)
(2) Of those 2.7m, 2.14m (or about 80%) are
in category 4: ie, they eat at McD's once
a week, but no more often than that .
So one can forget them.
(3) Of the remaining 531,000 (merely) - and
now one is approaching statistical
insignificance (531,000 = 2.4% of all
customers) - a mere 55,000 (0.24%) are in
category 2: nearly every day.
(4) Of that 55,000, 38,000 (69%) were males
of 19-24, whose EAR for energy, at the
lowest level, is on average 2,550
*COMA 41 xix Kcal/d*: at a more realistic level for
Table 1.1: that age group (PAL 1.7), their EAR
19-50 would be in the region of 3000 Kcal/d.
(5) Of the 531,000 in categories 2 and 3,
363,000 are aged 16-24 (68%); and 242,000
(46%3 are aged 16-18
(M:EAR: 2755 Kcal/d minimum)
(F: EAR: 2110 Kcal/d minimum)
(6) As Tables 19 and 20 show, particularly
the latter, heavy McD's usage is largely
the preserve of the 16-24s (most of them
* cf. Hawkes: (56%) males)*, after which comparatively
41:13:38-43 tender (and energetic) age, interest in
* does not McD's as an habitual* weekly source of
inc. 1 x low food declines rapidly: the number of
25-34s in categories 2 and 3 is just over
1/5th of the number of 16-24s in those
categories; whilst, from 35 onwards, the
numbers decline to insignificance.
(7) Prof. Conning's aphorism (P VI/6/13)
is thus shown to be well-judged:
- Not very many people in the UK
are using McD's food as a 'staple'!
- Those that are are of an age when
it doesn't matter in the least.
- The age-range is very narrow 16-24
- Beyond that age the frequency
(once a week or less) is, for any
significant no. of people,
immaterial.
Note: The above conclusions as to frequency and
age can be confirmed by a different route.
(i) OMNIMAS 1995 shows, that, of the total
no. of customers in 1995 (22.5m):
16 - 24s = 6.344m = 28%
25 - 44s = 10.790m = 48%
45 - 65+s = 5.730m = 2496
(ii) p.1 of AFI in Y V/3 shows- that, in
*ie 1993, the % of visits* by age group was:
volume
of sales
16 - 24: 47%
25 - 44: 43%
45 - 65+: 11% (=101%)
(iii) Thus (assuming the figs., in %s, to be
roughly the same in 1993 and 1995):
28% of the customers (16-24) yielded 47% of the visits
48% " " " (25-44) " only 43% " " "
and 24% " " " (45-65+) " " 11% " " "
(iv) This, too, emphasises the importance of
the 16-24s and the fairly rapid decline
of usage with age.
Therefore (8) Even making the assumption that eating McD's
food 'nearly every day; or even 'several times
a week' is a bad idea (which, on the evidence
of part 1 of this enquiry, is a false
assumption),
(a) the small no. of people actually doing
that;
(b) the ages of those people, and
(c) the short length of time for which they
are doing it
all mean that McD's food Poses no threat
whatever to the health of the adult
*And: Energy (16-65+) population in this country *
Protein
Fibre
Vits
Mins. . ?
(9) For the generality of McD's customers, who eat
there not > 1 x pw, the case is put beyond
doubt by some conclusions demonstrated in
XX of Prof. Crawford on his return
(25.6.96)* I used the analyses done by his
*269: 64 - 7 dept. which are behind his latest statement.
See Table 6 I took the McD's meal consisting of
ante. hamburger, FF(M) and coke: this gave a total
SF content of 6.32g (higher than the other
McD's meal).
I then took a 20 yr old male with an EAR
(minimum) of 2550 Kcal/d.
If his DRV for SF is 10% of 2550, then he can have
255 Kcal from SF/d 9 = 28.3 g/d x 7= 198.3 g/w
whereas 6.32g x 7= 44.24 g/w
This means that even if he ate this meal
every day for a week, McD's would be
contributing < ¼ (22.3%) of his SF 'load' for
the week! And if he ate it 1 x that week:
1/32 or 3.2%!
"Substantial" ?
"Dominant" ?
(TF: DRV 30% of 2550 Kcal = 765 = 85g.
This meal: 32g = 38% of DRV)
(85 x 7 = 595; 32 = 1/19 or 5.4%
of week's TF load!).
7.20 Children in the UK
OMNIMAS 1995.
(i) Of the 55,000 customers in category 2
(nearly every day : 7.18, ante), 40,000
had children.
(ii) But this does not mean that 40,000
customers took their children to McD's
nearly every day!
(iii) This is easy to see: 38,000 of the 55,000
in cat. 2 were males arced 19-24, leaving
8,000 35 - 44s, all M
6,000 45 - 54s, all F
3,000 55+s, all F = 17,000,
with no cat. 2s at all in the
25 - 34 age group and no F in the
19-24 age group.
(iv) Thus, even if all those 17,000 35 - 55+s
had children (unlikely), that still means
that 23,000 of the 38,000 19-24 yr old
males had children (if < 17,000 of the
older people had children, then > 23,000
of the 19-24 Ms must have done).
