Diagnosis and Possible Reversal of Pre-Diabetes: - Natural ...

More documents

Recommendations

Info

Editor’s Note: For a copy of Dr. Jaffe’s study, visit the Clinical Tools section of the Natural Medicine Journal (www.naturalmedicinejournal. com) and click on Clinical Insights. References 1 Jaffe R, Mani J, DeVane J, Mani H. Tolerance loss in diabetics: Association with foreign antigen exposure. Diabet Med. 2006;23(8):924-5. Early And Accurate Diagnosis is Critical Commentary by Mona Morstein, ND The medical diagnosis of pre-diabetes (PD) includes both standard evaluations, as well as a unique naturopathic test. The goal of early and accurate diagnosis is to determine if the patient is in a mild, moderate, or severe state of pre-diabetes. Early and accurate diagnosis helps determine how aggressive the treatment needs to be, and how much damage PD may have already caused the body. PD is often associated with metabolic syndrome, which is defined similarly by various organizations. The basic definition based on the American Heart Association (AHA)/Updated National Cholesterol Education Program (NCEP) consists of having three or more of the following traits: • Elevated waist circumference (men >40 inches; women >35 inches; lower for Asian populations) • Hypertriglyceridemia (>150 mg/dl) • Reduced HDL (men 100 mg/dl) Not all pre-diabetic patients have metabolic syndrome; however, simply having a fasting glucose level of 101–125 mg/dl can identify a patient as pre-diabetic. When I have a patient with a pre-diabetic glucose number, I reflex to a more comprehensive analysis of glucose regulation, which is justified in scientific literature. The Oral Glucose Tolerance Test is a standard lab test consisting of having a patient fast 12 hours, get a fasting glucose level, and then drink 75–100 g of a glucose drink, with repeated glucose blood draws over the next one, two, and three hours. I have personally adapted this test to a different format. I have patients fast for 12 hours and then test their fasting glucose and insulin levels. I then have them eat—preferably at a local fast food restaurant—one pancake with syrup and one hash brown. This gives the patient 100 g of refined sugar and grain carbohydrate, as well as saturated fat—the two top food groups that initiate insulin resistance. I am more interested in seeing what actual food does to people than just a glucose drink. I then have the patient return to the clinic 1.5 hours after eating for a second blood draw of glucose and insulin. Some other naturopaths at my clinic have patients get postprandial draws of one, two, and three hours, but I find that is very difficult for many patients, and it is time-consuming. For my interpretation of the patient’s condition, it also does not seem to help more than the solo 1.5-hour postprandial reading. Insulin levels are vital for understanding how much insulin resistance is occurring. How much insulin that is secreted, analyzed in combination with glucose levels, gives the clinician a very accurate way of determining if the patient’s insulin resistance and pre-diabetes status is mild, moderate, or severe. Russell Jaffe, MD, PhD, CCN, NACB, FRSM is a renowned early pioneer of Integrative Medicine. Starting as a Molecular Biochemist / Pathologist at Boston U Medical Center and the USPHS/ NIH he was the founding chairman of the Scientific Committee of the American Holistic Medical Association. Dr. Jaffe taught one of the first courses on using Eastern medical strategies in Western medicine. He has won many awards for his lifetime contributions to clinical medicine, biochemistry, immunology, methodology, and integrative health policy. He currently serves on the tasks forces that are modeling evidence based, affordable, effective, sustainable healthcare. He is chairman and CEO of PERQUE, LLC, ELISA/ACT Biotechnologies, LLC. He is also a Senior Fellow of the Health Studies Collegium Foundation. I also do a comprehensive CMP/CBC, including TSH/FT3/FT4, vitamin D (25OHVD), ferritin (to check for early liver inflammation indicating fatty liver), and A1C. It might be wise to also include fibrinogen to check on blood clotting risk, HS-CRP to analyze inflammation, and homocysteine to check for L-methylfolate bioavailability. The initial physical exam should include vitals, heart/lung evaluation, thyroid exam, search for skin tags or acanthosis nigricans, height, weight, waist circumference with BMI, body fat percentage (via scale such as Tanita or Bio-Impedance device), foot exam including edema/ pulses/lesions/neuropathy (using standard monofilament check), and abdominal exam to check for hepatomegaly. The patient should be