This presentation is an overview of our recent publication in the Appetite Journal. "Preclinical Evidence for the Addiction Potential of Highly Palatable Foods: Current Developments Related to Maternal Influence" by David Wiss, Kristin, Criscitelli, Mark Gold, and Nicole Avena.

1. Preclinical Evidence for the
Addiction Potential of Highly
Palatable Foods: Current
Developments Related to
Maternal Influence

3. OBESITY
• Contributing mechanisms:
• Changes in food supply
and dietary patterns
• Sedentary lifestyles
• Genetic susceptibility1,2
• Gene-environment
interactions resulting in
epigenetic modifications3,4
1. Farooqi, S., & O'Rahilly, S. (2006). Genetics of obesity in
humans. Endocrine Reviews, 27, 710-718.
2. Llewellyn, C., & Wardle, J. (2015). Behavioral susceptibility to
obesity: Gene-environment interplay in the development of
weight. Physiology and Behavior.
3. Rooney, K., & Ozanne, S. E. (2011). Maternal over-nutrition and
offspring obesity predisposition: Targets for preventative
interventions. International Journal of Obesity, 35, 883-890.
4. Skinner, M. K. (2011). Role of epigenetics in developmental
biology and transgenerational inheritance. Birth Defects Research,
93, 51-55.
5. Huang, J. S., Lee, T. A., & Lu, M. C. (2007). Prenatal
programming of childhood overweight and obesity. Maternal and
Child Health Journal, 11, 461-473.
Prenatal programming of
increased childhood overweight
and obesity has been
established in humans5

4. CURRENT FOOD ENVIRONMENT
• Encourages excessive
consumption of highly
processed foods
• Exaggerated levels of sugar,
fat, and salt
• Neuroadaptations in the
mesolimbic dopamine
reward pathways1,2,3
• Neurochemical and
behavioral alterations
mirroring drug addiction4
1. Avena, N. M., Rada, P., & Hoebel, B. G. (2008). Evidence for
sugar addiction: behavioral and neurochemical effects of
intermittent, excessive sugar intake. Neuroscience and
Biobehavioral Reviews, 32, 20-39.
2. Rada, P., Avena, N. M., & Hoebel, B. G. (2005). Daily bingeing
on sugar repeatedly releases dopamine in the accumbens shell.
Neuroscience, 134, 737-744.
3. Willuhn, I., Burgeno, L. M., Groblewski, P. A., & Phillips, P. E.
(2014). Excessive cocaine use results from decreased phasic
dopamine signaling in the striatum. Nature Neuroscience, 17,
704-709.
4. Murray, S., Tulloch, A., Gold, M. S., & Avena, N. M. (2014).
Hormonal and neural mechanisms of food reward, eating
behaviour and obesity. Nature Reviews: Endocrinology, 10, 540-
552.

5. PEDIATRIC OBESITY
• Growing prevalence1,2
• Prenatal/intrauterine???
• Preclinical evidence:
• Appetite regulation begins
during prenatal/perinatal
period3,4,5,6
1. Ng, M., Fleming, T., Robinson, M., Thomson, B., Graetz, N.,
Margono, C., ...Gakidou, E. (2014). Global, regional, and national
prevalence of overweight and obesity in children and adults during
1980–2013: A systematic analysis for the Global Burden of Disease
Study 2013. The Lancet, 384, 766-781.
2. Swinburn, B. A., Sacks, G., Hall, K. D., McPherson, K., Finegood, D.
T., Moodie, M. L., & Gortmaker, S. L. (2011). The global obesity
pandemic: shaped by global drivers and local environments. The
Lancet, 378, 804-814.
3. Ashino, N. G., Saito, K. N., Souza, F. D., Nakutz, F. S., Roman, E. A.,
Velloso, L. A., Torsoni, A. S., & Torsoni, M. A. (2012). Maternal high-
fat feeding through pregnancy and lactation predisposes mouse
offspring to molecular insulin resistance and fatty liver. Journal of
Nutritional Biochemistry, 23, 341-348.
4. Muhlhausler, B. S., Adam, C. L., Findlay, P. A., Duffield, J. A., &
McMillen, I. C. (2006). Increased maternal nutrition alters
development of appetite-regulating network in the brain. The FASEB
Journal, 20, E556-E565.
5. Shalev, U., Tylor, A., Schuster, K., Frate, C., Tobin, S., & Woodside,
B. (2010). Long-term physiological and behavioral effects of exposure
to a highly palatable diet during the perinatal and post-weaning
periods. Physiology & Behavior, 101, 494-502.
6. Sun, B., Purcell, R. H., Terrillion, C. E., Yan, J., Moran, T. H. (2012).
Maternal high-fat diet during gestation or suckling differentially
affects offspring leptin sensitivity and obesity. Diabetes, 61, 2833-
2841.

