In This Issue….

-   Vitamin D deficiency doubles the risk of Alzheimer disease
-   Does vitamin E affect blood sugar?
-   Antioxidant supplements reduce arterial stiffness
-   Is this common cause of neurological problems too often overlooked?
-   Low selenium lowers thyroid hormone
-   This anti-aging hormone is largely affected by mineral status

CLINICAL UPDATE – Vitamin D deficiency doubles the risk of Alzheimer disease

In this landmark study, blood levels of vitamin D were measured in 1658 elderly adults who were free from dementia or heart disease. Follow up more than five years later revealed that those with vitamin D deficiency (defined as 25-50 nmol/L) were over 50% more likely to have dementia (cognitive impairment that is milder than Alzheimers) and 70% more likely to have Alzheimers. When vitamin D levels fell below 25 nmol/L, which is what the authors called severe deficiency, the risk of dementia and Alzheimers rose even more to 125% and 122% respectively, meaning they are more than twice as likely to experience major cognitive dysfunction as they age when vitamin D levels are low.

In an unrelated but similar study, people over 70 were assessed for mild cognitive impairment and vitamin D levels. In this population, it was found that lower vitamin D correlated with cognitive decline, even in those without dementia. Although the mechanism of action for the protective role of vitamin D is still not totally clear, a new paper sheds some light on how this vitamin protects the brain, citing a anti-inflammatory role for vitamin D in pericytes, which are specialized brain cells that protect the blood-brain barrier.
(Neurology, August 2014)
(Dementia and Geriatric Cognitive Disorders, June 2014)
(Journal of Alzheimer Disease, June 2014)

LINK to ABSTRACT Vitamin D and the risk of dementia and Alzheimer disease.
LINK to ABSTRACT Serum 25-Hydroxyvitamin D and Cognitive Decline: A Longitudinal Study among Non-Demented Older Adults.
LINK to ABSTRACT Additional Clues for a Protective Role of Vitamin D in Neurodegenerative Diseases: 1,25-Dihydroxyvitamin D3 Triggers an Anti-Inflammatory Response in Brain Pericyte. 

CLINICAL UPDATE – Does vitamin E affect blood sugar?

In a meta-analysis of 14 randomized controlled trials that evaluated the influence of vitamin E (studies with combined antioxidants were excluded from this review) on glycemic control, the authors stated in their conclusion that “there is currently insufficient evidence to support a potential beneficial effect of vitamin E supplementation on improvements of HbA1c and fasting glucose and insulin concentrations in subjects with type 2 diabetes.”

However, when subgroups were analyzed, the conclusion was different. For example, in the text of the paper, the authors state “the subgroup analysis indicated that vitamin E supplementation significantly decreased both HbA1c and fasting insulin in studies with low serum vitamin E concentration and poorer glycemic control. Furthermore, larger vitamin E doses and longer study durations also benefited HbA1c and fasting insulin concentrations.”

This paradoxical statement confirms the inherent difficulty in testing vitamins in isolation for complex diseases using the randomized controlled trial paradigm from pharmaceutical trials.
(Public Library of Science, April 2014)

LINK to ABSTRACT Influence of vitamin E supplementation on glycaemic control: a meta-analysis of randomised controlled trials. LINK to FREE FULL TEXT 

CLINICAL UPDATE – Antioxidant supplements reduce arterial stiffness

A meta-analysis of randomized controlled trials on antioxidant supplementation and its effect on arterial stiffness concluded that antioxidant supplements have “a small, protective effect on arterial stiffness.” The authors noted that the benefit was larger on those people who had lower levels of antioxidants (in this case vitamins C and E) at baseline, suggesting that conflicting results in past studies may be due to varying baseline levels or dosages that end up obscuring potential effects.
(Journal of Nutrition, August 2014)

LINK to ABSTRACT Antioxidant Vitamin Supplementation Reduces Arterial Stiffness in Adults: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. 

CLINICAL UPDATE – Is this common cause of neurological problems too often overlooked?

Vitamin B12 deficiency is commonly associated with neurologic complications like tingling and numbness in the extremities. However, research suggests other micronutrient deficiencies cause similar clinical presentation but are often overlooked, particularly copper deficiency which will often manifest neurologically in much the same way as B12 deficiency. Two recent papers highlight that neurological complications from malabsorption, such as bariatric surgery or celiac, are often the result of vitamin or mineral deficiencies (B1, B12, copper, etc) which are too commonly overlooked but once diagnosed, are easily and inexpensively be treated.
(Handbook of Clinical Neurology, 2014)

LINK to ABSTRACT Neurologic manifestations of malabsorption syndromes.
The neurologic complications of bariatric surgery.

CLINICAL UPDATE – Low selenium lowers thyroid hormone

In this experiment, selenium deficiency had a major impact on the function of liver enzymes, in particular those that are involved in one-carbon metabolism reactions. Specifically, induced selenium deficiency reduced the activity of deiodinase enzymes in the liver that convert the precursor hormone T4 into the bioactive form of thyroid hormone T3, thus reducing serum thyroid hormone levels. In addition, enzymes that protect against lipid peroxidation (the selenoproteins glutathione reductase and thioredoxin reductase) were reduced in the presence of insufficient selenium.
(Journal of Nutritional Biochemistry, September 2014)

LINK to ABSTRACT Hepatic metabolite profiles in mice with a suboptimal selenium status. 

CLINICAL UPDATE – This anti-aging hormone is largely affected by mineral status

In this paper on the anti-aging hormone IGF-1 (insulin like growth factor 1), the role of zinc, selenium and magnesium in determining levels of IGF-1 is reviewed. Magnesium deficiency may down regulate IGF-1, according to the authors, via its role in reducing inflammatory enzymes. When magnesium is low, inflammation is high and anabolic hormones such as IGF-1 are down regulated. With respect to selenium, the authors propose a mechanistic link to IGF-1 via selenium’s role in converting thyroid hormone into its bioactive form. As thyroid hormone is reduced, a feedback system then down regulates growth hormone and IGF-1, linking selenium deficiency to its clinical presentation of muscle wasting. Finally, the link between zinc deficiency and reduced IGF-1 is thoroughly explored citing zinc’s role in quelling inflammation as a proposed mechanism for increasing IGF-1.
(Nutrients, October 2013)

LINK to ABSTRACT IGF-1, the cross road of the nutritional, inflammatory and hormonal pathways to frailty. LINK to FREE FULL TEXT