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Food addiction and obesity

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J.Neurol.Sci.[Turk]

Journal of Neurological Sciences [Turkish] 33:(2)# 48; 392-400, 2016

http://www.jns.dergisi.org/text.php3?id=960

Review

Food Addiction and Obesity

Reci MESERİ1, Ayşegül BİLGE2, Özge KÜÇÜKERDÖNMEZ3, Ender ALTINTOPRAK4

1
Ege Üniversitesi İzmir Atatürk Sağlık Yüksekokulu, Beslenme ve Diyetetik Bölümü, İzmir,
Turkey 2Ege Üniversitesi Hemşirelik Fakültesi, Ruh Sağlığı ve Hastalıkları Hemşireliği
Anabilim Dalı, İzmir, Turkey 3Ege Üniversitesi Tıp Fakültesi, Ruh Sağlığı ve Hastalıkları
Anabilim Dalı, İzmir, Turkey

Abstract
The aim of this review is to discuss the concept of food addiction and its association with
obesity. The DSM-5, published in May 2013, defines substance related and addictive
disorders as clinical disorders indicated by inappropriate substance use within the last 12
months that meets at least two of the following 11 criteria: impaired control (4 criteria), social
impairment (3 criteria), risky use (2 criteria) and pharmacological response (tolerance and
withdrawal, 2 criteria). An important novelty in the DSM-5 is that, even though it is not
induced by a chemical agent, a behavioral disorder, gambling, is classified as an addiction.
Eating and sex, instincts that are essential for survival and wellbeing, are also called natural
rewards. Dopamine, a reward neurotransmitter, regulates pleasurable and motivating
responses to food intake. Repeated stimulation of these reward pathways, as in substance
abuse, weakens control over food intake and causes compulsive food consumption. Imaging
studies have shown that obese people have impairments in the dopaminergic pathways that
regulate their control and reward systems. Studies indicate that even in post-prandial satiety,
obese people show reward response to hyper-palatable foods. Thus, food addicts' efforts to
lose weight are frustrated by addiction, and they have difficulty in adopting healthy nutritional
habits. Studies of food addiction have proliferated recently around the world, but very few
have been conducted in Turkey. Community-based studies of food addiction should be
conducted to determine its prevalence. Obese people who are also addicted to food should be
treated with multiple treatment methods.

Keywords: Food addiction, addiction, obesity, dopamine

Gıda Bağımlılığı ve Şişmanlık

Özet
Bu derlemenin amacı gıda bağımlılığı kavramını ve gıda bağımlılığının şişmanlıkla ilişkisini
tartışmaktır. Mayıs 2013'te basılan DSM-V'e göre ‘Madde Kullanımı ve Bağımlılık
Bozuklukları' son 12 ayda, bozulmuş kontrol (4 kriter), sosyal bozukluk (3 kriter), tehlikeli
olduğunu bildiği halde kullanmayı sürdürme (2 kriter), farmakolojik/klinik yanıt (tolerans ve
yoksunluk-2 kriter) olmak üzere toplam 11 kriterden en az ikisine sahip olma ile kendini
gösteren klinik bozukluğa yol açan uygunsuz madde kullanımı olarak tanımlanmaktadır.
DSM-V'deki önemli değişikliklerden biri, kimyasal etkisi olmasa da bir davranış
bozukluğunun (Kumar Oyna Bozukluğu) “Bağımlılık” başlığı altında değerlendirilmesidir.
Yemek yemek, seks gibi yaşamın sürdürülmesi için gerekli, insanlara mutluluk veren
içgüdüsel davranışlara doğal ödüller denilmektedir. Dopamin, ödül nörotransmitteri olarak

