42 s MEDIE
Review Al'licle
Sugar Intake and Diabetes Mellitus
A. R. P. WALKER
SUMMARY
Within the last century the prevalence and mortality rates
of diabetes and other degenerative diseases have in-
creased considerably. Simultaneously, there have been
marked alterations in the types and amounts of food con-
sumed. One of the most conspicuous dietary changes has
been the very considerable rise in sugar intake. Some re-
gard this change specifically as the factor most responsible
for the increase in diabetes. In this review, the relationship
between rises in sugar intake and prevalences of diabetes
and the bearing of sugar intake on obesity are discussed.
There is not enough evidence that a high intake of sugar
specifically promotes the development of diabetes, but
this does not imply that sugar intake is unimportant. Be-
cause of the high prevalence of obesity in some popula-
tions, restriction of sugar intake is as important as other
dietary restrictions.
S. Afr. med. l., 51, 842 (1977).
In many parts of the world there has been a dramatic
alteration in disease pattern, from one predominantly of
infections to one of degenerative diseases. The change
is evident from comparisons between (I) our ancestors
and ourselves, (ii) rural and urban populations in de-
veloping countries, and (iii) persons in developing coun-
tries and those who have settled in 'Western' countries.''
Conditions and diseases which have become more com-
mon are almost wholly caused by changes in environmental
factors. What factors have changed to such an extent
that at present over two-thirds of all deaths in Western
populations are due to coronary heart disease, cerebral
vascular disease, cancer, and diabetes mellitus? The most
important factor is diet, although other changes are con-
tributory in varying measure, e.g. alterations in physical
activity, cigarette smoking, atmospheric pollution, and
stresses linked with urbanization and rise in social status.
In the three contexts described, what dietary changes
have occurred or are occurring? Briefly, energy intake
increases. Intakes of protein and fat increase, especiaUy
in developing populations. Total carbohydrate intake faUs;
less bread and other cereals are eaten, and they tend to
be more refined; sugar intake increases several-fold. There
are changes in intakes of mineral salts and vitamins; con-
sumption of some nutrients rises, while that of others
Human Biochemistry Research Unit of the South African
Medical Research Council, South African Institute for
Medical Research, Johannesburg
A. R. P. WALKER, D.se.
Dare received: J December 1976.
E TYDSKRlF 4 Junie 1977
faUs. Fibre intake and bulk-forming capacity of diet
unequivocally decrease.
Of the diseases with increased prevalence and mortality
rates, one of the most prominent is diabetes. Of the dietary
changes that have occurred simultaneously, the increase
in sugar intake has perhaps been the most marked. Some
believe this dietary change to be the only cause of diabetes;
others, however, consider sugar intake. apart from its
energy contribution, to be irrelevant.
In seeking to assess the culpability of sugar, questions
which require answering are: is sugar the sole or principal
aetiological factor? Is it an influencing factor, or simply
an associated factor? Are people with a high sugar intake
more prone to diabetes than those with a low intake?
If individuals consume less sugar, do they thereby lessen
their chance of developing diabetes? Does increased or
reduced sugar intake by diabetic patients increase or re-
duce the severity of their disease? Attempts to answer
these and related questions form the burden of this review.
The topics to be discussed are: the increase in the
mortality rates and prevalence of diabetes; dietary and
non-dietary causative factors; the increase in sugar intake;
correlations between national sugar intakes and diabetes
mortality rates; observations on correlations between sugar
intake, glucose tolerance abnormality and diabetes in
particular population groups; sugar intake, obesity and
diabetes; experimental feeding studies on man and animals
and possible mechanisms involved in the development of
diabetes.
INCREASE IN DIABETES
Mortality
Diabetes was known to the ancients in India, China,
and Egypt' although Hippocrates did not mention the
disease.
At the turn of the century, diabetes ranked 27th as a
cause of death in the USA' Since then the mortality rate
of diabetes has steadily increased in orth America and
most European countries; in Denmark, for example, the
average annual death rate in men has nearly doubled since
1955 - 58. On the other hand, in England and Wales, from
1940 until 1955, the death rate of people of both sexes
over 45 years of age decreased.' In the USA, diabetes is
now the 5th leading cause of death by disease, and the 6th
of all causes. Its rank in order of lethality is lower in most
European countries. As to the true ranking position,
Tokuhata et al.' in the USA claim that the order should
be higher, since a large number of patients with diabetes
die from its complications, and these patients are usually
not counted as having died from the disease, according
4 June 1977 SA MEDICAL
to the existing system for reporting deaths. A survey of
10 170 death certificates in Pennsylvania indicated that
about l6~ of persons had diabetes at time of death, but
this was mentioned in only about half of the certificates
and in only 2,50 was death attributed to diabetes. The
highly important conclusion was reached that diabetes
'has a very poor visibility as a significant public health
problem."
When developing populations become urbanized and
more sophisticated, and when emigrants from developing
populations settle in Western countries, mortality rates
from diabetes rise in a varying degree."
Mortality among diabetics of all ages is excessive;
women are less fortunate than men and die much earlier
than non-diabetic women:
The increase in mortality due to diabetes is not simply
an effect linked with the ageing of populations, but is
readily apparent from age-specific data. An important
factor in the changing mortality pattern of diabetes is the
bearing of increased medical interest and progress on
the recognition of the disease. From the uncertainties
described, it will be clear that considerable caution must
be exercised in the use of mortality data to define aetio-
logical factors.
Prevalence
As stressed by Jackson," West'O and numerous other
authors, the major problem in estimating the prevalence of
diabetes lies in the varying criteria used in its diagnosis.
Keen" stated that 'if one appbes the various different
sets of criteria for the diagnosis of diabetes to a large
number of individuals in a given country, the calculated
rate of diabetes could vary at least as much as three or
four-fold and perhaps as much as ten-fold within that
country'. He added that 'with that much variation, one
can do some picking and choosing to find the figure
that best fits one's hypothesis'. A World Health Organi-
zation Expert Committee" on diabetes, in attempting to
clarify the confusion, simply aggravated it. Variations in
prevalence data are induced by differences in screening
procedures, glucose load, time of day when examined,
hours since last feeding, and the chemical method em-
ployed.
According to Malins: diabetes, when reckoned by con-
ventional criteria of glucose intolerance, is present in
between 2% and 6{, of the prosperous populations of the
world. According to West," 'In most affluent Western
societies, about 3{, of adults over thirty years of age have
known diabetes. roughly 3{, have undiscovered diabetes.
and very roughly lO{, will eventually become diabetic'.
The disease is uncommon before 20 years, and increases
with age. At 65 years and over, mild glucose intolerance
is very common; prevalences of 25{, in England," and
55'0 in an American group," have been reported. Usually,
but not invariably, diabetes is commoner in women than
in men.'"-'
Enormous differences prevail between certain popula-
tions. Medalie et al." found that 'There were marked
variations in incidence according to area of birth, with
men from Asia, North Africa and Israel exhibiting sig-
JOURNAL 843
nificantly higher rates than those from European coun-
tries'. As examples of additional contrasts, West"" re-
ported that 'In one group of Eskimo communities it ap-
pears that the rate of diabetes is less than I 0 even in the
older segment of the population. In several tribes of forth
American Indians more than 30% of middle-aged people
have diabetes. Thus, we have differences a great as 50-
fold: In South African populations. Walker" found the
prevalence of diabetes to be l{, and 32~ in groups of
elderly rural Blacks and urban Indians. respectively. Care
must be taken in making comparisons of prevalence of the
disease in different countries. West' has emphasized the
tremendous contrast between rates for known diabetes in
less privileged adult populations, compared with rates
for known and occult diabetes in privileged populations.
Prevalence and mortality tend to decrease in war-time,
simultaneously with alterations in diet and manner of
life."-" This phenomenon will be referred to further in
the discussion.
