Though the hunger-reduction phenomenon reported during ketogenic diets is well-known, the underlying molecular and cellular mechanisms remain uncertain. Ketosis has been demonstrated to exert an anorexigenic effect via cholecystokinin CCK release while reducing orexigenic signals e. The aim of this review is to provide a summary of our current knowledge of the effects of ketogenic diet KD on food control in an effort to unify the apparently contradictory data into a coherent picture. Hunger and satiety are two important mechanisms involved in body weight regulation. Even though humans can regulate food intake by will, there are systems within the central nervous system CNS that regulate food intake and energy expenditure. This complex network, whose control center is spread over different brain areas, receives information from adipose tissue, the gastrointestinal tract GIT, and from blood and peripheral sensory receptors. Mayer suggested that depletion of carbohydrate availability leads to hunger, and the hypothalamic centers with receptors sensitive to glucose levels might be involved in the short-term regulation of energy intake Mayer, In , Kennedy proposed the lipostatic hypothesis suggesting that lipid metabolites could also be involved in food regulation Kennedy, , and in , Mellinkoff studied the effects of protein metabolism suggesting an aminostatic hypothesis Mellinkoff et al.
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Ketogenic diets are well-established as a successful anticonvulsant therapy. Based on overlap between mechanisms postulated to underlie pain and inflammation, and mechanisms postulated to underlie therapeutic effects of ketogenic diets, recent studies have explored the ability for ketogenic diets to reduce pain. Pain is one of the most commonly indicated health-related factors leading to poor quality of life. Here we review correlative and direct evidence that ketogenic diets could offer a non-pharmacological option for reducing pain and inflammation. High-fat ketogenic diets have long been known to be effective against seizures, 4, 5 and metabolically the high fat, very low carbohydrate and restricted protein content limits available glucose and forces utilization of ketones for cell energy. Similar to epilepsy, pain is a condition that encompasses diverse underlying conditions. Why would one propose that ketogenic diets might also be useful in treating pain, a seemingly disparate condition? There are several lines of evidence, outlined below, that strongly suggest that metabolic approaches to pain could provide new clinical opportunities. Some of these mechanisms have been tested directly and additional research is ongoing. Multiple hypotheses undergird postulated hypoalgesic and anti-inflammatory effects of a ketogenic diet. Here we highlight four main postulated mechanisms. Reducing glycolytic metabolism appears to be anticonvulsant, whether it is accomplished by fasting, caloric restriction, high fat plus carbohydrate restriction the ketogenic diet, the modified Atkins diet, 4, 5 or specifically blocking glycolysis with 2-deoxyglucose.
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Portion Size, Energy Intake, and Obesity. Journal List Front Psychol v. For example, are there certain types of food products that non-Hispanic blacks buy more frequently? The presence of KBs in the blood and their elimination via urine causes ketonemia and ketonuria. Similar results were observed in a four-year study comparing energy restriction and portion control Flechtner-Mors et al. The nervous system and metabolic dysregulation: emerging evidence converges on ketogenic diet therapy. Implications, Comorbidities and Multiple Benefits Use of the ketogenic diet has spread internationally in recent years, and therefore it has become a therapy increasingly accessible to many different cultural traditions. How this kind of metabolic condition ketosis can affect satiety and hunger mechanisms is still a matter of debate. Eating is impacted not only by the biological responses that occur when the presence of food or even the smell of food triggers physiological. It will not reverse what has hap-.