Effects of Images Following Beverage Ingestion on Brain Activation
| Status: | Withdrawn |
|---|---|
| Conditions: | Obesity Weight Loss |
| Therapuetic Areas: | Endocrinology |
| Healthy: | No |
| Age Range: | 20 - 35 |
| Updated: | 4/21/2016 |
| Start Date: | August 2015 |
| End Date: | December 2016 |
The primary purpose of this study is to quantify activation of regions of the brain
associated with taste, appetite, and reward after viewing high sugar and high fat (HS/HF)
images compared to control images following ingestion of (1) an artificially sweetened
solution, (2) a sucrose solution, and (3) a tasteless control solution in normal weight vs.
obese women. This is a repeated measures study design; hence, data are collected on three
days corresponding to the three solutions. Body mass index (BMI) is a between subjects
measure.
1. After consuming an artificially sweetened solution and a sucrose solution compared to a
tasteless solution, viewing HS/HF food images vs. control images will result in higher
activation of taste pathways (frontal operulum and anterior insula (FO/AI)) in the
brain.
2. After consumption of a sucrose solution compared to an artificially sweetened solution
and a tasteless solution, viewing HS/HF food images vs. control images will result in
higher activation of regions of the brain associate with appetite (hypothalamus).
3. After consumption of a sucrose solution compared to an artificially sweetened solution
and a tasteless solution, viewing HS/HF food images vs. control images will result in
higher activation of regions of the brain associated with reward [amygdala, anterior
cingulate cortex (ACC), Orbitalfrontal Cortex (OFC), and ventral tegmental area (VTA),
striatum, insula] in obese but not normal weight women. After consuming an artificially
sweetened solution compared to a tasteless solution, viewing HS/HF images vs. control
images will result in no differences in activation of reward pathways of the brain.
associated with taste, appetite, and reward after viewing high sugar and high fat (HS/HF)
images compared to control images following ingestion of (1) an artificially sweetened
solution, (2) a sucrose solution, and (3) a tasteless control solution in normal weight vs.
obese women. This is a repeated measures study design; hence, data are collected on three
days corresponding to the three solutions. Body mass index (BMI) is a between subjects
measure.
1. After consuming an artificially sweetened solution and a sucrose solution compared to a
tasteless solution, viewing HS/HF food images vs. control images will result in higher
activation of taste pathways (frontal operulum and anterior insula (FO/AI)) in the
brain.
2. After consumption of a sucrose solution compared to an artificially sweetened solution
and a tasteless solution, viewing HS/HF food images vs. control images will result in
higher activation of regions of the brain associate with appetite (hypothalamus).
3. After consumption of a sucrose solution compared to an artificially sweetened solution
and a tasteless solution, viewing HS/HF food images vs. control images will result in
higher activation of regions of the brain associated with reward [amygdala, anterior
cingulate cortex (ACC), Orbitalfrontal Cortex (OFC), and ventral tegmental area (VTA),
striatum, insula] in obese but not normal weight women. After consuming an artificially
sweetened solution compared to a tasteless solution, viewing HS/HF images vs. control
images will result in no differences in activation of reward pathways of the brain.
In this pilot study, we will use functional magnetic resonance imaging (fMRI) to determine
the effects of high calorie visual food cues [i.e. images of foods that are high in both
sugar and fat (HS/HF), such as ice cream] on activation of taste, appetite, and reward
pathways in the brain following the separate ingestion of (1) an artificial sweetened
solution (2) a sucrose solution and (3) a tasteless solution in obese individuals. Obesity
rates are high among US adults with 33.8% of adults having a BMI of 30 or greater (1). The
prevailing belief is that homeostatic systems are in place to monitor energy homeostasis.
Sugar sweetened beverages appear to alter the homeostatic systems so that (1) metabolic
feedback signals do not function correctly or as intended (2), as little or no dietary
compensation is seen with energy from beverages (3), or (2) sweet and savory foods (sugar
sweetened beverages) override the system (i.e. hedonics) (2). Epidemiological data suggest
Americans are consuming 20-25% of their energy in beverage form which equates to ~430-535
kcal/day (3, 4). In most studies, sugar sweetened beverage intake has been shown to increase
weight (5, 6). While limited data are available, a meta-analysis in humans demonstrates that
the inclusion of aspartame compared to sugar reduces energy intake (7). A prospective study
found that weight loss maintainers utilize artificial sweeteners more than normal weight
individuals (8). This suggests artificial sweeteners may be a method to promote weight loss
in obese individuals. Public policy on sugar sweetened beverages is starting to be
reexamined, however, it is currently unknown what effect sugar sweetened beverage intake and
artificial sweetened solutions have on (1) taste, appetite, and reward regions of the brain
and (2) food cravings and related brain activation, among obese vs. normal weight
individuals. The aim of this study is to provide important data on why obese individuals
continue to consume sugar-sweetened beverages despite the associated negative health
outcomes. We hypothesize that this consumption is due to sugar sweetened beverages, but not
artificial sweeteners, activating reward pathways of the brain (hedonics).
