Stress and Childhood Obesity

Being a kid doesn’t necessarily mean having a carefree life, yet that’s how most adults view childhood. Because kids don’t have jobs, bills to pay, and children to raise what could they possibly have to worry about? More than we realize. Even the very young among us have stressors, slight though they may be. Stress is a function of the demands we face and our ability to handle them. Often it comes from outside sources. You know—family, job, friends, school, and expectations. Sometimes stress comes from inside, related to what we think we should do compared to what we actually do, say or think.

Today, kids have to learn scores of times more information than their parents did at the same age. That we can blame on an electronic era. And they have to learn these things in the same allotted time. Preschoolers get stressed when their moms leave them at daycare. As they get older, kids are pressured by academics and social position. After all, they need to fit in. Their lives get so hectic they seldom have time for themselves, for creative play, or even for relaxation. They are overscheduled with activities that would tax even the adult mind. Disturbing images on TV, news of wars, terrorism and natural disasters, and concerns for personal and family safety add to the burden. Illness, death and divorce don’t help.

All stressors are not created equal, and all people do not respond to stress the same way. Children often learn to handle stress from their parents. Sometimes that’s good; sometimes not. The idea that, “If it doesn’t kill me, it’ll make me stronger,” doesn’t apply to youngsters who’ve not yet developed a coping mechanism. What does this have to do with obesity, a childhood plague that’s more than doubled in the last few decades?  Lots.

A person’s reaction to stress will likely invoke the fight-or-flight (-or freeze) response as the primary means of dealing with a novel situation perceived as threatening. Children who overreact to stress will manufacture more cortisol than the body can dump, and that’s where the problem begins—emotional eating (Michels, 2012). Cortisol is a steroid hormone made by the adrenal glands, released in response to stress. Its main job is to increase blood sugar to power the fight-flight machinery. Cortisol counteracts insulin and contributes to insulin resistance (Goran, 2010) by lowering glucose transport to the cell membrane. Small increases in cortisol can provide a quick burst of energy in an emergency. At the same time it can heighten memory, briefly but powerfully enhance immunity and lower sensitivity to pain. But the return to normal is needed lest the body idle at high rpm’s. With our high-stress culture that has become the norm…chronic stress. That eventually induces impairment of cognitive function, suppresses thyroid activity, throws blood sugar out of whack, menaces bone density, elevates blood pressure, and actually lowers immune responses. And it increases deposition of abdominal fat, setting the stage for metabolic syndrome, depressed affect (Endocrine Society, 2009) (Dockray, 2009) and cardiovascular entanglement, even at a young age.

Children’s biological response to stressors was examined recently by researchers from Penn State and Johns Hopkins Universities.  A group of pre-teens was assigned public speaking and mathematical tasks with little preparation time allowed for either. Cortisol content of their saliva was measured before and after. Following the assignment, the children were offered an array of snack foods regardless of their hunger status. The amount of calories they consumed varied, but those with the highest body mass indexes, who also had the highest cortisol levels, consumed more calories, even in the absence of hunger, than did those with lower cortisol levels. The outcome suggests that children with poor response to stress are at risk for becoming overweight or obese (Francis, 2013). Other factors that contribute to eating in the absence of hunger include poverty, living in a violent environment and food insecurity.

The determination of childhood obesity needs to be made on an individual basis, not from a chart developed by an insurance company that focuses on only one ethnicity or population. Anthropometric measurements and family history need to be included in an evaluation. Pathologies need to be ruled out, genetics must be considered, and psychosocial factors scrutinized. The comorbidities of obesity are varied and many, and their prophylaxis calls for early intervention, some of which transcends diet. Overweight children face the same health conditions as their parents, with hypertension, discordant lipid panels, abnormal glucose levels, and elevated inflammation markers among them. Lifestyle changes, where parents are the managers, may be all that is needed. This may include dietary interventions that eliminate simple carbohydrates, especially sugars and refined starches common to the foods kids like the most. These foods will spike insulin, which will spike cortisol, which will encourage eating, which will add pounds. Avoiding pharmaceutical anorectic agents is strongly encouraged.

Mental stress is associated with emotional eating, which typically ignores healthy dietary patterns (Michels, 2013). Cortisol levels peak in the morning, but can remain elevated in stressful surroundings. Admittedly, some of those surroundings are beyond a parent’s control, so coping mechanisms are helpful. Without being a helicopter parent, it’s possible to create a comfortable atmosphere for a child, even when he is away from you. Teaching coping skills by example starts early. Believe it or not, kids watch, listen and emulate. There are three-year-olds with vocabularies that would make you wince. If kids can learn to be tense and confrontational, they can also learn to relax and to take things in stride.

Limiting cortisol manufacture might be as easy as increasing magnesium in thediet. How?  Vegetables. Essential fatty acids, music therapy and phospholipids,and even vitamin C and tea have been shown to curtail cortisol release (Rains,2011) (Arent, 2010) (Peters, 2001).

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