Lesson 8: Childhood and Adolescent – Health Implications and Appetite Dysregulation from Obesity

Table of Contents


Thus far I have discussed various considerations and implications within the preconception, pregnancy, and infancy/toddler stages of life with respect to future obesity risk, weight management, and at times various other aspects of health. Moving along chronologically, in this and the next five lessons I will discuss childhood obesity itself. Here I will discuss some of the various physiologic health consequences resulting from childhood obesity and its management; this includes current and long-term health risks as well as considerations of appetite regulation and how this differs between individuals with and without obesity.

Health implications associated with childhood obesity

There are many negative health effects associated with childhood obesity; I will discuss some of the health implications here.

Persistence of obesity over time

A 2016 systematic review and meta-analysis (“SR/MA”) including 16 publications (through the year 2013) evaluating the carryover of childhood obesity to adult obesity found that(Simmonds, 2016):

  • Children with obesity compared to those without were 5.2x more likely to become adults with obesity.
  • 55% of children with obesity will still have obesity in adolescence.
  • 70% of adolescents with obesity continue to have obesity when they are >30 years old.
  • 70% of adults with obesity did not have obesity in childhood or adolescence.

One recent study of children aged 6-11 years found that only 9% of those with obesity transitioned to the overweight category and 1% transitioned to the normal weight category over a median follow-up of 2.1 years.(Foster, 2023) In contrast, 23% and 28% of those in the overweight category transitioned to the normal weight and obesity categories, respectively, while 14% and 2% of those in the normal weight category transitioned to the overweight and obesity categories, respectively.

Thus, most children with obesity will continue to have obesity in the future, though many adults with obesity did not have obesity during childhood. As the above SR/MA is older and obesity rates have steadily increased over the last 5-10 years, it stands to reason that the numbers have increased over time. This has been estimated to occur in a couple of modelling studies, both indicating that the rates of adult obesity and in particular adult severe obesity when predicted from childhood obesity status will increase as time goes on.(Ward, 2017; Woo, 2020) Therefore, there is no reason to expect people to “outgrow” their obesity over time without making changes conducive to better health.

Note: Of interest, a 2018 scoping review attempted to determine a definition of metabolically healthy obesity in children, noting many definitions had been used previously.(Damanhoury, 2018) While opinions varied, the authors did note that the literature suggests many children with metabolically healthy obesity become metabolically unhealthy over time, with 1 study finding >30% transition over a 1 year period. Additionally, a 2019 review noted that individuals with metabolically healthy obesity, according to the consensus definition proposed in the prior review, may still have other abnormalities such as hepatic steatosis, increased carotid intima-media thickness, elevated inflammatory markers and in adulthood may have other cardiometabolic complications.(Vukovic, 2019)

Thus, even if children with obesity currently do not have signs of health complications by the standard metrics there is reason to think they may have other negative health markers or will transition to a metabolically unhealthy phenotype with worse health implications in the future if no effort is made towards improving health. There seems to be a particularly higher risk of developing diabetes long-term if obesity begins in childhood or adolescence.(Sidhu, 2023)

Health complications of childhood obesity

A 2016 review highlighted various physiologic changes that can occur with childhood obesity, noting(Armstrong, 2016):

  • The resting heart rate may increase due to impaired autonomic nervous system function.
  • Obesity onset prior to puberty can lead to an earlier peak height velocity and a ~1” decrease in final adult height.
    • Historically the literature more strongly indicated that obesity leads to early puberty in females, but more recent literature suggests this also occurs in males.(Huang, 2021; Li, 2022)
  • Decreased salivary flow rate and changes in the properties of saliva increase the risk of dental caries.
  • Larger tonsils and associated sleep-related breathing problems are more common.
  • Gynecomastia (breast tissue development) may present in ~40% of adolescent males with obesity.
  • A cervicodorsal hump may occur, pes planus (flat feet) is more common, lordosis is common and can cause low back pain, and gait abnormalities can develop that generate greater stress on the knees.
  • Acanthosis nigricans (darkened velvety skin on the neck and potentially axillae/stomach/elsewhere) indicates insulin resistance and when insulin resistance becomes more severe skin tags can develop within the acanthosis. Striae (stretch marks) also can become apparent over time.
  • Polycystic ovarian syndrome (“PCOS”) may be more likely to develop in females which can lead to menstrual irregularities, worsening acne, and male-pattern hair growth.
  • Yeast infections on the skin are more common as obesity increases transepidermal water loss & raises the skin pH.

