Essential fatty acids in breast milk of atopic mothers: comparison with non-atopic mothers, and effect of borage oil supplementation.

OBJECTIVE: To evaluate whether levels of n-6 long chain polyunsaturated fatty acids (LCPs) in human breast milk are related to the mother's atopic constitution, and whether a decreased level can be restored by gamma-linolenic acid supplementation. DESIGN: Cross-sectional study and dietary supplementation trial. SUBJECTS: 20 atopic mothers and 20 non-atopic mothers (controls), all lactating. SETTING: General population. INTERVENTIONS: The atopic mothers were randomly assigned to low (n=10) or high (n=10) dosage oral supplementation with oral borage oil for one week (230 or 460 mg gamma-linolenic acid (18:3n-6) per day). MAIN OUTCOME MEASURES: Essential fatty acid composition of the breast milk total fat fraction, determined by gas liquid chromatography. RESULTS: Arachidonic acid (20:4n-6) was lower in breast milk of atopic mothers compared with non-atopic mothers (0.39 wt% vs 0.46 wt%, difference -0.07% wt% (95% confidence limits -0.13, -0.01 wt%; P<0. 05). The ratio between linoleic acid and the sum of n-6 derivatives did not differ between these groups, indicating no difference in delta-6-desaturase (D6D) activity. Supplementation of the atopic mothers significantly increased the levels of gamma-linolenic acid and dihomo-gamma-linolenic acid in breast milk in a dose-related way, but the level of arachidonic acid was not increased. CONCLUSION: We found a decreased level of arachidonic acid in breast milk in atopic compared to non-atopic mothers, but no indication that the rate-limiting enzymatic step (D6D) is involved. Supplementation increased the precursor pool but did not restore the level of arachidonic acid. We conclude that atopy is related to a metabolic disturbance beyond the D6D enzymatic step. A low level of arachidonic acid in breast milk may be a risk factor for the development of atopy in the infant, especially when the possible underlying metabolic disturbance of EFA metabolism is inherited by the child. SPONSORSHIP: F Hoffman-La Roche (Basel, Switzerland) and Friesland Dairy Foods (Leeuwarden, The Netherlands).

The shape of the cumulative food intake curve in humans, during basic and manipulated meals.

The shape of the cumulative food intake curve of normal weight and obese women was studied during solid food lunches, artificially prolonged meals, and energetically enriched meals eaten in a laboratory setting. Subjects (86 normal weight, 50 obese) displayed consistent eating behaviour over 3-6 repeated meals, with marked differences between individuals. Aspects of eating behaviour were reflected in decelerated and nondecelerated (or linear) cumulative intake curves depending on changes or no changes in eating rate during the course of a meal, respectively. A change in eating rate was generally related to decrease in bite size, with bite rate remaining constant, from the third temporal quarter of the meal onwards, resulting in a decelerated cumulative intake curve. The nondecelerated (linear) cumulative intake curve does not show this change in eating rate: in the first three temporal quarters bite size and bite rate were constant, whereas in the fourth temporal quarter bite size decreased slightly, compensated by a small increase in bite rate. Intraindividual ranges for meal parameters such as chewing time per bite, bite interval and initial eating rate indicated consistency of individual eating behaviour. In manipulation experiments with a subset of 21 subjects in which meals were artificially prolonged by an interval of 8 min, the cumulative intake curves did not differ significantly from the original cumulative intake curves in 10 nondecelerated (linear) eaters, but showed a change towards nondecelerated curves in 8 out of 11 decelerated eaters.(ABSTRACT TRUNCATED AT 250 WORDS)

Obesity, restrained eating and the cumulative intake curve.

The cumulative intake curves of 50 obese and 86 normal weight women during test meals were related to body mass index, age and the three factors of Stunkard & Messick's questionnaire (Journal of Psychosomatic Research, 29, 71-83), cognitive restraint, disinhibition and perceived hunger. Eating behaviour was monitored by a concealed camera and rate of intake via an electronic balance built into the table under the plate. The eating behaviour of each subject was very consistent over a series of three or six lunches of the same solid food consumed solitarily in a constant environment, with marked differences between subjects. Differences in body mass index over the whole sample were not related to the shape of the cumulative intake curve during test meals. In multiple regression analysis, the normal-weight subjects who scored high on disinhibition of restraint in response to emotions and external influences showed a more nearly constant rate of intake. In a separate multiple regression, the overweight subjects with the same characteristic showed a decelerating rate of intake. Susceptibility to hunger had no discernible relationship to the shape of the cumulative intake curve in either normal or overweight subjects. We conclude that the shape of the cumulative intake curve can be attributed more to cognitive than to biological factors.