Porpoising this month

Four children, training for an April marathon (it’s not looking promising), and writing an Integrated Summary of Effectiveness for a client…I’m purposely porpoising this month.  I hope to be up for a breath and a post in April…cheers!

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Folic acid supplementation and ASD risk

Hot off the press folks:

Published this week in the Journal of the American Medical Association (JAMA), this paper is worth sharing as it suggests a link between maternal folic acid deficiency and risk for developing ASD: Surén P, Roth C, Bresnahan M, et al. Association Between Maternal Use of Folic Acid Supplements and Risk of Autism Spectrum Disorders in Children. JAMA. 2013;309(6):570-577. doi:10.1001/jama.2012.155925.

This isn’t the first study to suggest that folic acid or folate may play a role in ASDs.  Folate is a water-soluble B vitamin that acts as a coenzyme or cosubstrate in numerous biochemical reactions and genetic expression.  It is essential for health and reduces risk of birth defects.  However, folic acid must be converted to an active form before it is used by the body (see figure below).  Folinic acid is an active form of folate that is currently under investigation in several clinical trials to improve oxidative stress markers, behavior, and language in individuals with ASD.

One of these studies is being conducted at the Arkansas Children’s Hospital under the direction of Drs. Richard Frye (primary investigator) and S. Jill James (sub-investigator).  Both investigators have published numerous peer-reviewed papers that can be found by searching PubMed.  This study (NCT01602016) was designed to evaluate the effect of folinic acid supplementation on language improvement and behaviors in 130 children with ASD ages 3 to 14 years.  The study involves 3 phases:

  1. A baseline or screening phase to evaluate language impairment and eligibility.
  2. A 12-week, randomized, placebo-controlled, double-blind treatment period with folinic acid or placebo.
  3. A 12-week open-label extension period to provide folinic acid to all participants who complete the double-blind treatment phase.

Notably, this study is being conducted at the Arkansas Children’s Hospital, which is one of the participating centers in the Autism Treatment Network (ATN). What is the ATN? The ATN is a network of hospitals, physicians, researchers, and families at 17 locations across the United States and Canada. The ATN’s goal is to provide comprehensive, high-quality care by teams of healthcare professionals who understand ASDs and are experts at treating ASD-associated medical conditions such as sleep disturbances and gastrointestinal problems.  An ATN hospital would be my first choice in seeking medical care for my son.

Back to folate, my son seems to have benefited from folate supplementation.  He currently takes an active form of folate called L-methylfolate or Deplin®.  I expect more data from researchers in the future to support (or not) the use of folate as an intervention for at least a subset of children with ASDs.

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Cholesterol: When Less Is Not Better


Image source: freepik.com

If, like many Americans, you think that the lower your blood cholesterol, the healthier you would be… think again.  Cholesterol is important for a host of physiological functions in the body described briefly below:

  • Helps build myelin, which is a substance that protects and covers nerve cells so that impulses travel more quickly (Saher, Brugger et al. 2005);
  • Builds and maintains cell membranes, including important signaling areas called “lipid rafts” (Simons and Ehehalt 2002, Korade and Kenworthy 2008);
  • Influences the development and patterning of the central nervous system (see below);
  • Serves as a precursor compound in the production of steroid hormones, bile acids, neuroactive steroids, and vitamins (most notably, Vitamin D) (Porter 2008, Orth and Bellosta 2012).Source: Great Plains Laboratory
cholesterol formation_GreatPlainsLaboratory

Imagine source: Great Plains Laboratory

Low cholesterol is associated with mental health disorders, such as depression, anxiety, suicidal tendencies, impulsivity, and aggressive behavior (Partonen, Haukka et al. 1999).  Importantly, as it relates to this blog, some researchers suspect that abnormal cholesterol and sterol metabolism may also contribute to the development of autism spectrum disorders (Tierney, Bukelis et al. 2006, Lee and Tierney 2011).  It turns out that the prevalence of autism spectrum disorders is relatively high (~50 to 75%) among individuals with a genetic disorder called Smith-Lemli-Opitz syndrome (SLOS) (Tierney, Nwokoro et al. 2000, Sikora, Pettit-Kekel et al. 2006), a disorder which was first described in 1964 by Drs. Smith, Lemli, and Opitz (Smith, Lemli et al. 1964).  Notably, SLOS is characterized by low blood and tissue concentrations of cholesterol (less than 10mg/dL in severe cases) and elevated blood and tissue concentrations of the precursor compound to cholesterol, 7‑dehydrocholesterol (7-DHC) (Tint, Irons et al. 1994).  Individuals with SLOS have characteristic physical malformations, growth problems, and behavioral abnormalities including, but not limited to, the following: failure to thrive (poor weight gain), hypotonia (poor muscle tone), sleep problems, social and language delays, stereotyped behaviors, aggression (such as self-biting and head banging), and some delays in cognitive functioning (Kelley and Hennekam 2000, Tierney, Nwokoro et al. 2001).  Sound familiar?

