Hvorfor er overvekt hos barn alarmerende? Hva er det som skjer Overlege Dr.Med Bård Kulseng Regionalt senter for behandling av sykelig overvekt St. Olavs Hospital og NTNU

Hvorfor er overvekt hos barn alarmerende? Vi vet ikke sikkert hva overvekten kommer av og hvordan den skal bekjempes. Men den skyldes at et overskudd av kalorier bygger seg opp Den fører til redusert livskvalitet og sykdom. Den øker i befolkningen Den påvirker neste generasjon Den er en økonomisk og sosial belastning på vårt samfunn Påvirker stabilitet i vårt samfunn Øker forskjell i levekår

Nå har ca 1 av 4 fedme i Norge! Age 20+ H2: 18.6% H3: 23.5% Nå har ca 1 av 4 fedme i Norge! Age 20+ H2: 14.4% H3: 22.5%

Endring i insidenser og sykdomspanorama Har vi et helsevesen som er tilpasset nye utfordringer

Hvorfor endring i befolkningen Økt energi inntak (fett og sukker). Feil mat Mindre fysisk aktivitet Sykdom? Miljøforurensninger? Påvirket foster Arv og endring i gener som aktiveres ????????

En spiser for mange kalorier og sitter for mye i ro

Copyright © The American College of Physicians. From: Reduction in Obesity and Related Comorbid Conditions after Diet-Induced Weight Loss or Exercise-Induced Weight Loss in Men: A Randomized, Controlled Trial Ann Intern Med. 2000;133(2):92-103. doi:10.7326/0003-4819-133-2-200007180-00008 Figure Legend: Comparison of Change Scores between the Diet and Exercise Weight Loss Groups Date of download: 9/18/2013 Copyright © The American College of Physicians. All rights reserved.

Årsaker til fedme

Spisevaner og kosthold Røyking, snus og alkoholbruk Sosial ulikhet i helse og læring blant barn og unge Resultater fra den landsrepresentative spørreskjemaundersøkelsen ”Helsevaner blant skoleelever. En WHO-undersøkelse i flere land” Universitetet i Bergen Fysisk aktivitet Fritidsaktiviteter Spisevaner og kosthold Røyking, snus og alkoholbruk Subjektiv helse og velvære Skoletrivsel og skolestress Mobbing Skjermbasert atferd og problematisk dataspilling

Biology's influence during obesity development, treatment, and relapse. Biology's influence during obesity development, treatment, and relapse. Homeostatic systems adapt to prevent perpetual weight loss or gain when environmental and behavioral pressures change. The interplay of this balance between the changes in nonhomeostatic pressures and homeostatic adaptations is shown for the initial development and progression of obesity (A–C), during energy-restricted weight loss (D), during weight maintenance after weight loss (E), and during the relapse to obesity (F). Biology may play a more subtle, permissive role during the initial development of obesity, but it becomes a driving force for weight regain after weight loss. MacLean P S et al. Am J Physiol Regul Integr Comp Physiol 2011;301:R581-R600 ©2011 by American Physiological Society

Blundell. Disease Models & Mechanisms 5, 608-613 (2012) Fig. 2. A new formulation for appetite control. A proposed tonic signal for the drive to eat that reflects the body’s demand for energy arises (mainly) from FFM and RMR. In turn, this drive is under tonic inhibition from leptin, whose action reflects the amount of stored energy reserves in the body. As the amount of adipose tissue increases, leptin insensitivity occurs and this tonic inhibition is reduced. The drive to eat is periodically interrupted and suppressed by episodic signals in the form of peptides that are released from the GI tract in response to food consumption. The resulting pattern of eating is a consequence of the interactions between tonic and episodic physiological signals. The figure also illustrates the postulated effect of exercise on appetite control. Prolonged exercise displays a dual-process action by stimulating hunger (an effect that is highly variable between individuals) but also by increasing post-prandial satiety signalling (King et al., 2009) through an effect on GI peptides (Martins et al., 2010). See text for further description. Blundell. Disease Models & Mechanisms 5, 608-613 (2012)

