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In animal studies, sugar has been found to produce more symptoms than is required to be considered an addictive substance. Animal data has shown significant overlap between the consumption of added sugars and drug-like effects, including bingeing, craving, tolerance, withdrawal, cross-sensitisation, cross-tolerance, cross-dependence, reward and opioid effects. Sugar addiction seems to be dependence to the natural endogenous opioids that get released upon sugar intake. In both animals and humans, the evidence in the literature shows substantial parallels and overlap between drugs of abuse and sugar, from the standpoint of brain neurochemistry as well as behaviour.
DiNicolantonioJJ, etal. Br J Sports Med 2017;0:1–5. doi:10.1136/bjsports-2017-097971
In animal studies, sugar has been found to produce
more symptoms than is required to be considered an
addictive substance. Animal data has shown significant
overlap between the consumption of added sugars and
drug-like effects, including bingeing, craving, tolerance,
withdrawal, cross-sensitisation, cross-tolerance, cross-
dependence, reward and opioid effects. Sugar addiction
seems to be dependence to the natural endogenous
opioids that get released upon sugar intake. In both
animals and humans, the evidence in the literature shows
substantial parallels and overlap between drugs of abuse
and sugar, from the standpoint of brain neurochemistry
as well as behaviour.
It has been suggested that refined added sugars are
habit-forming just like cocaine, nicotine, alcohol,
tobacco and caffeine.1–3 In fact, chronic smokers
suppress their cigarette cravings better than their
food cravings.4 Some individuals report increased
sweet cravings after giving up cigarettes,5 likely
accounting for the typical weight gain associated
with quitting smoking.6 In fact, oral glucose may
even decrease tobacco cravings7 and withdrawal
discomfort.5 One study in cocaine-addicted individ-
uals noted that their liking and wanting for food
was even greater than that for cocaine.8 As sweet
foods are the most craved foods, this suggests that
the reward and cravings from added sugars might
be comparable to that of addictive substances.
Indeed, food cravings have significant overlap
with drug cravings,1–3 9 and animal studies show that
sweetness, such as sugar or saccharin, is preferred
even over that of addictive drugs like cocaine.10–14
Once sugar is introduced (even in lab rats already
addicted to cocaine) the rats will almost always
switch over to consuming sugar. This is because the
reward from sugar surpasses that of even cocaine.2
Consuming sugar produces effects similar to that of
cocaine,15–19 altering mood,20 possibly through its
ability to induce reward and pleasure,2 leading to
the seeking out of sugar.2 Others have shown that
foods high in sugar produce drug-like psychoactive
effects.2 21–23
A natural reward from sugar is another evolu-
tionary adaptation, as it would have driven humans
to search out and consume sugar whenever it
was found in the food supply.10 24 The increased
consumption of foods high in sugar (such as ripened
fruit and honey) would have increased the chances
for survival during periods of food scarcity, as sugar
helps us to lay down fat, and when found in nature
generally indicates foods that would have provided
ample amounts of calories.24 Those individuals with
the greatest fat stores likely had a strong evolu-
tionary advantage when it comes to survival during
times of food scarcity. Thus sugar cravings likely
imparted a strong evolutionary advantage.
Unfortunately humans never adapted to the
intense reward that follows the consumption of
highly refined added sugars, and the 24/7 availability
of these sugars provides us with little reprieve. In
other words, we can run from sugar but we cannot
hide. The most common forms of added sugar are
sucrose (table sugar) and high-fructose corn syrup.
Each contains the simple sugars glucose and fruc-
tose. This unnatural reward from consuming sugar
(surpassing that of drugs of abuse) over-rides our
self-control mechanisms predisposing us to sugar
addiction.10 Indeed, sweet substances are extremely
rewarding to humans and other mammals, but there
does appear to be genetic differences in the strength
of this preference for sweetness.10 25–29 And with the
recent ‘sweetening of the world’s diet’, there has
followed a dramatic rise in the consumption of
sugar.30–33 Added sugars have penetrated the food
supplies of virtually every isolated corner of the
The reason why we may not be able to give up
the sweet stuff is because sweet sensations are
one of the most intense sensory pleasures that
humans experience in the modern day.10 Our
seeking out of sugary substances exceeds any
metabolic need.10 And there is no physiological
requirement for consuming a single gram of added
sugar as there is technically no such thing as an
‘essential carbohydrate’ (unlike that for protein
or fat).34 Nonetheless as we previously discussed,
fructose consumption played a critical role in
human evolution. Although individuals can clearly
thrive and survive without any added sugars, the
human species likely would not have survived for
very long without the craving and consumption of
natural sources of fructose.
The issue of attractiveness of sweets in humans
is further complicated by the fact that individ-
uals perceive sweetness differently. The tendency
to experience addiction to refined sugars is likely
rooted in both the sweet taste perception and the
preference of each individual, likely reflecting
genetic factors.35 Thus although humans have the
ability to become addicted to sugar, the tendency to
do so is likely multifactorial.
Nowadays, sugar has been refined to the state of a
chemical-like substance. Indeed, when sugar cane is
crushed and drained of all its liquid contents, boiled
down to a syrup, shaken and then stripped of all its
vitamins, minerals and molasses, we are left with
pure white crystals. This extraction and refinement
process is similar to that of other addictive white
crystals, that is, cocaine from the coca leaf, and
opium from the poppy seed/pod.36 Thus, it is the
Sugar addiction: is it real? A narrativereview
James J DiNicolantonio,1 James H O’Keefe,1 William L Wilson2
To cite: DiNicolantonioJJ,
O’KeefeJH, WilsonWL.
Br J Sports Med Published
Online First: [please include
Day Month Year]. doi:10.1136/
1Saint Luke’s Mid America Heart
Institute, Kansas, USA
2Lahey Health and the Wilson
Institute of Neurobiology,
Burlington, USA
Correspondence to
DrJames JDiNicolantonio,
Saint Luke’s Mid America Heart
Institute, Kansas City, USA;
jjdinicol@ gmail. com
Accepted 1 August 2017
2DiNicolantonioJJ, etal. Br J Sports Med 2017;0:1–5. doi:10.1136/bjsports-2017-097971
refinement of sugar that significantly adds to its addictive prop-
During our evolutionary history we only had access to fruc-
tose in honey, fruits and certain vegetables, and in these sources
fibre and other substances are present that slow and limit the
absorption of the fructose. With low levels of fructose consump-
tion typical of our evolutionary history, about half is converted
to glucose and a quarter is converted to lactate. Very little fruc-
tose is converted into fat when consumption is at a low level
and fatty acid synthesis is also not upregulated. Thus throughout
our evolutionary history humans consumed a small amount of
fructose on a regular basis and this did not cross the fat storage
threshold. It is only when they occasionally binged on fructose
after finding a beehive or large supply of ripened fruit would they
store extra fat. Importantly, the natural antioxidants contained
in these natural foods would have decreased the formation of
‘inflammatory’ fat stores (unlike that with the consumption of
added sugars).