392
J.Neurol.Sci.[Turk]

adlandırılmaktadır, besin alımını güdüleyici yanıtları ve besinden alınan hazzı düzenler. Ödül
yollarının tekrar uyarılması, madde kötüye kullanımındaki benzer biyolojik mekanizmaları
uyararak gıda alımındaki kontrolü zayıflatmakta ve kompulsif gıda tüketimine yol açmaktadır.
Görüntüleme çalışmaları, şişman bireylerin ödül ve kontrol sistemlerini düzenleyen
dopaminerjik yolaklarında bozukluklar olabileceğini göstermiştir. Yapılan çalışmalarda
şişmanların doyduktan sonra bile yüksek enerjili besinlere ödül yanıt geliştirdiği, gıda
bağımlılığı olan bireylerin zayıflama konusundaki çabalarının da, bağımlılıkları nedeniyle
zarar gördüğü, sağlıklı beslenme alışkanlıkları kazanmakta güçlük çektikleri saptanmıştır.
Gıda bağımlılığı dünyada son yıllarda sıkça tartışılan bir konu olmakla birlikte ülkemizde bu
konuda yapılmış çalışmalar yok denecek kadar azdır. Toplumda gıda bağımlılığı ile ilgili
çalışmalar yürütülmeli, sıklığı saptanmalıdır. Gıda bağımlılığı olan şişman bireylerde ise
çoklu tedavi yöntemleri kullanılmalıdır.

Anahtar Kelimeler: Gıda bağımlılığı, bağımlılık, şişmanlık, dopamin

to data collected by the World Health

INTRODUCTION
Obesity is a health problem that is
increasingly more common both in Turkey
and in other parts of the world(3,22,27). This
problem is usually associated with poor
diets and a sedentary lifestyle(3). Obesity
may result in physical illnesses such as
diabetes and heart disease and mental
disorders such as depression and social
phobia(10,17,28). The fact that the
consumption of some foods is pleasure-
inducing, combined with the observation
that some people have difficulty
controlling the consumption of these foods,
despite an awareness of obesity-related
problems, indicates that some foods may
be addictive. Many of the major theories of
addiction also identify an important role of
stress in addiction processes(38). This
literature review shows that there are many
studies on food addiction, and that children
and adolescents are at particular risk of
developing this addiction. This review
aims to examine the relationship between
food addiction and obesity on the basis of
studies conducted in Turkey and other
countries.
Obesity and Mental Health
Obesity is a global epidemic. It is defined
as the accumulation of excessive bodily fat
that threatens physical and mental
wellbeing(22). Obesity is seen both in
developed and developing economies and
is increasingly more common. According
Organization (WHO), there are over 400
million obese and more than 1.6 billion
over-weight people in the world, and these
numbers are projected to reach 700 million
and 2.3 billion, respectively, in 2015(3).
The MONICA (Multinational MONItoring
of trends and determinants in
CArdiovascular disease) study conducted
by the WHO in six regions of Asia, Africa
and Europe over a 12-year period found
that in ten years, the frequency of obesity
increased by 10% to 30%(27).
Epidemiological studies show that
demographic factors such as age and
gender, socio-cultural factors such as
marital status and level of education,
biological factors, nutritional habits and
life-style factors such as smoking, alcohol
consumption and lack of physical
activity(3).
Childhood obesity is on the increase and in
the fight against obesity, the prevention of
child and adolescent obesity is a priority
health issue(16,19,37,46). Current childhood
obesity rates are reported to be 10 times
the rate they were in the 1970s. Unless
effective measures are taken, it is estimated
that the frequency of obesity will continue
to rise, and the number of obese children
and adolescents in Europe will reach 15
million(1,17). Childhood obesity rates
increased by 5% in the Unites States
between the years 1963 and 1970, and by
17% from 2003 to 2004(19). In a study