Due to the uncertainties involved in determining the
prevalence of diabetes such data must be used with
caution in defining aetiological factors.
NON-DIETARY CAUSATIVE FACTORS
The basic defect in diabetes is unknown. On clinical.
physiological, and genetic grounds, it is unlikely that a
single abnormality will explain all cases of diabetes and
all its complications."
The Genetic Factor
Joslin et al.," Marble' and many others regard heredity
as the most important factor in the onset of diabetes
mellitus. Little, however, is known about the mode of
genetic transmission." Falconer'" considered that an in-
heritable cause for proneness to diabetes decreases with
increasing age; under 10 years. he thought it to be 70-
SO{" at 50 years, 30 - 40{" the average being 35{,. In a
major study undertaken in Birmingham, it was stated that
'Only diabetes of early onset has a strong genetic back-
ground'. Its role at 30 - 49 years was 25 - 50{, of that at
0- 30 years." Epidemiological studies have strongly under-
lined that the genetic component evokes significant emer-
gence of diabetes only if environmental factors are pro-
pitious, i.e. only when a sophisticated diet and manner of
life are adopted.
Non-dietary Environmental Factors
Changes in physical activity. Diabetes 'increases with
physical idleness and with obesity, but is less evident
among those who regularly exert themselves" There is
no need to enlarge on the huge fall in physical activity
that has occurred since the time of our forefathers, a
century or more ago. In IS50, in the USA, 97" of energy
was supplied by animal power and human muscle; at
present the figure is less than l{,.'" Passmore'" has
characterized modern man. or at least Western modern
man, as 'Homo sedentarius'. Habitual physical activity is
decreasing in all three types of population enumerated
844 SA MEDIESE TYDSKRIF 4 Jume 1977

in the first paragraph. A recent report has described how Western countries are reported to have sugar intakes of
exercise alone can reduce weight, and benefit the obese.'" 20 - 40 g per day, e.g. in France, Italy, Sicily and Sardinia."
Groups with high daily consumptions in Britain include
bus drivers (118 g) and bus conductors (123 g).... In many
INCREASED SUGAR INTAKE less privileged developing populations daily sugar intake
Changes in diet were very briefly outlined in the intro- is extremely low; in Bangladesh, intake is about 10 g,
duction. Only changes in sugar intake will be considered and supplies 2 0 0 of calories.'o In most developing popu-
in detail. lations, however, sugar intakes are increasing, e.g. groups
According to Yudkin,31 mean consumption of 'natural' of rural and urban South African Blacks now consume
sugar several millenia ago was about 3 kg per year. Data mean of 60 - 80 g and 60 - 90 g per day, respectively."
given by Hollingsworth" are illuminating. In the UK in The influence of social class is variable. Tn the UK
1880, sugar and syrups supplied I I o~ of total available the class difference in sugar intake is slight; intake tends
food energy. The proportion then increased steadily, apart to fall with rise in prosperity." Tn 'younger' countries this
from the period of the last war; in 1903 - 13, it was 14~; is more marked. For example, in Johannesburg, mean in-
1934- 38, 15~; 1942, 11%; 1952, 14~; 1962, 170~; and take of sugar among Whites in the less prosperous southern
1972, 18~. From Hollingsworth's data, calculations in- part of the city, is about 120 - 140 g per day, as against an
dicate that approximate mean sugar intakes per person intake of about 80 - 100 g per day in the northern suburbs....
per year were: 1900, 36 kg; 1950,45 kg; and 1972, 150 Jn contrast, among Blacks, Coloureds, and Indians, sugar
kg. Information on present mean sugar intakes in several intake rises with increase in socio-economic state.
populations is given by the Food and Agriculture Or- Men usually consume more sugar than women; this
ganization;" some data are presented in Table I. Data prevails in young and middle-aged populations. As shown
on mortality rates from diabetes" are also given. These by Yudkin" and confirmed in investigations in South
will be discussed later. Africa,""" intake rises to a peak in late adolescence and
falls after the second decade; consumption decreases still
further with age.
TABLE I. SUGAR INTAKE AND D!ABETES MORTALITY RATES
In the assessment of sugar intake, it must be borne in
IN WESTERN POPULATIONS
mind that not all investigators have used a satisfactory
Mean sugar available questionnaire, such as that of Bett et al.'" Data on intakes
are therefore not wholly comparable. Despite widely
Diabetes divergent views on the role of sugar consumption in
Per capita Per capita r:lOrtality proneness to several diseases, there is meagre information
Country per diem per annum rate per on sugar intakes of representative segments of populations,
(g) (kg) 100000 and on trends in consumption. In recognition of this,
Denmark 139 50,4 12,8 Yudkin31 has stated that 'not even the sugar industry
UK 136 49,S 13,3 knows who is eating how much sugar and how much they
New Zealand 134 48,S 12,2 are changing'. In this connection there are discrepancies,
USA 134 48,5 19,2 apparent or real, between total sugar available national-
Netherlands 133 48,0 12,6 ly per capita and sugar intake as determined from dietary
Sweden 120 43,6 18,5 surveys of large series of households. For example, in
Switzerland 118 42,6 26,2 1961 in the UK, the former approach gave a figure of
Finland 113 40,8 14,0 about 148 g per day. Yet extensive studies of households
Germany 91 33,0 27,7 yielded a figure of about 84 g, namely 72 g sugar (pur-
France 88 31,8 16,7 chased as sugar) and 12 g from preserves." The difference,
Italy 72 26,3 20,7 148 - 84 g, i.e. 64 g, appears to be larger than can be
accounted for by items not always included in household
An important fact given In the report of the Food and surveys, or by meals eaten away from home." Keys'" has
Agriculture Organization" is that in several developing also drawn attention to this type of discrepancy. This
and underprivileged populations, mean. available daily further uncertainty emphasizes that data on sugar available
sugar intakes per person are high; e.g. Brazil III g, per capita in total populations must be used with con-
Colombia 124 g, Costa Rica 164 g, Ticaragua 146 g, siderable caution for epidemiological and aetiological
Uruguay 109 g, and Mauritius 103 g. Cleave,'" although purposes.
providing no evidence, has speculated that most of the
sugar in these countries is consumed in its 'natural' form, CORRELATION BETWEEN NATIONAL
and hence is less noxious. Yudkin," however, maintains SUGAR INTAKES AND MORTALITY RATES
that 'degrees of refining make virtually no difference to FROM DIABETES
the harmfulness of sugar'. In the UK, mean daily total
intakes in 'control' adult subjects reported in investigations Correlation coefficients are frequently estimated in in-
on sugar intake and coronary heart disease, varied vestigations on the role of dietary components in mortality
between 69 and 147 g.'"-" Yudkin 43 maintains that 'many rates from certain diseases. Table I depicts national sugar
persons consume less than 45 g and very many consume intakes and mortality rates from diabetes in a number of
more than 150 g per diem'. Some rural populations in Western countries. For most listed, there is no broad
4 June 1977 SA MEDICAL Jo R AL 845

association between sugar consumption and diabetes, such comes as prominent as among populations born in Israel.
