Is Type-2 Diabetes the Result of Toxic Fat?

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Toxic Fat and DiabetesIt’s no secret that type 2 diabetes is the result of insulin resistance, or that it is a major health epidemic in America and throughout the world. But new research is showing that there might be a previously unrecognized culprit: toxic fat.

Being overweight or obese are both big-time risk factors for type 2 diabetes, but they are not the only risk factors. They also don’t explain how skinny people, or those of “normal” weight can also acquire type 2 diabetes. In fact, you might be interested to hear that type 2 diabetes patients of normal or healthy weight are more likely to die than their heavier counterparts.

Previous research monitoring type 2 diabetes prevalence indicated that 12% of diagnoses between 1990 and 2011 were in people with normal weight. This is quite interesting because it shows there is likely a strong genetic component to a condition typically thought to be the result of lifestyle choices. This genetic component may be how the body’s fat cells function, and particularly the presence of toxins called ceramides.

The Diabetes Epidemic

An overwhelming number of Americans are currently living with diabetes, while a substantial number of others have pre-diabetes. Many of those with pre-diabetes will join the ranks of diabetic very soon. According to the Centers for Disease Control and Prevention (CDC), over 29 million Americans—9.3 percent of the population—are living with diabetes. Of course, not all cases are type 2 diabetes, but most are. Type 2 diabetes represents 90 to 95% of all diabetes diagnoses.

Type 1 diabetes used to be referred to as “childhood diabetes” or “early-onset diabetes,” and is basically a genetic condition sufferers are born with. It is irreversible and can only be managed throughout life. Those who have it are unable to produce the hormone insulin.

On the other hand, type 2 diabetes is something people contract later in life—although data indicates that people are increasingly being diagnosed at a younger age. People with type 2 diabetes produce insulin, but their bodies do not utilize it properly.

What Is Insulin?

Insulin is a hormone secreted by the pancreas when you consume sugar. It shuttles sugars to your cells, providing glucose for energy. In people with type 2 diabetes, insulin doesn’t really do its job. The glucose is not properly administered or assimilated by cells, and builds up in the bloodstream instead. This leads to elevated levels of blood sugar, and when they reach abnormal levels, diabetes is diagnosed.

Toxic Fat: A New Discovery to Spearhead Improved Treatment?

Recent research published in the journal Cell Metabolism shows that although body weight is a risk factor for type 2 diabetes, it’s not solely responsible for the condition. If it were, then those of normal weight or healthy people wouldn’t have the condition. The study, done by a research team from the University of Utah’s Department of Nutrition and Integrative Physiology, shows that it might not be how much fat a person has, but what kind of fat they have. A type of toxic fat metabolite, called ceramides, may play a major role in one’s risk for type 2 diabetes.

The researcher found that a buildup of ceramides prevents fat cells from working effectively and impairing cell metabolism, insulin response, nutrient absorption and calorie burning. It should be noted that this study looked at the effects of ceramides on mice.

When humans eat, calories are either burned as energy or stored as fat, which are technically energy reserves. For some people, however, the excess fat turns into ceramides. According to the lead researcher of the study, Scott Summers (PhD), when too many ceramides accumulate in fat tissue, it can reach a “tipping point.” This causes the fat tissue to stop working properly, spilling over into the blood vessels, heart, and other tissues.

Ceramides are not new on the scene and have previously been linked to diabetes. They’ve been noted to cause the death of pancreatic beta cells (which make insulin), increase insulin resistance, and reduce insulin gene expression.

Summers’ study has shown that when mice were injected with extra ceramide cells, they became insulin-resistant and unable to burn calories. On the other hand, mice that had lower numbers of ceramides didn’t develop the same symptoms.

This research suggests that thin or “healthy weight” people with diabetes, may have a genetic condition that predisposes them to create higher numbers of ceramides. Summers also pointed out that although being overweight and obese are common in American cases of type 2 diabetes, Asian countries have a higher number of diabetics, while having relatively low obesity rates.

What You Can Do

As of right now, there isn’t much you can do to alter what kind of fat you have, or your body’s propensity to produce ceramides. However, you can still greatly reduce the risk of type 2 diabetes by adopting an active lifestyle and limiting intake of excess calories and refined foods. When it comes to preventing diabetes, regulating blood sugar is the most important thing. This can be done through exercise, which is linked to improved glucose metabolism.

Eating foods rich in fiber, as well as avoiding high-sugar and highly-refined items like soda, white bread, candies, white flour, sugar, syrups, sauces, and other-sugar rich products that can add unused calories and increase blood sugar. Instead, opt for whole grains, vegetables, fruits, legumes, nuts, and spices and seasonings that are low in added sugars.


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Sources:
Adipocyte ceramides regulate subcutaneous adipose browning, inflammation, and metabolism, Bhagirath Chaurasia et al., Cell Metabolism, doi: http://dx.doi.org/10.1016/j.cmet.2016.10.002, published online 3 November 2016.
Role of ceramide in diabetes mellitus: evidence and mechanisms, Sehamuddin Galadari et al., Lipids in Health and Disease, doi: 10.1186/1476-511X-12-98, published online July 8, 2013.
Association of weight status with mortality in adults with incident diabetes, M. R. Carnethon et al., JAMA, doi: 10.1001/jama.2012.9282, published online August 8, 2012.