Antibiotics encourage obesity
Continued use of antibiotics in children can lead to obesity, changes in bone growth and altered gut bacteria, according to a new study in Nature Communications. The team stated that, in the USA, 262 million courses of antibiotics were prescribed to outpatients, that’s 842 per 1000 people a year, with use at its highest in children under 10. Estimates suggest children may have had 10 courses by this age. Antibiotics are well known to impact on microbial function, but little study has been done into how they affect host health during critical developmental stages.
The researchers mimicked childhood antibiotic use by using mice as their models. They found that early life pulsed antibiotic treatment (PAT) leads to short term increases in mouse weight and bone growth, whilst also leading to long-term changes in composition of gut bacteria. These changes included altering the species of the bacteria present and therefore the metabolic functions as well. Furthermore, they found that the bacteria in the antibiotic treated mice took much longer to adapt to new diets than those without antibiotics. The team remain cautious regarding the implication for humans though.
Read MoreBariatric surgery before pregnancy – Is this a solution to a big problem?
In the UK, 33% of pregnant women are overweight or obese and may experience gestational diabetes. Bariatric surgery commonly leads to greater and more sustained weight loss than do lifestyle approaches, and evidence that bariatric surgery can prevent, treat, or even “reverse” type 2 diabetes has increased enthusiasm for its use prior to pregnancy. However, there are also concerns that potential malnutrition or malabsorption resulting from these surgeries may lead to pregnancy complications.
In this article from America, pregnancy outcomes were examined in women from 2006 to 2011 who underwent bariatric surgery prior to pregnancy as compared with matched controls. (Early-pregnancy BMI in the control cohort was matched to pre-surgery BMI in the bariatric-surgery cohort). As compared with controls, women with a history of bariatric surgery had significantly lower incidences of gestational diabetes.
Obstetricians will most likely be seeing an increasing number of women who have undergone bariatric surgery before pregnancy although women are advised to delay conceiving until 12 to 24 months after surgery. But the current data, combined with previous reports, suggest that it may be prudent to monitor foetal growth in women who have undergone bariatric surgery, particularly in those who have had gastric bypass surgery.
The current study underscores that bariatric surgery has the potential to reduce the risks of gestational diabetes and large-for-gestational-age neonates but is also associated with some risks in pregnancy such as preterm birth, stillbirth, neonatal death, and major congenital malformations. Decisions regarding bariatric surgery in women of reproductive age should take into account the benefits and risks associated with this, not inconsequential procedure in terms of both pregnancy and long-term health.
Read MoreThe economic scale of obesity
In America, concern about the health risks, medical care costs, and other consequences of obesity has led to a host of policies and programmes implemented by companies, school districts, and governments to prevent and reduce obesity. It has also resulted in a large body of economic research on the causes and consequences of obesity, and on approaches to prevent and reduce obesity.
Economic solutions, taxes, incentives, and information, do not offer any single strategy that is likely to have more than a modest effect. Strategies like junk food taxes are promoted with projections that sound great, the hard economic truth is that these estimates are subject to many limitations. None are backed by solid evidence that they will have more than a modest effect and they may well have unintended consequences.
From this review the evidence suggests that there is no single dominant economic cause of obesity; a wide variety of factors may contribute a modest amount to the risk. In different groups and different circumstances, the effects may be large or insignificant. Studies of economic approaches to preventing obesity, such as menu labelling, taxes on energy-dense foods, and financial rewards for weight loss, see only modest effects on weight and thus a range of policies may be necessary to have a substantial effect on the prevalence of obesity.
Read MoreNew function of obesity gene revealed
In research published by the New England Journal of Medicine, scientists at Harvard and MIT found that by tweaking certain pieces of the DNA code in the gene region responsible for coding the fat mass and obesity-associated protein, known popularly as the “FTO gene” or the “obesity gene”, they could cause the body to accelerate metabolism and burn excess fat that otherwise would have remained stored.
The FTO region harbours the strongest genetic association with obesity, yet the basis of this association remains elusive. To test how faulty genetics were at play in weight gain, the researchers took fat samples from Europeans holding both the variant of the FTO gene region linked to obesity and a normal FTO gene. They discovered that, in those with obesity, the DNA code of the FTO gene was activating two other associated genes, IRX3 and IRX5. Those genes, in turn, were preventing fat from being burnt through a process known as thermogenesis, where fat cells get rid of energy in the form of heat, instead of storing it as fat. This happens naturally in those with healthy FTO gene regions.
Testing on mice using the Crispr/Cas9 system, which edits the faulty DNA code to the correct sequence, the scientists were able to install the correct code, thereby preventing the body from storing excess fat. The process has so far proved successful in reversing obesity in mice, but is yet to be tested on humans.
Read MoreChillies becoming hot topic in fight against obesity
Researchers in Australia have investigated the association between hot chilli pepper receptors (TRPV1) and the feeling of fullness in mice. As the stomach fills it begins to stretch, which activates nerves that inform the body that the stomach is filling and when it has reached capacity. The researchers found that this activity is regulated by TRPV1 receptors, also known as hot chilli pepper receptors. This builds on previous knowledge that capsaicin, the chemical that makes chillies hot, reduces food intake in humans.
The study also found that deletion of TRPV1 receptors dampened the response of gastric nerves to stretch. This resulted in a delayed feeling of fullness and consumption of more food, showing that the capsaicin mechanism is potentially vital in controlling how much food we eat. Dr Stephen Kentish, one of the study authors, hopes to ‘see how feasible this is as a potential treatment not just for obesity itself but maybe in the prevention of gaining weight.’ These exciting findings could inform further research in this area and lead to the development of novel therapies.
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