This modality can be contrasted with the emphasis of conventional medicine, which is to cure or mitigate disease, as reported by the American Holistic Health Association. For example, a conventional practitioner will follow an established algorithm for diabetes management that includes a medically established protocol centered on monitoring blood sugar and prescribing medications to balance it. An alternative medicine provider takes a personalized, whole-person approach that may include a prescription for changes in diet and exercise habits, stress reduction, and other lifestyle considerations. (The table below offers a comparison of alternative medicine with conventional medicine.)
Christina Kalberg is the Executive Director of the Diabetes Research Connection (DRC). She comes to DRC with over 10 years of experience as a senior-level executive effectively integrating passion and in-depth skill into well-crafted marketing, public relations, communications, operations and fundraising campaigns to directly fuel multi-million-dollar revenue growth. Christina is a strategist, deftly aligning staff and other stakeholders. She has a Bachelor’s degree in Journalism with an emphasis in Public Relations and a Master’s degree in Business Administration. Christina is also an adjunct professor for the marketing program at Point Loma Nazarene University, where she teaches Digital and Social Media Marketing.
Information on this website is provided for informational purposes only and is not intended as a substitute for the advice provided by your physician or other healthcare professional. You should not use the information on this website for diagnosing or treating a health problem or disease, or prescribing any medication or other treatment. Any third party offering or advertising on this website does not constitute an endorsement by Andrew Weil, M.D. or Healthy Lifestyle Brands.
Kelly Prinkey-Krupinski, 48 and an avid dog lover, has been struggling with adult onset Type 1 diabetes for 12 years. She said the disease runs her life. “It is a constant struggle,” she said. “My mind is always aware that every bite of food that I eat, every medicine I take, every illness and emotion I experience will affect my blood sugar. There is never a vacation from the constant balancing act to stay alive. It scares me to think of a time when I can't obtain the insulin that I must take 24-7. I would pray that there will be a cure in my lifetime. I just hate to think of the kids that struggle with Type 1 diabetes. This research with dogs sounds promising. As a dog lover myself, I would love to see if our canine friends can be cured. I'm excited to see the results.”
Benari, an Ashkenazi Jew, doesn’t fall into that category. But Cummings and other bariatric experts I spoke to said that surgery should be a possible option for any person whose diabetes isn’t improving. Cummings himself is currently working on a clinical trial in India of bariatric patients with BMIs as low as 25. And he expects similar trials will come down the pipeline.
Evidence linking hepatic insulin sensitivity to intraorgan triglyceride content has been steadily accumulating. In insulin-treated type 2 diabetes, insulin dose correlates with the extent of fatty liver (35), and in turn, this is associated with insulin sensitivity to suppression of hepatic glucose production (36). Decreasing the fat content of liver is associated with improvement in insulin suppression of glucose production and, thereby, with improvement in fasting plasma glucose (20,23).
The findings, reported in the journal Cell Metabolism, show the cells grown in the lab can reduce blood glucose levels to normal. Professor Evans added: “It was a little bit of a surprise to see that beta cells produce a high level of this regulator, but beta cells have to release massive amounts of insulin quickly to control sugar levels. It’s a very energy-intensive process.”
Mechanism of interaction between excess amounts of fatty acids, diacylglycerol, and ceramide and insulin action within the hepatocyte. Diacylglycerol activates PKCε and inhibits activation of IRS-1 by the insulin receptor. Ceramides cause sequestration of Akt2 by PKCζ and inhibit insulin control of gluconeogenesis. These mechanisms have recently been reviewed (99). FFA, free-fatty acid; TG, triacylglycerol.