Which woman has Type 2 diabetes?
Heads up National Institute on Aging….these older “lean” adults with diabetes who show a higher risk of mortality than their heavier counterparts may have gone YEARS without a diagnosis of diabetes….simply because of their “lean-ness.”
It’s unfortunate that type 2 diabetes has become stereotypes as “fat diabetes.” (Years ago type 2 was called “diabetes of old age” until younger and younger people developed the disease. As a result of assuming those with type 2 are overweight or obese, it is possible that these lean patients have had higher than normal blood sugar for years. During these years without a diagnosis, or treatment, high blood sugar wreaked havoc inside their bodies.
Years of higher than normal blood sugar will block and harden the arteries, cause inflammation of all blood vessels, increase AGE’s, lead to hypertension, high cholesterol, high triglycerides, low Vitamin D. If diabetes was not diagnosed as early as possible, you would expect to see heart attack, stroke, cancer, osteoporosis in these seemingly healthy, lean folks.
How do we solve this? LOOK at the fasting glucose of EVERY patient; overweight or lean. Readings over 99mg/dL mean pre diabetes…no matter the weight. And…if your patient is lean and has higher than normal blood sugar, they will be most likely prove to have type 1.5 diabetes and require insulin sooner than your overweight patients.
The reason for the increased mortality isn’t the patient’s lean-ness, it just may be under- treatment of his diabetes for a period of years prior to his diagnosis!.
Here’s the National Institute on Aging “study” results…beneath it Diane Kress’ article on type 1.5 diabetes.
Mortality Risk Higher in Normal-Weight Diabetes Patients
Muscle size may mediate the relationship between body mass index and mortality in type 2 diabetes
|WEDNESDAY, Oct. 29, 2014 (HealthDay News) — In older adults with type 2 diabetes, muscle size may mediate the association between body mass index (BMI) and mortality, according to research published online Oct. 14 in Diabetes Care.Rachel A. Murphy, M.D., of the National Institute on Aging in Bethesda, Md., and colleagues analyzed data from the AGES-Reykjavik cohort of participants, aged 66 to 96 years, with type 2 diabetes. The authors sought to investigate whether adipose tissue, muscle size, and physical function, which vary by weight, mediate associations between BMI and mortality. Participants were normal weight (18.5 to 24.9 kg/m², 117 participants), overweight (25.0 to 29.9 kg/m², 293 participants [referent group]), or obese (≥30.0 kg/m², 227 participants).The researchers found that, compared with overweight participants, there was no mortality risk for obese participants and an increased risk of mortality for normal-weight participants (hazard ratio [HR], 1.72; 95 percent confidence interval [CI], 1.12 to 2.64). After adjustment for adipose tissue and kneeextensor strength, these associations persisted. Mortality risk for normal-weight participants was attenuated after adjustment for thigh muscle (HR, 1.36; 95 percent CI, 0.87 to 2.11) and gait speed (HR, 1.44; 95 percent CI, 0.91 to 2.27). Further analysis confirmed that thigh muscle size mediated 46 percent of the relationship between normal weight and mortality risk.”In conclusion, the results illustrate the importance of identifying type 2 diabetes among normal-weight individuals and suggest that muscle size may help to explain relationships between BMI and mortality in type 2 diabetes,” the authors write.
Type 1.5 Diabetes? WHAT????? By Diane Kress, RD CDE
Most people have heard of gestational diabetes, type 1 diabetes, and type 2 diabetes.
Gestational diabetes can occur during pregnancy.
Type 1 diabetes, autoimmune in nature and usually occurring abruptly during the childhood/teen years, renders the pancreas incapable of producing insulin.
Type 2 diabetes has a genetic component, is influenced by environmental stressors like overweight, inactivity, high carb intake, and stress, and occurs most often in adulthood is characterized by inadequate insulin production and/or insulin resistance.
Over the past years, we’ve seen these solid lines of delineation become blurred with the discovery of what has been called type 1.5 diabetes or latent autoimmune diabetes of adults (LADA). Discovered in the 1970’s and more regularly discussed since the early 1990’s, many diabetes practitioners subscribe to its existence although there is not yet a classification for LADA.
