Where is lactase in the body

You may be asked not to have any milk or milk products for a short time to see if your symptoms get better. While lactose intolerance and irritable bowel syndrome IBS are two different conditions, both can cause similar symptoms for people who drink milk or eat milk products. This article explains why. There is no treatment that can help your body make more lactase.

But you can manage your symptoms by changing your diet. In the past, people who were lactose intolerant were told to avoid dairy products. Today, health experts suggest you try different dairy foods and see which ones cause fewer symptoms.

That way you can still get enough calcium and other important nutrients. He or she can suggest other foods to be sure you get enough calcium. You may need to take calcium supplements. Children with lactose intolerance should be seen by a healthcare provider. Children and teenagers need dairy foods.

Lactose intolerance can affect you every time you eat a snack or meal. So you need to be careful about the foods you eat every day. However, many people can tolerate a certain amount of lactose and don't need to completely avoid it. Lactose is often added to some boxed, canned, frozen, and prepared foods such as:. Call your healthcare provider if you have trouble managing your symptoms.

Some symptoms can be embarrassing. Your healthcare provider can work with you to help keep them under control. Health Home Conditions and Diseases. What is lactose intolerance? Lactose intolerance is not the same thing as having a food allergy to milk. What causes lactose intolerance? Here are some common causes of this condition: Lactose intolerance often runs in families hereditary. Symptoms may start during the teen or adult years. In some cases, the small intestine stops making lactase after an injury or after a disease or infection.

Some babies born too early premature babies may not be able to make enough lactase. This is often a short-term problem that goes away. For example, in a y follow up study, Sahi et al. In their study cohort, all previously identified lactose-malabsorbers also remained as such during the y follow-up period even though some of them continued consuming milk regularly. One notable exception to the aforementioned studies is a report from Bolin and Davis 58 describing a lower incidence of lactose malabsorption in Australian-born Chinese than indigenous Chinese living in Singapore.

Nevertheless, the overall evidence from cross-sectional studies seems to support the findings of the intervention studies that lactose absorption capacity does not depend on the availability of dietary lactose. Considering that the age of onset for lactase deficiency varies considerably between populations, studies examining the relation between milk consumption habits and intestinal lactase activity in young children are especially interesting.

Cook 59 reported that Ugandan children exhibited a gradual fall in lactose absorption capacity from birth to childhood irrespective of their milk intake. Similarly, in a study conducted in Thailand, continuous milk intake since infancy did not prevent a decline in lactose-absorbing capacity Furthermore, studies on Peruvian and Israeli children reported that the lactose-absorbing capacity in these populations was not related to milk consumption during childhood 61 , On the other hand, others have suggested that although lactase status is genetically determined, continued lactose intake after weaning could increase the age of onset for hypolactasia 51 , This is mostly supported by data showing that in populations where milk consumption is high, hypolactasia appears at a later age than in populations with low milk consumption 39 , 51 , 54 , 59 , 60 , 62— In a study cohort consisting of Mexican-American children and Anglo-American children, lactose malabsorption manifested earlier in the Mexican-American group who also consumed less milk than the Anglo-American children Bolin et al.

However, the causality of this relation is uncertain. In the only intervention study conducted in young children, milk supplementation for 1 y did not prevent or delay the development of hypolactasia This study was conducted in a Singaporean population where the prevalence of hypolactasia is high. Possibly, the observed variations in the age of onset for hypolactasia in different populations are under generic or epigenetic regulation and lactose intake does not influence this process.

Although endogenous lactase activities remain unchanged during lactose feeding, lactose-malabsorbers frequently report experiencing fewer and less severe GI symptoms as feeding progresses. This would suggest that some adaptive mechanisms relating to lactose processing occur during prolonged intake of lactose. In one of the first studies to demonstrate adaptation to lactose feeding, Johnson et al. In addition, when challenged with the maximum tolerated dose of lactose, 4 of these subjects exhibited no increase in breath H 2 concentration Subsequent investigations have produced similar findings: lactose-malabsorbing individuals show decreased breath H 2 concentrations after a lactose challenge following a lactose-feeding period 68—71 Table 2.

Although these reports have reported none or only minor improvements in GI symptoms, the findings imply that colonic microbes adapt to the presence of lactose in the colonic lumen.

