Added Sugar Intake and Brain Structure and Function
Conditions: Child Development
Sponsor: University of Kansas Medical Center

KUMC – HRPP- 03/12/2015 
 
Page 1 of 18
 
 
 
 
University of Kansas Medical Center 
RESEARCH PROTOCOL INVOLVING HUMAN SUBJECTS 
TEMPLATE WITH GUIDANCE 
 
Version date: 2/19/2024 
Principal Investigator: Holly Hull, PhD 
Study Title: Added sugar intake and brain structure and function 
Co- Investigator(s): Laura Martin, PhD 
 
 
 
I. 
Purpose, Background and Rationale 
A. Aim and Hypotheses 
1. The first 1000 days post-conception have been characterized as a critical window for 
brain development, during which much of the brain’s growth, structure, and function is 
set1. Key nutrients from maternal and infant dietary intake fuels these maturational 
processes, thus providing the potential underlying foundation for later cognitive 
development. Brain growth and development is particularly sensitive to poor nutrition 
during this window2; previous work detailed the effects of deficiencies in the status of 
folic acid, choline, iron, zinc, iodine, and long chain polyunsaturated fatty acids3. While 
nutrient deficiencies have been studied, less is known about the impact and timing of 
excess nutrition in relation to cognitive development4. 
 
2. Aim 1: Determine the relationship between added sugars (% calories) intake during 
pregnancy and infancy/toddlerhood (birth to 24 months) on brain structure and function. 
Hypothesis: added sugars intake will be negatively related to brain structure 
(hippocampal volume) and function (resting state functional connectivity and P3 
amplitude). We will explore how sex modifies this relationship. 
 
Aim 2: Determine the relationship between fructose (% calories) consumption during 
pregnancy and infancy/toddlerhood (birth to 24 months) on brain structure and function. 
Since some studies reported relationships with fructose independently, we will explore 
relationships with fructose separately. 
Hypothesis: fructose intake will be negatively related to brain structure (hippocampal 
volume) and function (resting state functional connectivity and P3 amplitude). We will 
explore how sex modifies this relationship. 
 
B. Background and Significance 
1. Study Significance: Brain development is a protracted process that begins in early 
gestation and continues into late adolescence. By the 8th week in gestation, the basic 
brain structures and the central nervous system are formed, and neuron production and 
migration are started5. From the 8th week until delivery, the cortical and subcortical 
structures form, including the major fiber pathways. In the third trimester, myelination 

KUMC – HRPP- 03/12/2015 
 
Page 2 of 18
 
 
 
 
and growth of the hippocampus increases rapidly until around18-24 months of age1. 
Rapid brain growth continues with a four-fold increase in brain size during early 
childhood, reaching 90% of full brain size by six years old. The first 1000 days post- 
conception have been characterized as a critical window for brain development, during 
which much of the brain’s growth, structure, and function is set1. During this time, the 
brain is particularly vulnerable to nutrient deficiencies, and such deficiencies can have a 
severe impact on cognitive development2,3. Promoting optimal development and 
cognition has clear individual benefits, but also has substantial economic impact6-8. The 
prevention of later developmental deficits is estimated to save $6B annually9,10. 
 
The concept that early development disproportionately affects later outcomes is widely 
accepted in the developmental sciences11-15, and the nutrition literature16-22. Thus far, 
most research has focused on key early life nutrient deficiencies2,4,16. Prenatal and 
postnatal long-chain polyunsaturated fatty acids (LCPUFA)23 docosahexaenoic acid (DHA) 
and arachidonic acid (AA), iron24-27, and zinc28-30 promote brain structure development, 
myelination, neurogenesis, neuronal migration, synaptogenesis and production of 
neurotransmitters. Iron deficiency is related to decreased language skills and fine-motor 
skills31,32 and supplementing iron, copper, and zinc improved attention measures33. 
Nutrient intake strongly supports the normal development of underlying neural structure 
and function that is critical for later cognitive development. While the effect of nutrient 
deficiencies is reported, the impact of excess nutrition is less studied. 
 
2. The impact of excess nutrient intake on brain development and function has garnered far 
less consideration compared to nutrient deficiencies. Data suggest that added sugars 
intake during pregnancy, infancy, and toddlerhood may interfere with the early formation 
of the brain structures that contribute to learning and memory34. Fructose is of particular 
interest here, as it is one of six monosaccharides represented in added sugars35, and is 
found in the diet as a sweetener commonly added to foods during processing in the form 
of high fructose corn syrup (HFCS) and sucrose, a disaccharide made of a glucose bound 
to a fructose36. HFCS is a low-cost sweetener commonly used in sugar sweetened 
beverages (SSB). The effect of fructose may be due to fructose metabolism not being 
tightly regulated like glucose metabolism36 leading to oxidative stress and an 
inflammatory response37. 
 
3. Literature Review: The literature suggests that added sugars intake in early life exceeds 
recommendations. Added sugars are defined as sugars and syrups added as an 
ingredient to foods during processing, preparation, or at the table, while total sugars 
include added sugars plus sugar naturally occurring in foods (e.g., fruit and milk)35. One 
added sugar in particular, fructose (e.g., high fructose corn syrup), has been investigated 
as a driver of the negative relationships reported between added sugars and health 
outcomes38. Pregnant women are recommended to consume <10% of calories/day from 
added sugars, whereas infants and toddlers (<24 months) are recommended to consume 
no added sugars39. Even so, pregnant women are reported to consume 15.8% of 
calories/day from added sugars40, and 6- to 24-month-olds to consume 1.4-7.2% of 
calories/day from added sugars41,42. Data in pregnant women and infants and toddlers 

KUMC – HRPP- 03/12/2015 
 
Page 3 of 18
 
 
 
 
found 70% of pregnant women39 and 97.3% of infants and toddlers consumed added 
sugars in each day43. While this is concerning given the relationships between added 
sugars intake and chronic disease development44-46, evidence is growing that early added 
sugars intake is also related to diminished cognitive function47.  
 
