1. Introduction

Milk is an important source of highly bioavailable calcium as well as protein of good nutritional quality. The main carbohydrate in milk, the disaccharide lactose, is hydrolyzed in the small intestine by the brush border enzyme lactase into glucose and galactose, which are subsequently absorbed [1]. Lactase activity is high in the newborn intestine but is genetically programmed to decrease from weaning, resulting in residual levels in adults. This situation, known as “primary hypolactasia” or “adult-type hypolactasia”, concerns around 75% of the world population and occurs earlier and faster in certain populations (such as the Thai population) than in others (such as the Finnish population) [1]. In Chile, it is estimated that 60-65% of the population is hypolactasic [2,3]. Primary hypolactasia is due to epigenetic events that result in the methylation of cytosine residues in the promoter area of the lactase gene. These DNA modifications inhibit the binding of transcriptional regulatory factors, leading to the progressive inhibition of lactase expression [4]. The remaining 25% of the world adult population is “lactase persistent”, i.e., adult intestinal lactase persists in these individuals in values similar to those of newborns. This phenomenon is due to specific mutations (single-base polymorphisms) which appeared in the human genome during the Neolithic age, the period in which human sedentarization, the domestication of cows, goats and sheep, and the beginning of dairy farming occurred [5]. Different mutations, which appeared at the same time in geographically distant populations (Northern Europe, sub-Saharan Africa, the Middle East, India and China) have been described, The presence of these mutations prevents the modification of cytosines, allowing the persistence of lactase gene expression throughout an individual’s entire life.

In hypolactasic subjects that consume milk, undigested lactose accumulates in the intestine where it can induce water secretion and eventually diarrhea, mainly due to its osmotic load [1]. Undigested lactose reaches the colon where it is fermented by the microbiota, generating gases such as hydrogen, which can cause bloating and abdominal pain, borborygmi and a higher frequency of rectal gas emission. In hypolactasic subjects, lactose can therefore be considered as a soluble dietary fiber. The eventual presence of digestive symptoms leads hypolactasic subjects to spontaneously reduce their consumption of milk and dairy products and, therefore, their intake of calcium and proteins of high biological value [1]. Although around 30% of hypolactasic individuals are lactose intolerant and develop digestive symptoms when they consume lactose-containing foods, most of them are tolerant and remain asymptomatic when consuming moderate amounts of milk (500 mL/d), probably due to the metabolic adaptation of their gut microbiota [6].

One way to continue consuming dairy products for intolerant people is, for example, to consume yogurt with live bacteria. Indeed, multiple clinical studies have shown that the lactase of yogurt bacteria continues hydrolyzing lactose in the human intestine, reducing the development of digestive symptoms [7]. Based on these studies, the European Food Safety Authority (EFSA) authorized a health claim stating that “the consumption of yogurt with live bacteria improves lactose tolerance in hypolactasic subjects” [8]. Similarly, many probiotics such as L. acidophilus NCFM express β-galactosidases that can hydrolyze lactose, preventing its subsequent fermentation and gas production [9,10]. Interestingly, a recent study in lactose-intolerant individuals reported that dietary supplementation with L. casei Shirota and B. breve Yakult for 4 weeks reduced their digestive symptoms and hydrogen excretion in a lactose hydrogen breath test performed upon completion of probiotic administration, an effect that persisted 3 months after discontinuing probiotic consumption [11]. Although Bifidobacterium spp. also express β-galactosidases [12,13] and could improve lactose intolerance, less clinical studies using this bacterial genus have been carried out in hypolactasic subjects, and none of them with B. bifidum. A limitation in the use of Bifidobacterium species is that they are oxygen-sensible, making it more difficult to reach and maintain high levels of these bacteria in food products [14].

Based on these antecedents, the aim of this study was to evaluate whether the acute and chronic intake of an ice cream containing high (107 CFU/g) or low levels (105 CFU/g) of the B. bifidum 900791 strain decreases breath hydrogen excretion and improves lactose intolerance in hypolactasic subjects.