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group_2_presentation_2_-_lactose_intolerance [2019/03/08 21:53] pateln25 [PATHOPHYSIOLOGY & CAUSES] |
group_2_presentation_2_-_lactose_intolerance [2019/03/09 12:07] (current) pateln25 |
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| ====== PRESENTATION SLIDES ====== | ====== PRESENTATION SLIDES ====== | ||
| + | [[https://drive.google.com/file/d/1IeEeMf0uSiA8cz5uAo_iFmvbIIjEkoA7/view?usp=sharing|External Link]] | ||
| ====== INTRODUCTION ====== | ====== INTRODUCTION ====== | ||
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| There are several ways to test for lactose intolerance including breath tests, blood tests, internal biopsies, and stool tests. When diagnosing, if the symptoms described line up with those of lactose intolerance, a lactose- free diet can be implemented. The diet can last up to 2 weeks and must not include any sources of lactose, especially from hidden sources. If the symptoms appear to be subtle, then further testing can be done using the techniques listed below. | There are several ways to test for lactose intolerance including breath tests, blood tests, internal biopsies, and stool tests. When diagnosing, if the symptoms described line up with those of lactose intolerance, a lactose- free diet can be implemented. The diet can last up to 2 weeks and must not include any sources of lactose, especially from hidden sources. If the symptoms appear to be subtle, then further testing can be done using the techniques listed below. | ||
| - | <box 40% round | > {{ :playground:7.png?450 |}} </box| Figure 4: Map of the world showing percentage of people affected by lactose intolerance. (Retrieved from: The University of Alabama, 2013)> | + | <box 40% round | > {{ :playground:7.png?450 |}} </box| Figure 4: The various tests used for diagnosing lactose intolerance.> |
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| This is similar to the lactose tolerance test but instead, it measures galactose instead of glucose levels. In a lactose tolerant individual, when lactose is ingested and broken down to glucose and galactose, the galactose in the blood is converted to glucose inside the liver (Villako & Maaroos, 1994). Ethanol delays the clearance of galactose from the circulation (Villako & Maaroos, 1994). A doctor will administer 500 mg of ethanol/kg body weight 10 min before providing the 50g lactose load to the patient (Villako & Maaroos, 1994). Galactose concentrations are measured at 0, 20, 40, 60 and 90 minutes (Patel & Minocha, 2000). If the patient has lactase deficiency and is unable to hydrolyze lactose and absorb its monosaccharides, the blood galactose levels do not usually increase. | This is similar to the lactose tolerance test but instead, it measures galactose instead of glucose levels. In a lactose tolerant individual, when lactose is ingested and broken down to glucose and galactose, the galactose in the blood is converted to glucose inside the liver (Villako & Maaroos, 1994). Ethanol delays the clearance of galactose from the circulation (Villako & Maaroos, 1994). A doctor will administer 500 mg of ethanol/kg body weight 10 min before providing the 50g lactose load to the patient (Villako & Maaroos, 1994). Galactose concentrations are measured at 0, 20, 40, 60 and 90 minutes (Patel & Minocha, 2000). If the patient has lactase deficiency and is unable to hydrolyze lactose and absorb its monosaccharides, the blood galactose levels do not usually increase. | ||
| - | ====== PATHOPHYSIOLOGY & CAUSES ====== | + | ====== CAUSES & PATHOPHYSIOLOGY====== |
| Lactose is a disaccharide found in milk and as a result, many processed foods such as cheese, chocolate, bread, and even sausages (Srinivasan & Minocha, 1998). Lactose gives milk its partially sweet taste but has no special nutritional importance for adults (Vesa //et al//., 2000). However, for infants, it is the most important source of energy, especially in the first year of their life when their primary source of food is their mothers’ milk. In fact, for infants, lactose provides almost half the total energy requirement (Vesa //et al.