The Link between Alcoholism and Obesity

July 30, 2014

The Link between Alcoholism and Obesity – The Prevailing Health Consequences

Obesity and Alcoholism are life threatening health conditions yet people are still not keen on healthy living habits that avoids and prevent such conditions

From the definitions of the two terminologies you may not see clearly the absolute similarities however these two conditions (alcoholism and obesity) may be much more correlated that you have ever imagined. If you look at the two conditions, you will realize that both are provoked by an episode of loss of control. It may not matter how the loss of control took place whether it was genetically instigated, propelled by environmental factors or it was just a moment of one’s weak moments does not count, the common denominator is there is a loss of control.

Many people suffering from these conditions normally invest heavily in the management of their addiction occasioned by various factors like struggling to maintaining control, feeling guilty or just juggling with when they will access their addictive elements that is alcohol or food. With this both conditions can grow progressively worse and when taken to the extreme can be life threatening.

The powerful ingredients making alcoholism and obesity to be similar are the contents of what causes their being addictive which are ethanol and food and how they work on the brain. For instance ethanol stimulates reward centers in the brain exactly the way sugar, salt and fat also do. It is because of this that people with a tendency of over-drinking may also have the same tendency to overeating.

The Link between Alcoholism and Obesity – Alcohol and Weight loss

Ignorantly people often say that alcohol consumption increases appetite and therefore alcohol consumers are motivated to eat more thereby gaining weight. This is not true since ethanol which is the key addictive ingredient in alcoholic drinks and fat from foods have approximately the same amount of calories however those people suffering from alcoholism have a tendency not to be affected by obesity primarily because they are often malnourished due to poor feeding habits having replaced a portion of their food calories with calories from alcohol

According to a study conducted in 2005 sampling regular alcohol consumers it was established that those who drank the smallest amount (i.e. one drink per day) with the extreme frequency (i.e. three to seven days per week) had a lower body mass index (BMI) than those who drank more occasionally, but in larger units. Even though we may not rely heavily on these findings they may indicate some relationship between over-drinking and overeating.

Connection between Alcoholism and Obesity

Early 2010 researchers from Washington University School of medicine released one of the most important findings regarding the connection between obesity and alcoholism. The study was based on two large alcoholism surveys previously done where 80,000 people participated in both. They then put proper control on all the factors of the study and the ultimate finding was that in quite recent survey those with a family history of alcoholism had a greater chance of being affected by obesity. For women, who had a 49 percent greater chance, this was especially true. One possible reason is that in trying to avoid the alcoholic behaviors observed in their families, people replace alcohol with a different addiction.

Surprisingly enough researchers did not find any connection or association between obesity and family history of alcoholism in the first survey. The fact that the link strengthened as much as it did in the relatively short amount of time between the two surveys suggests that environmental factors (the increase in sedentary times; the increased prevalence of fatty, sugary and salty foods in grocery stores and restaurants; and the reduced access to opportunities for activity) are involved. In brief a genetic risk might be submissive in a world that makes maintaining one’s weight a relatively straightforward task. But, change the environment to make unhealthy eating easier and being active harder, and the problem will become apparent.

Finally in their (researchers’) comments in their publication they focused on changes to our food environment, suggesting that obesity may be rising in “individuals vulnerable to addiction. This may be specifically the result of a changing food environment and the increased availability of highly palatable foods.”

The Link between Alcoholism and Obesity – Overlapping Brain Pathways

More and more, neuroscientists are finding similarities in the pathways that lead to excessive eating and dependence on alcohol and other drugs. Both obesity and alcohol addiction have been linked to the brain’s reward system. Overconsumption can trigger a gradual increase in the reward threshold, requiring more and more palatable high-fat food or strengthening alcohol to satisfy cravings. It is no secret that addiction and obesity the two major and most challenging health problems in U.S and many other nations across the globe today. It is therefore important that we learn from these research findings to not just keep talking but to put into practice some of the knowledge we have gathered about addiction to the study of overeating and obesity.

Every day possess an opportunity to learn something new and we are privileged to be learning more about how eating and drinking are indistinguishably connected at the physiologic level. These physiologic commonalities help to explain why the behaviors of excessive food intake and excessive alcohol consumption share so many similarities. Nonetheless, in appreciation of possible link between obesity and alcoholism we all have a duty to unlock the link and use the findings to understand, treat and most importantly prevent these two diseases from further damaging our societies and families.

It will finally take a collective approach for all of us to win this race. On your part you can contribute by talking to the experts like Dr. Dalal Akoury, Founder of AWAREmed Health and Wellness Resource Center concerning all that may be bothering you concerning these these health conditions. Doctor Akoury and her team of experts are there for you and your friends to ensure you are not just educated but well treated by offering exclusive NER Recovery Treatment to you, your friends, other physicians and health care professionals through training, clinical apprenticeships, webinars and seminars. Remember together we will win and celebrate having chosen to be a part of this truly successful and fast weight loss and addiction recovery treatment.

The Link between Alcoholism and Obesity – The Prevailing Health Consequences

Obesity and sugar addiction

March 13, 2014

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.

Obesity and sugar addiction-Neuroendocrine imbalances

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