instructed to fill out a week-long diet diary to track eating habits, accurately recording everything she/he eats and drinks for all meals/snacks. Bowel movement frequency, symptoms, and sleeping habits should also be recorded. Regarding the treatment of pre-diabetes, some clinicians fail to emphasize the importance of sleep in this patient population. Several well-designed studies, including a recent one this year from the Journal of Clinical Endocrinology, 1 have clearly demonstrated that lack of sleep causes insulin resistance and weight gain. Sleep directly affects the two main hormones that regulate human appetite: leptin and ghrelin. Leptin is made in the adipocytes and instructs a person to eat less food. When a person gets enough sleep, it raises leptin levels, which decreases the desire to eat. Conversely, low amounts of sleep lower leptin levels and can thus cause increased appetite. Ghrelin is another appetite hormone made in the stomach. Opposite to leptin, ghrelin tells the brain to eat more food. When people don’t get enough sleep, ghrelin levels increase and people crave high carbohydrate foods. Less sleep also causes an increase in cortisol output at night, which can cause hyperglycemia and initiate insulin resistance, another factor in abdominal weight gain and developing pre-diabetes and diabetes. Lastly, sleep is also needed for growth hormone (GH) to be fully secreted. Adult patients with low GH secretion are insulin resistant, due to several not wholly understood factors. If a patient presents with PD symptoms and has sleep problems, a sleep study should be performed. Instituting sleep hygiene is a necessary aspect of pre-diabetes treatment and includes turning off most lights in the house so melatonin output can be enhanced; establishing the same bedtime routine each night; not watching disturbing TV shows or even news at night before bed, which may cause mental/emotional upset; spending some time reading before bed to initiate sleep; ensuring the mattress and room temperature is conducive to the patient’s body; addressing problems such as partner snoring or restless legs that may be interrupting the patient’s sleep; urging the use of a continuous positive airway pressure (CPAP) if apnea is diagnosed; dealing with hormonal imbalances that ©2009 Natural Medicine Journal 1(2), October 2009 | Page 2
may be causing sleeping problems, such as elevated nighttime cortisol, or menopausal night sweats; using guided relaxation DVDs (or other stress relaxation techniques) to help induce sleep; and recommending occasional sleep aids, but avoiding nightly addiction to them. References 1 Nedeltcheva AV, Kessler L, Imerial J, Penev PD. Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance. J Clin Endocrinol Metab. 2009 Sep; 94(9):3242-51. Epub 2009 Jun 30. Addressing Chronic Inflammation With Two Key Dietary Supplements Commentary by Cheryl Myers, RN Many of my colleagues no longer support a pre-diabetes diagnoses, believing instead that any consistent fasting blood sugar (FBS) over 100 should be considered type 2 diabetes (albeit a milder form) and must be treated. Diabetes is most reversible in the earliest stages, when FBS is less than 125, which is the general range of the term “pre-diabetes.” Effective early identification of underlying causes is critical to the successful treatment of this condition. While the etiology of pre-diabetes is multifactorial, one consistent hallmark is chronic inflammation. This potential underlying cause is often not considered as fully as it should be in clinical practice. In a selfperpetuating, destructive cycle, hyperglycemia and insulin resistance beget inflammatory changes. According to one recent study, “insulin receptor substrates serine phosphorylation is a time-controlled physiological feedback mechanism in insulin signaling that is hijacked by metabolic and inflammatory stresses to promote insulin resistance.” 1 FBS consistently above normal and not contributable to non-diabetic factors is evidence of this process in action. In simpler terms, inflammation promotes insulin resistance, insulin resistance promotes hyperglycemia, and hyperglycemia promotes inflammation. It is important that this cycle be interrupted or pre-diabetes will evolve to diabetes in the majority of patients thus diagnosed. Two scientifically substantiated potent anti-inflammatories to consider clinically are curcumin and omega 3 fatty acids. Curcumin has been examined for its ability to prevent oxidative stress, modulate the immune system, and reduce inflammation—all of which has a positive impact on pre-diabetes. However, one area of particular interest is curcumin’s ability to inhibit and modulate specific kinases called c-Jun N-terminal kinases (JNKs, also called “stress-activated kinases” or SAPKs). JNKs modify the activity of certain proteins that are especially important in the development of insulin resistance, which is clinically the earliest stage in the development of type 2 diabetes. 