393
J.Neurol.Sci.[Turk]
conducted in the United States in 2007 and
2008, the percentage of children and
adolescents with BMIs above the 95th
percentile was found to be 16.8%(31). From
20% to 25% of adolescents in the Unites
States are reported to be obese(15,16), and
this figure is projected to rise to 30% by
2028 and to 40% by 2048(45).
According to Turkey's 2010 Childhood
Obesity Survey, conducted by member
states of the European Region of the World
Health Organization, the number of
overweight and obese people has
increased. Approximately 40% of its
population are overweight, and 15% are
obese(40).
In Turkey, childhood obesity is increasing.
Bereket et al. reviewed the studies
conducted between 2004 and 2010 and
showed that between 10% and 15% of
children and adolescents from 6-18 years
of age were overweight, and their rate of
obesity was between 2% and 7%(5).
Turkey's Health and Nutrition Survey
(2010), conducted by the Ministry of
Health, found that 14.3% of children and
adolescents from 6-18 years of age were
overweight, and their rate of obesity was
found to be 8.2%(24).
According to WHO data, overweight and
obesity are responsible for 80% of Type 2
diabetes, 35% of ischemic heart disease
and 55% of hypertension among adults in
Europe, causing more than a million deaths
a year(17). When mothers put on too much
weight during pregnancy, it may result in
their children being obese
adolescence(25,29), and childhood obesity
may lead to adulthood obesity, possibly
leading to chronic diseases such as
coronary disease, diabetes and
(15,16,46,48)
hypertension . Many studies find
that chronic diseases in adulthood are
associated with nutritional habits in
adulthood and adolescence(35,36,46).
Obesity creates mental disorders as well as
physical illness. Studies find that obese
people have significantly higher levels of
depression-proneness and body
dissatisfaction and lower self-esteem(10,28).
Body dissatisfaction also acts as an
intervening variable leading to lower levels
of self-esteem(41). According to a meta-
analysis conducted by De Wit et al. (2010),
obesity increases depression-proneness in
adults, especially among women(13). Obese
children and adolescents face
discrimination and labeling, which is
detrimental to their mental and social
wellbeing(47). Thus, obesity is an emerging
serious situation which effects both
physical and mental health.
Food Addiction as a Form of Substance
Addiction
The Psychodynamic and Behavioral
Causes of Addiction
According to Freud, the founding father of
classical psychoanalysis, addiction is
caused by problems during the oral stage
of psychosexual development that lead to
the development of an oral personality.
Excessive maternal attachment, greed,
despair, depression, sentimentality and
inconsistency are among the indicators of
this personality type. Among people with
this mental disorder, oral craving remains,
but changes direction later in life. Objects
such as water, milk and mother's breast are
replaced with alcohol, cigarettes, or some
other substance(32).
Behavioral models of substance abuse
underline the importance of learning in the
development of this disorder. Through
classical or operant conditioning, a
connection is formed between events and
in information related to these events, which
in turn reinforces substance use. For
example, alcohol consumption is
connected to numerous stimulants in the
environment in which alcohol is
consumed. The smell or taste of an
alcoholic drink is among the most
powerful of these stimulants. More subtle
stimulants include the physical
environment (such as bars) in which the
substance is consumed and the mental state
of the consumer. Substance abuse develops
as repeated substance use associated with
394
J.Neurol.Sci.[Turk]
environmental factors turns these factors
into conditioned stimuli. These learned
connections later create the idea and the
expectation that the substance will be used
whenever these stimulants are present(32).
Classification of Addiction
The fifth edition of the Diagnostic and
Statistical Manual of Mental Disorders
(DSM-5) treats addiction in the section on
“Substance-Related and Addictive
Disorders," which are defined as clinical
disorders indicated by inappropriate
substance use within the last 12 months
that meets at least two of the following 11
criteria: impaired control (four criteria),
social impairment (three criteria), risky use
(two criteria) and pharmacological/clinical
response (two criteria, tolerance and
withdrawal)(2,8). The DSM-5 treats
disorders related to the use of alcohol,
caffeine, cannabis, hallucinogens,
inhalants, opioids, sedative-hypnotics and
anxiolytics, stimulants, tobacco and other
substances in separate codes. One of the
most important changes in the DSM-5 is
that gambling addiction is included in this
section because it stimulates the reward
pathways in the brain, like substance
abuse, and results in similar behavior. This
is an important development because
repetitive, detrimental behavior that is
difficult to control is now treated as an
indication of an addictive disorder. Other
repetitive behaviors such as sex addiction,
exercise addiction and shopping addiction
are also discussed in the DSM-5, but not
included in this chapter because their
classification as formal disorders requires
further research(2,20).
Barry et al. (2009) adapted the DSM-5's
criteria for substance use disorder to
overeating(4). Table-1 shows this
adaptation.
Gearhardt et al. (2011) identified the
following common characteristics shared
395
by addictive substances and hyper-
palatable foods: they increase dopamine-
and opioid-related neural system activity,
trigger artificially heightened levels of
reward, rapidly enter blood circulation,
stimulate neurobiological systems, are
encountered by balancing mechanisms that
result in heightened tolerance, give rise to
desires that are triggered by symbols, are
difficult to stop consuming and continue to
be used despite harmful effects(18). There
seems to be agreement in the literature that
food addiction, like substance dependence
and alcohol dependence, results in elevated
tolerance, symptoms of withdrawal, risky
consumption and other health problems.
Can food be addictive?
Instinctive behaviors such as eating and
having sex that are necessary for the
survival of the species and are pleasure-
inducing are called natural rewards(12,21). In
pre-industrial societies, the typical diet
consisted of unprocessed or minimally
processed meat, whole grains, fruits and
vegetables. The consumption of meat
products and fruits with high levels of
protein, fat or sugar content was limited
due to their limited availability. In the
process of evolution, the human brain
adapted to this condition and developed
reward mechanisms to stimulate increased
consumption of high-calorie foods to
increase chances of survival. However, in
the last century, our lifestyles have
changed greatly, and due to developments
such as urbanization and advances in food
production, high-calorie foods are no
longer limited. To the contrary, the
consumption of processed, artificial, high-
calorie and high-fat foods has now become
commonplace(18).
J.Neurol.Sci.[Turk]

