FAO Nutrition Meetings Report Series 
    No. 46A WHO/FOOD ADD/70.36

    The content of this document is the result of the deliberations of the
    Joint FAO/WHO Expert Committee on Food Additives which met in Rome,
    27 May - 4 June 19691

    Food and Agriculture Organization of the United Nations

    World Health Organization

    1 Thirteenth report of the Joint FAO/WHO Expert Committee on Food
    Additives, FAO Nutrition Meetings Report Series, in press;
    Wld Hlth Org. techn.  Rep. Ser., in press.


    Biochemical aspects

    In vitro tests with lipase showed ready hydrolysis into stearic and
    lactic acid (Hodge, 1961). Rats fed the sodium or calcium salt
    excreted only traces of lactate in the faecal fat showed good
    utilization of the stearic acid moiety and of the calcium (Hodge,

    Experiments comparing the metabolism of a mixture of 1 stearic acid
    and C14 labelled lactic acid with stearoyl lactylate containing C14
    in the lactic acid moiety, showed that 58 per cent. of the C14 in the
    physical mixture was excreted in the first 24 hours as CO2 through
    the lungs and 61 per cent. of the lactic acid moiety similarly. There
    was no difference in C14 distribution and excretion in animals
    receiving lactate in either form. Thus lactate derived from stearoyl
    lactylate is metabolized normally after prompt and quantitative
    release prior to absorption (Hodge, 1961).

    Acute toxicity

    Four out of eight rats given 30 g/kg body-weight stearoyl lactylate
    acid died but all eight rats in each group given 20 g or 25 g/kg
    body-weight survived. This is not a true LD50 estimation because much
    unabsorbed material was found in the stomach of the dead animals
    (Hodge, 1961).

    Short-term studies

    Rat. Calcium stearoyl lactylate was fed to groups of five male rats
    at levels of 0.5 per cent., 2.0 per cent. and 12.5 per cent. in their
    diet for 43 days. At the two per cent. level and 12.5 per cent. level
    the relative liver weights were increased.

    In a similar experiment on groups of 10 male and 10 female rats
    calcium stearoyl lactylate was fed in the diet at levels of 0.5 per
    cent., 5.0 per cent. and 12.5 per cent. for 98 days. Growth was
    retarded at 5 per cent. and 12.5 per cent. and the relative weights of
    liver, stomach, heart, spleen and brain were increased at 12.5 per
    cent. No histological abnormalities were seen in kidneys, brain, lung,
    spleen and liver, but at the 12.5 per cent. level lipogranulomata were
    detected in the adipose tissue. No increase in stainable liver fat was
    seen. Urinalysis and blood morphology were normal. Radiological
    studies of femurs were normal indicating that the additional calcium
    in the diet had no effect on body load (Hodge, 1961). Ten male rats
    received five per cent. calcium stearoyl lactylate in their diet and
    developed slightly greater relative liver weights. On the other hand,
    20 male rats fed five per cent. sodium stearoyl lactylate showed no
    difference in relative liver weight between test and control rats.

    Twenty male rats received 5 per cent. sodium stearoyl lactylate for 28
    days with 20 controls on stock diet. After 28 days the experimental
    group was also returned to normal diet and observed for another three
    months. Groups of five rats were sacrificed 32, 60, 90 and 140 days.
    Relative liver weights were slightly higher in each test group except
    in animals examined after 90 days (Hodge, 1961).

    Further experiments were undertaken to elucidate the effect of
    different levels of calcium stearoyl lactylate on relative liver
    weights as well as the effect of the fat level of the diet ion
    relative liver weights. The relative liver weights became normal when
    rat's returned to stock diets.  When diets contained physical mixtures
    of stearic acid, lactic acid and calcium carbonate instead of calcium
    stearoyl lactylate they produced comparable relative liver weights
    Hodge, 1961).

    Groups of 25 rats received diets containing 0 per cent., 0.1, 1.0 per
    cent., 2 per cent., 3 per cent., 4 per cent., 5 per cent. and 7.5 per
    cent. of calcium stearoyl lactylate. At the two highest levels there
    was growth retardation with relative liver weight increase. Groups of
    five male rats were given diets containing either 15 per cent. lard or
    10 per cent lard + five per cent. calcium stearoyl lactylate for 30
    days. The test group grew at a lower rate but relative liver weights
    were less than in the controls. Groups of 10 rats received diets
    containing five per cent. of calcium palmityl lactylate or calcium
    oleyl lactylate for 30 days. All test groups grew slower and had
    markedly raised relative liver weights compared with five per cent.
    calcium stearoyl lactylate. Kidney weights were normal for all groups
    and histological examination of liver, kidneys and fatty tissues
    revealed no abnormalities in any of these groups (Hodge, 1961),

