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Is it safe to consume sugar if I have obesity?

It has been estimated that there are over one billion individuals worldwide who are currently obese and by the year 2030 this number is going to rise to 1.5 billion individuals if current trend continues. However the most common question is “Is it safe to consume sugar if I have obesity?” The fast answer is yes, but you need to be careful. Obesity was initially seen primarily in the wealthy countries, who would have been the only ones able to afford sugar, for example the rise in sugar intake in United Kingdom and United States closely correlates with the rise in obesity rates observed in these countries. Furthermore, the later introduction of sugar to developing countries also correlates with the later rise in their rates of obesity and comorbidities.

Nowadays it is an obesity pandemic. In the USA, it has been estimated that 33.8 % of adults, over 66 million individuals, are obese, while an additional 74 million are overweight. It is estimated that the prevalence of obesity grew a shocking 40 % over the last 30 years. In European countries, obesity ranges from 20 to 30% and the rates are even higher in Australia, South America, and the Middle East. Numerous studies linked the ingestion of added sugars to obesity. Why?

Unhealthy dietary habits, alone or in combination with other lifestyle-related factors can provide a ground for obesity. In most countries, dietary habits have been gradually changed from traditional to Westernized diets that contain a substantial amount of meat, high fat content, and sweet foods including desserts and sugar-sweetened beverages. Mice fed fructose-sweetened water gain more weight than do mice given the same calories as starch, which suggests that fructose may also slow the basal metabolic rate. So, fructose specifically does not stimulate insulin secretion or the production of the hormone (leptin) regulating long-term food energy balance, such that sugar tends not to satisfy the appetite and affects glucose metabolism, lipid profile and insulin resistance.

Any food with added sugars is calorie dense food without any nutrient value – no vitamins, minerals, fiber, protein, and fat. Pure simple carbohydrates… Proteins, fat, complex carbohydrates, fiber are necessary nutrients not only for wellbeing but also for an appropriate level of satiety in order not to consume an excessive amount of food.

Clinical studies have confirmed that sucrose intake (particularly fructose) can induce weight gain. Serum triacylglycerols (fatty substances transported in the blood in the form of lipoproteins) increased in young men who received a diet supplemented with 200 g sucrose per day, whereas concentrations did not increase when starch was the primary carbohydrate. Numerous studies have shown that patients with obesity have decreased taste perception, particularly for sweet tastes. A similar hypothesis has been proposed regarding evidence for reduced brain dopamine receptors in obesity and, in both cases, it is proposed that increased food consumption, and associated weight gain, resulting from the need to increase sensory and brain stimulation. There is also pre clinical evidence in rodents and fruit flies that dietary sugar content influences sweet taste perception. For example, in Drosophila melanogaster a high sugar diet led to the decreased response of ‘sweet taste sensing neurons’, resulting in diminished behavioral responses to sweet tastes. Importantly, reduction of sweet taste responses through neural manipulation resulted in overfeeding and obesity, further suggesting that sweet taste perception is a driver of obesity.

So, an association between sugar and obesity is likely to be attributed to multiple factors such as intake of a considerable amount of energy, less feeling of fullness, decreased taste perception, and reduced brain dopamine receptors, stimulating insulin secretion, and fat storage following the long-term consumption of sugar.

More information about Sugar and obesity you can find in this article:,little%20or%20no%20nutritional%20value.

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