Table 1. Applying substance dependence criteria to overeating disorder (based upon Barry et al.
(2009)

Substance dependence criterion Possible criterion for overeating

disorder
Criterion Example Example
Impaired control Alcoholic plans to stop at the Obese individual goes to a restaurant
local bar for one beer, ends up to eat one serving of salad, ends up
staying until closing and having eating a whole plate of fried
several drinks, makes repeated vegetables and dessert, keeps eating
unsuccessful attempts to stop after a large meal, makes repeated
drinking. unsuccessful attempts to diet.
Social impairment Alcoholic fails to show up at Obese individual loses self-esteem
work after a night of heavy because of labeling, which results
drinking, stops associating with from overeating, avoids going to the
non-drinking friends. beach, shopping for clothing, or places
where physical activity is required,
stops associating with slim people.
Risky use Alcohol dependent individual Obese individual continues to eat
continues to drink after being sugar and fatty foods after being
diagnosed with fatty liver. diagnosed with diabetes or
hypertension.
Pharmacological/ Tolerance: Alcohol dependent Tolerance: Obese individual requires
clinical response individual requires five drinks to very large servings to feel full instead
(tolerance and feel intoxicated instead of three. of smaller ones.
withdrawal) Withdrawal: Alcohol dependent Withdrawal: Dieter experiences
individual experiences symptoms symptoms of depression, smokes or
such as nausea and sweating drinks caffeinated beverages to
when he or she doesn’t have compensate, has headaches, feels
alcohol. restless and feels a strong desire to
stop dieting.

