Week 8 Journal Entry: Food Addiction
Food addiction is a somewhat controversial term. When considering that obesity is a significant issue in any field of practice, the Advanced Practice Nurse must be aware of current research and treatment discussions. Watch the video the following videos Week 8: Learning Materials from Dr. Mark Gold, who is a world-renowned expert on addiction-related diseases, and Ashley Gearhardt, PhD., a food addiction expert.
Video link #1: What is the evidence that food addiction exists https://youtu.be/t1QoVpetAOY
Video link #2: How did we get here and where are we going https://youtu.be/8M08uBjil9Q
Also, read the article (see attached pdf article) that discusses Food Addiction in general and then locate a second article that deals with your population specific program, i.e. family, pediatrics, women, psychiatric, geriatric, acute care, etc.
Note: MY SPECIFIC PROGRAM IS PSYCHIATRIC.
Note: Please, attach a pdf copy of the second article found.
– In your one-two page journal submission, discuss the concept of Food Addiction and possible scenarios or patients that you are likely to encounter in your practice as an APRN (Psychiatry Mental Health Nurse Practitioner)
– Finally, discuss your personal thoughts on food addiction – is this real or junk science? (Note: In my opinion is real) Why or why not? How do you intend to address obesity in your own practice?
The paper submission should be 500-750 words in length and in APA format.
– Please, this is a turnitin assignment (free of plagiarism)
– APA format
– Minimum 500 -750 words.
Note: My background for you to have as a reference: I am currently enrolled in the Psych Mental Health Practitioner Program, I am a Registered Nurse, I work at a Psychiatric Hospital, where I also work with this vulnerable population.
What Is the Evidence for “Food Addiction?” A Systematic Review
Eliza L. Gordon 1,* ID , Aviva H. Ariel-Donges 1, Viviana Bauman 1 and Lisa J. Merlo 2
2 Center for Addiction Research and Education, Department of Psychiatry, University of Florida, 1149 Newell Drive, Gainesville, FL 32610, USA; [email protected]
* Correspondence: [email protected]; Tel.: +1-352-273-5234
Received: 10 March 2018; Accepted: 6 April 2018; Published: 12 April 2018 ���������� �������
Abstract: The diagnostic construct of “food addiction” is a highly controversial subject. The current systematic review is the first to evaluate empirical studies examining the construct of “food addiction” in humans and animals. Studies were included if they were quantitative, peer-reviewed, and in the English language. The 52 identified studies (35 articles) were qualitatively assessed to determine the extent to which their findings indicated the following addiction characteristics in relation to food: brain reward dysfunction, preoccupation, risky use, impaired control, tolerance/withdrawal, social impairment, chronicity, and relapse. Each pre-defined criterion was supported by at least one study. Brain reward dysfunction and impaired control were supported by the largest number of studies (n = 21 and n = 12, respectively); whereas risky use was supported by the fewest (n = 1). Overall, findings support food addiction as a unique construct consistent with criteria for other substance use disorder diagnoses. The evidence further suggests that certain foods, particularly processed foods with added sweeteners and fats, demonstrate the greatest addictive potential. Though both behavioral and substance-related factors are implicated in the addictive process, symptoms appear to better fit criteria for substance use disorder than behavioral addiction. Future research should explore social/role impairment, preoccupation, and risky use associated with food addiction and evaluate potential interventions for prevention and treatment.
Keywords: food addiction; eating behavior; process addiction; systematic review
The term “addiction” is commonplace in present society, despite the lack of consensus on an established clinical definition (see Table 1 for definitions set forth by various health-related professional organizations). In clinical practice, there is no official diagnosis of “addiction.” Instead, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) states that the term may be used to describe severe substance use disorders .
Criteria for substance use disorder diagnoses include 11 biopsychosocial symptoms grouped into four categories (see Table 2) . Diagnostic criteria focus on the consequences (e.g., symptoms, distress, and impairment in daily functioning) of addictive disorders, however, research has provided insight into the actual process (e.g., the neurobiological correlates) of addiction. Some important findings focus on neurological factors related to reward and motivation, including DeltaFosB (∆FosB; a gene transcription factor), dopamine, and opioid expression [2–4].