But does sugar behave like a drug of abuse? It has been noted
that the same increase in dopamine D1 receptor binding and
decreased D2 receptor binding in the striatum that occur with
cocaine administration also occur with intermittent access to
sugar or glucose.17 Rats with intermittent access to sugar also
have the same decrease in D2 receptor mRNA in the nucleus
accumbens that occurs with morphine and cocaine. Moreover,
the same increase in μ-receptor binding that occurs with cocaine
and morphine occurs with intermittent sugar intake. And finally
the same release of dopamine and reduction in extracellular
acetylcholine in the nucleus accumbens (indicating tolerance)
that occurs with injecting morphine occurs with bingeing on
sugar.17 Figure 1 provides a schematic of sugar addiction.
The sugar–drug connection goes even further as ‘addiction
transfer’ may occur between sugar and drugs of abuse and
alcohol.37 Some overweight patients may transfer their addic-
tion to high-sugar foods over to addictive drugs after weight
loss surgery. In one study, weight loss surgery patients who
reported preweight loss surgery problems with high-sugar
foods were the most likely to have new-onset substance use
disorders after surgery.37 Box 1 summarises how added sugars
(refined sugar and high-fructose corn syrup) behave like drugs
of abuse.
In order to understand if sugar is addictive, we need to under-
stand drug addiction. Take for example opiate addiction, which
can be diagnosed if naloxone (an opiate antagonist) produces
subsequent withdrawal signs. Shockingly, this is exactly what
occurs when animals are fed sugar and then given naloxone.
More importantly, the withdrawal that occurs with naloxone in
these animals eating sugar is similar to that found with nico-
tine or morphine. Sugar addiction seems to be a dependence on
the body’s own natural endogenous opioids that get released on
sugar intake.38 Indeed, there are substantial parallels and overlap
Figure 1 Schematic of sugar addiction
Box1 How added sugars behave like addictive drugs of
Behaves like a chemical or drug—due to its ‘pure’ white
crystalline form, which is readily absorbable leading to
unique metabolic harms1
Habit-forming just like alcohol, tobacco, cocaine, nicotine,
tea, coffee and chocolate1–3
Induces reward and cravings comparable to addictive drugs,
being more rewarding than cocaine3
Alters mood,4 induces reward and pleasure,3 leading to the
seeking out of sugar3
Produces drug-like psychoactive effects3 5–7
Produces cravings comparable to that of cocaine, sex and
cigarettes3 8 9
Can produce dependence/addiction (eg, bingeing,
withdrawals and cravings) indicating sugar can be
DiNicolantonioJJ, etal. Br J Sports Med 2017;0:1–5. doi:10.1136/bjsports-2017-097971
between drugs of abuse and sugar, from the standpoint of brain
neurochemistry as well as behaviour.
So back to the question, is sugar addictive? The term addic-
tion is generally reserved for drugs of abuse (ie, cocaine, heroin,
morphine, nicotine and alcohol) and is many times used synon-
ymously with dependence.17 The Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition (DSM-5) defines
‘substance use disorder’ (ie, addiction) if at least two to three
criteria (symptoms) exist from a list of 11. This was a change
from DSM-IV, which categorised both substance abuse and
substance dependence as separate disorders, and substance
abuse only required one criterion. In DSM-5 these two catego-
ries have been combined into ‘substance use disorder’. It is also
interesting to note that binge eating disorder has been added to
DSM-5. Sweet and high-fat foods are preferred by those with
binge eating disorders and that those preferences are mediated
by the endogenous opioid system.39
In animal models, sugar produces more symptoms (eg, crav-
ings, bingeing, tolerance and withdrawal) than is required to be
considered an addictive substance.36 So we can be quite confident
that sugar is indeed addictive in animal models. In fact, animal
data demonstrate significant overlap between the consump-
tion of added sugars and drug-like effects,10 40–42 producing
(1) bingeing, (2) craving (a strong desire to ‘use’), (3) tolerance
(gradual escalation in intake with repeated use), (4) withdrawal
(adverse physiological signs with discontinuation of use), (5)
cross-sensitisation (increased response to drugs of abuse), (6)
cross-tolerance (animals become tolerant to the analgesic effects
of morphine after chronic intake of sugar and saccharin),43 44
(7) cross-dependence (suppression of withdrawal symptoms with
certain drugs),38 45 46 (8) reward47 48 (intense dopamine release
in the brain),17 49–51 and (9) opioid effects, such as the release
of endogenous opioids on consuming sweet substances,44 46 52
symptoms of narcotic withdrawal when an opiate blocker is
given, and other neurochemical changes in the brain.17 36
A person may become addicted to sugar due to dependence on
his or her own endogenously released opioids.38 This is particu-
larly revealing when looking at patients with anorexia who may
be ‘addicted to starvation’ by the same dependence pathway
that occurs when eating sugar (ie, addiction to endogenously
released opioids that occurs during starvation).53 If anorexia can
be classified as a disease, and is apparently the body’s addiction
to its own endogenously released opioids, then sugar addiction
(dependence to endogenously released opioids on consumption
of sweets) should also be able to fall under the classification of
a disease.
In the purest sense, addiction is simply a psychological depen-
dence, but also a physiological dependence to sugar.17 While
there is not a universal agreement for the definition of addic-
tion, certain characteristics must be present in order to diagnose
an addiction (ie, cravings, tolerance and withdrawal), otherwise
known as the ‘addiction triad’. In order for sugar to be truly
considered addictive, it must be able to induce a withdrawal.
And in order for humans to have withdrawals from sugar, a
threshold must be reached. Thus, a certain dose of sugar needs
to be consumed for a certain of time whereby neurochemical
changes occur in the brain. This period of time likely varies from
person to person based on genetic differences.
It just so happens that after several weeks to months of chronic
sugar intake, the period in between sugar intake may cause
‘dopamine deficiency’ in the brain due to downregulation of the
dopamine D2 receptors and a reduction in binding of dopamine
to those receptors.54 But why is dopamine deficiency in the brain
a problem?
When the brain is low in dopamine, this can then lead to
withdrawals. And it is the withdrawal that can lead to continued
perpetual sugar intake leading to addiction. But the withdrawals
from sugar are less obvious compared with addictive drugs.