Recent neurobiological studies examine disease is characterized by impaired

the relationship between food addiction
and obesity and discuss whether overeating
needs to be considered a form of
behavioral disorder because food
consumption is followed by certain types
of neurological activity(4). The focus in
these studies is on food's relationship with
reward pathways in the central nervous
system and with dopamine. Dopamine is a
reward neurotransmitter(23) and regulates
responses that stimulate food intake and
pleasure from food. A study that sheds
light on this issue was conducted with
Parkinson's disease patients. Parkinson's
movement due to dopamine deficiency and
is accompanied by cognitive, behavioral
and emotional disorders. Dagher et al.
(2009) found that Parkinson's disease
patients usually do not develop
dependencies, whereas some patients
treated with drugs such as levodopa, which
is a precursor of dopamine, develop
behavioral disorders such as gambling,
shopping and sex addiction(11).
Dopamine and dopaminergic pathways are
very important because they ensure
survival by motivating food intake. The

396
J.Neurol.Sci.[Turk]
mesencephalic dopamine system may
trigger a response to food stimulants even
in the presence of post-prandial satiety
signals and increase food consumption.
When this happens, eating behavior
switches from a homeostatic state to a
hedonic corticolimbic state(44). Recent
studies find that consumption of large
amounts of sugar and fat results in
overstimulation of the reward system of
the brain and increases dopamine release.
When appetizing foods are displayed,
reward mechanisms are activated and
dopamine release in the brain increases
automatically and reflexively, similar to
what happens in cases of substance
dependence. Foods rich with sucrose and
glucose have been found to activate the
brain's reward system and increase glucose
concentrations in the brain. Studies find
that the ventral striatum, prefrontal cortex
and amygdala are responsive to pleasure
from food. Repeated supraphysiological
stimulation of these reward pathways
triggers neurobiological adaptation by
stimulating biological mechanisms similar
to those seen in substance abuse.
Reward deficiency syndrome was
described as the chemical imbalances in
the brains reward system that result in
many behavioral disorders. According to
Blum and his colleagues, decreased
dopaminergic process may cause seeking
“reward” and abstinence behaviors. In
addition, in a study conducted on alcoholic
and non-alcoholic cadavers, they found out
that D2 receptor polymorphism (Taq 1A)
was associated with alcohol abuse which
lightened the studies that show the
association between genetic make-up and
addiction(6,33). According to a study
conducted by Blum and colleagues,
alcoholics have significantly more A1
allele compared to non-alcoholics who
have mainly A2 allele. The ones who carry
A1 allele have a lower density of dopamine
D2 receptors which result in anger, anxiety
and craving for substances(6,7). Noble et al.
found similar results for smoking; the
incidence of having A1 allele was higher in
397
smokers and past smokers than non-
smokers(30).
At the most basic level, weight gain occurs
when there is an imbalance of energy, that
is to say, when energy intake is greater
than energy expended. As a result, the cure
for obesity involves increasing energy
expenditure and limiting energy intake(4).
Although the relationship between energy
imbalance and obesity is simple at this
most basic level, obesity is a very complex
condition and is difficult to treat.
Studies conducted on twins or adoptees
showed that both genetic and
environmental factors may contribute to
obesity. As in alcoholics, in obese patients,
higher prevalence of Taq A1 allele was
found, resulting a lower density of
