Below is a list of interesting publications looking at the difference between people who are overweight/obese to healthy weight ppl in brain activity in response to food.
Things to keep in mind:
- Maybe it actually is not as simple as "willpower."
- Differences between one another. Having a knowledge of this difference could lead to a higher level of understanding why others are having a harder time, or stuck in a yo-yo cycle.
- Maybe weight loss if not just all about, insulin, macro's controlling hunger, and a certain nutritional plan.
- Maybe there is NOT "one right plan" out there for everyone.
- Maybe this is why it might be insensitive for you to bost about fitting into the size 4 bikini in a group designed to help the overweight/obese. Or placing body image pictures up when you have no history of being overweight/obese for a significant of time is not the same as when a person with this history places a post up about making it to some healthy weight BMI.
- This could be why persistence and surrounding yourself in a "culture of health" above all else might actually be the key. As you are literally battling against your own brain's functioning when you are overweight or obese.
- Things inside the "***" are my thoughts/notes/questions.
-These are mostly all small studies, granted there are many of them, and many to corroborate what others found. In fact, there are many more. So while not every single overweight or obese person has these changes, some might.
-I acknowledge BMI is a SCREENING TOOL, and does not actually convey the actual individual's health. It is possible to be of "normal" BMI and still have health issues.
Acronym Key & Other Helpful Reminders
OB = overweight or obese (sorry I know you are going to think of an OB patient, but super sorry, some of the studies use this same acronym, and I got too tired of having to write out "overweight or obese."
NW = normal weight, BMI <25
ppl = people
Underweight = <18.5
Normal weight = 18.5–24.9
Overweight = 25–29.9
Obesity = BMI of 30 or greater
Neural mechanisms associated with food motivation in obese and healthy weight adults. Martin LE1, et. al. Obesity (Silver Spring). 2010 Feb;18(2):254-60. https://www.ncbi.nlm.nih.gov/pubmed/19629052
N = 10 obese adults, mean BMI = 34.0, range = 30.2–38.1 kg/m2)
N = 10 HW adults, mean BMI = 22.1, range = 19.5–24.7 kg/m2
Each group was comprised of five female and five male participants and all participants were right‐handed.
Used fMRI to examine changes in the hemodynamic response in obese and HW adults while they viewed food and nonfood images in premeal and postmeal states.
During the premeal condition, obese participants showed increased activation in anterior cingulate cortex (ACC) and medial prefrontal cortex (MPFC).
The OB grp self-report measures of disinhibition were negatively correlated with premeal ACC activations and self-report measures of hunger were positively correlated with premeal MPFC activations.
After meal: obese participants also showed greater activation in the MPFC.
These results indicate that brain function associated with food motivation differs in obese and HW adults and may have implications for understanding brain mechanisms contributing to overeating and obesity, and variability in response to diet interventions.
***Pearl: evidence that obese ppl feel more motivation to eat food when seen, and less ability to say no to desirable food***
Widespread reward-system activation in obese women in response to pictures of high-calorie foods. Stoeckel LE1, et a.Neuroimage. 2008 Jun;41(2):636-47. doi: 10.1016/j.neuroimage.2008.02.031. Epub 2008 Mar 4.
N = 12 OB
N = 12 NW
Used fMRI to investigate activation of reward-system and associated brain structures in response to pictures of high-calorie and low-calorie foods
Results:
“analysis revealed that pictures of high-calorie foods produced significantly greater activation in the obese group compared to controls in medial and lateral orbitofrontal cortex, amygdala, nucleus accumbens/ventral striatum, medial prefrontal cortex, insula, anterior cingulate cortex, ventral pallidum, caudate, putamen, and hippocampus.”
“high-calorie vs. low-calorie foods, the obese group also exhibited a larger difference than the controls did in all of the same regions of interest except for the putamen.”
“...obese women exhibited greater activation in response to pictures of high-calorie foods in a large number of regions hypothesized to mediate motivational effects of food cues.”
