This substance has been evaluated for acceptable daily intake by
the Joint FAO/WHO Expert Committee on Food Additives in 1969, 1973,
1977 and 1980 (see Annex I, Refs. 19, 32, 43 and 54). Toxicological
monographs were issued in 1969 and 1973 (see Annex I, Refs. 20 and
Since the previous evaluation, additional data have become
available and are summarized and discussed in the following monograph.
The previously published monograph has been expanded and is reproduced
in its entirety below.
Absorption and metabolism
Karaya gum does not disintegrate or decompose appreciably in the
alimentary tract. In a study of 10 dogs, 95% of the orally
administered gum was recovered in the faeces. It absorbs a large
quantity of water and therefore acts as a mechanical laxative. It
tends to increase faecal nitrogen excretion, does not affect starch
digestion in the dog and does not inhibit the utilization of vitamin A
in rats (Ivy & Isaacs, 1938).
The caloric value was determined in groups of 10 rats fed for one
week 5 g basal diet with either 1 g and 3 g corn starch or 1 g and 3 g
karaya gum supplements. At the i g level, karaya gum only had 30% of
the caloric value of corn starch. At the 2 g level growth was very
depressed. The intestine was enlarged in all rats on gum (Anon.,
The action of 10 species of Bacteroides found in the human colon
on dietary fibre has been studied. Karaya gum is not utilized by these
bacteria and remains unchanged (Salyers et al., 1977).
Fermentations of 10 polysaccharides by species of the family of
Enterobacteriaceae were examined. Karaya gum was not fermented by any
of the strains tested. As food additive, karaya gum seems safe from
destruction by facultative fermenters (Ochuba &von Riesen, 1980).
Two groups of four male rats (365-459 g) were fed pelleted diet
containing 5% (w/w) karaya gum over a 24-hour period. Urine and faeces
from each animal were collected and weighed after 24, 48 and 72 hours.
Faeces were examined, after methanolysis, by GC-MS and the quantity
and monosaccharide composition of the faecal polysaccharides were
compared with the dose and original composition of the gum
polysaccharides. It was estimated that 95% of the gum consumed was
recovered as faecaI polysaccharide. Rhamnose was not detected in the
urine. The absence of this component demonstrates that it is not
liberated from karaya gum during its transit through the intestine.
These two findings indicate that extensive degradation involving
chains and chain terminations did not occur. The study has not
produced any evidence suggesting metabolic modification of karaya gum
in the intestinal tract of the rat when the gum is added to a normal
rat diet (Brown et al., 1982).
Special studies on mutagenicity
The host-mediated assay of karaya gum did not produce any
measurable mutagenic response or alteration in the recombination
frequency of Saccharomyces cerevisiae in either host-mediated assay
or the associated in vitro tests. The cytogenetic assay of karaya
gum exhibited no adverse effect on either metaphase chromosomes from
rat bone marrow or anaphase chromosomes from in vitro cultures of
human embryonic lung cells at any of the dose levels or time periods
tested. No consistent responses Occurred in the dominant lethal gum
test to suggest that karaya gum is mutagenic to the rat as a result of
this experimental procedure (Newell & Maxwell, 1972, available in
The acute oral LD50 of 12 food-grade gums (sodium and calcium
carragheenate, tragacanth, ghatti, locust bean, arabic, guar, karaya,
propylene glycol, alginate, furcellaran, agar-agar and Na
carboxymethylcellulose) was studied. Each material was administered by
gavage to five groups of 10 rats, with five males and five females in
each group. Vehicles utilized were water, mineral oil, corn oil and
soybean oil. The animals were fasted 18 hours prior to dosing with
food and water available ad libitum during the 14-day observation
period. LD50 values observed ranged from 2.6 to 18.0 g/kg with most
values in the 5-10 g/kg range. Generally, the rabbit was the most
sensitive species and the rat and mouse the least sensitive (Bailey et
al., 1976, available in summary only).
Examination of the intestine of rats fed 1 g karaya gum per day
for 91 days showed no gross abnormalities. There was no interference
with normal growth (Ivy & Isaacs, 1938).
Karaya gum was used in a six- to seven-week feeding study to
evaluate the effect on adaptive responses of nutritionally controlled
parameters in rats by feeding a fibre-free diet containing increasing
additions of polysaccharides (0, 10, 20 and 40%). In general, the
supplements reduced weight increases due to lower energy intakes. None
of the polysaccharides fed, however, decreased energy utilization.
Similarly, all polysaccharides increased small intestine length up to
about 30% without grossly altering mucosal protein and DNA per unit of
length. Concerning the effect on the large intestine, the addition of
karaya gum at 10, 20 and 40% level caused average increases of the
weight of the colon by a factor of 1.4, 1.9 and 2.9 respectively
(Elsenhaus et al., 1981).
Karaya gum was given to groups of 15 rats of each sex at levels
of 0 (control), 0.2, 1.0 and 5.0% (w/w) in the diet for 13 weeks (5%
is the top level recommended for substances that are not absorbed). An
increase in faecal bulk was seen in all treated groups throughout the
experiment. There was a decrease in weight gain at the highest dietary
level (significant only in the females) which was associated with a
marginal reduction in food conversion efficiency. Males given 1 or 5%
gum drank more than the controls and a transient increase in water
intake was seen in females given the highest level. The no-untoward-
effect level from this study was 5% of the diet, providing a mean
intake of approximately 4 g karaya gum/kg bw per day (Taupin &
Three dogs were fed 5 g unprocessed karaya gum daily for 30 days.
Defaecations were not frequent, faecal bulk and moisture were
increased but there was no obvious gastrointestinal irritation (Ivy &
Five rats were fed karaya gum in the diet for two years. Three
developed enlarged colon and ulceration (Hoelzel et al., 1941).