dopamine D2 receptors. Smith and
Robbins explains this phenomenon as, due
to low baseline dopamine D2 receptor
level which is the reward deficient state,
patient seeks for highly palatable food and
consumes it. This consumption yields to
down regulation of dopamine receptors
which leads to habituation of seeking and
consuming high palatable foods(39).
Moreover, drugs that blocks dopamine D2
receptors increase appetite which cause
weight gain(43). Imaging studies show that
in obese individuals, the dopaminergic
pathways that regulate reward and control
systems might be impaired(42). Thus,
reward deficiency syndrome may
contribute to obesity epidemic.
Studies of the diagnosis of food addiction
have found that specific regions of the
brain are stimulated during the anticipation
and the consumption of appetizing foods,
as they are in other addictions(34).
Likewise, studies with college students
have found that excessive overeating leads
to low stress tolerance like tobacco
addiction and substance dependencies, and
that food addiction is characterized by
strong impulses and cravings(26). In a study
of adults in weight loss programs,
Burmeister et al. (2013) found that food
addiction was accompanied by depression,
J.Neurol.Sci.[Turk]
emotional eating, excessive eating,
negative attitudes about weight, body
shame and low self-efficacy. Individuals
with high levels of food addiction are less
successful at losing weight and have
difficulty developing healthy eating habits,
and their efforts at weight loss are
hampered by addiction(9). In another study,
Dimitropoulus et al. (2011) found that
obese individuals develop reward response
to high-energy foods even after large
meals, whereas individuals with normal
weights do not display this response once
satiety is reached(14). These findings also
point out that there is a complex
associations between obesity and reward
system.
CONCLUSION
Nutrition is essential for survival, and
eating is a natural way to meet bodily
needs, but it becomes the cause of many
health problems when food is consumed in
excess of or less than what the body needs.
In recent years, there is a growing
recognition that hyper-palatable foods may
be addictive, and both genetic and
environmental factors may be responsible
for the increase in the prevalence of
obesity around the world. To counter
negative effects of obesity, families as well
as teachers, students and cafeteria workers
at schools should be educated about proper
nutrition, weight-loss counseling should
address issues of addiction as well as
energy imbalance and advanced studies
should be conducted on the prevalence of
and biological and genetic mechanisms
behind food addiction.
Correspondence to:
Reci Meseri
E-mail: recimeseri@yahoo.com
398
Received by: 27 August 2015
Revised by: 03 February 2015
Accepted: 15 March 2016
The Online Journal of Neurological
Sciences (Turkish) 1984-2016
This e-journal is run by Ege University
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Comments and feedback:
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Journal of Neurological Sciences (Turkish)
Abbr: J. Neurol. Sci.[Turk]
ISSNe 1302-1664
REFERENCES
1. Aksoydan, E. P., G. Inanc, N. Arslan, P. Alphan
Tufekci, E. Koksal, E. et al. (2011). Çocuk ve
Ergenlerde Ağırlık Yönetimi (Weight Management
in Children and Adolescents). Ankara Başkent
Üniversitesi
2. Association, A. P. (2013). American Psychiatric
Association: Diagnostic and Statistical Manual of
Mental Disorders. Arlington. 5th.
3. Bahia, L., E. S. Coutinho, L. A. Barufaldi, et al.
(2012). "The costs of overweight and obesity-related
diseases in the Brazilian public health system:
cross-sectional study." BMC Public Health 12: 440.
4. Barry, D., M. Clarke and N. M. Petry (2009).
