Archives for September 2011

Children With Autism And Gastrointestinal Symptoms Have Altered Digestive Genes

These changes may also affect the mix of bacteria present in the digestive tract

Researchers at the Center for Infection and Immunity (CII) at Columbia University’s Mailman School of Public Health and at the Harvard Medical School report that children with autism and gastrointestinal disturbances have altered expression of genes involved in digestion. These variations may contribute to changes in the types of bacteria in their intestines. Full study findings are reported online in the journal PLoS ONE.

Autism, which is defined by impairments in verbal and non-verbal communication, social interactions, and repetitive and stereotyped behaviors, affects approximately 1% of the population. Many children with autism have gastrointestinal problems that can complicate clinical management and contribute to behavioral disturbances. In some children, special diets and antibiotics have been associated with improvements in social, cognitive and gastrointestinal function.

The investigators found that children diagnosed with autism and gastrointestinal disturbances have abnormalities in levels of genes for enzymes that break down sugars and for molecules that transport them from the lumen of the intestine into the blood. These variations were also associated with changes in the bacterial composition of the intestine.

The researchers examined biopsies from 22 patients, 15 diagnosed with autism and seven typically developing children. They used real-time PCR to measure gene expression and genetic sequencing techniques to characterize the bacteria present in the intestines of each child.

Brent Williams, PhD, research scientist at CII and first author of the study, noted that, “whereas others have looked at bacterial composition of feces, our group was the first to characterize mucosal communities and to link findings to expression of genes important in carbohydrate metabolism and transport.”

“The findings are consistent with other research suggesting that autism may be a system-wide disorder, and provide insight into why changes in diet or the use of antibiotics may help alleviate symptoms in some children,” added Mady Hornig, MD, Director of Translational Research at the Center for Infection and Immunity.

“Although caution in interpretation is indicated because the sample size is small, our findings nonetheless provide a framework for developing and testing new hypotheses concerning the role of malabsorption and microflora in autism and related disorders,” said Ian Lipkin, MD, Director of the Center for Infection and Immunity.

 

Reference

Williams BL, Hornig M, Buie T, Bauman ML, Cho Paik M, et al. (2011) Impaired Carbohydrate Digestion and Transport and Mucosal Dysbiosis in the Intestines of Children with Autism and Gastrointestinal Disturbances. PLoS ONE 6(9): e24585. doi:10.1371/journal.pone.0024585

 

To Ditch Dessert, Feed The Brain

Brain reward regions are activated when glucose falls below normal levels (blue). In lean people -- but not obese people -- the prefrontal cortex which is involved in decision making and regulating impulses is activated (red) when glucose levels are normal.

If the brain goes hungry, Twinkies look a lot better, a study led by researchers at Yale University and the University of Southern California has found.

Brain imaging scans show that when glucose levels drop, an area of the brain known to regulate emotions and impulses loses the ability to dampen desire for high-calorie food, according to the study published online September 19 in The Journal of Clinical Investigation.

“Our prefrontal cortex is a sucker for glucose,” said Rajita Sinha, the Foundations Fund Professor of Psychiatry, and professor in the Department of Neurobiology and the Yale Child Study Center, one of the senior authors of the research.

The Yale team manipulated glucose levels intravenously and monitored changes in blood sugar levels while subjects were shown pictures of high-calorie food, low-calorie food and non-food as they underwent fMRI scans.

When glucose levels drop, an area of the brain called the hypothalamus senses the change. Other regions called the insula and striatum associated with reward are activated, inducing a desire to eat, the study found. The most pronounced reaction to reduced glucose levels was seen in the prefrontal cortex. When glucose is lowered, the prefrontal cortex seemed to lose its ability to put the brakes upon increasingly urgent signals to eat generated in the striatum. This weakened response was particularly striking in the obese when shown high-calorie foods.

“This response was quite specific and more dramatic in the presence of high-calorie foods,” Sinha said.

“Our results suggest that obese individuals may have a limited ability to inhibit the impulsive drive to eat, especially when glucose levels drop below normal,” commented Kathleen Page, assistant professor of medicine at the University of Southern California and one of the lead authors of the paper.

A similarly robust response to high-calorie food was also seen in the striatum, which became hyperactive when glucose was reduced. However, the levels of the stress hormone cortisol seemed to play a more significant role than glucose in activating the brain’s reward centers, note the researchers. Sinha suggests that the stress associated with glucose drops may play a key role in activating the striatum.