Although LADA is typically diagnosed in adulthood as type 2 diabetes, after 3-12 years, this type of diabetes seems to look more like type 1 diabetes. LADA has characteristics of both type 1 diabetes and type 2 diabetes.
A quick review of the differences between type 1, type 2, and LADA:
Type 1 diabetes is an autoimmune disease. A combination of genetic and environmental factors such as virus exposure or environmental toxins increases the risk of type 1 diabetes. An autoimmune response targets the destruction of the pancreas’ beta cells. In short order, the beta cells are rendered unable to produce life -sustaining insulin. People with type 1 diabetes do not respond to oral medications for blood sugar regulation and require insulin (injections or infusion) for life.
Although type 1 diabetes was once called juvenile diabetes (the majority of new diagnoses occur in childhood/teen years), adults can also develop type 1 diabetes.
Type 2 diabetes most often occurs in adults; although, children are increasingly being diagnosed with what used to be called adult onset diabetes. Type 2 diabetes is progressive in nature and fasting blood glucose may take years to elevate to the point of diabetes diagnosis. The progression to type 2 diabetes usually resembles: metabolic syndromeàpre diabetesàtype 2 diabetes. During the metabolic syndrome and pre diabetes years, it is possible to make lifestyle changes to help prevent the progression to type 2 diabetes.
In type 2 diabetes, three metabolic situations may be underway:
Many who develop type 2 diabetes are overweight at diagnosis, with fat stores concentrated around the middle (belly fat). This increased belly fat along with elevated cholesterol, triglycerides and blood pressure develops progressively during the years of “over production” of insulin.
Years of insulin over production and fat cell growth leads cells to become resistant to insulin. In fact, at this point, there may be high levels of insulin AND high levels of glucose in the blood. Over time, the over worked pancreas fatigues and eventually produces less insulin. Eventually, those with type 2 diabetes have insulin resistance and inadequate insulin production. All the while, the pancreas still produces insulin.
Type 1.5 diabetes accounts for roughly 10 percent of people with diabetes. It is estimated that 20 percent of those initially diagnosed as having type 2 diabetes actually have LADA. There is still uncertainty over how to define LADA, why it develops and progresses.
Often, a person with LADA may be lean or normal weight when diagnosed. Oral medications may initially work to decrease elevated blood sugar. Over time (in much shorter order than typical type 2s,) oral medications become ineffective. Blood sugar worsens and insulin must be prescribed to control high blood glucose.
Some diabetes practitioners recommend that in adult patients who present as lean or normal weight and have no known family history of type 2 diabetes, antibody testing should be performed to differentiate between type 2 diabetes and LADA.
Why would it be beneficial to “know in advance” if a person has type 2 or LADA? Well, think of it this way, many oral medications work by forcing the pancreas to produce more insulin. Sulfonylureas are one class of diabetes drugs that cause the pancreas to work harder. By prescribing more and more pancreas- provoking oral medications (to no avail), the medication would speed the demise of beta cells.
Also, if we keep a patient with LADA on a traditional diet for diabetes—calorie controlled/low fat—we are exposing the pancreas to an increased need to produce insulin caused by the high blood sugar rendered from the breakdown of 50-55% carb dieting. In the same way that some oral medications press the pancreas to produce more insulin, so, too, does the higher carbohydrate diet require more insulin production.
So, perhaps instead of it taking years for LADA to run its course and render the pancreas null and void, we can make lifestyle changes that can promote the health and wellness of this portion and decrease the need for insulin injections or infusions.
In the years it takes to prove that oral medications are not working, the patient is subjected to higher than necessary A1cs. The faster blood sugar is normalized, the better the long term outcomes. If insulin use is inevitable and orals can actually stress a pancreas that has begun to degrade, why not remove that excess stress from the pancreas and the body of the person with LADA?
The case could be made to first diagnose or recognize a patient with LADA and then begin appropriate treatment. Here are suggestions I give my would be “LADA” patients…
By resting the pancreas and normalizing blood sugar, we may be able to extend the lifespan of the LADA pancreas—from 5 years to perhaps 10 years or more. It’s important to remember that those with type 1 diabetes do not produce insulin, amylin, and may produce inadequate amounts of glucagon. It would be advantageous to keep the beta cells of the pancreas functioning as long as is possible—and not unnecessarily speed up their demise.
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