(v) Does one envisage, as a matter of
reality, that 23,000 (or more) 19-24 yr
old young men were taking their
children to McD's, on their own, nearly
every day?
(vi) Obviously not. What one envisages is a
young man of say, 20 or 21, who regularly
goes to McD's for his breakfast or his lunch
during the working week. He has a wife
and a small child at home (maybe 2, if he's
23 or 24). They all go to McD's, as a family,
from time to time (the wife might be,
for example, in cat.4 or lower).
(vii) The same sort of realistic approach can
be (should be) - used for category 3
(several times per week).
(viii) Of the 477,000 customers in cat. 3,
227,000 (47.6%) had children.
(ix) At the same time, of those 477,000,
242,000 were aged 16-18
and 83,000 were aged 19-24
(25+s: 152,000)
(x) Qq:
- how many of the 16 -18s are
likely to have had children at all?
*to
whom, - how many of the 234,000 19+s*
obviously, were likely to be to be taking
most of the their children several times a
227,000 with week.
children
must be (xi) Beyond categories 2 and 3, no
attrib. reason to enquire: children
visiting McD's once a week or less often
are of no concern at all.
7.21. Children in the US
(i) If, as suggested, the actual numbers
of children visiting McD's in 1991 (or in
any other year) was greater than
in Table 17, then, though the figs. given
in that table are for average frequency,
the chance that there were any significant
nos. of children visiting more than once
a week must be very small.
(ii) If so (and, probably, even if not,
limits ! ), then in the US, as in the UK,
one can, by the application of common
sense and experience, forget about
McD's so far as the health of children
concerned.
(iii) Thus if one goes back to the two 8 yr
olds in Table 4 (US: 1989/90), the fact
that they are getting, respectively 18. 5%
and 21% of their EARs for energy/d from
the TF content of that meal, or 6.9% and
7.8% from its SF content,is immaterial to
the q. whether
"eating McD's food may well make your
(children's) diet high in fat...".
8. Social Class
8.1 OMNIMAS 1995:
(1) Of McD's total no. of customers (22.511m. )
ABCIs = 10.038m = 44.6% of McD's total
C2DEs = 12.474m = 55.4% of " "
(2) Of the total eating-out population (EOP) (44.08m)
ABCIs = 18.412m = 41.8%
C2DEs = 25.669m = 58.2%
Therefore (3) ABCIs form a greater %, and C2DEs
a smaller %, of McD's customers than they
do, respectively, of the total EOP.
(4) Moreover
Of the 18.412m. ABCIs who ate out in 1995,
10.038m = 54.5% used McD's at least lx.
Whereas, of the 25.669m. C2DEs
who ate out in 1995,
12.474m = only 48.6% used McD's at least 1x.
(5) So McD's is, proportionately, more
popular with the ABCI eaters-out than it
is with the C2DEs.
(6) Heavy use amongst ABCls and C2DEs who use McD's.
]
So, again, there is very little to choose between the two groups
when it comes to the higher frequencies.
(7) The only area in which C2DEs out --score ABCls is in actual numbers that used
McD's in 1995: 12.474m v. 10.038m. But this may only reflect the fact (as the total
EoP numbers would suggest) that C2DEs outnumber the ABCls in the pop. as a
whole.
(8) So any suggestion that McD's is somehow the preserve of the undereducated, underpaid or underprivileged is completely exploded by these figures; and the conclusions sought be drawn by Prof. Crawford are, so far as McD's contribution to the diets of the population (by social class) is concerned, shown to be without foundation.
J. Mng. part (2)(ii)
X 1. The q. is :
"If eating McD's food may well make your diet
high in fat, etc., and low in fibre, etc.,
does that carry with it the very real risk that
you will suffer cancer of the breast or bowel or
heart disease as a result?"
2. Preliminary.
2.1 If the first 2 parts of this enquiry
- the content of the food and
- the frequency with which it is eaten
lead, as they do, to the conclusion that the
first part of the question - the premise - is
unsustainable, then it is tempting to suggest
that the second part is a sterile enquiry:-
If there is no real likelihood that
consumption of the food is going to make
people's diets high in fat, etc., and low
in fibre, etc., then the q. what the#
effect on their health might be if there
were such a likelihood, is, whilst
interesting, immaterial to the issue.
2.2 This is a real temptation, because, although
there has been a great deal of evidence about
the r/ship between diet and health, most
. . obviously cancer of the breast and colon,
nevertheless, the combined effect of parts 1
and 2 of this enquiry is really so strong that
a further enquiry into the r/ship between
consumption of McD's food and health is very
difficult to justify
- the more so when one considers that
McD's, as Pffs, don't actually have to
prove anything.
2.3 Not but what, I will, out of a proper sense of
caution, summarise what I take to be the
effect of the evidence in this part of the
case and try to produce a sensible answer to
the q.
2.4 In making that attempt, I shall concentrate on
the evidence of only four of the witnesses:
Prof. Naismith: nutrition.
Dr. Arnott : cancer.
Prof. Crawford: blood chemistry.
