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Vitamin A Dr.Mary Megson has used Vitamin A from Cod Liver Oil with apparent great success in ASD. Why would this be? For numerous years practitioners in Europe thought that goiter was caused by Vitamin A deficiency. However, while Vitamin A supplementation was able to reduce many of the accompanying symptoms, it wasn't able to get rid of all of them. Later, when it became known that iodine was the “suspect substance” in question, it was learned that thyroid status regulates Vitamin A metabolism. In current times biomedical research has gathered much knowledge on nuclear receptors and developmental toxicity bioassays which show how thyroid hormones modulate the biologic activity of retinoids (i.e. Kraft et al, 1994). The condition of low Free T3 (hypothyroidism) decreases the availability of retinol and/or its metabolism to retinoic acid, resulting in low Vitamin A levels. On the other hand, Vitamin A can influence thyroid hormones. This is due to the fact that the retinoic acid receptors share much with the T3 receptor - they belong to the same "superfamily" of G proteins. The TSH receptor itself contains distinct response elements for regulation by retinoids and T3 (Breen et al, 1997). This is why Vitamin A suppresses TSH levels (as shown by, i.e.: Darbon-Almirante et al, 1999; Breen et al, 1997; Coya et al, 1997). Just like in the case of iodine, the symptoms of Vitamin A excess may imitate the symptoms of Vitamin A deficiency - a so-called “paradoxal effect” In the liver, Vitamin A enhances T4 to T3 conversion (Morley et al, 1980) which is usually inhibited by such toxins as mercury or fluoride complexes. The TSH receptor is the lead activator of Gq/11 (Allgeier et al.1994). The TSH receptor can stimulate all 4 G-protein families (Laugwitz et al, 1996), and is known as the natural “universal” G protein - an activity entirely imitated by fluorides. Therefore it is clear why Vit A supplenmentation has also shown benefits in the treatment of “fluorosis”. Retinol binding protein (RBP) and TSH levels are inversely correlated. Mean RBP levels were significantly reduced in hypothyroid patients and the retinol/RBP ratio was also significantly different between euthyroid and hypothyroid children (Centanni et al, 1998). G/11: Novak et al (2000) examined the expression of phosphoinositide signaling proteins in human NT2-N cells, a well characterized model system for CNS neurons:
=============================================== Allgeier A, Offermanns S, Van Sande J, Spicher K, Schultz G, Dumont JE - "The human thyrotropin receptor activates G-proteins Gs and Gq/11" J Biol Chem 269(19):13733-5 (1994) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8188646&form=6&db=m&Dopt=r Breen JJ, Hickok NJ, Gurr JA - "The rat TSHbeta gene contains distinct Centanni M, Maiani G, Vermiglio F, Canettieri G, Sanna AL, Moretti F, Trimarchi F, Andreoli M - "Combined impairment of nutritional parameters and thyroid homeostasis in mildly iodine-deficient children" Thyroid 8(2):155-9 (1998) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9510124&form=6&db=m&Dopt=r Coya R, Carro E, Mallo F, Dieguez C - "Retinoic acid inhibits in vivo thyroid-stimulating hormone secretion" Life Sci 60(16):PL 247-50 (1997) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9096264&form=6&db=m&Dopt=r Dabon-Almirante CL, Damle S, Wadler S, Hupart K - "Related case report: in vivo suppression of thyrotropin by 9-cis retinoic acid" Cancer J Sci Am 5(3):171-3 (1999) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10367174&form=6&db=m&Dopt=r Kraft JC, Willhite CC, Juchau MR - "Embryogenesis in cultured whole rat embryos after combined exposures to 3,3',5-triiodo-L-thyronine (T3) plus all-trans-retinoic acid and to T3 plus 9-cis-retinoic acid" J Craniofac Genet Dev Biol 14(2):75-86 (1994) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8071425&form=6&db=m&Dopt=r Laugwitz KL, Allgeier A, Offermanns S, Spicher K, Van Sande J, Dumont JE, Schultz G - "The human thyrotropin receptor: a heptahelical receptor capable of stimulating members of all four G protein families" Proc Natl Acad Sci U S A 93(1):116-20 (1996) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8552586&form=6&db=m&Dopt=r Megson MN - "Is autism a G-alpha protein defect reversible with natural vitamin A?" Med Hypotheses 54(6):979-83 (2000) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10867750&form=6&db=m&Dopt=r FULL TEXT: CONGRESSIONAL TESTIMONY: Novak JE, Agranoff BW, Fisher SK - "Increased expression of Galpha(q/11) and of phospholipase-Cbeta1/4 in differentiated human NT2-N neurons: enhancement of phosphoinositide hydrolysis" J Neurochem 74(6):2322-30 (2000) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10820192&form=6&db=m&Dopt=r
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