Behavioral and biological indicators of addiction have also been observed in certain excessive behaviors , and research highlighting these similarities has sparked interest in addictive behavior more generally . The proposed “behavioral addictions” reflect dependence on a behavior or feeling
Nutrients 2018, 10, 477; doi:10.3390/nu10040477 www.mdpi.com/journal/nutrients
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brought about by an action, as opposed to a substance . Several studies have confirmed similarities between behavioral and substance addictions regarding ∆FosB, dopamine, and opioid expression; impaired control over the behavior; neglect of relationships and role obligations; and continued problematic behavior in the face of negative health outcomes [5,7]. As a result, the DSM-5 recently introduced a new diagnostic category, Non-Substance-Related Disorders, within the newly-named Substance-Related and Addictive Disorders section of the manual. This category currently includes only gambling disorder, however, several other behaviors were considered, including compulsive overeating [5,8], problematic sexual behavior , and excessive Internet gaming [5,9]. Although overeating was ultimately excluded from this category due to insufficient empirical evidence, discussion regarding the addictive potential of food has continued. Indeed, organizations such as the American Society of Addiction Medicine (ASAM) have chosen to include “food addiction” in their list of possible addictive disorders , and a number of studies have observed clear biological and behavioral similarities between drug use and overeating (i.e., altered dopamine expression, cravings, relapse to highly palatable food) [11–13]. In a review of food addiction studies in humans, Meule and Gearhardt  reported that four out of the 11 DSM-5 substance use disorder symptoms were empirically supported by studies of highly palatable food, and that the remaining seven symptoms were “plausible” based on the literature available at that time. Several additional studies on food addiction have been published since that review.
Table 1. Definitions of addiction.
English Oxford Dictionary  “Physically and mentally dependent on a particular substance.”
American Psychological Association 
“A chronic disorder with biological, psychological, social and environmental factors influencing its development and maintenance. Genes affect the degree of reward that individuals experience when initially using a substance (e.g., drugs) or engaging in certain behaviors (e.g., gambling), as well as the way the body processes alcohol or other drugs. Heightened desire to re-experience use of the substance or behavior, potentially influenced by psychological (e.g., stress, history of trauma), social (e.g., family or friends’ use of a substance), and environmental factors (e.g., accessibility of a substance, low cost) can lead to regular use/exposure, with chronic use/exposure leading to brain changes.”
American Society of Addiction Medicine 
“A primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviors. Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one’s behaviors and interpersonal relationships, and a dysfunctional emotional response. Like other chronic diseases, addiction often involves cycles of relapse and remission. Without treatment or engagement in recovery activities, addiction is progressive and can result in disability or premature death.”
American Psychiatric Association 
“A complex condition, a brain disease that is manifested by compulsive substance use despite harmful consequence. People with addiction (severe substance use disorder) have an intense focus on using a certain substance(s), such as alcohol or drugs, to the point that it takes over their life. They keep using alcohol or a drug even when they know it will causes problems. Yet a number of effective treatments are available and people can recover from addiction and lead normal, productive lives.”
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Table 2. Substance Use Disorder criteria, adapted from the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) .
1. Consuming a substance in greater amounts or over longer periods of time than intended. 2. Having a persistent desire or unsuccessfully attempting to decrease or limit substance use. 3. Spending a significant amount of time acquiring, using, or recovering from a substance. 4. Craving the substance or having a strong urge to use it.
5. Being unable to fulfill obligations at work, school, or home due to use of a substance. 6. Continually using a substance despite its effects causing or exacerbating persistent or recurrent social or
interpersonal problems. 7. Giving up or reducing social, occupational, or recreational activities due to substance use.
8. Continually using a substance in situations in which it is physically dangerous (e.g., driving under the influence of a substance).
9. Continually using a substance despite physical or psychological problems that are caused or made worse by the substance use.
10. Needing a substantially higher dose of the substance to achieve the desired effect; or experiencing a substantially reduced effect of the substance when the usual dose is consumed (i.e., tolerance).
