Cow's Milk Free Diet Research Articles

Cow's milk-free diet does not prevent diabetes in NOD mice

Cow's milk-free diet does not prevent diabetes in NOD mice

Cow's milk-free diet does not prevent diabetes in NOD mice.

Early dietary exposure to cow's milk proteins has been proposed as an important environmental factor in the development of IDDM both in humans and in diabetes-prone rodents. To examine the significance of cow's milk protein in IDDM, 120 NOD mice were maintained, starting from conception until sacrifice, on one of four diets: standard PMI Picolab Rodent Diet 20, a milk-free modification of the standard Picolab diet, a milk-free diet incorporating 0.036% bovine serum albumin (BSA), and a milk-free diet including 0.036% bovine IgG (BGG). The cumulative IDDM incidence at 7 months for these mice in a specific pathogen-free environment on the respective diets was 78, 93, 93, and 67% for females, and 17, 54, 17, and 0% for males. The ages of diabetes onset and insulitis scores were similar for mice on each diet. The unexpectedly lower incidence of IDDM in mice on the milk-free diet that included BGG raises the possibility this cow's milk protein might possibly have some protective effect against the development of IDDM in NOD mice. Our main finding was that the standard, milk-free, and BSA-containing diets resulted in comparable incidences of IDDM in NOD mice, demonstrating that neither cow's milk whey proteins in general nor BSA in particular are significantly important as etiologic dietary agents in IDDM in NOD mice.

FOUR CHILDREN AFFECTED BY IDIOPATHIC PARTIAL EPILEPSY IMPROVEMENT FOLLOWING A COW'S MILK PROTEINS FREE DIET.

The possibility that certain foods or allergens may induce convulsions has already been reported in the literature. None of these studies have,however,shown a close correlation between food allergy and epilepsy, most reports being anecdotical and open to various aetiological hypotheses. One exception is the investigation carried out by Crayton in 1981 using a double blind oral provocation test in a single patient in whom the epileptic crises were triggered by,or increased in frequency due to,sensitivity to certain foods (1). The present report concerns 4 children with idiopathic partial epilepsy,diagnosed by means of electroencephalography,with behavioural disorders (hyperactivity,sleep disorders and writing difficulties). In these patients,instead of using anticonvulsivant agents,treatment was based upon a cow's milk free-diet,working on the hypothesis that there could be a causal relationship between intolerance to this food item and the epileptic symptoms. Despite the absence of clinical signs typical of food allergy,all children presented a significantly positive skin reaction to prick tests for cow's milk protein. During the period in which this food item was excluded from the diet,but during which care was taken to ensure an adequate nutritional supply both from a qualitative and a quantitative viewpoint,none of the children presented critical manifestations. An improvement was observed in the children's behaviour and,moreover, the electroencephalographic anomalies disappeared. Upon double blind oral provocation tests,these patients did not present an immediate reaction,but only after a few days. Starting the controlled diet again led, in all cases,to disappearance of the neurological and behavioural symptoms,with a return to normal of the electroencephalogram. Studies were carried out in parallel on 23 children with benign myoclonic or rolandic epilepsy,who showed no benefit from the cow's milk-free diet. In conclusion,it would appear feasible to hypothesize the role of food intolerance in the onset of convulsive crises,even if limited to certain types of epilepsy such as the idiopathic partial form. The multifactorial aspects of idiopathic partial epilepsy,tend to suggest that the complex immunological mechanism regulating the allergic reaction may play an important role in the understanding of epileptic phenomena.

Gastroesophageal reflux and cow's milk allergy in infants: A prospective study

Recent reports have suggested that gastroesophageal reflux in pediatric patients may be caused by food allergy. The aim of our study was to determine the frequency of the association of gastroesophageal reflux with cow's milk protein allergy in patients win the first year of life. We studied 204 consecutive patients (median age, 6.3 months) who had been diagnosed as having gastroesophageal reflux on the basis of 24-hour continuous pH monitoring and histologic examination of the esophageal mucosa. Clinical history suggested diagnosis of cow's milk allergy in 19 infants, and 93 others had positive test results (serum IgE anti-lactoglobulin, prick tests, circulating or fecal or nasal mucus eosinophils) but did not have symptoms indicating cow's milk allergy. The cow's milk-free diet and two successive blind challenges confirmed the diagnosis of cow's milk allergy in 85 of the 204 patients with gastroesophageal reflux. The clinical presentations of the infants with gastroesophageal reflux alone were different, in view of the greater frequency of diarrhea (p less than 0.0001) and atopic dermatitis (p less than 0.0002). In all, gastroesophageal reflux was associated with, and probably caused by cow's milk allergy, in 85 of 204 cases (41.8%). Considering the frequency of this association, patients younger than 12 months old with symptoms of gastroesophageal reflux should be carefully examined to determine whether this disorder is primary or caused by cow's milk allergy.