//, 2000). Lactose is composed of the two monosaccharides, glucose and galactose (Vesa //et al//., 2000). Lactose is one third as sweet as the disaccharide sucrose (found in table sugar), which is made of glucose and fructose (Vesa et al., 2000). | Lactose is a disaccharide found in milk and as a result, many processed foods such as cheese, chocolate, bread, and even sausages (Srinivasan & Minocha, 1998). Lactose gives milk its partially sweet taste but has no special nutritional importance for adults (Vesa //et al//., 2000). However, for infants, it is the most important source of energy, especially in the first year of their life when their primary source of food is their mothers’ milk. In fact, for infants, lactose provides almost half the total energy requirement (Vesa //et al.//, 2000). Lactose is composed of the two monosaccharides, glucose and galactose (Vesa //et al//., 2000). Lactose is one third as sweet as the disaccharide sucrose (found in table sugar), which is made of glucose and fructose (Vesa et al., 2000). | ||
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| Lactose intolerance is the result of an inadequate amount of lactase production or none at all. This prevents the hydrolysis of lactose in the small intestine. The unabsorbed sugar will subsequently continue moving into the large intestine. The abundance of lactose sugar will osmotically attract water and electrolytes (from blood) into the intestine (Swagerty //et al.//, 2002). Under normal body conditions, the osmolarity in the intestinal lumen is higher than the osmolarity of the blood (Swagerty //et al.//, 2002). As a result, the fluid influx into the intestines of a lactose intolerant individual (after ingesting a lactose-rich meal) is approximately triple the predicted amount based on the osmolarity of the lactose by itself (Swagerty //et al.//, 2002). This abundance of water results in diarrhea (Swagerty //et al.//, 2002). In addition, lactose entering the colon is fermented (metabolized) by bacteria to produce short-chain fatty acids and gases (hydrogen, carbon dioxide, and methane). This leads to flatulence, bloating, pain, and even cramping (Srinivasan & Minocha, 1998). | Lactose intolerance is the result of an inadequate amount of lactase production or none at all. This prevents the hydrolysis of lactose in the small intestine. The unabsorbed sugar will subsequently continue moving into the large intestine. The abundance of lactose sugar will osmotically attract water and electrolytes (from blood) into the intestine (Swagerty //et al.//, 2002). Under normal body conditions, the osmolarity in the intestinal lumen is higher than the osmolarity of the blood (Swagerty //et al.//, 2002). As a result, the fluid influx into the intestines of a lactose intolerant individual (after ingesting a lactose-rich meal) is approximately triple the predicted amount based on the osmolarity of the lactose by itself (Swagerty //et al.//, 2002). This abundance of water results in diarrhea (Swagerty //et al.//, 2002). In addition, lactose entering the colon is fermented (metabolized) by bacteria to produce short-chain fatty acids and gases (hydrogen, carbon dioxide, and methane). This leads to flatulence, bloating, pain, and even cramping (Srinivasan & Minocha, 1998). | ||
| - | <box 40% round | > {{ :playground:4.png?400 |}} </box| Figure 6. Lactose fermentation in the colon by colonic bacteria to produce short-chain fatty acids and gasses (hydrogen, carbon dioxide, and methane) in individuals with lactose intolerance. (Retrieved from: IMD Labor Berlin)> | + | <box 40% round | > {{ :playground:4.png?400 |}} </box| Figure 6. Lactose fermentation in the colon by colonic bacteria to produce short-chain fatty acids and gasses (hydrogen, carbon dioxide, and methane) in individuals with lactose intolerance. (Retrieved from: IMD Labor Berlin, 2019)> |
