Folic Acid and Vitamin D (Calcitrio

Folic Acid and Vitamin D (Calcitriol)
Approximately 20 years ago, health agencies recommended that childbearing women supplement their diet with folic acid to reduce the risk of neural tube defects (NTD’s) and to facilitate proper neural tube closure, preventing Spina Bifida. Research has shown that folate can reduce the incidence of neural tube defects by about 70% and can also decrease the severity of these defects when they occur (Holmes 1988; Milunsky et al. 1989; Mulinare et al. 1988). Genetic polymorphisms of enzymes required to metabolize folate are common with autism and display up to 50% reduction in activity, hence attenuating the ability of folate to function in cellular processes (Scriver et al. 2000). The enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR) is required to convert folic acid into a form that can be utilized for methylation (Rogers 2008). By increasing maternal folic acid intake, there is an increased survival rate of children possessing a mutated MTHFR enzyme, C677T mutation. As a result, these children have a decreased enzymatic activity and, if not supplemented with folic acid during development, will eventually experience neurological regression and show an increased risk of autism. Thus, mutations in MTHFR have been associated with the development of autism. As mentioned, health agencies made recommendations to childbearing women that they should supplement their diet with folic acid to prevent neural tube defects (NTD’s). The recommended dose remains 400–1,000 lg. Although this supplement has decreased the rate of NTD’s, many feel that, as a result, autism is on the rise. Rogers (2008) investigates this hypothesis, and Fig. 4 displays the cases of autism from 1992 to 2007. Interestingly, the US Public Health Service has acknowledged a link between inadequate folic acid intake and neural tube defects, and in September 1992, recommended folic acid supplementation (Rogers 2008). It seems that genetic polymorphisms of folic acid metabolism enzymes are common, and attenuate the ability of folate to function (Scriver et al. 2000). A key enzyme methylenetetrahydrofolate reductase (MTHFR)—is the enzyme required for folate metabolism, whereas the presence of C677T mutant form has been linked to autism (Boris et al. 2004). The hypothesis by Rogers (2008) affirms that by increasing folic acid supplementation, birth rates of children containing MTHFR mutation(s) have increased. A normal or decreased folic acid status in fetuses with attenuated MTHFR activity results in increased risk of miscarriage, and, after birth, the children still require folic acid supplementation to compensate for reduced enzymatic activity. Folic acid plays, hence, an important role in proper methylation, which is important for gene silencing. The children who possess MTHFR mutations and do not receive folic acid supplementation are at risk for developing autism. Figure 5 displays the pathways involved in this hypothesis. This hypothesis explains how increasing folic acid supplementation alters the natural selection in favor of an adverse gene polymorphism, MTHFR C677T, which is found in high frequency in autism (Rogers 2008). A requirement of folic acid supplementation in children is, therefore, recommended for normal methylation and to promote a proper neurodevelopment. Moreover, hypotheses involving MTHFR implication with autism state that as a result of increased folic acid supplementation, natural selection has shifted in favor of progeny possessing a specific mutation(s) that would otherwise increase the risk of miscarriage in absence of folic acid supplementation. Simply, MTHFR enzyme metabolizes and activates folic acid for methylation, among other cellular functions, and attenuated phenotypes have negative effects on neuronal integrity. To overview the folic acid hypothesis, there is strong evidence that suggests this phenomenon is not coincidental. The environment influences responsive genes and, subsequently the genome. Vitamin D is a neurosteroid (McGrath et al. 2001) and follows this type of genetic organization (Cannell 2008). Calcitriol (activated vitamin D) deficiency in mice produces offspring with abnormal cell proliferation, and reduced expression of neuronal structure genes (Feron et al. 2005). Experimental studies showed that vitamin D deficiency dysregulates 36 proteins involved in mammalian brain development (Almeras et al. 2007). Importantly, vitamin D has also been shown to: (1) down-regulate neurologically harmful cytokines in the brain (Moore et al. 2005); (2) partially reverse brain damage (Burne et al. 2004); (3) increase cellular levels of the anti-oxidant glutathione (Garcion et al. 2002), which is capable of removing free radicals and also chelating heavy metals, including mercury (Kern and Jones 2006).
Cui et al. (2007) have determined that vitamin D is important for neural development and its deficiency negatively alters the brain structure and function. As mentioned, vitamin D, a neurosteroid, is considered to be an important regulator of cell proliferation in the developing brain, while

Kết quả (Việt) 1:

Axit folic và Vitamin D (Calcitriol)Approximately 20 years ago, health agencies recommended that childbearing women supplement their diet with folic acid to reduce the risk of neural tube defects (NTD’s) and to facilitate proper neural tube closure, preventing Spina Bifida. Research has shown that folate can reduce the incidence of neural tube defects by about 70% and can also decrease the severity of these defects when they occur (Holmes 1988; Milunsky et al. 1989; Mulinare et al. 1988). Genetic polymorphisms of enzymes required to metabolize folate are common with autism and display up to 50% reduction in activity, hence attenuating the ability of folate to function in cellular processes (Scriver et al. 2000). The enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR) is required to convert folic acid into a form that can be utilized for methylation (Rogers 2008). By increasing maternal folic acid intake, there is an increased survival rate of children possessing a mutated MTHFR enzyme, C677T mutation. As a result, these children have a decreased enzymatic activity and, if not supplemented with folic acid during development, will eventually experience neurological regression and show an increased risk of autism. Thus, mutations in MTHFR have been associated with the development of autism. As mentioned, health agencies made recommendations to childbearing women that they should supplement their diet with folic acid to prevent neural tube defects (NTD’s). The recommended dose remains 400–1,000 lg. Although this supplement has decreased the rate of NTD’s, many feel that, as a result, autism is on the rise. Rogers (2008) investigates this hypothesis, and Fig. 4 displays the cases of autism from 1992 to 2007. Interestingly, the US Public Health Service has acknowledged a link between inadequate folic acid intake and neural tube defects, and in September 1992, recommended folic acid supplementation (Rogers 2008). It seems that genetic polymorphisms of folic acid metabolism enzymes are common, and attenuate the ability of folate to function (Scriver et al. 2000). A key enzyme methylenetetrahydrofolate reductase (MTHFR)—is the enzyme required for folate metabolism, whereas the presence of C677T mutant form has been linked to autism (Boris et al. 2004). The hypothesis by Rogers (2008) affirms that by increasing folic acid supplementation, birth rates of children containing MTHFR mutation(s) have increased. A normal or decreased folic acid status in fetuses with attenuated MTHFR activity results in increased risk of miscarriage, and, after birth, the children still require folic acid supplementation to compensate for reduced enzymatic activity. Folic acid plays, hence, an important role in proper methylation, which is important for gene silencing. The children who possess MTHFR mutations and do not receive folic acid supplementation are at risk for developing autism. Figure 5 displays the pathways involved in this hypothesis. This hypothesis explains how increasing folic acid supplementation alters the natural selection in favor of an adverse gene polymorphism, MTHFR C677T, which is found in high frequency in autism (Rogers 2008). A requirement of folic acid supplementation in children is, therefore, recommended for normal methylation and to promote a proper neurodevelopment. Moreover, hypotheses involving MTHFR implication with autism state that as a result of increased folic acid supplementation, natural selection has shifted in favor of progeny possessing a specific mutation(s) that would otherwise increase the risk of miscarriage in absence of folic acid supplementation. Simply, MTHFR enzyme metabolizes and activates folic acid for methylation, among other cellular functions, and attenuated phenotypes have negative effects on neuronal integrity. To overview the folic acid hypothesis, there is strong evidence that suggests this phenomenon is not coincidental. The environment influences responsive genes and, subsequently the genome. Vitamin D is a neurosteroid (McGrath et al. 2001) and follows this type of genetic organization (Cannell 2008). Calcitriol (activated vitamin D) deficiency in mice produces offspring with abnormal cell proliferation, and reduced expression of neuronal structure genes (Feron et al. 2005). Experimental studies showed that vitamin D deficiency dysregulates 36 proteins involved in mammalian brain development (Almeras et al. 2007). Importantly, vitamin D has also been shown to: (1) down-regulate neurologically harmful cytokines in the brain (Moore et al. 2005); (2) partially reverse brain damage (Burne et al. 2004); (3) increase cellular levels of the anti-oxidant glutathione (Garcion et al. 2002), which is capable of removing free radicals and also chelating heavy metals, including mercury (Kern and Jones 2006).Cui et al. (2007) đã xác định rằng vitamin D là quan trọng cho sự phát triển thần kinh và thiếu tiêu cực làm thay đổi cấu trúc não và chức năng. Như đã đề cập, vitamin D, một neurosteroid, được coi là một điều quan trọng của sự gia tăng tế bào trong não đang phát triển, trong khi