Indeed, people are not visibly ‘strung-out’ on sugar, nor do they
have life-threatening or even physically apparent withdrawal
signs. But this does not mean that sugar withdrawal does not
exist in the brain. In fact, the lack of dopamine in the brain
during periods between sugar consumption has been suggested
to lead to attention deficit hyperactivity disorder (ADHD)-like
symptoms such as, hyperactivity, attention-deficit, distraction
and decreased performance.54 In essence, ADHD-type symp-
toms could be a sign of ‘withdrawal’ from eating refined added
In fact, obesity, ADHD and drug addiction to cocaine and
heroin all share the same downregulation of the dopamine D2
receptors in the brain. This suggests that all three conditions
have the same underlying issue (dopamine deficiency). During
periods off sugar, a mild state of depression may ensue due
to dopamine deficiency, which can be temporarily relieved by
consuming more sugar (hence the term ‘sugar fix’). This leads to
an endless and vicious cycle of dopamine highs and lows, perpet-
uating continued sugar intake and dependence on its intake.
Sugar and high glycaemic carbohydrates also have an effect on
brain serotonin. After consuming a meal high in sugar or carbo-
hydrates, there is a surge in brain serotonin. In other words,
people may overconsume sugar because it makes them feel better.
Over time this may lead to depletion of serotonin in the brain
perpetuating sugar dependence. As we have discussed, these
patients also tend to be dopamine-deficient with downregula-
tion of dopamine receptors. This combination may well explain
the association of obesity with many other brain disorders like
depression, anxiety disorders, bipolar disorder and ADHD.55
After consuming large amounts of sugar, a drop in blood
glucose may cause further sugar dependence. Throughout our
evolutionary history, low blood glucose levels meant ‘it’s time to
eat’, and if given the chance it made perfect sense to eat some-
thing with sugar or starch, the fastest way to restore normal
glucose levels. Ramped up hunger and sweet cravings were
Mother Nature’s means of accomplishing this critical task. But
today with a constant supply of added sugar readily available,
advocating the consumption of sugar as a treatment of low blood
glucose levels may make the situation worse. Since it is now
estimated that around 110 million Americans have insulin resis-
tance,56 much of the population could be at particular risk for
sugar addiction.
Sugar produces drug-like effects that may increase the risk for
drug addiction.17 Indeed, sugar may have a ‘gateway effect’ as it
cross-sensitises with drugs of abuse.17 However, these effects are
not always reproducible and more work in humans is required
to fully elucidate these effects. The consumption of sugar has
even caused an increase in the intake of alcohol during periods
of sugar abstinence.17 Rats given daily amphetamine injections
become hyperactive after tasting sugar.17 And this occurs even
when low doses of amphetamine are used. Sugar has also been
found to cross-sensitise with cocaine,17 and can lead to sensiti-
sation to the dopamine agonist quinpirole.17 These data suggest
4DiNicolantonioJJ, etal. Br J Sports Med 2017;0:1–5. doi:10.1136/bjsports-2017-097971
What is already known?
Substances of abuse are acknowledged throughout the
medical community to have the potential to be addictive.
Sugar consumption has increased in parallel with its
introduction in the food supply.
Sugar may drive increased food consumption, obesity and
What are the findings?
Animal studies have confirmed that the reward for sugar can
surpass that of cocaine.
In animal studies, sugar produces more symptoms than is
required to be considered an addictive substance.
In animal studies there is overlap between the consumption
of added sugars and drug-like effects (eg, bingeing, craving,
tolerance, withdrawal, cross-sensitisation, cross-tolerance,
cross-dependence, reward and opioid effects).
Sugar addiction may be a dependence to the natural
endogenous opioids that get released on sugar intake.
In both animals and humans there are substantial parallels
and overlap between drugs of abuse and sugar, from the
standpoint of brain neurochemistry as well as behaviour.
that sugar consumption may sensitise the brain dopamine system,
contributing to addiction and polysubstance abuse.17 More-
over, animals that prefer sweetness will self-administer cocaine
at a greater rate,17 which may be due to sugar’s dopaminergic,
cholinergic, opioid-mimicking effects and stimulant-mimicking
effects like dexamphetamine, methylphenidate and modafinil
(although smaller in magnitude).17
Postingestive glucose can activate the brain dopamine reward
circuit independently of sweet taste,57 and that sweet appetite
may even be stimulated by the presence of glucose in the gastro-
intestinal tract.58
Unlike drug or alcohol addiction, in general sugar addiction has
little direct negative social impact on individuals or their fami-
lies. Sugar addiction does have one clear impact on our collective
health—it makes us fat and metabolically sick. The fructose in
sucrose, honey, high-fructose corn syrup and fruits has little
impact on fat storage when it is consumed in small amounts.59
This was clearly how humans interacted with simple sugars most
of the time in the past. Our ancient ancestors would binge on
fruit or honey when it was available, but these episodes were
clearly sporadic. In today’s world with the 24/7 availability of
highly processed food loaded with added sugars, these episodes
of craving and bingeing would almost be constant, leading to a
markedly increased intake of fructose. Excessive consumption
of fructose promotes fat storage especially in the liver .60 This
supports the old adage ‘the dose makes the poison’.
Based on the aforementioned evidence, sugar meets many of
the criteria for a substance of abuse and could be potentially
addictive in humans. Changes that occur in the brain neuro-
chemistry with drugs are similar, although smaller in magnitude,
to those that result from sugar intake. Because of the nature of
addiction, simply telling people to consume less sugar is unlikely
to be successful. The focus of the medical profession should
be on finding treatments that suppress or eliminate these crav-
ings. Varenicline (Chantix) is approved by the Food and Drug
Administration as an aid to quitting cigarette smoking, and it
also markedly decreases cravings for sugar.61 There are a few
case reports suggesting that varenicline might be effective for
weight loss.
Certain supplements such as chromium picolinate and L-glu-
tamine have been reported to curb sweet cravings, but to date
research on these supplements has been limited. Chromium
picolinate appears to be especially effective for patients with
binge eating disorder and depression.62 Unfortunately as is the
case of many supplements, at the present time we are lacking
large controlled studies using these supplements.
In conclusion, now is the time to kick the habit and say
goodbye to the sweet stuff for good. Hopefully in the future we
will have more effective medical treatments that will help us in
this critical endeavour.
Contributors JJD performed the literature search and wrote the initial manuscript.
JHO’K and WLW reviewed, edited and wrote sections of the final manuscript.