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| Congenital lactose intolerance is very rare (Rusynyk & Still, 2001). In this form, babies are born with the inability to produce any lactase (Rusynyk & Still, 2001). As a result, the consumption of any amount of lactose is intolerable and even dangerous as their diarrhea can quickly lead to dehydration (Rusynyk & Still, 2001). This is a genetic, autosomal recessive condition, meaning that both the mother and father must pass on the same gene variant for their child to be affected (Vesa //et al//., 2000). This form of the disorder is generally apparent within a few days after birth. For these individuals, they must be fed a lactose-free diet (Rusynyk & Still, 2001). | Congenital lactose intolerance is very rare (Rusynyk & Still, 2001). In this form, babies are born with the inability to produce any lactase (Rusynyk & Still, 2001). As a result, the consumption of any amount of lactose is intolerable and even dangerous as their diarrhea can quickly lead to dehydration (Rusynyk & Still, 2001). This is a genetic, autosomal recessive condition, meaning that both the mother and father must pass on the same gene variant for their child to be affected (Vesa //et al//., 2000). This form of the disorder is generally apparent within a few days after birth. For these individuals, they must be fed a lactose-free diet (Rusynyk & Still, 2001). | ||
| - | {{ :playground:3.png?250 |}} | + | <box 30% round | > {{ :playground:3.png?250 |}} </box|Figure 7: Causes of secondary lactose intolerance (hypolactasia) by small intestine conditions (small bowel), conditions of other parts of the body (multisystem), and treatments (iatrogenic). (Retrieved from: Vesa et al., 2000)> |
| - | ====== TREATMENTS & LIFESTYLE ====== | + | |
| + | ====== TREATMENTS ====== | ||
| Lactose intolerance can be treated with simple dietary changes. The following are some of the strategies that can be used to reduce the amount of milk or daily products in his or her diet. | Lactose intolerance can be treated with simple dietary changes. The following are some of the strategies that can be used to reduce the amount of milk or daily products in his or her diet. | ||
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| ===== Dietary Management ===== | ===== Dietary Management ===== | ||
| - | Dietary management of lactose intake involves restricting the daily intake of lactose in order to reduce the onset of symptoms caused by lactose malabsorption (Shaukat et al., 2010). This restriction applies to all products containing the disaccharide lactose, which includes any dairy or dairy based products (Vesa et al., 2000). Lactose intolerance is caused by lactose malabsorption, which stems from lactose deficiency. Individuals with primary and secondary hypolactasia will express reduced concentrations of lactase enzyme in the small intestine (Mattar et al., 2012). These individuals can tolerate a varyingly small portion of lactose consumption, which can be determined via dietary management (Mattar et al., 2012). Dietary management involves restricting lactose digestion until symptoms of lactose intolerance are no longer present, which does not necessarily mean a complete shutdown of lactose consumption (Shaukat et al., 2010). Thus, these individuals are able to consume lactose within their varying limits. On the other hand, individuals with primary congenital alactasia lack the expression of lactase enzyme production, and as such, cannot tolerate any lactose consumption (Mattar et al., 2012). | + | Dietary management of lactose intake involves restricting the daily intake of lactose in order to reduce the onset of symptoms caused by lactose malabsorption (Shaukat //et al.//, 2010). This restriction applies to all products containing the disaccharide lactose, which includes any dairy or dairy based products (Vesa //et al.//, 2000). Lactose intolerance is caused by lactose malabsorption, which stems from lactose deficiency. Individuals with primary and secondary hypolactasia will express reduced concentrations of lactase enzyme in the small intestine (Mattar //et al.//, 2012). These individuals can tolerate a varyingly small portion of lactose consumption, which can be determined via dietary management (Mattar //et al.//, 2012). Dietary management involves restricting lactose digestion until symptoms of lactose intolerance are no longer present, which does not necessarily mean a complete shutdown of lactose consumption (Shaukat //et al.//, 2010). Thus, these individuals are able to consume lactose within their varying limits. On the other hand, individuals with primary congenital alactasia lack the expression of lactase enzyme production, and as such, cannot tolerate any lactose consumption (Mattar //et al.//, 2012). |