In adolescent rodents and humans, added sugars (including fructose) negatively 
impacted the hippocampal structure and connectivity48, increased hippocampal 
inflammation49, and impaired hippocampal-dependent memory50. Human data from the 
prenatal period and infancy are lacking, but one published study34 found greater maternal 
prenatal consumption of added sugars was related to poorer cortical organization, and 
greater maternal fructose intake during lactation was related to lower scores in the 
offspring on the Bayley-III Scales of Infant Development at 24 months old51. These 
preliminary studies are consistent with the hypothesis that added sugars intake during 
pregnancy, infancy, and toddlerhood may interfere with the development and early 
formation of neural circuits34, perhaps owing to increased oxidative 
stress/inflammation49,52,53 or decreased production of brain derived neurotrophic factor 
(supports brain development and circuit formation)52,54, leading to suboptimal cognitive 
outcome. This hypothesis was further supported by preliminary data from our own 
laboratory, which found that added sugars intake during the first two years of life was 
related to lower scores on standardized cognitive tests from 18 months to 6 years of age. 
The purpose of this proposal is to understand the relationship between maternal and 
early offspring (birth to 24 months) added sugars intake and brain structure and function 
at 5-6 years of age. 
 
In 7–11-year-old children48, increased intake of fructose and glucose was associated with 
increased right hippocampal CA2/3 subfield volume, and increased fructose intake was 
associated with mean diffusivity in the right cingulate-prefrontal cortex connections. This 
suggests an impact on hippocampal structure related to an increase in hippocampal 
inflammation. In the Project Viva cohort55, greater maternal prenatal intake of SSB was 
related to poorer offspring global intelligence. Greater maternal prenatal added sugars 
consumption was also related to lower newborn gray matter at 3 weeks old, including 
areas for later cognitive functioning34, suggesting an impact on formation of dendrites 
and synapses. This cohort was tested again at 24 months using the Bayley-III Scales of 
Infant Development56. Greater maternal SSB intake was related to lower scores on the 
Bayley-III. These data provide evidence for a relationship between maternal added 
sugars intake and the brain structures that are the foundation for future cognitive 
development. 
C. Rationale 
1. As described above, there is a growing body of evidence to suggest that excess added 
sugar intake negatively affects cognition. 
2. The innovation for this proposal involves a shift with respect to the theoretical approach 
around the relationship between cognition and nutrition. While the impact of key nutrient 
deficiencies on cognition is well documented, the relationship between excess intake (i.e., 
added sugars) and cognitive development has not been previously studied. Further, data 
are lacking on exposure timing relative to the impact on cognition and brain 

KUMC – HRPP- 03/12/2015 
 
Page 4 of 18
 
 
 
 
development. This proposal will investigate three time periods that are well established 
windows of brain development that are sensitive to nutrient exposures: the prenatal, 
infancy, and toddlerhood time periods. 
3. n/a – this study is not designed to improve the diagnosis or treatment of a disease 
II. 
Research Plan and Design 
A. Study Objectives: This purpose of this study is to fill a gap in the literature by providing an 
understanding of the relationship between added sugars and fructose intake during sensitive 
windows to brain structure and function. This project is unique because we can determine 
the effect of added sugars during three different times: pregnancy, infancy, and toddlerhood. 
 
Primary Aims: 
Aim 1: Determine the relationship between added sugars (% calories) intake during 
pregnancy and infancy/toddlerhood (birth to 24 months) on brain structure and function. 
 
Aim 2: Determine the relationship between fructose (% calories) consumption during 
pregnancy and infancy/toddlerhood (birth to 24 months) on brain structure and function. 
 
Secondary Aims: 
Secondary Aim 1: Determine the relationship between added sugars (% calories) intake 
during pregnancy and infancy/toddlerhood (birth to 24 months) on cognition. 
 
B. Study Type and Design: This is a non-interventional, observational study. 
 
Added sugar intake during pregnancy will be assessed using dietary data collected between 
12-20 wks gestation using the using the National Cancer institute (NCI) DHQ-II food 
frequency questionnaire (FFQ) or three 24-hour dietary recalls. 
 
Offspring dietary intake was collected at 2 weeks and at 6, 12, and 24 months by one 
multiple-pass 24-hour dietary recall administered to the child’s caregiver and collected by 
trained research staff. 
 
For the present study, we will collect three total dietary recalls: two weekday and one on the 
weekend. 
 
Brain structure and function will be measured using MRI and EEG assessments. Cognition will 
be measured using dimensional change card sort task and Peabody picture vocabulary test. 
 
C. Sample size, statistical methods, and power calculation 
1. n/a – randomization will not be used 
2. n/a – study will not be blinded 
3. The present study is pilot. The planned sample size is 45 subjects. 
D. Subject Criteria (See Vulnerable Populations appendix, if applicable): Participants 
who were previously enrolled in the ADORE GAINS study will be invited to participate in 
the present study when they are 5-6 years old. Participants will be both male and female 
and English or Spanish speaking. 
1. Inclusion criteria: Participated in ADORE GAINS. Age 5-6. 
2. Exclusion criteria: children who have received an autism diagnosis (per parent report) 
3. Withdrawal/Termination criteria: n/a 

KUMC – HRPP- 03/12/2015 
 
Page 5 of 18
 
 
 
 
4. Subjects may enter another research study while participating in this research study, as 
this study is observational only. 
 
E. Specific methods and techniques used throughout the study 
1. Laboratory tests: n/a 
2. Study Procedures: 
Dietary assessment: Three multiple-pass 24-hour dietary recall will be administered to 
the child/child’s caregiver and collected by trained research staff to characterize energy 
and nutrient intake of the child. 24-hour recalls accurately estimate dietary intake57,58 
and contain less reporting bias than diet records57,59. The recalls are entered into the 
Nutrition Data System for Research (NDS-R, version 2021, Minneapolis, MN) for macro- 
and micronutrient analysis including added sugars. 
 
Dimensional Change Card Sort (DCCS) task. This test is based on the basic paradigms of 
discrimination learning65,66, which was a focus of our laboratory’s research program 
during the 1990s67,68. This particular task is administered according to the protocol 
published by69, and has also been used in other nutritional studies, as well as in our 
research program on the development of attention in preschoolers70. Essentially, 
participants are presented with stimuli that can be sorted on various dimensions (e.g., 
shape or color). They are asked to sort the stimuli on one dimension (thus providing a 
measure of performance on that ability) but then are asked to reverse (i.e., “switch”) the 
rule. At that point, they must inhibit the previously activated rule in order to perform 
correctly under the new rules. For this particular task, children are presented a game in 
which they must sort 7 “red bunny” cards and 7 “blue car” cards into one of two boxes. 
One box is “labeled” with a red car and the other with a blue bunny. The child is asked 
to play either the “color game,” with red bunnies sorted (face down) into the “red car” 
box; blue cars sorted (face down) into the “blue bunny” box; or they are asked to play 
the “shape game,” with blue cars sorted (face down) into the “red car” box and red 
bunnies sorted (face down) into the “blue bunny” box. The protocol is to administer two 
practice trials, and then 6 trials with varying levels of support as needed (i.e., 
instructions may be repeated, or cards may be identified as a scaffold for the production 
of strategies) although the answers are never given to the child. If children perform 5 
out of 6 trials correctly, the game is switched to the opposite (i.e., shape-to-color or 
color-to-shape). Should the child successfully negotiates the switch, the task would 
proceed with the “border version” of the task, where half of 12 sorting cards have a black 
border around the picture, and the child is asked to play “color game” when the card has 
a black border and “shape game” when it does not; here, there are 12 trials, but no 
game-switch phase. Correct responses are recorded for each phase, and performance is 
also qualitative characterized as 0 (fail pre-switch phase), 1 (pass pre-switch, fail post- 
switch), 2 (pass the pre- and post-switch phases, but fail border phase), and 3 (pass all 
phases). The DCCS task will take approximately 15 minutes. 
 