Competing interests JJD is the author of The Salt Fix and operates the website
thesaltfix. com WLW sells a supplement that contains both L-glutamine and
chromium picolinate. JHO’K owns and operates a nutraceutical company.
Provenance and peer review Not commissioned; externally peer reviewed.
© Article author(s) (or their employer(s) unless otherwise stated in the text of the
article) 2017. All rights reserved. No commercial use is permitted unless otherwise
expressly granted.
1 Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet
Assoc 2010;110:1307–21.
2 Ahmed SH, Guillem K, Vandaele Y. Sugar addiction: pushing the drug-sugar analogy to
the limit. Curr Opin Clin Nutr Metab Care 2013;16:434–9.
3 Snow HL. Refined sugar: its use and misuse. The Improvement Era Magazine 1948:51.
4 Kober H, Mende-Siedlecki P, Kross EF, et al. Prefrontal-striatal pathway underlies
cognitive regulation of craving. ProcNatl Acad Sci 2010;107:14811–6.
5 Toll BA, Katulak NA, Williams-Piehota P, et al. Validation of a scale for the assessment
of food cravings among smokers. Appetite 2008;50:25–32.
6 Aubin H-J, Farley A, Lycett D, et al. Weight gain in smokers after quitting cigarettes:
meta-analysis. BMJ 2012;345:e4439.
7 West R, May S, McEwen A, et al. A randomised trial of glucose tablets to aid smoking
cessation. Psychopharmacology 2010;207:631–5.
8 Goldstein RZ, Woicik PA, Moeller SJ, et al. Liking and wanting of drug and non-drug
rewards in active cocaine users: the STRAP-R questionnaire. J Psychopharmacol
9 Nair SG, Adams-Deutsch T, Epstein DH, et al. The neuropharmacology of relapse to
food seeking: methodology, main findings, and comparison with relapse to drug
seeking. Prog Neurobiol 2009;89:18–45.
10 Lenoir M, Serre F, Cantin L, et al. Intense sweetness surpasses cocaine reward. PLoS
One 2007;2:e698.
11 Augier E, Vouillac C, Ahmed SH. Diazepam promotes choice of abstinence in cocaine
self-administering rats. Addict Biol 2012;17:378–91.
12 Cantin L, Lenoir M, Augier E, et al. Cocaine Is low on the value ladder of rats: possible
evidence for resilience to addiction. PLoS One 2010;5:e11592.
13 Kerstetter KA, Ballis MA, Duffin-Lutgen S, et al. Sex differences in selecting between
food and cocaine reinforcement are mediated by Estrogen. Neuropsychopharmacology
14 Morales L, Del Olmo N, Valladolid-Acebes I, et al. Shift of circadian feeding pattern
by high-fat diets Is coincident with reward deficits in obese mice. PLoS One
15 Ifland JR, Preuss HG, Marcus MT, et al. Refined food addiction: a classic substance use
disorder. Med Hypotheses 2009;72:518–26.
16 Gearhardt AN, Grilo CM, DiLeone RJ, et al. Can food be addictive? public health and
policy implications. Addiction 2011;106:1208–12.
17 Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and
neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev
18 Brown RJ, Rother KI. Non-nutritive sweeteners and their role in the gastrointestinal
tract. J Clin Endocrinol Metab 2012;97:2597–605.
19 Grayson BE, Seeley RJ, Sandoval DA. Wired on sugar: the role of the CNS in the
regulation of glucose homeostasis. Nat Rev Neurosci 2013;14:24–37.
20 Pretlow RA. Addiction to highly pleasurable food as a cause of the childhood obesity
epidemic: a qualitative internet study. Eat Disord 2011;19:295–307.
21 Rose N, Koperski S, Golomb BA. Mood food: chocolate and depressive symptoms in a
cross-sectional analysis. Arch Intern Med 2010;170:699–703.
DiNicolantonioJJ, etal. Br J Sports Med 2017;0:1–5. doi:10.1136/bjsports-2017-097971
22 Dallman MF. Stress-induced obesity and the emotional nervous system. Trends in
Endocrinology & Metabolism 2010;21:159–65.
23 Spring B, Schneider K, Smith M, et al. Abuse potential of carbohydrates for overweight
carbohydrate cravers. Psychopharmacology 2008;197:637–47.
24 Johnson RJ, Andrews P, Benner SA, et al. Theodore E. Woodward Award: the
evolution of obesity: insights from the mid-miocene. Trans Am Clin Climatol Assoc
25 Steiner JE. Human facial expressions in response to taste and smell stimulation. Adv
Child Dev Behav 1979;13:257–95.
26 Drewnowski A. Taste preferences and food intake. Annu Rev Nutr 1997;17:237–53.
27 Berridge KC. Food reward: brain substrates of wanting and liking. Neurosci & Rev
28 Sclafani A. Oral and postoral determinants of food reward. Physiol Behav
29 Keskitalo K, Knaapila A, Kallela M, et al. Sweet taste preferences are partly genetically
determined: identification of a trait locus on chromosome 16. Am J Clin Nutr
30 Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup
in beverages may play a role in the epidemic of obesity. Am J Clin Nutr
31 Bray GA, Popkin BM. Dietary sugar and body weight: have we reached a crisis in the
epidemic of obesity and diabetes?: health be damned! Pour on the sugar. Diabetes
Care 2014;37:950–6.
32 Malik VS, Popkin BM, Bray GA, et al. Sugar-sweetened beverages and risk
of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care
33 Popkin BM, Nielsen SJ. The sweetening of the world’s diet. Obes Res
34 Westman EC. Is dietary carbohydrate essential for human nutrition? Am J Clin Nutr
35 Reed DR, McDaniel AH. The human sweet tooth. BMC Oral Health 2006;6:S17.
36 DiNicolantonio JJ, Lucan SC, Season S. It's Everywhere and Addictive: The New York
Times, 2014.
37 Fowler L, Ivezaj V, Saules KK. Problematic intake of high-sugar/low-fat and high
glycemic index foods by bariatric patients is associated with development of post-
surgical new onset substance use disorders. Eat Behav 2014;15:505–8.
38 Colantuoni C, Rada P, McCarthy J, et al. Evidence that intermittent, excessive sugar
intake causes endogenous opioid dependence. Obes Res 2002;10:478–88.
39 Yanovski S. Sugar and fat: cravings and aversions. J Nutr 2003;133:835s–7.
40 Kelley AE. Memory and addiction: shared neural circuitry and molecular mechanisms.
Neuron 2004;44:161–79.
41 Levine AS, Kotz CM, Gosnell BA. Sugars: hedonic aspects, neuroregulation, and energy
balance. Am J Clin Nutr 2003;78:834s–42.