11. Experiencing negative physical and psychological symptoms when the substance is not consumed at the typical dose or frequency (i.e., withdrawal).
Note. To meet DSM-5 criteria for a substance use disorder, clinical distress or impairment must be evidenced by two or more of the above symptoms within a 12-month period. Severity is classified as mild (2–3 symptoms), moderate (4–5 symptoms), or severe (≥6 symptoms).
Nonetheless, there have been inconsistencies regarding the definition of food addiction. A variety of approaches have been used to measure it, such as self-report questionnaires ; patient self-identification ; and the Yale Food Addiction Scale (YFAS), which is currently the best available measure for evaluating food addiction based upon modified DSM criteria for substance use disorders [20,21]. Some have erroneously conceptualized food addiction as either obesity or binge eating [22–25], yet mounting evidence indicates that these constructs are distinct [26,27]. Though some individuals with obesity may display neurological and behavioral similarities to individuals addicted to drugs , estimates suggest that only approximately 24.9% of overweight/obese individuals report clinically-significant symptoms of food addiction and 11.1% of healthy-weight individuals also report these symptoms . Similarly, while food addiction symptoms are associated with binge eating behavior and account for 6–14.8% of the unique variance in binge eating disorder , current estimates suggest that only approximately 56.8% of individuals with binge eating disorder report clinically significant food addiction symptoms . Although there is substantial overlap between food addiction and binge eating symptoms, the two constructs are not synonymous [26,27].
The concept of food addiction remains controversial [25,30,31]. Some researchers question whether food or eating can be addictive if it is necessary to our survival , while others point out the common biological (e.g., brain reward pathways, ∆FosB expression), behavioral (e.g., relapse, using more than intended), and psychological (e.g., preoccupation, impaired control) similarities between the compulsive consumption of highly palatable foods and use of addictive drugs [2,32,33]. Nevertheless, critics and proponents alike agree that more research is needed to confirm the validity of food addiction [30,34]. A non-systematic review by Hone-Blanchet and Fecteau  comparing animal and human models of food addiction to characteristics of substance use disorder concluded that there was significant overlap between the two conditions, but that more research was needed. Extant published systematic reviews on the concept of food addiction have either conflated obesity with food addiction or excluded animal studies [22,28,29]. As such, a more recent and inclusive systematic review was needed. The present systematic review aimed to summarize the peer-reviewed empirical literature examining
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the evidence for food addiction in both animal and human studies. The chosen method involved assessing its association with key characteristics of addiction in relation to food: (a) neurobiological changes, (b) preoccupation with the substance, (c) impaired control, (d) social impairments, (e) risky use, (f) tolerance/withdrawal, (g) chronicity of the condition, and (h) relapse [1,10,17].
2. Materials and Methods
Data collection, review, reporting, and discussion were conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Statement [35,36]. The literature search was carried out in PubMed and PsychINFO databases using varying combinations of the following keywords: food addiction, addiction, process addiction, binge eating, hedonic eating, compulsive overeating, compulsive eating, eating behavior, food, eat, feeding behavior/psychology, food preferences, food habits, hyperphagia, eating disorders, obesity, overeat*. Meshterms were used in the PubMed search. Filters were used in both databases according to the study’s predetermined inclusion and exclusion criteria. Given that the “study type” filters on PubMed only identified articles in print, a second search was done using the same search terms without filters in order to identify recent articles published online before print. Additional studies were identified through review of the references listed in the identified articles. Due to the proliferative nature of research on food addiction, two searches were done: the first was completed on 29 June 2016, and the second was completed on 8 January 2018. Protocols were followed for both searches exactly as described above, with the exception that the second search included only articles published since 30 June 2016.
