Obesity and sugar addiction-Neuroendocrine imbalances

Obesity and sugar addiction-Sugar, sweetness or palatability

Sugar addiction is associated with obesity what you eat can have diverse effect on your life.

The concept of sugar addiction relies on rats given the choice between a palatable sucrose solution and a much less palatable chow. Naturally in such circumstances they consume sucrose. The question is whether it is sucrose, sweetness or palatability to which they are responding? It needs to be demonstrated that similar behavior could not be demonstrated with carbohydrate in general, artificial sweeteners or fat-rich palatable foods. Comparisons have been made between the reaction of rats to the provision of sucrose, a high-fat diet and a sweet-fat combination. The ability of the opioid antagonist naloxone to produce withdrawal symptoms was not observed with fat although it occurred when sucrose alone was provided, evidence that in this paradigm different types of palatable food produce different responses.

However, it appears that rats do not have a preference for sucrose consumption as there is a preference for sucrose in sham feeding studies, where after passing through the mouth it leaves the body, ensuring no post-ingestive effects occur. Dopamine is released from the nucleus accumbency with this procedure. The sweetness of fruit juices is rewarding as judged by “reward expectation-related neuronal activity” in the primate striatum, although it is produced by sugars other than sucrose.

There is a preference for artificial sweeteners that in turn have been shown to influence the activity of the nucleus accumbency. The intermittent access of rats to a saccharin solution rather than sucrose has also resulted in withdrawal symptoms when consumption stopped. It appears that in part at least there is a response not to sucrose but rather to a sweet taste.

More generally, is the response of a rat specifically to sweetness rather than palatability? Woolley questioned whether the opioid regulation of food consumption reflects the macronutrient content rather than flavor. They studied the consumption of two types of food pellets that differed in flavor although they were nutritionally identical. A μ-opioid receptor agonist injected into the nucleus accumbency increased the consumption of both pellets in a similar manner if they were tested when only one of the two foods was present. However, when both flavors of pellets were presented simultaneously, the agonist increased and the antagonist naltrexone selectively decreased the consumption of the preferred flavor. The authors suggested that based exclusively on flavor cues, opioid mechanisms in the nucleus accumbency increase the intake of palatable foods. Similarly the administration of naltrexone into the nucleus accumbency selectively decreased sucrose intake, although it had only a minimal influence on the consumption of less preferred chow. In addition a specific μ-agonist selectively increased the intake of sucrose, saccharin and a dilute saline solution. These findings demonstrated an important role for opioids in the nucleus accumbency in promoting the consumption of preferred palatable foods. When rats consumed a high-palatability sucrose solution the release of dopamine in the nucleus accumbency was dose dependent but palatable high-fat/sweet foods similarly induced dopamine release. The message is that it is palatability rather than sweetness or being sucrose that is critical in determining food preference.

This conclusion is supported by studying the impact of opioid drugs. As a generalization it has been known for many years that opioid agents enhance and opioid antagonists decrease feeding. In the rat the positive facial response to a sucrose solution was enhanced by morphine and decreased by opioid antagonists. The administration of morphine caused a short-term increase in food intake, and at least initially an increase in fat intake at the expense of carbohydrate.

The opioid antagonist, naloxone decreased fat rather than carbohydrate consumption in rats. As it is known that for many rats fat is more attractive than carbohydrates these finding are consistent with the view that opioid mechanisms influence the intake of palatable foods. Such a suggestion is supported by the study of initial food preferences. As there is variability amongst rats in their preferences for carbohydrate and fat Gosnell considered whether morphine was acting on food preferences. They distinguished fat-preferring from carbohydrate-preferring rats. Morphine increased carbohydrate intake in carbohydrate-preferring rats and increased fat intake in fat-preferring rats. Therefore morphine increased the intake of the preferred diet rather than a specific macronutrient. Similarly naloxone selectively decreased the intake of preferred foods and not sucrose content as would be predicted by the ‘sugar addiction’ hypothesis.

Obesity and sugar addiction-Sugar and reward mechanisms

Addictive drugs and palatable food both release dopamine from the nucleus accumbency.

The nucleus accumbency has different populations of neurons that are activated by natural and drug reinforcement. The release of dopamine by natural rewards, unlike drugs of abuse, undergoes rapid habituation.

Although the food-induced release of dopamine is markedly inhibited by pre-exposure to visual and olfactory stimuli that have been conditioned to food, similar visual and olfactory stimuli that had previously been conditioned to drugs of abuse strongly potentiate the dopaminergic reaction.

The suggestion, based on the animal evidence, is not that palatable foods are physically addictive but rather that a particular style of eating can produce a reaction to food that is similar to the response to drugs of abuse.

Obesity and sugar addiction-Comparisons of dopamine release induced by food and drugs of abuse

Although addictive drugs and palatable food both increase the release of dopamine from the nucleus accumbency it appears that they influence different populations of neurons. Such a conclusion is supported by studies in which either pharmacological manipulation or selective lesions reduce the self-administration of cocaine but do not influence the response to natural rewards. For example Caine and Koob used 6-hydroxydopamine to deplete the nucleus accumbency of dopamine and found a reduction in cocaine self-administration without altering the response to food.

Additional evidence arises from the study of the time scale of dopamine release. Dopaminergic functioning can be estimated using a range of methods. Recording the rate of firing of dopaminergic neurons allows the examination of functioning in a milli-second time frame. Similarly voltammetry measures dopamine release over sub-second periods. In contrast, microdialysis is used to estimate extra-cellular concentrations of dopamine over longer periods.

Finally research and studies will always be done on this topic obesity and addiction to find the scientific solution, nevertheless to achieve optimal weight loss in a record time efficiently and economically, it will be necessary to pay a visit to AWAREmed Health and Wellness Resource Center under Doctor Akoury’s where a lot of focus is put on Neuroendocrine Restoration (NER) to reinstate normality through realization of the oneness of Spirit, Mind, and Body, Unifying the threesome into ONE. This way you will get help fast while the endless researches and studies continue.