Peabody Picture Vocabulary Test (PPVT). Receptive vocabulary will be assessed using the 
PPVT-4. The PPVT-4 is a nationally standardized assessment of receptive vocabulary that 
has been shown to be fair with respect to cultural and economic status71. In this task, 

KUMC – HRPP- 03/12/2015 
 
Page 6 of 18
 
 
 
 
participants are shown pages depicting 4 pictorial choices. For each page, the examiner 
says a word, and the participant indicates, either by pointing or by stating a reference 
number, which picture best matches the word. Administration is simple and 
straightforward. The PPVT-4 yields a standard score normed with a mean of 100 and a 
standard deviation of fifteen. It takes about 30 minutes to complete. 
 
If one or both cognitive tests (DCCS and PPVT) are not completed at the second study 
visit for any reason, such as subject fatigue, the study team can ask the family if they 
are willing to come back at a later date for completion of the test(s). Compensation of 
an additional $50 would be provided if an additional visit is completed. 
 
Dual energy x-ray absorptiometry (DXA) scan: (Prodigy, Madison, WI, encore software 
version 13.60) will be used to measure body composition and regional AT distribution. 
The DXA is located within the Dietetics & Nutrition Clinic inside the Smith West building 
at KUMC. Using specific anatomic landmarks as previously described, regions including 
the arms, legs and trunk will be demarcated72. Calculations for FM in each region and 
summed for regions comprising the central (trunk) and peripheral (arms plus legs) will 
be completed. If a child moves during the scan the scan may need to be re-done but no 
more than 2 scans will be given over the duration of the study. The DXA scan takes 
about 10 minutes. 
 
If there is movement during the first DXA scan and the study team and/or parent does 
not think the child will lay still for a second scan, the family may be asked if they would 
come back a different day to complete a second DXA. As stated above, no more than 2 
scans will be given over the duration of the study. Compensation of an additional $50 
would be provided if an additional visit to repeat the DXA scan is completed. 
 
Anthropometry: Body weight will be assessed on a same calibrated scale (Detetco Scales, 
Webb City, MO). Standing height will be measured using a wall mounted stadiometer 
(Accu-Hite, Seca Corp, Hanover, MD). Subjects will remove shoes and be centered on the 
stadiometer. Height will be recorded to the nearest 0.1 cm. Two measurements will be 
taken and the average will be recorded. The measurements take about 5 minutes to 
complete. 
 
Skinfolds: Six skinfolds will be measured to represent AT distribution in order to compare 
to larger trials that do not have DXA. Dr. Hull has published using these methods to 
assess infant FM distribution73 and it has been argued skinfolds are a valid metric of 
regional FM74. All measurements will be collected using standardized procedures to our 
Laboratory and will take place on the same day as the body composition assessment by 
DXA using standardized procedures. All skinfolds will be identified using anatomical 
landmarks and taken on the right side of the body using Lange calipers (Beta 
Technology, Santa Cruz, CA). Skinfolds will be taken in order from head to toe and then 
repeated in that same order. If two skinfold measurements differ by more than 1 mm, a 
third measurement will be taken. The two measurements within 1 mm will be averaged 
and used for analysis. Biceps and triceps skinfolds will be measured at the midline of the 

KUMC – HRPP- 03/12/2015 
 
Page 7 of 18
 
 
 
 
anterior and posterior surface of the arm, respectively, on the mid-point between 
acromial process of the scapula and olecranon process of the ulna. Subscapular skinfold 
will be measured at the lower angle of the scapula. Suprailiac skinfold will be measured 
anteriorly to the midaxillary line and superiorly to the iliac crest, along the natural 
cleavage of the skin. The thigh skinfold will be measured at the mid-point between 
patella (kneecap) and inguinal crease at the anterior surface of the thigh. Flank skinfold 
will be measured immediately above the iliac crest at the mid-axillary line. Central FM 
will be calculated by adding the subscapular, suprailiac and flank skinfolds and dividing 
by two. Peripheral FM will be calculated by adding the thigh, biceps and triceps skinfolds 
and dividing by three. The skinfolds take about 15 minutes to complete. 
 
If the anthropometric and/or skinfold measurements are not completed at the second 
study visit, for any reason, the study team can ask the family if they are willing to come 
back at a later date for completion of the measurements. Compensation of an additional 
$50 would be provided if an additional visit is completed. 
 
3. Measuring height and weight are part of usual care for this population. No other 
procedures are part of usual care. None of the tests or measurements will be billed to 
insurance. 
4. n/a – no tissue samples will be collected 
5. Timeline: 
Procedure 
Study Visit 2 
Questionnaires 
x 
Diet Recall (3 total) 
x 
MRI acclimation scan 
MRI scan 
EEG 
Card sorting game 
x 
Picture vocabulary test 
x 
Anthropometry & skinfolds 
x 
DXA scan 
x 
 
F. Risk/benefit assessment: No appreciable risk of physical, psychological, social, legal or 
other harm is expected. 
Physical risk: The DXA exposes the subject to a small amount of radiation during the 
scan. One DXA scan is equivalent to approximately 2 hours of natural background 
radiation. To minimize radiation exposure, no more than two DXA scans will be 
completed for this study. Subjects may feel a light pinch when calipers are used to 
measure skinfolds. Study staff will be adequately trained and use gentle techniques to 
minimize discomfort.  
1. Psychological risk: Some children may get tired during the cognition tests and not 
perform at their best 
2. Social risk: n/a 
3. Economic risk: n/a 

KUMC – HRPP- 03/12/2015 
 
Page 8 of 18
 
 
 
 
4. Potential benefit of participating in the study 
a. n/a – no direct benefit to the individual subject or parent 
b. n/a – no direct benefit to the population from which the subject is drawn 
c. The information gained in this study will fill a gap in the literature by providing an 
understanding of the relationship between added sugar intake during a sensitive 
window of brain development. This data will help inform public health 
recommendations for added sugar intake and inform when interventions should 
occur. 
 