| + | ===== Adaptation ===== | ||
| + | Frequent consumption of lactose products can lead to adaptation by colonic bacteria (Mattar //et al.//, 2012). Small amounts of lactose consumption in regular intervals throughout the day can promote a favorable microbiome for lactose digestion (Mattar //et al.//, 2012). In essence, this can reduce lactose intolerance, allowing individuals with primary or secondary hypolactasia to consume higher doses of lactose over time (Mattar //et al.//, 2012). Furthermore, the ingestion of live yogurt cultures containing lactobacilli can improve lactose consumption (Mattar //et al.//, 2012). Lactobacilli can aid in the digestion of lactose, thus reducing lactose malabsorption (Mattar //et al.//, 2012). | ||
| - | ===== Lactase Supplements ===== | ||
| - | |||
| - | When dietary restriction of lactose consumption is not a suitable option, lactase supplements are available (Mattar et al., 2012). Lactase enzyme produced industrially by fungi of the genus Aspergillus, are suitable supplements to the lactase produced in the small intestines of humans (Mattar et al., 2012). This enzyme in the form of beta-galactosidase tablets, is available over the counter in several countries. The beta-galactosidase tablets must be taken at the time of lactose consumption in order to effectively aid in the digestion of lactose (Mattar et al., 2012). In addition, most available forms of this tablet are pH sensitive and are only active in acidic environments such as that of the stomach (Mattar et al., 2012). It is important to not that excessive acidity can denature the enzyme so consumption while fasting is not recommended (Mattar et al., 2012). | ||
| - | |||
| - | ===== Adaptation ===== | ||
| - | |||
| - | Frequent consumption of lactose products can lead to adaptation by colonic bacteria (Mattar et al., 2012). Small amounts of lactose consumption in regular intervals throughout the day can promote a favorable microbiome for lactose digestion (Mattar et al., 2012). In essence, this can reduce lactose intolerance, allowing individuals with primary or secondary hypolactasia to consume higher doses of lactose over time (Mattar et al., 2012). Furthermore, the ingestion of live yogourt cultures containing lactobacilli can improve lactose consumption (Mattar et al., 2012). Lactobacilli can aid in the digestion of lactose, thus reducing lactose malabsorption (Mattar et al., 2012). | ||
| ===== Lactose Substitutes ===== | ===== Lactose Substitutes ===== | ||
| - | Individuals with primary or secondary hypolactasia can tolerate varying concentrations of lactose consumption, which is often considerably lower than lactose tolerant individuals (Mattar et al., 2012). Thus, dietary modifications for these individuals often involve the consumption of lactose-reduced or lactose-free substitutes (Mattar et al., 2012). Milk has many lactose-free substitutes that are available in wide distribution across the world. These substitutes include soy milk, almond milk, coconut milk, rice milk, hazelnut milk, hemp milk, and many other variants (Shaukat et al., 2010). | + | Individuals with primary or secondary hypolactasia can tolerate varying concentrations of lactose consumption, which is often considerably lower than lactose tolerant individuals (Mattar //et al.//, 2012). Thus, dietary modifications for these individuals often involve the consumption of lactose-reduced or lactose-free substitutes (Mattar //et al.//, 2012). There are many products currently on the market that are lactose-free. Many of them are also based on legumes, seeds and grains. These include almond, rice, hazelnut hemp, soy, sunflower, oat, and coconut milks (Shaukat //et al.//, 2010). They are available in original or other flavors as sweetened and unsweetened. |