Articles were included if their stated purpose was to test the validity of the food addiction construct, and if they fulfilled the following modified PICOS (Participants, Interventions, Comparisons, Outcomes, and Study Design) criteria [35,36]. Acceptable participants included humans or animals of any age with no specific limitations on disease or diagnosis. Only quantitative, empirical, peer-reviewed studies published in the English language were included. The American Psychological Association’s defines “quantitative” studies as those which “provide numerical representation of observations for the purpose of describing and explaining the phenomenon studied followed by the application of . . . statistical methods” , (“Quantitative Study”). Therefore, studies using self-report measures that produced a numerical outcome (e.g., Likert scale, yes/no, hunger ratings) were considered quantitative. Empirical studies were defined as those “based on . . . systematic observation, or experiment, rather than theory or general philosophical principle”  (“Empirical Study”). Studies examining any type of intervention or comparison (e.g., randomized control trial, cross-sectional) within these constraints were included in order to accurately reflect the heterogeneous nature of the existing literature. Studies could be published online or in print, and no limits were set on date of publication. Finally, because not all overweight/obese individuals or individuals with eating disorders report addiction-like symptoms related to food , studies defining food addiction solely by weight, BMI, or eating disorder diagnosis were excluded.
Articles selected from PubMed and PsychINFO were reviewed first by title, then abstract, and finally full article for relevancy and eligibility using the inclusion criteria described above. The first author independently assessed study eligibility, and articles whose eligibility was unclear were reviewed by two experienced obesity researchers. The last included study was identified in January 2018. A flowchart for study inclusion is depicted in Figure 1.
The data extraction form used for this study was modeled after forms used in similar systematic reviews (e.g., ) and was modified for the current paper. The following data were extracted: author/year of publication, study type, sample characteristics, number of subjects in treatment/control groups, main independent variable(s), and main outcome variable(s). Two of the current authors assessed risk of bias on the study level using a modified combined scoring system based on those reported by Jamaty and colleagues  and Pursey and colleagues . These scoring systems were combined in order to include relevant criteria for both animal  and human  studies. Criteria included questions about sample selection, study design, and reporting of findings. The authors
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gave answers of “Yes”, “No”, or “Unclear” regarding each question for every article included in the review. An answer of “non-applicable” was given for the question “Was there sufficient description of the groups?” if a study did not have multiple groups. Quality scores were obtained by summing the number of “Yes”, “No”, and “Unclear” ratings, then calculating the ratio of “Yes” ratings to the sum of the “No” and “Unclear” ratings combined. “Not applicable” ratings were not included in the calculation of the overall quality rating. Disagreements between authors were discussed until a resolution was agreed upon.
Figure 1. Study selection flow diagram, presented according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement [35,36].
The original database search produced a total of 2421 articles, and the updated search produced 577 articles. Three additional articles describing eight studies were identified from references in other papers. After removing duplicate references and excluding articles that did not meet the predetermined inclusion criteria, a total of 35 articles and 52 studies were identified (see Figure 1 and Appendix, Table A1). Primary reasons for exclusion were study objective (i.e., did not aim to evaluate the validity of the food addiction construct) and study type (i.e., not a quantitative empirical study). Publishing dates of included articles ranged from 1999 to 2017. Twenty articles (comprising 22 studies) involved human participants and 15 articles (comprising 30 studies) involved animal subjects (i.e., rats, mice, and monkeys). Forty-nine studies focused on the addictive potential of certain foods, five studies focused on the addictive potential of eating patterns, and two studies focused on the addictive potential of both certain foods and eating patterns.
As seen in Appendix, Table A2, quality scores for included articles ranged from 0.8 (lowest ratio of “Yes” ratings to “No” ratings plus “Unclear” ratings)  to a perfect score (all “Yes” ratings) [40–43]. Three articles disclosed competing financial interests, including Coca-Cola , the International Sweeteners Association , sugar industry relations , pharmaceutical companies [13,40] and involvement in addiction/impulse disorder organizations . Nineteen articles reported no competing interests and 13 made no statement (see Table A2). As competing financial interests may bias study conclusions , data should be objectively considered with this context in mind.
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Of the 35 articles (52 studies) included in this review, 31 articles (47 studies) reported results supporting the criteria for addiction, two articles (two studies) were mixed, and two articles (three studies) reported unsupportive findings (see Appendix, Table A3). Results examining support for each pre-specified addiction characteristic were evaluated separately and are described below.