The prevalence of SLOS and other sterol disorders among individuals with ASD is unknown.  In blood samples from 100 boys and girls with autism, obtained from the Autism Genetic Research Exchange repository, no samples had sterol levels consistent with SLOS, but abnormally low blood cholesterol concentrations (less than 100 mg/dL) were measured in 19 of 100 (19%) samples (Tierney, Bukelis et al. 2006), suggesting that abnormal sterol metabolism is present in at least a subset of individuals with ASD.

Now, let’s review why cholesterol is important.  Listed below are reasons that researchers think low cholesterol may contribute to ASD (Lee and Tierney 2011):

  • Low cholesterol may affect the fate of how brain cells develop and later communicate by impairing sonic hedgehog (SHH) signaling during embryonic development.  SHH helps direct the pattern of the nervous system and limbs during embryonic development.

    lipid raft

    Image source: nigms.nih.gov

  • Low cholesterol may disrupt cell membrane signaling regions by disrupting membrane “lipid rafts” that serve as platforms for cell signaling and direct neuronal networks in the brain.

Anecdotal evidence suggests that cholesterol can improve many areas of functioning in individuals with SLOS (Elias, Irons et al. 1997, Irons, Elias et al. 1997).  However, no relationship between autism behaviors and cholesterol concentration was observed in a group of 14 children (aged 3 to 16 years) with SLOS (Sikora, Pettit-Kekel et al. 2006), nor did long-term dietary cholesterol supplementation improve developmental functioning in this same population (Sikora, Ruggiero et al. 2004).

To further investigate the link between cholesterol and autism, the Eunice Kennedy Shriver National Institute of Child Health and Human Development is sponsoring an ongoing, multicenter (Johns Hopkins, NIH Clinical Center, and Ohio State), randomized, double-blind, placebo-controlled study in 900 children (wow!) with ASD aged 4 to 12 years (“Cholesterol in ASD: Characterization and Treatment”; Clinical.Trials.gov Identifier: NCT00965068).  As of the time of this post (February 2013), this study was still actively recruiting study participants.  The primary goals of this study are listed below:

  1. Measure and characterize cholesterol concentrations in this large group of children with ASD.
  2. Evaluate the relationship between behavioral symptoms of autism with cholesterol concentrations (low, medium, high).
  3. Determine if adding cholesterol to the diet will improve behavioral and other characteristics in children with ASD who have low cholesterol.

The strength of the study described above is that it meets many of the “gold standard” study design criteria; it is randomized, double-blind, placebo-controlled, and large (900 participants!).  Therefore, the results of this study will hold significant weight with mainstream clinicians and researchers IF the integrity of study conduct is maintained.  Upon completion, the study administration and disposition will be carefully evaluated by asking questions similar to the following:

  • Did the number of participants enrolled into the study meet the target enrollment?
  • How many of the randomized participants completed the study as planned?
  • Did all enrolled participants meet the entrance criteria as planned?
  • Were participants compliant with the study protocol?
  • Was the treatment blind broken for any reason?

The autism community needs more “gold standard” studies.  I wish these investigators luck, because a study of this size with a heterogeneous population of individuals who notoriously have feeding issues will be a lot of work…a common problem for those trying to conduct high-quality studies in the ASD population.