In another experiment, groups of three rats were fed karaya gum
at first at 10%, gradually increasing to 25% in the diet over their
life span. Controls of five and seven animals received low residue
diets. No caecal ulceration was found in this experiment (Carlson &
OBSERVATIONS IN MAN
Forty-six female and 46 male subjects took karaya gum granules
for one week at levels equivalent to 7 g/day. Seven subjects had
abdominal discomfort (Ivy & Isaacs, 1938). Ingestion or inhalation was
reported to have caused allergy. Sixteen cases of allergic sensitivity
to inhalation of the gum used as a wave set and to oral ingestion as a
laxative were reported. Symptoms included hay fever, asthma,
dermatitis and gastrointestinal distress (Figley, 1940). In a
comparison with carob bean gum as a laxative in 10 human subjects,
karaya gum was found to be transformed to a gelatinous state at a
higher level in the intestine and to be transported more rapidly
through the intestinal tract (Holbrook, 1951). A case of allergic
respiratory symptoms (nasal congestion, coughing and wheezing)
following exposure to karaya gum powder has been reported in a
27-year-old female nurse employed for three years as an enterostomal
therapist (Wagner, 1980).
The administration of karaya gum to human subjects and the
effects on glucose absorption, caecal and colonic function and routine
haematological and biochemical measurements were studied. Karaya gum
was administered to five fit male volunteers (aged 30-56 years), free
of gastrointestinal disease and symptoms, over a 21-day period. The
dose of 10.5 g was well tolerated. Karaya gum had no significant
effect on wet and dry stool weight, faecal constituents or transit
time. Also, there was no increase in bacterial metabolic activity. It
would appear that the molecule is not significantly degraded during
its passage through the human colon. Karaya gum appears to have little
metabolic effect upon the host: glucose tolerance is not significantly
altered after its ingestion and haematological and biochemical indices
remain unchanged (Eastwood et al., 1982).
Karaya gum is not degraded by strains of bacteria found in the
human colon. An especially designed metabolic study in the rat
demonstrated that karaya gum does not undergo any metabolic
modification in the intestinal tract.
The available short-term study in the rat showed no evidence of
adverse effects at the 5% level. The effects noted in feeding trials
were those expected of a non-metabolized polymeric substance acting as
a bulking agent.
The new data submitted indicate that karaya gum, even ingested in
a relatively large dose, has no toxic effect and also has little
metabolic action of consequence.
Level causing no toxicological effect
Rat: 5% (50 000 ppm) in the diet, equal to 4000 mg/kg bw.
Estimate of temporary acceptable daily intake for man
0-20 mg/kg bw.
FURTHER WORK OR INFORMATION
Required by 1985
Submission of the results of a short-term feeding study in a
Anon. (1964) Unpublished report (No. 3110860/1) from the Wisconsin
Alumni Research Foundation to Stein, Hall & Co.
Bailey, D. E., Morgareidge, K. & Collins, T. X. (1976) Comparative
acute oral toxicity of twelve food grade gums in the mouse, rat,
hamster and rabbit. Food and Drug Res. Labs, Inc., New York; US
Food and Drug Administration, Washington, D.C. - Abst. 15th
Annual Meeting of the S.O.T., Toxicol. appl. Pharmacol., 37,
Brown, P. H., Pringuer, M. A. & Anderson, D. M. W. (1982) A study of
the fate of gum karaya in the rat, Toxicol. Lett., 13,
Carlson, A. J. & Hoelzel, F. (1948) Prolongation of the life span of
rats by bulking agents in the diet, J. Nutr., 36, 27-40
Eastwood, M. A., Brydon, W. G. & Anderson, D. M. W. (1982) The effects
of gum karaya in man. Unpublished report submitted by INGAR to
Elsenhaus, B., Blume, R. & Caspary, W. F. (1981) Long-term feeding of
unavailable carbohydrate gelling agents. Influence of dietary
concentration and microbiological degradation on adaptive
responses in the rat, Am. J. Clin. Nutr., 34, 1837-1848
Figley, K. D. (1940) Karaya gum hypersensitivity, J. Am. Med. Ass.,
Hoelzel, F., Costel, E. & Carlson, A. J. (1941) Production of
intestinal lesions by feeding karaya gum and other materials to
rats, Am. J. dig. Dis., 8, 266-270
Holbrook, A. A. (1951) The behaviour of carob gum in the
gastrointestinal tract of man, Am. J. dig. Dis., 18, 24-28
Ivy, A. C. & Isaacs, B. L. (1938) Karaya gum as a mechanical laxative.
An experimental study on animals and man, Am. J. dig. Dis.,
Newell, G. W. & Maxwell, W. A. (1972) Mutagenic effects of sterculia
gum (karaya). Stanford Res. Inst.; US Nat. Tech. Inf. Ser., PB
Rep. 1972, No. 221823/8. From Govt. Rep. Announce (US) 1973, 73
(17) 45; C.A. 80: 10842s, 1974
Ochuba, G. U. &von Riesen, V. L. (1980) Fermentation of
polysaccharides by Klebsiellae and other facultative bacilli,
Appl. Environ. Microbiol., 39, 988-992
Salyers, A. A. et al. (1977) Fermentation of mucin and plant
polysaccharides by Bacteroides from the human colon, Appl.
Environ. Microbiol., 33, 319-322
Taupin, P. J. Y. & Anderson, D. M. W. (1982) Subchronic toxicity
study in rats fed gum karaya, Fd Chem. Toxicol., 20, 513-517
Wagner, W. (1980) Karaya gum hypersensitivity in an enterostomal
therapist, J.A.M.A., Feb. 1, 243, No. 5, 432