An fMRI study of obesity, food reward, and perceived caloric density. Does a low-fat label make food less appealing? Ng J1, et.al.Appetite. 2011 Aug;57(1):65-72.
https://www.ncbi.nlm.nih.gov/pubmed/21497628
N= 17 obese young women
N = 17 lean young women.
Used fMRI
OB, “showed greater activation in somatosensory... gustatory..., and reward valuation regions in response to intake and anticipated intake of milkshake versus tasteless solution, though there was little evidence of reduced striatal activation.
OB…“also showed greater activation in the Rolandic operculum, frontal operculum, and vmPFC in response to isocaloric milkshakes labeled regular versus low-fat.
Results suggest that hyper-responsivity of somatosensory, gustatory, and reward valuation regions may be related to overeating and that top-down processing influence reward encoding, which could further contribute to weight gain.
***Pearl another good reminder to not use food rewards in kids, it’s not guaranteed to avoid obesity in the kids, but seems reasonable if parents have weight issues they need to be extra careful to not food reward (“reward encode” their brains).***
Relation of reward from food intake and anticipated food intake to obesity: a functional magnetic resonance imaging study. Stice E1, et. al. J Abnorm Psychol. 2008 Nov;117(4):924-35.
https://www.ncbi.nlm.nih.gov/pubmed/19025237
N = with 33 adolescent girls: 7 were classified as obese (>95% BMI)
11 were classified as lean (<50%),
15 participants fell in between these two extremes.
(mean age = 15.7, SD = 0.9).
(Used fMRI)
The “obese adolescent girls showed greater activation bilaterally in the gustatory cortex...and in somatosensory regions... in response to anticipated intake of chocolate milkshake (vs. a tasteless solution) and to actual consumption of milkshake (vs. a tasteless solution)...”
“...obese adolescent girls also showed decreased activation in the caudate nucleus in response to consumption of milkshake versus a tasteless solution, potentially because they have reduced dopamine receptor availability.”
...“hypofunctioning of dopamine-mediated reward circuitry may cause individuals to overeat to compensate for this reward deficit, which through conditioning produces greater anticipatory food reward and heightened development of the somatosensory cortex.”
…“we also found that participants with a higher BMI showed less activation in the striatum in response to food consumption relative to those with a lower BMI, which is consistent with the proposal that obese individuals may experience less phasic dopamine release when consuming food relative to lean individuals.”
***IE anticipation of reward is elevated, but when eat reward is not actually what was anticipated leading to increased intake to get correct dopamine(feel good) response***
#ItIsNotAsGoodAsItLooks
"Results suggest that individuals who show greater activation in the gustatory cortex and somatosensory regions in response to anticipation and consumption of food, but who show weaker activation in the striatum during food intake, may be at risk for overeating and consequent weight gain."
***Pearl: Multipleseparatee neural pathways are at play when it comes to wanting to eat and volume of food that will be then eaten***
#ItIsNOTJustAboutTheVolumeOfFood
#ItsLikelyMoreAboutYourNeuroPathways
Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Stice E1,et.al. Science. 2008 Oct 17;322(5900):449-52.
https://www.ncbi.nlm.nih.gov/pubmed/18927395
Data from two functional magnetic resonance imaging studies
Results, “implies that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.”
Individual differences in reward drive predict neural responses to images of food. Beaver JD1,et.al. J Neurosci. 2006 May 10;26(19):5160-6.
https://www.ncbi.nlm.nih.gov/pubmed/16687507
N = seven females and five males,
Mean age of 22 ± 2.4 years.
Participants were restricted from eating for 2 h before the testing session.
“Using functional magnetic resonance imaging, we report that individual variation in trait reward sensitivity (as measured by the Behavioral Activation Scale) is highly correlated with activation to images of appetizing foods (e.g., chocolate cake, pizza) in a fronto-striatal-amygdala-midbrain network.”
“Our findings demonstrate that there is considerable personality-linked variability in the neural response to food cues in healthy participants and provide important insight into the neurobiological factors underlying vulnerability to certain eating problems (e.g., hyperphagic obesity).”