  1. Compagnone, N. A. and S. H. Mellon (2000). “Neurosteroids: biosynthesis and function of these novel neuromodulators.” Front Neuroendocrinol 21(1): 1-56.
  2. Elias, E. R., M. B. Irons, A. D. Hurley, G. S. Tint and G. Salen (1997). “Clinical effects of cholesterol supplementation in six patients with the Smith-Lemli-Opitz syndrome (SLOS).” Am J Med Genet 68(3): 305-310.
  3. Irons, M., E. R. Elias, D. Abuelo, M. J. Bull, C. L. Greene, V. P. Johnson, L. Keppen, C. Schanen, G. S. Tint and G. Salen (1997). “Treatment of Smith-Lemli-Opitz syndrome: results of a multicenter trial.” Am J Med Genet 68(3): 311-314.
  4. Kelley, R. I. and R. C. Hennekam (2000). “The Smith-Lemli-Opitz syndrome.” J Med Genet 37(5): 321-335.
  5. Korade, Z. and A. K. Kenworthy (2008). “Lipid rafts, cholesterol, and the brain.” Neuropharmacology 55(8): 1265-1273.
  6. Lee, R. W. and E. Tierney (2011). “Hypothesis: the role of sterols in autism spectrum disorder.” Autism Res Treat 2011: 653570.
  7. Majewska, M. D. (1992). “Neurosteroids: endogenous bimodal modulators of the GABAA receptor. Mechanism of action and physiological significance.” Prog Neurobiol 38(4): 379-395.
  8. Nishimori, K., Y. Takayanagi, M. Yoshida, Y. Kasahara, L. J. Young and M. Kawamata (2008). “New aspects of oxytocin receptor function revealed by knockout mice: sociosexual behaviour and control of energy balance.” Prog Brain Res 170: 79-90.
  9. Orth, M. and S. Bellosta (2012). “Cholesterol: its regulation and role in central nervous system disorders.” Cholesterol 2012: 292598.
  10. Partonen, T., J. Haukka, J. Virtamo, P. R. Taylor and J. Lonnqvist (1999). “Association of low serum total cholesterol with major depression and suicide.” Br J Psychiatry 175: 259-262.
  11. Paul, S. M. and R. H. Purdy (1992). “Neuroactive steroids.” FASEB J 6(6): 2311-2322.
  12. Porter, F. D. (2008). “Smith-Lemli-Opitz syndrome: pathogenesis, diagnosis and management.” Eur J Hum Genet 16(5): 535-541.
  13. Reversi, A., V. Rimoldi, S. Brambillasca and B. Chini (2006). “Effects of cholesterol manipulation on the signaling of the human oxytocin receptor.” Am J Physiol Regul Integr Comp Physiol 291(4): R861-869.
  14. Saher, G., B. Brugger, C. Lappe-Siefke, W. Mobius, R. Tozawa, M. C. Wehr, F. Wieland, S. Ishibashi and K. A. Nave (2005). “High cholesterol level is essential for myelin membrane growth.” Nat Neurosci 8(4): 468-475.
  15. Sikora, D. M., K. Pettit-Kekel, J. Penfield, L. S. Merkens and R. D. Steiner (2006). “The near universal presence of autism spectrum disorders in children with Smith-Lemli-Opitz syndrome.” Am J Med Genet A 140(14): 1511-1518.
  16. Sikora, D. M., M. Ruggiero, K. Petit-Kekel, L. S. Merkens, W. E. Connor and R. D. Steiner (2004). “Cholesterol supplementation does not improve developmental progress in Smith-Lemli-Opitz syndrome.” J Pediatr 144(6): 783-791.
  17. Simons, K. and R. Ehehalt (2002). “Cholesterol, lipid rafts, and disease.” J Clin Invest 110(5): 597-603.
  18. Smith, D. W., L. Lemli and J. M. Opitz (1964). “A newly recognized syndrome of multiple congenital anomalies.” J Pedatrics 64: 210-217.
  19. Tierney, E., I. Bukelis, R. E. Thompson, K. Ahmed, A. Aneja, L. Kratz and R. I. Kelley (2006). “Abnormalities of cholesterol metabolism in autism spectrum disorders.” Am J Med Genet B Neuropsychiatr Genet 141B(6): 666-668.
  20. Tierney, E., N. A. Nwokoro and R. I. Kelley (2000). “Behavioral phenotype of RSH/Smith-Lemli-Opitz syndrome.” Ment Retard Dev Disabil Res Rev 6(2): 131-134.
  21. Tierney, E., N. A. Nwokoro, F. D. Porter, L. S. Freund, J. K. Ghuman and R. I. Kelley (2001). “Behavior phenotype in the RSH/Smith-Lemli-Opitz syndrome.” Am J Med Genet 98(2): 191-200.
  22. Tint, G. S., M. Irons, E. R. Elias, A. K. Batta, R. Frieden, T. S. Chen and G. Salen (1994). “Defective cholesterol biosynthesis associated with the Smith-Lemli-Opitz syndrome.” N Engl J Med 330(2): 107-113.
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More on Vitamin D…

Related to my post on Vitamin D and autism spectrum disorders, see Dr. Mark Hyman’s article: “Vitamin D – Why You are Probably NOT Getting Enough.”