A 2021 review noted that childhood obesity increases the risk of obstructive sleep apnea, type 2 diabetes mellitus (“T2DM”), hyperlipidemia, hypertension, non-alcoholic fatty liver disease (“NAFLD”), and metabolic syndrome.(Kansra, 2021) In children age 4-9 years, one study found obesity significantly increased the risk of prediabetes, NAFLD, and hyperlipidemia.(Pedicelli, 2022) Disrupted sleep (more common in obesity with sleep-disordered breathing) can lead to increases in ghrelin (the “hunger hormone”) and emotional eating. This also contributes to systemic oxidative stress & inflammation, contributing to long-term health complications. A 2021 review detailed some of the ways that obesity can lead to various cardiometabolic health conditions.(Drozdz, 2021) The authors note:

  • Obesity has been associated with signs of atherosclerosis in children, in part due to pro-inflammatory substances formed in adipose tissue that can cause endothelial damage and increase vascular stiffness.
  • Elevated total cholesterol, triglycerides, blood pressure, and body mass index (“BMI”) as young as age 9 years contributes to elevated adult carotid intima-media thickness, and this relationship strengthens throughout adolescence. This increases the risk of heart disease.
  • The sympathetic nervous system can be activated by both insulin resistance and leptin resistance as well as sleep-disordered breathing; all of these factors are more common in obesity. This will contribute to increased aldosterone secretion and salt-sensitive hypertension. Adipose tissue can also directly contribute to aldosterone activity, leading to this same effect. As a result, children with obesity have a much higher risk of hypertension than children without obesity.

Tip: The authors of the last review did find some encouraging results in the literature. Increased levels of cardiorespiratory fitness (“CRF”) seem to compensate for some of the negative effects of increased body fat. Additionally, most of the risk of T2DM, hypertension, dyslipidemia, and carotid artery atherosclerosis from having childhood obesity will disappear if the children no longer have obesity by adulthood. I discuss more of these latter results in the next section.

I want to emphasize the fact that higher levels of CRF seem to mitigate the negative health effects of obesity. There is evidence this applies to other aspects of fitness as well.(de Lima, 2022) At any level of obesity, increased general fitness correlates with health benefits and mitigates the risks of obesity. For this reason, it makes sense to emphasize increasing fitness as part of any weight management intervention designed to improve overall health.

Many of the known complications of childhood obesity have been summarized in the figures below:

Reproduced from: Calcaterra V, Verduci E, Pascuzzi MC, Magenes VC, Fiore G, Di Profio E, Tenuta E, Bosetti A, Todisco CF, D’Auria E, Zuccotti G. Metabolic Derangement in Pediatric Patient with Obesity: The Role of Ketogenic Diet as Therapeutic Tool. Nutrients. 2021 Aug 16;13(8):2805. doi: 10.3390/nu13082805. PMID: 34444964; PMCID: PMC8400548.
Reproduced from: Marcus C, Danielsson P, Hagman E. Pediatric obesity-Long-term consequences and effect of weight loss. J Intern Med. 2022 Dec;292(6):870-891. doi: 10.1111/joim.13547. Epub 2022 Aug 5. PMID: 35883220; PMCID: PMC9805112.

Impact of childhood obesity on adult health

Several reviews have evaluated the impact of childhood obesity on future adult health:

Pre-2021 reviews:

  • A 2019 review noted that childhood obesity increases the future risk of cardiovascular disease, cardiometabolic disease, and cancer, with increasing risk if obesity persists through puberty.(Weihrauch-Blüher, 2019) The authors recommend attempting to normalize obesity prior to puberty to help mitigate these risks.
  • A 2020 SR/MA evaluated the impact of changing weight status from childhood to adulthood on cardiovascular risk factors and health outcomes in adulthood, including 52 articles.(Sun, 2020) When transitioning from excess body weight in childhood to normal weight in adulthood, the authors found that the odds ratio of developing T2DM remains elevated at 1.37. However, while the odds ratios for developing hypertension, dyslipidemia, NAFLD, metabolic syndrome, high carotid intima-media thickness, and cardiovascular disease were all between 1.12-1.60, none of these were statistically significant. In contrast, for individuals with excess weight in childhood who remain with excess weight in adulthood, the odds ratio for T2DM was 3.94 and for the remaining conditions listed above were 2.83-10.61 (all of these were statistically significant).

