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.
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 this is an older analysis 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.
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 figure below:
Impact of childhood obesity on adult health
Several reviews have evaluated the impact of childhood obesity on future adult health:
- 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.
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.
Appetite dysregulation in obesity:
- 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.
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