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Lactase Persistence is the tendencies of man to react to lactose.

Lactase

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Lactase is the enzyme through which we are capable of digesting lactose which is made up of simple sugars, glucose and galactose. Lactase breaks them into their separate parts to be easily used. Lactase is an enzyme generally in little children. Beginning at ages 2-5 as a majority of people mature they no longer produce lactase and they become incapable of digesting lactose leading to many clinical symptoms we describe as lactose intolerance and lactose malabsorption. [1][2][3]

Lactase Non-Persistence

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Lactase non-persistence is another word for lactose malabsorbers or in other words those that no longer produce enough lactase to break down lactose in dairy products therefore resulting in complications. The three major complications include adult-type hypolactasia, CLD and lactose intolerance.[4] [5]

Hypolactasia

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Adult-type[6][7] hypolactasia is also known as Lactase non-persistence. Adult-type hypolactasia is the normal process in mammals, in this case human, to begin producing less lactase enzyme after the switch from a mother’s milk to other forms of nourishment. Evolutions or mutations have occurred though throughout human development allowing less than half of the human population to retain lactase activity through their life. It is theory that these populations have gained an advantage in survival because they can gain the extra nutrients from the ability to digest milk, lactose, and the forms of other nutrients mankind uses for sustenance.

Congenital Lactase Deficiency

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Congenital lactase deficiency or CLD is a gastrointestinal disorder in the newborn. This disorder is seen in babies throughout the world but a high concentration in Finland suffers from congenital lactase deficiency. [8]

Lactose Intolerance

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Lactose Intolerance[9] is different from other lactose malabsorber disorders because along with the inability to break down lactose comes unpleasant gastrointestinal problems. When those of with lactose intolerance consume large of dairy products passes into the large intestine where the resident facultative bacteria flora acts upon it to break it down. The lactose is broken down by the bacteria into acetic, butyric, propionic and fatty acids. These new products are used by the intestinal cells to be used as substances put to use in the metabolism process. Other by-products of the breakdown of lactose are carbon dioxide, hydrogen and methane. These latter mentioned by-products cause gassy, bloated, and/or nauseous feelings. Another symptom of lactose intolerance is diarrhea. [10]

Other Lactase Maldigestion

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In many other developments of lactose maldigestion people maintain small amounts of lactase production but not enough to prevent some difficulties. This small amount of lactase and other friendly bacteria in the stomach allow for this issue to be addressed with many ways that are used to tame or “cure” other forms of lactose mal-digestion and lactose intolerance. [11][12][13]

Dealing with lactose Malabsorption and intolerance

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Because of an experiment made at Meharry Medical Center in Nashville, Tennessee it is believed that to extent lactose intolerances can be overcome. By extent it is meant that people can develop a maximum tolerated dose. This means that although people may gain discomfort from the lactose in dairy products they will be able to gain a tolerance amount or certain concentration of lactase so that they will fill no discomfort within these bounds. It is a great thing to acquire an ability to digest dairy products because they are a source of a large amount of nutrients. There are many requested ways to deal with lactose malabsorption and Intolerance they are listed below. [14][15]

Developing a Tolerance

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One way to develop a small tolerance or remove discomfort is to drink milk more often but in smaller amounts, because this allows the lactase that may be present to not be overwhelmed and cause problems. It also allows friendly bacteria to gain abilities to help. [16] Eating dairy products with other meals or snacks can also help because it will take longer for the stomach to get through digesting giving more time for small amounts of lactase and friendly bacteria to break down lactose. Another way to be able to utilize nutrients in dairy products, which contain lactose, is to slowly increase your intake. This process will make it so your digestive system will develop to be able to handle lactose over time.[17]

Alternatives to High Lactase

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Another alternative to high lactose dairy products are dairy products where lactose has decayed or been processed already. Hard cheeses generally have the lactose removed during their making process. Also any yogurt with active cultures will have bacteria that contain enzymes that will digest lactose even in your digestive tract. Leave these yogurts out in room temperature for thirty minutes because these bacteria become dormant and inactive when refrigerated.