Prof. Campbell: nutritional chemistry
(Prof Wheelock has been largely incorporated
in parts 1 and 2).
2.5 These are what I call 'proper' experts:
they have
(i) the necessary academic and
professional qualifications; and
(ii) the necessary experience in their respective fields.
2.6 Where so difficult and important a subject as
the relationship (if any) between diet and
cancer is concerned, or the degree of risk of
heart disease generated by diet, no less than
a 'proper' expert is worth attention.
2.7 Thus I shall ignore, without implying anything
at all about their qualifications to speak
about other matters elsewhere, the following:
*By qualification Barnard : none of the necessary
and experience qualifications* (and anyway
(practice), a wholly unbalanced in his
psychiatrist. presentation of the relevant
* As to this, see material*).
his XX (whole)
on Days 34-36.
Cox : no qualifications (if, indeed,
he was giving e. about
nutrition at all - seemed to
have more to say about
marketing) .
Cannon : ditto: no better placed than
any other intelligent laymen
to deduce - as J. must do -
the answers (if any) from the
work of the true experts.
Bronhy : Somewhat different, in
that she does work in
nutrition. But it turned out
her work was more
educational than scientific
and that she did not propose
herself as an expert in any of
the relevant disciplines.
2.7.1 A word in passing about the assertion* that
*DM: all or most of the Pffs' witnesses on this
topic (and others) are in some way
'compromised' by an association with McD's or
the food industry, whereas the Ds' witnesses
are all completely independent, having, as it
were, descended from Olympus to explain to
the Court why McD's food is so unhealthy.
2.7.2 Pffs' witnesses
Wheelock: Professor of Food Science,
retained by McD's to advise
them on nutrition.
Naismith: Emeritus Professor of Nutrition
at KCL (etc. ): no connection
with McD's.
Arnott: Consultant in Radiotherapy
and Oncology at Bartis (etc.): no
connection with McD's.
2.7.3 Defts' witnesses
Barnard: Consultant to PETA (animals) and
* 37:62:39-60 an associate of both Cox* and
*256:20: 6-9 Campbell*.
Cox: Correspondent for Campbell in this
*Campbell (1): country* and an associate of
PB IC/H/3 Barnard (see above), both of
whom are cited in Cox's book,
Encyclopaedia of Vegetarian Living,
whose 'credo' (p. 1 ) is the refusal
to eat animals.
*256:6:3-14 Campbell: Associate of Crawford* (and
Barnard and Cox: see above); also
co-Chairman of Cannon's
organisation's Diet and Cancer
*Cannon (2) Project. *
PD IA/8
Crawford: Associate of Campbell (see above).
Cannon: Associate of Campbell (see above); also,
via the London Food
Commission/ National Food
Alliance, of Lobstein
*55:49:18-60 (and Dibb, Millstone). *
(possibly also
Gellatley)
2 . 7 .4 Not that any of this is terribly sinister.
Simply that it makes a nonsense of DM's
adulation of his witnesses' supposed
'independence' (and of his silly, and
offensive, assertion that the Pffs' witnesses
*More later are 'tainted')*. In fact, one has a suspicion,
under Malice: grounded both on their mutual associations
it is assumed and on the nature of their evidence, that the
that he spoke Ds' witnesses may be part of a dedicated
for HS, too. 'anti-animal-fat' clique or coterie
(motivated, in some cases - Cox, possibly
Barnard, - by a concern for animals rather
than human health) which saw this trial as a
convenient platform for the promulgation of
its views. Which is not to say that their
views are, for this reason alone, to be
disregarded (they are wrong because the -
evidence shows them to be wrong); simply
that their supposed status as wholly
independent Olympians may not be entirely
credible.
3. Going back to the meaning -
What is a "very real risk"?
3.1 A "real risk" is one that has been
demonstrated or established. It can be
observed to have real consequences.
3.2 A "very real risk" describes the degree of the
risk: deny its existence at your peril!
3.3 So, perhaps, "very + real" = "serious" or "strong".
3 .4 Thus -
1933: The Nazis in Germany may present
a threat to European stability.
1938: The Nazis are a real threat to peace in Europe.
1940: The Nazis are a very real threat to
continued existence of this country.
3.5 In addition, two kinds of 'risk' must be
distinguished:
(1) If there is more than a fanciful
possibility that, eg, diet will in due
course be found to have a role in the
aetiology of cancer, even though that
role has not been established, then, in
one sense, the person who pays no
attention to what he eats is taking a
* = "It may be so. 'risk', viz, the risk that the possibility*
On the other hand, it - or hypothesis* - will turn out to be
may not be so". out to be the fact.
That is not, in this context, a
real risk, still less a very real risk.
(2) A real risk - a fortiori, a very real
risk, - is one which is known to
accompany a particular activity:
- eg, the risk of death or injury
involved in mountaineering or
riding a motorbike without a
crash helmet
- or, closer to home, the risk of
cancer or heart disease
- involved in ~ smoking
cigarettes.
(3) Thus a real risk is one which has been
identified, established (demonstrated)
and accepted by all reputable authorities
over a period of time.
