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The worldwide decline in vitamin intake is contributing to the increase in the number of overweight people. Scientists at the French research institutes INSERM and INRA draw this conclusion from an animal study in which they gave mice half of the amount of vitamins that the animals require. Thanks a lot, food industry.

Not enough
A few weeks ago it was on the American site of NutraIngredients.com: scientists Balz Frei, Walter Willett and Bruce Ames warned against the negative way in which the mass media and scientists portray nutritional supplements with added vitamins and minerals. [nutraingredients-usa.com 03-Jun-2014]

It is so that studies have occasionally found that heavy users of these supplements have a slightly higher risk of developing cancer or cardiovascular disease. But statistics show that large groups of people in modern societies are getting far fewer minerals and vitamins than textbooks recommend.

Ninety percent of Americans consume too little vitamin D and vitamin E; sixty percent get too little magnesium, and fifty percent don’t consume the recommended amount of calcium and vitamin A. And that’s just a few examples. Multi-vitamins are a cheap and simple way of compensating for these deficiencies.

Overweight
One of the things that vitamins do is to help convert nutrients into energy, and French researchers wondered whether a diet with too few vitamins might encourage overweight. They conducted an experiment with mice, giving them half of the amount of vitamins usually contained in their food for a period of 12 weeks.

And indeed, although the animals’ energy intake didn’t increase as a result of the vitamin shortage, they did become fatter.

White bars: mice given standard feed; black bars: mice given too few vitamins.

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The vitamin shortage made the cells less sensitive to insulin, and reduced the amount of the fat sensor PPAR-alpha synthesised in the liver – and thus also reduced the fat burning. The researchers also observed evidence of the reduced fat burning in the mice’s blood. The vitamin shortage reduced the concentration of the ketone beta-hydroxybutyrate, a substance released when fatty acids are burned.

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Conclusion
“Our study in mice suggests a role for vitamin insufficiency in obesity, although extensive further work is still required”, the researchers write. “Vitamin deficiency based on consumption of inexpensive but vitamin-poor foods may play a role in body weight and adiposity management. Our study contributes to the recommendation of a healthy diet composed of diverse food products with high vitamin density, such fruit and vegetables, whole-grain cereals and fish products.”

Multivitamin restriction increases adiposity and disrupts glucose homeostasis in mice.

Abstract

A strong association between obesity and low plasma concentrations of vitamins has been widely reported; however, the causality of this relationship is still not established. Our goal was to evaluate the impact of a multivitamin restriction diet (MRD) on body weight, adiposity and glucose homeostasis in mice. The mice were given a standard diet or a diet containing 50 % of the recommended vitamin intake (MRD) for 12 weeks. At the end of the experiment, total body weight was 6 % higher in MRD animals than in the control group, and the adiposity of the MRD animals more than doubled. The HOMA-IR index of the MRD animals was significantly increased. The adipose tissue of MRD animals had lower expression of mRNA encoding adiponectin and Pnpla2 (47 and 32 %, respectively) and 43 % higher leptin mRNA levels. In the liver, the mRNA levels of Ppar? and Pgc1? were reduced (29 and 69 %, respectively) in MRD mice. Finally, the level of ?-hydroxybutyrate, a ketonic body reflecting fatty acid oxidation, was decreased by 45 % in MRD mice. Our results suggest that MRD promotes adiposity, possibly by decreasing adipose tissue lipolysis and hepatic ?-oxidation. These results could highlight a possible role of vitamin deficiency in the etiology of obesity and associated disorders.

PMID: 24858304 [PubMed]

Source: http://www.ncbi.nlm.nih.gov/pubmed/24858304

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