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Vitamin D and Autism Spectrum Disorders: Is there a link?

Sunshine in Greece

Sunshine in Greece (Photo credit: Guillaume Cattiaux)

Vitamin D, the “sunshine vitamin”, is considered a hormone by most experts. Following exposure to the sun’s ultraviolet B (UVB) radiation, the skin produces significant quantities of Vitamin D in a relatively short period of time. However, Vitamin D production in the skin is affected by many environmental factors, including the following:

  • Latitude [1]
  • Air pollution [2, 3]
  • Cloud cover [4]
  • Season [1]
  • Skin pigmentation [5]
  • Age [6]
  • Body mass index [7]
  • Sun screen use [8]
  • Various medications, including anti-epileptic and steroid medications [9]

Unfortunately, very little Vitamin D is obtained in our modern day diet. Although Vitamin D can be obtained through dietary sources, such as fatty fish or fortified foods, the quantity of Vitamin D in these sources is quite variable and most people today do not obtain a sufficient quantity of Vitamin D through diet [10, 11]. As a result, Vitamin D deficiency and insufficiency among adults and children are considered a pandemic by some experts [12, 13], particularly in certain populations such as those with darker skin pigmentation [14, 15]. Vitamin D deficiency and insufficiency appears to be associated with increased risks for a number of diseases, including hypertension, diabetes, allergies, cancer, and depression [16-21].

In addition to its well-known effects on bone health and prevention of rickets, Vitamin D has wide-ranging extra-skeletal effects, including, but not limited to, the immune system [22-24], brain development and function [25-28], and gene regulation [29]. Thorough reviews of Vitamin D and its effects are freely available from the National Institutes of Health, Office of Dietary Supplements (http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/) and the Vitamin D council, a non-profit organization whose mission is to increase public and professional awareness of the health benefits of Vitamin D (http://www.vitamindcouncil.org). Additionally, thousands of peer-reviewed publications can be accessed through the U.S. National Library of Medicine’s PubMed search engine (http://www.ncbi.nlm.nih.gov/pubmed) (my personal favorite!), including hundreds of papers that have been published by Michael F. Holick from Boston University Medical Center (for review, see [30] and evidence-based recommendations from the Endocrine Society’s Clinical Practice Guidelines [31]). Currently, the optimal dose of Vitamin D for a given population is under debate among medical and scientific experts [32, 33], so don’t be surprised to hear more about this “vitamin” in the future and its importance for other diseases, including, but not limited to, cancer, cardiovascular disease, diabetes, chronic obstructive pulmonary disease, and autoimmune diseases.

So, what does Vitamin D have to do with autism spectrum disorders (ASD)? Current evidence has not established Vitamin D as a cause for ASD, but findings from epidemiological studies, associative studies, small clinical studies, and some case reports do indicate that maternal Vitamin D deficiency is associated with the development of ASD in some cases (note that “associated” with autism is different than “causes” autism). The theory that Vitamin D deficiency may play a role in ASDs was first proposed by Dr. John Cannell in the May 2007 Vitamin D Council newsletter (www.vitamindcouncil.org; Accessed December 2012) and later reviewed by Dr. Cannell in peer-reviewed papers published in 2008 [34] and 2010 [35]. His reviews provide a compelling argument and describe data from a variety of associative and epidemiological studies that indicate that Vitamin D deficiency, particularly maternal Vitamin D deficiency, contributes to the development of ASDs. Listed below are some of the links between Vitamin D and ASD:

  • County-level autism prevalence rates in three US states were greatest in areas with more rain and clouds [36]. Notably, clouds and rain antagonize UVB’s Vitamin D-producing action in the skin.
  • The prevalence of autism is less among those living in rural areas than in urban areas, where tall buildings and more pollution impede UVB exposure, and thereby, reduce Vitamin D production [37].
  • Prevalence rate of ASD appears to be greater among children of mothers with darker skin pigmentation or melanin, which effectively reduces UVB production of Vitamin D [38, 39]. In another epidemiological study, the rate of ASD was shown to be higher among infants from immigrant mothers with dark skin than with lighter skin [40, 41].
  • ASD prevalence increases among children born at higher latitudes [42] where the sun’s UVB radiation is less, and therefore, Vitamin D production is less.
  • High seafood consumption has been linked with fewer cases of ASDs despite the fact that it is polluted with mercury and other toxins [43, 44]. Furthermore, fatty fish contains significant quantities of Vitamin D, and Vitamin D may protect the genome against damage from environmental toxins [45].
  • Autism has been reported to be more common among mothers who took antiepileptic drugs during their pregnancy [46, 47]. This class of medications is one of the few drug classes that have been shown to reduce Vitamin D concentrations.

