Hugh
mellitus foods1’ M.D.,
Trowel!,3
it has
of diabetes that
been
suggested
diets.
From
in England
directly
from
diabetes
mellitus and
These
54%
data
protective.
death
Recent
dietary
foods diets
by oral
amounts
years fiber
were
experimental
high-carbohydrate previously
the
agents
of insulin.
cause
and
of Clinical
and
studies
or moderate Am.
Wales
of diabetic
J. Clin.
Nutr.
but
31: S53-S57,
31: OCTOBER
1954
those
men those
1957
starchy
have
shown
men
who had
by
died
55%
National
mellitus,
who
who
Standardized
to
high-fiber
in many not
tolerance if they ate
of high-fiber of diabetes
that had
in
flour.
namely
that
foods
were
high-fiber, been
previously
treated received
1978.
Epidemiological
Nutrition
only
in
diabetes.
in susceptible
excluded.
until
that
mellitus
of insulin,
were
1941
etiology
factor
reported
production
hyperglycemic
of diabetes doses
rates
conversely
incidence against
that carbohydrate but was decreased
deaths from
of the and
increased protect
is a diabetogenic
death
the
the
might
demonstrated diets
fell
with
hypothesis
remission
background
Journal
food
complication
coincided
and
diets
diabetes
diabetogenic
A study of noninfective disease in Africa reported that diabetes mellitus had been rare in rural Africans from 1920 through 1960 but had become common in urban blacks (1). It was suggested, “merely as a speculation,” that the rarity of diabetes in rural Africans might be related to their low-fat, high-carbohydrate diets since carbohydrate foods increased carbohydrate tolerance (2, 3). In addition, African rural diets contained many high-fiber starchy foods; possibly these were protective factors with respect to diabetes (1). On October 20, 1972, the future contributors to a proposed book on refined carbohydrate foods and disease (4) presented various papers to a symposium held in London under the auspices of the McCarrison Society. One of the papers outlined certain historical aspects of food processing. Another paper propounded a hypothesis that fiber-depleted starchy food was a diabetogenic factor in susceptible phenotypes and that high-fiber starchy food was protective (5). This may be called the dietary-fiber hypothesis of the etiology of diabetes melhitus (6). The American
Africans
starchy
Wales,
in England
These
starchy
low-fiber
all cardiovascular
rates
in women.
in rural
ago experimental studies if they ate high-carbohydrate
mellitus;
suggested
fiber-depleted
large
of
high-carbohydrate
that
high-fat
1940
mellitus
high-fiber,
years adults
diabetes
African
rarity
suggested
human phenotypes. Many was increased in healthy
men
fiber
2
The
Africans
Conversely
The
dietary
F.R. CP.
ABSTRACT urban
and
data
in England
There were two basic reasons leading to the formation of this hypothesis. The first lay in the personal experience of a total’ inability to find a single case of g!ycosuria during 6 years’ medical work in Kenya from 1929 to 1935 (7). At a slightly later date, only three cases of diabetes were detected in the first 1000 Nairobi African black autopsies (8). In the 1930’s there were few obese Kenya Highland blacks (7); 40 years hater a visit to East Africa revealed many grossly obese African blacks in every large town and a diabetes clinic in every city. The second reason behind the dietary fiber hypothesis hay in a close relationship with Professor Harold Himsworth, without whose support a book on kwashiorkor (protein-energy malnutrition) would not have been written (9). Himsworth (2, 3) had made many From the Department of Medicine and Pediatrics, Makerene University and Uganda Government, Uganda. 2 Address reprint requests to: Dr. Hugh Trowell, Woodgreen,
Fordingbnidge,
Hampshire
SP6
2AZ,
England. Formerly
1978,
pp. S53-S57.
Consultant
Printed
Physician.
in U.S.A.