2 Curcumin is a known inhibitor of JNKs and therefore could be a powerful tool in reversing the metabolic processes that lead to insulin resistance and subsequent prediabetes. 3 Biochemistry aside, from a treatment perspective, curcumin has been shown quite efficacious in the prevention of cardiovascular disease, one of the unfortunate potential sequela of diabetes as well as diabetic retinopathy, a leading cause of blindness. 4 , 5 Preliminary research indicates that curcumin may help prevent diabetic neuropathy. 6 Omega 3 fatty acids also have proven anti-inflammatory properties. In a recent study, 148 men with impaired glucose tolerance and/or impaired fasting blood glucose were followed for 12 months after counseling in dietary fat quality. At the end of the study, 92 subjects reverted to normal Mona Morstein, ND, graduated from National College of Natural Medicine where she also did a year residency in Family Practice. She then moved to Great Falls, Mont., where she had a private practice for 13 years before joining Southwest College of Naturopathic Medicine (SCNM). She is Chair of the Nutrition Department, associate professor, and clinical supervisor at SCNM. Dr. Morstein is a general practitioner who uses numerous modalities and has focuses on diabetes, gastroenterology, and women’s health. glucose levels and 56 remained in prediabetic status. None of the participants progressed to full diabetes. Additionally, it was noted that subjects in the highest tertile of omega-3:omega-6 fatty acid ratio showed the highest chance of improving glucose disturbances (2.51, 1.01-6.37). 7 Therefore, incorporating more fatty fish into the diet and/or supplementing with omega 3 fatty acids can have a profound impact on ameliorating blood sugar changes associated with type 2 diabetes, and studies indicate a higher omega 3:omega 6 ratio is protective against progression to diabetes. Given the strong correlation between inflammation and prediabetes, I feel it is imperative that clinicians address this issue in this patient population. The scientific literature provides us with enough substantiation to incorporate curcumin and omega 3 fatty acids into the dietary supplement program of the pre-diabetic patient, along with applicable dietary and lifestyle counsel. References 1 Tanti JF, Jager J. Cellular mechanisms of insulin resistance: role of stressregulated serine kinases and insulin receptor substrates (IRS) serine phosphorylation. Curr Opin Pharmacol. 2009 Aug 13.) 2 Kaneto H. The JNK pathway as a therapeutic target for diabetes. Expert Opin Ther Targets. 2005;9(3):581-92. 3 Moon DO, Jin CY, Lee JD, et al. Curcumin decreases binding of Shiga-like toxin-1B on human intestinal epithelial cell line HT29 stimulated with TNFalpha and IL-1beta: suppression of p38, JNK and NF-kappaB p65 as potential targets. Biol Pharm Bull. 2006;29(7):1470-5. 4 Wongcharoen W, Phrommintikul A. The protective role of curcumin in cardiovascular diseases. Int J Cardiol. 2009;133(2):145-51. 5 Kowluru RA, Kanwar M. Effects of curcumin on retinal oxidative stress and inflammation in diabetes. Nutr Metab (Lond). 2007;4:8. 6 Osawa T. Nephroprotective and hepatoprotective effects of curcuminoids. Adv Exp Med Biol. 2007;595:407-23. 7 Sartorelli DS, Damião R, Chaim R, Hirai A, Gimeno SG, Ferreira SR. Dietary omega-3 fatty acid and omega-3: omega-6 fatty acid ratio predict improvement in glucose disturbances in Japanese Brazilians. Nutrition. 2009 Jul 30. Cheryl Myers, RN, is recognized as an expert in the health and dietary supplement field. She writes, gives public appearances, and is in charge of scientific affairs and education for EuroPharma, Inc. Cheryl graduated from Purdue University, and also has clinical certifications in oncology and gerontology, and has a second degree in psychology. Cheryl’s nationally published articles have addressed a variety of health applications for natural products, and Cheryl has been a featured guest on radio shows, and is frequently interviewed by a variety of periodicals, including the New York Times, Wall Street Journal, Prevention Magazine, and Healthy Living. ©2009 Natural Medicine Journal 1(2), October 2009 | Page 3
Page 1: Diagnosis and Possible Reversal of

Diagnosis and Possible Reversal of Pre-Diabetes: - Natural ...

Create successful ePaper yourself

Delete template?

Save as template?