Reduced or No Lactase

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If all other techniques of “taming” your malabsorption and lactose intolerance fail consider the expensive alternative. There are many reduced-lactose milks and cheese available these include Lactaid, and Dairy Ease. [18]

Medicine Solutions

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Another expensive options are droplets for your milk which will break down the lactose before consumption. These droplets on average eliminate two thirds of the lactose in a glass of milk after twenty four hours of being left out to sit. Milk or reduced-lactose milk will taste sweeter because when lactose is broken down it is made into sweeter forms of sugar.[19] Pills and capsules are another way to help with the consumption of lactose because they provide digestive enzymes for your body that will break down lactose. These tablets should be taken right before consumption of dairy products because the affects wear off quickly. [20]

Evolution

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There are several different observations along the evolution and development of lactase persistence. Lactase persistence is seen by some as a result of culture evolution when it comes to the career of dairying. Cultures that kept cattle and other milk animals tended to develop a growing number of milk-using and lactose friendly adults which would in turn increase the amount of those devoting themselves to raising their livestock. [21][22] Another theory behind the evolution and growth of the lactase persistent gene is it is caused by pressures. It has been observed that there is a high concentration of lactase persistent adults in Northern Europe today. In past populations and harsh conditions pressures may have led to the development and the survival of lactase persistent adults. This theory is supported by the fact that many bones of past populations that have suddenly become extinct like the Greenland Viking colony have shown weak bone stuctures, and it is know that they had a little skin exposure to the sun so less vitamin D production so therefore the people would have benefited from the development of lactase persistence. [23][24]

A final theory behind the lactase persistent gene is that of dependency. In the Sahara-Arabian Peninsula it is observed to have a large concentration of lactase persistent adults. Scientists believe that because of harsh conditions this gene would give adults a selective advantage because they would be able consume large quantities of milk and gain they needed nutrients to survive. This allowed more to survive with the lactase persistent gene producing more youth and a culture with lactase persistence as dominant.[25][26][27]

Nutritional Implications

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Dairy products are a large source of nutrients, being rich in protein, calcium, and carbohydrates. Because of the high nutritional value in dairy products it can be very unhealthy, even dangerous, for any children to be lactose intolerant. The solution for lactose intolerant children and infants are formulas made from soybeans. Due to the ability for adults to gain all the nutrients in dairy from other sources, animals and plants or even fermented milk products, it is not necessary to have actual dairy products in their diet if they are lactose intolerant. But there are many lactose-free dairy products being developed and put in to the market for those with the lactase deficiency. [28]