as prevails between sugar intake and coronary heart Cohen considers the large increase in sugar intake to be
disease." Indeed, several countries in the lower range of the primary causative factor. He noted that 'Individuals
intake, e.g. Switzerland, Germany and Italy, have high or groups with different genetic sensitivity to a high sucrose
mortality rates from diabetes. However, if all countries, intake, may develop high or retain normal blood glucose
developing and Western, are considered together, then values on consuming the same amount of sucrose. This
certainly the diabetes mortality rate rises with increase in explains why, in the same community, only a certain per-
sugar intake. Discrepancies exist in the case of sugar- centage of the population will develop diabetes, while
producing South American countries; Uruguay and Costa others will not'. In discussing changes in the diet of the
Rica have mean daily intakes per capita of 109 and 164 g; Yemenites, Keen" commented that 'From less than 10
death rates from diabetes are given as 17,4 and 9,4 per grammes a day their sucrose intake went up to 80 or so
lOO 000.'" Duration of consumption, of course, is a highly grammes a day. Even so, and despite the greater pre-
important factor. Uncertainties over the validity of the valence of diabetes among them, they were eating only
information on sugar intakes and lethality thus preclude about two-thirds as much sugar as the indigenous popu-
firm conclusions from correlation coefficient data on the lation. Sucrose intake was, of course, only one of the many
relationship between sugar intake and diabetes. changes in the way of life in Israel. The immigrants were
It must be stressed that there are major limitations to more sedentary. They ate more fat and were exposed to
the interpretations that can be made from correlation a variety of other stresses, dietary and social.' He thus
coefficient investigations of this type. Firstly, there are considered that there was a range of choices to explain
the uncertainties, as already indicated, on national nutrientthe increased diabetes rate. The studies of diabetes in Israel
intakes and mortality rates. More important, it cannot by Kahn et al." and by Medalie et al."''o have provided no
be ignored that studies thus far undertaken have not been support for the view that level of sugar intake is critical
very fruitful in their yield of knowledge on the causation - 'there is no evidence to confirm the theory that dia-
of degenerative diseases. Mortality from coronary heart betes is due only to excess of sugar ingestion'.
disease is several times higher than that from diabetes. Polynesians. Detailed studies on groups of these people
Yet although the relationship between national intakes of and New Zealanders have shown that sophistication of diet
particular nutrients and mortality data for coronary heart is associated with a rising prevalence of obesity and
disease has been very intensively investigated, there is stilldiabetes. In one report. Prior'n described how 'Pukapukans
enormous controversy over which food component bears living on subsistence economy, on an atoll near the equator,
the chief responsibility."35.5<l.".53 Armstrong and Doll'" re-
with around 40 of their calories from sucrose, have
cently stressed that 'correlations should be taken only as diabetic prevalence rates that do not differ significantly
suggestions for further research and not as evidence of from the Carterton Europeans (in ew Zealand) who
causation or as basis for preventive action'. are obtaining around 13,:' of calories from sucrose'.
South African Blacks. In rural areas, sugar intake, pre-
SUGAR INTAKE, GLUCOSE TOLERANCE viously very low, has risen and averages approximately
ABNORMALITY AND DIABETES 60 - 80 g per day..... Diabetes remains rare, Glucose tolerance
abnormality is present in about I % of the elderly.1S In urban
Epidemiological Observations areas, sugar intake is higher, but still less than that of
Whites. Surveys indicate that some groups of urban Blacks
Population groups with Iow sugar intakes and low have almost the same prevalences of diabetes as Whites.' In
prevalences of diabetes. These include primitive and de- one study of elderly Blacks in Johanm ;burg, glucose
veloping populations, e.g. Eskimoes, Navajo Indians, tolerance abnormality was present in about 6" H Analogous
Yemenite newcomers to Israel," and rural African Blacks"" observations have been made on Blacks in Rhodesia ,"
Population groups with low sugar intakes and moderate Groups with moderate or high intakes of sugar who
prevalences of diabetes. These include Chinese in Hong- have high prevalences of diabetes. USA Indians: Studies
Kong whose sugar intake is reported to be about 15 g on several groups of American Indians",,,,G3 revealed that
per day, but in whom the prevalence of diabetes has been among Cherokee Indians sugar intake suppljed about
stated to be much the same as that in Western popula- I O~~ of energy. Of persons aged 34 years and over, glu-
tions."":;;; Kalahari Bushmen, who are hunter-gatherers, are cose tolerance abnormality was present in 25 %.
accustomed to a very low sugar intake; yet Joffe et al." South African Indians: As with Indians who have
noted that some Bushmen exhibited glucose intolerance settled in Fiji, East and Central Africa, and elsewhere,
and significantly impaired insulin secretion. South African Indians are unusually prone to dev~lop
Populations in transition. Yemenites in Israel have been diabetes. Among Indians in the Transvaal, with mean
studied intensively by Co hen et al.",58 The Yemenites have sugar intakes of about 80 g per day, glucose tolerance ab-
been described as changing from a limited energy and normality was found in 21 % of subjects of 25 years and
sucrose intake to the high energy diet, rich in sugar, over." In Cape Town, Jackson et al." reported that in a
adopted by them in the so-called developed countries. particular group of Tamil Indians, of the same age group,
The principal difference in the Yemenite diet has been glucose tolerance abnormality was present in 38~. Studies
the change from 0% to 20:' calories derived from sugar. by Campbell"' on sugar intake and abnormalities in an
Whereas diabetes is virtually absent in new immigrants, Indian population in Tongaat, Natal, yielded similar
the disease, in the course of one to two decades, be- findings.
 846 SA MEDIESE
From the foregoing it is apparent that while a rise in
the prevalence of diabetes is associated with increasing
sophistication of diet, including increased sugar intake,
specific levels of sugar intake are associated with a wide
range of prEvalences of diabete. This has been re-
peatedly emphasized by We t.'o.",.,
Correlation between Sugar Intake and Glucose
Tolerance Abnormality
Diabetes is least common where carbohydrate con-
sumption is highest, as among most primitive and deve-
loping populations. West" stated that 'detailed analysis
revealed that the impressive negative correlation was with
starch consumption and not sugar consumption, .. Many
still think that high starch diets enhance risk of dia-
betes. While these data do not prove that eating starch
protects one from developing diabetes, the results cer-
tainly give no support to the notion that starch con-
sumption increases risk of diabetes.' Keen," on the basis
of his own studies and those of others,'';'" asked, 'Is the
risk of becoming diabetic affected by sugar consumption?
May I set forth alternative possibilities? Conceivably,
eating sucrose might be a way of preventing diabetes.'
He continued 'Our own studies indicate that, within
populations, if anything, there is an inverse relationship
between the stated sugar intake and various measures of
"diabeticity" or impaired glucose tolerance. This fits with
the unexpected inverse correlation between estimates of
sucrose intake, carbohydrate and calorie intake, and
obesity.'
In Edinburgh, Baird'" took pre-diagnosis histories from
93 maturity-onset diabetics who had just come to the clinic;
similar data were collected from 183 of their siblings, and
from 283 siblings of non-diabetic subjects. She calculated,
inter alia, the amount of added sugar that each of these
groups habitually took in their diet. Calculated average
sugar intake in the diabetics did not differ from that of
the siblings of non-diabetics. She was unable to find any
single item of diet which correlated with the degree of
glucose tolerance/intolerance, a conclusion also reached
by others."'" In fact, Baird ,noted there to be a small
inverse correlation between added sugar consumption
and the degree of glucose intolerance. In Durban, Booyens
er al.'" evaluated the diet of a small group of people whose
father and mother were both diabetic, prior to any
knowledge or testing of diabetes. These workers found
no relationship between prEvious sugar intake and whether
the person on subsequent testing turned out to be diabetic.
In this field, neither Cleave nor Yudkin have published
observations. or, as far as can be ascertained, have
Cohen and associate workers reported data on settled
Yemenites in Israel in respect of whether those who de-
veloped diabetes had higher sugar intakes compared with
those who were not affected.
From what has been discussed, it will be apparent that
evidence is lacking that in individuals a higher than average
intake of sugar specifically promotes glucose tolerance
abnormality and diabetes. There is, as indicated, some
evidence to the contrary.
TVDSKRIF 4 ]unie 1977
SUGAR I TAKE, OBESITY A D DIABETES
According to Joslin er al.~J 'overweight is the most common
factor in the aetiology of diabetes'. West" considers that
'environmental factors play a key part in the emergence
of diabetes in population groups and in individuals. And
of these environmental factors, I think that the toral
calorie inrake and the extent of acliposiry that mayor may
not develop are the key factors.- In their study at Bedford.