3.1. Neurobiological Correlates of Addiction
Sharma, Fernandes, and Fulton  showed that rats placed on a 12-week high-fat diet of primarily hydrogenated coconut oil, maltodextrin, sucrose, and casein had significantly higher ∆FosB, dopamine D2 receptor, and brain-derived neurotropic factor expression, and lower dopamine D1 receptor expression, in the NAc. These changes were observed before the onset of obesity and were linked to behaviors suggestive of anhedonia. The authors concluded that the brain changes may have put the animals at greater risk for addictive-like symptoms such as relapse. No human studies reported findings related to ∆FosB.
Colantuoni and associates  compared brain chemistry changes in rats with intermittent, excessive glucose intake to rats given a normal diet of chow. They found that exposure to the highly palatable food in an intermittent eating pattern caused increased activation of dopamine D1 (p < 0.05) and µ-opioid-1 receptors (p < 0.05), as well as decreased binding of dopamine D2 receptors, in the dorsal striatum (p < 0.05). Adams and colleagues  found that rats given a high-fat/low-sucrose diet (primarily lard) also had decreased D2 receptor expression in the NAc, but those given a low-fat/high-sucrose diet did not (high fat diet: F = 11.1, p = 0.009; high sucrose diet F = 3.8, p = 0.074). Reduced D2 receptor expression (p < 0.01) in the striatum (along with other indicators of down-regulation of reward functioning) was also observed in rats who volitionally overate highly palatable foods (bacon, sausage, cheesecake, pound cake, frosting, chocolate) in a study by Johnson and Kenny . Authors of each study concluded that their results were consistent with findings in substance use disorder literature.
In humans, Davis and associates  found that individuals who met the YFAS cutoff suggesting clinically significant food addiction symptoms had higher multi-locus genetic profile (MLGP) scores associated with increased dopamine signaling (p = 0.023), and that the relationship between the MLGP scores and food addiction was mediated by reward-driven eating (95% CI: 0.00–1.12). Davis, Levitan, Kaplan, Kennedy, and Carter  showed that an appetite suppressant that blocked dopamine functioning was not effective in adults who screened positive for food addiction on the YFAS compared with controls, suggesting altered dopamine signaling strength in adults with more food addiction symptoms similar to what is seen among adults with substance use disorders.
3.1.3. Opioid Expression
Opioid receptors were reported to play a role in food reward in rats. Le Merrer and Stephens  found that rats conditioned on sugar sweetened pellets no longer responded to the conditioned reward when given an opiate antagonist (naltrexone; dose effect: F2,32 = 1.72, non-significant). Newman, Pascal, Sadeghian, and Baldo  showed that rats who were fed sweetened shortening daily ate significantly more standard chow than rats not fed the palatable food when given a µ-opioid receptor agonist (DAMGO), suggesting that opioid receptor activity may be associated with overeating and consumption of highly palatable foods.
As a measure of opioid function, Daubenmier and colleagues  analyzed the effects of an acute opioid blockade drug (naltrexone) on cortisol and nausea in overweight/obese women. They found that women who engaged in more emotional and restrained eating had greater levels of cortisol (r = 0.37, p < 0.05), and women who engaged in binge eating had greater levels of nausea in response
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to the drug (p = 0.048), suggesting that these individuals “may have a down-regulated opioidergic system” (p. 99). Cambridge and associates  similarly found a significant role for the µ-opioid receptor system in motivation for food reward; they observed that a µ-opioid receptor antagonist reduced motivation for, but not liking of, high calorie foods (e.g., chocolate) in people with obesity and moderate binge eating (p < 0.05). Although the authors did not conclude that their results supported food as an addictive substance, they did indicate a role for the µ-opioid system in food-related reward.
