Lactose intolerance, also known as lactose malabsorption, is a clinical condition with identifiable signs and symptoms after ingesting dietary products that include the disaccharide lactose.
Normally, the lactase enzyme, located in the small intestine brush border, hydrolyzes lactose upon intake into glucose and galactose. The symptoms of lactose intolerance include bloating and soreness in the abdomen, nausea, flatulence, loose stools, and borborygmi.
Epidemiology
Although it is a common condition, lactose intolerance is uncommon in children under five. Young adults and adolescents are most frequently affected. Approximately 65% of individuals worldwide are lactose intolerant. Among several racial and ethnic groups, lactose intolerance varies in prevalence.
Hispanics, Asians, and African Americans are most likely to experience it, whereas European Americans are least likely to. Although the age-related fall in lactase activity often peaks during childhood, it has sometimes been observed to occur later, in adolescents, especially in Whites.
Patients of mixed ethnicity have a low lactase non-persistence, whereas the native ethnic group has a higher prevalence. Many patients first observe intolerance symptoms in late adolescence or early adulthood, and the condition often manifests itself gradually and subtly at first.
Anatomy
Pathophysiology
The brush border of the small intestine mucosa contains the lactase enzyme. Unabsorbed lactose accumulates in the gut due to lactase deficiency. Osmotic diarrhea is the outcome, which is an inflow of fluid into the gut lumen.
Hydrolysis of lactose into simple sugars occurs when intestinal bacteria digest lactose-producing gas (carbon dioxide, hydrogen, and methane) that is not absorbed. As a result, the lumen experiences an increase in fluid flow. These pathways’ combined impact causes a variety of abdominal symptoms.
Etiology
Low levels of enzyme can cause lactase insufficiency, which prevents lactose from being hydrolyzed into components that can be absorbed, such as glucose and galactose. The four main causes of lactase deficiency are as follows.
Primary Lactase Deficiency
It is the most typical cause of lactase insufficiency, also called non-persistence. With advancing age, lactase enzyme activity gradually decreases. Infancy signifies the beginning of the loss in enzyme function, while adolescence or early adulthood marks the onset of symptoms. Recent research has revealed that lactase persistence results from mutation, whereas lactase non-persistence is of the ancestral form (typical Mendelian inheritance).
Secondary Lactase Deficiency
Injury to the intestinal mucosa can result from several viral, inflammatory, or other conditions, leading to secondary lactase deficiency. Common causes include Celiac disease, Ulcerative Colitis, Gastroenteritis, Antibiotics, and chemotherapy.
Developmental Lactase Deficiency
It occurs in newborns delivered prematurely between 28 and 37 weeks of gestation. Due to the infant’s undeveloped gut, lactose cannot be hydrolyzed. Age-related improvements in this condition are attributed to the development of the gut and the resulting appropriate lactase activity.
Congenital Lactase Deficiency
Due to autosomal recessive genetics, lactase enzyme activity has decreased or been absent from birth. It appears in a newborn following milk consumption. It is an uncommon cause of the insufficiency, and little is known about its genetics.
Genetics
Prognostic Factors
The prognosis for lactose intolerance is good. With dietary changes alone, most patients see a significant improvement in their indications and symptoms. Osteopenia may result from lactose intolerance. The LCT-13910C>T gene variation of lactose intolerance in Whites is associated with vitamin D insufficiency.
Lactose intolerance, also known as lactose malabsorption, is a clinical condition with identifiable signs and symptoms after ingesting dietary products that include the disaccharide lactose.
Normally, the lactase enzyme, located in the small intestine brush border, hydrolyzes lactose upon intake into glucose and galactose. The symptoms of lactose intolerance include bloating and soreness in the abdomen, nausea, flatulence, loose stools, and borborygmi.
Although it is a common condition, lactose intolerance is uncommon in children under five. Young adults and adolescents are most frequently affected. Approximately 65% of individuals worldwide are lactose intolerant. Among several racial and ethnic groups, lactose intolerance varies in prevalence.
Hispanics, Asians, and African Americans are most likely to experience it, whereas European Americans are least likely to. Although the age-related fall in lactase activity often peaks during childhood, it has sometimes been observed to occur later, in adolescents, especially in Whites.
Patients of mixed ethnicity have a low lactase non-persistence, whereas the native ethnic group has a higher prevalence. Many patients first observe intolerance symptoms in late adolescence or early adulthood, and the condition often manifests itself gradually and subtly at first.
The brush border of the small intestine mucosa contains the lactase enzyme. Unabsorbed lactose accumulates in the gut due to lactase deficiency. Osmotic diarrhea is the outcome, which is an inflow of fluid into the gut lumen.
Hydrolysis of lactose into simple sugars occurs when intestinal bacteria digest lactose-producing gas (carbon dioxide, hydrogen, and methane) that is not absorbed. As a result, the lumen experiences an increase in fluid flow. These pathways’ combined impact causes a variety of abdominal symptoms.