- Thus our Govt. is able to compel the
tobacco companies (even the French! ) to
print stark warnings on cigarette
packets:
*Qv on RR's Gitanes 'Smoking causes cancer'*
(attached). 'Smoking causes heart disease'*
- This does not mean that everyone who
smokes will get cancer or CHD. But it
does mean that all those that do smoke
run a real risk (perhaps a very real
risk) of doing so
- in greater or less degree, no
doubt, according to their genes,
their weight, their life-style, and so on.
(4) The qq. arising in this case are different for cancer and CHD: (i) For cancer and diet, the q. is, Does the given diet carry with
it a (very) real risk of cancer at all? (ii) For CHD, the q. is, What is the degree of (real)
risk which that diet carries? 4. CHD 4.1 The Pffs' admission: (1) That there is a considerable amount of
evidence of a relationship between a diet
high in saturated fat and sodium, and
(In writing: obesity, high blood pressure and heart
15.12. 93) disease; and
(2) That that relationship is causal in
(RR in Ct) nature.
4.2 Note that this says nothing of diabetes: nor
does the leaflet: nor shall I. It is
irrelevant.
4.3 The admission is an admission that there is a
real risk - not a theoretical or hypothetical
one - of suffering CHD (etc) if your diet is
high in SF and Na.
4.4 But it makes no concession as to the degree of
risk; nor as to the relative importance of SF
and Na in creating that risk.
4.5 As to this last q. (SF v Na):
It seems tolerably clear that 'high' Na
intakes do not, for most people, present the
same degree of risk as high SF intakes, at
any rate so far as CHD is concerned (stroke
might be different, but that is outwith this
case):
- See, eg, COMA 46:6.6.8 on p 138.
- and Naismith:
- Hypertension on p.7 of his
*252:21 report*;
- Day 253: 31-2, as to the
effect of lowering systolic blood
pressure by 2 or 3 mg
(misstatement/misprint for 2-3
mm/Hg?) by dietary Na reduction
vs. benefits to be obtained by use
of drugs.
4.6 So far as SF intakes are concerned, the q. is
more complicated:
(1) How much SF?
(2) For how long?
(3) What other factors are/may be
important in increasing/ reducing
risk?~
4.7 Q. (1) above: how much?
No clear answer. So the 'best bet' is
probably COMA 41 :3.4.18 on p. 49 (1991)
(10% of EAR for energy in Kcal/d); endorsed
by COMA 46(1994), which is, of course,
specific to CVD: R.2.1 on p.1.
4.8 Q. (2) above: for how long?
4.8.1 CHD is, in general, a disease of later life;
which is (obviously) one reason why its
incidence is greater in more affluent
*more accurately: societies (people live longer)*:
more people live
long enough to
get CHD.
*OV/26 (i) WHO Report (1990), p.28*.
(ii) Naismith: 252:54(end)-55:16
57 (ens J)
253: 22-24
(iii COMA 46: pp 42-3:
- Contrast Tables 2.5a and 2.5b
- Take, eg, Males in England:
2.5a (under 65s):
*Total Rate: c. 92/100,000* pop by 1990
52,000 <1/1000 (1087)
2.5b (all ages):
* Total Rate: c. 290/100,000* pop by 1990.
164,000 >1/350 (345)
- This means that once you get past
65, your chances of dying from
CHD increase dramatically. And
this is so for both sexes in all
parts of the UK.
- This is confirmed by Fig. B .3 in
App. B on p.181, which breaks
down the rates in different age
-groups under 65:
Males: 35-44: c. 30/100,000 (1/3333) 1990
(E&W
only)
45-54: c.160/100,000 (1/625)
55-64: c.500/100,000 (1/200)
- And the rate no doubt increases with age after 65.
4.8.2 What is not clear - nor ever could be, because
individuals vary so much - is the
frequency/amount: years ratio between intake
of, say, SF and the Onset of CHD.
- For example, what accounts for the
*Total 30/100,000* deaths amongst 35-44s?
17,000
Genetics?
Vast quantities of SF in early life?
Lack of exercise?
Smoking?
(more later) Lack of fruit and vegetables?
Congenital weaknesses?
etc. etc.
4.8.3 The only conclusion one can safely draw is
that, since the risk of death from CHD
increases sharply with age, whatever role diet
plays in the creation of that risk (and it is
accepted it plays a role), a considerable no.
of years must pass before it has its effect
for the majority of people who eventually
suffer from CHD.
4.8.4 And that is why (amongst other reasons) the
age/frequency figures for McD's customers
are important.
4.8.5 So the ans. to q. (2) is:
no precise estimate can be achieved, but,
since, in general, CHD is a condition of
late development, many years.
*252:22:42-8 4.8.6 Professor Naismith put it like this:*
Q(HS): Consistent advice has been that a
high consumption of sat. fats
increases the risk of heart
disease. Is that not right?
A: That is so, yes. That has been
consistent for probably 30 years.
Not simply high consumption; a diet
that is high in fat consumed over a
life-time is more likely to cause
heart disease than one that is low
in saturated fats.