6. HYPOTHALAMUS & HORMONES
• Arcuate nucleus (ARC)
• Integration site1
• Appetite-related signals
• Glucose
• Triglyceride
• Insulin
• Leptin
• Orexigenic hormones
• Neuropeptide Y (NPY)
• Agouti-related protein (AgRP)
• Anorexigenic neurons2
• Proopiomelanocortin (POMC)
1. Bauer, P. V., Hamr, S. C., & Duca, F. A. (2015). Regulation of
energy balance by a gut-brain axis and involvement of the gut
microbiota. Cellular and Molecular Life Sciences.
2. Hahn, T. M., Breininger, J. F., Baskin, D. G., & Schwartz, M. W.
(1998). Coexpression of Agrp and NPY in fasting-activated
hypothalamic neurons. Nature Neuroscience, 1(4), 271-272.

7. HYPOTHALAMUS & HORMONES
• Metabolic state influences
reward system by linking
homeostatic mechanisms
(hypothalamus) with
reward pathways
(midbrain & cortex)1,2
• Rise in obesity rates in
part explained by early life
nutritional imbalances3
1. De Araujo, I. E., Deisseroth, K., Domingos, A. I., Friedman, J.,
Gradinaru, V., & Ren, X. (2011). Leptin regulates the reward value
of nutrient. Nature Neuroscience, 14, 1562-1568.
2. Coll, A. P., Farooqi, S., & O'Rahilly, S. (2007). The hormonal
control of food intake. Cell, 129, 251-262.
3. Ramamoorthy, T. G., Begum, G., Harno, E., & White, A. (2015).
Developmental programming of hypothalamic neuronal circuits:
Impact on energy balance control. Frontiers in Neuroscience,
9(126).

8. HYPOTHALAMUS & HORMONES
• Insulin
• Works with dopamine (DA) in the
ventral tegmental area (VTA) to
orchestrate motivation to engage
in consumptive behavior1
• Calibrates reward
• Increased DA reuptake through DAT
• Leptin
• Signals to reduce energy intake
and increase expenditure2,3
• Inhibiting NPY
• Stimulating POMC
1. Mebel, D. M., Wong, J. C. Y., Dong, Y. J., &
Borgland, S. L. (2012). Insulin in the ventral
tegmental area reduces hedonic feeding and
suppresses dopamine concentration via increased
reuptake. Behavioral Neuroscience, 36, 2336-
2346.
2. Morton, G. J., Meek, T. H., & Schwartz, M. W.
(2014). Neurobiology of food intake in health and
disease. Nature Reviews Neuroscience, 15(6), 367-
378.
3. Shan, X., & Yeo, G. S. H. (2011). Central leptin
and ghrelin signalling: Comparing and contrasting
their mechanisms of action in the brain. Reviews
in Endocrine and Metabolic Disorders, 12, 197-
209.

9. HYPOTHALAMUS & HORMONES
• Leptin
• Modulates DA circuits to generate
behavioral response
• Reduced expression of leptin receptors
in VTA & hypothalamus lead to increased
effort-based feeding & intake1
• High fat diets (HFDs) can induce
leptin resistance2
• Increased potential for leptin
resistance in postnatal period:3
• Abnormal appetite reg., glu intolerance,
altered reward sensitivity, obesity
1. Hommel, J. D., Trinko, R., Sears, R. M.,
Georgescu, D., Liu, Z., Gao, X., Thurmon, J.
J., Marinelli, M., & DiLeone, R. J. (2006).
Leptin receptor signaling in midbrain
dopamine neurons regulates feeding.
Neuron, 51, 801-810.
2. Pandit, R., Mercer, J. G., Overduin, J., la
Fleur, S. E., & Adan, R. A. H. (2012).
Dietary factors affect food reward and
motivation to eat. Obesity Facts, 5, 221-
242.
3. Shalev, U., Tylor, A., Schuster, K., Frate,
C., Tobin, S., & Woodside, B. (2010). Long-
term physiological and behavioral effects
of exposure to a highly palatable diet
during the perinatal and post-weaning
periods. Physiology & Behavior, 101, 494-
502.

