Dr. Binod Gupta
Lactose intolerance is the inability of the human body to digest the lactose present in our foods, especially in milk and dairy products. It is synthesised in the mammary glands. The term, lactose intolerance, is more of a relative than absolute term.
Lactose, a milk disaccharide consisting of glucose and galactose must be broken down in the small intestine by the enzyme lactase (β-galactosidase) in order for its constituents, galactose and glucose, to be absorbed. The lactase is present on the surface of the mucosa of the small intestine with the highest concentration being in the mid jejunum. Lactose that is not digested transits to the lower small intestine and large intestine, thus creating the potential for symptoms (Matthews, Waud, Roberts, & Campbell, 2005).
The production of the enzyme lactase declines significantly after weaning in all mammals. Consequently, many adult humans become unable to digest lactose properly as they mature. There is a greater incidence of lactose intolerance in adults from countries that traditionally do not have a strong dairy industry. The prevalence of lactose intolerance is very high (almost 100%) in Asian countries, above 50% in south America and Africa, and is approximately 53% among Mexican Americans and 80% among African American
The gene in humans that controls lactase production, and hence lactose tolerance/intolerance, is labeled C/T-13910. Lactase deficiency may occur due to primary, secondary and congenital causes.
Primary lactase deficiency: Primary lactase deficiency is the normal post-weaning loss of the majority of intestinal lactase and is the most common cause of lactose intolerance (Heyman, 2006).
Secondary lactase deficiency: Secondary lactase deficiency is a transient deficiency of lactase that occurs as a consequence of damage to the lining of the small intestine, caused by medications, disease, surgery or radiation therapy to the enterocytes (Savaiano & Levitt, 1987; Scrimshaw & Murray, 1988b; Srinivasan & Minocha, 1998).
Congenital lactase deficiency: Infants born prematurely are more likely to have lactase deficiency because an infant's lactase levels do not increase until the third trimester of pregnancy.
Not all people with lactase deficiency have digestive symptoms, but those who do may have lactose intolerance. Most people with lactose intolerance can tolerate some amount of lactose in their diet. Symptoms tend to occur between 30 minutes and 2 hours after the ingestion of the lactose containing food (Rusynyk & Still, 2001), and can manifest clinically as an incident of lactose intolerance (Matthews et al., 2005).
Symptoms include gastrointestinal distress, diarrhea, and flatulence, frequent watery stools, bloating due to hydrogen, carbon dioxide and methane production by bacteria. Sometimes, there are abdominal pain, distension and visceral cramping due to excess gas production (He et al, 2006).
It can be suspected by its symptoms initially and conformed by different tests (Moore, 2003). As hydrogen is produced when colonic bacteria hydrolyze unabsorbed lactose, the hydrogen breath test has become the most widely used technique for diagnosis of lactose malabsorption (Casellas, Varela, Aparici, Casaus, & Rodriguez, 2009).
Clinical symptoms: The hydrogen breath test has been proven to be far more reliable than clinical history in the diagnosis of lactose intolerance (Dipalma & Narvaez, 1988). There are frequently discrepancies with regards to clinical history due to individuals who believe themselves to be lactose malabsorbers and prove not to be, whilst others prove to be lactose malabsorbers when they think they are not (Dipalma & Narvaez, 1988; Suarez, Savaiano, & Levitt, 1995a).
Hydrogen breath test: The measurement of breath hydrogen after ingestion of 25-50g of lactose after overnight fasting is the most sensitive and specific tolerance test available (Swagerty
et al., 2002).
The test is based on the principle that unabsorbed lactose in the colon is detectable in pulmonary excretion of hydrogen and other gases (Arola, 1994). A rise in breath hydrogen concentration greater than 20 ppm over baseline after lactose ingestion over 3-6 h suggests lactose intolerance.
Lactose intolerance should not be thought of as a disease, but instead the normal physiologic pattern in all mammals (McBean & Miller, 1998; Stephenson & Latham, 1974; Swagerty et al., 2002) and there is no reliable way to prevent or reverse it. But, there are different ways to live with lactose intolerance. What works for one person might not work for another. Because there is no cure for lactose intolerance, controlling your symptoms is mostly up to you.
About 44% of lactose intolerant women regain the ability to digest lactose during pregnancy. This might be caused by slow intestinal transit and intestinal flora changes during pregnancy. Lactose intolerance might be managed in following ways-
With dietary changes
Supplements of lactase enzyme
Adaptation to increasing amounts of milk. The amount of change needed in the diet depends on how much lactose a person can consume without symptoms.
Experts recommend four general principles in dealing with lactose intolerance as below-
Avoidance of dietary lactose
Substitution to maintain nutrient intake
Regulation of calcium intake
Use of enzyme substitute.
There are a few remedies that may help you minimize your lactose intolerant symptoms-
Determine your level of lactose intolerance
Consider lactase products, stick with small servings at a time
Don't eat dairy foods alone
Choose lactose-reduced or lactose-free milk & dairy products
Take a lactase enzyme supplement just before you eat dairy products
Drink juices that are fortified with calcium
Yogurts that contain active cultures are easier to digest and much less likely to cause lactose problems, learn to read food labels. Enzymatic lactase supplementation may have an advantage over avoiding dairy products, in that alternative provision does not need to be made to provide sufficient calcium intake, especially in children.
(Dr Gupta is a dairy-vet consultant)