Decreased caudate response to milkshake is associated with higher body mass index and greater impulsivity. Babbs RK1, et.al. Physiol Behav. 2013 Sep 10;121:103-11.
https://www.ncbi.nlm.nih.gov/pubmed/23562867
Two studies:
N = 25: 13 OB + 12 HW
N = 14
…“conclude that the inverse correlation between BMI and caudate response to milkshake is associated with impulsivity but not food reward. These findings suggest that response to milkshake in the dorsal striatum may be related to weight gain by promoting impulsive eating behavior.”
***IE: they found an association that as BMI goes up, the neurological impulse to eat also goes up***
Obese children show hyperactivation to food pictures in brain networks linked to motivation, reward and cognitive control. Holsen LM, et. al. Int J Obes (Lond). 2010 Oct;34(10):1494-500.
https://www.ncbi.nlm.nih.gov/pubmed/20440296
N: 10 healthy weight children (<85% percentile), and 10 obese children (>95%)
Functional magnetic resonance imaging (fMRI) scans were conducted twice: when participants were hungry (pre-meal) and immediately after a standardized meal (post-meal). During the fMRI scans, the participants passively viewed blocked images of food, non-food (animals) and blurred baseline control.
Conclusion:
"Obese children were hyper-responsive to food stimuli as compared with HW children. In addition, unlike HW children, brain activations in response to food stimuli in obese children failed to diminish significantly after eating. This study provides initial evidence that obesity, even among children, is associated with abnormalities in neural networks involved in food motivation, and that the origins of neural circuitry dysfunction associated with obesity may begin early in life."
***Evidence weight maint, avoidance of weight gain are harder for an obese person...my question would be does this even worsen as BMI increases more and more, or more is this effect harder to reverse the higher the BMI is when a person is on a weight loss “journey”??***
Attentional bias to food images associated with elevated weight and future weight gain: an fMRI study. Yokum S1, et. al. Obesity (Silver Spring). 2011 Sep;19(9):1775-83. doi:
N = 35 adolescent girls lean to obese
“Results indicate that overweight is related to greater attentional bias to food cues and that youth who show elevated reward circuitry responsivity during food cue exposure are at increased risk for weight gain.”
***Maybe why as an adult we want that Birthday cake so badly!!! Despite knowing as Physicians it is store bought, it will be dry, it will leave a weird film in your mouth, it is highly processed, it is bad for our body...yet we want it!! Is it because as a child we did not know these things plus we did not have a developed palate so that cake did actually taste good + cake was eaten during times of happiness --->increased reward circuitry***
#KnowledgeIsPower
***This might be reasoning to argue Against “moderation” and FOR “abstaining from some foods in order to either break these old maladaptive nueologic pathways, or at least build and make stronger healthier pathways allowing us to know we are ok without that food, ever!!” #BOOM
#DidSheJustSAYSTOPEATINGCAKE #DONTYOUTAKEAWAYMYCAKE 😉
Greater corticolimbic activation to high-calorie (HCal) food cues after eating in obese vs. normal-weight adults. Dimitropoulos A1, et al. 2012 Feb;58(1):303-12. doi: 10.1016/j.appet.2011.10.014. Epub 2011 Oct 30.
https://www.ncbi.nlm.nih.gov/pubmed/22063094
N = 22 overweight/obese (OB) and 16 (NW) individuals participated in a fMRI task examining neural response to visual cues of high- and low-calorie foods before and after eating.
Findings: suggest that for OB individuals, HCal food cues show sustained response in brain regions implicated in reward and addiction even after eating. Moreover, food cues did not elicit similar brain response after eating in the NW group suggesting that neural activity in response to food cues diminishes with reduced hunger for these individuals.
