Nutr Rev

Human adult-onset lactase decline: an update.

Lee MF. Krasinski SD.
Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, USA.
Human adult-onset lactase decline is a biologic feature characteristic of the maturing intestine in the majority of the world's population. The digestion and absorption of lactose, the major carbohydrate in milk and also the main substrate for lactase, is often variable, a consequence of lactase levels, gastric emptying rate, and colonic salvage. Although commercially available "lactase" products alleviate symptoms in many lactose-intolerant people, a greater understanding of this variability in lactose tolerance could lead to interventions that reduce the rate of gastric emptying and/or increase the proliferation of lactose-metabolizing bacteria in the colon, leading to more efficient lactose utilization. Adult-onset lactase decline appears to be a risk factor for developing osteoporosis, owing to avoidance of dairy products or interference of undigested lactose with calcium absorption. Elderly with both adult-onset lactase decline and atrophic gastritis or those undergoing anti-ulcer treatment may have an increased risk of low calcium absorption owing to the lack of gastric acid that facilitates calcium uptake. Thus, lactose-intolerant elders should monitor their calcium nutrition status carefully.

Gastrointestinal alcohol dehydrogenase.

Year 1998
Seitz HK. Oneta CM.
Department of Medicine, Salem Medical Center, Heidelberg, Germany.
Alcohol dehydrogenase (ADH) consists of a family of isozymes that convert alcohols to their corresponding aldehydes using NAD+ as a cofactor. The metabolism of ethanol by gastrointestinal ADH isozymes results in the production of acetaldehyde, a highly toxic compound that binds to cellular protein and DNA if not further metabolized to acetate by acetaldehyde dehydrogenase isozymes. Acetaldehyde seems to be involved in ethanol-associated cocarcinogenesis. The metabolism of retinol and the generation of retinoic acid is a function of class I and class IV ADH, and its inhibition by alcohol may lead to an alteration of epithelial cell differentiation and cell growth and may also be involved in ethanol-associated gastrointestinal cocarcinogenesis.