Sucrose and artificial sweetners Previously it has been found that there is an altered
hypothalamic response to glucose ingestion in obese humans (9). In obese humans, brain
activation seems impaired; i.e., it was lower and delayed compared to lean subjects. This
study lacked a functional contrast and had higher noise and less accuracy than current fMRI
blood-oxygen-level-dependent (BOLD) technology and only the hypothalamus was analyzed (9).
The current study and future studies from this pilot and feasibility work will further
determine if dietary sugar responses are differentially regulated in obese individuals
possibility contributing to the over consumption of sugar sweetened beverages in obese
adults.
Frank et al. concluded that taste pathways are activated with sucralose and sucrose taste in
younger normal weight women (10). Only sucrose recruited reward pathways but appetite
pathways were not documented due to either lack of significance or examination (10). This
study will confirm beverage ingestion opposed to tasting evokes a similar reward response
and also examines appetite and reward pathways in obese individuals.
The effects of caloric vs. non caloric sweetener on taste activation were previously
examined in normal weight men (11). During the non-caloric solution tasting, 2 caloric
tastants were also consumed. These caloric tastants could invoke differential cephalic phase
responses altering the results (12). Consumption of the artificial sweetener or the caloric
solution increased activation of the insula, middle OFC, lateral OFC and amygdala. With the
artificial sweetener, there was greater activation of the OFC (11). Next, the effects of
sweet taste (2.4 mL) in younger male and female diet soda drinkers was examined (13). Water
was utilized as the rinse and baseline for the comparison between diet and regular soda. In
these persons, higher right orbitalfrontal cortex brain activation response in non-caloric
compared to caloric solution was observed (13). These previous studies utilized only normal
weight participants and taste to examine for the effects of artificial sweeteners on brain
response. The current study examines obese individuals and solution ingestion to observe
differences in brain activation. Overall there are differential brain responses to caloric
vs. non-caloric sweetener in normal weight individuals thus previously authors suggested
that more research needs to be performed as to the effectiveness of artificial sweeteners at
decreasing energy intake.
Obesity Women were shown food picture cues of high energy foods. The high energy foods
produced significantly greater activation in the brain reward regions in obese compared to
normal weight control women (14). Differences between groups included ACC, VTA, nucleus
accumbens (NAc), amygdala, ventral pallidum (Vent Pall), Caudate, and Putamen (14).
Postmeal, obese individuals, but not normal weight individuals, increase activation of the
putamen (part of striatum) and amygdala suggesting these regions may play a role in
overeating (15) which is why these regions are incorporated into the current study
hypothesis. These cross-sectional studies are important as previously Murdaugh et. al (16)
found that obese individuals that were not successful at short term weight loss or longer
term weight loss maintenance had greater activation of reward pathway brain regions. While
speculative, artificial sweeteners may reduce cravings by not activating reward pathways
especially in obese persons. This grant will help provide pilot data to further elucidate
this important question.
the effects of high calorie visual food cues [i.e. images of foods that are high in both
sugar and fat (HS/HF), such as ice cream] on activation of taste, appetite, and reward
pathways in the brain following the separate ingestion of (1) an artificial sweetened
solution (2) a sucrose solution and (3) a tasteless solution in obese individuals. Obesity
rates are high among US adults with 33.8% of adults having a BMI of 30 or greater (1). The
prevailing belief is that homeostatic systems are in place to monitor energy homeostasis.
