4/18/2013 Disclosures Facts & Fiction about Pediatric Obesity - - PDF document

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Facts & Fiction about Pediatric Obesity Treatm ent: Nutrition & Metabolic Health Im provem ent

Luis A. Rodríguez, RD, CNSC UCSF Benioff Children’s Hospital & WATCH Clinic May 20 13

Disclosures

 I have nothing to disclose

Outline

 Adult and Pediatric Obesity Trends  Health Consequences Associated with Obesity  Genetics vs. Environmental Changes  Fats, Proteins and Carbohydrates (sugars)  Meal Trends, and Locations  Screening Obesity and Metabolic Markers  Nutritional Recommendations  Other Recommendations  Summary

1999

Obesity Trends* Am ong U.S. Adults BRFSS, 1 9 9 0 , 1 9 9 9 , 2 0 0 9

( * BMI 3 0 , or about 3 0 lbs. overw eight for 5 ’4 ” person) 2009 1990 No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

Pediatric Obesity Epidemic

(M. de Onis et al., 2010)

Pediatric Obesity Epidemic

4/18/2013 2 Pediatric Obesity Epidemic Pediatric Obesity Epidemic

Im m ediate Health Problem s Im m ediate Health Problem s Chronic Health Conditions Chronic Health Conditions  Asthma  Sleep Apnea  Skin Infections  Joint Pain  Hypertension  Type 2 Diabetes  Hypercholesterolemia  Hepatic Steatosis  Menstrual Abnormalities  Heart Disease  PCOS  Lower Self-Esteem and

Confidence

Health Consequences Associated with Childhood Obesity and Unhealthy Eating

• Genetic Syndromes
• Prader-Willi
• Laurence-Moon/Bardet-Biedl
• Alstrom
• Turner’s
• Ruvalcaba

Genetics and Hormonal Defects

• Developmental Programming
• Prenatal Undernutrition (SGA) (Barker, 2004)
• Dutch Famine Study (Roseboom et al., 2001)
• Prematurity
• Overnutrition (LGA, GDM) (Boney et al., 2005)
• Direct relationship of maternal
• besity with child obesity.

(Whitaker, 2004)

Genetics and Hormonal Defects Environmental Changes

 Food Supply Macronutrient Changes

 Fats  Proteins  Carbohydrates

 Meal Trends, and Locations  Food Addictions?  Decreased Physical Activity Levels

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Dietary Energy in Food Supply

Kcal/ day per person (Putnam, 2002) ↑340 kcal/day

Macronutrient Changes over past 3 Decades

 Fat

 Total Kcal % decreased from 40%  30% since 1980’s

 Protein

 Stable at about 15%

 Carbohydrate

 Starch 49  51%  Fructose 8  12-15%

(Chanmugam et al, 2003)

Fats

Dietary Fat Dietary Source Medicinal Value or Danger Omega-3 Fatty Acids Wild fish, flaxseed oil Anti-inflammatory, lowers serum TG, repairs membranes Monounsaturated Fatty Acids Olive and canola oil Stimulates Liver Metabolism, reduces atherogenesis Polyunsaturated Fatty Acids Vegetable oils Anti-inflammatory, excess amount can cause immune dysfunction Saturated Fatty Acids Grass-fed animal meats, milk and dairy products, egg yolks Atherogenic in Familial Hypercholesterolemia Medium-chain triglycerides Palm oil, coconut oil, palm kernel

• il

Energy source, some suggestion

• f stimulation of atherosclerosis

Omega-6 fatty acids Farm-raised animals and fish (corn and soy fed) Atherosclerosis, insulin resistance, immune dysfuncion, pro-inflammatory Trans fats Synthetic, processed food Atherosclerosis, NASH

(Lustig, 2012; Perito et al., 2013)

Fats

 Women’s Health Initiative  Randomized controlled, prospective study from

1993-1998.

 ~50,000 post-menopausal women.  Goal to decrease Fat Calories and increase F/V and

• grains. Fat decreased by 8%.

 No significant risk reduction in CHD, stroke or CVD. (Howard et al, 2006)

Proteins

 Branched Chain Amino Acids (L, I, V)  Essential Amino Acids  High concentration in corn  Increased insulin resistance d/t bypassing

glycogen storage

 Patients with metabolic syndrome have

higher bloodstream levels (Lustig, 2012; Newgard et al., 2009)

Sugar (Fructose)

• Increases nutrient consumption
• Attenuated Ghrelin response
• Reduced Insulin response, low Leptin rise.
• NASH pathogenesis and progression
• Liver is primary site for metabolism
• Fructose bypasses rate-limiting step of glycolysis
• Preferentially metabolized to acetyl coA
• Provides substrate for FFA
• Increases Visceral Fat

(Teff et al., 2004) (Perito et al., 2013) (Elliot,2002; Lustig, 2012)

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Fructose

 Increased consumption

 37gm fructose/day (1977-1978) 8% Kcal Intake  55gm fructose/day 10.2% Kcal Intake  78gm fructose/day 12% Kcal Intake (Adolescents)

(Vos et al., 2008)

Sugar (Fructose)

 American Heart Association Recommendation for

Optimal Cardiovascular Health

 Women 21gm sugar/day (1,800 Kcal/day)  Men 38gm sugar/day (2,200 Kcal/day)

(Johnson et al., 2009)

Fiction

 “Beating obesity will take action by all of us, based

• n one simple com m on sense fact: All calories

count, no matter where they come from, including Coca-Cola and everything else with calories…”

• The Coca Cola Company, 2013

Fiction Fiction Fact Fact  A Calorie is A Calorie  Calorie output is tightly

regulated and dependant on the quantity and quality of ingested calories.