England, Keen" noted that diabetics between 40 and 70
years were fatter than non-diabetics. Pyorala et al."
found the incidence of diabetes to be 4,3 times greater in
obese than in non-obese men; almost the same figure has
been reported for women." Matins' has pointed out that
'It is, in fact, impossible to produce diabetes by over-
feeding alone, even in experimental animals, and some
other factor seems to be required,' Medley" maintains
that 'obesity per se is not a cause of diabetes. The cause
of the common association between the two conditions may
be that obesity acts as a precipitating factor in those al-
ready predisposed to diabetes; or that obesity is a con-
sequence of the pre-diabetic state.' In a Leading Article
in Lancel' it was stated that 'diabetes is largely dependent
on prevalence of obesity, but in communities where obesity
is common, other environmental and genetic factors inter-
act with obesity to determine both the occurrence and
time of appearance of diabetes in the individual'.
Cohen" takes the view that obesity in relation to dia-
betes is a 'side issue'. According to West,,,,l1 'when we
matched fat Cherokees of orth Carolina, in whom dia-
betes is rife, with equally fat Whites, we found that the
Whites had the same amount of diabetes'. . . 'Inter-
racial differences in prc:valences of diabetes were small
when racial groups were matched for adiposity.' In
Johannesburg obesity is much more common in Black
compared with White women, but prevalence of diabetes
remains lower in Black women:' Jacksons in Cape Town
has also noted that obesity in Black compared with White
women is less often associated with diabetes. However,
duration of changes in diet and of physical activity are
strongly influential in the relationship under discussion. lo
The Bearing of Sugar Intake on Obesity
Yudkin35 maintains that 'The proof of the pudding is in
the eating.. , Many people lose weight very simply by
giving up sugar, or by severely restricting it.' There is,
however, a dearth of published controlled studies on
representative segments of population groups which vali-
date this belief.
Tn South Africa, studies on Black. Coloured, Indian
and White schoolchildren revealed that mean weights
and heights, respectively, do not differ significantly in
those whose sugar intake falls into the upper third.
from those in the lower third." This was also true of
groups of urban Black, Coloured, and Indian women in
the age group 30 - 39 years. These observations are in
agreement with those made in the etherlands by
Bruggeman and Visser,"' who concluded that there was
no significant correlation between sugar intake and obesity.
Evidently a rise in sugar intake is matched by a reduction
4 June 1977 SA MEDICAL
in the intake of non-sugar foods. In a report by a Com-
mittee of the Nutrition Council in the Tetherlands, it was
concluded that 'there was no reason to suppose that sugar
plays a primary role in the causation of atherosclerotic
disease or obesity, or that it affects life expectancy.'''
It is important to note, as already indicated, that there
is some evidence that an inverse correlation may prevail
between sugar intake and obesity. This unexpected re-
lationship was apparent in the investigation of Richardson."
Accordingly, Keen" stated that 'if sucrose intake is linked
with genesis of diabetes, either directly, or indirectly by
way of the production of obesity, then it is probably only
in a few predisposed individuals that this is likely to occur'.
No reports appear to be available on representative
groups of populations who have voluntarily lowered their
intake of sugar, while continuing to consume their other-
wise everyday diet. Ashwell"" recently commented on the
popularity and measure of success attained by slimming
clubs; but Yudkin" asserted that 'we do not have any
hard information about the success rate of any of the
slimming clubs... we do not know the number of people
who went, what their problem was, how overweight they
were, how long they stayed and what was their success'.
Bray," also Garrow,SJ emphasized that just as slimming
clubs ought to publish their results, so ought obesity
clinics and private physicians. Booth" commented 'It has
been suggested that it would be difficult to prove anything
physicians and nutritionists have done has had any real
effect yet'.
From the foregoing information, it is apparctlt that
evidence is lacking that sugar intake, apart from its con-
tribution of calories, is specifically promotive of over-
weight, obesity, and diabetes.
EXPERIMENTAL SHORT-TERM STUDIES ON
MAN
ln man no long-term study on diabetes and differing
sugar intakes has been carried out. Several short-term in-
vestigations have, however, been pursued. In some of these
trials, glucose tolerance abnormalities were found to
be higher on high sugar/Iow starch diets than those on
low sugar/high starch diets. Changes in glucose tolerance
levels, however, were slight. In other studies no changes
or converse changes were observed.
Szanto and YudkinS5 reported that high and low sugar
regimens, lasting 14 days, had no significant effect on the
glucose tolerance test, serum cholesterol or phospholipid.
They noted, however, that one-third of subjects on a high
sugar in take developed 'sucrose-induced hyperinsulinism'
Those who exhibited hyperinsulinism experienced a mean
weight gain increment 5 times greater than that of the
remainder on the high sugar regimen. This observation
precludes attaching full blame for the change to the
alteration in intake of sugar. They also reported that
patients with peripheral vascular disease exhibited sig-
nificantly greater insulin activity than control subjects with
the same sugar intake. These workers therefore concluded
that in only a proportion of individuals does a higher
sugar intake promote diabetes or ischaemic heart disease.
Subsequently, Yudkin" stated that a high sugar intake
10 RNAL 847
for periods longer than 14 days did impair glucose
tolerance in experimental subjects and maintained that
there were increases in serum cholesterol and trigly-
cerides in all subjects every time they did the experiment.
ln the investigation of Szanto and Yudkin,S5 the mean
daily intake of sugar on the high sugar diet was 438 g,
which is three to six times the mean intake of adults in
sophisticated Western populations. Judging from data on
Whites in Johannesburg, the amount of sugar mentioned
is consumed by less than I ':'0 of adults. Whether glucose
tolerance abnormality or 'sucrose-induced hyperinsulinism'
would be evoked significantly by sugar intakes within
the broad ranges of everyday consumption is a matter
for speculation.
Cohen et al.'" fed diets with a high sugar content to Israeli
volunteers for a period of 21 days. At the end of this
time, they found a slight impairment of glucose tolerance,
compared with the corresponding situation when a high
bread/low sugar diet was eaten. On the high sugar diet.
the total intake was 231 g per day, which is three times
higher than the mean sugar intake in lsrael, and would
be consumed habitually by only a very small fraction
of the adult population. Anderson" has examined in de-
tail the results of the studies described; he did not con-
sider the conclusion reached to be warranted.
In Cape Town, Mann er al." studied the effect of
iso-caloric exchange of dietary sugar and starch on fasting
serum lipids, postprandial insulin secretion and alimentary
lipaemia in human subjects. Sugar or starch intakes were
140 g per day and the observation period was 56 days.
When starch replaced sugar, there were no significant
differences in fasting serum lipid concentrations or re-
active insulin, nor in the insulin response and alimentary
lipaemia after a standard mixed breakfast.
From experiments lasting 28 days Dunnigan et al."'
concluded that glucose tolerance, plasma insulin, and
serum lipids, were not significantly altered by the sub-
stitution of sucrose for starch at levels of sugar intake
comparable to those in Western diets. Anderson et al. 90
demonstrated that short periods (up to 10 weeks) on a
high sugar diet (supplying up to 800~ of energy) lead to
improvement in glucose tolerance. Kelsay et al:' investi-
gated the effects of diets with high glucose and fructose
contents in 7 young women for a period of 28 days. Of
the carbohydrate moiety (which supplied 50% of energy),
85% was composed of glucose, sugar or a mixture of
sugars and starches (the control diet). The amount of
glucose or sugar consumed daily was 212 g per day. It was
found that on the regimens described, compared with the
control diet, data on fasting blood glucose, and glucose and
insulin responses, did not differ significantly. Lutjens et al."
gave normal subjects equivalent amounts of glucose,
sucrose, and carbohydrates in the form of bread and
starch on separate occasions. The glucose and insulin
values showed no significant difference in these persons
after they had been loaded with the various carbohydrates.