Sugar sweetened beverages appear to alter the homeostatic systems so that (1) metabolic
feedback signals do not function correctly or as intended (2), as little or no dietary
compensation is seen with energy from beverages (3), or (2) sweet and savory foods (sugar
sweetened beverages) override the system (i.e. hedonics) (2). Epidemiological data suggest
Americans are consuming 20-25% of their energy in beverage form which equates to ~430-535
kcal/day (3, 4). In most studies, sugar sweetened beverage intake has been shown to increase
weight (5, 6). While limited data are available, a meta-analysis in humans demonstrates that
the inclusion of aspartame compared to sugar reduces energy intake (7). A prospective study
found that weight loss maintainers utilize artificial sweeteners more than normal weight
individuals (8). This suggests artificial sweeteners may be a method to promote weight loss
in obese individuals. Public policy on sugar sweetened beverages is starting to be
reexamined, however, it is currently unknown what effect sugar sweetened beverage intake and
artificial sweetened solutions have on (1) taste, appetite, and reward regions of the brain
and (2) food cravings and related brain activation, among obese vs. normal weight
individuals. The aim of this study is to provide important data on why obese individuals
continue to consume sugar-sweetened beverages despite the associated negative health
outcomes. We hypothesize that this consumption is due to sugar sweetened beverages, but not
artificial sweeteners, activating reward pathways of the brain (hedonics).
Sucrose and artificial sweetners Previously it has been found that there is an altered
hypothalamic response to glucose ingestion in obese humans (9). In obese humans, brain
activation seems impaired; i.e., it was lower and delayed compared to lean subjects. This
study lacked a functional contrast and had higher noise and less accuracy than current fMRI
blood-oxygen-level-dependent (BOLD) technology and only the hypothalamus was analyzed (9).
The current study and future studies from this pilot and feasibility work will further
determine if dietary sugar responses are differentially regulated in obese individuals
possibility contributing to the over consumption of sugar sweetened beverages in obese
adults.
Frank et al. concluded that taste pathways are activated with sucralose and sucrose taste in
younger normal weight women (10). Only sucrose recruited reward pathways but appetite
pathways were not documented due to either lack of significance or examination (10). This
study will confirm beverage ingestion opposed to tasting evokes a similar reward response
and also examines appetite and reward pathways in obese individuals.
The effects of caloric vs. non caloric sweetener on taste activation were previously
examined in normal weight men (11). During the non-caloric solution tasting, 2 caloric
tastants were also consumed. These caloric tastants could invoke differential cephalic phase
responses altering the results (12). Consumption of the artificial sweetener or the caloric
solution increased activation of the insula, middle OFC, lateral OFC and amygdala. With the
artificial sweetener, there was greater activation of the OFC (11). Next, the effects of
sweet taste (2.4 mL) in younger male and female diet soda drinkers was examined (13). Water
was utilized as the rinse and baseline for the comparison between diet and regular soda. In
these persons, higher right orbitalfrontal cortex brain activation response in non-caloric
compared to caloric solution was observed (13). These previous studies utilized only normal
weight participants and taste to examine for the effects of artificial sweeteners on brain
response. The current study examines obese individuals and solution ingestion to observe
differences in brain activation. Overall there are differential brain responses to caloric
vs. non-caloric sweetener in normal weight individuals thus previously authors suggested
that more research needs to be performed as to the effectiveness of artificial sweeteners at
decreasing energy intake.
Obesity Women were shown food picture cues of high energy foods. The high energy foods
produced significantly greater activation in the brain reward regions in obese compared to
normal weight control women (14). Differences between groups included ACC, VTA, nucleus
accumbens (NAc), amygdala, ventral pallidum (Vent Pall), Caudate, and Putamen (14).
Postmeal, obese individuals, but not normal weight individuals, increase activation of the
putamen (part of striatum) and amygdala suggesting these regions may play a role in
overeating (15) which is why these regions are incorporated into the current study
hypothesis. These cross-sectional studies are important as previously Murdaugh et. al (16)
found that obese individuals that were not successful at short term weight loss or longer
term weight loss maintenance had greater activation of reward pathway brain regions. While
speculative, artificial sweeteners may reduce cravings by not activating reward pathways
especially in obese persons. This grant will help provide pilot data to further elucidate
this important question.
Inclusion Criteria:
- Female
- 20-35 years old (inclusive)
- Weigh less than 350 lbs
- Weight stable (>±5 kg in the last 6 months).
- Body mass index (BMI) between 20-25 kg/m2 or 30-35 kg/m2.
- Willing to fast for 10 hours prior to examination.
- Right handed.
Exclusion Criteria:
- Diagnosis (by self report) of diabetes
- Diagnosis (by self report) of neurological condition
- Current or past alcohol or drug abuse problem.
- Smoking
- Have internal metal medical devices including cardiac pacemakers, aortic or cerebral
aneurysm clips, artificial heart valves, ferromagnetic implants, shrapnel, wire
sutures, joint replacements, bone or joint pins/rods/screws/clips, metal plates,
metal fragments in your eye, or non-removable metal jewelry such as rings.
- Unable or unwilling to complete the imaging procedures for the duration of the MRI
scan due to claustrophobia or other reason.
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