| - | Milk provides a good source of nutrients essential for bone mineralization and growth. This is especially important during peak growth periods. Some nutrients found in milk include: protein, calcium, vitamin D, vitamin A, vitamin B12, riboflavin and phosphorus. | + | Individuals avoiding foods containing milk may lose source essential nutrients from their diet, and therefore foods must be chosen with care to replace these lost nutrients. In some cases, cross-reactivity may occur when the proteins in one food are similar to the proteins in another. When that happens, the body's immune system sees them as the same. There is a high degree of cross-reactivity between cow's milk and the milk from other mammals such as goat and sheep. Studies show the risk of allergy to goat's milk or sheep's milk in a person with cow’s milk allergy is about 90%. The risk is much lower, about 5%, for allergy to mare's milk which is less cross-reactive with cow's milk. |
| - | There are many products currently on the market that are lactose-free. This is a good option for those that don't want to give up their favorite milk products. There are more options on the way. The lactose-free food market is predicted to grow 11.10 percent between 2017 and 2021.Individuals avoiding foods containing milk may lose source essential nutrients from their diet, and therefore foods must be chosen with care to replace these lost nutrients. In some cases, cross-reactivity may when the proteins in one food are similar to the proteins in another. When that happens, the body's immune system sees them as the same. There is a high degree of cross-reactivity between cow's milk and the milk from other mammals such as goat and sheep. In studies, the risk of allergy (resulting in symptoms) to goat's milk or sheep's milk in a person with cow’s milk allergy is about 90%. The risk is much lower, about 5%, for allergy to mare's milk which is less cross-reactive with cow's milk. | + | === Milk Ingredients === |
| + | |||
| + | Always read the entire ingredient label to look for the names of milk. Milk ingredients may be within the list of the ingredients or could be listed in a “Contains: Milk” statement beneath the list of ingredients. Advisory statements such as “may contain milk” or “made in a facility with milk” are voluntary and not required by any labeling law. It is recommend for the individual to consult their doctors if they consume products with these labels. | ||
| - | Foods from the meat and alternative food category can provide the proteins necessary to meet daily requirements However, to replace calcium the individual may need to consume a lots of non-dairy foods containing calcium which may be more than they are cable of consuming. Furthermore, calcium fortified juices can provide additional calcium but are not a good source of other nutrients. | + | <box 50% round | > {{ :playground:33f0310b003e9be91c52d92f7c34c3b3_3_.png?500 |}} </box|Figure 8: A list of milk ingredients. (Retrieved from: Kids with Food Allergies, 2019)> |
| - | Many milk alternatives are also based on legumes, seeds and grains. These include rice, hemp, soy, sunflower, oat, and coconut milks. Those not allergic to nuts may also consider nut milks (the most common of which is almond milk). Most of these milks can be substituted one-for-one in recipes. Many are available in original or other flavors. They are also available in sweetened and unsweetened varieties. Generally, the unsweetened and unflavored versions work best as substitutes in recipes. The following are some examples of milk alternatives based on legumes, seeds and grains. | + | ===== Lactase Supplements ===== |
| - | Soy milk | + | When dietary restriction of lactose consumption is not a suitable option, lactase supplements are available (Mattar //et al.//, 2012). Lactase enzyme produced industrially by fungi of the genus Aspergillus, are suitable supplements to the lactase produced in the small intestines of humans (Mattar //et al.//, 2012). This enzyme in the form of beta-galactosidase tablets, is available over the counter in several countries. The beta-galactosidase tablets must be taken at the time of lactose consumption in order to effectively aid in the digestion of lactose (Mattar //et al.//, 2012). In addition, most available forms of this tablet are pH sensitive and are only active in acidic environments such as that of the stomach (Mattar //et al.//, 2012). It is important to not that excessive acidity can denature the enzyme so consumption while fasting is not recommended (Mattar //et al.//, 2012). |
| - | Fortified rice milk | + | |
| - | Fortified grain or seed milks (oat milk, flax milk) | + | |