3.1.4. Other Neurobiological Changes
In a controlled study conducted on primates, Duarte and colleagues  found that chocolate induced a persistent conditioned place preference response usually only seen in response to drug rewards. Monkeys who received chocolate spent more time in environments where they had previously received chocolate, whereas controls showed no place preference (F1,13 = 13.59, p = 0.003, η2p = 0.53). Conditioning persisted even after a 15-day follow-up (F1,13 = 4.31, p = 0.06, η2p = 0.26), indicating that chocolate, like drugs, can be used for this type of conditioning. In rats, Le Merrer and Stephens  found that an AMPA receptor antagonist blocked the conditioned response to sweetened pellets (F2,34 = 3.02, non-significant) in a manner comparable to drugs of abuse. Additionally, Newman and colleagues  suggested that gamma-aminobutyric acid (GABA) receptor activity may be implicated in food addiction; they found that rats given a daily dose of sweetened shortening ate significantly more standard chow than rats not fed the palatable food when given muscimol, a GABA agonist that induces feeding (ps < 0.01).
In a study comparing rats genetically prone to obesity against rats resistant to obesity, Mary Brown and colleagues  reported a significant role for the NAc glutamatergic system in driving overeating (ps < 0.05), similar to the glutamatergic mechanisms seen in animal models of relapse to drug addictions. Additionally, Pérez-Ortiz and associates  found that rats fed a high-fat diet (primarily lard, casein, and sucrose), exhibited increases in potential biomarkers of addiction (fumarate hydratase, ATP synthase subunit alpha, and transketolase) in the NAc (p < 0.05). Adams and colleagues , however, found that a high fat diet (primarily lard) reduced activity of cAMP response element-binding protein (CREB; F1,10 = 5.4, p = 0.042) and its activated form (pCREB; F1,10 = 5.9, p = 0.036) in the NAc, contrary to their prediction.
In an electroencephalographic (EEG) study by Imperatori and colleagues , participants with three or more food addiction symptoms on the YFAS exhibited brain changes similar to those in people with addictive disorders (e.g., increased functional connectivity in fronto-parietal areas; ps < 0.05). A functional magnetic resonance imaging (FMRI) study by Gearhardt and colleagues  found that YFAS symptom scores were correlated with increased activation in the amygdala, cingulate cortex, and medial orbitofrontal cortex when participants were anticipating consumption of a chocolate milkshake. When participants received the milkshake, those with higher YFAS scores had greater activation in the dorsolateral prefrontal cortex (p = 0.007) and caudate (p = 0.004) and less activation in the lateral orbitofrontal cortex (p = 0.009) compared to those with lower YFAS scores. Gearhardt and colleagues concluded that this pattern of increased activation in areas of the brain related to reward and decreased activation in areas related to inhibition is similar to that seen in substance dependence.
De Ridder and colleagues  compared resting-state EEG brain activity between (1) adults with obesity who endorsed more than three YFAS symptoms (“High YFAS”), (2) adults with obesity who endorsed less than three YFAS symptoms (“Low YFAS”), (3) adults without obesity or food addiction (“Lean controls”), and (4) adults without obesity but with alcohol use disorder (“Alcohol addiction”). Positive correlations were found between YFAS symptoms and the rostral anterior cingulate cortex (rACC) for theta (r = 0.23, p = 0.041) and beta3 (r = 0.22, p = 0.041) frequency bands. Increased gamma activity in the rostral anterior cingulate cortex (rACC) extending to the dorsal medial prefrontal cortex (dmPFC) was associated with increased hunger ratings in the High YFAS group only (r = 0.72, p = 0.002), and increased alcohol craving in the Alcohol addiction group (r = 0.72, p = 0.002), while the rACC was negatively correlated with hunger in the Low YFAS group. Conjunction analyses
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further revealed similarities between the High YFAS group and the Alcohol addiction group in the ACC/dmPFC and precuneus (Z = 2.24, p = 0.013), sgACC, orbitofrontal cortex (OFC), and temporal lobe (fusiform/parahippocampal area) (Z = 2.78, p = 0.003). No correlations were found between the Low YFAS and Alcohol addiction groups. The authors concluded that there were significant neurobiological similarities between persons with food addiction symptoms and alcohol dependence.
In a gustatory cue exposure trial among overweight/obese adolescents, Feldstein Ewing and associates  found that consumption of high-calorie …
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