Department of Psychiatry, University of Florida College of Medicine & McKnight Brain Institute, Gainesville, FL, USA.
Med Hypotheses. 2009 Dec;73(6):892-9. doi: 10.1016/j.mehy.2009.06.049. Epub 2009 Jul 29.
One plausible explanation for the controversy that surrounds the causes and clinical management of obesity is the notion that overeating and obesity may only be a couple of "symptoms" associated with a yet to be discovered medical disorder.
To introduce the Salted Food Addition Hypothesis. This theory proposes that salted food acts in the brain like an opiate agonist, producing a hedonic reward which has been perceived as being only peripherally "flavorful", "tasty" or "delicious". The Salted Food Addition Hypothesis also proposes that opiate receptor withdrawal has been perceived as "preference," "urges," "craving" or "hunger" for salted food.
The Salted Food Addiction Hypothesis is made manifest by individually presenting a basic review of its primary coexisting components; the Neurological Component and the Psychosocial Component. We also designed a prospective study in order to test our hypothesis that opiate dependent subjects increase their consumption of salted food during opiate withdrawal.
The neuropsychiatric evidence integrated here suggests that salted food acts like an, albeit mild, opiate agonist which drives overeating and weight gain. The opiate dependent group studied (N=27) developed a 6.6% increase in weight during opiate withdrawal.
Salted Food may be an addictive substance that stimulates opiate and dopamine receptors in the brain's reward and pleasure center more than it is "tasty", while salted food preference, urge, craving and hunger may be manifestations of opiate withdrawal. Salted food and opiate withdrawal stimulate appetite, increases calorie consumption, augments the incidence of overeating, overweight, obesity and related illnesses. Obesity and related illnesses may be symptoms of Salted Food Addiction.
围绕肥胖的原因和临床管理而产生的争议有一个合理的解释，即暴饮暴食和肥胖可能只是尚未发现的医学疾病的几种“症状”。
介绍加盐食物假说。该理论提出，加盐食物在大脑中的作用类似于阿片类激动剂，产生一种愉悦的奖励，这种奖励被认为只是外围的“有味道”、“美味”或“可口”。加盐食物假说还提出，阿片受体戒断被感知为对加盐食物的“偏好”、“冲动”、“渴望”或“饥饿”。
通过单独呈现其主要共存成分的基本综述，即神经成分和心理社会成分，使加盐食物成瘾假说显现出来。我们还设计了一项前瞻性研究，以检验我们的假设，即阿片类药物依赖者在阿片类药物戒断期间会增加对加盐食物的摄入。
这里整合的神经精神病学证据表明，加盐食物的作用类似于阿片类药物激动剂，尽管作用温和，但会导致暴饮暴食和体重增加。我们研究的阿片类药物依赖组（n=27）在阿片类药物戒断期间体重增加了 6.6%。
加盐食物可能是一种成瘾物质，它刺激大脑奖励和愉悦中心的阿片类和多巴胺受体的作用超过了它的“美味”，而加盐食物的偏好、冲动、渴望和饥饿可能是阿片类药物戒断的表现。加盐食物和阿片类药物戒断会刺激食欲，增加热量摄入，增加暴饮暴食、超重、肥胖和相关疾病的发生率。肥胖和相关疾病可能是加盐食物成瘾的症状。