42 Volkow ND, Wise RA. How can drug addiction help us understand obesity? Nat
Neurosci 2005;8:555–60.
43 D’Anci KE, Kanarek RB, Marks-Kaufman R. Duration of sucrose availability
differentially alters morphine-induced analgesia in rats. Pharmacol Biochem Behav
44 Lieblich I, Cohen E, Ganchrow JR, et al. Morphine tolerance in genetically selected rats
induced by chronically elevated saccharin intake.Science 1983;221:871–3.
45 Rudski J, Billington CJ, Levine AS. A sucrose-based maintenance diet increases
sensitivity to appetite suppressant effects of naloxone. Pharmacol Biochem Behav
46 Kanarek RB, Mathes WF, Heisler LK, et al. Prior exposure to palatable solutions
enhances the effects of naltrexone on food intake in rats. Pharmacol Biochem Behav
47 Volkow ND, Fowler JS, Wang GJ, et al. Imaging dopamine’s role in drug abuse and
addiction. Neuropharmacology 2009;56:3–8.
48 Dopamine WRA. learning and motivation. Nat Rev Neurosci 2004;5:483–94.
49 Hajnal A, Smith GP, Norgren R. Oral sucrose stimulation increases accumbens
dopamine in the rat. Am J Physiol Regul Integr Comp Physiol 2004;286:31R–7.
50 Pontieri FE, Tanda G, Orzi F, et al. Effects of nicotine on the nucleus accumbens and
similarity to those of addictive drugs. Nature 1996;382:255–7.
51 Di Chiara G, Imperato A. Drugs abused by humans preferentially increase synaptic
dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl
Acad Sci U S A 1988;85:5274–8.
52 Cohen E, Lieblich I, Bergmann F. Effects of chronically elevated intake of different
concentrations of saccharin on morphine tolerance in genetically selected rats. Physiol
Behav 1984;32:1041–3.
53 Aravich PF, Rieg TS, Lauterio TJ, et al. β-endorphin and dynorphin abnormalities in rats
subjected to exercise and restricted feeding: relationship to anorexia nervosa? Brain
Res 1993;622:1–8.
54 Johnson RJ, Gold MS, Johnson DR, et al. Attention-deficit/hyperactivity disorder: is it
time to reappraise the role of sugar consumption? Postgrad Med 2011;123:39–49.
55 Wurtman RJ, Wurtman JJ. Brain serotonin, carbohydrate-craving, obesity and
depression. Obes Res 1995;3:477S–80.
56 DiNicolantonio JJ, O’Keefe JH, Lucan SC. Added fructose: a principal driver of type 2
diabetes mellitus and its consequences. Mayo Clin Proc 2015;90:372–81.
57 Tellez LA, Han W, Zhang X, et al. Separate circuitries encode the hedonic and
nutritional values of sugar. Nat Neurosci 2016;19:465–70.
58 Han W, Tellez LA, Niu J, et al. Striatal dopamine links gastrointestinal rerouting to
altered sweet appetite. Cell Metab 2016;23:103–12.
59 Sun SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell
us. Nutr Metab 2012;9:89.
60 Schwarz JM, Noworolski SM, Erkin-Cakmak A, et al. Effects of dietary fructose
restriction on liver fat, De Novo Lipogenesis, and insulin kinetics in children with
obesity. Gastroenterology 2017.
61 Shariff M, Quik M, Holgate J, et al. Neuronal nicotinic acetylcholine receptor
modulators reduce sugar intake. PLoS One 2016;11:e0150270.
62 Brownley KA, Boettiger CA, Young L, et al. Dietary chromium supplementation for
targeted treatment of diabetes patients with comorbid depression and binge eating.
Med Hypotheses 2015;85:45–8.
... According to Wiss et al. (41), alcohol consumption and smoking may induce sugar cravings by stimulating appetite through the biochemical mechanisms of neurotransmitters (e.g., dopamine, opioid peptides, and serotonin). Dinicolantonio et al. (42) proposed that sugar may have drug-like psychoactive effects, inducing dependence and/or addiction; that is, substance abuse and sugar are cross-sensitized, which may lead sugar to have a potential "gateway effect" on substance abuse (42). Considering the high prevalence of alcohol consumption and smoking among adolescent boys, there is a need for strategies to reduce alcohol and smoking consumption among adolescents. ...
... According to Wiss et al. (41), alcohol consumption and smoking may induce sugar cravings by stimulating appetite through the biochemical mechanisms of neurotransmitters (e.g., dopamine, opioid peptides, and serotonin). Dinicolantonio et al. (42) proposed that sugar may have drug-like psychoactive effects, inducing dependence and/or addiction; that is, substance abuse and sugar are cross-sensitized, which may lead sugar to have a potential "gateway effect" on substance abuse (42). Considering the high prevalence of alcohol consumption and smoking among adolescent boys, there is a need for strategies to reduce alcohol and smoking consumption among adolescents. ...
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This study aimed to identify sex-based differences in the individual and environmental factors associated with sugar-sweetened beverage (SSB) consumption among Korean high school students. Secondary data were obtained from the 15th (2019) Korea Youth Risk Behavior Web-based Survey. In this study, we analyzed data from 13,066 high school students (5,874 boys and 7,192 girls) who answered questions regarding SSB consumption and individual and environmental factors. Complex sampling analysis (descriptive statistics and logistic regression analysis) was conducted using the SPSS Statistics 26.0 software. Most adolescents (97% boys and 95.2% girls) reported having consumed SSBs in the last seven days. Individual factors, such as increased stress, sleep dissatisfaction, and fast-food intake (more than thrice a week) were positively associated with SSB consumption among adolescent boys and girls. Environmental factors like high education levels (above college) of mothers were negatively associated with SSB consumption among both boys and girls. Furthermore, current alcohol consumption, smoking, low vegetable intake (less than thrice a week) in boys, and more than 2 h a day of screen-based sedentary behavior in girls were positively associated with SSB consumption. According to the results, individual factors associated with SSB consumption varied according to the sex of adolescents. Thus, sex differences in factors associated with SSB consumption in adolescents should be considered as basic knowledge for developing strategies for reducing SSB consumption.
... Sucrose, a common constituent of an energydense diet, is one of the major dietary components employed in various forms and amounts to meet the psychological desire has been shown to result in dietary assault and health complications (Jensen et al., 2018a). Its addition to foods, such as candies, soft drinks, and ice cream, has continued to cause non-communicable pandemic disease and sustained dramatic increase, occasioned by addiction (DiNicolantonio et al., 2018). Consequently, a high sucrose diet remains one of the leading causes of global health burden, especially in developed societies (DiNicolantonio et al., 2018). ...