G. Location where study will be performed: All study visits will occur at the KU Medical 
Center main campus in Kansas City, KS. The study visit will occur at Dr. Hull’s research 
laboratory in the SmithWest building. All participants will be assigned a non-identifiable 
subject number. Subjects’ records will be stored electronically on the KUMC RedCap server. 
All paper records will be kept in Dr. Hull’s locked research laboratory. Only approved study 
team members have access to this area. 
 
H. Collaboration (with another institution, if applicable): n/a 
 
I. Single IRB Review for a Multi-site study (if applicable): n/a – not a multi-site study 
1. For which sites will KUMC serve as the IRB of record? n/a 
2. Indicate which study activities will occur at each site. If all study procedures will be 
identical across study sites, state this. n/a 
3. Describe how you will assess the capacity of each site to perform the research (e.g., 
expertise, staffing, space, equipment, etc.) If applicable, include site evaluation tools in 
your IRB submission. n/a 
4. Describe how the lead investigators will ensure that all participating sites use the IRB- 
approved version of the protocol, consent, recruitment materials and other study 
documents. n/a 
5. Describe how the lead investigators will communicate with and disseminate new 
information to other sites (e.g., training meetings, regularly-scheduled conference calls, 
notifications, etc.) n/a 
6. Describe how the lead investigator will assess protocol compliance, unanticipated 
problems and adverse events at other sites. n/a 
7. Name the member of the KUMC study team who will be the point of contact to coordinate 
oversight and communication with the sites. n/a 
 
J. Community-Based Participatory Research (if applicable) 
1. Participants and the nature of their involvement: n/a 
2. Cultural issues: n/a 
3. Origin of the research question: n/a 
4. Risks and Benefits: n/a 
5. Study Description and Process: n/a 
6. Return of results: n/a 
7. Sustainability: n/a 
 
K. Personnel who will conduct the study, including: 

KUMC – HRPP- 03/12/2015 
 
Page 9 of 18
 
 
 
 
1. Indicate, by title, who will be present during study procedure(s): 
a. Sarah Crawford: Study Coordinator, all visit procedures 
b. Laura Castro de Santiago: Bilingual Study Coordinator, all visit procedures 
c. Jill Shaddy-Gouvion: Research Personnel, will perform cognitive testing 
2. Primary responsibility for the following activities, for example: 
a. Determining eligibility: Sarah Crawford, Laura Castro de Santiago 
b. Obtaining informed consent: Sarah Crawford, Laura Castro de Santiago,  
c. Providing on-going information to the study sponsor and the IRB: Sarah Crawford, 
Laura Castro de Santiago 
d. Maintaining participant's research records: Sarah Crawford, Laura Castro de 
Santiago 
e. Completing physical examination: n/a 
f. Taking vital signs, height, weight: Sarah Crawford, Laura Castro de Santiago 
(height and weight only) 
g. Drawing / collecting laboratory specimens: n/a 
h. Performing / conducting tests, procedures, interventions, questionnaires: Sarah 
Crawford, Laura Castro de Santiago, Jill Shaddy-Gouvion 
i. Completing study data forms: Sarah Crawford, Laura Castro de Santiago 
j. Managing study database: Sarah Crawford, Laura Castro de Santiago 
 
L. Assessment of Subject Safety and Development of a Data and Safety Monitoring 
Plan 
1. Elements of the plan include: 
a. Persons/groups who will review the data (study team; independent safety 
monitor, data monitoring committee or formal DSMB): PI and study team 
b. Data/events that will be reviewed: n/a 
c. Frequency of review: n/a 
d. Types of analyses to be performed: n/a 
e. Safety-related triggers that would cause the PI to stop or alter the study: n/a 
2. n/a – non-interventional study, no anticipated adverse events related to the study 
3. n/a – non-interventional study, no anticipated adverse events related to the study 
 
III. 
Subject Participation 
A. Recruitment: 
1. Subjects will be recruited from the ADORE GAINS study cohort if they agreed to future 
contact on the informed consent form at the time of consent for that study. 
2. Study coordinators and graduate research assistants will contact potential participants by 
phone. The study will be explained using the recruitment script (pending IRB approval). 
3. n/a – no advertisements or flyers will be used for recruitment 

KUMC – HRPP- 03/12/2015 
 
Page 10 of 18
 
 
 
 
4. The recruitment diagram and recruitment postcard will be sent to potential participants 
who express interest when spoken to on the phone and agree to have the materials sent 
electronically. These handouts are intended to provide a simple, visual overview of what 
the entails. They will be accompanied by the more detailed verbal explanation provided 
by the study team via phone. 
 
B. Screening Interview/questionnaire: The general health screener will be sent to parent 
to complete. This has questions to assess MRI safety and if the child has been diagnosed 
with autism. 
 
C. Informed consent process and timing of obtaining of consent 
1. Sarah Crawford, Laura Castro de Santiago will be in charge of obtaining written consent. 
2. The consent process will occur via phone or in a private room with only approved study 
personnel present. The electronic consent form is structured in different sections 
including study purpose, study procedures, risks and benefits, additional information 
(cost, payment, funding, voluntary reminder), privacy protection, stopping the study, 
and lastly the consent page with signature fields. Each section is a different page, so the 
interviewee has to advance to the next section. The interviewer will verbally explain each 
section to the potential participant. By structuring the form in sections, participants 
receive small amounts of information at a time making it easier to understand. It also 
creates a natural pause after each section, at which time the interviewer will give the 
participant the opportunity to ask any questions. After the consent interview, participants 
will be given the opportunity to think about the decision and discuss privately with their 
spouse/partner if applicable. If consent interview occurs in-person, the study team 
member will step out of the room should they want time to think/discuss privately. If the 
consent occurs via phone, a second phone call will be scheduled to actually sign the 
consent if they choose to do so. 
3. All subjects will be minors, therefore a legal guardian will give informed consent for all 
subjects. 
 
D. Alternatives to Participation: As stated in the consent form, a parent can choose not to 
have their child participate. 
 
