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Overweight and Obesity as it Relates to Pediatric Airway Dysfunction

When we are addressing the progression of sleep disordered breathing (SDB) to Upper Airway Resistance Syndrome (UARS) to Obstructive Sleep Apnea (OSA), in children, it’s imperative we bring pediatric overweight and obesity into the forefront. In our culture obesity had reached epidemic proportions and continues to climb. Not unlike adults, children with obesity have a 46% increased risk of progressing to OSA compared to their normal-weight peers. In fact, about half of all people with OSA are overweight, and for those with both conditions, losing 10 percent of your body weight can reduce AHI by 26-32%. Conversely, patients with mild OSA who gain 10% more body weight are at a six-fold risk of disease progression.  For both children and adults, weight loss is one of the first lifestyle remedies physicians recommend when treating OSA. Unfortunately, it’s much easier prescribed than accomplished.

Researchers continue to point to the bidirectionality of this relationship. Weight gain worsens the progression of SDB and OSA, but in turn, these sleep/airway disorders make weight loss significantly more difficult.   This viscous cycle is frustrating for patients, parents and for all medical/dental professionals who are engaged in helping patients improve either condition.

Weight Gain and OSA:

During weight gain, fat is deposited in the tongue, soft palate and lateral pharyngeal walls results in enlargement of these tissues upper airway resistance and progression of SDB to OSA. (1) The tongue plays perhaps the most critical role in airway patency which can examine another time, when we look at physical development.

You might ask why a child with OSA experiences more difficulty with weight loss.  Satiety hormones related to obesity are altered by OSA.  Ghrelin, the appetite stimulant that causes the stomach to growl is elevated.  Sleep deprivation also stimulates Leptin resistance.  Remember that the satiety hormone Leptin, is produced in the adipose cells and communicate with the hypothalamus to tell us when we’ve consumed enough.  Leptin resistance and Ghrelin production stimulate increased appetite and more calorie consumption.  

Not so incidentally, increased sugar consumption (particularly fructose) also disrupts the satiety hormone balance, so a reduction in sugar consumption becomes a necessary part of the SDB/OSA solution.

Glucose Regulation

Insulin resistance is the precursor to, and the etiology of Type 2 Diabetes and it effects 150 million Americans. Based on a large body of evidence, OSA seems to be associated with impaired glucose tolerance (3), not to mention the most significant culprit in our climbing Diabetes rates. Here’s how:

There is complex relationship between adipose tissue, insulin action (sensitivity) and glucose homeostasis.   This gives us the ability to survive when food supplies are scarce.  (4)

Insulin is released from the pancreas to offset a rise in blood glucose.  Now that we gulp and gobble an average of 22 teaspoons of sugar a day, our sensitivity to insulin is impaired and the insulin pump works overtime until it burns out it’s producer, the beta cells.   All the while, excess glucose gets transported to our adipose cells for deposition and storage.  

Fructose (the sugar molecule that has cloaked commercial foods) is processed in the liver.  Its toxicity and fat deposition there causes the slow silent killer, NAFLD, non-alcoholic fatty liver disease. Currently 20% of all children and 40% of obese children are afflicted with NAFLD.

Adiponectin is another fat cell derived hormone that improves glucose control and lipid metabolism and may reduce inflammation and atherosclerosis. Levels of adiponectin are reduced in both obesity and OSA.(2)

Overweight and Obese children are significantly more likely to carry that into adulthood, putting them at risk for health threats beyond OSA. In fact, it’s now estimated that 75% of our health care dollars are spent on treatment of preventable, non-communicable disease primarily  metabolic syndrome. Metabolic syndrome is a cluster of conditions including increased hypertension, lack of glycemic control, excess body fat around the waist, and abnormal cholesterol or triglyceride levels. Approximately 8.3% of normal weight patients can develop metabolic syndrome vs. 29.9% of obese.  There is more prevalence among those who develop central obesity (represented by abdominal fat), regardless of their overall weight. (5)

Calling all health professionals! Our ability to work in partnership with children and their families—to mitigate weight gain—gives us opportunities to alter the course of human disease.

What Can WE Do?

The primary cause of obesity, metabolic syndrome, diabetes, cardiovascular disease and even OSA is, in a word, SUGAR!   Our commercial fructose consumption, in the absence of it’s antidote (natural plant fiber) is killing us.  There is an enormous body of evidence around these facts.   If you haven’t yet read Robert Lustig’s book Fat Chance or watched his YouTube video called “Sugar the Bitter Truth”, stop reading and do it. 

As a dental profession we don’t have to have an advanced degree in nutrition to counsel patients on this because sugar talk has always been in our expertise.  Before the obesity epidemic there was…… Caries…. and we learned to talk about sugar as a root cause. Unfortunately, now there’s no magic bullet we can add to the water, like we did with fluoride, to drive down the rates of metabolic illness.   And the commercial food and drug industries aren’t about to stimulate a health reform. So it really is up to us!

Please grow your pediatric examination far beyond mirror and explorer. Learn to recognize SDB/airway disorders.  Notice weight gain.  Stay curious longer.  Take a simple diet inventory on all your pediatric patients.  With no judgment, only love, ask what they eat and drink in a day.  Hand people great resources to help families learn how to reduce sugar and white flour and discover how to increase consumption of nutrient dense whole foods. (Believe me they are confused and need guidance!) And help them forge commitments with you as their accountability partner. Changing the health trajectory of a child’s life is perhaps the most profound gift we can ever give!

P.S.  Do all this, as if the future of our country depended on it….because it does! With our help, the health of our people can once again be our greatest asset.  

Susan Maples, DDS

Dr. Susan Maples leads a successful, total health, insurance-independent dental practice in Holt, Michigan. She brings preventive and restorative dental expertise, a passion for mouth-body total health, a master’s degree in business/marketing, and 30+ years of experience in private practice. She is the creator and founder of Total Health Academy, a complete online solution for dental teams to integrate all aspects of Total Health Dentistry, author of BlabberMouth! 77 Secrets Only Your Mouth Can Tell You To Live a Healthier, Happier, Sexier Life, developer of the Hands-On Learning Lab™ and SelfScreen.net. Susan currently serves on the Governing Board of the American Academy of Oral Systemic Health (AAOSH).

Email: Susan@drsusanmaples.com

Resources

(1) Godoy, Ivan R B et al. “Fat accumulation in the tongue is associated with male gender, abnormal upper airway patency and whole-body adiposity.” Metabolism: clinical and experimental vol. 65,11 (2016): 1657-1663. doi:10.1016/j.metabol.2016.08.008

(2) Zeng, Fanfang et al. “Association of adiponectin level and obstructive sleep apnea prevalence in obese subjects.” Medicine vol. 96,32 (2017): e7784. doi:10.1097/MD.0000000000007784

(3) Mesarwi, Omar et al. “Sleep disorders and the development of insulin resistance and obesity.” Endocrinology and metabolism clinics of North America vol. 42,3 (2013): 617-34. doi:10.1016/j.ecl.2013.05.001

(4) Kahn, B B, and J S Flier. “Obesity and insulin resistance.” The Journal of clinical investigation vol. 106,4 (2000): 473-81. doi:10.1172/JCI10842

(5)  Lee, Soo Cheng et al. “Metabolic syndrome among non-obese adults in the teaching profession in Melaka, Malaysia.” Journal of epidemiology vol. 27,3 (2017): 130-134. doi:10.1016/j.je.2016.10.006