“The key seems to be eating healthy foods that maintain glucose levels,” Sinha said. “The brain needs its food.”

 

Reference

Page KA, Seo D, Belfort-Deaguiar R, Lacadie C, Dzuira J, Naik S, Amarnath S et al. Circulating glucose levels modulate neural control of desire for high-calorie foods in humans. J Clin Invest 2011 Sep 19. [Epub ahead of print]

 

Diabetes May Significantly Increase Your Risk of Dementia

People with diabetes appear to be at a significantly increased risk of developing dementia, according to a study published in the September 20, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology.

“Our findings emphasize the need to consider diabetes as a potential risk factor for dementia,” said study author Yutaka Kiyohara, MD, PhD, of Kyushu University in Fukuoka, Japan. “Diabetes is a common disorder, and the number of people with it has been growing in recent years all over the world. Controlling diabetes is now more important than ever.”

People with diabetes were more likely to develop Alzheimer’s disease and other types of dementia, such as vascular dementia, which occurs when there is damage to blood vessels that eventually deprive the brain of oxygen.

For the study, a total of 1,017 people who were age 60 and older were given a glucose (sugar) tolerance test after an overnight fast to determine if they had diabetes. Study participants were monitored for an average of 11 years and then tested for dementia. During the study, 232 people developed dementia.

The study found that people with diabetes were twice as likely to develop dementia as people with normal blood sugar levels. Of the 150 people with diabetes, 41 developed dementia, compared to 115 of the 559 people without diabetes who developed dementia.

The results remained the same after the researchers accounted for factors such as high blood pressure, high cholesterol and smoking. The risk of dementia was also higher in people who did not have diabetes, but had impaired glucose tolerance, or were “pre-diabetes.”

In addition, the study found the risk of developing dementia significantly increased when blood sugar was still high two hours after a meal.

 

Reference

Matsuzaki T, Sasaki K, Hata J, Hirakawa Y, Fujimi K, Ninomiya T et al. Association of Alzheimer disease pathology with abnormal lipid metabolism: The Hisayama Study. Neurology 2011; 77 (11): 1068-1075.

 

Feed Your Head

Psychiatrists Abram Hoffer (1917 – 2009) and Humphry Osmond (1917 – 2004) met in Saskatchewan in 1951, and embarked on a quest to do what traditional psychiatry deemed impossible: to find a cure for schizophrenia. Their work spawned a number of directions for research, many of which are only gaining acceptance in wider circles now.

Their primary contribution to psychiatry was a theory about treating people suffering from mental illness using nutrition. Hoffer and Osmond set out to prove that the symptoms of schizophrenia could be controlled with healthy, unprocessed food and large doses of vitamins.

Linus Pauling (1901 – 1994) was an American scientist, peace activist, two-time Nobel Prize winning author and educator. Pauling & Hoffer became friends and together advocated for mega-doses of niacin, vitamin C and other nutrients in the treatment of all kinds of disease. Pauling came up with the name “Orthomolecular” for this new, yet ancient, form of treatment. Orthomolecular means “the right molecules in the right amounts.”

Hoffer, Osmond and Pauling were way ahead of their time. Their work coincided with a general movement towards de-institutionalization in mental health, releasing patients back into the community with no real support system. At the same time, economic changes were bringing budget cuts to all aspects of health care in North America.

This was also the dawn of the age of Big Pharma. Multi-national pharmaceutical corporations sprung up in the 1950s and 60s, introducing new anti-psychotic drugs that made it possible to control, if not actually help, the mentally ill. Consumers put their faith in the idea of the “magic bullet” and since then, psychiatry has been largely controlled by the pharmaceutical industry.

For their efforts, Hoffer, Osmond, Pauling & hundreds of like-minded doctors were condemned by their peers.

The tide is turning: a growing wave of consumer demand is driving an orthomolecular resurgence. Doctors and patients are being slowly won over by a simple idea that makes more sense every day: WE ARE WHAT WE EAT. Documentary from 2010.

Watch the full documentary now:

Vaccines and Brain Development (Lecture)

Centers for Disease Control and Prevention (CDC) officials claim vaccines are safe and effective. Is that true? If vaccines are safe, why did the incidence of autism increase from one case of autism in 10,000 American children to one case of autism in 150 American children after the massive childhood vaccination program began? If childhood vaccines are safe, why are 560,000 vaccinated children afflicted with autism while nonvaccinated Amish and Mennonite children rarely have the disease? Why has the incidence of asthma, allergies, autoimmune disease, Type I diabetes, and neurologic conditions dramatically increased in vaccinated children?

