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AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS fundamental clinical imbalance are essential to address the modern plague of diabesity. The causes of diabesity are not the same for every person. For some, diabesity may be simply a result of poor diet. For others, it may be due to environmental toxins, chronic inflammation, digestive imbalances, chronic stress, or even food sensitivities. This is why we must take a comprehensive approach to understanding, diagnosing, and treating these fundamental clinical imbalances that drive diabetes, insulin resistance, and most chronic diseases. Functional Medicine Approach to Diabesity: Case Studies Obesity (diabesity) is a complex, multi-factorial, multi-gene disorder with dynamic web-like physiological imbalances affecting gene expression and phenotype. A systemic approach directed at removing the impediments to optimal function (diet, toxins, allergens, infections, stress) and providing the ‚ingredients‛ for optimal health (whole foods, micronutrients, light, air, water, movement, rhythm, sleep, connection, community, meaning and purpose) based on the model of Functional medicine xcviii provides a roadmap for diagnosis and treatment of the underlying clinical imbalances at the root of obesity and chronic disease. The functional clinical imbalances are influenced by the environment including diet and nutritional status on core functional systems - hormonal/metabolic, immune/inflammatory, digestive, detoxification, mitochondrial energetics and redox status, structural and psycho-spiritual. These diagnostic and treatment principles are illustrated in the following cases. Case 1: Inflammation, Obesity and Diabetes S.R. is a 67-year-old woman with a 10-year history of type 2 diabetes. Her weight was 233 pounds with a BMI of 36 and waist to hip ratio 0.91. Her past medical history was significant for hypertension, angina, reflux, rheumatoid arthritis and lupus, hypothyroidism, chronic allergies and sinusitis, and depression. Her medications included metformin, benazepril, fluoxetine, pravastatin, bio-identical hormone replacement, 50 cetrizine, lansoprazole, levothyroxine, naproxen, a multivitamin glucosamine, and calcium with D. She is a widow who lives alone and is estranged from her family. She is a recovering alcoholic with a history of childhood sexual abuse. Her diet consisted predominately of refined carbohydrates including bread, pasta, muffins and ice cream. She does no exercise. Her medical symptom questionnaire (MSQ) was 86. Functional diagnostic assessment revealed hyperinsulinemia of 23 (nl < 5), glucose of 140 mg/dl and HbA1c of 6.8. Her high sensitivity C-reactive protein was elevated at 10.6 (nl < 1) and her sedimentation rate was 20. Her antinuclear antibodies were 1:80 speckled pattern. On a statin her total cholesterol was 198 mg/dl, LDL-C 119 mg/dl, HDL-C 54 mg/dl and triglycerides 199 mg/dl. She had a fatty liver with an elevated gamma glutamyl transferase (GGT) of 40. Organic acid analysis revealed impaired fatty acid and carbohydrate metabolism, and mitochondrial dysfunction as well as impaired detoxification and dysbiosis with small intestinal bacterial overgrowth (SIBO). Treatment consisted of low glycemic load, high fiber, phytonutrient rich, allergen elimination (gluten and diary), whole foods plant based diet and moderate exercise of 30 minutes of walking daily. Digestive imbalances were treated by stopping NSAID, proton pump inhibitor, herbal antimicrobials, probiotics, glutamine and an antiinflammatory rice based medical food for treating dysbiosis. Oral estrogen was changed to vaginal to reduce fat deposition and inflammation. Antidepressant was changed from fluoxetine to buproprion to improve appetite control. In addition to her multivitamin, she was treated with coenzyme Q10 and alpha lipoic acid (antioxidants and mitochondrial co-factors) as well as Bcomplex and milk thistle for fatty liver and enhanced detoxification. After 2 years of treatment, she lost 45 pounds. Her medical symptoms score (MSQ) reduced from 86 to 6. Her C-reactive protein reduced from 10.6 to 2.8, total cholesterol from 198 to 171, triglycerides from 199 to 88, and HDL-C increased from 57 to 65. Her insulin reduced from 23 to 11, fasting glucose from 140 to 103 and hemoglobin A1c from 6.8 to 5.7 and GGT from 40 to 17. 2012
AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS Organic acids showed normalization of fat and carbohydrate metabolism and citric acid cycle normalized as did the markers of impaired detoxification and dysbiosis. Case 2: Treatment Resistant Obesity and Diabetes J.L was a 59-year-old African American female college dean with obesity and diabetes. She had a history of hypertension, obstructive sleep apnea, and hyperlipidemia. She presented with severe fatigue unable to drive, watch television, exercise or cook for herself. Her BMI was 35 at 190 pounds. Despite maximal intensive medical therapy, she remained hypertensive with a blood pressure of 160/104 and was about to start insulin therapy and retire because she could no longer fulfill her work obligations. Her hemoglobin A1c was 10.1. She was on atorvostatin, metformin, glyberide metopropol, aspirin, lotrel (amlodipine and benazepril) and a multivitamin. She was single, a non-smoker, exercised irregularly and ate prepared and microwavable foods and sweets at night. Her laboratory evaluation revealed urine 3+ glucose, fasting glucose 312, hemoglobin A1c 10.1. Her 25 OH vitamin D was 17 ng/ml (normal 45-100). She had elevated liver function tests with an ALT of 56. Urine microalbumin was negative. On a statin, her total cholesterol was 186 mg/dl, HDL 54 mg/dl, LDL 122 mg/dl, TG 101 mg/dl. However, on nuclear magnetic resonance spectroscopy, she had predominately small LDL (1320/1608) and HDL particles. Her cardio C-reactive protein was 0.7, homocysteine 6.4, fibrinogen 311, and her Lp(a) was elevated at 423 (normal < 30). She had elevated lipid peroxides of 2.2 nmol/mL (nl
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