In vitro lymphocyte proliferation with milk and a casein–whey protein hydrolyzed formula in children with cow's milk allergy

Discordant results have been reported about the role of lymphocyte proliferation assays in patients with cow's milk allergy. We studied the peripheral blood mononuclear cell response of 10 children with cow's milk allergy by means of a lymphocyte proliferation test to determine the diagnostic value of this assay, the clinical tolerance of a new therapeutic hydrolyzed formula, and the evolution of lymphocyte proliferation after 3 months of a cow's milk–free diet with the hydrolyzed formula. The lymphocyte proliferation at the time of diagnosis in the patients with cow's milk allergy was not statistically different from the results in the control group. The proliferation test performed after 3 months of diet with the hydrolyzed formula and restriction of cow's milk protein showed that the cellular proliferation remained globally the same compared with the proliferation at the time of diagnosis. The hydrolyzed formula proteins induced a lower cellular proliferation than milk proteins in patients with cow's milk allergy. Our results suggest that the lymphocyte proliferation test cannot be recommended for diagnostic purposes. However, in patients with cow's milk allergy the proliferation test affirmed the absence of immunogenicity of the hydrolyzed formula because it induced no significant T-cell activation. ( J Allergy Clin Immunol 1995;96:549-57.)

The role of cow's milk protein intolerance in steroid-resistant nephrotic syndrome.

The role of cow's milk protein intolerance in steroid-resistant nephrotic syndrome was evaluated in 17 children. Cow's milk was excluded from the diet for at least 14 days without changing previously ineffective prednisone dosage. Six patients with minimal change or mesangial proliferation went into remission 3 to 8 days after elimination of cow's milk. After a period of 2-3 weeks of remission, cow's milk challenge was positive in three patients. After one year on a cow's milk-free diet, two of six patients became milk tolerant and are in remission of NS, one of six became steroid-dependent, two of six are still unable to tolerate cow's milk and are in remission on a cow's milk-free diet and one of six children was lost from observation. The role of cellular mechanisms in steroid-resistant nephrotic syndrome is suggested.

Cow milk-sensitive enteropathy: Predisposing factors and treatment

Cow milk-sensitive enteropathy is a temporary disorder of infancy characterized by a variably abnormal small intestinal mucosa while milk is in the diet. This abnormality is reversed by a cow milk-free diet, only to recur on challenge. Important predisposing factors are age (< 3 years), transient IgA immunodeficiency, atopy, and early bottle feeding. The disorder is diagnosed histologically by evidence of mild-to-moderate partial villous atrophy with thin, often patchy mucosa. For an accurate clinical diagnosis, challenge with the offending food after a demonstrated response to cow milk elimination is critical. When available, serial small intestinal bowel biopsies related to elimination and challenge are also important. Treatment is elimination of cow milk and all foods based on cow milk, and substitution of cow milk feedings with commercially available formulas free of cow milk protein. Five types of cow milk substitutes are described; only nutritionally complete formulas are recommended. Later, a milk challenge will determine the timing of safe reintroduction of cow milk to the diet, at a time when the child is gaining weight, thriving, and symptom free. This dietary treatment is always temporary; reintroduction of a normal diet is nearly always possible between 1 and 2 years of age.

Soy Milk Induced Nutritional Rickets: A Case Report

A two-year-old boy is described with iatrogenically induced nutritional rickets. Without adequate dietetic advice he had been placed on a cow's milk free diet from eight months and given a nutritionally inadequate soy milk from a health food store.

Evaluation of a casein and a whey hydrolysate for treatment of cow's-milk-sensitive enteropathy.

A casein and a whey hydrolysate were evaluated in the management of 18 children with cow's-milk-sensitive enteropathy. This diagnosis was based upon clinical features, an abnormal small intestinal mucosa, i.e. an enteropathy, and a clinical response to cow's milk elimination. Two infants refused to take the whey hydrolysate. The median weight gain was higher in children given whey hydrolysate (19.4 g/day) than the casein hydrolysate (9.8 g/day). All children responded to cow's milk elimination and most had a significant improvement in small intestinal morphology after a cow's-milk-free diet. There was some advantage for the whey hydrolysate on morphometric analysis of their small intestinal mucosal response.