Why do obstetricians give pregnant women influenza vaccines that contain a toxic dose of mercury? Why do newborn children receive Hepatitis B vaccine in the nursery when there is no medical justification for the immunization?

Dr. Russell Blaylock (born 1945) is a board certified neurosurgeon, author and lecturer. He is a former clinical assistant professor of neurosurgery at the University of Mississippi Medical Center and is currently a visiting professor in the biology department at Belhaven College. His discussion addresses those, and many other, issues. If you are concerned about your health, and the health of your family, you must watch this video.

This lecture was given in October 2008 at the Radio Liberty Seminar.

 

 

Vaccination: The Hidden Truth

To summarize in broad terms, instead of resulting in prophylaxis, meaning prevention, all responses to vaccines actually fall under the broad umbrella of anaphylaxis, which means sensitisation, the OPPOSITE of immunization. In this extremely informative video (1998), fifteen people, including Dr. Viera Scheibner (a PhD researcher), five medical doctors, other researchers, reveal what is really going on in relation to illness and vaccines. Ironically, the important facts come from the orthodox medicine’s own peer-reviewed research.

With so much government and medical promotion of vaccination for prevention of disease, the video is clearly devoted to presenting the other side of the issue that parents and others are not being told. The result is a damning account of the ineffectiveness of vaccines and their often harmful effects. It declares that parents are not being told the truth by the media, the Health Department and the medical establishment, with a medical doctor, Dr. Mark Donohoe, confessing that “It is a problem for me that I am part of a profession that is systematically lying to people…”

The video presents well documented answers to questions like: Was it really vaccines that saved us? Why are they only counterproductive? How are many statistics misleading? What do vaccines contain? What are they doing to our organs, immune systems, even our genes? Are childhood diseases really dangerous to healthy children? Why does vaccination continue? What are our rights? Can vaccine damage be evaluated and countered? What is the true key to immunity?

The video raises the fundamental question of whether we should be trying to prevent childhood diseases anyway, in that they contribute to the development of a healthy immune system. If what the video says is true, why is vaccination pushed so heavily by the government authorities? (Excerpt from vaccination.inoz.com)

 

Thimerosal (Ethylmercury), Vaccines and Autism

Charlie Crist, the Governor of Florida alarmed at the growing rate of Autism and its effect on the children and families of the State of Florida as well as the economic impact on healthcare and educational systems, commissioned by Executive Order 08-36 (March 7, 2008) the Autism Task Force, a broad Panel of individuals from both private and public sectors, to examine and evaluate the risks to the children and economy of the State of Florida.

On September 24-25, 2008 Governor Crist’s Task Force on Autism Spectrum Disorders convened at the University of South Florida in Tampa, Florida. These are highlights from the two day conference.

The use of thimerosal (ethylmercury), a preservative used in vaccinations, was the hot topic of the two day conference.

FACT:

Mercury and its compounds are hazardous to humans.

Ethylmercury, mercury’s most dangerous compound, is used extensively in vaccines as a preservative and anti-bacterial agent.

 

 

Immunoexcitotoxicity and Autism Spectrum Disorders (Lecture)

Dr. Russell L. Blaylock (born 1945) is a board certified neurosurgeon, author and lecturer. He is a former clinical assistant professor of neurosurgery at the University of Mississippi Medical Center and is currently a visiting professor in the biology department at Belhaven College.

The autism spectrum disorders (ASD) are a group of related neurodevelopmental disorders that have been increasing in incidence since the 1980s. Despite a considerable amount of data being collected from cases, a central mechanism has not been offered. A careful review of ASD cases discloses a number of events that adhere to an immunoexcitotoxic mechanism. This mechanism explains the link between excessive vaccination, use of aluminium and ethylmercury as vaccine adjuvants, food allergies, gut dysbiosis, and abnormal formation of the developing brain.

 

 

Read More

 

Autism, No Vaccines No Autism

“We have a fairly large practice. We have about 30,000 or 35,000 children that we’ve taken care of over the years, and I don’t think we have a single case of autism in children delivered by us who never received vaccines,” said Dr. Mayer Eisenstein (2009), Homefirst’s medical director who founded the practice in 1973. Homefirst doctors have delivered more than 15,000 babies at home, and thousands of them have never been vaccinated.

