Vitamin D pills’ effect on healthy bones queried.


Healthy adults do not need to take vitamin D supplements, suggests a study in The Lancet which found they had no beneficial effect on bone density, a sign of osteoporosis.

But experts say many other factors could be at play and people should not stop taking supplements.

University of Auckland researchers analysed 23 studies involving more than 4,000 healthy people.

The UK government recommends children and over-65s take a daily supplement.

The New Zealand research team conducted a meta-analysis of all randomised trials examining the effects of vitamin D supplementation on bone mineral density in healthy adults up to July 2012.

The supplements were taken for an average of two years by the study participants.

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I’m not surprised they didn’t find any evidence of the effects of vitamin D on bone density because there are so many other factors involved…”

Dr Laura Tripkovic University of Surrey

Bone mineral density is a measure of bone strength and measures the amount of bone mineral present at different sites in the body. It is often seen as an indicator for the risk of osteoporosis, which can lead to an increased risk of fracture.

The trials took place in a number of different countries including the UK, the US, Australia, Holland, Finland and Norway.

Although the results did not identify any benefits for people who took vitamin D, they did find a small but statistically significant increase in bone density at the neck of the femur near the hip joint.

According to the authors, this effect is unlikely to be clinically significant.

Free up resources

Prof Ian Reid, lead study author, from the University of Auckland, said the findings showed that healthy adults did not need to take vitamin D supplements.

“Our data suggest that the targeting of low-dose vitamin D supplements only to individuals who are likely to be deficient could free up substantial resources that could be better used elsewhere in healthcare.”

Writing about the study in The Lancet, Clifford J Rosen from the Maine Medical Research Institute agrees that science’s understanding of vitamin D supports the findings for healthy adults, but not for everyone.

“Supplementation to prevent osteoporosis in healthy adults is not warranted. However, maintenance of vitamin D stores in the elderly combined with sufficient dietary calcium intake remains an effective approach for prevention of hip fractures.”

The Department of Health currently recommends that a daily supplement of vitamin D of 10 micrograms (0.01mg) should be taken by pregnant and breastfeeding women and people over 65, while babies aged six months to five years should take vitamin drops containing 7 to 8.5 micrograms (0.007-0.0085mg) per day.

Additional factors

Dr Laura Tripkovic, research fellow in the department of nutritional sciences at the University of Surrey, said the study was important but very specific.

“I’m not surprised they didn’t find any evidence of the effects of vitamin D on bone density because there are so many other factors involved in osteoporosis, like genes, diet and environment.

“To pin it all on vitamin D… it’s difficult to do that.”

Dr Tripkovic said it was no good taking vitamin D supplements if people didn’t also maintain a healthy, balanced diet containing calcium and take plenty of exercise.

She said most healthy people should be able to absorb enough vitamin D naturally, through sunshine and diet.

“But if people are worried about their vitamin D levels then a multi-vitamin tablet would do. If you have bone pain and muscle aches then you should go and see your GP and discuss it.”

We get most of our vitamin D from sunlight on our skin, but it is also found in certain foods like oily fish, eggs and breakfast cereals.

However, taking too much vitamin D in the form of supplements can be harmful because calcium can build up and damage the kidneys.

Experts advise taking no more than 25 micrograms (0.025mg) a day.

The UK guidance is currently being reviewed.

Iodine deficiencies during pregnancy linked to lower IQ in offspring.

Iodine deficiencies during pregnancy may have negative neurocognitive outcomes among offspring, according to findings by researchers in the United Kingdom that were published in The Lancet.

Pregnant women and those planning a pregnancy should ensure adequate iodine intake; good dietary sources are milk, dairy products and fish. Women who avoid these foods and are seeking alternative iodine sources can consult the iodine fact sheet that we have developed, which is available on the websites of the University of Surrey and the British Dietetic Association. Kelp supplements should be avoided, as they may have excessive levels of iodine,” Sarah C. Bath, PhD, RD, of the department of nutritional sciences at the University of Surrey, said in a press release.

Bath and colleagues analyzed stored samples of urinary iodine concentrations from 1,040 first-trimester pregnant women, measures of IQ from the offspring aged 8 years and reading ability at age 9 years. The mother-child pairs were collected from the Avon Longitudinal Study of Parents and Children (ALSPAC).

The researchers defined mild-to-moderate iodine deficiency as a median urinary iodine concentration of 91.1 mcg/L (interquartile range [IQR], 53.8-143; iodine-to-creatinine ratio of 110 mcg/g; IQR, 74-170).