E. Costs to Subjects: n/a – all study tests and procedures will be provided by the study. No 
study-related procedures will be billed to insurance. A subject’s health insurance status will 
not impact their ability to participate.  
 
F. How new information will be conveyed to the study subject and how it will be 
documented: New information will be conveyed to the study subject in writing, via a letter. 
A dated copy of the letter will be kept in their research record to document that the 
information was provided. Reconsent will occur if required by the IRB. 
 
G. Payment, including a prorated plan for payment: Subjects will receive $100 per visit 
attended. The reimbursement will be requested to the ClinCard after each study visit is 
completed. If a subject chooses to withdraw, they will only receive compensation for the 
study visit(s) completed. Reimbursement for travel expenses may be available, but will need 

KUMC – HRPP- 03/12/2015 
 
Page 11 of 18
 
 
 
 
to be pre-approved by the PI. 
 
H. Payment for a research-related injury: Treatment for research-related injury will be 
provided at usual charge. Claims will be submitted to the subject’s health insurance policy, 
government program, or other third party. The subject will be billed for any costs not 
covered by the insurance. 
 
IV. 
Data Collection and Protection 
A. Data Management and Security: 
1. In addition to the PI, Co-I, and IRB-approved study team members, data monitors and 
auditors from the IRB and regulatory authorities will have access to study data. 
2. To maintain confidentiality, subjects will be given a non-identifiable study ID number. 
Research records containing identifiable information will be kept in Dr. Hull’s locked 
research laboratory. All study records will be retained for 25 years, per university policy 
for pediatric studies. 
3. Subjects will be identified by their study ID number. 
4. The study coordinators will maintain and have access to the information that links the 
subject’s identity to their study ID number. 
5. Data will be linked to the subject using their assigned study ID number. 
6. Data will be stored on the KUMC RedCap server and university P-drive. Only IRB- 
approved study team members will have access to the data. 
7. iPads may be used for electronic data entry during study visits. All data collected via iPad 
will be entered into RedCap and stored on the KUMC RedCap server. A study specific 
iPad will be used to take and temporarily save photos of children during the DXA scan. 
The iPad is passcode protected and only approved members of the study team have 
access. After each visit, photos will be saved to the university P-drive and deleted from 
the iPad. If the parent consents yes to the future use of photos, photos will be kept on 
the P-drive for possible future use in presentations and publications of the research in 
accordance with the optional multimedia consent and KUMC multimedia authorization 
form. If the parent consents no to the future use of photos, all photos of the participant 
will be deleted after sharing them with the participant as a memento of their 
participation. 
8. n/a – no identifiable data will be sent outside KUMC 
 
B. Sample / Specimen Collection: n/a – no samples will be collected 
 
C. Tissue Banking Considerations: n/a – no samples will be collected, therefore no samples 
will be available to bank 
D. Procedures to protect subject confidentiality: There is no appreciable risk of loss of 
confidentiality. Subjects will be made aware of persons who may see their protected health 
information in the informed consent document and may choose not to enroll in the study 
based on the information provided them in accord with 2003 HIPAA regulations. The 
patient’s confidentiality will be maintained and will not be made publicly available to the 
extent permitted by the applicable laws and regulations. 
 

KUMC – HRPP- 03/12/2015 
 
Page 12 of 18
 
 
 
 
E. Quality Assurance / Monitoring 
1. All data entry will verified by a second study team member using the original source 
document to ensure data are accurate, consistent, complete and reliable. 
2. n/a – no plans to have ongoing third-party monitoring 
 
V. 
Data Analysis and Reporting 
A. Statistical and Data Analysis: The data analysis plan for each primary aim is described 
below. There are no planned interim analyses. 
1. Aim 1 analysis: Determine the relationship between added sugars (grams and % 
calories) intake during pregnancy and infancy/toddlerhood (birth to 24 months) on brain 
structure and function. Brain structure will be quantified as brain volume in Freesurfer. 
Based on prior studies, we will examine the Pearson correlation between hippocampal 
brain volume and added sugars intake during pregnancy and infancy/toddlerhood. 
Exploratory analyses will examine correlations with added sugars intake and brain 
volume in inhibitory control brain regions (i.e., dorsal anterior cortex) and reward related 
regions (i.e., ventromedial prefrontal cortex). Brain function will be quantified as resting 
state functional connectivity within the default mode network which includes prefrontal 
and parietal regions as well as the attention and salience networks. Pearson correlations 
will examine the relationship between functional connectivity metrics and added sugars 
intake. Brain function during the EEG Food Go/NoGo task will be quantified as the 
amplitude of the P3 and N2 components and correlations will examine the relationship 
between P3/N2 amplitudes and added sugars. Analyses will be corrected for multiple 
comparisons using a Bonferroni correction. 
2. Aim 2 analysis: Determine the relationship between fructose (grams and % calories) 
consumption during pregnancy and infancy/toddlerhood (birth to 24 months) on brain 
structure and function. As in Aim 1 analyses, brain structure will be quantified as 
Freesurfer volumes, brain function will be quantified as resting state connectivity, and 
brain activation during the EEG Food Go/NoGo Task. Correlations will be used to examine 
the relationship between brain measures and fructose consumption. 
 
B. Outcome: We hypothesize that added sugars and fructose intake will be negatively related 
to brain structure (hippocampal volume) and function (resting state functional connectivity 
and P3 amplitude). The strength of the correlations and level of significance will determine if 
there is a relationship between variables being tested. 
 
C. Study results to participants: Study participants will be informed of the overall study 
results via a letter, which will be mailed after the study and analysis is complete. Participants 
will not be given their individual results from study procedures; however, this information 
may be made available upon request, with approval by the PI. 
 
D. Publication Plan: The present study is a pilot. This project was submitted as a June 2022 
R01 and received positive reviews. It will be resubmitted in November 2022 with the hope of 
receiving R01 funding to extend the study to the entire ADORE GAINS cohort. We hope by 
getting more participants to complete the cognitive tests and body composition 
measurements that we will have a large enough sample to publish results relating to those 

KUMC – HRPP- 03/12/2015 
 
Page 13 of 18
 
 
 
 
measurements. Any publications would further support the R01 application. 
 
