Abstract
True lactose intolerance (symptoms stemming from lactose malabsorption) is less common than is widely perceived, and should be viewed as just one potential cause of cows’ milk intolerance. There is increasing evidence that A1 beta-casein, a protein produced by a major proportion of European-origin cattle but not purebred Asian or African cattle, is also associated with cows’ milk intolerance. In humans, digestion of bovine A1 beta-casein, but not the alternative A2 beta-casein, releases beta-casomorphin-7, which activates μ-opioid receptors expressed throughout the gastrointestinal tract and body. Studies in rodents show that milk containing A1 beta-casein significantly increases gastrointestinal transit time, production of dipeptidyl peptidase-4 and the inflammatory marker myeloperoxidase compared with milk containing A2 beta-casein. Co-administration of the opioid receptor antagonist naloxone blocks the myeloperoxidase and gastrointestinal motility effects, indicating opioid signaling pathway involvement. In humans, a double-blind, randomized cross-over study showed that participants consuming A1 beta-casein type cows’ milk experienced statistically significantly higher Bristol stool values compared with those receiving A2 beta-casein milk. Additionally, a statistically significant positive association between abdominal pain and stool consistency was observed when participants consumed the A1 but not the A2 diet. Further studies of the role of A1 beta-casein in milk intolerance are needed.
Highlights
There is a widespread assumption within both general society and among healthcare professionals that the dominant cause of milk intolerance is insufficient lactase enzyme activity
The in vivo release of BCM-7 from each liter of bovine milk will depend on the protein content of the (which is in turn affected by the breed, animal feeding and component standardization procedures during milk, the proportion of A1 and A2 beta-casein, and possibly the specific gastrointestinal during milk processing), the proportion of A1 and A2 beta-casein, and possibly the specific conditions of the individual
It is important to note the considerable advancements relating to A1 beta-casein and BCM-7 that have been made since the European Food Safety Authority (2009) report on the possible health effects of beta-casomorphins and BCM-7 [10]
Summary
There is a widespread assumption within both general society and among healthcare professionals that the dominant cause of milk intolerance is insufficient lactase enzyme activity. The evidence, as summarized in the 2010 National Institutes of Health consensus statement on lactose intolerance and health, is that “many who self-report lactose intolerance show no evidence of lactose malabsorption. The cause of their gastrointestinal symptoms is unlikely to be related to lactose” [1]. There is an increasing body of evidence that bovine beta-casomorphin-7. (BCM-7), derived from A1 beta-casein, is an important contributor to milk intolerance syndrome. It is that evidence that we discuss here, including the potential for interactions between lactose intolerance and A1 beta-casein intolerance
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