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Sunday, 15 December 2013

Retinol (The animal forms of vitamin A) Health Benefits

Retinol Health Benefits
Retinol, one of the animal forms of vitamin A, is a yellow, fat-soluble substance, a diterpenoid and an alcohol converted to vitamin A and and the retinyl ester derivative of the alcohol stored mostly in liver, when eating animal food sources, such as liver and egg yolk. When converted to retinoic acid, vitamin A is essential for skin health, teeth remineralization, bone growth.and the process of cell differentiation, hence, the growth and development of embryos Retinoic acid via the retinoic acid receptor.
1. Early Organogenesis
Retinoic acid, a derivative of vitamin A, is an essential component of cell-cell signaling during vertebrate organogenesis. In early development retinoic acid functions as a trunk organizer by providing an instructive signal for posterior neuroectoderm and foregut endoderm and a permissive signal for trunk mesoderm differentiation. At later stages, retinoic acid contributes to the development of the eye and other organs. Recent efforts suggest that retinoic acid acts primarily in a paracrine manner and provide insight into the cell-cell signaling networks that control differentiation of pluripotent cells.(25)
2. Endodermal organ
Endoderm organ primordia become specified between gastrulation and gut tube folding in Amniotes, the others two layers are the ectoderm (outside layer) and mesoderm (middle layer), with the endoderm as the intermost layer. The team at Swiss Institute for Experimental Cancer Researchshowed that retinoic acid (RA) signaling coordinates the position of different endoderm organs along the antero-posterior axis in chick embryos and could serve as a basis for the differentiation of specific endodermal organs from ES cells.(26)
3. Anti cancers
In a  a study to assess the feasibility and impact of two dietary interventions for ovarian cancer survivors, conducted by University of Houston and University of Texas MD Anderson Cancer Center, supports the feasibility of designing dietary interventions for stages II-IV ovarian cancer survivors and provides preliminary evidence that a low fat high fiber diet and a diet supplemented with encapsulated FVJC may increase phytonutrients in ovarian cancer survivors, after 6 months, total serum carotenoid levels and α- and β-carotene concentrations were significantly increased in both groups (P<0.01); however, β-carotene concentrations were increased more in the FVJC group. Serum β-cryptoxanthin levels, fiber intake (+5.2g/day), and daily servings of juice (+0.9 servings/day) and vegetables (+1.3 servings/day) were all significantly increased in the LFHF group (all P<0.05). Serum levels of albumin, lutein and zeaxanthin, retinol, and retinyl palmitate were significantly increased in the FVJC group (all P<0.05). No changes in cancer antigen-125, anthropometry, or HRQOL were observed.(27)
4. The Hox genes
The study by National Institute for Medical Research, Mill Hill, London, indicated that retinoids can affect the expression of Hox genes in cell linesand embryonic tissues; the hindbrain and branchialregion of the head are particularly sensitive to theteratogemc effects of retinoic acid. The presence ofendogenous retinoic acid, together with the distributionof retinoid binding proteins and nuclear receptorsin the developing embryo, strongly suggest thatretinoic acid is a natural morphogen in vertebrate development(28)
5. Prostate cancer
In the study to investigae the retinoids, the natural or synthetic derivatives of Vitamin A (retinol), are essential for the normal development of prostate and have been shown to modulate prostate cancer progression in vivo as well as to modulate growth of several prostate cancer cell lines. 9-cis-retinoic acid and all-trans-retinoic acid are the two most important metabolites of retinol, showed that showed that 9-cis-retinoic acid and all-trans retinoic acid enhanced the assembly of connexin32 into gap junctions. Our results further showed that 9-cis-retinoic acid and all-trans-retinoic acid prevented androgen-regulated degradation of gap junctions, post-translationally, independent of androgen(29)
6. Etc.
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