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  • Psychobiological Traits in The Risk Profile For Overeating and Weight Gain

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    Davis, C. 2009 Int J Ob

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    Psychobiological traits in the risk profile for overeating and weight gain

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    Davis, C. 2009 Int J Ob

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    13 просмотров5 страниц

    Psychobiological Traits in The Risk Profile For Overeating and Weight Gain

    Загружено:

    eduardobar2000
    Davis, C. 2009 Int J Ob

    Авторское право:

    © All Rights Reserved
    Скачайте в формате PDF или читайте онлайн в Scribd
    Отметить как неприемлемый контент
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    rere! jana of Obes (200 33, 549-53 2009 Macnian Pubs ied Mighs ed C507. 065/09_ $3200 Sisal REVIEW Psychobiological traits in the risk profile for overeating and weight gain C Davis!? 1343 Bethune College, York University, Toronto, Ontario, Canada and *The Centre for Addiction and Mental Health, Toronto, Ontario, Carada (Our dramatically changed food environment ~since petiods in our history when food sources were highly constrained has presented new challenges for obesity research, For example, these alterations have strongly emphasized the physiological differences between the homeostatic and the hedonic regulation of food intake the latter being largely responsible for the pronounced increase in obesity in the past few decades, There is also increasing agreement that compulsive overeating shares many patalels with addiction disorders such as drug abuse. These factors have also fostered a renewed interest in identifying individual differences in personally and motivational systems that increase the risk for overeating and weight qain in our population, Reward sensitivity has been the focus of a recent body of compelling research, with evidence favoring two seemingly ‘Opposite points of view. On the one hand, studies have found support for a link between low reivard sensitivity and obesity, whereas other evidence suggests that a strong appetitive motivation feads to overeating and weight gain. Arguments are provided to reconcile these apparently disparate theories, Finally, the role of impulsivity and is links with symptoms of attention deficit/hyperactivity disorder are discussed, as well as their respective toles in the risk profile for obesity. Interational journal of Obesity (2009) 33, $49-S$3; doi:10,1038/}jo.2009.72, Keywords: psychobiolagy, reward sensitivity, impulsivity; ADHD Introduction “There is increasing ageoement that excessive food consump= ‘hon has many similatties to addiction disorders such as drag abuse, in part, because both activate the same brain reward mechanisms. ‘They also have comparable clinical features, such as their escalating compulsion, he symptoms of tolerance and withdrawal, and the overwhelming cravings that contribute to repeated relapses after periods of restraint fr abstinence. "The family transmission pattern of binge cating and substance dependence disorders also indicates a shared etiology unbke their respective associations with other psychopathologies, which appear fo be transmitted independently? Different from arug abuise, however, the concept of food addiction isa relatively recent phenomenon, and one whose ‘emergence roughly coincided with the dramatic al ‘our food environment over the past two generations. Human ‘energy sources are no longer constrained as they were historically. Instead, we have a supertluty of relatively cheap and energy-dense fod, with is nearly untimited availability, ation in Comespondence: 01 € Davis, 343 Bethune College, Yok Univeral, Trent, nano, canal, M3} 7P3 alec In addition, the food industry appears to have focused on ‘iF natural desire for sugar and fat by increasing many-fod their ‘close’ in much of what we eat each day.* Such changes hhave substantially exaggerated the physiologic distinction between homeostatic hunger that which follows 2 period fof relatively prolonged food deprivation..and hedonic hunger, which occurs in the absence of privation. ‘he latter ‘ largely regulated by the palatability and rewarding properties oF food, and Is believed to play a caltical sole In ‘woight gaint Although the prevalence of obesity has doubled over the past few decades, its morbid! form (badly mass index (BMI) >40} has seen an alanning fourfold Increase,? Consequently, it is not unusual for curent research samples to inchide obese participants with BMIS as high as 60 or 70, The wiclening BMI range for obesity, and in. some cases its early age of onset, suggests a condition that Is likely to have causally relevant subtypes, It has even been suggested that some cases of obesity should be included as @ mental disorder In Plagnostic and Statistical Mamuial= Version V." 1 behooves us, therefore, 10 focus our reseaicl efforts an finding biologically based moderator variables that distinguish one form of obesity from another. In addition, and despite the unprecedented number of consumer temp= lations facing all of us, thete Is great population variability in daily food Intake with many individuals able to remain in intial ara of Obey yc is re CDs ‘energy balance and to malnsain & healthy amount of body fat. Henee, another major challenge for obesity researchers, is to identity the factors that foster one individual's prone ness {0 Weight gain, oF buffer another from the same fate Although 3 comprehensive risk facior profile for obesity must consider the social and cultural parameters of an individual psychological tisk vatlables that have an established biological and therefore heritable underpinning, experience, this study will focus on cevtain Reward sensitivity Individual differences in the sensitivity oF reactivity of the nnesocorticolimbie pathway have been steongly implicated in the risk for drug addictions.” The research is divide however, concerning. the tion, One argument favors the view that a reward deficiency synarome fsa key rik factor The premise is that addictive substances are used as a form of ‘sellmedtication’ used to boost a shuggish or fryo-funetioning. rewae syster and (6 increase heconie capacity. Recently, these same arguments hhave boon extended tothe risk for obesity.” On account of the ausal direction of this associa central role of dopamine in the activation of the common reward pathway, vulnerability research has lgely comee trated on the funetional avallabity of this neurotransmitter inv the Drain. Much of the obesity evidence supporting a ‘reward deficiency syndrome’ viewpoint has derived from ber genet ng approaches. examining dopamine D2 receptor levels and alleles of the DRD2 gene, which regulate their expression." ‘The most frequently studied polymorphism of the D2 receptor is the iw. For many years, f/f was thought to be located nthe Samntranslated region of DRD2. However, recently it was shown that this singlemucteotide polymorphisi does not reside In DRD2, but in a neighboring gene called Ankyr containing kinase 1 {ANKKD.' It iy not known how this marker influences DRD2. expression or whether the ANKK? gene is biologieally connected to the DROZ heen suggested that individuals with the TagiA + allele Uthot is, AI/AT and A1/A2 genotypes) have seduced brain dopamine function compared with those with the AI allele {that is, the A2/A2 genotype) because of a 30-40% reduction In D2 receptor density in the strlatal region of the former group." On aecount of its. association with fewer D2 receptors, the AL allele has been elated to reduced mesolimbic brain dopamine signaling, ancl deficient ability {o experience naiural reward. Some studies have found a higher frequency of he A allele and lower striatal receptor densities. in obese Individuals."""* “These ndings are typically explained by the speculation that an insensi revvard system fosters the overcating of energy-

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