www.medscape.org This article is part of a CME/CE certified activity. The complete activity is available at: /viewprogram/32316 CME/CE Information CME/CE Released: 01/31/2012; Valid for credit through 01/31/2013 Target Audience This activity is intended for clinicians such as physicians, nurse practitioners, school nurses, and dietitians as well as coaches, teachers, and daycare providers. Goal The goal of this activity is to review comorbidities associated with pediatric obesity and provide strategies for their prevention and management. Learning Objectives Upon completion of this activity, participants will be able to: Identify serious obesity-related comorbidities and the risk factors that are associated with their development in children who are overweight or obese. 1. Describe specific strategies used by clinicians who successfully diagnose and manage obesity-related comorbidities in children 2. Credits Available Physicians - maximum of 0.75 AMA PRA Category 1 Credit(s)™ Nurses - 0.75 ANCC Contact Hour(s) (0 contact hours are in the area of pharmacology) All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Accreditation Statements For Physicians Medscape, LLC is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. Medscape, LLC designates this enduring material for a maximum of 0.75 AMA PRA Category 1 Credit(s)™ . Physicians should claim only the credit commensurate with the extent of their participation in the activity. Medscape, LLC staff have disclosed that they have no relevant financial relationships. Contact This Provider For Nurses Eating for 2: Maternal Nutrition and Childhood Obesity (print... http://www.medscape.org/viewarticle/757304_print 1 of 14 3/1/12 1:57 PM
Transcript
www.medscape.org
This article is part of a CME/CE certified activity. The complete activity is available at:/viewprogram/32316
CME/CE Information
CME/CE Released: 01/31/2012; Valid for credit through 01/31/2013
Target Audience
This activity is intended for clinicians such as physicians, nurse practitioners, school nurses, and dietitians aswell as coaches, teachers, and daycare providers.
Goal
The goal of this activity is to review comorbidities associated with pediatric obesity and provide strategies fortheir prevention and management.
Learning Objectives
Upon completion of this activity, participants will be able to:
Identify serious obesity-related comorbidities and the risk factors that are associated with theirdevelopment in children who are overweight or obese.
1.
Describe specific strategies used by clinicians who successfully diagnose and manage obesity-relatedcomorbidities in children
2.
Credits Available
Physicians - maximum of 0.75 AMA PRA Category 1 Credit(s)™
Nurses - 0.75 ANCC Contact Hour(s) (0 contact hours are in the area of pharmacology)
All other healthcare professionals completing continuing education credit for this activity will be issued acertificate of participation.
Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Accreditation Statements
For Physicians
Medscape, LLC is accredited by the Accreditation Council for Continuing Medical Education (ACCME) toprovide continuing medical education for physicians.
Medscape, LLC designates this enduring material for a maximum of 0.75 AMA PRA Category 1 Credit(s)™ .Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Medscape, LLC staff have disclosed that they have no relevant financial relationships.
Contact This Provider
For Nurses
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Author
Daniel L. Marks, MD, PhD
Associate Professor, Pediatrics, Oregon Health and Science University, Portland, Oregon
Disclosure: Daniel L. Marks, MD, PhD, has disclosed no relevant financial relationships.
Dr. Marks does intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnosticsapproved by the FDA for use in the United States.
Dr. Marks does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics notapproved by the FDA for use in the United States.
Editor
Kristin M. Richardson
Senior Scientific Director, Medscape, LLC
Disclosure: Kristin M. Richardson has disclosed no relevant financial relationships.
Gina K. Kaeuper
Freelance Scientific Director, Knoxville, TN
Disclosure: Gina K. Kaeuper has disclosed no relevant financial relationships.
Laura A. Feiker
Clinical Editor, Medscape, LLC
Disclosure: Laura A. Feiker has disclosed no relevant financial relationships.
CME Reviewer
Nafeez Zawahir, MD
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Download Slides
CME Clinical Director, Medscape, LLC
Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.
Nurse Planner
Laurie E. Scudder, DNP, NP
Nurse Planner, Continuing Professional Education Department, Medscape, LLC; Clinical Assistant Professor,School of Nursing and Allied Health, George Washington University, Washington, DC
Disclosure: Laurie E. Scudder, DNP, NP, has disclosed no relevant financial relationships.
Slide 1.
Daniel Marks, MD: Hello. This is Dr Daniel Marks. I am an associate professor of Pediatric Endocrinology atOregon Health and Science University and Doernbecher Children’s Hospital in Portland, Oregon. I would like towelcome you to this audio webcast titled, “Eating for 2: Maternal Nutrition and Childhood Obesity.”
