Obesity Care

Sugar free drinks no better than full sugar drinks

With the UK introducing a levy on sugary drinks, expected to take effect in 2018, much research as to the effects of ‘sugar-free’ drinks is currently underway. One study from Imperial College London has found that sugar free drinks are no more helpful for maintaining weight than their full-sugar counterparts. Artificially-sweetened beverages (ASBs) are used as alternatives to full-sugar drinks and are often called ‘diet’ versions, to this end many consumers perceive them as the healthier option. However, this study found that there is no solid evidence to support this theory.

Sugar-sweetened beverages (SSBs) make up a third of UK teenagers’ sugar intake, and nearly half of all sugar intake in the USA, they contain few essential nutrients and have been proven to increase levels of obesity and diabetes. ASBs make up a quarter of the global sweetened beverages market; however they are not taxed to the same extent as SSBs, perhaps because of their perceived ‘healthiness’. The researchers suggest that ASBs might trigger compensatory food intake by stimulating sweet taste receptors and resulting in overconsumption of other foods. Whilst there is no direct evidence for a role of ASBs in weight gain, the researchers did not find any evidence suggesting that they were involved in weight loss when compared to their full sugar versions. The authors clearly stated that ASBs may be contributing to the global obesity crisis and should not be promoted as part of a healthy diet.

Eating routinely may help shed fat

A recent study was conducted at the University of Alabama to determine whether changing a person’s eating schedule could help them lose weight. This is one of the first human tests of early time-restricted feeding (eTRF) and it found that this type of meal timing can reduce swings in hunger and alter fat burning patterns. With eTRF people eat their last meal of the day by mid-afternoon and do not eat again until breakfast the next morning; essentially, the study suggests that eating during a much smaller window of time than one usually does can lead to weight loss. eTRF is associated with an 18-hour fasting period, the researchers claim that this keeps appetite levels more even throughout the day.
It is known that many aspects of the metabolism function to their optimum level at the beginning of the day; this diet seeks to exploit that and align with the circadian clock of the body. This study was conducted in 11 men and women with excess weight over four days, food intake was monitored as was calorie burning. Although eTRF did not alter the number of calories burned, it did reduce daily hunger swings and increased fat burning levels during night. This study was performed in a small sample size, therefore more research must be undertaken in this area in order to better understand its mechanisms and reliability.

Does good-tasting food directly cause weight gain?

A new study from the Monell Center in Philadelphia has found that desirable food in and of itself does not lead to weight gain. The study used mouse models in order to research the effects of good tasting food on overeating. Previous studies have shown that mice will show an affinity for tasty human foods such as chocolate chip cookies and crisps. However, this study aimed to examine whether the taste of food actually drives overeating. The researchers designed a series of experiments that assessed what types of food the mice liked; they then placed different groups of mice on a variety of diets. They found that the mice that ate the sweet and oily foods were no heavier than those that ate the plain foods.

These results were repeated over a period of six weeks, however food choice and overeating are complex mechanisms, many factors come in to play and therefore these results must be understood as being part of a much larger area of research. The study authors are hopeful that the results show that it is possible to create foods that are both healthy and good-tasting; however this research must be furthered to get to that point.

Vitamin D improves gut flora and metabolic syndrome

A study published in Frontiers in Physiology has found that a high-fat diet alone is not enough to trigger metabolic syndrome, it must be accompanied by a Vitamin D deficiency. Metabolic syndrome is defined by a group of risk factors that can lead to diabetes and heart disease, these include obesity, high blood sugar levels, high blood pressure and high cholesterol. The study itself was conducted in mice models and found that vitamin D deficiency caused an imbalance in gut flora, contributing to fatty livers and the symptoms that make up metabolic syndrome. Vitamin D deficiency can decrease the production of defensins, which are anti-microbial molecules that help to regulate gut flora.

If these outcomes can be repeated in humans it seems that exposure to the sun and consuming vitamin D supplements could be a feasible approach to preventing metabolic syndrome. The authors of the study are keen to continue this area of research so that more can be done to fully understand the role of vitamin D and vitamin D supplements in the development and prevention of metabolic syndrome.

Overweight affects DNA methylation

A new study published in Nature has found that overweight and obesity can lead to changes in your DNA, thereby changing how that gene is expressed. Whilst genes do not change over the course of our lives, the way that they are expressed can, and our lifestyles directly influence this, this is known as epigenetics. Up until recently, there have been few studies assessing the impact of overweight on epigenetics; however with increasing rates of obesity, this topic is becoming more and more important.

This research was carried out by an international team who examined possible correlations between BMI and epigenetic changes. Blood samples of over 10,000 European people were taken, and the team identified 207 different gene loci that were epigenetically dependant on BMI in the first group of individuals, and they then confirmed 187 of these loci in the next group. Further research confirmed that the changes were a consequence of being overweight, and were not the cause. Significant changes were also seen in the genes that are responsible for inflammation. The researchers are hoping that their results will aid the development of new strategies to predict and prevent obesity-related conditions, and also the consequences of obesity.

Leaving college with more than just a degree

A recent study has examined the weight trajectories of US college students and has found that, on average, a college student gains an extra 10 pounds during their studies. Published in the Journal of Nutrition Education and Behaviour, the study measured student BMI at the beginning and end of their first and second years, then once again after their fourth year. Twenty three per cent of the students were overweight when they started college, whilst 41% were by the end of their senior year. The increase in weight was not the only worry for the study authors, who highlighted that obese young adults are at risk of a variety of health conditions.

The authors also found that weight gain was observed over all four years of college, not limited to a particular year. Meaning that weight loss interventions need to be able to target multiple cohorts of students, rather than just the first year, which is what many of the current interventions do. Fruit and vegetable intake of the students was also below the recommended intake. The study authors hope that new behavioural strategies will target the college population in order to help curb the obesity epidemic.