Figure 1 The “limbic triangle Figure 1  The “limbic triangle.” Three areas of the CNS conspire to drive food intake and reduce physical activity, resulting in persistent weight gain. The ventromedial hypothalamus (VMH) transduces the leptin signal from adipocytes to reduce energy intake and increase energy expenditure; however, hyperinsulinemia prevents leptin signaling, promoting the “starvation response.” The ventral tegmental area (VTA) transduces the leptin signal to reduce dopamine neurotransmission to the nucleus accumbens (NA), reducing food intake; however, hyperinsulinemia prevents leptin signaling here as well, increasing dopamine and promoting the “reward” of food. The amygdala transduces fear and stress, which results in increased cortisol release from the adrenal cortex. The elevated cortisol also drives energy-rich food intake and promotes insulin resistance, further interfering with leptin signaling at the other two CNS sites. Thus, activation of any aspect of the limbic triangle turns on a positive feedback loop, promoting continued weight gain and obesity. CHO, carbohydrate; REE, resting energy expenditure; SNS, sympathetic nervous system. 23

The next generation of patients

Individuality and epigenetics in obesity Periods of life in which DNA methylation processes take place. Erasure of methylation imprints is almost exclusively of two stages: primordial germ cells and blastocyst development. Maternal care, ageing and different environmental factors (such as dietary components, some toxins and drugs, inflammation and perhaps physical activity) regulate the methylation processes in the different periods of life. © This slide is made available for non-commercial use only. Please note that permission may be required for re-use of images in which the copyright is owned by a third party. Obesity Reviews Volume 10, Issue 4, pages 383-392, 21 APR 2009 DOI: 10.1111/j.1467-789X.2009.00595.x http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2009.00595.x/full#f1

Bariatric surgery for mothers protects offspring from obesity Born before (48) Mother’s surgery (BMI 48) Before after (172) mothers’ surgery (BMI 31) * Bariatric surgery for mothers protects offspring from obesity Caloric restriction during pregnancy may affect development of offspring. This study followed the growth to adolescence of offspring of obese mothers who gave birth prior to, or following substantial weight loss following bariatric surgery (biliopancreatic diversion [BPD]). The prevalence of overweight or obesity was markedly and significantly lower among children born post-surgery, compared to those born pre-surgery. The difference appeared to be gender specific, with most of the effect occurring in boys. Kral JG, Biron S, Simard S et al. Large maternal weight loss from obesity surgery prevents transmission of obesity to children who were followed for 2 to 18 years. Pediatrics 2006;118:e1644-9. † Normal weight Overweight Obese Underweight % of offspring in weight categories: *p=0.005 vs. after surgery; †p=0.006 for overweight + obese vs. after surgery. Kral JG et al. Pediatrics 2006;118:e1644-9.

Acantosis nigrans

Obesity complikations increases the risk of early death CMAJ. 2011 October 4; 183(14): e1059–e1066.

Konklusjon Årsakene til fedme hos barn er sammensatte Antall barn med fedme er for høyt Barnefedme fører til redusert helse hos barnet og risikoen drar barnet med seg i voksen alder Barnefedme har konsekvenser for et bærekraftig samfunn

BARIATRISK KIRURGI – LEVEUTSIKTER Sjöström L et al: SOS-studien 1987 – 2001 I kirurgigruppen betyr dette en reduksjon i justert hazard ratio for død på 29% Forskjellen synes særlig å gjelde AMI og cancer Adams TD et al: 1984 – 2002 (Utah, USA) 2,7% døde i kirurgigruppen og 4,1% i kontrollgruppen Sykdomsspesifikk mortalitet i kirurgigruppen red. med Coronarsykdom 56% Diabetes 92% Cancer 60%