They concluded that 'For patients with diabetes mellitus
this means that it is entirely superfluous to prescribe
a "sugar"-free diet, when other carbohydrates are allowed.'
In Antarctica, Roberts" investigated the effects of a
sugar-free diet on serum lipids of 18 men for 300 days
 848 SA MEOIESE
and reported a fall of about 1O~0 in serum triglyceride
levels. Ryan'" regarded this relatively slight fall as very
disappointing, in view of the propitiousness of the cir-
cumstances. Unfortunately no data were given of changes
in glucose tolerance or related variables.
From the studies described, it is concluded that ex-
perimental sugar consumption, within the ranges of intake
of the majority of Western populations, does not cause
impairment of glucose tolerance.
SHORT-TERM EXPERIME TAL
OBSERVATIONS 0 ANIMALS
Christophe"" investigated the effects of diets with high
sugar, fructose, glucose and starch contents (supplying
70 0 0 of energy) on special strains of obese and non-
obese mice fed ad libitum for 45 days. He found that the
effect of a high sugar diet on the plasma level of immuno-
reactive insulin was intermediate between that of high
fructose and high glucose diets. Hackel et al."" carried out
observations on the sand rat and noted that when animals
changed from their normal vegetable diet to a laboratory
diet which contained 53 0 :' energy as dextrin, most de-
veloped glycosuria, a marked decrease in glucose tolerance,
and elevated plasma insulin. Vrana" found that serum
insulin concentration after oral glucose administration
was higher in rats fed a sugar diet than in rats fed a
starch diet. aismith and Rana'"' fed groups of rats to
appetite for 50 days on diets containing starch, fructose,
glucose, maltose or sucrose. 0 significant difference in
blood glucose was found between the groups. Coltart and
Crossley" examined the influence of sugar on glucose
and fructose tolerance in baboons; when animals were
fed on a 75~~ sugar, fat-free diet for 91 days, it was
found, on testing the animals with a sugar meal, that
glucose tolerance was improved but fructose tolerance
impaired.
Perhaps the best-known investigations on experimental
animals are those of Cohen." Conclusions reached in-
cluded the following: 'These studies demonstrate that in
a selected population (of rats) with genetic predisposi-
tion, high sucrose intake leads to the appearance of dia-
betes, while the same population fed a starch diet remains
normal. The diabetes appearing in our experimental animals
has the closest parameters with human adult-onset dia-
betes, namely, hyperglycaemia, glycosuria, diabetic-enzy-
matic pattern, serum insulin, peripheral insulin resistance,
and retinal and renal vascular complications. It also shows
the need for the interaction of both genetic factor(s)
and metabolic changes in diabetes to induce the onset of
the vascular complications. By changing the diet and pre-
venting the metabolic changes in the individual with
genetic tendency to develop vascular complications, it
may be possible to prevent the appearance of vascular
changes. The experiments with animals duplicate our
observations in Yemenites, in whom we observed an in-
creased prevalence of diabetes on transition from a limited
caloric and sucrose intake to the high caloric. rich-in-
sucrose diet adopted by them in the so-called developed
countries.' The experimental diets included 25 - 72b sugar;
in human diets, these concentrations would afford about
TYDSKRIF 4 Junie 1977
150 g and 430 g per diem. It must be reiterated that studies
were made on selected populations of rats with genetic
predisposition.
Diabetes in experimental animals may be produced
by numerous types of diet, e.g. diets high in protein,
in fat, and low in carbohydrates (including sugar).'
As with tudies on the bearing of sugar intake on glu-
cose tolerance abnormality and diabetes in man, it is
difficult to assess the precise relevance to man of the
findings in animal studies, in which. in the main, sugar
has been fed at unphysiologically high doses.
POSSIBLE MECHANISMS INVOLVED IN
DIABETES DEVELOPMENT
In deficiency diseases such as iron deficiency anaemia,
goitre, and rickets, raising the intake of the appropriate
nutrient alone is effective for cure and prophylaxis. The
specific metabolic mechanisms involved are relatively
straightforward. In some diseases of excess, such as fluo-
rosis, the mechanism of the element's involvement appears
simple. In conditions which are not wholly due to nutri-
tional excess, such as obesity, diabetes and coronary
heart disease, the respective mechanisms of metabolic
involvement of nutrients are far more complex. This is
due in part to the varying role and operation of non-
dietary factors, and in part to the lack of knowledge of
the precise potential noxiousness of different components
of the diet when consumed in excess. In experiments on
animals and man, some mechanisms have been suggested
to account for the role of sugar compared with that of
other carbohydrate components. Yet the precise bearing
of different dietary components on pancreatic function.
and in particular on insulin production and beta-cell
activity, remains uncertain. According to Knowles'oo 'The
mechanism of development of diabetes mellitus is not
known'. This inadequacy of knowledge is largely the reason
for ignorance of the diet most suitable for diabetics;
this topic will be considered in the Discussion. The lack
of unanimity of results of experimental investigations
obtained by different groups of workers renders it diffi-
cult to define mechanisms of the metabolic involvement of
specific carbohydrate foods (in proportions and amounts
found in everyday diets of populations) in the develop-
ment of diabetes.
DISCUSSION
It might be imagined that in view of the vehemence with
which sugar is condemned by some and the assurance
with which benefits from reduction in sugar intake are
often claimed or implied, there would be ample unequi-
vocal supporting evidence on all these scores. Yudkin 31
urges 'It is highly desirable that every effort should be
made to reduce sugar consumption drastically'. Coben"
'recommends cutting down to a minimum the use of sucrose
and other refined sugars to about 5~6 of the carbohydrate
intake' (about 15 g sugar per day).... 'This curtailment. ..
should be applied from birth'. According to Ziegler1 1
'reduction in sugar consumption in the early states of
potential diabetes mellitus may give a possibility of a
4 June 1977 SA MED1CAL
reaL prophylaxis against diabetes and perhaps also against
other forms of illness of civilization'.
Requirements to Establish a Disease as due to
Nutritional Excess
Criteria for the establishment of a nutritional deficiency
disease have been listed by Yudkin."" as follows: (i)
evidence of low intake of the nutrient; (ii) evidence that
the nutrient concerned is involved metabolically in the
development of specific stigmata; (iii) proof that by
increasing the intake of the nutrient, prevalence of specific
stigmata is reduced or eliminated. Undoubtedly the
same criteria may be used in respect of diseases of nutri
tional excess. Thus, to establish that a particular nutrient
consumed to excess favours, or results in, a particular
condition or disease, requirements are: (i) proof of a
habitually high consumption of the nutrient; (ii) proof of
the nutrient's specific metabolic involvement in the de
velopment of the particular disease; and (iii) proof that
when the intake of the nutrient is significantly reduced.
prevalence of the disease falls. What are the results when
these criteria are applied to the issue of sugar intake and
diabetes?
None would dispute that current intakes of sugar. corn
pared with those in the past, have greatly increased. Next,
as to specific metabolic involvement of sugar compared
WJth other nutrients in the development of diabetes, this
is a highly controversial subject, as has already been indi
cated. Certainly, in some species of animals and in some
experimental dietary contexts, glucose tolerance abnor-
mality is more common when a regimen is composed
mainly of sugar in comparison with one composed mainly
of starch. Furthermore, in some experiments using parti.
cular strains of animals. a high sugar diet compared with a
high starch diet has been shown to be associated with vascu.
lar stigmata stated to be similar to lesions seen in human
diabetics. However, in experiments on humans it appears
that only in the presence of very high sugar intakes is im-
paJrment of glucose tolerance demonstrable. In none of
the investigations undertaken in which sugar was fed
at levels prevailing in everyday nutrition was there im
pairment of glucose tolerance, or of serum immunore
active insulin response. Moreover, as already described,
results of some studies undertaken have indicated that
glucose tolerance is imoroved with a rise in sugar intake.