Notes

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  1. ^ Pattersen, David K. “Lactose Intolerance”. Cambridge World of Food.2000. V.1. p 2000-1062
  2. ^ Di Stefano, M; Terulla, V; Tana, P; Mazzocchi, S; Romero, E; Corazza, G.R. “Genetic Test For Lactase Non-Persistence And Hydrogen Breath test: Is Genotype Better Than Phenotype To Diagnose Lactose Malabsorption?”. Digestive and Liver Disease. 2009. Vol.41(7). P474-479.
  3. ^ Karamanolis, G; Tack, J. “Nutrition and Motility Disorders”. Best Practice & Research Clinical Gastroenterology. 2006. Vol.20(3). P485-505.
  4. ^ Szilagyi, A; Malolepszy, P; Hamard, E; Xue, X; Hilzenrat, N; Ponniah, M; MacNamara, E; Chong, G. “Comparison of a real-Time Polymerase Chain Reaction Assay for Lactase Genetic Polymorphism With Standard Indirect Tests for Lactose Maldigestion”. Clinical Gastroenterology and Hepatology. 2007. Vol.5(2). P192-196.
  5. ^ Szilagyi, A; Malolepszy, P; Hamard, E; Xue, X; Hilzenrat, N; Ponniah, M; MacNamara, E; Chong, G. “Comparison of a real-Time Polymerase Chain Reaction Assay for Lactase Genetic Polymorphism With Standard Indirect Tests for Lactose Maldigestion”. Clinical Gastroenterology and Hepatology. 2007. Vol.5(2). P192-196.
  6. ^ Dore, M.P.; Pedroni, A; Peltonen, L; Enattah, N; Tadeu, V; Delitala, G; Caballli-Sforza, L; Obinu, D. .”Prevalence of Lactase Persistence and the Performance of a New Non Invasive Genetic test In adult Patients”. Digestive and Liver Disease. 2008. Vol.40. pS63.
  7. ^ Dore, M.P.; Pedroni, A; Peltonen, L; Enattah, N; Tadeu, V; Delitala, G; Caballli-Sforza, L; Obinu, D. “A Novel Non Invasive genetic test to Diagnose Hypolactasia in adult Patients”. Gastroenterolotgy. 2008. Vol.134(4). pA-673.
  8. ^ Behrendt, M; Kelser, M; Hoch, M; Naim, H.Y. “Impaired trafficking and Subcellular Localization of a Mutant Lactase associated with congenital Lactase Deficiency”. Gastroenterology.2009. Vol.136(7). P2295-2303.
  9. ^ Pattersen, David K. “Lactose Intolerance”. Cambridge World of Food.2000. V.1. p 2000-1062
  10. ^ Troelsen, J.T. “Adult-type Hypolactasia and Regulation of Lactase Expression”. BBA-general Subjects.2005. Vol.1723(1-3). p19-32.
  11. ^ Troelsen, J.T. “Adult-type Hypolactasia and Regulation of Lactase Expression”. BBA-general Subjects.2005. Vol.1723(1-3). p19-32.
  12. ^ Behrendt, M; Kelser, M; Hoch, M; Naim, H.Y. “Impaired trafficking and Subcellular Localization of a Mutant Lactase associated with congenital Lactase Deficiency”. Gastroenterology.2009. Vol.136(7). P2295-2303.
  13. ^ Klotz, Arthur P. “Gastrointestinal Symptons And Intestinal Lactase Deficiencies??? A Word Of Caution”. The American Journal of Digestive Diseases. 1967. Vol.12(4). P421-423.
  14. ^ Casiglione, F; Di Girolamo, E; Ciacci, C; Caporaso, N; Pasquate, L; Cozzolino, A; Tortora, R; Testa, A; Rispo, A. “Lactose Malabsorption: Clinical of Breath Test Diagnosis?”. The European e-Journal of clinical Nutrition and Metabolism.2008. Vol.3(6). Pe316-e320.
  15. ^ Patel, YT; Minocha, A. “Lactose Intolerance: Diagnosis and Management.” Caomprehensive Therapy.2000. Vol.26(4). P246-50.
  16. ^ Patel, YT; Minocha, A. “Lactose Intolerance: Diagnosis and Management.” Caomprehensive Therapy.2000. Vol.26(4). P246-50.
  17. ^ Patel, YT; Minocha, A. “Lactose Intolerance: Diagnosis and Management.” Caomprehensive Therapy.2000. Vol.26(4). P246-50.
  18. ^ Patel, YT; Minocha, A. “Lactose Intolerance: Diagnosis and Management.” Caomprehensive Therapy.2000. Vol.26(4). P246-50.
  19. ^ Sinden, A.A; Sutphen, JL. “Dietary Treatment of Lactose Intolerence in Infants and Children”. Journal of the American Dietetic Association.1991. Vol.91(12). P1567-71.
  20. ^ Patel, YT; Minocha, A. “Lactose Intolerance: Diagnosis and Management.” Caomprehensive Therapy.2000. Vol.26(4). P246-50.
  21. ^ Itan, Yuval; Jones, Bryony; ingram, Catherine; Swallow, Dallas; Thomas, Mark. “A Worldwide correlation of Lactase Persistence Phenotype and Genotypes”. BMC Evolutionary Biology. 2010. Vol.10(1). P36.
  22. ^ Gerbault, Pascale; Moret, Celine; Currat, Mathias; Sanchez-Maza, Alicia; O’Rourke, Dennis. “Impact of Selection and Demography On the Diffusion of Lactase Persistence”. 2009. Vol.4(7).
  23. ^ Itan, Yuval; Jones, Bryony; ingram, Catherine; Swallow, Dallas; Thomas, Mark. “A Worldwide correlation of Lactase Persistence Phenotype and Genotypes”. BMC Evolutionary Biology. 2010. Vol.10(1). P36.
  24. ^ Gerbault, Pascale; Moret, Celine; Currat, Mathias; Sanchez-Maza, Alicia; O’Rourke, Dennis. “Impact of Selection and Demography On the Diffusion of Lactase Persistence”. 2009. Vol.4(7).
  25. ^ Sinden, A.A; Sutphen, JL. “Dietary Treatment of Lactose Intolerence in Infants and Children”. Journal of the American Dietetic Association.1991. Vol.91(12). P1567-71.
  26. ^ Itan, Yuval; Jones, Bryony; ingram, Catherine; Swallow, Dallas; Thomas, Mark. “A Worldwide correlation of Lactase Persistence Phenotype and Genotypes”. BMC Evolutionary Biology. 2010. Vol.10(1). P36.
  27. ^ Gerbault, Pascale; Moret, Celine; Currat, Mathias; Sanchez-Maza, Alicia; O’Rourke, Dennis. “Impact of Selection and Demography On the Diffusion of Lactase Persistence”. 2009. Vol.4(7).
  28. ^ Sinden, A.A; Sutphen, JL. “Dietary Treatment of Lactose Intolerence in Infants and Children”. Journal of the American Dietetic Association.1991. Vol.91(12). P1567-71.