New potential therapeutic target receptor identified

A team of scientists from King’s College London and Imperial College London have identified a receptor called FFAR2 that may be used in the fight against obesity, publishing their study in Nature Reviews Endocrinology. They tested a high fat diet, containing fermentable carbohydrate, against a control diet on mice. The results showed that the mice on the fermentable carbohydrate diet were protected against obesity. However, this protection was lost in FFAR2 knockout mice; those with the FFAR2 receptor showed an increase of 130% in satiety, this was associated with increased levels of hormone peptide YY and PYY, which furthers the feeling of fullness.

It is already known that supplementation of a diet with non-digestable carbohydrates can reduce appetite, however this is one of the first studies to identify a specific receptor in relation to its role in reducing food intake and protecting against obesity in this way. The study authors are hoping to further explore this area, with the hope of creating either a dietary or pharmaceutical means to change the cellular make up and involved FFAR2 in a therapeutic way. Further to this, work can now begin on developing a food system, with this knowledge, that is attractive to the general population.

Untreated Obesity causing cost increase

The Milken Institute recently released figures that displayed the economic cost of obesity to the USA. Obesity now costs the USA $1.4 trillion dollars, the vast majority of the money arises from the complications that are associated with a higher BMI. This in turn relates to the diseases that are common for untreated obesity. Interestingly, the evidence-based medicine expenditure was negligible in comparison to the other costs. Furthermore, the $64 billion dollars spent on diet and weight loss products was seen to be having little impact in the long-term.

The data shows that more must be done in the way of evidence-based research so that the prevention of obesity becomes a reality as does the avoidance of complications. Whilst the report calls for a collaborative effort by stakeholder, it also acknowledges the complexity of the problem as a whole. Therefore, the report goes on to say that whilst big actors must develop preventative measures, it is also down to personal responsibility in order to help make the change within the world.

Sugar substitute may not promote weight loss

A team of researchers from Massachusetts General Hospital have found a possible mechanism that may help explain why aspartame, a sugar substitute, does not help promote weight loss. Their report was published in Applied Physiology, Nutrition and Metabolism, and it explains that phenylalanine, a breakdown product of aspartame may interfere with the actions of an enzyme which prevents metabolic syndrome. Using mouse models, the researchers found that a diet with aspartame actually increases weight, whilst a non-aspartame diet does not.

During this study, a series of experiments was carried out, with one showing that the activity of an enzyme, known as IAP, was greatly reduced when added to a solution containing an aspartame sweetened drink, this was not the case in the sugar sweetened drink. This is particularly worrying as sugar substitutes are often used to promote weight loss by limiting the consumption of sugar. Now a number of epidemiological studies are looking into whether these substitutes are genuinely effective. The researchers want to highlight that other mechanisms may be involved, and this is only one such mechanism that may point to the use of artificial sweeteners being counter-productive.

Large BMI increase during puberty may predispose to death by cardiovascular disease later in life

A study published in The Lancet Diabetes & Endocrinology has found that boys with a large increase in BMI during puberty are at an increased risk of death due to CVD in later life. The study itself included over 37,000 men born between 1945 and 1961, and the change in BMI was calculated using BMI values at 8 and 20 years of age. The aim of the study was to evaluate the contribution of BMI for cardiovascular mortality, with the focus being the developmental period of puberty.

There was no increase in cardiovascular risk for those who were overweight before puberty, or those whose BMI normalised during puberty. BMI normally increases during puberty, however this study found that when BMI increases by more than 7 units, the risk of cardiovascular mortality later in life is also increased; this is by 22 per cent for every extra BMI unit. The researchers are now urging schools to monitor their students’ BMIs to ensure that they do not suffer from cardiovascular complications in the future.

Does fatty food cause mental health issues?

A recent study published in Molecular Psychiatry has found that excess fatty intake can affect the cognitive function of brains. This study was conducted in mice, and found that diets rich in fat reduce levels of an important protein called reelin that helps synapses in the brain signal to one another, resulting in possible cognitive and psychiatric issues. Reelin deficiency is also a feature of brain disorders such as schizophrenia and Alzheimer’s disease. The researchers saw changes as early as four weeks into the experiments, after the mice had been fed high-fat diets. The cognitive results were evident even before the animals started gaining weight. Interestingly, the results were only seen in mice that were adolescent and not fully adult mice.

The changes were mostly evident in the prefontal cortex of the mice, in humans, this is associated with decision making, expressing personality and controlling social behaviour. With the supposed drop in the quality of diets over the past few decades, this study has found some worrying results. Furthermore, the study found the results to be particularly pronounced in adolescent mice, in humans this is a period where people will start to make their own decisions about food, especially with increased calorific needs, the researchers have suggested that more education must therefore be provided about the potential pitfalls in choosing high fat diets.

Diet and exercise improves kidney function in fatty liver patients

Non-alcoholic steatohepatitis (NASH) is characterised by excess fat in the liver that can cause inflammation and scarring. This may progress to cirrhosis and liver cancer; it can also compromise kidney function. A recent study has found that patients with confirmed NASH, who were put on a low-calorie/fat diet and participated in an exercise programme, experienced reduced liver inflammation and an improved kidney function.

These results were seen after controlling for compounding factors such as diabetes, hypertension and medications. However, the exact mechanism by which these outcomes were made is not fully understood yet. The researchers have hypothesised that oxidative stress, insulin sensitivity,inflammation, and vascular endothelial function all have roles to play. Hopefully, more research will be done in this area to fully understand the therapeutic benefits of such programs for patients with NASH.