Accordingly. the requirement of evidence that excessive
consumption of sugar per se is involved in the develop
ment of diabetes has not been met.
Turning to the third requirement, i.e. proof that a
sustained lowering of sugar intake results in a decrease
in the prevalence of, or mortality from, diabetes - this
obviously is the preeminently critical issue. Jt was em
bodied in a question put by Senator Schweiker'" to Cohen
at the USA Senate Committee hearings: 'Can you cite
an example of a human population where the addition of
sugar or the removal of sugar correlates with the rate of
diabetes?' Cohen was unable to answer the question, nor
was 1t answered by any of the other authorities who gave
eV1dence at the hearings. Furthermore, no specific infor.
matlOn on this issue is given in the contributions (books,
JOURNAL 49
papers) of those who urge gros reduction In presentday
levels of sugar consumption.
The item of evidence most frequently quoted in the
above connection is the fall in diabetes occurrence and
mortality in Britain. and in Scandinavian and other coun
tries during the last war. The decrease was attributed to
the decrease in fat intake by Himsworth'" and by Childs:"
and to the decrease in sugar intake by Cleave." Campbell'~'
and others. It is thought by Trowell" to have been related
to the increase in crude fibre intake. In Britain. during the
war period. mean fat intake fell by 25'" and sugar by
33 v" .'" Lt must be pointed out. however. that the diabete
incidence also fell in Japan during the blockade at the
end of the war.'"; Yet in that country. according to Keen."
'Sugar restriction can have played little, if any part. in
view of the very limited prior use of sucrose in Japan'.
The third requirement of evidence that diabetes is in
part a disease which stems specifically from excessive
sugar consumption, and can be remedied by sugar re-
striction. has not been met.
Yudkin'" has stated that there are many people in
Britain who are accustomed to sugar intakes below .+5 g
per day and very many who consume more than 150 g
per day. There should therefore be no insuperable practical
problem in assembling. and intensively studying. appro
priate segments of populations accustomed to grossly
contrasting sugar intakes. It is therefore extremely dis-
appointing that relatively straightforward epidemiological
studies of this type should not yet have been undertaken,
thereby leaving clinical, metabolic and other ditrerences
between contrasting groups as matters largely of conjecture.
This, unfortunately. is the aspect of the subject of sugar
intake and diabetes in which dearth of knowledge is most
conspicuous. The inadequacy of knowledge on diet and
diabetes is insufficiently appreciated. Tn recognition of this
lack, in a Special Report on Principles of utrition and
Dietary Recommendations for Patients with Diabetes Mel
litus.""J it is stated: 'there are no controlled prospective
studies which provide evidence for choosing the optimal
proportion of dietary carbohydrates and fat with regard
to long term complications in any type of diabetic popu
lation'. Further, in a Leading Article'": in Lancer it was
stated: 'A multitude of different dietary regimens has been
proposed, including restriction of fat intake. the elimina
tion of all dietary sucrose, restriction or elevation of
carbohydrate intake and alterations of eating pattern,
with frequent small feeds replacing infrequent large meals.
However, this wealth of confusing and sometimes contra-
dictory advice has not yet been accompanied by a properly
conducted study to demonstrate convincingly that any
particular diet is superior.' According to Ryan,'O' 'As
things stand now, no one knows what the ideal diabetic
diet is. T think there is more unsubstantiated dogma in
diabetes than in any other area of endocrinology.' Wolf'''''
maintains, 'At present there is no room for dogmatic
positions on etiology or therapy' of diabetes.
As against these forthright statements on inadequa-
cies of knowledge regarding the most suitable diet for the
treatment of the disease (or for its avoidance), it is
illuminating that according to the survey of TruswelI et
 50 SA 1EDIESE
al.,"O the huge bulk ( -+"0) of diabetic clinics in Britain
'aim to restrict sllero e completely'. West.''' too, noted that
experts still advise re triction or complete exclusion of
refined sugars.
Questions Posed ID the Introduction
In the Introduction. questions were put regarding the
specific blameworthiness of sugar for the high current
frequencies of glucose tolerance abnormality and diabetes
in Western and urban developing populations. From
what has been discussed, the culpability of sugar is un-
proved. In nutritional diseases such as kwashiorkor. rickets,
scurvy, pellagra. beri-beri. iron deficiency and other anae-
mias. and goitre, it has not been difficult (in retrospect)
to fully establish these as being due to specific insufficiency
of particular nutrients. However, with a disease such as
diabetes, it is considered that a correspondingly precise
apportionment of blame is out of the question. Firstly,
diabetes, as is frequently emphasized, is a disease of
'multifactorial genetic influence'.' Secondly, the increasing
prevalence of diabetes has been associated with changes
in diet, not only in intake of sugar (and other refined
carbohydrate foods). but of fat, protein and crude fibre.
Further. the changes in prevalence of the disease have
also been associated with decreasing physical activity, with
undoubted ramifications in the increasing prevalence of
obesity. In view of the number of variables involved an
aphorism of the great Virchow'" is singularly appos'ite:
'How then can one with certainty determine which of
two concurrent phenomena is cause and which effect,' and
whether either is in fact cause and both are not simul-
taneous effects of a third factor or. indeed. that each is
not the effect of two quite distinct causes?'
What of Future Intakes of Sugar?
While specific implication of sugar in the causation of
diabetes is unproved, this certainly does no! imply that
level of intake of sugar, a highly palatable source of
energy, is unimportant. Obesity in adult populations, not
only in Western countries but in urban areas in developing
countries. is very common. Among adults, energy intake
is usually excessive, and intakes of some nutrients (protein,
fat, calcium), are roughly double the physiological re-
quirements. Whjle the ill-effects of obesity, unless severe,
may have been exaggerated,m doubtless obesity is a real
risk to health. In a recent Leading Article"" in the British
N!edical Journal it was stated that 'It may be true ... that
obesity itself does not necessarily increase the risk of
coronary heart disease. How then should the physician
advise the overweight patient? The answer would seem to
be that, though overweight may be an independent risk
factor, there are many compelling grounds for weight
reduction. In the first place, a diseased heart should not
be subjected to the unnecessary strain of moving an
overweight body. Secondly, obesity is associated with the
development of hypertension. hyperlipidaemia, and dia-
betes, all of which are aetiologically important in coronary
heart disease, and overweight reduction should be the
TYDSKRIF 4 J lInie 1977
first (and is often the most successful) treatment for these
onditions.' When restriction of energy intake is called
for (although, as Mann'" has pointed out, 'it rarely
works'), should sugar intake be reduced preferentially, or
should reductions be made in intakes of all food compo-
nents?
Many have argued that since sugar contributes energy
only, then for reduction of energy intake, the consump-
tion of this foodstuff should be preferentially reduced.
This view is highly plausible. Yet, is it likely that among
individuals in Western populations a reduction in intake
of, say, 50 g sugar per day, compared with a reduction
of 50 g in the intake of other foodstuffs. would promote
undernutrition with respect to essential nutrients? Yudkin"
has stated, 'although as far as r know nobody has de-
monstrated nutritional deficiency in individuals that are
accustomed to taking large quantities of sugar, I feel
that this is largely due to the fact that we are not very
good at detecting mild deficiencies'. It could be rejoined,
equally, that mild deficiencies are not apparent because they
are not there to be detected, bearing in mind the present
advanced state of knowledge on clinical, biochemical, and
other assessments of nutritional status. It is important to
note that Kouwenhoven and Drijver,'" in short-term
studies, showed weight reduction to be three-fold greater
when they employed a regimen in which intakes of all
dietary foodstuffs were decreased, compared with a regimen
in which only carbohydrate foods were restricted. Further-
more, cholesterol levels feU on the former, but rose on
the latter regimen. These observations provide no support
for other workers, e.g. Pfeiffer.'" who aver that in seeking
weight reduction by restriction of energy intake, prime
consideration should be given to reduction of sugar
intake.