After adjusting for 21 socioeconomic, parental and child factors as confounders, data indicated that children of women with an iodine-to-creatinine ratio of less than 150 mcg/g were more likely to have scores in the lowest quartile for verbal IQ (OR=1.58; 95% CI, 1.09-2.3), reading accuracy (OR=1.69; 95% CI, 1.15-2.49) and reading comprehension (OR=1.54; 95% CI, 1.06-2.23) vs. those of mothers with ratios of at least 150 mcg/g. Furthermore, scores continued to dwindle when the less than 150-mcg/g group was subdivided, researchers wrote.

In an accompanying commentary, Alex Stagnaro-Green, MD, MHPE,professor of medicine and obstetrics and gynecology at the George Washington University School of Medicine and Health Sciences, andElizabeth N. Pearce, MD, associate professor of medicine at Boston University School of Medicine, wrote that this study, along with previous research, represents a call-to-action because of the documented link between iodine deficiency and poor neurocognitive outcomes.

 “Absence of a public health policy in the face of clear documentation of moderate iodine deficiency and strong evidence of its deleterious effect on the neurodevelopmentof children is ill advised,” they wrote. “Nor should unmonitored and adventitious dietary iodine sources continue to be relied on.”

Source: Endocrine Today

Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC)



As a component of thyroid hormones, iodine is essential for fetal brain development. Although the UK has long been considered iodine replete, increasing evidence suggests that it might now be mildly iodine deficient. We assessed whether mild iodine deficiency during early pregnancy was associated with an adverse effect on child cognitive development.


We analysed mother—child pairs from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort by measuring urinary iodine concentration (and creatinine to correct for urine volume) in stored samples from 1040 first-trimester pregnant women. We selected women on the basis of a singleton pregnancy and availability of both a urine sample from the first trimester (defined as ≤13 weeks’ gestation; median 10 weeks [IQR 9—12]) and a measure of intelligence quotient (IQ) in the offspring at age 8 years. Women’s results for iodine-to-creatinine ratio were dichotomised to less than 150 μg/g or 150 μg/g or more on the basis of WHO criteria for iodine deficiency or sufficiency in pregnancy. We assessed the association between maternal iodine status and child IQ at age 8 years and reading ability at age 9 years. We included 21 socioeconomic, parental, and child factors as confounders.


The group was classified as having mild-to-moderate iodine deficiency on the basis of a median urinary iodine concentration of 91·1 μg/L (IQR 53·8—143; iodine-to-creatinine ratio 110 μg/g, IQR 74—170). After adjustment for confounders, children of women with an iodine-to-creatinine ratio of less than 150 μg/g were more likely to have scores in the lowest quartile for verbal IQ (odds ratio 1·58, 95% CI 1·09—2·30; p=0·02), reading accuracy (1·69, 1·15—2·49; p=0·007), and reading comprehension (1·54, 1·06—2·23; p=0·02) than were those of mothers with ratios of 150 μg/g or more. When the less than 150 μg/g group was subdivided, scores worsened ongoing from 150 μg/g or more, to 50—150 μg/g, to less than 50 μg/g.


Our results show the importance of adequate iodine status during early gestation and emphasise the risk that iodine deficiency can pose to the developing infant, even in a country classified as only mildly iodine deficient. Iodine deficiency in pregnant women in the UK should be treated as an important public health issue that needs attention.

Source: Lancet



Interlinks between sleep and metabolism.


Lack of sleep is increasingly associated with weight gain and metabolic problems. Interfaces between the pathways that regulate circadian timing and metabolism might underlie these adverse health effects. Jill Jouret reports.

Getting a good night’s sleep is a basic, but often eluded, prescription for good health. Modern lifestyles provide opportunities for 24 h activity, and minimising sleep is often thought to be a harmless, efficient, or merely necessary means to accommodate schedules. However, feeling tired at night is more than an instruction to rest. Behaviour and physiology are intricately linked to light and dark cycles, and an internal timing mechanism has evolved to ensure that physiological processes occur at optimum times in a 24 h cycle. Maintaining the synchrony of this endogenous circadian clock seems to have wide-ranging health implications.

Although the mechanisms are not fully clear, evidence is mounting that insufficient sleep and disruption in circadian rhythms contribute to pathogenesis of metabolic disorders, cardiovascular disease, and cancer. Worldwide, metabolic syndrome is on the rise, as is the introduction of artificial light and activity into night-time hours. Epidemiological and clinical studies have shown that short-duration and poor-quality sleep predict development of type 2 diabetes and obesity, suggesting that sleep, circadian rhythms, and metabolic systems are interconnected.

In mammals, circadian rhythms are generated centrally by the suprachiasmatic nuclei in the anterior hypothalamus. Light perception by the retina synchronises these single-celled oscillators, generating rhythmic outputs that regulate sleep and wakefulness, feeding and energy expenditure, and glucose homoeostasis. This central clock also sends signals via direct innervation and humoral factors to clock components in peripheral tissues, thus maintaining the circadian timing of an array of physiological processes. Transcription—translation feedback loops implicating specific clock genes lead to a roughly 24 h cycle.