***NW people have decreased sensation of reward after eating ---> why they have better satiety after a meal????***
Reward activity in satiated overweight women is decreased during unbiased viewing but increased when imagining taste: an event-related fMRI study. Frankort A1, et. al. Int J Obes (Lond). 2012 May;36(5):627-37. doi: 10.1038/ijo.2011.213. Epub 2011 Nov 8.
https://www.ncbi.nlm.nih.gov/pubmed/22064161
N = 14 OB (mean BMI: 29.8 , ranging from 27-38
15 HW (mean BMI: 21.1, ranging from 18-25
Method:
All women were placed in OCPs to take out differences in hormonal regulation
***Holy heck, now that is thorough!!****
fMRI images taken in the early afternoon (they just ate lunch 1-1.5 hours prior to entering MRI), images of palatable and unpalatable high-calorie and low-calorie food pictures were shown while in the MRI.
First they just showed a mixture of types of aforementioned categories of eating, pictures of foods , no instructions. Then shown images also with instruction to imagine tasting the food too.
***this study design is different in that it was a mix of “healthy” and “unhealthy” food images, not just “unhealthy” desirable foods one after the other.***
Conclusion:
1)The OB grp had a greater reward response when told to imagine tasting the food.
This, “may represent an increased reward response induced by high-calorie palatable food.”
2)During viewing without instructions there was reduced reward activation in the OB participants compared with those with a HW may reflect avoidance of high-calorie palatable food stimuli.
***yes you read that correctly...the OB group had less of a reward response when just seeing food, but then had an increase in reward response when told to imagine the taste of food!!! ***
Theory 1 to explain:
They proposed the reason was the OB ppl are more use to weighing if food healthy or not, if they should or should not eat it, thus decreasing the “reward effect,” but then once the OB ppl actually imagined the taste, it was over the reward effect was more.
More interesting is they think the OB patients avoidance of the images was an automatic thing, not a cognitive effort to avoid the food as if a cognitive effort another part of the brain would have lit up essentially.
Theory 2 to explain
Previous studies have shown that it takes longer for OB ppl to diminish the response to a repeated taste stimulus + other studies have shown a greater effect of sensitization on responding for food in OB children.
***side note: this food sensitization is seen in OB adults and kids, and why it is not always good advice to tell a person/child with OB to snack before going to a party….as you may be making the situation worse***
Therefore, it is possible that the OB ppl were sensitized by the unbiased viewing condition and therefore showed an elevated response during taste imagination, whereas the HW were already diminishing the response to the food after unbiased viewing and therefore showed a decreased response during taste imagination.
Theory 3, this one more of a confounding factor:
“...due to the elapsed time during runs 1 and 2 … approx 35 min of unbiased viewing)...Increased hunger in the OB group could thus have led to the elevated response during taste imagination in this group.”
Dorsal striatum and its limbic connectivity mediate abnormal anticipatory reward processing in obesity.Nummenmaa L1, et. al. PLoS One. 2012;7(2):e31089. doi:
https://www.ncbi.nlm.nih.gov/pubmed/22319604
N = 19 morbidly obese
N= 16 HW
Measured regional brain glucose uptake in subjects with PET during euglycemic hyperinsulinemia, and with (fMRI) while anticipatory food reward was induced by repeated presentations of appetizing and bland food pictures.
findings suggest that enhanced sensitivity to external food cues in obesity may involve abnormal stimulus-response learning and incentive motivation subserved by the dorsal caudate nucleus, which in turn may be due to abnormally high input from the amygdala and insula and dysfunctional inhibitory control by the frontal cortical regions. These functional changes in the responsiveness and interconnectivity of the reward circuit could be a critical mechanism to explain overeating in obesity.
***meaning more reward incentive to eat, and less ability to say no to the food stimulus***
Differential activation of the dorsal striatum by high-calorie visual food stimuli in obese individuals. Rothemund Y1, et. al. Neuroimage. 2007 Aug 15;37(2):410-21. Epub 2007 May 18.
https://www.ncbi.nlm.nih.gov/pubmed/17566768
N = 13 obese
N = 13 HW
Used fMRI and manipulated food motivation by presenting visual food stimuli differing in their caloric content and energy density.
