The Surprising Truth About Wheat, Carbs, and Sugar – Your Brain’s Silent Killers
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To add insult to injury, I should also point out that insulin can be viewed as an accomplice to the events that unfold when blood sugar cannot be managed well. Unfortunately, insulin doesn’t just escort glucose into our cells. It’s also an anabolic hormone, meaning it stimulates growth, promotes fat formation and retention, and is a pro-inflammatory hormone. When insulin levels are high, other hormones can become adversely affected, either increased or decreased due to insulin’s domineering presence. This, in turn, plunges the body further into unhealthy patterns of chaos that cripple its ability to recover its normal metabolism.
Genetics are certainly involved in whether or not a person becomes diabetic, and genetics can also determine at what point the body’s diabetes switch gets turned on, once its cells can no longer tolerate the high blood sugar. For the record, type-1 diabetes is a separate disease thought to be an autoimmune disorder—accounting for only 5 percent of all cases. People with type-1 diabetes make little or no insulin because their immune system attacks and destroys the cells in the pancreas that produce insulin, so daily injections of this important hormone are needed to keep blood sugars balanced. Unlike type 2, which is usually diagnosed in adults after their bodies have been abused by too much glucose over time, type-1 diabetes is typically diagnosed in children and adolescents. And unlike type 2, which is reversible through diet and lifestyle changes, there is no cure for type 1. That said, it’s important to keep in mind that even though genes strongly influence the risk of developing type-1 diabetes, the environment can play a role, too. It has long been known that type 1 results from both genetic and environmental influences, but the rising incidence over the last several decades has led some researchers to conclude that environmental factors are increasingly involved in the development of type 1 and may be more important than genetic predisposition.
What we’re beginning to understand is that insulin resistance, as it relates to Alzheimer’s disease, sparks the formation of those infamous plaques that are present in diseased brains. These plaques are the build-up of an odd protein that essentially hijacks the brain and takes the place of normal brain cells. And the fact that we can associate low levels of insulin with brain disease is why talk of “type-3 diabetes” is starting to circulate among researchers. It’s all the more telling to note that obese people are at a much greater risk of impaired brain function, and that those with diabetes are at least twice as likely to develop Alzheimer’s disease.
This statement is not meant to imply that diabetes causes Alzheimer’s disease, only that they both share the same origin. They both spring from foods that force the body to develop biological pathways leading to dysfunction and, farther down the road, illness. While it’s true that someone with diabetes and another person with dementia may look and act differently, they have a lot more in common than we previously thought.
In the last decade, we’ve witnessed a parallel rise in the number of type-2 diabetes cases alongside obesity. Now, however, we’re starting to see a pattern among those with dementia, too, as the rate of Alzheimer’s disease increases in sync with type-2 diabetes. I don’t think this is an arbitrary observation. It’s a reality we all have to face as we shoulder the weight of soaring healthcare costs and an aging population. New estimates indicate that Alzheimer’s will likely affect 100 million people by 2050, a crippling number for our health care system that will dwarf our obesity epidemic. The prevalence of type-2 diabetes, which accounts for 90 to 95 percent of all diabetes cases in the US, has tripled in the past forty years.