Molecular links between circadian and metabolic pathways have been identified and many hormones implicated in metabolism and energy balance exhibit circadian oscillation—eg, expression and secretion of leptin, a hormone that signals satiety, peaks at night. The complex signalling systems that govern glucose homoeostasis and metabolism of fatty acids, cholesterol, bile acids, and toxins receive inputs from the local and central circadian clocks, allowing cells to anticipate metabolic reactions in a 24 h period. In-vitro studies show that metabolic cues can be transmitted to core components of the circadian clock. Such crosstalk suggests a mechanism by which eating (and possibly sleeping) patterns could shift innate circadian timing.

study published in March, 2013, by a group at the University of Surrey (Guildford, UK) highlighted the interconnection between sleep, circadian rhythmicity, and metabolism. Whole-blood RNA samples were taken from participants after a week of restricted nightly sleep (5·7 h) and also after a week of adequate sleep (8·5 h). Transcriptome analysis showed that 711 genes were upregulated or downregulated by insufficient sleep, including genes associated with circadian rhythms and metabolism.

Sleep restriction also reduced the total number of genes with circadian expression profiles, implying that even a week of poor sleep can disrupt the body’s intricate physiological timing.

Melatonin, a key regulator of sleep, could be an important link connecting circadian timing and insulin signalling. Melatonin production is suppressed by light, and peaks around 3—5 h after sleep onset; it regulates the sleep—wake cycle by lowering body temperature and causing drowsiness, and also inhibits insulin secretion by pancreatic β cells. A 2013 case-control studywithin the Nurses’ Health Study cohort showed that, compared with women in the highest category of melatonin secretion, women in the lowest category had about a twice the risk of developing type 2 diabetes (after controlling for demographic, lifestyle, and other risk factors). Previous studies have shown that single nucleotide polymorphisms of the melatonin receptor are also associated with an increased risk of type 2 diabetes.

More clinical research is needed to characterise this association between sleep, melatonin concentrations, and type 2 diabetes, and to elucidate, for example, whether melatonin supplementation has a role in treatment. Irregular and extended working hours are a reality for many industries, and epidemiological studies have shown lower melatonin concentrations in night-shift workers than in day-shift workers and an increasing risk of type 2 diabetes with number of years of shift work. For this substantial proportion of the workforce, more solutions are needed to prevent people from falling into economically driven health traps.

Insufficient sleep is a risk factor for weight gain and obesity, in addition to type 2 diabetes, and understanding the underlying mechanisms could help to guide novel weight-loss strategies. A study published on April 2, 2013, showed that eating behaviours, particularly night-time eating, contributed to weight gain during sleep loss. Whole-room calorimetry measured daily energy expenditure in adults undergoing 5-day cycles of inadequate (5 h) or adequate (9 h) nightly sleep. Energy expenditure was about 5% higher with insufficient sleep, but increased food intake more than compensated for this energetic cost. In the sleep-loss condition, participants ate a smaller breakfast but consumed 42% more calories as after-dinner snacks, leading to weight gain. The study investigators suggested that participants’ eating patterns during sleep loss resulted from a delayed circadian phase—ie, a later onset of melatonin secretion at night, assessed by hourly blood samples from an intravenous catheter—which might have led to a circadian drive for more food intake. Furthermore, the time between waking and melatonin offset was longer in the 5 h sleep condition; thus, participants awoke during an earlier circadian phase (while still in biological night) and might have been less hungry for breakfast. Previous studies have suggested that disrupted signalling of satiety and hunger hormones leads to the overeating associated with insufficient sleep; however, in both the 5 h and 9 h conditions, excessive food intake was accompanied by appropriate increases in the satiety hormones leptin and peptide YY and decreases in ghrelin, which stimulates hunger.

Future studies should examine how sleep deprivation leads to delays in circadian phase and how circadian timing of meals affects energy metabolism. For the millions of people whose working week necessitates a disrupted sleep schedule, a physiological drive for more food intake, the availability of high-calorie foods, and exhaustion leading to less physical activity overall could be a potent formula for weight gain.

Whether for work, play, or travel, voluntary sleep curtailment has become endemic; however, restricted sleep seems to interfere with the crosstalk between complex physiological and circadian networks that have evolved to couple our bodily functions with the Earth’s 24 h rotation. Many more issues deserve investigation, such as the differential effects on health of acute versus chronic sleep deprivation, and how light exposure mediates the effects of sleep loss. As more evidence emerges of the circadian orchestration of metabolism, perhaps the time has come for sleep to figure more prominently in treatment and public health guidelines.

Source: Lancet