Tuesday , November 21 2017
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Obesity

Obesity and Diabetes: Diabetes patients are considered obese when they have a Body Mass Index over 30. Such patients are at greater risk for a host of other problems cardiovascular disease, cancer, sleep apnea, and poor quality of life. Tremendous research is being done to control, manage, and reverse obesity in diabetics and the educated healthcare professional can help.

Time Will Tell What Patient Will Do

Male, 21 years of age has class III obesity, binge eating disorder, fatty liver, and asthma, and was recently diagnosed with type 2 diabetes. It is his freshman year at a college away from home. He eats in the cafeteria, and has no refrigerator or stove in his room. He visits today after not taking metformin or GLP-1 agonist since at starting school. He is under a lot of stress and states the food at school is terrible, unhealthy, and not diabetes-friendly at all. Note, he has been taught a lower carb meal plan. He says he is not taking Glucophage or Victoza; each of them at low doses gives him terrible diarrhea. He states he checks his glucose twice a week, with fastings in the 90-100 range. He is up 10 pounds since our last visit in September.

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When Losing Weight, Warn ’em!

I work in obesity medicine. As many of us know, losing weight isn't the problem for most, but weight regain is. As the saying goes for many, you can't be rich enough or thin enough. Many of our patients come in with unrealistic goals regarding their weight loss, and don't give themselves enough credit for the weight they have lost. Many, for many reasons, regain.

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Denial: Numbers Don’t Lie

Woman, 64 years of age. History of Class II Obesity and hyperlipidemia. While she had obesity, her glucose levels were elevated. A1C 8.2%. She followed a lower carb meal plan, was active, took metformin and a GLP-1, a statin and an ACE-I. She lost 22% total body weight. A1C then remained in the 6-6.5% range for 3 years on this treatment plan. Over the past 8 months, due to insurance and her statement of denial that she ever really had diabetes, she stopped taking her glucose-lowering medication, statin, and ACE-I, wasn’t as strict with meal plan or activity, and stopped checking her glucose, but did not gain back her weight.

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A New Paradigm in the Understanding and Treatment of the Metabolic Syndrome: Targeting Alterations within the Biological Clock System

The prevalence of obesity and insulin resistance syndrome, rare only a century ago in most geographic locals of the world are now disorders whose prevalence represents the majority of humans in westernized countries on planet Earth. This simple observation strongly suggests that factors other than or in addition to genetic mutations/alterations are facilitating this rapid onset in disease occurrence world wide. Although the insulin resistance syndrome is viewed by the medical community as a defect of normal physiology, a plethora of available evidence indicates that the insulin resistant condition evolved among vertebrates as a survival strategy to enable increased survivability of ensuing, predictable seasons of low/no food (including glucose) availability.

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Introduction: Anthony Cincotta

I am a neuroendocrinologist by training, having received my Bachelor’s degree in biochemistry and molecular biology from the University of California, Santa Barbara and Master’s and Doctorate degrees from Louisiana State University (LSU) in physiology under the mentorship of Dr. Albert H. Meier. It was at LSU that my interest in the biological clock system and its role in the regulation of metabolic physiology was sparked by the revolutionary discoveries and elucidations made by Dr. Meier’s lab concerning biological clock mechanisms regulating physiology. He and his group in the early 1960s were the very first to demonstrate the existence in any organism of circadian rhythms of physiological responses to neuroendocrine factors. At LSU, I began investigating the possibility that modern human pathology of the metabolic syndrome (and several other progressive pathologies) was not a result of any “genetic defect” but of an environmentally induced (e.g., diet, stress, sleep-wake architecture) alteration of circadian neuroendocrine information presented to the clock system that then responded to direct the body to the obese/insulin resistant state as a survival response to such information.

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