10. HYPOTHALAMUS & HORMONES
• Ghrelin
• Homeostatic appetite
regulation
• Hedonic eating1,2
• Alters DA neurons in VTA3,4
• Maternal HFD during
prenatal/lactation increases
ghrelin in offspring5
1. Abizaid, A., Liu, Z., Andrews, Z. B., Shanabrough, M.,
Borok, E., Elsworth, J. D., ...Horvath, T. L. (2006). Ghrelin
modulates the activity and synpatic input organization of
midbrain dopamine neurons while promoting appetite.
The Journal of Clinical Investigation, 116, 12.
2. Naleid, A. M., Grace, M. K., Cummings, D. E., & Levine,
A. S. (2005). Ghrelin induces feeding in the mesolimbic
reward pathways between the ventral tegmental area and
the nucleus accumbens. Peptides, 26, 2274-2279.
3. Dickson, S. L., Egecioglu, E., Landgren S., Skibicka, K. P.,
Engel, J. A., & Jerlhag (2011). The role of central ghrelin
system in reward from food and chemical drugs. Molecular
and Cellular Endocrinology, 340, 80-87.
4. Skibicka, K. P., Hansson, C., Alvarez-Crespo, M., Friberg,
P. A., & Dickson, S. L. (2011). Ghrelin directly targets the
ventral tegmental area to increase food motivation.
Neuroscience, 180, 129-137.
5. Slupecka, M., Romanowicz, K., & Wolinski, J. (2016).
Maternal high-fat diet during pregnancy and lactation
influences obestatin and ghrelin concentrations in milk and
plasma of wistar rat dams and their offspring. International
Journal of Endocrinology, 2016, 5739763.

11. HYPOTHALAMUS & HORMONES
“Neurodevelopment in utero is influenced by
maternal feeding patterns via perturbations in
insulin, leptin, and ghrelin signaling. These hormones
interact with the development of reward system,
particularly in the VTA, impacting the homestatic and
hedonic mechanisms that govern feeding behavior.
Nutritional imbalances during pregnancy have the
potential to stimulate reward-based eating in the
offspring”

12. FETAL UNDER-NUTRITION
• Linked to adult adiposity
• Dutch hunger famine1 (human)
• Lipid profile, CHD, T2DM,
cognition
• Intergenerational2
• Remodeling hypothalamic
structures3
• Altered gene expression3
• Satiety hormones
• Alteration of HPA axis4
• Predictive adaptive response
1. Roseboom, T. J., Painter, R. C., van Abeelen, A. F. M.,
Veenendaal, M. V. E., & de Rooij, S. R. (2011). Hungry in the
womb: What are the consequences? Lessons from the
Dutch famine. Maturitas, 70, 141-145.
2. Jimenez-Chillaron, J. C., Isganaitis, E., Charalambous, M.,
Gesta, S., Pentinat-Pelegrin, T., Faucette, R. R., ...Patty, M.
(2009). Intergenerational transmission of glucose
intolerance and obesity by in utero undernutrition in mice.
Diabetes, 58, 460-468.
3. Langley-Evans, S. C., Bellinger, L., & McMullen, S. (2005).
Animal models of programming: Early life influences on
appetite and feeding behavior. Maternal and Child
Nutrition, 1, 142-148.
4. Zhang, L., Xu, D., Zhang, B., Liu, Y., Chu, F., Guo, Y.,
...Wang, H. (2013). Prenatal food restriction induces a
hypothalamic-pituitary-adrenocortical axis-associated
neuroendocrine metabolic programmed alteration in adult
offspring rats. Archives of Medical Research, 44, 35-345.