VI. 
Literature Cited 
1. Fox SE, Levitt P, Nelson CA, 3rd. How the timing and quality of early experiences influence 
the development of brain architecture. Child Dev. Jan-Feb 2010;81(1):28-40. 
doi:10.1111/j.1467-8624.2009.01380.x 
2. Wachs TD, Georgieff M, Cusick S, McEwen BS. Issues in the timing of integrated early 
interventions: contributions from nutrition, neuroscience, and psychological research. Ann N 
Y Acad Sci. Jan 2014;1308:89-106. doi:10.1111/nyas.12314 
3. Cusick SE, Georgieff MK. The Role of Nutrition in Brain Development: The Golden 
Opportunity of the "First 1000 Days". The Journal of pediatrics. Aug 2016;175:16-21. 
doi:10.1016/j.jpeds.2016.05.013 
4. Schwarzenberg SJ, Georgieff MK, Committee On N. Advocacy for Improving Nutrition in the 
First 1000 Days to Support Childhood Development and Adult Health. Pediatrics. Feb 
2018;141(2)doi:10.1542/peds.2017-3716 
5. Bowman SA, Clemens JC, Friday JE, Moshfegh AJ. Food Patterns Equivalents Database 2017- 
2018: Methodology and User Guide. Food Surveys Research Group, Beltsville Human 
Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture, 
Beltsville, 
6. Malik VS, Hu FB. Fructose and Cardiometabolic Health: What the Evidence From Sugar- 
Sweetened Beverages Tells Us. Journal of the American College of Cardiology. Oct 6 
2015;66(14):1615-1624. doi:10.1016/j.jacc.2015.08.025 
7. US Departments of Health and Human Services and Agriculture. 2020-2025 Dietary 
Guidelines for Americans, 9th edition. . 
https://www.dietaryguidelines.gov/sites/default/files/2020- 
12/Dietary_Guidelines_for_Americans_2020-2025.pdf Accessed August 23, 2021 
8. Cioffi CE, Figueroa J, Welsh JA. Added Sugar Intake among Pregnant Women in the United 
States: National Health and Nutrition Examination Survey 2003-2012. Journal of the 
Academy of Nutrition and Dietetics. May 2018;118(5):886-895 e1. 
doi:10.1016/j.jand.2017.10.021 
9. Kong KL, Burgess B, Morris KS, et al. Association Between Added Sugars from Infant 
Formulas and Rapid Weight Gain in US Infants and Toddlers. The Journal of nutrition. Jun 1 
2021;151(6):1572-1580. doi:10.1093/jn/nxab044 
10. Herrick KA, Fryar CD, Hamner HC, Park S, Ogden CL. Added Sugars Intake among US 
Infants and Toddlers. Journal of the Academy of Nutrition and Dietetics. Jan 
2020;120(1):23-32. doi:10.1016/j.jand.2019.09.007 
11. Kong KL, Burgess B, Morris KS, Faith MS, Paluch RA. High intake of added sugars is linked to 
rapid weight gain in infancy, breastfeeding >/=12 months may protect against this: A 
preliminary investigation. Pediatr Obes. Mar 2021;16(3):e12728. doi:10.1111/ijpo.12728 
12. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. Added sugar intake and 
cardiovascular diseases mortality among US adults. JAMA Intern Med. Apr 2014;174(4):516- 
24. doi:10.1001/jamainternmed.2013.13563 
13. Luger M, Lafontan M, Bes-Rastrollo M, Winzer E, Yumuk V, Farpour-Lambert N. Sugar- 
Sweetened Beverages and Weight Gain in Children and Adults: A Systematic Review from 
2013 to 2015 and a Comparison with Previous Studies. Obes Facts. 
2017;10(6):674-693. doi:10.1159/00 

KUMC – HRPP- 03/12/2015 
 
Page 14 of 18
 
 
 
 
14. Dello Russo M, Ahrens W, De Henauw S, et al. The Impact of Adding Sugars to Milk and Fruit 
on Adiposity and Diet Quality in Children: A Cross-Sectional and Longitudinal Analysis of the 
Identification and Prevention of Dietary- and Lifestyle-Induced Health Effects in 
15. Francis H, Stevenson R. The longer-term impacts of Western diet on human cognition and 
the brain. Appetite. Apr 2013;63:119-28. doi:10.1016/j.appet.2012.12.018 
16. Clark KA, Alves JM, Jones S, et al. Dietary Fructose Intake and Hippocampal Structure and 
Connectivity during Childhood. Nutrients. Mar 26 2020;12(4)doi:10.3390/nu12040909 
17. Hsu TM, Konanur VR, Taing L, et al. Effects of sucrose and high fructose corn syrup 
consumption on spatial memory function and hippocampal neuroinflammation in adolescent 
rats. Hippocampus. Feb 2015;25(2):227-39. doi:10.1002/hipo.22368 
18. Noble EE, Hsu TM, Liang J, Kanoski SE. Early-life sugar consumption has long-term negative 
effects on memory function in male rats. Nutr Neurosci. Apr 2019;22(4):273-283. 
doi:10.1080/1028415X.2017.1378851 
19. Berger PK, Monk C, Bansal R, Sawardekar S, Goran MI, Peterson BS. Association of Prenatal 
Sugar Consumption with Newborn Brain Tissue Organization. Nutrients. Jul 16 
2021;13(7)doi:10.3390/nu13072435 
20. Berger PK, Plows JF, Jones RB, et al. Associations of maternal fructose and sugar-sweetened 
beverage and juice intake during lactation with infant neurodevelopmental outcomes at 24 
months. The American journal of clinical nutrition. Dec 10 2020;112(6):1516-1522. doi 
21. Sanguesa G, Cascales M, Grinan C, et al. Impairment of Novel Object Recognition Memory 
and Brain Insulin Signaling in Fructose- but Not Glucose-Drinking Female Rats. Mol 
Neurobiol. Aug 2018;55(8):6984-6999. doi:10.1007/s12035-017-0863-1 
22. Bukhari SHF, Clark OE, Williamson LL. Maternal high fructose diet and neonatal immune 
challenge alter offspring anxiety-like behavior and inflammation across the lifespan. Life Sci. 
Mar 15 2018;197:114-121. doi:10.1016/j.lfs.2018.02.010 
23. Agrawal R, Noble E, Vergnes L, Ying Z, Reue K, Gomez-Pinilla F. Dietary fructose aggravates 
the pathobiology of traumatic brain injury by influencing energy homeostasis and plasticity. J 
Cereb Blood Flow Metab. May 2016;36(5):941-53. doi:10.1177/0271678X15606719 
24. Stiles J, Jernigan TL. The basics of brain development. Neuropsychol Rev. Dec 
2010;20(4):327-48. doi:10.1007/s11065-010-9148-4 
25. Doyle O, Harmon CP, Heckman JJ, Tremblay RE. Investing in early human development: 
timing and economic efficiency. Econ Hum Biol. Mar 2009;7(1):1-6. 
doi:10.1016/j.ehb.2009.01.002 
26. Conti G, Heckman J, Pinto R. The Effects of Two Influential Early Childhood Interventions on 
Health and Healthy Behaviour. Econ J (London). Oct 2016;126(596):F28-F65. 
doi:10.1111/ecoj.12420 
27. Campbell F, Conti G, Heckman JJ, et al. Early childhood investments substantially boost adult 
health. Science. Mar 28 2014;343(6178):1478-85. doi:10.1126/science.1248429 
28. Shireman TI, Kerling EH, Gajewski BJ, Colombo J, Carlson SE. Docosahexaenoic acid 
supplementation (DHA) and the return on investment for pregnancy outcomes. 
Prostaglandins, leukotrienes, and essential fatty acids. Aug 2016;111:8-10. 
doi:10.1016/j.plefa.2016.05.008 
29. Adamo AM, Zago MP, Mackenzie GG, et al. The role of zinc in the modulation of neuronal 
proliferation and apoptosis. Neurotox Res. Jan 2010;17(1):1-14. doi:10.1007/s12640-009- 
9067-4 