“The results indicate that in obese individuals simple visual stimulation with food stimuli activates regions related to reward anticipation and habit learning”... Additionally, high-calorie food images yielded BMI-dependent activations in regions associated with taste information processing (anterior insula and lateral orbitofrontal cortex), motivation (orbitofrontal cortex), emotion as well as memory functions (posterior cingulate).
Collectively, the results suggest that the observed activation is independent of the physiological states of hunger and satiation, and thus may contribute to pathological overeating and obesity. Some of the observed activations (dorsal striatum, orbitofrontal cortex) are likely to be dopamine-mediated.
***meaning obese people not only have to fight increased hunger hormones, and decreased satiety, but also have areas of the brain lighting up...emotions, memory, taste information, motivation...that didn’t light up for HW people***
fMRI reactivity to high-calorie food pictures predicts short- and long-term outcome in a weight-loss program. Murdaugh DL1, et.al. Neuroimage. 2012 Feb 1;59(3):2709-21.
https://www.ncbi.nlm.nih.gov/pubmed/22332246in
N = 25 obese
Method: followed the ppl before and after a 12-week psychosocial weight-loss treatment and at 9-mo follow-up. fMRI.. "in response to viewing high-calorie food vs. control pictures."
"In those obese individuals who were least successful in losing weight during the treatment, we found greater pre-treatment activation to high-calorie food vs. control pictures in brain regions implicated in reward-system processes.."
"Furthermore, less successful weight maintenance at 9-mo follow-up was predicted by greater post-treatment activation in such brain regions as insula, ventral tegmental area, putamen, and fusiform gyrus."
"In summary, we found that greater activation in brain regions mediating motivational and attentional salience of food cues in obese individuals at the start of a weight-loss program was predictive of less success in the program and that such activation following the program predicted poorer weight control over a 9-mo follow-up period."
***Not sure what this practically means, not like everyone is going to get a fMRI just before a plan to see if higher or lower change of "failing" on the plan. As even if the person shows a "lower chance" is that really a reason to not even try? More I just thought this was interesting.***
J Neurosci. 2010 Sep 29;30(39):13105-9.
Weight gain is associated with reduced striatal response to palatable food.
Stice E1, Yokum S, Blum K, Bohon C.
https://www.ncbi.nlm.nih.gov/pubmed/20881128
N = 26 young OB women
Showed people images of a glass of water or milkshake. No eating 4-6 hrs before imaging
“Results indicated that women who gained weight over a 6 month period”...noted as >2.5% increase in BMI, N = 8 …. “showed a reduction in striatal response to palatable food consumption relative to weight-stable women.”
“Collectively, results suggest that low sensitivity of reward circuitry”... ***IE didn’t get as much reward as would be expected***... “increases risk for overeating and that this overeating may further attenuate responsivity of reward circuitry in a feedforward process.
***overeating in OB people contributes to neuro changes that make it easier to continue to gain***
***This study was limited in a couple ways, it more just is another small one amongst others that show these neuro changes in response to increased weight gain/overeating in those who are OB***
Neuroimage. 2012 Oct 15;63(1):415-22.
Nucleus accumbens response to food cues predicts subsequent snack consumption in women and increased body mass index in those with reduced self-control. Lawrence NS1, Hinton EC, Parkinson JA, Lawrence AD.
fMRI
“Food cue related activity in the nucleus accumbens was related to subsequent snack food consumption”…BUT… “it was associated with increased BMI in individuals reporting low self-control” (People who felt they had control of eating, didn’t gain
“However, both nucleus accumbens activation and snack food consumption were unrelated to self-reported hunger, or explicit wanting and liking for the snack.”
"Food cue reactivity in the ventromedial prefrontal cortex" led to "hunger, but not with consumption."
“Our data provide support for theoretical models that advocate a 'dual hit' of increased incentive salience attribution to food cues and poor self-control in determining vulnerability to overeating and overweight.”