13. MATERNAL OVER-FEEDING
• Overweight phenotype
• More pronounced impact the
closer to birth1,2
• “Metabolic imprinting”3
• Reduced energy expenditure4
• Greater size, weight, fat mass
• Higher risk for metabolic
disorder
• Evidence implicated DA and
opioid systems5
1. Ashino, N. G., Saito, K. N., Souza, F. D., Nakutz, F. S.,
Roman, E. A., Velloso, L. A., Torsoni, A. S., & Torsoni, M. A.
(2012). Maternal high-fat feeding through pregnancy and
lactation predisposes mouse offspring to molecular insulin
resistance and fatty liver. Journal of Nutritional
Biochemistry, 23, 341-348.
2. Muhlhausler, B. S., Adam, C. L., Findlay, P. A., Duffield, J.
A., & McMillen, I. C. (2006). Increased maternal nutrition
alters development of appetite-regulating network in the
brain. The FASEB Journal, 20, E556-E565.
3. Sullivan, E. L., Smith, M. S., & Grove, K. L. (2011).
Perinatal exposure to high-fat diet programs energy
balance, metabolism and behavior in adulthood.
Neuroendocrinology, 93, 1-8.
4. Stefanidis, A., & Spencer, S. J. (2012). Effects of neonatal
overfeeding on juvenile and adult feeding and energy
expenditure in the rat. PLoS ONE, 7(12).
5. Grissom, N. M., & Reyes, T. M. (2013). Gestational
overgrowth and undergrowth affect neurodevelopment:
Similarities and differences from behavior to epigenetics.
International Journal of Developmental Neuroscience, 31,
406-414.

14. LACTATION
• Early postnatal period critical
for programming appetite and
body fat mass
• HFD during suckling linked to
leptin resistance1
• Composition of milk regulator in
development/maturation of
appetite control2
• Highly palatable diet3
• Altered feeding patterns
• Higher hypothalamic DA
• Delayed satiety
Gestation and lactation in mice are
typically 3 weeks each
1. Sun, B., Purcell, R. H., Terrillion, C. E., Yan, J., Moran,
T. H. (2012). Maternal high-fat diet during gestation or
suckling differentially affects offspring leptin sensitivity
and obesity. Diabetes, 61, 2833-2841.
2. Bayol, S. A., Farrington, S. J., & Stickland, N. C.
(2007). A maternal 'junk food' diet in pregnancy and
lactation promotes an exacerbated taste for 'junk food'
and a greater propensity for obesity in rat offspring.
British Journal of Nutrition, 98, 843-851.
3. Wright, T. M., Fone, K. C., Langley-Evans, S. C., &
Voigt, J. P. (2011). Exposure to maternal consumption
of cafeteria diet during the lactation period
programmes feeding behaviour in the rat.
International Journal of Developmental Neuroscience,
29, 785-793.

15. UNDER- AND OVER-FEEDING
“Both fetal under- and over-nutrition have potential
to impact the appetite-regulating neural network in
the hypothalamus, implicating both the DA and
opioid systems in the intergenerational risk for
obesity and other metabolic disorders. Additionally,
the early postnatal period (influenced by quality of
milk during lactation) has also been shown to create
neuroendocrine imbalances, which can delay
feelings of satiety and lead to hyperphagia in the
offspring.”

16. INTRAUTERINE PROGRAMMING
• Maternal exposure to highly
palatable foods
• Impact on reward processing
well into adulthood
• Pre- and postnatal
• Altered behavior in offspring
• DA reward system1,2
• Mu-opioid receptor3
• Fetuses of HFD rodents4,5
• Hyperleptinemia
• Hyperinsulinemia
• Increased impulsivity6,7,8,9
1. Kendig, M. D., Ekayanti, W., Stewart, H., Boakes, R. A., & Rooney, K.
(2015). Metabolic effects of access to sucrose drink in female rats and
transmission of some effects to their offspring. PloS One, 10, e0131107.
2. Naef, L., Moquin, L., Dal Bo, G., Giros, B., Gratton, A., & Walker, C. D.
(2011). Maternal high-fat intake alters presynaptic regulation of dopamine
in the nucleus accumbens and increases motivation for fat rewards in the
offspring. Neuroscience, 176, 225-236.
3. Carlin, J., George, R., & Reyes, T. M. (2013). Methyl donor
supplementation blocks the adverse effects of maternal high fat diet on
offspring physiology. PLoS ONE, 8(5), e63549.
4. Gupta, A., Srinivasan, M., Thamadilok, S., & Patel, M. S. (2009).
Hypothalamic alterations in fetuses of high fat diet-fed obese female rats.
Journal of Endocrinology, 200, 293-300.
5. Mitra, A., Alvers, K. M., Crump, E. M., & Rowland, N. E. (2009). Effect of
high-fat diet during gestation, lactation, or postweaning on physiological
and behavioral indexes in borderline hypertensive rats. American Journal of
Physiology: Regulatory, Integrative and Comparative Physiology, 296(1),
R20-R28.
6. Adams, W. K., Sussman, J. L., Kaur, S., D'souza, A. M., Kieffer, T. J., &
Winstanley, C. A. (2015). Long-term, calorie-restricted intake of a high-fat
diet in rats reduces impulse control and ventral striatal D2 receptor
signalling - two markers of addiction vulnerability. Behavioral Neuroscience,
42, 3095-3104.
7. Grissom, N. M., Herdt, C. T., Desilets, J., Lidsky-Everson, J., Reyes, T. M.
(2015). Dissociable deficits of executive function caused by gestational
adversity are linked to specific transcriptional changes in the prefrontal
cortex. Neuropsychopharmacology, 40, 1353-1363.
8. Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction.
Neuropsychopharmacology, 35, 217-238.
9. Liu, J., Lester, B. M., Neyzi, N., Sheinkopf, S. J., Gracia, L., Kekatpure, M., &
Kosofsky, B. E. (2013). Regional brain morphometry and impulsivity in
adolescents following prenatal exposure to cocaine and tobacco. JAMA
Pediatr, 167, 348-354.

