Vitamin D intake and vitamin D status of Australians

The main source of vitamin D for Australians is exposure to sunlight. Thus, levels of serum 25-hydroxyvitamin D3, the indicator of vitamin D status, vary according to the season and are lower at the end of winter.

In Australia and New Zealand, the prevalence of vitamin D deficiency varies, but is acknowledged to be much higher than previously thought. One study found marginal deficiency in 23% of women, and another frank deficiency in 80% of dark-skinned and veiled women. The groups at greatest risk of vitamin D deficiency in Australia are dark-skinned and veiled women (particularly in pregnancy), their infants, and older persons living in residential care.

Only a few foods (eg, fish with a high fat content) contain significant amounts of vitamin D. In Australia, margarine and some milk and milk products are currently fortified with vitamin D.

The average estimated dietary intake of vitamin D for men is 2.6–3.0 µg/day and for women is 2.0–2.2 µg/day. The estimated dietary requirement of vitamin D is at least 5.0 µg/day and may be higher for older people.

Adequate intake of vitamin D is unlikely to be achieved through dietary means, particularly in the groups at greatest risk, although vitamin D-fortified foods may assist in maintaining vitamin D status in the general population.

An appropriate health message for vitamin D needs to balance the need for sunshine against the risk of skin cancer.

Altering the redox state of skeletal muscle by glutathione depletion increases the exercise-activation of PGC-1α

We investigated the relationship between markers of mitochondrial biogenesis, cell signaling, and antioxidant enzymes by depleting skeletal muscle glutathione with diethyl maleate (DEM) which resulted in a demonstrable increase in oxidative stress during exercise. Animals were divided into six groups: (1) sedentary control rats; (2) sedentary rats + DEM; (3) exercise control rats euthanized immediately after exercise; (4) exercise rats + DEM; (5) exercise control rats euthanized 4 h after exercise; and (6) exercise rats + DEM euthanized 4 h after exercise. Exercising animals ran on the treadmill at a 10% gradient at 20 m/min for the first 30 min. The speed was then increased every 10 min by 1.6 m/min until exhaustion. There was a reduction in total glutathione in the skeletal muscle of DEM treated animals compared to the control animals (P < 0.05). Within the control group, total glutathione was higher in the sedentary group compared to after exercise (P < 0.05). DEM treatment also significantly increased oxidative stress, as measured by increased plasma F2-isoprostanes (P < 0.05). Exercising animals given DEM showed a significantly greater increase in peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α) mRNA compared to the control animals that were exercised (P < 0.05). This study provides novel evidence that by lowering the endogenous antioxidant glutathione in skeletal muscle and inducing oxidative stress through exercise, PGC-1α gene expression was augmented. These findings further highlight the important role of exercise induced oxidative stress in the regulation of mitochondrial biogenesis.