... Its addition to foods, such as candies, soft drinks, and ice cream, has continued to cause non-communicable pandemic disease and sustained dramatic increase, occasioned by addiction (DiNicolantonio et al., 2018). Consequently, a high sucrose diet remains one of the leading causes of global health burden, especially in developed societies (DiNicolantonio et al., 2018). Impaired lipids metabolism and regulation proceeds the pathogenesis of the non-alcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD), and neurodegenerative disorders such as Alzheimer's disease (AD) (Bruce et al., 2017). ...
... The 85 most accepted methods of sugar addition are sucrose and high-fructose corn syrup, which are 86 widely used nowadays. Moreover, the extraction and refinement process of sugar into white crystal 87 (refined sugar) is similar to cocaine from coca leaf (DiNicolantonio, O'Keefe, & Wilson, 2018). 88 J o u r n a l P r e -p r o o f ...
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Refined sugar is a processed product containing 99% sucrose, which is obtained from sugarcane (70%) or sugar beet (30%). In modern societies, sugar continues to play a significant role in the diet, recognised not only for its flavour and special sweetening properties but also for its role in food preservation. On the other hand, a high consumption of refined sugar is associated with non-communicable diseases and many health issues such as a high risk of dental caries, overweight and neurodevelopmental disorders in children. Alternatives like unrefined sugars have generated a lot of interest as a healthy substitute due to their nutraceutical properties. This paper is aimed to review the beneficial effects of sugar derived from natural sources and highlight health problems that could be caused by refined processed sugar. Refined sugar is frequently used in variety of items including processed foods, soft drinks or ice creams although it is considered unhealthy due to its high salt and sugar content as well as added fats and artificial coloring. Natural sugars are preferred because they have a high nutritional value and a high concentration of healthy compounds, which offset the negative effects of refined sugar. Therefore, removing refined sugar or at least reducing its consumption should be promoted as a healthier option in food choices.
... More importantly, food addiction, such as SUD, is characterized by seeking and compulsive behaviours. Thus, bingeing sweet food or long-term exposure of HSD to rodents let to overweight or obesity [194], whereas sucrose or sugar withdrawal predispose them to behaviour similar to depression and anxiety [120,143]. Fructose (8% solution) given for 21 days to male rats increased bingeing behaviour following a long-term intermittent access model and decreased NAc shell neuron activation [195]. ...
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Carbohydrates are important macronutrients in human and rodent diet patterns that play a key role in crucial metabolic pathways and provide the necessary energy for proper body functioning. Sugar homeostasis and intake require complex hormonal and nervous control to proper body energy balance. Added sugar in processed food results in metabolic, cardiovascular, and nervous disorders. Epidemiological reports have shown enhanced consumption of sweet products in children and adults, especially in reproductive age and in pregnant women, which can lead to the susceptibility of offspring’s health to diseases in early life or in adulthood and proneness to mental disorders. In this review, we discuss the impacts of high-sugar diet (HSD) or sugar intake during the perinatal and/or postnatal periods on neural and behavioural disturbances as well as on the development of substance use disorder (SUD). Since several emotional behavioural disturbances are recognized as predictors of SUD, we also present how HSD enhances impulsive behaviour, stress, anxiety and depression. Apart from the influence of HSD on these mood disturbances, added sugar can render food addiction. Both food and addictive substances change the sensitivity of the brain rewarding neurotransmission signalling. The results of the collected studies could be important in assessing sugar intake, especially via maternal dietary patterns, from the clinical perspective of SUD prevention or pre-existing emotional disorders. Methodology: This narrative review focuses on the roles of a high-sugar diet (HSD) and added sugar in foods and on the impacts of glucose and fructose on the development of substance use disorder (SUD) and on the behavioural predictors of drugs abuse. The literature was reviewed by two authors independently according to the topic of the review. We searched the PubMed and Scopus databases and Multidisciplinary Digital Publishing Institute open access scientific journals using the following keyword search strategy depending on the theme of the chapter: “high-sugar diet” OR “high-carbohydrate diet” OR “sugar” OR “glucose” OR “fructose” OR “added sugar” AND keywords. We excluded inaccessible or pay-walled articles, abstracts, conference papers, editorials, letters, commentary, and short notes. Reviews, experimental studies, and epidemiological data, published since 1990s, were searched and collected depending on the chapter structure. After the search, all duplicates are thrown out and full texts were read, and findings were rescreened. After the selection process, appropriate papers were included to present in this review.
Résumé Cette dernière décennie, l’industrie agroalimentaire a largement adapté son offre avec la généralisation de produits contenant des édulcorants pour remplacer les sucres ajoutés ou sucres libres et, ainsi, limiter les apports caloriques tout en maintenant l’appétence aux produits. Cependant, nombre de données observationnelles questionnent l’efficacité et la sécurité de cette stratégie. En effet, les édulcorants semblent présenter des avantages et des inconvénients sur les plans du comportement alimentaire et des conséquences métaboliques. Cette disparité des résultats semble pouvoir s’expliquer par les mécanismes d’action et l’impact spécifique des différentes molécules édulcorantes. En effet, bien que tous les édulcorants ciblent les mêmes récepteurs cellulaires, il faut rappeler que chaque édulcorant peut différer dans sa structure chimique, son profil pharmacocinétique et, plus important encore, dans son activité pharmacologique, et ainsi induire des réponses physiologiques ou pathologiques propres. De manière générale, les méta-analyses indiquent une augmentation du risque de développer un diabète de type 2 lorsque la consommation de ces édulcorants est importante, mais les données expérimentales ne sont pas aussi tranchées. Cet article présente les mécanismes d’action des édulcorants les plus utilisés et les différents effets associés à la consommation d’édulcorants sur le comportement alimentaire et ses conséquences sur la gestion du poids et le contrôle métabolique.
When a pet dies, owners can experience similar levels of grief as when a human dies. Previous research indicates the role of continuing bonds (CB) when a pet is alive. To understand the impact of these bonds after the pet has died, we conducted a systematic narrative synthesis according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines (PRISMA). Findings were heterogenous, yet there were still parallels in the literature. CB can sometimes aggravate and intensify grief experiences, particularly when pet grief is perceived as disenfranchised grief. However, identifying appropriate bonds can be useful to moderate the intensity of grief and be a valuable mechanism of support. CB can also help post-traumatic growth of owners.
