Visit her site (linked from her name above) to learn how your medicine cabinet can kill you.

The report by Hyppönen and Power in this issue of the Journal (1) highlights a [...]]]> Authors: Reinhold Vieth, Heike Bischoff-Ferrari, Barbara J Boucher, Bess Dawson-Hughes, Cedric F Garland, Robert P Heaney, Michael F Holick, Bruce W Hollis, Christel Lamberg-Allardt, John J McGrath, Anthony W Norman, Robert Scragg, Susan J Whiting, Walter C Willett and Armin Zittermann

The report by Hyppönen and Power in this issue of the Journal (1) highlights a frustrating and regrettable situation for nutrition researchers. In the early 1970s, the same serum 25-hydroxyvitamin D [25(OH)D] concentrations reported by Hyppönen and Power were thought to be indicative of “healthy” white adults in the United Kingdom (2). However, during those early years after the discovery of 25(OH)D, the adequacy of its serum concentration was based simply on whether the concentration was enough to prevent osteomalacia or rickets. Three decades later, we know that 25(OH)D concentrations relate to many other aspects of health, including fracture risk, bone density, colon cancer, and even tooth attachment (3); we also know that much higher concentrations of 25(OH)D are needed to prevent adverse outcomes. Indeed, in the 1958 British birth cohort, lower 25(OH)D is associated with a higher percentage of hemoglobin A1C (a measure of long-term glucose concentration), which further emphasizes the need to maintain optimal 25(OH)D concentrations.

Human diets do not provide sufficient vitamin D; if they did, the abovementioned associations between health and serum 25(OH)D concentrations would not be so routinely observed. The vitamin D provided by foods and supplements is overwhelmed by the effect of skin exposure to ultraviolet B light. Geography, season, skin color, and sun-related behavior are the main predictors of vitamin D nutritional status (6-10). Correction of low 25(OH)D concentrations can happen only if some or all of the following are implemented: the encouragement of safe, moderate exposure of skin to ultraviolet light; appropriate increases in food fortification with vitamin D; and the provision of higher doses of vitamin D in supplements for adults.

Evaluation of most relations of health and disease that involve vitamin D leads to the conclusion that a desirable 25(OH)D concentration is ≥75 nmol/L (30 ng/mL) (3-5). If a concentration of 75 nmol/L is the goal to be achieved by consumption of vitamin D, then why is it so rare for members of the population to accomplish this? One reason is that almost every time the public media report that vitamin D nutrition status is too low, or that higher vitamin D intakes may improve measures of health, the advice that accompanies the report is outdated and thus misleading. Media reports to the public are typically accompanied by a paragraph that approximates the following: “Current recommendations from the Institute of Medicine call for 200 IU/d from birth through age 50 y, 400 IU for those aged 51–70 y, and 600 IU for those aged >70 y. Some experts say that optimal amounts are closer to 1000 IU daily. Until more is known, it is wise not to overdo it.” The only conclusion that the public can draw from this is to do nothing different from what they have done in the past.

Supplemental intake of 400 IU vitamin D/d has only a modest effect on blood concentrations of 25(OH)D, raising them by 7–12 nmol/L, depending on the starting point. To raise 25(OH)D from 50 to 80 nmol/L requires an additional intake of {approx}1700 IU vitamin D/d (11). Safety is the first priority when giving advice to increase supplementation or fortification with any nutrient. A recent review in this Journal applied the risk assessment method used by the Food and Nutrition Board to update the safe tolerable upper intake level (UL) for vitamin D (12). The method focuses on the risk of hypercalcemia. The conclusion was that the UL for vitamin D consumption by adults should be 10 000 IU/d (12). This indicates that the margin of safety for vitamin D consumption for adults is >10 times any current recommended intakes.

The balance of the evidence leads to the conclusion that the public health is best served by a recommendation of higher daily intakes of vitamin D.

Emphasis mine. Originally published June 2007. http://www.ajcn.org/cgi/content/full/85/3/649

(CBS) If you’ve been diagnosed “probable” or “presumed” 2009 H1N1 or “swine flu” in recent months, you may be surprised to know this: odds are you didn’t have H1N1 flu.

In fact, you probably didn’t have flu at all. That’s according [...]]]> US swine flu reporting is inaccurate according to research published by CBS:

(CBS) If you’ve been diagnosed “probable” or “presumed” 2009 H1N1 or “swine flu” in recent months, you may be surprised to know this: odds are you didn’t have H1N1 flu.