 

Why You Need More Vitamin D. A Lot More

by William B. Grant, Ph.D. 

Vitamin D has emerged as the nutrient of the decade. Numerous studies have found benefits for nearly 100 types of health conditions. These health benefits include reduced risk of bone diseases, many types of cancer, cardiovascular disease (CVD), diabetes mellitus, bacterial and viral infectious diseases, and autoimmune diseases such as multiple sclerosis,[1] neurological conditions such as cognitive dysfunction,[2] and improved athletic and physical performance.[3]

Sunshine, Skin, Sunburn, and Sunscreen

The primary source of vitamin D for most people is solar ultraviolet-B (UVB) light. Skin pigmentation has adapted to where a population lives for a thousand years or more as those with skin too dark or light do not survive as well as those with the appropriate skin pigmentation.[4]Dark skin protects against the harmful effects of UV, but also blocks the UVB from penetrating deeply enough into the skin to produce vitamin D from 7-dehydrocholesterol. Those with lighter skin can produce vitamin D more rapidly, but are more prone to melanoma and other skin cancer. Sunscreens block UVB and thus limit vitamin D production. While sunscreens are useful in reducing risk of sunburning, they do not block the long wave UV (UVA) as well as UVB. UVA is linked to risk of melanoma. Wearing sunscreen when there is no danger of burning can actually increase the risk of melanoma.[5]

Understanding Vitamin D Research

Since vitamin D production is the primary source of vitamin D, ecological and observational studies have been very useful in teasing out the effects of vitamin D on health. There are two types of ecological studies, based on geographical and temporal (over time) variations. In geographical studies, populations are defined geographically and both health outcome and risk-modifying factors are averaged for each geographical unit. Statistical analyses are then used to determine the relative importance of each factor. The first paper linking UVB and vitamin D to reduced risk of colon cancer was published in 1980.[6] This link has now been extended to about 15 types of cancer in the United States with respect to average noontime solar UVB doses in July.[7] Solar UVB doses in July are highest in the Southwest and lowest in the Northeast.[8]Mortality rates are generally lowest in the Southwest and highest in the Northeast.[9] Similar results have been found in Australia, China, France, Japan, Russia, and Spain, and the entire world.[10]

In temporal studies, seasonal variations in health outcomes are sought. A good example of a seasonal effect linked to solar UVB doses and vitamin D is influenza, which peaks in winter.[11]

Observational studies are generally of three types: case-control, cohort, and cross-sectional. In case-control studies, those diagnosed with a disease have serum 25-hydroxyvitamin D [25(OH)D] level or oral vitamin D intake determined at that time and are compared statistically with others with similar characteristics but without that disease. In cohort studies, people are enrolled in the study and the vitamin D index determined at that time. The cohort is followed for a number of years and those who develop a specific disease are compared statistically with matched controls who did not. The main problem with cohort studies is that the single value of the vitamin D index may not relate to the time in the individual’s life when vitamin D had the most impact on the disease outcome. Cross-sectional studies are essentially snapshots of a population and look at various factors in relation to the prevalence of health conditions. As biochemistry can be affected by health status, such studies provide less reliable information on the role of UVB and vitamin D on health outcome.

The role of vitamin D in CVD and diabetes mellitus type 2 have largely been studied using cohort studies. Significantly reduced risk of CVD and diabetes mellitus incidence have been reported in a number of studies in the past three years.[12]

Health policy officials like to see randomized controlled trials (RCTs) reporting health benefits with limited adverse effects. RCTs are certainly appropriate for pharmaceutical drugs which, by definition, are artificial substances that the human body has no experience with. RCTs with vitamin D are problematic for a number of reasons. For one, many RCTs used only 400 IU/day vitamin D3, which is much lower than the 10,000 IU/day that can be produced with whole-body exposure to the midday sun in summer, or 1500 IU/day from casual sunlight exposure in summer.[13] For another, there are both oral and UVB sources of vitamin D, so the amount taken in the study will compete with the other sources. There is considerable individual variation in serum 25(OH)D for a given oral vitamin D intake.[14] Unfortunately, serum 25(OH)D levels are generally not measured in oral vitamin D RCTs.