Although these findings are promising, the Vitamin D hypothesis isn’t supported by all research data [48, 49]. The problem is that most studies that have been completed at the time of this writing are not prospectively designed, randomized, blinded, and of sufficient size to conclude one way or another about the role of Vitamin D in ASDs. Although Vitamin D deficiency is unlikely to be the sole contributing factor to development of ASD, data from the sources cited above (along with others) are suggestive that Vitamin D deficiency may contribute to some of the medical problems observed in individuals with ASD, including immune system imbalances [50, 51], neurocognition delays [25], language delays [52], and reduced bone mineral density [53, 54].

The good news is that two active clinical studies are currently investigating the role of Vitamin D in ASDs:

  • The first study is entitled: “Vitamin D to Prevent Autism in Newborn Siblings.” In this study, researchers from the Oregon Health and Science University are investigating whether administering Vitamin D3 to approximately 40 mothers who already have at least one child with autism and who are pregnant will prevent the recurrence of autism in the newborn sibling. Mothers will be given 4000 IU/day Vitamin D3 during their pregnancy and 6000 IU/day while breastfeeding. If the mothers are not breastfeeding, infants will be given 400 IU/day up until 1 year and then 1000 IU/day after 1 year up until 3 years of age. In this study, treatment with Vitamin D3 is being given in an “open-label” fashion during the pregnancy and while breastfeeding. In other words, all participants in the study will receive Vitamin D and know that they are being given Vitamin D; and the researchers will also know that their subjects are being given Vitamin D. The study has not yet started recruiting and is expected to be completed by the end October 2017. ClinicalTrials.gov Identifier: NCT01366885 (http://www.clinicaltrials.gov/ct2/show/NCT01366885?term=autism+AND+Vitamin+D&rank=1).
  • The second active study is entitled “Open Label Clinical Trial of Vitamin D in Children With Autism.” This is another open-label study (see description in paragraph above); it is being conducted by researchers from the University of California, San Francisco. In this study, increasing doses of Vitamin D3 (up to a maximum of 10,000 IU/day) will be administered to 20 male and female 3 to 8-year-old subjects with ASD and Vitamin D deficiency. The dose of Vitamin D will be titrated to achieve blood concentrations of Vitamin D near the high range of normal. This study is currently recruiting and is expected to be completed by December 2013. This exploratory study will give preliminary information with respect to the safety and effectiveness of Vitamin D3 in children with ASD. Clinical Trials.gov identifier: NCT01535508 (http://www.clinicaltrials.gov/ct2/show/NCT01535508?term=autism+AND+Vitamin+D&rank=2).

Unfortunately, these two studies are not sufficient to prove or disprove the role of Vitamin D as an intervention to prevent ASD or to improve ASD symptomology. But, they are a start. Because both of these studies are rather small and “open-label”, the results won’t hold a significant weight of evidence among mainstream clinicians to support its use as a prevention or treatment of ASDs. However, if results are promising, these studies could lead to the design of randomized, blinded, placebo-controlled studies, which are considered the gold standard for establishing evidence among mainstream physicians and scientists.

The Vitamin D hypothesis resonates with me because only my oldest boy (1 of 4 children) has been diagnosed with ASD. Notably, during my pregnancy with him, I spent much of my time indoors while working long hours in an office setting. With my three subsequent pregnancies, I spent more time outdoors as I had reduced my working hours from full-time to part-time status. My son with ASD had documented failure to thrive between ages 4 to 6 years, along with bowed legs. At age 6, his Vitamin D levels were below normal (and this was the first time that a physician had measured his circulating Vitamin D concentrations). My son now takes approximately 5000 IU/day Vitamin D3 in the winter, which has increased his blood concentrations to a mid-to-high blood concentration. Since starting Vitamin D supplements, he rarely is sick. He is also growing at an average rate for males his same age. These anecdotal observations are not direct evidence that Vitamin D caused my son’s development of autism, but I think providing extra Vitamin D to achieve high-normal blood concentrations has certainly improved his health, and as a result, improved his day-to-day functioning and concentration. Until data shows otherwise, my son will continue taking his Vitamin D.