KUMC – HRPP- 03/12/2015 
 
Page 15 of 18
 
 
 
 
30. Yelland LN, Gajewski BJ, Colombo J, Gibson RA, Makrides M, Carlson SE. Predicting the effect 
of maternal docosahexaenoic acid (DHA) supplementation to reduce early preterm birth in 
Australia and the United States using results of within country randomized controlled 
31. Bornstein MH, Esposito G. Beyond cry and laugh: toward a multilevel model of language 
production. Behav Brain Sci. Dec 2014;37(6):548-9; discussion 577-604. 
doi:10.1017/S0140525X13003968 
32. Meredith RM. Sensitive and critical periods during neurotypical and aberrant 
neurodevelopment: a framework for neurodevelopmental disorders. Neurosci Biobehav Rev. 
Mar 2015;50:180-8. doi:10.1016/j.neubiorev.2014.12.001 
33. Knudsen EI. Sensitive periods in the development of the brain and behavior. J Cogn 
Neurosci. Oct 2004;16(8):1412-25. doi:10.1162/0898929042304796 
34. Colombo J. The critical period concept: research, methodology, and theoretical issues. 
Psychol Bull. Mar 1982;91(2):260-75. 
35. Bornstein MH. Sensitive periods in development: interdisciplinary perspectives 
(Crosscurrents in contemporary psychology series). 1st edition ed. Psychology Press, Taylor 
and Francis Group 2014. 
36. Colombo J, Gustafson KM, Carlson SE. Critical and Sensitive Periods in Development and 
Nutrition. Annals of nutrition & metabolism. 2019;75 Suppl 1:34-42. 
doi:10.1159/000508053 
37. Barker DJ, Eriksson JG, Forsen T, Osmond C. Fetal origins of adult disease: strength of 
effects and biological basis. International journal of epidemiology. Dec 2002;31(6):1235-9. 
38. Barker DJ. The Fetal Origins of Type 2 Diabetes. Annal of Internal Medicine. February 16 
1999;130(4):322-324. 
39. Barker DJ. Fetal origins of coronary heart disease. BMJ (Clinical research ed. Jul 15 
1995;311(6998):171-4. 
40. Barker DJ. The fetal origins of adult hypertension. J Hypertens Suppl. Dec 1992;10(7):S39- 
44. 
41. Barker DJ, Gluckman PD, Godfrey KM, Harding JE, Owens JA, Robinson JS. Fetal nutrition 
and cardiovascular disease in adult life. Lancet. Apr 10 1993;341(8850):938-41. 
42. Barker DJ, Osmond C. Infant mortality, childhood nutrition, and ischaemic heart disease in 
England and Wales. Lancet. May 10 1986;1(8489):1077-81. 
43. Innis SM. Dietary omega 3 fatty acids and the developing brain. Brain Res. Oct 27 
2008;1237:35-43. doi:10.1016/j.brainres.2008.08.078 
44. Tran PV, Kennedy BC, Lien YC, Simmons RA, Georgieff MK. Fetal iron deficiency induces 
chromatin remodeling at the Bdnf locus in adult rat hippocampus. American journal of 
physiology Regulatory, integrative and comparative physiology. Feb 15 2015;308(4):R276- 
82. doi: 
45. Carlson ES, Tkac I, Magid R, et al. Iron is essential for neuron development and memory 
function in mouse hippocampus. The Journal of nutrition. Apr 2009;139(4):672-9. 
doi:10.3945/jn.108.096354 
46. Greminger AR, Lee DL, Shrager P, Mayer-Proschel M. Gestational iron deficiency differentially 
alters the structure and function of white and gray matter brain regions of developing rats. 
The Journal of nutrition. Jul 2014;144(7):1058-66. doi:10.3945/jn.113.187732 
47. Lozoff B, Beard J, Connor J, Barbara F, Georgieff M, Schallert T. Long-lasting neural and 

KUMC – HRPP- 03/12/2015 
 
Page 16 of 18
 
 
 