    The appearance of lipogranulomata and the increased relative liver
    weight are related to the excessive intake of abnormal proportions of
    long-chain fatty acids. The balance between saturated and unsaturated
    fats (S:U ratio) in the human diet is about 0.6 if the diet contains
    30 - 40 per cent. fat. Rats fed diets containing 35 - 50 per cent.
    saturated fatty acid products (palmitic acid, stearic acid,
    ethylstearate, monoglycerides and acetylated monoglycerides of
    hydrogenated lard) develop localized fat necrosis with formation of
    lipogranul omata. The condition is preventable by simultaneous feeding
    of cornoil and reversible by a return to normal diet (Cox & De Eds,
    1958; Herting & Crain, 1958; Ambrose et al., 1958).

    Groups of five rats were maintained for periods up to six months on
    diets containing varying levels of calcium stearyl dilactylate (3 per
    cent. - 25 per cent.) and stearoyl lactylic acid (8 per cent. - 22 per
    cent.). The total fat content was 20 per  cent. The outcome depended
    on the S:U ratio. The added fats were chosen to give ratios from 0.6
    to 4.4. Growth was depressed with increasing percentage of calcium
    stearoyl lactylate at 16 per cent. and higher levels and with 14 per
    cent, and above, for the acid. Mortality was high at levels of 20 per
    cent. and above. Relative liver weights were normal at S:U ratios of

    0.6 (17 per cent. fat + 3 per cent. calcium stearoyl lactylate or 17
    per cent. fat + 2.6 stearoyl lactylic acid) but rose with higher
    ratios. Lipogranulomata appeared at ratio values beyond 1.4. The
    iodine number of depot fats reflected the variation in S:U ratio of
    the diet.  Restoration to the basal ration containing 20 per cent. fat
    caused disappearance of lipogranulomata in four - six months. No
    histopathological abnormalities were seen (Hodge et al., 1964). In a
    repeat experiment with 40 male and 40 female rats fed 25 per cent.
    calcium stearoyl lactylate or 118 per cent. stearoyl lactylic acid in
    their diet, all animals developed severe lipogranulomata with high
    mortality. Recovery was rapid if animals were placed on basal diet
    containing 20 per cent. fat (half cornoil, half lard). Growth rate
    recovered and any deaths occurring were unrelated to the diet (Hodge,

    Dog. One male and three female beagles were fed a diet containing
    7.5 per cent. calcium stearoyl lactylate; another group of one male
    and three females acted as controls.  After two years no noteworthy
    differences were observed between the two groups. Urinalysis and
    haematological findings remained normal. No gross or microscopic
    tissue changes were found attributable to administration of calcium
    stearoyl lactylate. Liver weights were within normal range; nor did
    the livers differ in moisture, protein, lipids, ash or glycogen. Other
    organ weights were also normal. No adverse effects were observed in
    one dog receiving sodium stearoyl lactylate in his diet for one month
    at a level of 7.5 per cent., then increased to 12.5 per cent. for two
    weeks and to 15 per cent. for another month. No changes occurred in
    the blood; organ weights and the microscopic appearance of the tissues
    were normal (Hodge, 1961).

    Long-term studies

    None available.


    The metabolism of these substances has been studied satisfactorily.
    Despite the absence of long-term feeding studies it is possible to
    proceed with their evaluation. Extensive short-term studies in rats
    have shown that at levels below two per cent. in the diet there is no
    effect on growth or relative liver weight. The dog appears to be a
    less sensitive species. It would be desirable to carry out metabolic
    studies in man to ascertain species differences.


    Level causing no toxicological effect in the rat.

    0.5 per cent. (=  5000 ppm) in the diet equivalent to 250 mg/kg body-
    weight per day.

    Estimate of acceptable daily intake for man

                                            mg/kg body-weight

    Temporary acceptance                          0 - 2.5

    Further work required by June 1972

    See specification Ref. 19, Annex 1.


    Ambrose, A. M., Robbins, D. J. & Cox, A. J. (1958) Fd Res., 23, 536

    Cox, A. J. & De Eds, F. (1958) Amer. J. Path., 34, 263

    Herting, D. C. & Crain, R. C. (1958) Proc. Soc. exp. Biol. (N.Y.),
    98, 347

    Hodge, H. C., Maynard, E. A., Downs, W. L. & Panner, B. (1964) 
    Toxic. appl. Pharmac., 6, 350

    Hodge, H. C. (1961) Unpublished report to the C. J. Patterson Co.
    submitted by Markel, Hill & Byerley, 1969

    See Also:
       Toxicological Abbreviations