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  3. Agarwal, K.S., et al., The impact of atmospheric pollution on vitamin D status of infants and toddlers in Delhi, India. Arch Dis Child, 2002. 87(2): p. 111-3.
  4. Engelsen, O., et al., Daily duration of vitamin D synthesis in human skin with relation to latitude, total ozone, altitude, ground cover, aerosols and cloud thickness. Photochem Photobiol, 2005. 81(6): p. 1287-90.
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  7. Wortsman, J., et al., Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr, 2000. 72(3): p. 690-3.
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  9. Zhou, C., et al., Steroid and xenobiotic receptor and vitamin D receptor crosstalk mediates CYP24 expression and drug-induced osteomalacia. J Clin Invest, 2006. 116(6): p. 1703-12.
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  11. Moore, C.E., M.M. Murphy, and M.F. Holick, Vitamin D intakes by children and adults in the United States differ among ethnic groups. J Nutr, 2005. 135(10): p. 2478-85.
  12. Holick, M.F., The vitamin D epidemic and its health consequences. J Nutr, 2005. 135(11): p. 2739S-48S.
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  15. Collins-Fulea, C., K. Klima, and G.R. Wegienka, Prevalence of low vitamin D levels in an urban midwestern obstetric practice. J Midwifery Womens Health, 2012. 57(5): p. 439-44.
  16. Ganji, V., et al., Serum vitamin D concentrations are related to depression in young adult US population: the Third National Health and Nutrition Examination Survey. Int Arch Med, 2010. 3: p. 29.
  17. John, E.M., et al., Vitamin D and breast cancer risk: the NHANES I Epidemiologic follow-up study, 1971-1975 to 1992. National Health and Nutrition Examination Survey. Cancer Epidemiol Biomarkers Prev, 1999. 8(5): p. 399-406.
  18. Judd, S.E., et al., Optimal vitamin D status attenuates the age-associated increase in systolic blood pressure in white Americans: results from the third National Health and Nutrition Examination Survey. Am J Clin Nutr, 2008. 87(1): p. 136-41.
  19. Kositsawat, J., et al., Association of A1C levels with vitamin D status in U.S. adults: data from the National Health and Nutrition Examination Survey. Diabetes Care, 2010. 33(6): p. 1236-8.
  20. Sharief, S., et al., Vitamin D levels and food and environmental allergies in the United States: results from the National Health and Nutrition Examination Survey 2005-2006. J Allergy Clin Immunol, 2011. 127(5): p. 1195-202.
  21. Vaughan, C.P., et al., Vitamin D and lower urinary tract symptoms among US men: results from the 2005-2006 National Health and Nutrition Examination Survey. Urology, 2011. 78(6): p. 1292-7.
  22. Cantorna, M.T., J. Zhao, and L. Yang, Vitamin D, invariant natural killer T-cells and experimental autoimmune disease. Proc Nutr Soc, 2012. 71(1): p. 62-6.
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  24. Hewison, M., Vitamin D and immune function: an overview. Proc Nutr Soc, 2012. 71(1): p. 50-61.
  25. Eyles, D.W., T.H. Burne, and J.J. McGrath, Vitamin D, effects on brain development, adult brain function and the links between low levels of vitamin D and neuropsychiatric disease. Front Neuroendocrinol, 2012.
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  29. Norman, A.W., et al., 1,25(OH)2-vitamin D3, a steroid hormone that produces biologic effects via both genomic and nongenomic pathways. J Steroid Biochem Mol Biol, 1992. 41(3-8): p. 231-40.
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Welcome to my blog!

(Photo by Becky Brown; www.beckybrownphotography.com)

This site is dedicated to my son, John, and all the other individuals diagnosed with an autism spectrum disorder who deserve better medical care.  Each and every day, I ask myself, “Am I doing everything for my child with autism?”  Our journey the past 10 years has been long and hard, but I see a bright future for my son…and it is on this site that I want to discuss some of the promising interventions for autism spectrum disorders that are currently under investigation.  Coming soon…Vitamin D!

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