| - | Fortified nut milks (almond or cashew milk) | + | |
| - | Fortified coconut milk | + | |
| - | Any of these milk substitutes can be used, if tolerated. Make sure they are a good source of calcium and additional nutrients. Review the nutrition information on the package to check the amount of protein, which should be 8 grams per 8 ounce serving. Soy or rice milk can be used for children who are eating a variety of other foods. The soy or rice milk must be calcium fortified or contain 30 percent calcium. | ||
| - | When cooking, you can substitute non-dairy margarine or oils (in equal amounts) for butter. Soy-based, coconut-based, and pea-based yogurt, sour cream, and cream cheese products are available at many grocery stores. Milk-free ice creams and other products are also available. Be sure to check the ingredient statements to make sure that they contain no milk ingredients | + | ====== REFERENCES ====== |
| - | How to Read a Label for Milk | + | |
| - | Always read the entire ingredient label to look for the names of milk. Milk ingredients may be within the list of the ingredients. Or milk could be listed in a “Contains: Milk” statement beneath the list of ingredients. Advisory statements such as “may contain milk” or “made in a facility with milk” are voluntary. Advisory statements are not required by any labeling law. It is recommend for the individual to consult their doctors if they consume products with these labels. | + | Arola, H. (1994). Diagnosis of Hypolactasia and Lactose Malabsorption. //Scandinavian Journal of Gastroenterology//, 29(sup202), 26–35. doi:10.3109/0036552940909174 |
| + | Fang, L., Ahn, J. K., Wodziak, D., & Sibley, E. (2012). The human lactase persistence-associated SNP− 13910* T enables in vivo functional persistence of lactase promoter–reporter transgene expression. //Human Genetics//, 131(7), 1153-1159. doi: 10.1007/s00439-012-1140-z | ||
| - | ====== REFERENCES ====== | + | IMB Labor Berlin: Lactose Intolerance. (2019). Retrieved from https://www.imd-berlin.de/en/special-areas-of-competence/food-intolerances/lactose-intolerance.html |
| - | Arola, H. (1994). Diagnosis of Hypolactasia and Lactose Malabsorption. Scandinavian Journal of Gastroenterology, 29(sup202), 26–35. doi:10.3109/0036552940909174 | + | Itan, Y., Jones, B. L., Ingram, C. J. E., Swallow, D. M., & Thomas, M. G. (2010). A worldwide correlation of lactase persistence phenotype and genotypes.// BMC Evolutionary Biology//, 10, 36. doi: /10.1186/1471-2148-10-36 |
| - | Fang, L., Ahn, J. K., Wodziak, D., & Sibley, E. (2012). The human lactase persistence-associated SNP− 13910* T enables in vivo functional persistence of lactase promoter–reporter transgene expression. Human genetics, 131(7), 1153-1159. doi: 10.1007/s00439-012-1140-z | + | |
| - | Itan, Y., Jones, B. L., Ingram, C. J. E., Swallow, D. M., & Thomas, M. G. (2010). A worldwide correlation of lactase persistence phenotype and genotypes. BMC Evolutionary Biology, 10, 36. doi: /10.1186/1471-2148-10-36 | + | Itan, Y., Powell, A., Beaumont, M. A., Burger, J., & Thomas, M. G. (2009). The origins of lactase persistence in Europe. //PLoS Computational Biology//, 5(8), e1000491. doi: 10.1371/journal.pcbi.1000491 |
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| Lactose Intolerance: Background, Pathophysiology, Etiology. (2017). Retrieved from https://emedicine.medscape.com/article/187249-overview | Lactose Intolerance: Background, Pathophysiology, Etiology. (2017). Retrieved from https://emedicine.medscape.com/article/187249-overview | ||
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| - | Mattar, R., de Campos Mazo, D. F., & Carrilho, F. J. (2012). Lactose intolerance: diagnosis, genetic, and clinical factors. Clinical and experimental gastroenterology, 5, 113-121. doi: 10.2147/CEG.S32368 | + | Mattar, R., de Campos Mazo, D. F., & Carrilho, F. J. (2012). Lactose intolerance: diagnosis, genetic, and clinical factors. //Clinical and Experimental Gastroenterology//, 5, 113-121. doi: 10.2147/CEG.S32368 |
