Randomized clinical trial of soy formula with and without added fiber in antibiotic-induced diarrhea.

OBJECTIVE: The objective of this study was to examine the effects of soy formulas with and without added soy fiber in children who developed diarrhea while receiving antibiotics. DESIGN: In a masked, randomized parallel study, older infants and toddlers were fed commercial soy formulas with or without added soy fiber for 10 days on occurrence of diarrhea during the administration of antibiotics. Subjects were stratified by feeding (formula versus cow's milk). The primary variables were duration of diarrhea, stool characteristics, and intake. Secondary variables were weight and spit-up. RESULTS: All 45 children who completed the 10-day study received >30% of their caloric intake from formula. Fiber intake from other foods did not differ between groups and averaged 0.5 g/day. Total median fiber intake of the group fed the formula with added fiber was 6.53 g/day. The mean duration of diarrhea was 25.1 +/- 5.2 hours for children fed the formula with added fiber and 51.6 +/- 10.7 hours for those fed the regular formula (P =.0013). CONCLUSION: The duration of antibiotic-induced diarrhea in children fed the soy formula with added soy fiber was significantly reduced.

Influence of purine intake on uric acid excretion in infants fed soy infant formulas.

OBJECTIVE: These studies tested the hypothesis that increasing intake of purines, delivered as RNA from soy protein-based infant formula, would increase urinary uric acid excretion in infants. METHODS: Study One examined the influence of feeding on serum uric acid in a total of 178 infants from four separate trials with infants fed commercial and experimental soy-based and milk-based infant formulas or human milk. Studies Two and Three compared the effect of a standard purine soy formula (STD Purine; 180 mg purines/L from RNA) and a reduced purine soy formula (Reduced Purine; 65 mg purines/L; 26 mg/L from RNA and 39 mg/L from ribonucleotides) on urinary uric acid excretion in infants. In Study Two, 11 infants ranging in age from 16 to 128 days of age were fed both formulas in a random crossover design. Complete 72-hour urine collections were done at the end of each 11-day feeding period. Urinary uric acid excretion was expressed as mmol/day. In Study Three, 33 infants were enrolled before eight days of age and randomized to one of the formulas one week later. Spot urine samples were collected at 28 and/or 56 days of age and urinary uric acid concentration was expressed as mmol/mmol creatinine. RESULTS: In Study One, each of the feedings resulted in mean serum uric acid levels within normal reference ranges. Soy formula led to higher serum uric acid levels than human milk, and human milk to levels indistinguishable from cow milk-based formulas. In Study Two, infants excreted significantly more uric acid in the urine when fed the STD Purine formula compared to the Reduced Purine formula (0.86+/-.04 vs. 0.57+/-.04 mmol/d) (p = 0.006). In Study Three, infants fed the STD Purine formula had a significantly higher concentration of uric acid in their urine compared to those fed the Reduced Purine formula (2.1+/-0.2 vs. 1.4+/-0.1 mmol uric acid/mmol creatinine) (p = 0.0001). CONCLUSION: These data indicate that healthy infants can digest RNA and subsequently absorb the liberated purine ribonucleotides as determined by urinary uric acid concentration.

Growth of newborn, term infants fed soy formulas for 1 year.

Few studies have measured long-term growth in infants fed soy protein-based formulas. The effect of nucleotide (NT) supplementation of soy protein-based infant formulas on growth is unknown. Growth was therefore evaluated in healthy term infants fed a soy protein-based formula (SOY; n = 73), SOY with added NT (72 mg added NT/L) at human milk (HM) levels (SOYN, n = 73), or mixed feeding (MF, n = 67) in a randomized, masked, parallel 1-year feeding study. The MF group (a nonrandomized reference group) was fed HM exclusively from birth to 2 months of age followed by HM and/or a standard milk-based formula (Similac with Iron with no supplemental NTs) to 1 year of age. Results indicated that growth (weight, length, and head circumference) was normal and comparable among the three groups. All three groups had similar plasma albumin (at 2 months of age) and hemoglobin levels (at 12 months of age). Thus, this study demonstrated similar growth in the first year of life among infants fed MF feeding or soy formula with or without supplemental NTs.

Use of soy fiber in acute diarrhea in infants and toddlers.

Soy fiber has been shown to reduce the duration of watery stools during acute diarrhea caused by bacterial and viral pathogens in underdeveloped countries. A randomized blinded clinical trial was conducted with middle-class American children to assess the efficacy of soy fiber-supplemented infant formula. Stool characteristics, intake, and weight were recorded. Infants > 6 months of age (n = 44) fed soy fiber-supplemented formula (Isomil DF) had a significantly shorter estimated median duration of diarrhea (9.7 hours vs. 23.1 hours) than those fed soy formula (Isomil). The use of fiber-supplemented soy formula may reduce the duration of diarrheal symptoms in U.S. infants more than 6 months of age with acute diarrhea.

Effect of dietary fiber (soy polysaccharide) on the severity, duration, and nutritional outcome of acute, watery diarrhea in children.