More recent reviews:

  • A 2021 review specifically discussed the carryover of childhood obesity into adult medical complications.(Malhotra, 2021) The authors noted that childhood obesity increases the risk of several adult complications, such as metabolic syndrome, T2DM, hypertension, NAFLD, several cancers (pancreatic, kidney, ovarian, colon, and more), and hidradenitis suppurativa, but resolving obesity by early adulthood substantially mitigates or even eliminates this excess risk. Childhood obesity also increases the risk of early-onset atherosclerosis as well as atrial fibrillation, atrial flutter, and higher carotid intima-media thickness in adults, but achieving a normal BMI by early adulthood mitigates these risks as well. Childhood obesity does increase the risk of PCOS and infertility in adulthood, as well as pregnancy-induced hypertension, gestational diabetes mellitus, and preeclampsia, and other conditions such as psoriasis, lupus, and depression. There is a strong correlation between childhood obesity and asthma development (both in childhood and later in adulthood), and obesity also modifies the susceptibility to air pollution and tobacco exposure.
  • A 2021 SR evaluated the association of pediatric obesity with morbidity and mortality in young adulthood (<45 years old).(Horesh, 2021) The authors found that childhood overweight and obesity associates with increased risks of T2DM, several types of cancer, metabolic syndrome, hypertension, coronary artery disease, heart failure, and mortality secondary to kidney disease and infection. Much of the increased risk disappears in individuals who are able to obtain a healthy-range BMI by early adulthood but elevated risk does persist particularly for T2DM, cancer, and cardiovascular mortality.
  • A 2022 SR generally found that being born with a low BMI or developing a high BMI during childhood associated with future health risk, but many studies do not adjust for the BMI at adulthood and no studies adequately assessed the impact of childhood body composition differences on future health outcomes.(Bander, 2022)
  • A 2023 SR/MA found childhood obesity increases the risk of developing and dying from cancer in adulthood by ~30%.(Mohammadian Khonsari, 2023)

Note: A 2021 SR included 9 studies assessing the effect of weight regain after loss on cardiometabolic health in children with obesity.(Vermeiren, 2021) The authors assessed body composition, waist circumference, blood pressure, inflammatory markers, insulin & glucose metrics, and lipid & cholesterol metrics. Overall, there was no clear evidence of a harmful effect of weight regain after loss, with parameters not seeming to exceed the baseline values for most variables in most studies, and at times there were sustained benefits even after weight regain. This body of literature is relatively small and more research is needed, but at this point any concerns of harmful physiologic effects of weight regain after weight loss do not seem to outweigh the benefits of the weight loss itself.

Of note, there may still be risks of weight regain if it leads to a higher peak weight, which can more readily happen when people engage in restrictive diets with non-sustainable lifestyles.

I will discuss more regarding if children should aim to lose weight or maintain their current weight as they continue to grow taller in Lesson 11.

Appetite dysregulation associated with obesity

The more traditional health considerations discussed in the last section are not the only consequences of childhood obesity. There is a substantial body of research indicating that individuals with obesity or genetically prone to developing obesity have different appetite characteristics than individuals without obesity and that adolescents in general may have difficulty with appetite regulation. For those curious, I am including brief summaries of some of the recent published literature in the expandable box below, and for those who do not wish to read through all of this information I am including the key points and general takeaways underneath the expandable box.

General appetite dysregulation in youth:

  • In a 2017 SR of studies evaluating the link between subjective appetite rating and subsequent energy intake, 21 studies were included in youth populations (aged 4-17 years) and there was no link observed in 11 of the 21 studies.(Holt, 2017) This dissociation was also observed in adults. Thus, there seems to be a distinction between perceived appetite and resultant energy intake.
  • A 2018 cohort study examined 925 twin pairs and estimated BMI heritability at 4 years of age.(Schrempft, 2018) BMI heritability was 86% in the higher-risk home environments but just 39% in the lower-risk home environments. The authors noted from prior research that the heritability of BMI increases throughout childhood.
  • In a 2019 editorial, the authors noted that a recent twin study in children aged 7-15 years found genetic factors explained 80% of the association between poorer executive function and higher BMI.(Gowey, 2019) This indicates that some individuals will have a strong genetic predisposition to behavioral traits that associate with an elevated BMI.
  • A 2021 SR/MA evaluating food addiction in youth populations examined 18 studies and found that an estimated 15% of youth show signs of food addiction (19% of youth with overweight or obesity).(Yekaninejad, 2021)
  • A 2021 review of the satiety quotient (essentially calculated after consuming a meal as the change in subjective appetite divided by the energy content of the meal) found this to be a potentially invalid and unreliable metric in adolescents.(Fillon, 2021)
  • A 2021 study examining adolescents aged 12-14 years without obesity found 15% of them were susceptible to sensitization to high-energy-dense foods and this associated with an increase in BMI over a 2-year period.(Temple, 2021) Sensitization to low-energy-dense foods did not have an influence on BMI.
  • A 2023 study examining children ages 7-8 years who had a healthy weight and differing risk of obesity found that those with poorer measures of executive functioning had a greater response to the portion size effect.(Keller, 2023) The authors speculate that if this is replicated it may prove helpful to target behavioral and emotional regulation to better manage excessive food availability.
  • A 2023 study including children on average 4.9 years old found that when given the opportunity they served similar volumes of snack foods to themselves regardless of their underlying energy density, and when eating self-selected amounts of these servings they consumed on average 84 kcal from pretzels and 29 kcal from strawberries, indicating the appearance of the food rather than its energy density guides the amount consumed.(Diktas, 2023)

