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Childhood Obesity and Poor Blood Sugar Control

Posted by Greg Kester on

What’s driving the obesity pandemic?

September has been deemed National Childhood Obesity Awareness Month, an ironic title considering that obesity is so common. It seems that most discussions on public health or chronic disease are punctuated with the growing concern over the nation’s expanding waistline, and for good reason. Yet while the overall rate of obesity in the US is still alarmingly high (over 35% of adults are obese and almost 70% are overweight), there is actually some good news to report. The adult obesity rate, which has been steadily climbing for decades, is beginning to taper off, and the childhood obesity rate has actually plateaued, according to the State of Obesity.

Considering the smorgasbord of research and programs aimed at reversing the obesity trend, you might think it’s about time for some results. Between 1980 and 2012, the obesity rate for adolescents ages 12-19 more than quadrupled, increasing from 5% to 21% (for 6-11 year olds, the rate increased from 7% to 18% during this same time frame). This is particularly concerning because an obese child is likely to become an obese adult and suffer many of the health complications associated with obesity.

What causes obesity?
Ask an average person what causes obesity, and you’ll likely hear some variation of “too much food and not enough exercise.” Ask an academic or researcher what causes obesity and the response will probably sound something like, “Obesity is complex disorder that is influenced by a variety of genetic, environmental, behavioral, and sociological factors, which may lead to energy imbalance and excessive weight gain.” Both responses are partially true, yet neither actually tells us how or why these factors lead to weight gain.

Cause and Effect
Researchers spend a lot of time trying to “prove” cause and effect. Determining whether a change in A causes a change in B, or vice versa, can make all the difference, especially when it comes to disease processes. It has long been assumed that obesity causes diabetes. Indeed, the two conditions are so often found together that health professionals have coined the term “diabesity.” It’s also been assumed that obesity is caused by excess calories, and that obesity, in turn, leads to insulin resistance and eventually, type 2 diabetes**. However, we may have been mistaken about the direction of “cause and effect” linking obesity and diabetes. Consider this statement from an article published in the Harvard Gazette called Obesity? Diabetes? We’ve Been Set Up:

“Today, roughly 30% of overweight people have [diabetes], and 85% of diabetics are overweight.”

Take 30 seconds to read this statement again and think about it. If excessive weight caused diabetes, you would expect these statistics to be reversed, but as it is, a much higher percentage of diabetics are overweight than overweight people are diabetic. This observation lends some critical insight into the “diabesity” issue. Read on.

The typical recommendation for someone with insulin resistance and at risk for type 2 diabetes is to lose weight. While this is not bad advice per se, it may be putting the cart before the horse. Consider this: obesity may actually be a normal (yes, that’s normal) physiological response to insulin resistance similar to how a fever is a normal physiological response to an infection. We know of course that that getting a fever does not cause an infection, but vice versa. Likewise, obesity may actually be a symptomof poor blood sugar control rather than a result of excessive calorie intake.

The way your body processes energy from food and regulates weight is complex, involving numerous biochemical pathways, nutrients, and hormones, a major one being insulin. Along with other hormones (like those that regulate appetite), insulin functions to maintain energy balance and keep weight stable. However, perpetual blood sugar spikes (from excessive amounts of refined carbs) and physical inactivity can eventually lead to insulin resistance. When a person becomes insulin resistant, their pancreas starts producing larger than normal quantities of insulin, which promotes fat storage. Meanwhile, their cells are not able to absorb sugar from the bloodstream efficiently, causing hyperglycemia. Furthermore, an individual may experience “insulin resistant hunger,” due to the fact that insulin plays a major role in appetite regulation.

Why does this matter?
Obesity is physically noticeable. Insulin resistance is not. Despite what you might assume, an obese person that is insulin sensitive may actually be healthier than a lean individual with insulin resistance. That’s certainly not to say that obesity is desirable. On the contrary, it increases the risk for a host of other health ailments, namely cardiovascular disease. But here’s the key takeaway from all this: the best way to address the diabesity issue is to first improve insulin sensitivity. What might this look like practically?

More exercise: Consider this – working muscle takes up glucose at 20 times the rate of resting muscle. Even a single bout of exercise can make muscle cells more sensitive to insulin for up to 16 hours after exercising.

Cut the refined sugar: Refined sugar in the diet causes the blood sugar to spike, resulting in a spike in insulin. When this “spike” happens frequently (eating tons of starch at every meal), it can lead to long term problems.

​Consume/ supplement with nutrients to support insulin sensitivity: We mentioned earlier that your body requires nutrients for energy regulation. Some nutrients are required for insulin to properly “signal” the cell. If these nutrients are not present, insulin sensitivity will be impaired. Other non-nutrient compounds have shown to improve insulin sensitivity in clinical trials, like berberine (from barberry) and curcumin (from turmeric).

Get adequate sleep: Sleep deprivation has a significant effect on insulin sensitivity. In a study published in the Annals of Internal Medicine in which participants were sleep deprived on 4 of the 8 nights they spent in a lab, their insulin sensitivity dropped by an average of 16%. Chronic sleep deprivation may, over time, lead to insulin resistance and type 2 diabetes.

​Consider your food environment: Let’s return to the academic’s response for “what causes obesity?”. The academic is right to say that environmental and behavioral factors play a role in obesity. Certain “cues,” like the sight or smell of food, can actually stimulate biochemical changes in the body, and in turn, our behavior. Too often, our food environment is very conducive to overeating, and worse, overeating foods high in fat and sugar (which stimulate the reward centers of the brain). Do yourself a favor and don’t buy or stock foods in your home or workplace that will tempt you until they’re gone.

**For those interested, the traditional understanding linking obesity and insulin resistance is that obesity results in elevated levels of non-esterified fatty acids (NEFA), which at high levels will impair insulin sensitivity. However, recent data suggests there is actually very little correlation between adiposity and NEFA. While obesity individuals certainly have more adipose tissue, the enzymes involved in triglyceride lipolysis (i.e. those that increase NEFA) appear to be down-regulated in obesity, resulting in normal physiological levels of NEFA even in obese individuals.

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