My goals today will be first to discuss the evidence for fetal metabolic programming in humans. I will start offwith a discussion of some basic epidemiology trying to demonstrate that fetal metabolic programming occurs.Next, I will discuss current environmental challenges during pregnancy and lactation, primarily the consumptionof large amounts of non-nutritive sweeteners and animal fat. I will discuss the role of breastfeeding in childhoodmetabolic programming and flavor preference modeling, and then very briefly mention a few developmental
Eating for 2: Maternal Nutrition and Childhood ObesityCME/CEDaniel L. Marks, MD, PhD
Posted: 01/31/2012
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aspects of how children learn to eat.
Slide 2.
First, I am going to discuss the evidence that metabolic programming occurs in human pregnancies, and willuse the Dutch Hunger Winter as an example of nutritional programming in humans. The data here is very clearand the story is compelling, although a bit sad. In the mid 1940s during World War II, the area that is now theNetherlands was occupied by Germany. At that time, the Allies conducted an effort called Operation MarketGarden in an attempt to liberate the German-occupied portion of the country. Unfortunately, this effort failed andwas followed then by a blockade of food imports to this part of Europe. A very harsh winter ensued, furtherlimiting access to food.
For a period of time (about 3 to 4 months) all people in this area were limited very strictly in the amount and typeof calories that they consumed. At the lowest point, the consumption was from 400 to 800 calories per day ofvery poor nutrition. This caloric restriction included women who were pregnant and women who were lactating,and, because of the availability of detailed clinical records, we were able to follow up on a cohort of offspring ofthese mothers to see what impact starvation during pregnancy had on the child’s outcome as they proceeded toadulthood. What was clearly shown was that exposure to famine during mid or late gestation resulted inimpaired glucose tolerance and a propensity to develop type 2 diabetes mellitus later in life. In contrast,exposure to famine early in gestation led to full-blown metabolic syndrome, with an atherogenic lipid profile,obesity, and an increased risk of coronary heart disease and other associated problems. These changes werethought to be due to lasting chemical modification of genes in the developing fetus that resulted in permanentso-called programmed changes in gene expression. This has now been defined as epigenetics.
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Slide 3.
Now, I would like to transition to discussing the modern nutritional challenges during pregnancy. Obviously weare not dealing, fortunately, with many periods of starvation in our environment; what we are in fact dealing withis the overconsumption of simple sugars and proinflammatory fatty acids, and by that I primarily mean animalfats and certain soy products. Over time, our consumption of simple sugars has risen dramatically. By 2001 wewere consuming around 150 pounds per year of simple sugars; our consumption is up towards about 180pounds per year now. What happens if we have a pregnancy that is challenged not by nutritional deprivation butinstead by the increased consumption of simple sugars in addition to the increased consumption of animal-typefat, the n-6 or proinflammatory fatty acids?
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Slide 4.
The first thing we can acknowledge is that the consumption of this kind of diet would lead to excessive maternalweight gain, and this in turn appears to have a dramatic increase in risk in the offspring vis-à-vis theirdevelopment of obesity and its attendant metabolic complications. If we look at recent epidemiological data, wefind that for women who start their pregnancy with a normal BMI, if they gain somewhere around 0.3 to maybe0.4 kilograms per week, that appears to be sort of the sweet spot where all risks are minimized—the risk of achild developing obesity later in life and also of having a child who is either small or large for their gestationalage at delivery. On the other hand, if the mother enters the pregnancy either overweight or obese, as nearly athird of our population of women of childbearing age are these days, what we find is that the weight gain rate atwhich these risks are minimized is less, and in fact approaches zero, or, for obese women, may even be lessthan zero. It appears that we can no longer apply the standard guidelines for weight gain during pregnancywhen the mothers are overweight or obese before pregnancy. They probably need to gain less weight in orderto minimize risks.
Slide 5.
We can also look at preclinical models that show that maternal diet leads to a variety of problems during thedevelopment of the fetus. In one study, a sample biopsy from a liver of a developing nonhuman primate isstained with a red stain to show fat. If the primate “mom” is on a typical high-fat “Western” diet, there istremendous deposition of this red stain in the liver of the baby as it develops. In fact, the baby is developingfairly severe fatty liver disease before it is even born. Furthermore, this leads to tremendous increases inoxidative stress markers and the death of liver cells. This is a clear example of how maternal diet can be veryhard on the baby’s liver.
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Slide 6.
