Sugar: How Bad is Bad? Part 2: Hyperglycemia, Metabolic Syndrome, Insulin Resistance, and Type II Diabetes
Being "hangry" is a a blood sugar handling thing
Eating refined carbohydrates and sugar every day (riding the blood sugar rollercoaster nonstop), leads to a condition where insulin can no longer keep blood sugar levels stable. In fact, blood sugar levels are typically low because now when they drop, the pancreas struggles to get them back up. This state is called hypoglycemia. Hypoglycemic people typically get shaky and irritable if they miss a meal, and have an insistent hunger that must be fed NOW. You might use caffeine or nicotine to suppress sugar cravings. You might eat sweets instead of balanced meals. Symptoms of hypoglycemia can include mental sluggishness, insomnia, irritability, inability to complete routine tasks, blurry vision, and even seizures.
The adrenal glands kick in and send cortisol to the rescue. Cortisol breaks down muscle tissue in order to get what it needs to increase blood sugar levels. But cortisol is something of an emergency hormone, meant to help us make it through stressful events. It is not really designed to constantly be handling blood sugar levels. Cortisol surges naturally give us an urge to refuel (eat), so if you are experiencing blood sugar handling issues due to poor diet, weight gain can occur.
Too much cortisol and the world starts to look competitive to the body–a place of win-lose, or fight-or-flight. We tend to call that a Type A person, but it can also be a person in a constant state of stress. Too much need for cortisol wears out the adrenal gland–what we call HPA-D (formerly known as adrenal fatigue).
Back in the caveman days, cortisol and adrenaline saved us in emergencies. If a big animal was coming at him and he needed to run away, adrenaline increased his heart rate and blood pressure, lending to almost superhuman strength to run far and fast. Caveman was in motion, and he used up that burst of sugar. But today, a dinner of spaghetti followed by a slice of cake can be recognized by the body as “an emergency.” We don’t burn it off because we are not in motion--we are sitting down, enjoying a nice glass of wine at the restaurant.
When it comes to sugar dysregulation, hypoglycemia is the first step. Hypoglycemia gives us circulatory problems, peripheral neuropathies, high triglycerides, high LDL, and more weight stored as belly fat. Belly fat isn’t just a matter of its cosmetic appearance. It is dysfunctional tissue sending dysfunctional messages that contribute to obesity, diabetes, and heart disease.
Chronic hypoglycemia can lead to metabolic syndrome. Metabolic syndrome is defined by the following risk factors:
- Abdominal obesity
- High cholesterol and triglycerides
- High blood pressure
- Insulin resistance
- The tendency to form blood clots
- Inflammation
Chronic hypoglycemia is caused by eating too many carbohydrates. Therefore, metabolic syndrome could easily be called “excess carbohydrate disease.” In fact, some researchers have gone as far as defining metabolic syndrome as “those physiologic markers that respond to a reduction in dietary carbohydrate” [1].
Continued consumption of sugar, and the chronic demand for high levels of insulin that goes along with it, will eventually wear out the pancreas, such that the body can no longer produce insulin at all (insulin resistance). This is adult-onset diabetes, or what is called type 2 diabetes.
Never before in the history of mankind have we had such a constant need to lower blood sugar. This is why the CDC projects that 1 in 3 children born in 2000 will develop type 2 diabetes. If this shocks you, it really shouldn’t. When you leave the house, it’s not hard to physically see where our world is headed in terms of health.
In summary: Sugar causes hyperglycemia. Chronic hyperglycemia causes metabolic syndrome. The metabolic syndrome causes insulin resistance. Insulin resistance causes type 2 diabetes.
Sugar is bad.
Stay tuned for the science behind the reasoning.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2359752/?tool=pubmed
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