"Obesity and its relationship to addictions: is
overeating a form of addictive behavior?" Am J
Addict 18(6): 439-451.
5. Bereket, A. and Z. Atay (2012). "Current status of
childhood obesity and its associated morbidities in
Turkey." J Clin Res Pediatr Endocrinol 4(1): 1-7.
6. Blum, K., J. G. Cull, E. R. Braverman, et al. (1996).
"Reward Deficiency Syndrome." American Scientist
84(2): 132-145.
7. Blum, K., P. K. Thanos and M. S. Gold (2014).
"Dopamine and glucose, obesity, and reward
deficiency syndrome." Front Psychol 5: 919.
8. Blumenthal, D. M. and M. S. Gold (2010).
"Neurobiology of food addiction." Curr Opin Clin
Nutr Metab Care 13(4): 359-365.
9. Burmeister, J. M., N. Hinman, A. Koball, et al.
(2013). "Food addiction in adults seeking weight
loss treatment. Implications for psychosocial health
and weight loss." Appetite 60(1): 103-110.
10. Caldwell, M. B., K. D. Brownell and D. E. Wilfley
(1997). "Relationship of weight, body
J.Neurol.Sci.[Turk]
dissatisfaction, and self-esteem in African American
and white female dieters." Int J Eat Disord 22(2):
127-130.
11. Dagher, A. and T. W. Robbins (2009). "Personality,
addiction, dopamine: insights from Parkinson's
disease." Neuron 61(4): 502-510.
12. Davis, C. and J. C. Carter (2009). "Compulsive
overeating as an addiction disorder. A review of
theory and evidence." Appetite 53(1): 1-8.
13. de Wit, L., F. Luppino, A. van Straten, et al. (2010).
"Depression and obesity: a meta-analysis of
community-based studies." Psychiatry Res 178(2):
230-235.
14. Dimitropoulos, A., J. Tkach, A. Ho, et al. (2012).
"Greater corticolimbic activation to high-calorie
food cues after eating in obese vs. normal-weight
adults." Appetite 58(1): 303-312.
15. Donnelly, J. E., D. J. Jacobsen, J. E. Whatley, et al.
(1996). "Nutrition and physical activity program to
attenuate obesity and promote physical and
metabolic fitness in elementary school children."
Obesity Research 4(3): 229-243.
16. Elliott, K. G., C. L. Kjolhede, E. Gournis, et al.
(1997). "Duration of breastfeeding associated with
obesity during adolescence." Obesity Research 5(6):
538-541.
17. Europe, W. H. O. R. O. f. (2007). The Challenge of
Obesity in the WHO European Region and the
Strategies for Response
18. Gearhardt, A. N., C. Davis, R. Kuschner, et al.
(2011). "The addiction potential of hyperpalatable
foods." Curr Drug Abuse Rev 4(3): 140-145.
19. Godoy-Matos, A. F., E. P. Guedes, L. L. Souza, et al.
(2009). "Management of obesity in adolescents:
state of art." Arq Bras Endocrinol Metabol 53(2):
252-261.
20. Hebebrand, J., O. Albayrak, R. Adan, et al. (2014).
""Eating addiction", rather than "food addiction",
better captures addictive-like eating behavior."
Neurosci Biobehav Rev 47: 295-306.
21. Hone-Blanchet, A. and S. Fecteau (2014). "Overlap
of food addiction and substance use disorders
definitions: analysis of animal and human studies."
Neuropharmacology 85: 81-90.
22. James, P. T. (2004). "Obesity: the worldwide
epidemic." Clin Dermatol 22(4): 276-280.
23. Junghanns, K., C. Veltrup and T. Wetterling (2000).
"Craving shift in chronic alcoholics." Eur Addict
Res 6(2): 64-70.
24. Kurumu, T. S. B. T. H. S. (2013). Türkiye Sağlıklı
Beslenme ve Hareketli Hayat Programı 2014-2017
(Turkey's Healthy Nutrition and Energetic Living
Program 2014-2017). Ankara
25. Laitinen, J., A. Jaaskelainen, A. L. Hartikainen, et
al. (2012). "Maternal weight gain during the first
half of pregnancy and offspring obesity at 16 years:
a prospective cohort study." BJOG 119(6): 716-723.
26. Lee, A. and S. E. Gibbs (2013). "Neurobiology of
food addiction and adolescent obesity prevention in
low- and middle-income countries." J Adolesc
Health 52(2 Suppl 2): S39-42.
27. Molarius, A., J. C. Seidell, S. Sans, et al. (1999).
"Varying sensitivity of waist action levels to identify