Future Research
It is desirable to obtain more satisfactory knowledge
on prevalences of glucose tolerance abnormality and dia-
betes, as affected by sex, age and ethnic group. Endeavours
should continue to be made in a variety of contexts and
populations, to increase our knowledge of the long-term
health patterns in those with high compared with those
with low intakes of sugar. The acquisition of this know-
ledge is imperative, in view of the fact that in the not
too distant future, the increase in world population will
compel greater reliance on the consumption of carbo-
hydrate foods, including sugar. Keen" has stated that in
communities 'our main attack should be to try to define
sucrose-sensitive diabetes-susceptible individuals, if they
exist'.
Another aspect which merits investigation concerns
the role of fibre-depleted diets and the occurrence of dia-
betes. As diets have risen in refined cereal and sugar
contents, they have .decreased in their content of fibre-
containing foods. Trowell'" has recently put forward a
'dietary fibre hypothesis of the aetiology of diabetes
mellitus', and Jenkins et al.,m also Kiehm et al.,'''' have
reported falls in blood glucose levels when fibre-rich food
components were added to the diet.
4 June 1977 EDl AL JOUR AL

5~. Cuhen. A. Tt:ltelhaulll. A. :lnd ~ahtc:rni~. R. t 1~72) ,\h:tahuil'lll

Finally, it must be repeated that, in the main, no 21, 2r.
matter how fruitful are the re ult of future research. "l) Kahn, H. A .. Herman. J. B.. MeJahe. J. H .. NC:llh.:ld. H "
Rbs. E. and Goldbourt, (19711: J. chrun. Di,., 23. 017.
diabete is a disea e of multifactorial aetiology. It is hO. MeJalie. J. H .. Papier. C. M., GolJhollrt, U. and Ham:lIl. H
unwarrantable therefore to expect that increased know- (191'): Arch. int. Med.. 135. 11.
01. Prior, I. A. M. ill Hilkbrand, .. ed. (1974): Up. 61.," p. 4.
ledge of the predisposing causes of the disease will fully 02. Wi ks. A. C. Il. and Jone,. J. J. (1974): Postgrad. med. J .. 50. 05"
63. Wt. K. M. and Kalbfleiseh, 1. M. (1971): Diabete<. 20, 99.
explain times of emergence, prevalence. ex difference. 6..L Jackson. \V. P. U .. van Mieghem. \V .. Marine. N.. Keller. P. and
and individual susceptibilitie . Edelstein. I. (1974): . Afr. med. 1.. 48. I 39.
0:. Campbell. G. D. ill Ostman. J. and Miln<r, R. G. D .. eds (1909)
Diabetes (proeeedings of the 6th Congress of the International
Diabetes Federation, oekhoIm 1967), p. 693. Amsterdam: Excerpta
REFERENCE iedica Foundation.
66. Abrams, M. E.. larretl. R. l .. Keen, H., Boyn... D. R. :lull
I. Burkitl, D. P. (1973): Brit. med. J., I. 274. Crossley. J. N. (1969): Brit. med. 1.. I. 599.
2. Walker, A. R. P. (1974): Ann. intern. Med., 80, 663. 07. Keen. H .. Jarrett. R. J. and Fuller. J. H. (1974): Diabetulugiea.
3. Marble. A. ill Marble. A .. White. P., Bradley, R. F. and Krall, L. P. 10, 372.
eds (1973): los/in's Diobetes Mellitus, 11th ed., p. 1. Philadelphia: o Reid. D. D .. Brett. G. Z .. Hamilton. P. J. S.. Jarrett. R. J.
Lea &. Febiger. Keen. H. and Rose. G. A. (1974): lancet. I, 409.
4. Marks, H. H. and Krall, L. P. (1973): Ibid .. p. 209. 69. Baird. J. D. (1973): Proe. nutr. oc .. 32. 199.
5. Warren, M. D. and Corfield, A. (1973): Lancet, I, r 11. 70. Booyens. 1.. Frank. M. de V .. de Waal. V. M .. Camphell. G IJ
6. Trowell. H. C. (1974): Ibid., 2, 99 and Goldberg. M. D. (1970): Afr. med. J. 44. 271.
7. Tokuhata, G. K .. Miller, W .. Digon. E. and Hartman. T. (1975): 71. Keen. H. (1964): Proc. roy. oe. Med .. 57. 190.
J. chron. Di .. 28. 23. 72. Pyorala, K., Lehlovirta, E. and TIomaki, L. (1974): Acta endoer.,
Jackson. W. P. U. (1970): Acta diabet. lat.. 7, 361. 181, suppl., p. 23.
9. M,lins. J. M. 11974): Lancet. 2, 1367. 73. Rimm. A. A .. Werncr. L H .. Yserloo. B. V. and Ber..tein. R. A
10. West, K. M. (1972): Acta diabet. lat., 9. supp!. 1, p. 40-. (1975): Publ. Hlth Rep .. 90, 44.
11. Keen. H. in Hillebrand, S. S., ed (1974): Is rhe Risk of Becomillg 74. Medley. D. R. K .. (196-): Quart. J. Med .. 34. Ill.
Diabetic Affected by Sugar COHsumplion? p. 14. Belhesda, l\1ary 75. leading Article (1971): lancet. I. 3 I.
land: Intem:ninflal Sugar Research FOllndation. 76. Walker. A. R. P. (1974): S. Afr. med. J .. 48, 10-0.
12. Report of a WHO Expert Committee (1965): Diabetes Mellitus (WHO 77. 8rllggeman. F. J. and Visser, \N. (1973): Papa prc::scntc:J at Lh\.'
Tech. Rep. Ser. o. 310). Geneva: World Health Organization. 7th International Sugar Meeting. Paris. 22 November 1973.
13. West, K. M. in Hillebrand, S. S., ed, (1974): Op. eIt.," p. 1. 78. Dalderup. lo M. and van H~ard. W. B. (1971): Vueding. 32. 569.
14. Working Party (1963): Brit. med. 1., 2, 655. 79. Ri hardson. J. F. (1972): Brit. J. Nutr.. 27, 449.
15. Burch. G. E. and O'Meallie. L. P. (1967): Amer. J. med. Sci .. O. Ashwell. M. M .. Burland. W. lo. Samuel. P. D. and Yudkin. JoO
254, 602. eds (1974): Obesity. p. 359. London: Churchill Li\'ing~tont'.
16. Medalie, J. H .. Papier. C., Herman, J. B.. Goldbourt, U .. Tamir. I. Yudkin, J. (197'+): Ibid .. p. 360.
'eufeld. H. N. and Riss, E. (1974): Israel J. med. i., 10, I. 82. Bray. G. A. (1974): IbiJ., p. 361.
17. West. K. M. (1974): Diabetes. 23. 41. 3. Garrow. J. S. (1974): Ibid .. n. 301.
18. Walker. A. R. P. (1966): S. Afr. med. J .. 40, 14. 84. Booth, C. C. (1974): Ibid., p. 369.
19. Himsworth, H. P. (1949): Proc. roy. oc. Med., 42, 323. 85. Szanto, and Yudkin. J. (I 69): Pustgrad. med. J .. 45. 002.
20. Childs, P. (1972): Brit. J. urg., 59, 669. 86. Cohen. A. l..Teitelbaum. A .. Balogh. M. and Groen. J. J. (19601:
21. Cleave. T. L. (1974): The accharine Disease. Bri tol: John Wright Amer. J. clin. I mr.. 19. 59.
&. Sons. 7. Anderson, J. W. ill Hillebrand, S. ., ed. (1974): Op. eIt." ,
22. Ehrlich. R. M. (1974): Pediat. Clin. . Amer., 21. 71. p. 44.
23. Joslin, E. P., Dublin, L T. and Marks, H. H. (1935): Amer. J. i\1ann, J. I., Trllswell. A. S., Hendricks. D. A. and Manning. F.
med. Sci., 189, 163. (1970): Lancet. J. 70.