***I wished they also looked at the area that has to do with ‘self-control” as I wonder if these same people did have decreased activation in the areas that allow you to say “no,” (ie “ self-control”).***
Neuroimage. 2010 Oct 1;52(4):1696-703. Body mass correlates inversely with inhibitory control in response to food among adolescent girls: an fMRI study. Batterink L1, Yokum S, Stice E.
N = 39 adolescent girls (M age = 15.7)
Used fMRI
"Results suggest that hypofunctioning of inhibitory control regions and increased response of food reward regions are related to elevated weight."
***IE decreased ability to say no to food, while also having another area activate looking for a reward***
Others I didn't even go through!!
Neseliler S, Han JE, Dagher A. The use of functional magnetic resonance imaging in the study of appetite and obesity. In: Harris RBS, ed. Appetite and food intake: central control. Boca Raton, FL: The British Institute of Radiology.; 2017.
| Geha P, Cecchi G, Todd Constable R, Abdallah C, Small DM. Reorganization of brain connectivity in obesity. Hum Brain Mapp 2017; 38: 1403–20. doi: https://doi.org/10.1002/hbm.23462 |
García-García I, Jurado MÁ, Garolera M, Marqués-Iturria I, Horstmann A, Segura B, et al. Functional network centrality in obesity: a resting-state and task fMRI study. Psychiatry Res 2015; 233: 331–8. doi: https://doi.org/10.1016/j.pscychresns.2015.05.017
Berthoud HR. Metabolic and hedonic drives in the neural control of appetite: who is the boss? Curr Opin Neurobiol 2011; 21: 888–96. doi: https://doi.org/10.1016/j.conb.2011.09.004
| Page KA, Seo D, Belfort-DeAguiar R, Lacadie C, Dzuira J, Naik S, et al. Circulating glucose levels modulate neural control of desire for high-calorie foods in humans. J Clin Invest 2011; 121: 4161–9. doi: https://doi.org/10.1172/JCI57873 |
| Kroemer NB, Krebs L, Kobiella A, Grimm O, Vollstädt-Klein S, Wolfensteller U, et al. (Still) longing for food: insulin reactivity modulates response to food pictures. Hum Brain Mapp 2013; 34: 2367–80. doi: https://doi.org/10.1002/hbm.22071 |
Wallner-Liebmann S, Koschutnig K, Reishofer G, Sorantin E, Blaschitz B, Kruschitz R, et al. Insulin and hippocampus activation in response to images of high-calorie food in normal weight and obese adolescents. Obesity 2010; 18: 1552–7. doi: https://doi.org/10.1038/oby.2010.26
Grosshans M, Vollmert C, Vollstädt-Klein S, Tost H, Leber S, Bach P, et al. Association of leptin with food cue-induced activation in human reward pathways. Arch Gen Psychiatry 2012; 69: 529–37. doi: https://doi.org/10.1001/archgenpsychiatry.2011.1586
Batterham RL, ffytche DH, Rosenthal JM, Zelaya FO, Barker GJ, Withers DJ, et al. PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans. Nature 2007; 450: 106–9. doi: https://doi.org/10.1038/nature06212
Simon JJ, Wetzel A, Sinno MH, Skunde M, Bendszus M, Preissl H, et al. Integration of homeostatic signaling and food reward processing in the human brain. JCI Insight 2017; 2. doi: https://doi.org/10.1172/jci.insight.92970
Lopez RB, Milyavskaya M, Hofmann W, Heatherton TF. Motivational and neural correlates of self-control of eating: a combined neuroimaging and experience sampling study in dieting female college students. Appetite2016; 103: 192–9. doi: https://doi.org/10.1016/j.appet.2016.03.027
Endnotes:
This is not an exhaustive review. Each article was screened for what seem to be the most interesting points. For a more depth analysis, please go to the original source and read away.
And as always this website is meant for educational/informational purposes only. It is not here to treat any medical issues.
Thank you for taking the time to compile and summarize these studies. Very useful information.