One man's meat...

There is a view that because lactose intolerance is clinically so similar to irritable bowel syndrome (IBS), there is little point distinguishing between the two.1 The problem with patients is that they refuse to fit neatly into our diagnostic categories. Either that or our definitions of clinical conditions are not as neat as we consider them to be.

 

What is lactose intolerance?

It is important to distinguish between lactose intolerance and cow's milk allergy (CMA), in which specific IgG and IgA immunoglobulins are detectable. These two conditions can co-exist. In a sample of school children, 14% of those with CMA were found to be lactose intolerant compared with 3% of those without CMA.2

 

All mammals are exposed to lactose during breast-feeding but most lose the ability to produce lactase (the enzyme, lactase-phlorizin hydrolase) after weaning. In fact, lactose intolerance, rather than being a disease, is the normal state for most of humanity. Only the majority of people with European ancestry have the peculiar habit of continuing to drink milk into adulthood and possess the physiological ability to digest it. It has been shown that the standard lactose test is not a reliable predictor of an individual's ability to consume moderate amounts of milk (see Table 1).

 

Table 1. Lactose intolerance or Lactase persistence?

 

Ethnic group         Lactose maldigestion4 Lactase persistence?

 

Native Americans             79%                      21%

African Americans 75%                      25%

Hispanic Americans          51%                      49%

Caucasian Americans       21%                      79%

 

 

The phrase lactose maldigestion is therefore used to describe patients who have symptoms even when they ingest amounts of lactose less than the standard test for 'lactose intolerance'. Most Asians, Africans and people from the Middle East do not continue to produce lactase into adult life.3 In other words, a condition known as 'lactase persistence' could be ascribed to the majority of European origin (column three merely shows the percentage without lactose maldigestion).

 

What we call lactose intolerance or adult hypolactasia is inherited through a single autosomal recessive gene.5 Yet, since hypolactasia is so common, it seems a little unfair to describe lactose malabsorption and lactase deficiency as 'chronic organic pathologic conditions characterized by abdominal pain and distention, flatulence, and the passage of loose, watery stools'.6

 

When adults who have no endogenous source of lactase drink cows milk, the lactose is metabolized by gut flora and hydrogen is produced. This is not the same as cow's milk allergy. With suitable equipment, the hydrogen can be detected on the breath but a positive result is not a diagnosis of lactose intolerance. Whereas, malabsorption of lactose can be determined by a breath test or jejunal biopsy, intolerance can be confirmed by a lactose challenge: feeding the patient lactose and waiting for a response, which may not be immediate. A misdiagnosis of refractory IBS is possible if the link between diet and their symptoms is not identified.6 Whereas doctors tend not to recommend exclusion diets unless absolutely necessary, it may be worth trying a lactose-free diet for a week to see if the patient feels better.

 

The hydrogen breath test is carried out on an outpatient basis in hospitals. A drink containing lactose is given and the breath is analyzed at regular intervals. The test is not suitable for infants or young children because of the risk of diarrhoea. Smoking and certain foods and medicines that could affect the accuracy of test results should be avoided before testing.

 

Life with low lactase

There can be degrees of lactase deficiency, leading to degrees of lactose tolerance. However, lactose intolerance can lead to inadequate absorption of important nutrients, deficiency disorders and less than optimal weight gain. Rather than avoid milk, it may be beneficial for some patients to take a lactose-hydrolyzed milk powder. This may be given to avoid the symptoms associated with lactose intolerance.7

 

An alternative to this technological fix is to use yoghurt or other probiotic cultures in fermented or unfermented milk. These can improve lactose absorption and reduce symptoms of intolerance.8 It can be no coincidence that where milk is consumed outside Europe, it is often in the form of fermented milk or yoghurt. A wide range of lactase-containing products are available from health food shops and the local pharmacist should be able to recommend a reasonably priced product that can be added to lactose-containing foods.

 

Reactions to lactose can be severe. In one unusual case it was found that not only hydrogen but also a butane compound were present in the breath. Both are toxic and the patient suffered from lethargy, headache, tachycardia, eczema and muscle pain. It is postulated that similar reactions could occur with other sugars, even glucose.9

 

 

An argument to test

For some patients, therefore, it seems very important to investigate the association between foods and symptoms. With the appropriate clinical approach it could save a lot of trouble for patients with IBS and save time and money on treatment.

 

In a study of patients with functional gastrointestinal disorders, 24% had a positive hydrogen breath test and most of these responded to dietary measures.10 Some people with lactase deficiency may have no symptoms with a moderate amount of milk in their diet. However, it has been proposed that a lactose breath test be included in the diagnostic work-up for all cases of IBS.11

 

If a quarter of IBS patients respond to dietary intervention that would certainly ease the burden. In the United States, it has been estimated that 20% of the population has IBS, and although the majority of these do not consult their doctor, IBS accounts for 25% of visits to US gastroenterologists and up to 12% of consultations in primary care.12

 

References

1.        Parker TJ, et al . Irritable bowel syndrome: is the search for lactose intolerance justified? Eur J Gastroenterol Hepatol 2001; 13(3): 219-25

2.        Kokkonen J, Tikkanen S, and Savilahti E. Residual intestinal disease after milk allergy in infancy. J Pediatr Gastroenterol Nutr 2001; 32(2): 156-161

3.        Sahi T. Genetics and epidemiology of adult-type hypolactasia. Scand J Gastroenterol Suppl 1994; 202: 7-20

4.        Scrimshaw NS, and Murray EB. The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance. Am J Clin Nutr 1988; 48(4 Suppl): 1079-1159

5.        Sahi T. Hypolactasia and lactase persistence. Historical review and the terminology. Scand J Gastroenterol Suppl 1994; 202: 1-6

6.        Shaw AD, Davies GJ. Lactose intolerance: problems in diagnosis and treatment. J Clin Gastroenterol 1999; 28(3): 208-216

7.        Neaverson MA. The clinical significance of lactose intolerance. Aust Fam Physician 1980; 9(10): 747-750

8.        de Vrese M, et al. Probiotics compensation for lactase insufficiency. Am J Clin Nutr 2001; 73(2 Suppl): 421S-429S

9.        Matthews SB, and Campbell AK. When sugar is not so sweet. Lancet 2000; 355(9212): 1330

10.    Enck P, ef a/. Prevalence of lactose malabsorption among patients with functional bowel disorders. Z Gastroenterol 1990; 28(5): 239-241

11.    Vernia P, Di Camillo M, and Marinaro V. Lactose malabsorption, irritable bowel syndrome and self-reported milk intolerance. Dig Liver Dis 2001; 33(3): 234-239

12.    Schuster MM. Defining and diagnosing irritable bowel syndrome. Am J Manag Care 2001; 7(8 Suppl): S246-51