EFFECTS F GLIADIN ON THE INTESTINAL MUCOSA IN PATIENTS WITH CELIAC DISEASE (CD)

The influences of gliadin on the function of the intestinal mucosa were studied in children with enteral protein intolerances in a prospective study. Group la* CD, n=14, gluten free diet for 1-2 months (m), histol. findings: type II-III according to SHMERLING. Group 1b: n=8, diet for 10-36 m, type I-II. Group II: Cow's milk protein intolerance, n=7, cow's milk free diet for 1-2 m, type II-III. Method: The netto water flux and the absorption and digestion rates of sugars were determined by perfusion of the upper jejunum immediately before and 2 up to 6 and 24 hrs after enteral infusion of gliadin. Result: 24 hrs after gliadin infusion the digestion and absorption rates of carbohydrates decrease only in the patients with time of treatment of 1-2 m whereas there are no effects in the patients with treatment logner than 10 m. The netto water secretion increases immediately after starting the gliadin infusion independent on time of treatment. Conclusion: the data suggests that different cell populations are influenced by gliadin in CD-patients.

Cow's Milk Whey Protein Elicits Symptoms of Infantile Colic in Colicky Formula-Fed Infants: A Double-Blind Crossover Study

There are several causes of infantile colic. The aim of this study was to evaluate, under controlled conditions, whether bovine whey proteins can elicit symptoms of infantile colic in colicky formula-fed infants. The mean age for entering the study was 6.4 weeks and the mean age for colic debut was 3.7 weeks. In 24 of 27 infants with severe colic, the symptoms disappeared when they were given a cow's milk-free diet (Nutramigen). These 24 infants were entered into a double-blind crossover study. The infants (receiving cow's milk-free diet) were given the contents of identical capsules with each meal during day 6. The same procedure was repeated on day 10. The capsules contained either whey protein powder (with Nutramigen added) or human albumin powder (with Nutramigen added). Eighteen infants receiving the whey protein-containing capsules reacted with colic, two infants receiving placebo reacted with colic (P less than .001), and four infants did not react at all. Crying hours per day for the 24 infants were 5.6 hours for formula-fed infants and 0.7 hour for cow's milk-free diet-fed infants (P less than .001). Crying hours per day were 3.2 hours for the infants receiving whey protein capsules and 1.0 hour for those receiving placebo (P less than .001). In conclusion, bovine whey protein can elicit symptoms of infantile colic in colicky formula-fed infants.

Prospective study of colitis in infancy and early childhood.

Ten of a total of 106 children with chronic inflammatory bowel disease seen between 1973 and 1983 were aged 3 years or less (9%). These are the subject of this study. Colonoscopy and biopsy revealed ulcerative colitis in two, Crohn's disease in two, cow's milk-induced colitis in two, and colitis of indeterminate type in four. The children were followed up and reassessed 2 years post-treatment. The four children with ulcerative colitis and Crohn's disease were asymptomatic 6 months after treatment with sulfasalazine and/or prednisolone. The two breast-fed infants with allergic colitis who were treated with cow's milk-free diet in baby and mother showed clinical, endoscopic, and histological resolution. One of the remaining four children with indeterminate colitis is well and off all treatment, and two are well with minimal symptoms and taking sulfasalazine. One child continued to have frequent relapses and subsequently had subtotal colectomy performed with clinical improvement. Histopathology showed features suggestive of intestinal Behcet's disease. The present study shows that colonoscopy and mucosal biopsy allow a firm diagnosis to be established in 60% of cases of this selected group of very young children. In our experience colitis in infancy and early childhood appears to be a heterogeneous group of conditions. An initial assessment of indeterminate colitis should be followed with multiple mucosal biopsies to attempt further categorization.

Cow's milk protein allergy and gastro-oesophageal reflux.

Evidence for cow's milk allergy was looked for prospectively in 15 children with recurrent vomiting. Whereas radiological examination showed gastro-oesophageal reflux to be present in all patients, 3 out of 15 children presented an enteropathy associated with an increased number of IgE plasmocytes in small intestinal biopsy tissue. These three patients did not improve with conventional medical therapy but a striking improvement occurred within 24 h on a cow's milk-free diet. We conclude that diagnostic confusion between gastro-oesophageal reflux and cow's milk allergy can occur and that the presence of IgE plasmocytes in small intestinal biopsy tissue indicates IgE-mediated cow's milk protein allergy. All cases of "intractable" gastro-oesophageal reflux should be suspected of cow's milk allergy and investigated accordingly.

Dietary bovine beta-lactoglobulin is transferred to human milk.