17. INTRAUTERINE PROGRAMMING
• Maternal HFD from last week of
gestation until weaning:
• Decreased expression of presynaptic
D2 autoreceptors in NAc
• Effects observed 2 months after
offspring weaned & returned to
control diet
• Early life nutritional programming
lasting impact on DA neurons
• Changes in circulating insulin,
leptin, ghrelin (interaction with DA)
Naef, L., Moquin, L., Dal Bo, G., Giros, B.,
Gratton, A., & Walker, C. D. (2011).
Maternal high-fat intake alters presynaptic
regulation of dopamine in the nucleus
accumbens and increases motivation for fat
rewards in the offspring. Neuroscience,
176, 225-236.

18. INTRAUTERINE PROGRAMMING
• Low maternal protein
• Increased food intake1
• Increased anxiety2
• Increased attention to
reward-predicting cues3
• Hallmark of addiction
• Higher preference for foods
rich in fat, sugar, and salt4
1. Whitaker, K. W., Totoki, K., & Reyes, T. M. (2012). Metabolic
adaptations to early life protein restriction differ by offspring sex
and postweaning diet in the mouse. Nutrition, Metabolism &
Cardiovascular Diseases, 22(12), 1067-1074.
2. Ramirez-Lopez, M. T., Vazquez, M., Bindila, L., Lomazzo, E.,
Hoffman, C., Blanco, R. N., ...Gomez de Hera, R. (2016). Exposure
to a highly caloric palatable diet during pregestational and
gestational periods affects hypothalamic and hippocampal
endocannabonoid levels at birth and induces adiposity and
anxiety-like behaviors in male rat offspring. Frontiers in Behavioral
Neuroscience, 9(339).
3. Grissom, N. M., Herdt, C. T., Desilets, J., Lidsky-Everson, J.,
Reyes, T. M. (2015). Dissociable deficits of executive function
caused by gestational adversity are linked to specific
transcriptional changes in the prefrontal cortex.
Neuropsychopharmacology, 40, 1353-1363.
4. Bayol, S. A., Farrington, S. J., & Stickland, N. C. (2007). A
maternal 'junk food' diet in pregnancy and lactation promotes an
exacerbated taste for 'junk food' and a greater propensity for
obesity in rat offspring. British Journal of Nutrition, 98, 843-851.

19. DRUG ADDICTION
• Rats fed highly palatable diets
during prenatal and pre-
weaning affects responses to
• Amphetamine
• Increased locomotor activity
• Sensitized response
• Alcohol
• Increased consumption
• Food exposure during critical
periods of neurodevelopment
impact consumption behavior
Bocarsly, M. E., Barson, J. R., Hauca, J. M., Hoebel, B. G.,
Leibowitz, S. F., & Avena, N. M. (2012). Effects of perinatal
exposure to palatable diets on body weight and
sensitivity to drugs of abuse in rats. Physiology &
Behavior, 107, 568-575.