(emphasis added)
4.9 But the degree of (real) risk is another
matter. This is what q.(3) addresses:
What other factors are/may be important in
increasing/reducing risk?
4.9.1 It is clear that the causes of CHD are
"multifactorial" - through obviously some of
the risk factors are likely to be related in
some cases
e.g. lack of exercise and obesity.
(see later) .
4.9.2 For the full range of possibilities it is
necessary to consult the evidence of Prof.
Naismith who summed the whole thing up at
252 : 22:26-40
- SF is only one of many factors.
4.9.3 The full range, according to Naismith - some
bad, some good (protective: Pj - is:
252: 7(and 23): Smoking (more
important than diet)
7: Genetics
7: Folic acid (P)
7: anti-oxidants (P)
8: stress
*The French 16-18: alcohol(P)*
paradox: 23: fruit and veg (more important
more later. than reducing fat consumption)
(P)
37: potassium (P)
253: 16: physical activity (P)
16: obesity.
4 . 9 .4 Thus, assuming the same intake of SF and
the same genetic predisposition, the fat:
person who smokes cigarettes, takes little
exercise and eats few vegetables or fruits is,
if his habit/life-style persists for a long
time, at much greater risk than the thin
person who doesn't smoke, - is physically
*Dr Arnott: has "a good intake of fruit and vex.'!*
254: 6 and 62
4.9.5 An important point about obesity.
If obesity is an important 'risk factor' for
CHD (which it is), and if increasing obesity
in men (2 x) over the last 10 years cannot be
Naismith: attributed to a change in diet,* then the
253:16 'culprit' is likely to be lack of exercise.
4.9.6 This is not to say that fat (whether SF or
PUFA) may not contribute to obesity, or that
obesity is the only deleterious consequence of
a high SF diet (increased serum LDLs, eg) .
But what it illustrates is that reasonable
quantities of fat (inc. SF) do no harm
provided that the rest of the consumer's
life-style (including, but by no means
confined to, his diet) is reasonably well
-balanced.
4.9.7 The French paradox (and the German)
See the composite sheet taken from COMA 46.
4.9.8 This is not a fanciful exercise. However
'crude' the intake figures may be, the
contrast between the intakes of supposedly
'unhealthy' foods and the incidence of CHD
mortality in France and Germany, on the one
hand, and the UK, on the other, is really
very striking (all the experts, inc. Crawford
and Campbell, agreed that, if the figs . were
accurate, the amounts by which French and
German intakes of the 'unhealthy' foods exceed
ours are significant). Nor is the contrast
confined to the figures for intakes. It also
extends (as one would expect, if the figs. for
intakes are broadly accurate)-$o the supposed
indices of risk for CHD: blood cholesterol,
blood pressure and body weight.
4 . 9 . 9 So what is the explanation? No-one can say,
it seems (hence "paradox").
- More fruit and vegetables?
- More wine/beer/alcohol generally?
- Less smoking?
- Less stress?
- Different gene pools?
4.9.10 The important point to be drawn from this is
not that SF is not a 'risk factor' (it is accepted
by everyone that it is), but
(i) that it bears out Prof. Naismith's emphasis on the multifactorial character of the aetiology of CHD; and
(ii) that it illustrates very vividly the dangers of using cross-population studies for anything other than hypothesis - generation .
4.10 Finally, .
4.10.1 Despite McD's rapid expansion in this country and throughout the world over the last 20 years or more, CHD mortality rates have been declining during that time, not only in this country, but in the USA and Australia as well:
COMA 46: Fig 2.6 on p.46
What the reasons for this might be is anybody's guess:
- arlier diagnosis?
- better treatment?
- less smoking?
- more exercise?
- less SF?
- more vegetables?
But it is interesting that in the USA, in particular, where McD's have by far their largest market (proportionately as well as numerically), and where fast-foods and hamburgers in particular, are more firmly entrenched in the way of life than elsewhere, the rate had by 1988 declined to well under 200/100,000 and was very considerably lower than ours.
4.10.2 None of this is to say that 290/100,000
164,000 deaths from CHD in this country in
1990 - or, more particularly, 52,000 amongst
men under 65 and 15,000 (26/100,000)
amongst females under 65 - is anything to be
pleased about - or ignored.
4.10.3 But what it does suggest is that the almost hysterical obsession with fat, and particularly animal fat, which may be seen in some quarters (Barnard, Cox, eg) is s scientifically unjustified - and socially irresponsible: a alarmist.
Much better the dispassionate balanced view of Naismith, Wheelock,
COMA 41 AND 46:
A diet which is high in fat, and particularly
SF, and low in fruit and vegetables does carry with it a real risk that if you persist in such a diet for many years you may get heart disease. Therefore, balance your diet, and your life-style, give up smoking, and you will reduce the risk considerably.
*3. 2-3
+"Serious" is
here used to
connote degree.
In the
qualitative
sense, any risk
of death from CHD
is serious!
4.10.4 All of which is to say that the degree of risk, though real, and though obviously more than slight, does not warrant the description veer real: for, as suggested earlier*, those words must import a flavour of serious+ danger.