Interestingly, these bacterial taxa do not produce H 2 during carbohydrate fermentation, which likely explains the observed reduction in breath H 2 concentrations after lactose feeding These results suggest that when dietary lactose reaches the colon, it stimulates the growth of lactose-fermenting bacteria, but whether this reduces intolerance symptoms to lactose is still a matter of debate. Studies have shown decreased flatulence during a lactose challenge following a lactose-feeding period, possibly because of microbial changes leading to reduced colonic gas production 68 , Colonic adaptation is also supported by a study showing that supplementing lactose-intolerant individuals with a prebiotic increases the proportion of lactose-fermenting bacteria, which leads to decreased abdominal pain when lactose is reintroduced in the diet 75 , Taken together, however, these studies mainly report only minor improvements in 1 intolerance symptom with no changes in other GI symptoms 68 , 70 , Moreover, Briet et al.

Another explanation could be individual differences in the composition of microbiota that contribute to GI symptom development after lactose intake. Nevertheless, these studies show that lactose feeding increases the proportion of intestinal bacteria capable of hydrolyzing lactose and decreases colonic H 2 production, trends that might lead to some alleviation of intolerance symptoms in lactose-malabsorbers.

This colonic adaptation to lactose feeding appears to be reversible, i. However, despite colonic adaptation, the nutritional benefit of lactose for these individuals would still remain low compared with lactase-persistent individuals. Intervention studies investigating colonic adaptation in humans after a lactose-feeding period.

Studies that have measured changes in endogenous lactase activity after an intervention period consistently show a lack of enzyme induction, suggesting that lactose intake does not affect an individual's lactase activity. Although these studies are scarce and have relatively few subjects, data from cross-sectional studies support the theory of purely genetic regulation.

However, a few questions remain open. Firstly, the existing intervention studies have mainly been conducted on subjects from populations with a high prevalence of hypolactasia.

This implies that most of the subjects in these studies are genetically homozygous for lactase deficiency, meaning that their ability to express lactase might have already been compromised permanently. Perhaps extending these analyses to include genetic polymorphisms with varying lactase activities would produce a wider range of outcomes.

Secondly, considering that the age of onset for hypolactasia varies extensively between populations, it would certainly be of interest to investigate the genetic or epigenetic factors that trigger the downregulation of lactase expression at a certain age in different populations.

Contrary to endogenous lactase, the capacity of colonic microbes to process lactose can adapt to increased flux of lactose into the colonic lumen. Colonic adaptation occurs mainly in lactase-deficient individuals and is possibly responsible for the increased tolerance to lactose after a lactose-feeding period, but this matter is still being debated and requires more detailed investigations.

Nevertheless, in lactose-malabsorbing individuals, withdrawing lactose from the diet might lead to the loss of adaptation and subsequently lower the threshold for intolerance symptoms when lactose is reintroduced. Overall, however, it remains unclear if lactose intake leads to colonic adaptation in all lactose-malabsorbers and what are the possible differences between adapters and nonadapters.

In addition, the microbial alterations contributing to colonic adaptation after lactose feeding should be investigated more thoroughly. The sole author was responsible for all aspects of this manuscript and declares no conflict of interests.

This review was funded by the Foundation for Nutrition Research. The funder had no role in the literature search, data gathering, and interpretation, and had no say in the final content of this manuscript. Lactose and lactase—who is lactose intolerant and why? J Pediatr Gastroenterol Nutr. Google Scholar. Lactose malabsorption and intolerance: a review. Food Funct. Lactase non-persistence and lactose intolerance. Curr Gastroenterol Rep. Simoons FJ.

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Letters: Lack of effect of rat milk on intestinal lactase activity in the postweaning rat. Acta Physiol Lat Am. Effect of prolonged nursing on the activity of intestinal lactase in rats. When lactose from the intestine contents comes into contact with the active site of lactase, it is broken down into glucose and galactose.

The SGLT1 transmembrane protein Sodium-Glucose Linked Transporter 1 , transports glucose or galactose via facilitated diffusion from the intestine into the enterocyte. Then GLUT2 Glucose Transporter 2 transports glucose or galactose via diffusion from the enterocyte to the bloodstream. If lactose is not broken down in the small intestine, as is the case in lactose intolerant individuals, it is passed into the large intestine. This leads to several problems that are characteristic of lactose intolerance.

The high concentration of lactose in the large intestine creates an osmotic gradient, which causes large volumes of water to move from the blood into the gut as the system begins to equalize the solute concentrations on either side of the intestine wall. This excess water leads to cramping and diarrhea, which causes pain and can lead to dehydration.

Furthermore, when lactose is not broken down by lactase in the small intestine it can be consumed by bacteria that live in the large intestine. Many of these bacteria use the process of sugar fermentation to produce ATP. The fermentation process produces large amounts of gaseous by-products, such as methane, carbon dioxide, and hydrogen.