Appetite dysregulation in obesity:

Pre-2020 literature:

  • A 2016 SR/MA found that children with obesity compared to children with normal weight had lower baseline levels of ghrelin (the primary hunger hormone) and smaller changes in ghrelin and peptide YY (a satiety hormone) after consuming a meal.(Nguo, 2016) These hormones did not correlate well with self-reported appetite.
  • A 2019 study took 135 individuals aged 14-17 years at baseline and provided them milkshakes of different compositions (low fat + low sugar, low fat + high sugar, high fat + low sugar, and high fat + high sugar) while undergoing functional MRIs of their brains, repeating this yearly for 3 years.(Yokum, 2019) 36 of these individuals ultimately had a >10% increase in BMI while 31 had <2% change in BMI. The subset of adolescents who gained the most weight had two interesting findings. First, at baseline (prior to weight gain) they had elevated activation of taste processing regions. Second, after gaining weight they had decreased neural responses in brain regions associated with encoding taste information (suggesting decreased responsivity of regions associated with taste & reward processing of palatable foods). This was particularly evident with the high-fat milkshakes.
    • Thus, it may be helpful to avoid high-fat and by extension high-fat/high-sugar foods to avoid blunting of taste & reward responsivity to decrease the risk of future weight gain.

More recent literature:

  • A 2020 review noted there are several traits in infants, toddlers, and children that are associated with a higher risk of overweight and obesity, such as high reactivity to foods, low self-regulation, inability to control impulses, poorer emotional self-regulation, and inability to delay gratification.(Smith, 2020) These aspects of emotional regulation in conjunction with added stress are highly linked to low physical activity, emotional eating, irregular & disrupted sleep, and later development of obesity.
  • A 2020 SR evaluated 147 studies examining the self-regulation failure hypothesis from a dual process models perspective for childhood overweight & obesity treatment.(Kemps, 2020) The authors noted that automatic processes (drive by stimuli) reach a peak during adolescence while regulatory processes show the greatest improvement at ages 6-10 years. Thus, in adolescence impulsivity increases. The majority of the studies showed an association between strong automatic processes and/or weak regulatory processes in youth with overweight or obesity. Overall, there were more studies supporting this model in children than in adolescents and there are few studies directly targeting interventions towards this model.
  • A 2021 review of 23 neuroimaging studies examined dysregulated eating behavior associated with obesity risk in youth.(Smith, 2021) The authors found that youth with obesity seem to have inefficient functioning of the frontal brain regions, thus requiring greater effort during conflict monitoring and when exerting control over eating behavior. In addition to this, children with obesity may also have decreased sensitivity to hunger and satiety cues, leading to a greater tendency to eat in response to external cues (ie, when large portions of foods are available). There also seems to be an imbalance between regulatory and reward regions, and this collectively associates with greater eating in the absence of hunger.
  • A 2021 narrative review of appetite self-regulation in early childhood highlighted that appetite self-regulation declines by the preschool ages, children who are less able to delay gratification are more likely to have overweight and obesity, and most children can only partially compensate for the increased caloric consumption when provided extra amounts of food.(Russell, 2021) Of note, while substantial individual differences occur, there are correlations over time within individuals for eating in the absence of hunger, food responsiveness, and satiety responsiveness (correlations r ~ 0.35-0.45). Children with overweight and obesity show less activation in the prefrontal brain regions associated with self-control & inhibition, and there is evidence that the maturation of these areas is altered by excessive consumption of calorie-dense foods.