Human milk from 38 mothers was analysed by radioimmunological method for content of bovine beta-lactoglobulin. Detectable amounts (5-33 micrograms/l) of immunoactive beta-lactoglobulin were found in 18 human milk samples. Milk from 3 mothers, whose infants suffered from infantile colic contained high amounts of beta-lactoglobulin (32, 18 and 14 micrograms/l respectively). With the mothers on a cow's milk free diet the contents fell to non-detectable amounts in two mothers and to 6 micrograms/l in the third. All three infants became free from colic.

Gastrointestinal occult hemorrhage and gastroduodenitis in cow's milk protein intolerance.

We are reporting on four infants with cow's milk protein intolerance who presented with hypochromic anemia and occult gastrointestinal hemorrhage. Esophagogastroduodenoscopy revealed erosive gastritis or gastroduodenitis in all cases. Management with a cow's milk-free diet led to a favorable clinical and hematological outcome; the endoscopic inflammatory image disappeared after the cow's milk-free diet trial. Challenge with cow's milk led to gastrointestinal symptoms and to impaired D-xylose absorption. The data presented suggest that some patients with cow's milk intolerance may have gastroduodenitis resulting in occult gastrointestinal hemorrhage and hypochromic anemia.

Do pre- and postchallenge small intestinal biopsies help to diagnose cow's milk protein intolerance?

Twelve infants suspected of cow's milk protein intolerance were challenged with cow's milk after at least one month of cow's milk-free diet. The challenge was clinically positive in seven. Small intestinal biopsies were taken with a multipurpose capsule both pre- and postchallenge (at 24 h) in eight, prechallenge in three, and postchallenge in one. Two or three biopsy specimens were taken at the same time in 15 of the 20 biopsy occasions. The morphology of the mucosa could vary from normal to slight damage at the same biopsy occasion. No difference was found in morphology judged by light microscopy between pre- and postchallenged biopsies. Light microscopy of small intestinal biopsies taken before and at 24 h after milk challenge seems of doubtful value as a routine diagnostic means in cow's milk protein intolerance.

Cow's milk intolerance presenting as necrotizing enterocolitis: E. de Peyer and J. Walker-Smith. Helv Paediatr Acta 32:509–515, 1977

Case history is reported of an infant who was changed from breast to bottle feeding at fourth day of life, who on ninth day developed bilious vomiting and bloody diarrhoea. Later gas was found in colonic wall on X-ray. Necrotizing enterocolitis was diagnosed and infant managed with total intravenous alimentation. On recovery although she tolerated breast milk, return to cow's milk formula lead to return of bloody diarrhoea. Subsequently she thrived on a cow's milk-free diet based on chicken meat formula. At four months after total of 15 ml cow's milk she had an acute anaphylactic reaction. She recovered and is well on milk-free diet. Thus, this infant has recovered from necrotizing enterocolitis but has evidence of persistent cow's milk protein intolerance. The hypothesis is put forward that in this child cow's milk protein played a major role in the pathogenesis of necrotizing enterocolitis.

UPPER AIRWAY OBSTRUCTION AND HEART FAILURE IN PATIENTS WITH HEINER'S SYNDROME

Two conditions, right heart failure secondary to upper airway obstruction and pulmonary hemosiderosis with serum precipitins to cow's milk (Heiner's Syndrome), have been simultaneously documenred in 3 children. A total of 6 patients with Heiner's Syndrome were found by screening for multiple precipitins in 160 consecutive children with idiopathic chronic lung disease. All 6 were black; 3 were infants and 3 were 1-4 years of age. All had normal or elevated serum immunoglobulins, normal sweat chlorides, and AA or AS hemoglobin. None were clearly predisposed to aspiration. All displayed typical manifestations of Heiner's Syndrome; recurrent pulmonary infiltrates (6/6), hemosiderin-laden macrophages (5/6), intermittent wheezing (4/6), eosinophilia (4/6), iron deficiency (4/6), and failure to thrive (4/6). The 3 older patients also manifested chronic rhinitis, large adenoids, evidence of right heart failure, hypercapnia and acidosis during sleep, and pulmonary/systemic resistance ratios of 1/2 to 1/3 with resultant mean pulmonary artery pressures from 35-45 mmHg. Symptomatic therapy, a cow's milk-free diet, and adenoidectomy when indicated led to improvement in all patients. Heiner's Syndrome and upper airway obstruction with pulmonary hypertension may be two stages, early and delayed, of the same process. Early dietary intervention may prevent cardiac complications and CO2 narcosis in children with this process.