This chapter summarizes the main health risks associated with an increased sugar consumption, mainly including studies investigating sucrose and glucose, and to a lesser extent to other carbohydrates. Literature data links high dietary sugar intake to obesity, metabolic and cardiovascular disease, dental caries, and also micronutrient dilution or hyperactivity in children, while an increased consumption of sugar-sweetened beverages is an important causal factor for diabetes mellitus. Various expert bodies recommend a maximum daily sugar intake of 25–50 g (5–10% of energy intake), but current reports point to large variations depending on the physio-pathological status, diet or lifestyle.
Chocolate is the most desired food in the world, and it has always been considered as a pleasant food, sought after both for hedonistic reasons and for its role as a “panacea” for mood and affectivity. Multiple features of “the food of Gods” can explain how it is induced/increased to induce/increase the desire to eat it. Its unique orosensory qualities (i.e., taste, smell, aroma, and texture) mostly contribute to explaining the commonly shared acceptability of chocolate craving. Furthermore, chocolate determines a peculiar brain activity, activating analogous brain areas and neurobiological mechanisms than substances of abuse. Chocolate contains various biologically active components such as methylxanthine, biogenic amines, and cannabinoid-like fatty acids, all of which arguably own both biological and emotional activity. Chocolate may be consumed as a form of self-medication for dietary lacks or to compensate low levels of neurotransmitters implicated in the regulation of mood, appetite, and behavior. Chocolate consumption and cravings are often parossistic and vary along with hormonal fluctuations related to the menstrual cycle, which suggests a hormonal relationship. This chapter focuses on chocolate characteristics, by focusing on their relationships with the neurobiological mechanisms, which may contribute to maintaining chocolate addiction and craving.
Overindulgence, excessive consumption, and a pattern of compulsive use of natural rewards, such as certain foods or drugs of abuse, may result in the development of obesity or substance use disorder, respectively. Natural rewards and drugs of abuse can trigger similar changes in the neurobiological substrates that drive food- and drug-seeking behaviors. This review examines the impact natural rewards and drugs of abuse have on perineuronal nets (PNNs). PNNs are specialized extracellular matrix structures that ensheathe certain neurons during development over the critical period to provide synaptic stabilization and a protective microenvironment for the cells they surround. This review also analyzes how natural rewards and drugs of abuse impact the density and maturation of PNNs within reward-associated circuitry of the brain, which may contribute to maladaptive food- and drug-seeking behaviors. Finally, we evaluate the relatively few studies that have degraded PNNs to perturb reward-seeking behaviors. Taken together, this review sheds light on the complex way PNNs are regulated by natural rewards and drugs and highlights a need for future studies to delineate the molecular mechanisms that underlie the modification and maintenance of PNNs following exposure to rewarding stimuli.
The consumption of sugar-sweetened beverages (SSBs) in China is rising rapidly and has become a major source of added sugar, which may pose a threat to human health. Intervention policies represented by consumption tax may be introduced to reduce sugar consumption. Few studies have addressed the consumption tax on SSBs in emerging countries like China, where beverage consumption is increasing considerably. Based on the scanner data of Chinese urban households from 2014 to 2017, this paper used the Quadratic Almost Ideal Demand System (QUAIDS) model to estimate the Marshallian (uncompensated) price elasticity of various beverages. We then conducted a simulation of the effect of the consumption tax on the consumption of sugar-sweetened beverages. The simulation results under different tax rates suggest that the tax on SSBs will significantly reduce the consumption of SSBs and bring about a slight increase in the consumption of diet drinks, thereby promoting beverage consumption in the low-calorie direction. This effect was particularly obvious in low-income groups with a smaller tax burden, unlike the situation in developed countries represented by the U.S. The findings imply that the consumption tax on SSBs is conducive to lowering added sugar intake and, as a result, reducing obesity. China should levy a consumption tax on SSBs and all sugar-sweetened foods in the future. Tax revenue can be used to fund research and development to reduce the production costs of sugar-free foods and encourage healthy eating behavior.
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Background & Aims Consumption of sugar is associated with obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease, and cardiovascular disease. The conversion of fructose to fat in liver (de novo lipogenesis, DNL) may be a modifiable pathogenetic pathway. We determined the effect of 9 days of isocaloric fructose restriction on DNL, liver fat, visceral fat (VAT), subcutaneous fat, and insulin kinetics in obese Latino and African American children with habitual high sugar consumption (fructose intake more than 50 g/day). Methods Children (9–18 years old; n = 41) had all meals provided for 9 days with the same energy and macronutrient composition as their standard diet, but with starch substituted for sugar, yielding a final fructose content of 4% of total kcal. Metabolic assessments were performed before and after fructose restriction. Liver fat, VAT, and subcutaneous fat were determined by magnetic resonance spectroscopy and imaging. The fractional DNL area under the curve value was measured using stable isotope tracers and gas chromatography/mass spectrometry. Insulin kinetics were calculated from oral glucose tolerance tests. Paired analyses compared change from day 0 to day 10 within each child. Results Compared with baseline, on day 10, liver fat decreased from a median of 7.2% (inter-quartile range, 2.5%–14.8%) to 3.8% (inter-quartile range, 1.7%–15.5%)(P<.001) and VAT decreased from 123 cm³ (inter-quartile range, 85–145 cm³) to 110 cm³ (inter-quartile range, 84–134 cm³) (P<.001). The DNL area under the curve decreased from 68% (inter-quartile range, 46%–83%) to 26% (inter-quartile range, 16%– 37%) (P<0.001). Insulin kinetics improved (P<.001). These changes occurred irrespective of baseline liver fat. Conclusions Short-term (9 day) isocaloric fructose restriction decreased liver fat, VAT, and DNL, and improved insulin kinetics in children with obesity. These findings support efforts to reduce sugar consumption. no: NCT01200043
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Excess sugar consumption has been shown to contribute directly to weight gain, thus contributing to the growing worldwide obesity epidemic. Interestingly, increased sugar consumption has been shown to repeatedly elevate dopamine levels in the nucleus accumbens (NAc), in the mesolimbic reward pathway of the brain similar to many drugs of abuse. We report that varenicline, an FDA-approved nicotinic acetylcholine receptor (nAChR) partial agonist that modulates dopamine in the mesolimbic reward pathway of the brain, significantly reduces sucrose consumption, especially in a long-term consumption paradigm. Similar results were observed with other nAChR drugs, namely mecamylamine and cytisine. Furthermore, we show that long-term sucrose consumption increases α4β2 * and decreases α6β2* nAChRs in the nucleus accumbens, a key brain region associated with reward. Taken together, our results suggest that nAChR drugs such as varenicline may represent a novel treatment strategy for reducing sugar consumption.