OBJECTIVE: To assess the effects of dietary fiber (soy polysaccharide) on the severity, duration, and nutritional outcome of acute, watery childhood diarrhea. METHODS: A total of 34 hospitalized Peruvian male infants between 2 and 24 months of age were randomly assigned to receive a soy-protein isolate, lactose-free formula with added soy polysaccharide (group SF, n = 19) or the same diet without added fiber (group S, n = 15). The consumption of formulas, stool amount and consistency, absorption of macronutrients, and change in anthropometric status were measured. RESULTS: Children in both groups were initially similar with regard to age, nutritional status, and prior duration and severity of diarrhea. Four patients in group SF (21%) and two in group S (13%) failed therapy because of recurrent dehydration or severe purging (P = .67). Formula intakes increased slightly during hospitalization (P = .03), but did not vary by dietary group (P = .73). Stool outputs declined significantly (P < .001) during hospitalization, but there were no significant differences by dietary group in either stool wet weight (P = .83) or dry weight (P = .87). Estimated median durations of liquid stool excretion after hospitalization were 43 hours in group SF and 163 hours in group S (P = .003). There were no significant differences in fractional or net absorption of macronutrients or change in anthropometric status by dietary group. CONCLUSIONS: Soy polysaccharide, while not affecting stool output, macronutrient absorption, or nutritional status during acute, watery childhood diarrhea, significantly and markedly reduced the duration of liquid stool excretion.

Prolactin concentrations in serum and milk of mothers with and without insulin-dependent diabetes mellitus.

Diabetes may affect the secretion of prolactin, the principal lactogenic hormone. Because adequate amounts are critical to the establishment of lactation, we assessed the prolactin status of 33 women with insulin-dependent diabetes mellitus (IDDM), 33 women without diabetes, and 11 reference women participating in a study of lactation from 2 to 84 d postpartum. Circulating concentrations of serum prolactin declined temporally for all women and did not differ significantly among any of the groups. During the first postnatal week, milk immunoreactive prolactin concentrations were lower for women with IDDM than for control and reference women and the inverse relationship between lactose and milk prolactin, which was significant at day 2 postpartum for reference women, was delayed until day 14 postpartum for women with IDDM. Early breast-feeding activity, increased breast-feeding frequency, and good glycemic control enhance prolactin secretion and should be promoted during lactation in women with IDDM.

A review of the hormone prolactin during lactation.

The principal lactogenic hormone, prolactin, secreted by the anterior pituitary is critical to the establishment of lactation, milk macronutrient content and milk production. The concentration of circulating prolactin increases during pregnancy so that by the end of gestation, levels are 10 to 20 times over normal amounts. However, prolactin is prevented from exerting its effect on milk secretion by elevated levels of progesterone. Following clearance of progesterone and estrogen at parturition, copious milk secretion begins. The minimal hormonal requirements for normal lactation to occur are prolactin, insulin and hydrocortisone. Prolactin stabilizes and promotes transcription of casein mRNA; may stimulate synthesis of alpha-lactalbumin, the regulatory protein of the lactose synthetase enzyme system; and increases lipoprotein lipase activity in the mammary gland. Prolactin levels decrease as lactation is established but nursing stimulates prolactin release from the pituitary which promotes continued milk production. Prolactin is secreted into milk at levels representative of the average circulating concentration. The physiological significance of milk prolactin to the infant is uncertain. Prolactin exists in three heterogenic forms which possess varying biological activity. The monomer with a molecular weight of 23 kDa is found in greatest quantity and is the principal biologically active form. The pattern of heterogeneity changes during pregnancy to favor even more monomer in proportion to the dimer. However, during lactation, the proportion of the monomer in circulation decreases in response to selective uptake of the monomer by the mammary gland. Over 90 percent of the prolactin in milk is present as the monomer. Prolactin may exert some of its biological effect by a shift in the ratio of active to less active forms of the molecule.

Quality-specific taste changes in multiple sclerosis.

Taste sensitivity in 79 patients with multiple sclerosis (MS) and 65 age- and sex-matched control subjects was measured with a sip-and-spit, suprathreshold scaling, magnitude estimation procedure using six concentrations each of sodium chloride, sucrose, citric acid, and quinine hydrochloride. Results were analyzed with a taste scoring system and by plotting psychophysical functions (log concentration versus log magnitude estimate) normalized to 1.0 M sucrose. Gender did not affect taste scores, but age was inversely related, so the results were analyzed by an analysis of covariance with age as the covariant. There was a significant alteration in taste sensitivity in the subjects with MS for sodium chloride and quinine hydrochloride stimuli but not for sucrose and citric acid; these results were confirmed by a separate analysis of the psychophysical functions. Some of the MS taste scores correlated with MS functional and physical disability scores. Taste sensitivity was not correlated with clinical history or presence of facial symptoms.

Zinc in multiple sclerosis.

Zinc profiles were examined in 68 patients with multiple sclerosis, 62 normal volunteers, and 13 patients with other neurological diseases. Plasma zinc levels were slightly increased in patients with multiple sclerosis and significantly increased in those with other neurological impairments (p less than 0.01), compared with control subjects. Albumin-bound as well as protein-bound zinc levels were normal in all groups tested. The alpha 2 macroglobulin-bound zinc level was significantly lower (p less than 0.01) in patients with multiple sclerosis than in control subjects. Erythrocyte-bound zinc levels were significantly increased (p less than 0.05) in patients with multiple sclerosis when compared with control subjects. Erythrocyte-bound zinc was normal in patients with other neurological impairments. Because erythrocyte-bound zinc levels are relatively independent of daily fluctuations in dietary zinc intake, an increase in these values may suggest alterations in the control mechanisms governing zinc compartmentalization in patients with multiple sclerosis.