 A Calorie Burned is a

Calorie Burned.

Calories Where Do People Eat When They Eat Out?

0% 5% 10% 15% 20% 25% 30% 35% 40% 45% 50%

Source: “Factors Influencing Lunchtime Food Choices among Working Americans”. 2009

Fast Food

 1/3 of U.S adults eat fast food  Longitudinal studies show fast food

intake predicts weight gain and increased risk for T2D

 Fast food restaurants overrepresented in

poorer neighborhoods; healthy alternatives harder to find

 Prevalence: 2.5/mile2 vs. 1.5/mile2

 Low SES associated with increased fast

food consumption

(Garber, Lustig, 2011)

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 Sugar

 Rodent Models demonstrate binging,

withdrawal (teeth chattering, tremors, shakes and anxiety)

 Seeking and craving  Cross-Sensitization  Human Studies also suggest sugar is addictive

with withdrawal

 Fructose increases liver and muscle insulin

resistance (Sung et al., 2011; Perito et al., 2013)

 Blocks leptin’s ability to extinguish mesolimbic

dopamine signaling

Photo from cbsnews.com

(Garber, Lustig, 2011)  Caffeine

 “Flavoring agent”  Increases salience of high rewarding

beverage.

 Well established psychological & physiological

dependence across age spectrum.

Is Fast Food Addictive?

(Garber, Lustig, 2011)

Photo from: http://www.islandcrisis.net

Is Fast Food Addictive?

 Environmental Cues

 Required to create addictive patterns  Powerful external Stimuli trigger reward in animal and human  Vulnerability to environmental cues may explain differences in

ability to follow a “diet”  Ads

 3-5 per 30 minutes during prime time TV.

(Brown, 2002) (Garber, Lustig, 2011)

Exercise

 33%

 Percentage of youth who are actual couch

potatoes, engaging in little or no leisure-time physical activity whatsoever  2/ 3

 Proportion of teens that don’t meet the

minimum recommended levels of physical activity of one hour a day of moderate to vigorous activity  >2-3

 Daily number of hours children spend

watching TV; more time than on any other single activity except sleeping  <6%

 Percentage of high schools requiring daily PE

Fiction Fiction Facts Facts  Exercise alone causes

significant weight loss

 Exercise—even in absence of

weight loss—decreases hepatic steatosis, and other lipotoxicity markers.

 Exercise builds muscle and

stimulates new mitochondrial development and improves insulin sensitivity

 Increases liver’s Krebs cycle

speed

Exercise

(Perito et al. 2013) (Lustig, 2012)

Screening and Identification of Pediatric Obesity

 Children 0-24 months use WHO Growth Standards

 >97th%ile for weight for length

 Children >2 years use CDC BMI curves

 85-95th%ile: Overweight  >95th%ile: Obese

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Metabolic Markers

 Physical Assessment

 Acanthosis Nigricans (Axilla, neck, flexural areas)  Marker of hyperinsulinemia

 Lab values

 Fasting insulin, fasting BG, HgA1C  ALT  Uric Acid  Fasting Cholesterol Panel

Unhealthy Food Patterns

 Beverages

 Soda, Juice (any kind), energy drinks, coffee drinks

 Foods

 Fast food, pre-packaged, processed foods

 Food environment

 Eating in front of TV, chaotic environment, on the go

 Stress eating, binge eating, disordered eating D I E T AN D E X E R CI S E !

Clinical Treatment

…W H AT?

WATCH Clinic (Weight Assessment for Teen and Child Health)

Nutritional Recommendations

 ½ of your plate non-starchy Vegetables and Fruit  ¼ of your plate Whole Grains

 Cereals >5gm fiber/serving  Breads >3gm fiber/serving  Other packaged >3gm fiber/~100Kcal

 ¼ of your plate Proteins High in Fiber or Healthy Fat

 Legumes, Nuts, wild fish, free range beef/poultry, eggs and dairy  Plain, added-sugar free dairy