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Sugar exerts its potent reinforcing effects via both gustatory and post-ingestive pathways. It is, however, unknown whether sweetness and nutritional signals engage segregated brain networks to motivate ingestion. We found in mice that separate basal ganglia circuitries mediated the hedonic and nutritional actions of sugar. During sugar intake, suppressing hedonic value inhibited dopamine release in ventral, but not dorsal, striatum, whereas suppressing nutritional value inhibited dopamine release in dorsal, but not ventral, striatum. Consistently, cell-specific ablation of dopamine-excitable cells in dorsal, but not ventral, striatum inhibited sugar's ability to drive the ingestion of unpalatable solutions. Conversely, optogenetic stimulation of dopamine-excitable cells in dorsal, but not ventral, striatum substituted for sugar in its ability to drive the ingestion of unpalatable solutions. Our data indicate that sugar recruits a distributed dopamine-excitable striatal circuitry that acts to prioritize energy-seeking over taste quality.
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Data from animal experiments and human studies implicate added sugars (eg, sucrose and high-fructose corn syrup) in the development of diabetes mellitus and related metabolic derangements that raise car-diovascular (CV) risk. Added fructose in particular (eg, as a constituent of added sucrose or as the main component of high-fructose sweeteners) may pose the greatest problem for incident diabetes, diabetes-related metabolic abnormalities, and CV risk. Conversely, whole foods that contain fructose (eg, fruits and vegetables) pose no problem for health and are likely protective against diabetes and adverse CV outcomes. Several dietary guidelines appropriately recommend consuming whole foods over foods with added sugars, but some (eg, recommendations from the American Diabetes Association) do not recom-mend restricting fructose-containing added sugars to any specific level. Other guidelines (such as from the Institute of Medicine) allow up to 25% of calories as fructose-containing added sugars. Intake of added fructose at such high levels would undoubtedly worsen rates of diabetes and its complications. There is no need for added fructose or any added sugars in the diet; reducing intake to 5% of total calories (the level now suggested by the World Health Organization) has been shown to improve glucose tolerance in humans and decrease the prevalence of diabetes and the metabolic derangements that often precede and accompany it. Reducing the intake of added sugars could translate to reduced diabetes-related morbidity and premature mortality for populations. ª 2015 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2015;nn(n):1-10
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Sugar-sweetened drinks have been associated with several health problems. In the point narrative as presented below, we provide our opinion and review of the data to date that we need to reconsider consumption of dietary sugar based on the growing concern of obesity and type 2 diabetes. In the counterpoint narrative following our contribution, Drs. Kahn and Sievenpiper provide a defense and suggest that dietary sugar is not the culprit. Data from the National Health and Nutrition Examination Survey and U.S. Department of Agriculture dietary surveys along with commercial Homescan data on household purchases were used to understand changes in sugar and fructose consumption. Meta-analyses and randomized clinical trials were used to evaluate outcomes of beverage and fructose intake. About 75% of all foods and beverages contain added sugar in a large array of forms. Consumption of soft drinks has increased fivefold since 1950. Meta-analyses suggest that consumption of sugar-sweetened beverages (SSBs) is related to the risk of diabetes, the metabolic syndrome, and cardiovascular disease. Drinking two 16-ounce SSBs per day for 6 months induced features of the metabolic syndrome and fatty liver. Randomized controlled trials in children and adults lasting 6 months to 2 years have shown that lowering the intake of soft drinks reduced weight gain. Recent studies suggest a gene-SSB potential relationship. Consumption of calorie-sweetened beverages has continued to increase and plays a role in the epidemic of obesity, the metabolic syndrome, and fatty liver disease. Reducing intake of soft drinks is associated with less weight gain.
Reductions in calorie intake contribute significantly to the positive outcome of bariatric surgeries. However, the physiological mechanisms linking the rerouting of the gastrointestinal tract to reductions in sugar cravings remain uncertain. We show that a duodenal-jejunal bypass (DJB) intervention inhibits maladaptive sweet appetite by acting on dopamine-responsive striatal circuitries. DJB disrupted the ability of recurrent sugar exposure to promote sweet appetite in sated animals, thereby revealing a link between recurrent duodenal sugar influx and maladaptive sweet intake. Unlike ingestion of a low-calorie sweetener, ingestion of sugar was associated with significant dopamine effluxes in the dorsal striatum, with glucose infusions into the duodenum inducing greater striatal dopamine release than equivalent jejunal infusions. Consistently, optogenetic activation of dopamine-excitable cells of the dorsal striatum was sufficient to restore maladaptive sweet appetite in sated DJB mice. Our findings point to a causal link between striatal dopamine signaling and the outcomes of bariatric interventions.
Dietary chromium supplementation for the treatment of diabetes remains controversial. The prevailing view that chromium supplementation for glucose regulation is unjustified has been based upon prior studies showing mixed, modest-sized effects in patients with type 2 diabetes (T2DM). Based on chromium's potential to improve insulin, dopamine, and serotonin function, we hypothesize that chromium has a greater glucoregulatory effect in individuals who have concurrent disturbances in dopamine and serotonin function - that is, complex patients with comorbid diabetes, depression, and binge eating. We propose, as suggested by the collective data to date, the need to go beyond the "one size fits all" approach to chromium supplementation and put forth a series of experiments designed to link physiological and neurobehavioral processes in the chromium response phenotype. Copyright © 2015. Published by Elsevier Ltd.
Bariatric or weight loss surgery (WLS) patients are overrepresented in substance abuse treatment, constituting about 3% of admissions; about 2/3 of such patients deny problematic substance use prior to WLS. It is important to advance our understanding of the emergence of substance use disorders (SUDs) – particularly the New Onset variant -- after WLS. Burgeoning research with both animal models and humans suggests that “food addiction” may play a role in certain forms of obesity, with particular risk conferred by foods high in sugar but low in fat. Therefore, we hypothesized that WLS patients who reported pre-WLS problems with high-sugar/low-fat foods and those high on the glycemic index (GI) would be those most likely to evidence New Onset SUDs after surgery. Secondary data analyses were conducted using a de-identified database from 154 bariatric surgery patients (88% female, Mage = 48.7 yrs, SD = 10.8, Mtime since surgery = 2.7 yrs, SD = 2.2 yrs). Participants who endorsed pre-surgical problems with high-sugar/low-fat foods and high GI foods were at greater risk for New Onset SUD in the post-surgical period. These findings remained significant after controlling for other predictors of post-surgical SUD. Our findings provide evidence for the possibility of addiction transfer among certain bariatric patients.