Low levels of enzyme can cause lactase insufficiency, which prevents lactose from being hydrolyzed into components that can be absorbed, such as glucose and galactose. The four main causes of lactase deficiency are as follows.
Primary Lactase Deficiency
It is the most typical cause of lactase insufficiency, also called non-persistence. With advancing age, lactase enzyme activity gradually decreases. Infancy signifies the beginning of the loss in enzyme function, while adolescence or early adulthood marks the onset of symptoms. Recent research has revealed that lactase persistence results from mutation, whereas lactase non-persistence is of the ancestral form (typical Mendelian inheritance).
Secondary Lactase Deficiency
Injury to the intestinal mucosa can result from several viral, inflammatory, or other conditions, leading to secondary lactase deficiency. Common causes include Celiac disease, Ulcerative Colitis, Gastroenteritis, Antibiotics, and chemotherapy.
Developmental Lactase Deficiency
It occurs in newborns delivered prematurely between 28 and 37 weeks of gestation. Due to the infant’s undeveloped gut, lactose cannot be hydrolyzed. Age-related improvements in this condition are attributed to the development of the gut and the resulting appropriate lactase activity.
Congenital Lactase Deficiency
Due to autosomal recessive genetics, lactase enzyme activity has decreased or been absent from birth. It appears in a newborn following milk consumption. It is an uncommon cause of the insufficiency, and little is known about its genetics.
The prognosis for lactose intolerance is good. With dietary changes alone, most patients see a significant improvement in their indications and symptoms. Osteopenia may result from lactose intolerance. The LCT-13910C>T gene variation of lactose intolerance in Whites is associated with vitamin D insufficiency.
Lactose intolerance, also known as lactose malabsorption, is a clinical condition with identifiable signs and symptoms after ingesting dietary products that include the disaccharide lactose.
Normally, the lactase enzyme, located in the small intestine brush border, hydrolyzes lactose upon intake into glucose and galactose. The symptoms of lactose intolerance include bloating and soreness in the abdomen, nausea, flatulence, loose stools, and borborygmi.
Although it is a common condition, lactose intolerance is uncommon in children under five. Young adults and adolescents are most frequently affected. Approximately 65% of individuals worldwide are lactose intolerant. Among several racial and ethnic groups, lactose intolerance varies in prevalence.
Hispanics, Asians, and African Americans are most likely to experience it, whereas European Americans are least likely to. Although the age-related fall in lactase activity often peaks during childhood, it has sometimes been observed to occur later, in adolescents, especially in Whites.
Patients of mixed ethnicity have a low lactase non-persistence, whereas the native ethnic group has a higher prevalence. Many patients first observe intolerance symptoms in late adolescence or early adulthood, and the condition often manifests itself gradually and subtly at first.
The brush border of the small intestine mucosa contains the lactase enzyme. Unabsorbed lactose accumulates in the gut due to lactase deficiency. Osmotic diarrhea is the outcome, which is an inflow of fluid into the gut lumen.
Hydrolysis of lactose into simple sugars occurs when intestinal bacteria digest lactose-producing gas (carbon dioxide, hydrogen, and methane) that is not absorbed. As a result, the lumen experiences an increase in fluid flow. These pathways’ combined impact causes a variety of abdominal symptoms.
Low levels of enzyme can cause lactase insufficiency, which prevents lactose from being hydrolyzed into components that can be absorbed, such as glucose and galactose. The four main causes of lactase deficiency are as follows.
Primary Lactase Deficiency
It is the most typical cause of lactase insufficiency, also called non-persistence. With advancing age, lactase enzyme activity gradually decreases. Infancy signifies the beginning of the loss in enzyme function, while adolescence or early adulthood marks the onset of symptoms. Recent research has revealed that lactase persistence results from mutation, whereas lactase non-persistence is of the ancestral form (typical Mendelian inheritance).
Secondary Lactase Deficiency
Injury to the intestinal mucosa can result from several viral, inflammatory, or other conditions, leading to secondary lactase deficiency. Common causes include Celiac disease, Ulcerative Colitis, Gastroenteritis, Antibiotics, and chemotherapy.
Developmental Lactase Deficiency
It occurs in newborns delivered prematurely between 28 and 37 weeks of gestation. Due to the infant’s undeveloped gut, lactose cannot be hydrolyzed. Age-related improvements in this condition are attributed to the development of the gut and the resulting appropriate lactase activity.
Congenital Lactase Deficiency
Due to autosomal recessive genetics, lactase enzyme activity has decreased or been absent from birth. It appears in a newborn following milk consumption. It is an uncommon cause of the insufficiency, and little is known about its genetics.
The prognosis for lactose intolerance is good. With dietary changes alone, most patients see a significant improvement in their indications and symptoms. Osteopenia may result from lactose intolerance. The LCT-13910C>T gene variation of lactose intolerance in Whites is associated with vitamin D insufficiency.
www.ncbi.nlm.nih.gov/books/NBK532285/
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