Thus, there are a few key points to take away from this:

  • Children and adolescents, regardless of their weight status, can have difficulty with self-regulation around food, particularly when excessive amounts of highly palatable options are available, as appetite ratings as well as satiety after eating do not always correlate well with the amount of calories that are actually consumed.
  • When these highly palatable food options are available, this suboptimal “food environment” significantly increases the heritability of obesity, implying that the underlying genetic predisposition that drives increased appetite and caloric consumption takes full effect when the opportunity arises.
  • Children with obesity in particular have greater difficulty as they have dysregulation of their appetite and satiety hormones and they have poorer executive function (thus they have more difficulty inhibiting the drive to eat food that is available). These difficulties seem to increase in adolescence as both impulsivity as well as opportunities for obtaining highly palatable foods increase during this time period.
  • Regular consumption of high-fat and likely other palatable foods influence the development of brain pathways to increase sensitization to these foods (thus increasing the desire for them) while simultaneously dulling the sensations resulting from their consumption (meaning more needs to be consumed for the same effect).

Overall, this demonstrates the importance of providing appropriate portion sizes, limiting access to highly palatable foods, and utilizing structured eating to help overcome impulsivity and an inability to self-regulate food intake. It is important to begin these healthy eating habits early in childhood to help prevent the alterations in brain development that seem to occur in a subset of children who are surrounded by a suboptimal food environment resulting in excessive consumption of highly palatable foods.

For children who have already been exposed to a suboptimal food environment and are currently dealing with obesity or troublesome appetite self-regulation as a whole, improvements can still be made with appropriate structure, portion sizes, food selection choices, and focusing on mindful eating. Mindful eating entails:

  • focusing on internal cues revolved around eating, such as hunger, appetite, satiation, and satiety, to help teach the body to understand what it does and does not need
  • removing the external cues that would provoke dysregulated eating, examples include:
    • highly palatable non-nutritious food options should be out of sight
    • meals should be consumed without being distracted by screens to make it easier to respond to the sensation of satiation
    • consuming meals with the family and having conversations can slow the pace of eating, allowing the body time to generate appetite and satiation signals in response to what you are actively consuming such that these signals can help you realize when you have consumed enough food

Tip: Increased time spent viewing screens associates with decreased satiety, increased consumption of unhealthy/energy-dense snacks, decreased consumption of fruits and vegetables, and poorer sleep patterns.( Smith, 2020; Motevalli, 2021) Enforcing family rules (particularly with screen time) leads to less obesogenic behaviors as this aids self-regulation.(Koletzko, 2020) Thus, decreasing screen time can be helpful, and it will also allow more time for physical activity (though screens can be watched with some physical activity such as using a treadmill or an elliptical machine).

If a child is struggling with appetite regulation and/or obesity, and you feel that the health behaviors worsen when watching screens, it is appropriate to limit the overall screen time or set limits in some other capacity to directly address the underlying cause of the unhealthy behaviors.


In this lesson I presented literature describing the physical health consequences of obesity as well as the hope-inducing literature suggesting that treating obesity effectively by early adulthood largely mitigates the long-term associated health risks. I also presented literature suggesting there are differences in appetite regulation between those with and without obesity, helping to show why some people struggle with obesity more than others, which should help to alleviate some of the shame and guilt associated with having obesity. This knowledge also allows smarter choices to help address appetite dysregulation as described above.

In the next lesson I will discuss the psychological aspects of childhood obesity and its treatment in more detail.