| - | Misselwitz, B., Pohl, D., Frühauf, H., Fried, M., Vavricka, S. R., & Fox, M. (2013). Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment. United European gastroenterology journal, 1(3), 151-159. doi: 10.1177/205064061384463 | + | Misselwitz, B., Pohl, D., Frühauf, H., Fried, M., Vavricka, S. R., & Fox, M. (2013). Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment. //United European Gastroenterology Journal//, 1(3), 151-159. doi: 10.1177/205064061384463 |
| - | Patel, Y. T., & Minocha, A. (2000). Lactose intolerance: Diagnosis and management. Comprehensive Therapy, 26(4), 246–250. doi:10.1007/s12019-000-0025-6 | + | Patel, Y. T., & Minocha, A. (2000). Lactose intolerance: Diagnosis and management. //Comprehensive Therapy//, 26(4), 246–250. doi:10.1007/s12019-000-0025-6 |
| Prevalence of lactose intolerance. (2013). Retrieved from https://www.food-intolerance-network.com/food-intolerances/lactose-intolerance/ethnic-distribution-and-prevalence.html | Prevalence of lactose intolerance. (2013). Retrieved from https://www.food-intolerance-network.com/food-intolerances/lactose-intolerance/ethnic-distribution-and-prevalence.html | ||
| - | Ridefelt, P., & Håkansson, L. D. (2005). Lactose intolerance: Lactose tolerance test versus genotyping. Scandinavian Journal of Gastroenterology, 40(7), 822–826. doi: 10.1080/0036552051001576 | + | Ridefelt, P., & Håkansson, L. D. (2005). Lactose intolerance: Lactose tolerance test versus genotyping. //Scandinavian Journal of Gastroenterology//, 40(7), 822–826. doi: 10.1080/0036552051001576 |
| - | Rusynyk, R. A., & Still, C. D. (2001). Lactose intolerance. Journal of the American Osteopathic Association, 101(4 supplement 1), 10S. | + | Rusynyk, R. A., & Still, C. D. (2001). Lactose intolerance. //Journal of the American Osteopathic Association//, 101(4 supplement 1), 10S. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/11392211 |
| - | Simoons, F. J. (1969). Primary adult lactose intolerance and the milking habit: A problem in biological and cultural interrelations. The American Journal of Digestive Diseases, 14(12), 819–836. doi: 10.1007/BF02233204 | + | Simoons, F. J. (1969). Primary adult lactose intolerance and the milking habit: A problem in biological and cultural interrelations. T//he American Journal of Digestive Diseases//, 14(12), 819–836. doi: 10.1007/BF02233204 |
| - | Simren, M., & Stotzer, P. O. (2006). Use and abuse of hydrogen breath tests. Gut, 55(3), 297-303. doi:10.1136/gut.2005.075127 | + | Simren, M., & Stotzer, P. O. (2006). Use and abuse of hydrogen breath tests.// Gut//, 55(3), 297-303. doi:10.1136/gut.2005.075127 |
| - | Shaukat, A., Levitt, M. D., Taylor, B. C., MacDonald, R., Shamliyan, T. A., Kane, R. L., & Wilt, T. J. (2010). Systematic review: effective management strategies for lactose intolerance. Annals of internal medicine, 152(12), 797-803. doi: 10.7326/0003-4819-152-12-201006150-00241 | + | Shaukat, A., Levitt, M. D., Taylor, B. C., MacDonald, R., Shamliyan, T. A., Kane, R. L., & Wilt, T. J. (2010). Systematic review: effective management strategies for lactose intolerance. //Annals of Internal Medicine//, 152(12), 797-803. doi: 10.7326/0003-4819-152-12-201006150-00241 |
| - | Solomons, N. W., García-Ibañez, R., & Viteri, F. E. (1980). Hydrogen breath test of lactose absorption in adults: the application of physiological doses and whole cow’s milk sources. The American Journal of Clinical Nutrition, 33(3), 545–554.doi:10.1093/ajcn/33.3.545 | + | Solomons, N. W., García-Ibañez, R., & Viteri, F. E. (1980). Hydrogen breath test of lactose absorption in adults: the application of physiological doses and whole cow’s milk sources. //The American Journal of Clinical Nutrition//, 33(3), 545–554.doi:10.1093/ajcn/33.3.545 |
| - | Srinivasan, R., & Minocha, A. (1998). When to suspect lactose intolerance: symptomatic, ethnic, and laboratory clues. Postgraduate medicine, 104(3), 109-123. doi: 10.3810/pgm.1998.09.577 | + | Srinivasan, R., & Minocha, A. (1998). When to suspect lactose intolerance: symptomatic, ethnic, and laboratory clues. //Postgraduate Medicine//, 104(3), 109-123. doi: 10.3810/pgm.1998.09.577 |
| - | Swagerty, D. L., Walling, A. D., & Klein, R. M. (2002). Lactose intolerance. American family physician, 65(9), 1845-1860. | + | Swagerty, D. L., Walling, A. D., & Klein, R. M. (2002). Lactose intolerance. //American Family Physician//, 65(9), 1845-1860. |
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