 Healthy Fats

 Olive/Canola Oils

Meals

 Breakfast

 Veggie Omelet, fruit, whole grain toast  Old Fashion oatmeal, nuts, banana, milk

 Lunch

 Cold Sandwich on whole grain bread, chicken breast/roast

beef, vegetables, cheese, fruit, water to drink

 Mixed greens salad with olive oil and vinegar, beans,

tomatoes, cucumbers, whole grain bread  Dinner

 Wild salmon/free range beef or poultry, brown rice, mixed

sautéed vegetables

 Whole grain pasta with tomatoes, bell peppers, onion, grilled

chicken, mixed greens salad with olive oil/vinegar

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Snacks

 Mix a protein with a non-starchy vegetable or fruit

 Mixed nuts with carrots  Plain yogurt, with banana  Cottage cheese with mixed berries  Plain milk or milk substitute with fruit  Hummus with bell peppers, cucumbers  Celery with peanut butter  Cheese stick with cherry tomatoes

Other Recommendations

 Wait 20 minutes before offering 2nd portions  Control home environment by limiting “treats”  Everyone at home follows same recommendations  Remove TV from Child/Teenage Room  Enroll in any type of entertaining, fun, sustainable,

regular physical activity with goal of 60 minutes/day

Summary

 Calories are NOT created equal. Unique nutrients

contribute to metabolic disease, even in absence of

• besity—trans fats, fructose.

 Follow WATCH Clinic Plate Model  Avoid processed foods (trans fats, low fiber, high sugar)  Avoid all sweetened beverages; only drink water, plain milk or

plain milk substitutes, and plain teas  Exercise improves cardiometabolic health, even in the

absence of weight loss.

References

 A. K. Garber, Lustig R. H. (2011) “ Is Fast Food Addictive?” Curr. Drug

Abuse Rev. 4, 146-162.

 Brown JD, Witherspoon EM. The mass media and American

adolescents’ health. J Adoles Health. 2002 Dec;31 (6 Suppl): 153-70.

 B. V. Howard et al., “Low-Fat Dietary Pattern and Risk of

Cardiovascular Disease: The Women’s Health Initiative Randomized Controlled Dietary Modification Trial,” JAMA 295 (2006): 655-66; B.

• V. Howard et al., “Low-Fat Dietary Pattern and Weight Change over 7

Years: The Women’s Health Initiative Dietary Modification Trial,” JAMA 295 (2006) 39-49.

References

 C. B. Newgard et al., “A Branched-Chain Amino Acid-Related Metabolic

Signature That Differentiates Obese and Lean Humans and Contributes to Insulin Resistance,” Cell Metab. 9 (2009): 311-26.

 C. M. Boney et al., “Metabolic Syndrome in Childhood: Association with

Birth Weight, Maternal Obesity, and Gestational Diabetes,” Pediatrics 115 (2005): e290-e96.

 D. J. Barker, “The Development Origins of Chronic Adult Disease,”

Acta Paediatr. Supp. 93 (2004): 26-33.

 K. C. Sung et al., “Interrelationship Between Fatty Liver and Insulin

Resistance in the Development of Type 2 Diabetes,” J. Clin. Endocrinol.

• Metab. 96 (2011): 1093-97.

 M. B. Vos et al., “Dietary Fructose Consumption Among US Children

and Adults: The Third National Health and Nutrition Examination Survey,” Medscape J. Med. 10, (2008): 160.

References

 M. de Onis et al., “Global Prevalence and Trends of Overweight and

Obesity Among Preschool Children,” Am . J. Clin. Nutr. 92 (2010): 1257-64.

 P. Chanmugam et al., “Did Fat Intake in the United States Really

Decline Between 1989-1991 and 1994-1996?” J. Am . Diet Assoc. 103 (2003): 867-72.

 Perito ER, Rodriguez LA, Lustig RH. “Dietary management of non-

alcoholic steatohepatitis.” Current Opinion in Gastroenterology, March 2013. Invited review, submitted November 2012.

 R.J.F. Loos et al., “Genome-wide Association Studies and Human

Population Obesity,” in Obesity Before Birth, R.H. Lustig ed. (New York: Springer, 2010), pp. 95-112.

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References

 R.K. Johnson et al., “Dietary Sugars Intake and Cardiovascular Health:

A Scientific Statement From the American Heart Association. Circulation.” 2009 Sep 15; 120 (11):1011-20.

 Robert H. Lustig, Fat Chance: Beating the Odds Against Sugar,

Processed Food, Obesity, and Disease. New York: Penguin, 2012.

 S. J. Olshansky et al., “A Potential Decline in Life Expectancy in the

United States in the 21st Century,” New Engl. J. Med. 352 (2005): 1138- 45.

 Teff K, et al. Dietary Fructose Reduces Circulating Insulin and Leptin,

Attenuates Posprandial Suppression of Ghrelin, and increases Triglycerides in Women. J Clin Endocr Metab (2004): 89:2963-2972.

 T. J. Roseboom et al., “Effects of Prenatal Exposure to the Dutch

Famine on Adult Disease in Later Life: An Overview,” Mol. Cell.

• Endocrinol. 185 (2001): 93-98.

 Whitaker, R. “Predicting Preschooler Obesity at Birth: The Role of

Maternal Obesity in Early Pregnancy,” Pediatrics. (2004): 114; e29.