I would also like to point out that we need to understand the types of fats that are being consumed and not justthe amount of fat consumed. N-6 fatty acids are proinflammatory and are thought to be causal of conditions likecoronary artery disease, whereas the n-3s, the fish-oil fatty acids, are protective. We can look at the n-6 to n-3fatty acid ratio (the n-6s being the bad fat and the n-3s being the good fat), and if we look at the maternal diet,we find that if mom is on a high-fat diet, then her n-6 to n-3 fatty acid ratio is very high. That is not particularlysurprising. Unfortunately, what we find is that the placenta does not protect the fetus from this abnormal andpathological ratio of fatty acids. If we look at the n-6 to n-3 ratio in the baby, it is elevated, indicating again thatmom’s diet can lead to a proinflammatory lipid profile in the baby. This is not a benign outcome. There arestudies now which show that higher amounts of fish-oil-type fats [n-3] found in mom’s diet are very beneficial inlowering the risk for the baby developing, for example, obesity and other attendant complications, whereas then-6 acids convey a much higher risk.1,2
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Slide 7.
I would like to move on now to discuss breastfeeding. Historically, breastfeeding has been linked to a lower riskfor childhood obesity, as I will show you. However, I must also point out that a lot has changed over time. Thefirst question is simply: Does breastfeeding make a difference? Is there any evidence? There is a very cleardose-response relationship between the amount of breastfeeding that a mom does and the risk of childhoodobesity, such that there is nearly a 3-fold change in the child’s risk of developing obesity as the time spentbreastfeeding increases from never to periods longer than 12 months.
Slide 8.
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Furthermore, there are some examples of diseases that are associated with obesity in susceptible populations,such as type 2 diabetes, in which the risk of this outcome is decreased by virtue of the period of time spentbreastfeeding. However, we need to look very carefully at these studies and realize that many of them werepublished in the mid to late 1990s. We were looking at adults who were as much as 40 years to even 50 yearsold, and what this really tells us is the impact of breast milk that was generated in the 1950s, not in 2012. I thinkwhat we need to consider is the possibility that breast milk in the current environment is going to convey adifferent risk.
Slide 9.
We can show, for example, that during lactation, infant fatty acids are very strongly linked to maternal fatty acidsand that this is conveyed via the breast milk. So, if we look back at that n-6 to n-3 fatty-acid ratio, the higher it isin mom, then the higher it is in the breast milk and the higher it is in the baby. So, the bottom line is, if mom isconsuming unhealthy fats, so is the baby and that is reflected in their development.
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Slide 10.
Furthermore, there are very clear studies that demonstrate that flavors experienced by mom either duringpregnancy or during lactation are transferred to the baby and those become preferred flavors for that baby’slifetime. There is one very nice example in which moms were asked to consume carrot juice or water at 6 timesduring the day throughout the last trimester of pregnancy and the period of lactation. At the time that the babywas being weaned to solid food, the babies were given their rice cereal mixed with either carrot juice or water.What was very clearly shown is that if mom had consumed carrot juice during the last trimester of pregnancy orthroughout lactation, then the baby had a strong increase in preference for carrot juice as part of its diet. This isagain an example of what we call flavor-preference modeling and it is independent of genetics and simplyreflective of something that happens by virtue of mom’s dietary experience.
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Slide 11.
I would like to point out a few other important things regarding the development of a child’s dietary preferences.As a child develops from weaning and through the first several years of life, there is a tremendous amount oflearning that goes on in regards to the type of diet that they will consume for the rest of their life, and this ishighly modifiable by their educational experience as they move forward. I do not really have time to go throughall of the details here, but I will give just a couple of quick examples. Reward tremendously increases foodpreference and this has a permanent effect. So if we said to a child, for example, “if you finish your homework,then you can have this treat,” that treat becomes an increased preferred food for the rest of their life simplybecause it was used as a reward. On the other hand, if we were to use bribery to try and get a child to eat afood—the classic example being, “if you finish your peas, you can go out and play,” that actually will decreasethe child’s preference for that food, again for their lifetime. These kinds of learning experiences have beenstudied over and over again and appear to have a very powerful effect on the baby’s lifetime risk of developingobesity and poor diet consumption.
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Slide 12.
I would like to thank you for participating in this activity. Remember, this is just one of the 3 parts required forcompletion of this CME/CE program. Please listen to all 3 parts to earn your CME/CE credit and checkMedscape Education often to continue to participate in the Children’s Health, Fitness, and Nutrition Initiative. Toproceed to the online CME/CE test, please click on the Earn CME/CE Credit link on this page. Thank you againfor your time.
Supported by an independent educational grant from Sanford Health.
This article is part of a CME/CE certified activity. The complete activity is available at:/viewprogram/32316
Boucher O, Burden MJ, Muckle G, et al. Neurophysiologic and neurobehavioral evidence of beneficialeffects of prenatal omega-3 fatty acid intake on memory function and school age. Am J Clin Nutr.2011;93:1025-1037. Abstract
1.
Donahue SMA, Rifas-Shiman SL, Gold DR, Jouni ZE, Gillman MW, Oken E. Prenatal fatty acid statusand child adiposity at age 3 y: results from a US pregnancy cohort. Am J Clin Nutr. 2011;93:780-788.Abstract
2.
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