Put another way, it would be sufficient to indicate the degree of risk of CHD which, on the evidence, the 'wrong' kind of diet, in itself, may create simply to describe it as a real risk.
If you then added to diet, all, or some, of:
- smoking
- obesity
- lack of exercise
- stress
you might be justified in describing the risk as very real.
5.0 Cancer
5.1 The q. was:
Does a diet which is high in fat, etc, and low in fibre, etc, carry with it a real risk of cancer of the breast or bowel?
5.2 'Real' emphasised in order to distinguish the
risk in q. from the 'risk' that hypothesis and
theory may mature into accepted fact in the
future.
5.3 The key witness is Dr Arnott; first, because
*the other the study of cancer and its causes are part
part is its of his life's work*; second, because his
treatment opinions are in accordance with all the
authorities whose duty it is to consider such
qq. and report their conclusions to the public in order that the public may be enabled to know what they should do (or not do) in the interests of good health; and, third, because his I impartiality and objectivity cannot be impugned (despite w which,-both HS and DM made the attempt*).
*254 : 6:14 (HS);
254 : 59:41-5
(DM): more later under
Malice.
5.4 Dr Arnott summarised the state of scientific
knowledge about the relationship between diet
and cancer on numerous occasions, both in
1994 and when he returned in May 1996. The
most comprehensive summary is perhaps that
given on 22.5.96 (Day 254:4:3 -- 5:42),
ending with this:
"What we have seen in all the studies regarding diet a and cancer is inconsistency in the results, and that is what I have tried to say all along. We do not know what the relationship between diet and cancer is. It is certainly not a clear-cut relationship, particularly r regarding cancer of the breast and bowel. If we were expecting to see evidence of a stronger relationship, I think all of the studies would have been more consistent than they have been".
5.4.1 Thus, in Dr Arnott's view, the overall picture
has become even cloudier than it was when he
gave evidence 2 years earlier.
5.5 The views of the national and international authorities:
(separate) 1982: Diet, Nutrition and Cancer, NRC(US): p.5
Then 6 years pass and we find that even that kind of (qualified) confidence seems to have ebbed away:
(own file) 1988: US Surgeon - Gen. 's Report: pp 224-5
(DI/2/58) 1989: UK response to EECis
"Europe against Cancer"
Initiative: Health
Education Authority: pp 18-19; 27
(bar chart)
(O IV/2/26) 1990: FAO/WHO - p 62, 3.3, 3.3.3, 3.3.6
- cf 3.3.5
pp. 90 and 91,
paras 4.1.2 and 4.1.3
1991: COMA 41 3.5-3.5.6, p.52
(PB IA/11/ 1991: Cancer of the Colon and Rectum: National
ref 6: Cancer Institute (US) : pp. 6 and 7
Barnard (2) ) (both pages of text)
5.5.1 The idea that the panels of experts who are
responsible for these reports . and
recommendations are somehow creatures of the
food industry or otherwise too craven to tell
the public what it needs to know for the sake
of its health is self-evidently absurd (as
well as offensive to the experts concerned).
5.6 The key word in all of this is "consistency" (or "inconsistency").
5 . 7. Thus, when Sir Richard Doll first published
his findings on smoking amongst doctors and
lung cancer, people could no doubt say (and
did) that this was only one study, that it was
too soon to tell, and so on. But as the years
have passed, the evidence supporting a
positive relationship has been (virtually) all
one way, with the result that, for some years
now, it has been possible to assert with
confidence that the one is a cause of the
other, even though the precise mechanism of
causation was not known (and the same would
be true of smoking and CHD). This is why,
on the 1-10 scale of risk which Dr. Arnott
*17: 58-9 described in July 1994*, he felt able to put
smoking and lung cancer at the top (10). In
other words, the evidence has been
consistent over a long period of time; with
the result that all responsible scientists
(inc. medical men) feel able to say that
smoking cigarettes in any quantity gives rise
to a real risk of lung cancer.
5.8 But with diet and the risk of cancer of the
breast and bowel, the evidence has been
inconsistent and conflicting. Thus Dr Arnott
gave the following scores on his scale (in
ascending order of 'risk'):
1. Fat and breast cancer.
2. Calorie intake and bowel cancer.
3. Fat and colon cancer.
3. Calorie intake and breast cancer.
4. Plant fibre as a protection (from both
cancers ) .
All those scores were in the 'pale grey' area
of the scale, that is, "meriting continuing
*17: 59:13-15 investigation, but certainly not proven facts"*
(whereas smoking and lung cancer, at 10, was
'black': x is almost certainly the cause of y.)
5.9 The scientific papers which have been studied
during this case simply bear this out. And
that includes Prof. Campbell's China study (of
which more later). The only thing which has
changed since 1994 is that fruit and veg.
might now merit a slightly higher score as a
protective element (more later).
5.10 The general pattern is:
(i) cross-population studies have suggested an association between diet and the 2
cancers;
(ii) So have some animal studies, and some prospective (cohort) studies; but
(iii) many of the case-control and, in particular, the prospective studies do not support an association.