Nonetheless, there have been several vitamin D RCTs that found significant health benefits beyond preventing falls and fractures.[15] These include ones for cancer,[16],[17] influenza and colds,[18] type A influenza,[19] and pneumonia.[20]

Important Benefits of Vitamin D

The evidence of beneficial roles of UVB and vitamin D for a large number of health conditions have recently been posted at the Vitamin D Council’s website.

In addition to an overview of the literature, the website also includes a feature to pull up a large number of titles on each condition from www.pubmed.gov .

Sufficient information is currently available from observational studies with support from ecological studies and RCTs to determine relationships between serum 25(OH)D levels and incidence rates for breast and colorectal cancer,[21] CVD,[22] and influenza.[23] Risk decreases rapidly for small increases in 25(OH)D for those with initial values below 10 ng/ml (25 nmol/L), then decrease at a slower rate to levels above 40 ng/ml (100 nmol/L). These relations have been used to estimate the change in mortality rates and life expectancy if population mean serum 25(OH)D levels were raised from current levels of 20-25 ng/ml (50-63 nmol/L) to 45 ng/ml (113 nmol/L). For the U.S., it was estimated that 400,000 deaths/year could be delayed,[24] which is about 15% of all deaths/year. For the entire world, it was estimated that the reduction in all-cause mortality rates would correspond to an increased life expectancy of two years.[22]

The mechanisms whereby vitamin D reduces the risk of disease are largely understood. For cancer, they include effects on cellular differentiation and proliferation, angiogenesis and metastasis.[25] For infectious diseases, they include induction of cathelicidin and defensins [26]and shifting cytokine production from proinflammatory T-helper 1 (Th1) cytokines to Th2 cytokines.[27] For CVD, they may include reducing blood pressure and keeping calcium in the bones and teeth and out of the vascular tissues.[28] For diabetes mellitus type 2, they may include improving insulin sensitivity.[29]

Current Government-Sponsored Recommendations are Too Low

In spite of the large and expanding body of scientific evidence that vitamin D has many health benefits, the US Institute of Medicine issued a report in November 2010 claiming that the evidence was strong only for effects on bones.[30],[31] The reason given was lack of convincing randomized controlled trials on other health conditions. The one on cancer showing a 77% reduced risk of all-cancer incidence between the ends of the first and fourth years involved 1100 IU/day vitamin D plus 1450 mg/day calcium.[16] However, the IOM Committee relied on the findings from the start of the study, which was not statistically significant. In addition, the IOM Committee pointed to observational studies reporting a U-shaped serum 25(OH)D-disease incidence relation as a reason to be concerned about higher doses of vitamin D. However, these studies used a single serum 25(OH)D value from the time of enrollment followed by follow-up times as long as 17 years. Two studies reported that the sign of the correlation between disease outcome and serum 25(OH)D level changes from negative to positive after seven-to-15 years.[32],[33] Thus, the U-shaped relations are not reliable and should not be used as the basis for policy decisions, especially since the Committee refused to consider the largely beneficial findings from observational studies.

How Much Vitamin D Do We REALLY Need?

The IOM committee set the recommended vitamin D intake at 600 IU/day for those under the age of 70 years and 800 IU/day for those over 70, and stated that 20 ng/ml (50 nmol/L) was an adequate level. The scientific consensus is that oral intake should be 1000-5000 IU/day vitamin D with a goal of 30-40 ng/ml (75-100 nmol/L).[34] The vitamin D research community has responded to the IOM report on vitamin D with over 60 letters and articles in peer-reviewed journals pointing out the absurdity and illogic of the IOM report.[35] The Endocrine Society published a paper recommending 1500-2000 IU/day and 30 ng/ml.[36] Meanwhile, members of the IOM Committee have been publishing articles in mainstream journals promoting their report.

(William Grant, PhD, is the director of the Sunlight, Nutrition, and Health Research Center (SUNARC)in San Francisco, California. The author receives funding from the UV Foundation, the Sunlight Research Forum, Bio-Tech-Pharmacal, the Vitamin D Council, and the Vitamin D Society of Canada.) 

(Orthomolecular Medicine News Service, September 16, 2011)

 

References:

1. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-81.

2. Llewellyn DJ, Lang IA, Langa KM, Melzer D. Vitamin D and cognitive impairment in the elderly U.S. population. J Gerontol A Biol Sci Med Sci. 2011;66(1):59-65.

3. Cannell JJ, Hollis BW, Sorenson MB, Taft TN, Anderson JJ. Athletic performance and vitamin D. Med Sci Sports Exerc. 2009;41(5):1102-10.