 
behavioral effects of iron deficiency in infancy. Nutrition reviews. May 2006;64(5 Pt 2):S34- 
43; discussion S72-91. doi:10.1301/nr.2006.may.s34-s43 
48. Bhatnagar S, Taneja S. Zinc and cognitive development. Br J Nutr. May 2001;85 Suppl 
2:S139-45. doi:10.1079/bjn2000306 
49. Adamo AM, Oteiza PI. Zinc deficiency and neurodevelopment: the case of neurons. 
Biofactors. Mar-Apr 2010;36(2):117-24. doi:10.1002/biof.91 
50. Tamura T, Goldenberg RL, Hou J, et al. Cord serum ferritin concentrations and mental and 
psychomotor development of children at five years of age. The Journal of pediatrics. Feb 
2002;140(2):165-70. doi:10.1067/mpd.2002.120688 
51. Beard JL, Connor JR. Iron status and neural functioning. Annual review of nutrition. 
2003;23:41-58. doi:10.1146/annurev.nutr.23.020102.075739 
52. Colombo J, Zavaleta N, Kannass KN, et al. Zinc supplementation sustained normative 
neurodevelopment in a randomized, controlled trial of Peruvian infants aged 6-18 months. 
The Journal of nutrition. Aug 2014;144(8):1298-305. doi:10.3945/jn.113.189365 
53. Stipanuk MH, Caudill MA. Biochemical, physiological, and molecular aspects of human 
nutrition. 3rd ed. Elsevier; 2013:xix, 948 p. 
54. Zhang DM, Jiao RQ, Kong LD. High Dietary Fructose: Direct or Indirect Dangerous Factors 
Disturbing Tissue and Organ Functions. Nutrients. Mar 29 2017;9(4)doi:10.3390/nu9040335 
55. Cohen JFW, Rifas-Shiman SL, Young J, Oken E. Associations of Prenatal and Child Sugar 
Intake With Child Cognition. Am J Prev Med. Jun 2018;54(6):727-735. 
doi:10.1016/j.amepre.2018.02.020 
56. Berger PK, Fields DA, Demerath EW, Fujiwara H, Goran MI. High-Fructose Corn-Syrup- 
Sweetened Beverage Intake Increases 5-Hour Breast Milk Fructose Concentrations in 
Lactating Women. Nutrients. May 24 2018;10(6)doi:10.3390/nu10060669 
57. Conway JM, Ingwersen LA, Vinyard BT, Moshfegh AJ. Effectiveness of the US Department of 
Agriculture 5-step multiple-pass method in assessing food intake in obese and nonobese 
women. The American journal of clinical nutrition. May 2003;77(5):1171-8. 
58. Blanton CA, Moshfegh AJ, Baer DJ, Kretsch MJ. The USDA Automated Multiple-Pass Method 
accurately estimates group total energy and nutrient intake. The Journal of nutrition. Oct 
2006;136(10):2594-9. doi:136/10/2594 [pii] 
59. Hebert JR, Hurley TG, Chiriboga DE, Barone J. A comparison of selected nutrient intakes 
derived from three diet assessment methods used in a low-fat maintenance trial. Public 
Health Nutr. Sep 1998;1(3):207-14. doi:S1368980098000330 [pii] 
60. Somerville LH, Bookheimer SY, Buckner RL, et al. The Lifespan Human Connectome Project 
in Development: A large-scale study of brain connectivity development in 5-21 year olds. 
Neuroimage. Dec 2018;183:456-468. doi:10.1016/j.neuroimage.2018.08.050 
61. Dosenbach NUF, Koller JM, Earl EA, et al. Real-time motion analytics during brain MRI 
improve data quality and reduce costs. Neuroimage. Nov 1 2017;161:80-93. 
doi:10.1016/j.neuroimage.2017.08.025 
62. Delorme A, Makeig S. EEGLAB: an open source toolbox for analysis of single-trial EEG 
dynamics including independent component analysis. J Neurosci Methods. Mar 15 
2004;134(1):9-21. doi:10.1016/j.jneumeth.2003.10.009 
63. Lopez-Calderon J, Luck SJ. ERPLAB: an open-source toolbox for the analysis of event-related 
potentials. Front Hum Neurosci. 2014;8:213. doi:10.3389/fnhum.2014.00213 

KUMC – HRPP- 03/12/2015 
 
Page 17 of 18
 
 
 
 
64. Szabo-Reed AN, Breslin FJ, Lynch AM, et al. Brain function predictors and outcome of weight 
loss and weight loss maintenance. Contemporary clinical trials. Jan 2015;40:218-31. 
doi:10.1016/j.cct.2014.12.008 
65. Kendler T. (1979). Development of discrimination learning: A levels-of-functioning 
explanation. In H Reese (Ed.), Advances in child development and behavior (pp. 83-117). 
New York: Academic Press. 
66. Reese HW, Lipsitt L. (1970). Experimental child psychology. New York: Wiley. 
67. Coldren JT, Colombo J. (1994). The nature and processes of preverbal learning: Implications 
from nine-month-old infants' discrimination problem solving. Mon Soc Res Child Devel, 
59(4, #249). 
68. Colombo J, Mitchell DW, Coldren JT, Atwater JD. (1990). Discrimination learning during the 
first year of life: Stimulus and positional cues. J Exp Psychol: Learn Mem Cog, 16, 98-109. 
69. Zelazo PD. The Dimensional Change Card Sort (DCCS): a method of assessing executive 
function in children. Nat Protoc. 2006;1(1):297-301. doi:10.1038/nprot.2006.46. 
70. Coldren JT, Colombo J. (2008, under review). Attention as a cueing function during 
kindergarten children’s dimensional change task performance. Infant and Child 
Development. 
71. Washington JA, Craig HK. Performances of At-Risk, African American Preschoolers on the 
Peabody Picture Vocabulary Test-III. Lang Speech Hear Serv Sch. 1999 Jan 1;30(1):75-82. 
doi: 10.1044/0161-1461.3001.75. PMID: 27764292. 
72. Yim JE, Heshka S, Albu JB, Heymsfield S, Gallagher D. Femoral-gluteal subcutaneous and 
intermuscular adipose tissues have independent and opposing relationships with CVD risk. J 
Appl Physiol (1985). 2008 Mar;104(3):700-7. doi:10.1152/japplphysiol.01035.2007. 
73. Carlsen EM, Renault KM, Nørgaard K, Nilas L, Jensen JE, Hyldstrup L, Michaelsen KF, Cortes 
D, Pryds O. Newborn regional body composition is influenced by maternal obesity, 
gestational weight gain and the birthweight standard score. Acta Paediatr. 2014 
Sep;103(9):939-45. doi:10.1111/apa.12713. 
74. Sanz N, Diaz M, López-Bermejo A, Sierra C, Fernández A, de Zegher F, Ibáñez L. Newborns 
with lower levels of circulating polyunsaturated fatty acids (PUFA) are abdominally more 
adipose. Pediatr Obes. 2014 Jun;9(3):e68-72. doi: 10.1111/j.2047-6310.2013.00200.x 
 
 
 

KUMC – HRPP- 03/12/2015 
 
Page 18 of 18
 
 
 
 
APPENDIX I: VULNERABLE POPULATIONS 
 
I. 
Cognitively or decisionally impaired individuals: n/a 
 
II. 
Children: We are targeting children aged 5-6 who previously participated in the ADORE GAINS 
study. All recruitment and consenting procedures will be targeted toward the parents, as the 
child will be too young to assent. No child will attain age 18 years while in the study, so no re- 
consent will be required. 
 
III. 
Pregnant women: n/a 
 
IV. 
Prisoners: n/a 
 
V. 
Students and/or Employees: 
A. n/a 
B. n/a 
C. n/a