20. GENETICS
• Epigenomic state1
• Maternal behavior
• Environmental programming
• Nutrition insults during
pregnancy passed to 2nd/3rd
generations2
• DNA methylation
• Biochemical process
involving covalent addition
of a methyl group at the 5’
position of cytosine in DNA
1. Weaver, I. C. G., Cervoni, N., Champagne, F. A., D'Alessio, A.
C., Sharma, S., Seckl, J. R., ...Meaney, M. J. (2004). Epigenetic
programming by maternal behavior. Nature Neuroscience, 7(8),
847-854.
2. Ponzio, B. F., Carvalho, M. H. C., Fortes, Z. B., & Franco, M. D.
C. (2011). Implications of maternal nutrient restriction in
transgenerational programming of hypertension and
endothelial dysfunction across F1-F3 offspring. Life Sciences,
90, 571-577.

21. GENETICS
• DNA methylation
• Maternal HFD
• Altered expression of DA and
opioid-related genes1
• Hypomethylation
• Transgenerational perpetuation
of addictive symptomatology &
subsequent obesity
• Maternal cocaine during 2nd
& 3rd trimester2
• Hypomethylation
• Hypermethlyation
• Modify gene expression
1. Vucetic, Z., Kimmel, J., Totoki, K., Hollenbeck, E., & Reyes, T.
M. (2010). Maternal high-fat diet alters methylation and gene
expression of dopamine and opioid-related genes.
Endocrinology, 151(10), 4756-4764.
2. Novikova, S. I., He, F., Bai, J., Cutrufello, N. J., Lidow, M. S., &
Undieh, A. S. (2008). Maternal cocaine administration in mice
alters DNA methylation and gene expression in hippocampal
neurons of neonatal and prepubertal offspring. PLoS ONE, 3(4),
e1919

22. INTRAUTERINE PROGRAMMING
“Early life nutritional programming can have a lasting impact
on behavior via the reward system (including DAT) and
MOR. Elevated blood levels of insulin and leptin in the
offspring of overfed mothers can lead to states of resistance
and subsequent weight gain. Hormonal influence on DA
neurons may lead to symptoms of addiction-like eating
(impulsivity, attentional bias, incentive salience).
Furthermore, epigenetic modifications stemming from
nutritional insults during pregnancy have the potential to
become transgenerational. Changes in DNA methylation
appear to modify genetic expression of DAT and MOR,
preprogramming the rewarding properties of highly
palatable foods.”

23. DISCUSSION
• “Addiction transfer” via
dysregulation of reward systems
begins to develop in utero
• Maternal ingestion of foods
known to induce addictive-like
eating can impact fetal
neurodevelopment and
subsequent ingestive behavior

24. DISCUSSION
• Timing of nutritional insult
• Most sensitive time window for
developmental programming
• Gestation, lactation
• Metabolic dysfunction stemming from
nutritional exposures can occur
independent of postnatal nutrition1
• Junk food consumed during
pregnancy can have lasting effects
on offspring (persist into adulthood)
• Body weight, food & drug preference2
1. Ashino, N. G., Saito, K. N., Souza, F. D.,
Nakutz, F. S., Roman, E. A., Velloso, L. A.,
Torsoni, A. S., & Torsoni, M. A. (2012).
Maternal high-fat feeding through
pregnancy and lactation predisposes
mouse offspring to molecular insulin
resistance and fatty liver. Journal of
Nutritional Biochemistry, 23, 341-348.
2. Bocarsly, M. E., Barson, J. R., Hauca, J.
M., Hoebel, B. G., Leibowitz, S. F., &
Avena, N. M. (2012). Effects of perinatal
exposure to palatable diets on body
weight and sensitivity to drugs of abuse
in rats. Physiology & Behavior, 107, 568-
575.

25. CONCLUSIONS
• Neuroadaptations within reward
related centers of brain contribute
to hedonic hyperphagia
• Given what we know about food
addiction, it is likely that a mother
who consumes junk food during
gestation will do so during lactation
• Also likely to create post-natal food
environment with these foods
Composite effect

26. CONCLUSIONS
• A greater understanding of
addiction transfer will help us
develop effective interventions
to combat the obesity pandemic
• Monitoring dietary intake during
pregnancy can become an
important preventative measure
• Macros should be balanced
• Reduced exposure to highly
palatable foods

27. QUESTIONS?