S53
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Diabetes starchy
TRO
S54
ing
steadily
from
21
period
from
1861
finally
to
in
per
million
during
the
through 1870 to 103 per million in 1914; they remained steady at 104 in 1915, fell to 98 in 1916, to 82 in 1917, and 78
1918;
the
rates
rose
to
83
in
1919 and 89 in 1920 (11). The introduction of insulin in 1921 provided a temporary check in the peacetime rise of the diabetes mortality rate; it also affected the interpretation of the data. Diabetes
mortality
rates
in England
Diabetes mortality rates fell in England and Wales during World War I and again in World War II. This phenomenon has been studied in depth on three occasions. In 1943, Stocks (11) (Registrar-General’s Office) analyzed diabetes mortality trends in England and Wales from 1861 to 1942. He
described the registration difficulties that had arisen during the first 4 decades of this century when the deaths of all diabetics from whatever cause had been recorded as diabetes deaths. Preference had been given to diabetes, rather than to other causes such as cancer or infectious diseases. In 1938 the RegistrarGeneral pioneered a fundamental change in the rules concerning the certification of diabetes deaths. Beginning in 1940 a diabetes death signified that the person had died more from diabetes than from any other disease. For instance cardiovascular complications causing death in a diabetic person were excluded from the recorded diabetes deaths from that time on (12). In 1943 Stocks reviewed the falling diabetes death rates that were accompanying World War II. He suggested that decreased sugar consumption was probably the major factor (11). The second study was made by Himsworth in 1948 in an examination of the falling diabetes mortality rates in women in England and Wales since 1941. He analyzed female diabetes death rates from 1900 to 1947, the data before 1940 having been adjusted by the Registrar-General’s correction factors (3). He added recent data for the years 1943 through 1947 to the existing data of Stocks (11). Himsworth considered that the falling diabetes death rates confirmed the suggestion of his previous experimental studies; i.e., a highcarbohydrate, low-fat diet retards the appearance of maturity-onset diabetes in susceptible persons (2, 3). Himsworth also pointed out that rationing had not apparently retarded the appearance of diabetes in susceptiblepersons who were under the age of 45; there had been no fall in their death rates during the recent period of food restrictions. The third study was made in 1965 when Cleave and Campbell (13) re-examined the data of Stocks (1!) and Himsworth (3); they presented a graph published by the latter upon which was superimposed a new line for sugar consumption. This graph depicted diabetes mortality rates and sugar data completed in 1947, although the analysis of etiological factors by Cleave and Campbell was made in 1965. These investigators ascribed the fall in diabetes mortality to decreased sugar consumption, as did Stocks some 22 years previously (11); they reported neither the diabetes mortality rates from 1948
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/10/S53/4656121 by University of Glasgow user on 15 September 2018
to the study of carbohydrate metabolism and the epidemiology of diabetes in relation to diet. He had studied the reduction in diabetes mortality during periods of war. For instance the diabetes crude mortality rates during World War I had fallen most in Germany and slightly less severely in England and Wales; there had been only a slight fall in the United States, Italy, and Japan, and none in Australia (3). During the war, food shortages had been most severe in those countries in which diabetes mortality had fallen most and far less severe in countries in which mortality fell least. When cereal supplies decrease, the milling rate is raised. During peacetime the 70% wheat flour milling extraction rate passes 70% of refined low-fiber flour for human consumption and diverts 30% of high-fiber middhings for cattle foodstuffs. During all modern wars, the extraction rate has been raised to 80 or even 90%, and more cereal foods are passed to man. When the milling extraction rate rises slightly, the fiber content of the flour rises considerably. During World War I the United States extraction rate was raised to 75% and other cereals were added; in Canada the rate rose to 81%; in Denmark much high-fiber barley meal and rye meal were added; in England the extraction rate rose to 81 to 90% during 1917 to 1918, but reverted to 70% in January 1919 (10). The English standardized female (reported) diabetes death rates had been riscontributions
WELL
DIABETES
MELLITUS
FIBER
S55
notypes. All available evidence suggests that there is considerable variation in the response of different phenotypes, both in animals and in man, for there is a considerable variation in genetic susceptibility. Experimental
studies
in small
rodents
Various studies (6, 12, 15) have shown that diets having a how ratio ofunavaihable dietary fiber to available energy (called the dietary F:E ratio) are diabetogenic for the rodent species concerned if the F:E ratio of these diets is lower than the F:E ratio of the diets to which this particular rodent species has adapted in its own natural environment (6). Thus sand rats, accustomed to eating the fibrous but how-energy food of the desert with a high F:E ratio, developed obesity and diabetes when fed ad libitum cereal chows of lower F:E ratio, but not if they were fed ad libitum vegetables of higher F:E ratio. Commercial random-bred mice developed obesity, hyperglycemia, even a diabetes melhitus syndrome, when fed how-fiber (30 units/day
Complete
Partial
None
14 6
13 6
0 0
1 0
9 3 5
9 0 0
0 3 (1)
0 0 5
and
requirements, in three men 40 to 55 insulin Fasting
requiring
those
TABLE 2 Triglyceride response of seven diabetic patients fed low-fiber low-carbohydrate (43% energy) diet 7 days, then low-fiber, high-carbohydrate (75% energy) diet for 7 days, and finally high-fiber, high-carbohydrate (75% energy) diet for 10 days (23) Low carbohy. drate 43 Low
No. of patients Duration, days Crude fiber g/day Dietary fiber” g/day Triglyceride mg/dl Increased, number
Decreased, “Neutral
fiber
7 7 4.3 9.1 189
number detergent
.
High
carbo
Low
fiber
7 7 8.8 21 199 5
2 estimations.
hydrate
High
for
75
fiber
7 10 18 60 139 0 7
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/10/S53/4656121 by University of Glasgow user on 15 September 2018
men
ward diets
energy
carbohydrate
adults
(21).
hyperglycemic
bolic drate
75 to 85%
improved
WELL
DIABETES
MELL1TUS
10. II.
14.
15.
16.
Himsworth studies of for continued
for his diabetes secre-
TROWELL,
London: 306-311. 2.
3.
6. 7. 8. 9.
Disease 1960, pp.
in Africa. 199, 217,
Proc.
Roy.
Soc. Med.
P. Diabetes mortality factors affecting it. J. H. C. Diabetes and Wales 1920-
TROWELL,
2: 998,
WIDDOWSON.
