Investigation of the Acute Digestive Symptoms Caused by Milks with Different Beta-casein Protein Variants in Dairy Intolerant Persons
thesisposted on 03.01.2019, 19:21 by Muhammed O. Sermet
Cows’ milk generally contains two types of β-casein, A1 and A2 types. A2 beta-casein is recognized as the original beta-casein variant because it was present before a proline to histidine point mutation occurrence in the polypeptide chain at 67th position. A1 and A2 are processed differently by digestive enzymes, and once milk or milk products are consumed, a seven-amino acid bioactive opioid peptide, beta-casomorphin-7, is released as a result of incomplete digestion of A1-beta-casein. This is a single-dose, randomized and double-blinded study. Participants received four different treatments (Regular milk, A2 milk, Jersey cow milk, and lactose free milk) in a randomized order. The lactose free milk acted as a negative control. This study aimed to evaluate tolerance to milks containing different levels of A2 β-casein (Jersey and A2 milks) as compared to commercial A1 (regularmilk containing both A1 and A2 β-casein) and lactose-free milk controls in lactose digesters and maldigesters. Seven subjects completed this double-blinded, randomized, crossover trial. Lactose malabsorption (LM) was determined by breath hydrogen test and milk intolerance were assessed by validated questionnaires. Treatments were fed as a single dose with a 6-day washout period to minimize any residual effects. Each subject was fed milk containing 0.5 g lactose per kg body weight. The pilot data from the seven subjects does strongly suggest greater hydrogen production from commercial A1 milk as compared to lactose-free, A2 and Jersey milks. Regular milk containing high A1 β-casein produced significantly higher hydrogen compared to lactose-free milk from 2 hours until 5hours. This suggests biologically relevant differences in lactose digestion among these milks. In addition, Jersey milk produced significantly higher hydrogen compared to lactose-free milk similar to regular milk between 2 and 6 hours while A2 milk was acting similar to lactose-free milk and did not result in increased hydrogen throughout the same time intervals. Taken together, these results suggest that the amount of A2 β-casein in Jersey milk was not adequate to attenuate the increased hydrogen concentration while pure A2 milk was effective. In this pilot clinical trial, abdominal pain, bloating, flatulence, diarrhea, fecal urgency and total GI symptoms were reported as measures of digestive discomfort. Although the mean values of total GI symptom scores were numerically lower on the lactose free, pure A2 and Jersey group compared to regular milk group, none were statistically different. With seven subjects reported in this pilot data, and a calculated sample size requirement of 26, we can interpret trends that ultimately could result in significant differences as additional subjects complete this protocol.