In fact, you probably didn’t have flu at all. That’s according to state-by-state test results obtained in a three-month-long CBS News investigation.

This sheds a new light on yesterdays post. Perhaps Europe is not having a lower infection rate than the US – as their statistics are so completely off the mark.

In France, flu cases rose in early September, then stayed at about 160 per 100,000 people until late October, when numbers started [...]]]> The New Scientist reports that the common cold may have reduced the infection rates of Swine Flu in Europe this autumn accounting for the lower infection rates than the USA (Full story here) :

In France, flu cases rose in early September, then stayed at about 160 per 100,000 people until late October, when numbers started rising again. The delayed rise was puzzling, says Jean-Sebastien Casalegno of the French national flu lab at the University of Lyon.

He reports that the percentage of throat swabs from French respiratory illnesses that tested positive for swine flu fell in September, while at the same time rhinovirus, which causes colds, rose (Eurosurveillance, vol 14, p 19390). He told New Scientist that in late October, rhinovirus fell – at the same time as flu rose. He suspects rhinovirus may have blocked the spread of swine flu via a process called viral interference.

This is thought to occur when one virus blocks another. “We think that when you get one infection, it turns on your antiviral defences, and excludes the other viruses,” says Ab Osterhaus at the University of Rotterdam in the Netherlands.

How important such interference is in viral epidemics is unclear, however: there are also cases in which there is no interference, and people catch two viruses at the same time. Normally, we don’t get a chance to see how rhinovirus affects flu, as flu epidemics usually strike in winter, whereas rhinovirus hits when schools start (late summer in the northern hemisphere)

It appears the common cold is not so common after all but quite a clever virus. It can outwit the deadly swine flu.

Kinney DK, Barch DH, Chayka B, Napoleon S, Munir KM.

Genetics Laboratory, McLean Hospital, 115 Mill St., Belmont, MA 02478, USA; Department of Psychiatry, Harvard Medical School, 25 Shattuck St., Boston, MA 02115, USA.

Recent research has discovered that a number of genetic risk factors for autism are de novo mutations. Advanced parental age at the [...]]]> From: http://www.ncbi.nlm.nih.gov/pubmed/19699591

Kinney DK, Barch DH, Chayka B, Napoleon S, Munir KM.

Genetics Laboratory, McLean Hospital, 115 Mill St., Belmont, MA 02478, USA; Department of Psychiatry, Harvard Medical School, 25 Shattuck St., Boston, MA 02115, USA.

Recent research has discovered that a number of genetic risk factors for autism are de novo mutations. Advanced parental age at the time of conception is associated with increased risk for both autism and de novo mutations. We investigated the hypothesis that other environmental factors associated with increased risk for autism might also be mutagenic and contribute to autism by causing de novo mutations. A survey of the research literature identified 9 environmental factors for which increased pre-conceptual exposure appears to be associated with increased risk for autism. Five of these factors – mercury, cadmium, nickel, trichloroethylene, and vinyl chloride – are established mutagens. Another four – including residence in regions that are urbanized, located at higher latitudes, or experience high levels of precipitation – are associated with decreased sun exposure and increased risk for vitamin D deficiency. Vitamin D plays important roles in repairing DNA damage and protecting against oxidative stress – a key cause of DNA damage. Factors associated with vitamin D deficiency will thus contribute to higher mutation rates and impaired repair of DNA. We note how de novo mutations may also help explain why the concordance rate for autism is so markedly higher in monozygotic than dizygotic twins. De novo mutations may also explain in part why the prevalence of autism is so remarkably high, given the evidence for a strong role of genetic factors and the low fertility of individuals with autism – and resultant selection pressure against autism susceptibility genes. These several lines of evidence provide support for the hypothesis, and warrant new research approaches – which we suggest – to address limitations in existing studies. The hypothesis has implications for understanding possible etiologic roles of de novo mutations in autism, and it suggests possible approaches to primary prevention of the disorder, such as addressing widespread vitamin D deficiency and exposure to known mutagens.

*Emphasis mine.

The Swine Flu vaccination contains mercury. This research also confirms the known “widespread vitamin D deficiency”. Four of the nine risk factors include environmental aspects likely to cause vitamin D deficiency.