5.11 All these kinds of studies have their
disadvantages:
(i) cross-population studies are too crude:
- they tend to. be based on 'food
disappearance' figures,
- they cannot take account of variations in diet and life-style across the different populations
studied,
- their chief value is for hypothesis - generation .
(ii) animal studies are chiefly valuable as a means of testing mechanisms: eg, the effect of high calorie/high fat diets on promoting tumours which have been deliberately induced in pure-bred species which have a known susceptibility to particular carcinogens.
- If they are used as a means of drawing conclusions about the role of diet in human physiology, they are dangerously unreliable.
- Again they are hypothesis-generators
- if this is possible in
animals, may it, or something
like it, be happening in
humans ?
(iii) Case-Control studies may study too few people for too short a period and may be distorted: by variations (or changes) in the diets of the cases, brought about by the mere fact that they are cases.
(iv) Cohort (prospective) studies may study too small a range of dietary intakes (too homogeneous) and, except in the very longest examples, may be too short. Nevertheless, they are probably the most reliable: *0 IV/ 2/26 Wheelock, Arnott, WHO (P62)*, Hill(1995, p.4) + +Behind Arnott (2) and Kinlen (1991, p 464); also Prof. Walker°.
Y V/12
O IV/2/7
° 26:31:4-30
5.12.1 Another problem (upon which Dr Arnott and Prof. Campbell agree) is that it is, in the end, impossible to disentangle the various elements of diet in such a way as to enable one to inculpate any particular element or elements .
5 .12 . 2 Thus there is a debate (which at present is wholly inconclusive) whether, if diet is implicated in either of these cancers,
(a) the 'villains' may be:
- fat
- saturated fat
- total energy intake
- cooking methods
- or something else
entirely; or a combination.
(b) or the 'goodies'
- fibre
- antioxidants (eg Vit C,
Vit E)
- micro-nutrients in fruit and veg (same thing?)
- calcium
- selenium
- n-3 PUFAs from oily fish
- Some unidentified
substances in Chinese
vegetables (!)
*Aspirin?: - or something else entirely*; Thun ( 1992 ) - or a combination.
OIV/2/19
(c) or whether what you need is a combination of all or some of both ( (a) and (b).
5.12.3 Dr Arnott gave a good example of this
problem*
*254 : 69:5-9
(perhaps
referring to "Experiments have been done which show
Kritchevsky that high calorie intake and low fat
(1984): intake animals get breast cancer more
O IV/2/11) frequently than animals who are given
high fat diet and low calorie intake."
(emphasis added)
5.12.4 Another striking example is the Finnish/NY
*O IV/2/25 study by Reddy et al (1978)*
(Colon cancer) - It was assumed (on the basis of other
- work) that the Finns were low-risk and the New Yorkers high-risk for colon cancer.
- For the 2 populations, the levels of fat and protein intake were the same, but the sources of fat were different (dairy v. meat) and the Finns' intake of cereal products (fibre) was greater.
- In the result, if the assumption was correct, there is no way of telling what,
* Perhaps calcium if anything*, in the differences in diet
in the Finns' dairy might account for the differences in
food? See: risk.
Morson (1990),
O IV/141 p.600,
1st Col.; and
Arnott : 17:46:22-5.
5.13.1 Prof. Campbell seemed to deprecate what he called the 'reductionist' approach, that is, the search for particular elements in the diet
which, separately or together, might be identified with confidence as increasing or reducing the risk of these cancers.
5.13.2 But, with respect to a distinguished scientist, he must be wrong about that. For it is not until you can say with some confidence that this, that or the other element or elements are likely (at least) to be concerned that you have the foundation for an assertion that diet is causally (as opposed to historically or accidentally) associated with these cancers. For it is not until you have reached that minimum position that you can assert the "biological plausibility" which Prof. *256:10:51-11:12 Campbell himself regarded as necessary.* Unless or until you are in that position, you remain in the position which, for all the detail of his China study, Prof . Campbell necessarily still finds himself today:
"These data are suggestive of the hypothesis that . . . "
or even
"they lend some support to the existing hypothesis that..."
5.13.3 The reason why such precision is necessary is that diet (unlike tobacco-smoking orb lack of exercise, which, qualitively, are unitary concepts) is an almost infinitely variable concept:
- thus, in relation to CHD, one can now say that a diet which is high in saturated fat (and, probably, low in fruit and veg. ) carries a real *for the reason, risk of disease*.
amongst others,
that the biological
mechanisms are
largely
established.
- but one cannot say the same of a diet which is high in fat (simpliciter) . the Greeks, Spanish, Italians
- If, therefore, one is going to propose that a diet of one kind or another is causally related to cancer of one kind or another, one has got to try and identify the particular element(s) in the diet (such as SF in relation CHD) from which it may plausibly be concluded the risk is derived.
- Unless you do this, you risk missing the
key Elements and, in the process, finding that your over-general proposition is unsustainable. *
*For example, if
you inculpate
'animal fat',
and people
therefore stop
eating dairy
produce, you. may
simply find,
in the end,
that all you
have achieved
is the removal
of significant
protective
elements from
the diet.
