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Low Carb Breckenridge 2017 is open to all including the general public, health, nutrition and fitness enthusiasts, scientific community and healthcare professionals.

For healthcare professionals, this live activity, Low Carb Breckenridge 2017, with a beginning date of 02/24/2017, has been reviewed and is acceptable for up to 19.25 Prescribed credit(s) by the American Academy of Family Physicians. Physicians should claim only the credit commensurate with the extent of their participation in the activity. AAFP Prescribed credit is accepted by the American Medical Association as equivalent to AMA PRA Category 1 credit(s)™ toward the AMA Physician’s Recognition Award. When applying for the AMA PRA, Prescribed credit earned must be reported as Prescribed, not as Category 1.

Event Page: http://denversdietdoctor.com/low-carb-breckenridge-2017/
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Friday, February 24 • 3:15pm - 3:45pm
The way to man’s heart is through the stomach (CME approved)

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For many clinicians, low-carbohydrate diets are rapidly becoming the first line of treatment for cardiometabolic diseases. However, debate remains around whether restricting dietary carbohydrates constitutes a treatment of the root cause of the disease, or whether the (often dramatic) results are only due to effective symptom control. By restricting carbohydrates in the face of impaired glucose tolerance and insulin resistance, we may simply be covering up the symptoms rather than truly curing the disease. While this distinction may not be important for most patients, it must be considered when faced with cases where health does not improve as expected after adopting a low-carbohydrate lifestyle. One potential cause of worsening cardiometabolic disease in the “low carb” patient is the presence of gram-negative lipopolysaccharide (LPS) endotoxinaemia. Both clinical and experimental endotoxinaemia result in hyperinsulinaemia and changes to the lipid profile. However, rather than being directly responsible for heart disease, these responses appear to be adaptive physiological changes as a result of LPS-induced inflammation, which then become mal-adaptive in the setting of chronic endotoxinaemia. Hyperinsulinaemia and insulin resistance may therefore have a similar aetiology to the previously-favoured cholesterol hypothesis of heart disease. Importantly for those using low-carb diets in their patients, a high-fat (i.e. low carb) diet may increase the translocation of LPS into the blood stream, exacerbating inflammation-induced metabolic disease. Rather than focusing on a single reductionisttheory, by integrating gut health and bacterial endotoxinaemia into cardiometabolic disease models, it is possible to combine multiple “competing” theories of heart disease (i.e. elevated cholesterol, hyperinsulinaemia, inflammation, and arterial intimal changes) into a larger picture, and explain why a traditional low carb diet may not always be the best approach to treating heart disease.


Friday February 24, 2017 3:15pm - 3:45pm
1) Forrest Room