subjects with overweight or obesity in 19
populations of the WHO MONICA Project." J Clin
Epidemiol 52(12): 1213-1224.
399
28. Mond, J., P. van den Berg, K. Boutelle, et al. (2011).
"Obesity, body dissatisfaction, and emotional well-
being in early and late adolescence: findings from
the project EAT study." J Adolesc Health 48(4):
373-378.
29. Moreira, P., C. Padez, I. Mourao-Carvalhal, et al.
(2007). "Maternal weight gain during pregnancy
and overweight in Portuguese children." Int J Obes
(Lond) 31(4): 608-614.
30. Noble, E. P., S. T. St Jeor, T. Ritchie, et al. (1994).
"D2 dopamine receptor gene and cigarette smoking:
a reward gene?" Med Hypotheses 42(4): 257-260.
31. Ogden, C. L., M. D. Carroll, B. K. Kit, et al. (2012).
"Prevalence of obesity and trends in body mass
index among US children and adolescents, 1999-
2010." JAMA 307(5): 483-490.
32. Ögel, K. (2010). Sigara, Alkol ve Madde Kullanım
Bozuklukları: Tanı, Tedavi ve Önleme (Tobacco,
Alchol and Substance Use Disorders: Diagnosis,
Treatment and Prevention). İstanbul Yeniden
Yayınları
33. Sahpolat, M. A., M. Kokacya, M.H. Copoglu S.U.
(2014). "Ödül Eksikliği Sendromu (Reward
Deficiency Syndrome)." Bağımlılık Dergisi (Journal
of Dependence) 15(2): 85-90.
34. Salamone, J. D. and M. Correa (2013). "Dopamine
and food addiction: lexicon badly needed." Biol
Psychiatry 73(9): e15-24.
35. Schneider, D. (2000). "International trends in
adolescent nutrition." Soc Sci Med 51(6): 955-967.
36. Siega-Riz, A. M., T. Carson and B. Popkin (1998).
"Three squares or mostly snacks--what do teens
really eat? A sociodemographic study of meal
patterns." J Adolesc Health 22(1): 29-36.
37. Simsek, E., S. Akpinar, T. Bahcebasi, et al. (2008).
"The prevalence of overweight and obese children
aged 6-17 years in the West Black Sea region of
Turkey." International Journal of Clinical Practice
62(7): 1033-1038.
38. Sinha, R. (2008). "Chronic stress, drug use, and
vulnerability to addiction." Ann N Y Acad Sci 1141:
105-130.
39. Smith, D. G. and T. W. Robbins (2013). "The
neurobiological underpinnings of obesity and binge
eating: a rationale for adopting the food addiction
model." Biol Psychiatry 73(9): 804-810.
40. TC. Sağlık Bakanlığı Türkiye Halk Sağlığı Kurumu,
T. M. E. B., Hacettepe Üniversitesi (2013). Çocukluk
Çağı Obezite Araştırması 2013 Ön Raporu (COSI-
TR) (Childhood Obesity Survey 2013-Preliminary
Report) Ankara
41. van den Berg, P. A., J. Mond, M. Eisenberg, et al.
(2010). "The link between body dissatisfaction and
self-esteem in adolescents: similarities across
gender, age, weight status, race/ethnicity, and
socioeconomic status." J Adolesc Health 47(3): 290-
296.
42. Volkow, N. D., G. J. Wang and R. D. Baler (2011).
"Reward, dopamine and the control of food intake:
implications for obesity." Trends Cogn Sci 15(1):
37-46.
43. Wang, G. J., N. D. Volkow, J. Logan, et al. (2001).
"Brain dopamine and obesity." Lancet 357(9253):
354-357.
44. Wang, G. J., N. D. Volkow, P. K. Thanos, et al.
(2009). "Imaging of brain dopamine pathways:
 J.Neurol.Sci.[Turk]

implications for understanding obesity." J Addict

Med 3(1): 8-18.
45. Wang, Y., M. A. Beydoun, L. Liang, et al. (2008).
"Will all Americans become overweight or obese?
estimating the progression and cost of the US
obesity epidemic." Obesity (Silver Spring) 16(10):
2323-2330.
46. Wang, Y. and T. Lobstein (2006). "Worldwide trends
in childhood overweight and obesity." Int J Pediatr
Obes 1(1): 11-25.
47. Wardle, J. and L. Cooke (2005). "The impact of
obesity on psychological well-being." Best Pract Res
Clin Endocrinol Metab 19(3): 421-440.
48. Whitaker, R. C., J. A. Wright, M. S. Pepe, et al.
(1997). "Predicting obesity in young adulthood from
childhood and parental obesity." N Engl J Med
337(13): 869-873.

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