4. Jablonski NG, Chaplin G. Colloquium paper: human skin pigmentation as an adaptation to UV radiation. Proc Natl Acad Sci U S A. 2010;107 Suppl 2:8962-8.

5. Gorham ED, Mohr SB, Garland CF, Chaplin G, Garland FC. Do sunscreens increase risk of melanoma in populations residing at higher latitudes? Ann Epidemiol. 2007;17(12):956-63.

6. Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol. 1980;9(3):227-31.

7. Grant WB, Garland CF. The association of solar ultraviolet B (UVB) with reducing risk of cancer: multifactorial ecologic analysis of geographic variation in age-adjusted cancer mortality rates. Anticancer Res. 2006;26(4A):2687-99.

8. Leffell DJ and Brash DE: Sunlight and skin cancer. Sci Am. 275(1): 52-53, 56-59, 1996. (accessed March 9, 2011).

9. Devesa SS, Grauman DJ, Blot WJ, Pennello GA, Hoover RN, Fraumeni JF Jr: Atlas of Cancer Mortality in the United States, 1950-1994. NIH Publication No. 99-4564, 1999.

10. Grant WB, Mohr SB. Ecological studies of ultraviolet B, vitamin D and cancer since 2000. Ann Epidemiol. 2009;19(7):446-54.

11. Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, Garland CF, Giovannucci E. Epidemic influenza and vitamin D. Epidemiol Infect. 2006;134(6):1129-40.

12. Parker J, Hashmi O, Dutton D, Mavrodaris A, Stranges S, Kandala NB, Clarke A, Franco OH. Levels of vitamin D and cardiometabolic disorders: systematic review and meta-analysis. Maturitas. 2010;65(3):225-36.

13. Hyppönen E, Power C. Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors. Am J Clin Nutr. 2007;85(3):860-8.

14. Garland CF, French CB, Baggerly LL, Heaney RP. Vitamin D supplement doses and serum 25-hydroxyvitamin D in the range associated with cancer prevention. Anticancer Res 2011:31:617-22.

15. Bischoff-Ferrari HA, Willett WC, Wong JB, Stuck AE, Staehelin HB, Orav EJ, Thoma A, Kiel DP, Henschkowski J. Prevention of nonvertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Arch Intern Med. 2009;169(6):551-61.

16. Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007;85(6):1586-91.

17. Bolland MJ, Grey A, Gamble GD, Reid IR. Calcium and vitamin D supplements and health outcomes: a reanalysis of the Women’s Health Initiative (WHI) limited-access data set. Am J Clin Nutr. 2011 Aug 31. [Epub ahead of print]

18. Aloia JF, Li-Ng M. Re: epidemic influenza and vitamin D. Epidemiol Infect. 2007;135(7):1095-6; author reply 1097-8.

19. Urashima M, Segawa T, Okazaki M, Kurihara M, Wada Y, Ida H. Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren. Am J Clin Nutr. 2010;91(5):1255-60.

20. Manaseki-Holland S, Qader G, Isaq Masher M, Bruce J, Zulf Mughal M, Chandramohan D, Walraven G. Effects of vitamin D supplementation to children diagnosed with pneumonia in Kabul: a randomised controlled trial. Trop Med Int Health. 2010;15(10):1148-55.

21. Grant WB. Relation between prediagnostic serum 25-hydroxyvitamin D level and incidence of breast, colorectal, and other cancers. J Photochem Photobiol B, 2010;101:130-136.

22. Grant WB. An estimate of the global reduction in mortality rates through doubling vitamin D levels. Eur J Clin Nutr, 2011;65:1016-1026.

23. Sabetta JR, DePetrillo P, Cipriani RJ, Smardin J, Burns LA, Landry ML. Serum 25-hydroxyvitamin d and the incidence of acute viral respiratory tract infections in healthy adults. PLoS One. 2010;5(6):e11088.

24. Grant WB. In defense of the sun: An estimate of changes in mortality rates in the United States if mean serum 25-hydroxyvitamin D levels were raised to 45 ng/mL by solar ultraviolet-B irradiance. Dermato-Endocrinology, 2009;1(4):207-14.

25. Krishnan AV, Feldman D. Mechanisms of the anti-cancer and anti-inflammatory actions of vitamin D. Annu Rev Pharmacol Toxicol. 2011;51:311-36.