Click here to proceed to Lesson 9


  1. Armstrong S, Lazorick S, Hampl S, Skelton JA, Wood C, Collier D, Perrin EM. Physical Examination Findings Among Children and Adolescents With Obesity: An Evidence-Based Review. Pediatrics. 2016 Feb;137(2):e20151766. doi: 10.1542/peds.2015-1766. Epub 2016 Jan 27. PMID: 26817935.
  2. Bander A, Murphy-Alford AJ, Owino VO, Loechl CU, Wells JC, Gluning I, Kerac M. Childhood BMI and other measures of body composition as a predictor of cardiometabolic non-communicable diseases in adulthood: a systematic review. Public Health Nutr. 2022 Oct 24:1-28. doi: 10.1017/S136898002200235X. Epub ahead of print. PMID: 36274635.
  3. Calcaterra V, Verduci E, Pascuzzi MC, Magenes VC, Fiore G, Di Profio E, Tenuta E, Bosetti A, Todisco CF, D’Auria E, Zuccotti G. Metabolic Derangement in Pediatric Patient with Obesity: The Role of Ketogenic Diet as Therapeutic Tool. Nutrients. 2021 Aug 16;13(8):2805. doi: 10.3390/nu13082805. PMID: 34444964; PMCID: PMC8400548.
  4. Damanhoury S, Newton AS, Rashid M, Hartling L, Byrne JLS, Ball GDC. Defining metabolically healthy obesity in children: a scoping review. Obes Rev. 2018 Nov;19(11):1476-1491. doi: 10.1111/obr.12721. Epub 2018 Aug 28. PMID: 30156016.
  5. de Lima TR, Martins PC, Moreno YMF, Chaput JP, Tremblay MS, Sui X, Silva DAS. Muscular Fitness and Cardiometabolic Variables in Children and Adolescents: A Systematic Review. Sports Med. 2022 Jan 12. doi: 10.1007/s40279-021-01631-6. Epub ahead of print. PMID: 35020179.
  6. Diktas HE, Roe LS, Keller KL, Rolls BJ. The effects of snack foods of different energy density on self-served portions and consumption in preschool children. Appetite. 2023 Jun 1;185:106527. doi: 10.1016/j.appet.2023.106527. Epub 2023 Mar 11. PMID: 36907517.
  7. Drozdz D, Alvarez-Pitti J, Wójcik M, Borghi C, Gabbianelli R, Mazur A, Herceg-Čavrak V, Lopez-Valcarcel BG, Brzeziński M, Lurbe E, Wühl E. Obesity and Cardiometabolic Risk Factors: From Childhood to Adulthood. Nutrients. 2021 Nov 22;13(11):4176. doi: 10.3390/nu13114176. PMID: 34836431; PMCID: PMC8624977.
  8. Fillon A, Beaulieu K, Mathieu ME, Tremblay A, Boirie Y, Drapeau V, Thivel D. A systematic review of the use of the Satiety Quotient. Br J Nutr. 2021 Jan 28;125(2):212-239. doi: 10.1017/S0007114520002457. Epub 2020 Jul 3. PMID: 32616106.
  9. Foster BA, Latour E, Lim JY, Weinstein K. Weight trajectories and obesity remission among school-aged children. PLoS One. 2023 Sep 20;18(9):e0290565. doi: 10.1371/journal.pone.0290565. PMID: 37729125; PMCID: PMC10511102.
  10. Gowey MA, Dutton GR. It’s not all in your head: Genetic underpinnings of the relationship between executive function and BMI. Am J Clin Nutr. 2019 Oct 1;110(4):793-794. doi: 10.1093/ajcn/nqz175. PMID: 31380558; PMCID: PMC6766437.
  11. Holt GM, Owen LJ, Till S, Cheng Y, Grant VA, Harden CJ, Corfe BM. Systematic literature review shows that appetite rating does not predict energy intake. Crit Rev Food Sci Nutr. 2017 Nov 2;57(16):3577-3582. doi: 10.1080/10408398.2016.1246414. PMID: 27736161.
  12. Horesh A, Tsur AM, Bardugo A, Twig G. Adolescent and Childhood Obesity and Excess Morbidity and Mortality in Young Adulthood-a Systematic Review. Curr Obes Rep. 2021 Sep;10(3):301-310. doi: 10.1007/s13679-021-00439-9. Epub 2021 May 5. PMID: 33950400.
  13. Huang A, Roth CL. The link between obesity and puberty: what is new? Curr Opin Pediatr. 2021 Aug 1;33(4):449-457. doi: 10.1097/MOP.0000000000001035. PMID: 34173790.
  14. Kansra AR, Lakkunarajah S, Jay MS. Childhood and Adolescent Obesity: A Review. Front Pediatr. 2021 Jan 12;8:581461. doi: 10.3389/fped.2020.581461. PMID: 33511092; PMCID: PMC7835259.
