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Systematic review
Sufficient evidence that 12 g of lactose is tolerated by most adults with lactose malabsorption and intolerance but insufficient evidence on the effectiveness of therapeutical strategies tested so far
  1. Massimo Montalto1,
  2. Antonella Gallo1
  1. Institute of Internal Medicine, Catholic University, Rome, Italy
  1. Correspondence to Massimo Montalto
    Institute of Internal Medicine, Catholic University, Largo A. Gemelli, 8, 00168, Rome, Italy; mmontalto{at}

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Lactose malabsorption is a very common condition caused by a deficiency of the intestinal enzyme that hydrolyses lactose into its components, galactose and glucose. High concentrations of lactase are physiologically present in neonates whereas, after weaning, a genetically programmed and irreversible reduction in its activity occurs in a majority of the world's population. Therefore, hypolactasia should not be considered a disease but rather a common pattern in human physiology. The presence in the colonic lumen of malabsorbed lactose does not necessarily result in gastrointestinal symptoms. When this condition is related to uncomfortable clinical manifestations as bloating, abdominal pain and diarrhoea, ‘lactose intolerance’ occurs. At present, the management of this condition is still an open matter.


Shaukat and colleagues' systematic review examines two important aspects of this topic: the assessment of the maximum tolerable dose of lactose and the interventions to reduce symptoms in patients with lactose intolerance. The authors independently selected and reviewed the relevant studies obtained from appropriate literature databases and clinical trial registers, and they conducted the systematic review rigorously. Thirty-six randomised studies met the inclusion criteria.


The authors' analysis concludes that persons with lactose intolerance or malabsorption can ingest 12 g of lactose without experiencing relevant symptoms. Moreover, the relevant role of ingestion of lactose with other nutrients is particularly stressed. In fact, the tolerated amount of lactose increases to about 20 g when administered with other nutrients. Finally, ingestion of 50 g of lactose provokes symptoms in most individuals.

Regarding the strategies of managing patients with lactose malabsorption and intolerance, the authors analyse different studies involving lactose-reduced and hydrolysed formulations, lactase supplements, probiotics and colonic adaptation. They conclude that there is insufficient evidence to support any of these approaches.


To date, the maximum tolerable dose of lactose has not been unequivocally established. It is thought that most lactose maldigesters can tolerate lactose amounts below 12 g (ie, the amount present in a cup of milk).1 However, gastrointestinal symptoms have been reported after ingestion of smaller doses of lactose.2 3 Furthermore, in clinical practice, it is very common to find lactose maldigesters who believe that the ingestion of a minimal amount of sugar (eg, white coffee) can produce gastrointestinal symptoms.

It is possible that the difficulties in correctly establishing the threshold level for symptom onset are because of many variables that can impact on it, such as residual lactase activity, individual sensibility to the intestinal wall distension, rate of gastric emptying, small-intestinal transit time, colonic microflora and its adaptation to chronic lactose ingestion, etc. Psychological factors can also play a pivotal role in lactose intolerance, since it is common to find subjects who erroneously attribute the occurrence of symptoms to some foods, such as lactose, notoriously assumed to be responsible for gastrointestinal disorders.

As regarding management of lactose malabsorption and intolerance, it has been widely reported that the clinical aspect should be considered more relevant than the H2 excretion; in fact, in malabsorber patients with intolerance, since there is no evidence of adverse effects of lactose maldigestion other than gastrointestinal symptoms, the major end point is to resolve the clinical picture. Just for this reason, treatment should be reserved exclusively for intolerant subjects.1

We appreciated the authors' effort to provide clear definitions regarding the different aspects of this condition, such as the differences between lactose malabsorption and intolerance, since many (not experienced in this field) physicians still do not adequately discern them. In the last few years, several approaches have been studied to avoid the consequences of a too often suggested (also by many physicians) strict lactose-free diet.4 Nevertheless, as remarked by the authors, none of these strategies has been sufficiently supported by evidence.

Moreover, we agree with Shaukat and colleagues regarding the numerous biases found in the available studies. In particular, some studies enrolled patients on the basis of documented malabsorption (by a positive hydrogen breath test) rather than on intolerance, thus failing to identify the ‘true’ intolerants. In addition, criteria to evaluate intolerance symptoms are heterogeneous and not standardised. Finally, doses of lactose are often different among the various studies, thus limiting the possibility to pool and generalise results and to provide definitive conclusions.

As a consequence, this review does not help the production of treatment guidelines. Therefore, the therapeutic management of lactose malabsorption still remains an open and debated topic. We think that a long-lasting lactose-free diet should be discouraged. Rather, a temporary avoidance of milk and dairy products from the diet should be initially undertaken in order to obtain symptom remission. Subsequently, to assure an adequate intake of essential nutritional substances, a gradual re-introduction of dairy products considering the individual threshold dose should be advised. Until evidence-based indications are introduced, we believe that at least the ingestion of lactose with other nutrients should be encouraged.


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  • Competing interests None.