26. Liu PT, Stenger S, Tang DH, Modlin RL. Cutting edge: vitamin D-mediated human antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction of cathelicidin. J Immunol. 2007;179(4):2060-3.

27. Cantorna MT, Mahon BD. Mounting evidence for vitamin D as an environmental factor affecting autoimmune disease prevalence. Exp Biol Med (Maywood). 2004;229(11):1136-42.

28. Zagura M, Serg M, Kampus P, Zilmer M, Eha J, Unt E, Lieberg J, Cockcroft JR, Kals J. Aortic stiffness and vitamin D are independent markers of aortic calcification in patients with peripheral arterial disease and in healthy subjects. Eur J Vasc Endovasc Surg. 2011 Aug 24. [Epub ahead of print]

29. Alvarez JA, Ashraf AP, Hunter GR, Gower BA. Serum 25-hydroxyvitamin D and parathyroid hormone are independent determinants of whole-body insulin sensitivity in women and may contribute to lower insulin sensitivity in African Americans. Am J Clin Nutr. 2010;92(6):1344-9.

30. Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium; Ross AC, Taylor CL, Yaktine AL, Del Valle HB, editors. Dietary Reference Intakes for Calcium and Vitamin D. Washington (DC): National Academies Press (US); 2011.

31. Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, Durazo-Arvizu RA, Gallagher JC, Gallo RL, Jones G, Kovacs CS, Mayne ST, Rosen CJ, Shapses SA. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96(1):53-8.

32. Lim U, Freedman DM, Hollis BW, Horst RL, Purdue MP, Chatterjee N, Weinstein SJ, Morton LM, Schatzkin A, Virtamo J, Linet MS, Hartge P, Albanes D. A prospective investigation of serum 25-hydroxyvitamin D and risk of lymphoid cancers. Int J Cancer. 2009;124(4):979-86.

33. Robien K, Cutler GJ, Lazovich D. Vitamin D intake and breast cancer risk in postmenopausal women: the Iowa Women’s Health Study. Cancer Causes Control. 2007;18(7):775-82.

34. Souberbielle JC, Body JJ, Lappe JM, Plebani M, Shoenfeld Y, Wang TJ, Bischoff-Ferrari HA, Cavalier E, Ebeling PR, Fardellone P, Gandini S, Gruson D, Guérin AP, Heickendorff L, Hollis BW, Ish-Shalom S, Jean G, von Landenberg P, Largura A, Olsson T, Pierrot-Deseilligny C, Pilz S, Tincani A, Valcour A, Zittermann A. Vitamin D and musculoskeletal health, cardiovascular disease, autoimmunity and cancer: Recommendations for clinical practice. Autoimmun Rev 2010;9:709-15.

35. Heaney RP, Grant WB, Holick MF, Amling M. The IOM Report on Vitamin D misleads. J Clin Endocrinol Metab. eLetter. (4 March 2011)

36. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad MH, Weaver CM. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab, 2011;96(7):1911-30.

 

For More Information:

For additional information on vitamin D, the reader is directed to PubMed to search “vitamin D” along with any keyword of interest. Some representative papers found there, with free access, are listed below. Papers published in the Journal of Orthomolecular Medicine are (still) not listed on PubMed. All J Orthomolecular Med papers may all be accessed at the Journal’s free archive.

Adams JS, Hewison M. Update in vitamin D. J Clin Endocrinol Metab. 2010 Feb;95(2):471-8. Review.

Bikle DD. Vitamin D: newly discovered actions require reconsideration of physiologic requirements. Trends Endocrinol Metab. 2010 Jun;21(6):375-84. Epub 2010 Feb 10. Review.

Herr C, Greulich T, Koczulla RA, Meyer S, Zakharkina T, Branscheidt M, Eschmann R, Bals R. The role of vitamin D in pulmonary disease: COPD, asthma, infection, and cancer. Respir Res. 2011 Mar 18;12:31. Review.

Hewison M. Vitamin D and the immune system: new perspectives on an old theme. Endocrinol Metab Clin North Am. 2010 Jun;39(2):365-79, table of contents. Review.

Raman M, Milestone AN, Walters JR, Hart AL, Ghosh S. Vitamin D and gastrointestinal diseases: inflammatory bowel disease and colorectal cancer. Therap Adv Gastroenterol. 2011 Jan;4(1):49-62.

Zhang R, Naughton DP. Vitamin D in health and disease: current perspectives. Nutr J. 2010 Dec 8;9:65. Review.