Pitman,
Breads,
1956, pp. 58-64. in
Hyg.
mellitus 1970 and
186 1-1942 Camb. 43: death food
and 242,
rates in supplies.
1974.
Coronary
T. L., AND Thrombosis,
0. D. CAMPBELL. Diabetes, and the Saccharine Disease. Bristol: John Wright, 1966, pp. 15-59. Ministry of Agriculture, Fisheries and Food. Food consumption levels in the United Kingdom. Board Trade J. 194: 753, 1968. TROWELL, H. C. Dietary fibre, ischaemic heart disease and diabetes mellitus. Proc. Nutr. Soc. 32: 151, 1973. TROWELL, H. C., D. A. T. SOUTHGATE, T. M. S. WOLEVER, M. A. GASSULL AND D. J. A. JENKINS. Dietary fibre re-defined. Lancet 1: 964, 1976. JENKINS, D. J. A., A. R. LEEDS, M. A. GASSULL, R. COCHET AND 0. M. M. ALBERTI. Decrease in post-
prandial
insulin
CLEAVE,
and glucose
concentrations
by guar
pectin.
pectin 20.
42: 323, 1949.
D. P., AND H. C. TROWELL. Refined CarFoods and Disease: Some Implications of Fibre. New York: Academic Press, 1975. TROWELL, H. C. Dietary fibre, coronary heart disease and diabetes mellitus. Part 1. Historical aspects of fibre in the food of western man, and Part 2. Coronary heart disease and diabetes mellitus. Plant Foods Man 1: 11,92, 1973-1974. TROWELL, H. C. Dietary-fiber hypothesis of the etiology of diabetes mellitus. Diabetes 24: 762, 1975. TROWELL, H. C. Obesity in the western world. Plant Foods Man 1: 157, 1973-1974. VINT, F. W. Post-mortem findings in natives of Kenya. E. Afn. Med. J. 13: 322, 1936-1937. TROWELL, U. C., J. N. P. DAVIES AND R. F. A. DEAN. Kwashiorkor. London: Edward Arnold, 1954.
London:
Ann. Internal Med. 86: 20, 1977. 18. JENKINS, D. J. A., A. R. LEEDS, T. M. S. WOLEVER, M. A. GASSULL, D. V. 00FF, K. 0. M. M. HocKADAY AND T. D. R. HOCKADAY. Unabsorbable carbohydrates and diabetes: decreased post-prandial hyperglycaemia. Lancet 2: 172, 1977. 19. JENKINS, D. J. A., A. R. LEEDS, H. HOUSTON, L. HINKS, 0. M. M. ALBERTI AND J. H. CUMMINGS. Carbohydrate tolerance in man after six weeks of
administration. J. W.,
ANDERSON,
R.
Proc.
Nutn.
H.
HERMAN
Soc. 36: 624, 1977. AND
D.
ZAKIM.
Effect of high glucose high sucrose diets on glucose tolerance of normal men. Am. J. Clin. Nutr. 26: 600,
BURKITF,
bohydrate Dietary
5.
Non-infective Arnold,
HIMSWORTH, H. P. The dietetic factor determining the glucose tolerance and sensitivity to insulin of healthy men. Clin. Sci. 2: 66, 1935. HIMSWORTH, H. P. Diet in the aetiology of human
diabetes. 4.
H. C. Edward
STOCKS,
and
References 1.
17.
E. M.
and Brown.
Lancet 13.
AND
White
England
24). The author thanks Sir Harold epidemiological and experimental mellitus and Mrs. Priscilla Milton tarial assistance.
R. A.,
MCCANcE,
some 1944. 12.
S57
FIBER
1973. 21.
J. D.,
BRUNZELL,
R. L. LERNER,
D. PORTE,
JR.
AND
E. I. BIERMAN. Effect of fat free high carbohydrate diet on diabetic subjects with fasting hyperglycemia. Diabetes 23: 138, 1974. 22.
T.
KIEHM,
0.,
J.
W.
ANDERSON
AND
K.
WARD.
Beneficial effects of a high carbohydrate high fiber diet on hyperglycemic diabetic men. Am. J. Clin. Nutr. 29: 895, 1976. 23. ANDERSON, J. W. High polysacchanide diet studies in patients with diabetes and vascular disease. Cereal Foods 24.
World
ANDERSON,
22: 12, 1977. J. W. Effect of carbohydrate
and high carbohydrate diabetes. Am. J. Clin.
diets on men with Nutr. 30: 402. 1977.
restriction
chemical
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/10/S53/4656121 by University of Glasgow user on 15 September 2018
capillaries. This should aid tissue perfusion. No reports have been received of changes in the vascular complications of diabetes. Special attention was paid to the question of whether the improvement of glucose metabolism was related to increased insulin secretion. Further studies by Anderson have indicated that insulin responses are lower in patients eating high-fiber, high-carbohydrate (75% energy) diets than those observed in patients eating how-fiber, moderate-carbohydrate (44% energy) diets. Improvement in carbohydrate tolerance does not appear to be related to increased insulin secretion but to increased sensitivity to available insulin (23,
AND