  15. Keller KL, Pearce AL, Fuchs B, Hallisky K, Rolls BJ, Wilson SJ, Geier C, Rose EJ. Children with lower ratings of executive functions have a greater response to the portion size effect. Appetite. 2023 Apr 13;186:106569. doi: 10.1016/j.appet.2023.106569. Epub ahead of print. PMID: 37059397.
  16. Kemps E, Goossens L, Petersen J, Verbeken S, Vervoort L, Braet C. Evidence for enhancing childhood obesity treatment from a dual-process perspective: A systematic literature review. Clin Psychol Rev. 2020 Apr;77:101840. doi: 10.1016/j.cpr.2020.101840. Epub 2020 Mar 4. PMID: 32172004.
  17. Koletzko B, Fishbein M, Lee WS, Moreno L, Mouane N, Mouzaki M, Verduci E. Prevention of Childhood Obesity: A Position Paper of the Global Federation of International Societies of Paediatric Gastroenterology, Hepatology and Nutrition (FISPGHAN). J Pediatr Gastroenterol Nutr. 2020 May;70(5):702-710. doi: 10.1097/MPG.0000000000002708. PMID: 32205768.
  18. Li Y, Gao D, Liu J, Yang Z, Wen B, Chen L, Chen M, Ma Y, Ma T, Dong B, Song Y, Huang S, Dong Y, Ma J. Prepubertal BMI, pubertal growth patterns, and long-term BMI: Results from a longitudinal analysis in Chinese children and adolescents from 2005 to 2016. Eur J Clin Nutr. 2022 May 6. doi: 10.1038/s41430-022-01133-2. Epub ahead of print. PMID: 35523866.
  19. Malhotra S, Sivasubramanian R, Singhal V. Adult obesity and its complications: a pediatric disease? Curr Opin Endocrinol Diabetes Obes. 2021 Feb 1;28(1):46-54. doi: 10.1097/MED.0000000000000592. PMID: 33229926.
  20. Marcus C, Danielsson P, Hagman E. Pediatric obesity-Long-term consequences and effect of weight loss. J Intern Med. 2022 Dec;292(6):870-891. doi: 10.1111/joim.13547. Epub 2022 Aug 5. PMID: 35883220; PMCID: PMC9805112.
  21. Mohammadian Khonsari N, Shahrestanaki E, Ehsani A, Asadi S, Sokoty L, Mohammadpoor Nami S, Hakak-Zargar B, Qorbani M. Association of childhood and adolescence obesity with incidence and mortality of adulthood cancers. A systematic review and meta-analysis. Front Endocrinol (Lausanne). 2023 Jan 19;14:1069164. doi: 10.3389/fendo.2023.1069164. PMID: 36742402; PMCID: PMC9892178.
  22. Motevalli M, Drenowatz C, Tanous DR, Khan NA, Wirnitzer K. Management of Childhood Obesity-Time to Shift from Generalized to Personalized Intervention Strategies. Nutrients. 2021 Apr 6;13(4):1200. doi: 10.3390/nu13041200. PMID: 33917383; PMCID: PMC8067342.
  23. Nguo K, Walker KZ, Bonham MP, Huggins CE. Systematic review and meta-analysis of the effect of meal intake on postprandial appetite-related gastrointestinal hormones in obese children. Int J Obes (Lond). 2016 Apr;40(4):555-63. doi: 10.1038/ijo.2015.256. Epub 2015 Dec 21. PMID: 26686004.
  24. Pedicelli S, Fintini D, Ravà L, Inzaghi E, Deodati A, Spreghini MR, Bizzarri C, Mariani M, Cianfarani S, Cappa M, Manco M. Prevalence of prediabetes in children and adolescents by class of obesity. Pediatr Obes. 2022 Feb 10:e12900. doi: 10.1111/ijpo.12900. Epub ahead of print. PMID: 35144324.
  25. Russell A, Russell CG. Appetite self-regulation declines across childhood while general self-regulation improves: A narrative review of the origins and development of appetite self-regulation. Appetite. 2021 Jul 1;162:105178. doi: 10.1016/j.appet.2021.105178. Epub 2021 Feb 24. PMID: 33639246.
  26. Schrempft S, van Jaarsveld CHM, Fisher A, Herle M, Smith AD, Fildes A, Llewellyn CH. Variation in the Heritability of Child Body Mass Index by Obesogenic Home Environment. JAMA Pediatr. 2018 Dec 1;172(12):1153-1160. doi: 10.1001/jamapediatrics.2018.1508. PMID: 30285028; PMCID: PMC6396810.