24. Rimoin, D. L. (1967): Diabetes. 16, 346. 89. Dunnigan. M. G .. Fyfe. T., McKiddie. 1. T. and Cro.bie. S. M.
25. Falconer, D. . (1967): Ann. Hum. Genet.. 31, I. (1970): Clin. -i .. 38. I.
26. College of General Practitioners (1965): Brit. med. J.. I, 960. 90. Anderson. J. \v.. Herman. R. H. and Zakim. D. (1973): Amer.
27. Cohen, A. M. (1973): Evidence at Hearings before the Select Com- J. cl in. fmL. 26. 60').
mittee of the US Senate on Nutritional and Human Need (Pan 2. 91. Kelsay. J. L.. Behall. K. 1.. Holden. J. M. and Prather. E.
Sugar in Diet. Diabete and Heart Diseases), p. 160. \Vashington: (1974): Ibid .. 27, 926.
US Government Printing Jffice. 92. Lutjens. A .. VerleuL H. and Plooij. M. (1975): Clin. chim. Acta.
28. Time 14 July 1975. p. 46. 62, 239.
29. Passmore. R. (1966): Amer. Heart 1.. 7J, 579. 93. Robem. A. M. (1973): Lancet. I. 1201.
30. Gwinup. G. (1975): Arch. intern. Med., 135, 676. 94. Ryan, W. G. ill Schwartz. T. B., Ryan. W. G. and Becker. F. 0 ..
31. YlIdkin, J. (1973): Evidence at Hearings before lhe Select Commitlee eds (1974): The Year Book of Elldocrill%g.... p. 301. Chicago:
of the US Senate on Nutrition and Human Needs (part 2: Sugar Year Book Medical Publishers.
in Diet, Diabetes and Heart Diseases), p. 224. Bethesda. Maryland: 95. ChriSlophe. J. ill Hillebrand, S.. ed. (1974): Op. cil.". p. 5H.
US Government Printing Office. 96. Hackel. D. B.. Frohman. L.. 1ikat. E.. le Bovitz. H. E... hmidl
32. Hollingsworth, D. (1974): Nutr. Revs.. 32, 353. Nielsen, K. and Kinne}'. T. D. (1966): Diabetes. 15, 10-.
33. Food and Agriculture Organization, (1969): The Scace of Food alld 97. Vrana. A. (1973): Phv iol. bohemoslnv .. 22. 445.
Allricu/ture. Rome: Food and Aericulwre Orll~nization. 9 . I ai mith, D. J. and Rana, I. A. (1974): utr. Metab., 16, 2 5.
34. Annual Global Data on Mortality, 1967 - 1969 (1971): Wld Hlth 99. Coltart. T. 1. and Crossley. J. N. (1970): Clin. i.. 38. 427.
stat. Rep.. 24, 22. 100. Knowles. H. C. (196 ): Fed. Proc.. 27, 945.
35. Yudkin, J. (1972): Pure Whice alld Deadly. London: Davis-Poynter. 101. Ziegler, E. (1967): Helv. pediat. Acta, 22, 360.
36. Yudkin, J. and Morland. J. (1967): Amer. J. clin. Nutr.. 20, 503. 102. Yudkin, J. (1961): The Practitioner, 187. 150.
37. Papp. O. A., Padilla, L. and Johnson. A. L. (1965): Lancet. 2, 259. 103. Senator Schweiker (1973): Question at Hearing before the Select
3 Paul, 0.. MacMillan, A.. McKean, H. and Park, H. (1968): Committee of the US Senate on Nlltrition and Human Needs (Part
Ibid., 2, 1049. 2: ugar in Diet, Diabetes and Heart Diseases). p. 204. Washing
39. Finegan, A., Hickey. T.. Mallrer, B. and Mulcahy, R. (1968): Amer. ton: US Government Printing Office.
J. clin. Nutr.. 21, 143. 104. Campbell. G. D. (1973): Ibid., p. 20
40. Howel!. R. W. and Wilson. D. G. (1969): Brit. med. 1.. 3, 145. 105. Goto. Y.. Nakayama, Y. and Vagi. T. (1958): Diabete. 7. 133.
41. Burns-Cox. C. J .. Doll, R. and Ball. K. P. (1969): Brit. Heart J. 106. Bierman. E. L.. Albrink. M. 1.. Arkv. R. A .. Connor. W. 1' ..
31, 485. DaYlOn. S.. pritz. N. and S'einber~. D. (1971): Ihid .. 20. 633.
42. 1RC Working Party (1970): lancet. 2, 1265. 107. leading Article (1974): Lancet. I. 39
43. Yudkin, J. (1969): Ibid., 2, 1072. 10 Rvan. W. G. ill chwarlz. T. B.. Ryan. \\'. G. and Beckcr. F. 0 ..
44. Walker, A. R. P .. Holdsworth. C. 1. and Walker. E. J. (1971): ed (1975): Op. eIc., p. 236.
S. Afr. med. J .. 45, 516. 109. Wolf, S. in Wolf . and Berte, B. B., eds (1975): Advances ill
45. j\!arr. J. W. and Heady, 1. A. (1964): lancet, 2, 146. Experimental Medicine ond Biology, vol. 65, p. 145. New York:
46. National Food Survey Committee (1963): Domestic Food Consump- Plenum Press.
tion and Expenditure, /96/, p. 13. London: HrvlS0. 110. Truswell. A. S.. Thomas. B. J. and Brown. A. M. (191'): Ilrit.
47. Walker, A. R. P. (1976): Unpublished STudies. med. J .. 4, 7.
48. Bett, D. G. G., Morland, J. and Yudkin, J. (1967): Brit. med. J., Ill. West. K. M. (1975): Nutr. Rev.. 33. 193.
3. 153. 112. Virchow. R. (1847): Quoted from Rather. L. J. (1956): Am",. J.
49. Walker. A. R. P. (1971): Atherosclerosis. 14. 137. Med .. 21. -7.
50. Key. A. (1971): Ibid .. 14, 193. 113. Gubner. R. S. (1973): Afr. med. 1.. 47, '6H
51. Arteriosclerotic and Degenerative Heart Disease (1969): Wrld 114. leading Article (1973): Brit. med. 1.. I. 566.
Hlth Stat. Rep., 22. 462. 11-. M,nn. G. V. (1974): ew En~1. J. Med .. 291. 226.
-2. Turner, R. and Ball, K. (1973): Lancet, 2, 1137. 116. Kouwenhoven, T. and Drijver. A. (1973): Voeding, 34, 1 O.
-3. Annstrong. B. K .. Mann, J. I., Adelstein, A. M. and Eskin. F. 117. PfeitIer, E. F. (1973): Acta Endocrinologica, 173, supp!., p. I.
(191'): J. chron Dis., 28, 45-. 11 Trnwell. H. C. (191'): Diabetes. 24. 762.
54. Armstrong, B. and Doll, R. (1975): Int. J. Cancer. 15. 617. 119. Jenkins, D. J. A., Leeds, A. R., Wolever, T. M. S., Goff, D. V.
55. McFadzean. A. J. S. and Yeung, R. (196 ): Diabete. 17, 219. Albeni. K. G. M. M .. Gassull, M. A. and Hockaday. T. D. R.
56. Barnes. R. J. (1974): Lancet, I, 355. (1976): Lancet. 2. 172.
57. JotIe, B. I., Jackson, W. P. U., Thomas, M. E., Toyer. M. G .. 120. Kiehm, T. G., Anderson, J. W. and Ward. K. (1976): Amer. J.
Keller. P. and Pimstone. B. I. (1971): Brit. med. J .. 4, 21l6. clin. Nutr.. 29. R95