5.13.3 This is not to belittle the work of Prof. Campbell and his colleagues. It may (when it is complete) turn out to be a very valuable contribution to the debate.
But if I were a scientist, I'd be thinking that it raised more questions than it answered - some of which are suggested by a q. (answered in the affirmative) which *256 :59: 14-36 J. asked -Campbell*:
Fat?
Animal Fat?
Vegetables?
What vegetables?
Chinese vegetables?
What in vegetables?
What in which vegetables?
What in which Chinese vegetables?
And if I were seeking an ens. to the q, does a high fat/low fibre diet carry a real risk of cancer?, I'd want to know, in the light of existing evidence, the answers to at any rate some of those qq.
5.13.5 Test the matter in this way:
*I have read - Suppose I am a learned* and responsible
and digested scientist. I might be an epidemiologist,
all the relevant a nutritionist, a biochemist or an
material. oncologist.
- I am given Prof. Campbell's article about the China study and the chapters in the
book written by him. I read them with care. A number of things strike me at once:
(1) Smoking seems not to have been taken into account.
(2) There is a weak positive correlation between fat intake and breast cancer. (article: 11585,Col.l)
(3) There is a weak inverse correlation between large bowel cancer and dietary carbohydrate and fibre intake (article: 11585,Col.2)
(4) Plasma ascorbate (vit.C) shows the
strongest inverse association
*but for males, with cancers*: (book: p.97)
not females:
the 'confounder'
might be smoking
(256:48): i.e. vit.C protects
against the effects
smoking.
- I then read Yuan (1995) and Hunter (1996) .
And I conclude that really nothing has changed, except that a stronger protective role for (fruit and) vegetables is beginning to emerge as a
possibility, perhaps displacing the old favourite, fibre.
5.13.6 This demonstrates why, as Dr. Arnott said, one must look for consistency over time and not be misled by the promise of one particular study: for, as soon as that has appeared, along come others which cast doubt on it (thus Campbell (1994), followed by Yuan (1995) and Hunter (1996)).
5.13.7 The studies which best illustrate the validity of Dr. Arnott's account of current knowledge
are:
(1) Breast cancer
Kinlen (1987) O IV/2/9
Kinlen (1991) 7
Jones (1987) 23
Willett (1992) 5
Kushi (1992) 24
Ip (1993) Behind Crawford (1) in PB IA/9
Campbell (1994) Behind Campbell in PB IC/H/5(?)
(also colon)
Yuan (1995) Behind Campbell in PB IC/H/5(?)
Hunter (1996) Behind Arnott (2) in Y V/12
(2) Colon Cancer
Reddy (1978) O IV/2/25
Willett (1989) Behind Crawford (1) in PB IA/9
(also breast)
Willett (1990) 0 IV/2/3
Morson (1990) 14
Thun (1992) 19
Shibata (1992) 20
(3) General
Doll (1988) O IV/2/16
Albanes (1987) 12
Hill (1995) Behind Arnott (2) in Y V/12
As to this last (Hill), see in particular pp 3-10; 18-21; 22-4; and 28 - end. See also Table 5 on p.11, which shows that, despite the differences in diet between the UK and France and Germany (see composite COMA chart and 4.9.8 - 10, ante), the death rates from large bowel cancer in men are virtually the same; whereas, if the hypotheses about diet and cancer were correct, one might expect the French and German mortality rates to be significantly higher.
5.13.8 These studies and articles (and others), taken together and read carefully and objectively, lead to this conclusion and this conclusion only:
5.14 Conclusion
There may be a causal relationship between diet and cancer of the breast and bowel. On the other hand, there may not be. The question is unanswered and requires further research. At the moment, we do not know whether it is so; still less do we know how it might be so.
I transpose the origins' q. (having regard to the burden of proof in this action and the weight of the scientific evidence) as follows:
Can it be shown that a diet which is high in fat, sugar, animal products and sodium, and low in fibre, vitamins and minerals, gives rise to a very real risk that you will suffer cancer of the breast or bowel?
Plainly, it cannot be. Nor can it even be shown that there is a risk in such a diet which is real. There is a theoretical risk, and the theory is certainly more than fanciful: but that is as far as current learning, objectively regarded, will allow the proposition to be pushed.
J Mng. part 2
IX 1. The qq. are (in shorthand):
(1) Do McD's know that their food is very unhealthy?
(2) Do they hide that fact?
(3) Do they lie to their customers about the nutritional value of
their food?
2. This is easily answered:
(1) You can't know what isn't true.
(2) You can't hide a fact which isn't one.
(3) You can't lie about something which you don't know is false.
3. Against the formidable factual background recently rehearsed, see what McD's do say about their food and its place in its customers' lives:
*Note Arnott's (1) UK: 1985: P VI/5*
comments 8
on these 1989: 6*
at 17:60-1
1993: Nutrition:
* front of P VI a question of balance:*
*P VI/16 and 17 (2) US: 1982} identical*
1984}
*P III /2/ 60-4 (3) Annual Report 1990:*
* Note Wheelock's
comments on
this at 14: 64-5. (4) On the evidence, these statements are both accurate fair - and pretty comprehensive.
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