  27. Sidhu SK, Aleman JO, Heffron SP. Obesity Duration and Cardiometabolic Disease. Arterioscler Thromb Vasc Biol. 2023 Oct;43(10):1764-1774. doi: 10.1161/ATVBAHA.123.319023. Epub 2023 Aug 31. PMID: 37650325; PMCID: PMC10544713.
  28. Simmonds M, Llewellyn A, Owen CG, Woolacott N. Predicting adult obesity from childhood obesity: a systematic review and meta-analysis. Obes Rev. 2016 Feb;17(2):95-107. doi: 10.1111/obr.12334. Epub 2015 Dec 23. PMID: 26696565.
  29. Smith JD, Fu E, Kobayashi MA. Prevention and Management of Childhood Obesity and Its Psychological and Health Comorbidities. Annu Rev Clin Psychol. 2020 May 7;16:351-378. doi: 10.1146/annurev-clinpsy-100219-060201. Epub 2020 Feb 25. PMID: 32097572; PMCID: PMC7259820.
  30. Smith KE, Luo S, Mason TB. A systematic review of neural correlates of dysregulated eating associated with obesity risk in youth. Neurosci Biobehav Rev. 2021 May;124:245-266. doi: 10.1016/j.neubiorev.2021.02.013. Epub 2021 Feb 12. PMID: 33587960.
  31. Sun J, Xi B, Yang L, Zhao M, Juonala M, Magnussen CG. Weight change from childhood to adulthood and cardiovascular risk factors and outcomes in adulthood: A systematic review of the literature. Obes Rev. 2021 Mar;22(3):e13138. doi: 10.1111/obr.13138. Epub 2020 Sep 1. PMID: 32875696.
  32. Temple JL, Ziegler AM, Crandall AK, Mansouri T, Hatzinger L, Barich R, Epstein LH. Sensitization of the reinforcing value of high energy density foods is associated with increased zBMI gain in adolescents. Int J Obes (Lond). 2021 Nov 30:1–7. doi: 10.1038/s41366-021-01007-w. Epub ahead of print. PMID: 34848836; PMCID: PMC8631696.
  33. Vermeiren E, Bruyndonckx L, De Winter B, Verhulst S, Van Eyck A, Van Hoorenbeeck K. The effect of weight regain on cardiometabolic health in children with obesity: A systematic review of clinical studies. Nutr Metab Cardiovasc Dis. 2021 Aug 26;31(9):2575-2586. doi: 10.1016/j.numecd.2021.05.020. Epub 2021 May 29. PMID: 34172320.
  34. Vukovic R, Dos Santos TJ, Ybarra M, Atar M. Children With Metabolically Healthy Obesity: A Review. Front Endocrinol (Lausanne). 2019 Dec 10;10:865. doi: 10.3389/fendo.2019.00865. PMID: 31920976; PMCID: PMC6914809.
  35. Ward ZJ, Long MW, Resch SC, Giles CM, Cradock AL, Gortmaker SL. Simulation of Growth Trajectories of Childhood Obesity into Adulthood. N Engl J Med. 2017 Nov 30;377(22):2145-2153. doi: 10.1056/NEJMoa1703860. PMID: 29171811.
  36. Weihrauch-Blüher S, Schwarz P, Klusmann JH. Childhood obesity: increased risk for cardiometabolic disease and cancer in adulthood. Metabolism. 2019 Mar;92:147-152. doi: 10.1016/j.metabol.2018.12.001. Epub 2018 Dec 5. PMID: 30529454.
  37. Woo JG, Zhang N, Fenchel M, Jacobs DR Jr, Hu T, Urbina EM, Burns TL, Raitakari O, Steinberger J, Bazzano L, Prineas RJ, Jaquish C, Juonala M, Ryder JR, Daniels SR, Sinaiko A, Dwyer T, Venn A. Prediction of adult class II/III obesity from childhood BMI: the i3C consortium. Int J Obes (Lond). 2020 May;44(5):1164-1172. doi: 10.1038/s41366-019-0461-6. Epub 2019 Oct 9. PMID: 31597933; PMCID: PMC7141944.
  38. Yekaninejad MS, Badrooj N, Vosoughi F, Lin CY, Potenza MN, Pakpour AH. Prevalence of food addiction in children and adolescents: A systematic review and meta-analysis. Obes Rev. 2021 Jun;22(6):e13183. doi: 10.1111/obr.13183. Epub 2021 Jan 6. PMID: 33403795; PMCID: PMC8244111.
  39. Yokum S, Stice E. Weight gain is associated with changes in neural response to palatable food tastes varying in sugar and fat and palatable food images: a repeated-measures fMRI study. Am J Clin Nutr. 2019 Dec 1;110(6):1275-1286. doi: 10.1093/ajcn/nqz204. PMID: 31535135; PMCID: PMC6885480.
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