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Unified Field Theory of Diseases of Civilization

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1 Unified Field Theory of Diseases of Civilization

2 Credentials Private Practice, Family Medicine and Bariatric Medicine in Northeast Kansas Medical Director, University of Kansas Weight Control Program (VLCD-very low calorie liquid diet) Consultant, Duke Diet and Fitness Center Consultant, Atkins Nutritionals, Inc. Consultant, Veronica Atkins Clinical Faculty, University of Kansas Medical School Diplomate of the American Society of Bariatric Physicians Past President, American Society of Bariatric Physicians Fellow, American Society of Bariatric Physician Co-author, lay press diet book Co-author, “Dietary Treatment of the Obese Individual” and “Medical Treatment of Pediatric Obesity” in Handbook of Obesity Treatment. Partner: Innovative Metabolic Solutions

3 Credentials Behavioral
40 + years training animals including cats, dogs, horses, and one chicken. I have participated in the training of 10 nationally ranked agility dogs including the #2 beagle (2 years) and #1 Norfolk Terrier (8 years) Currently employed by Joan Meyer (Triune Training) AKC World Agility Team member 2001, 2003, 2008. I specialize in behavior problems as well as the biomechanics of the working animal.

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5 Its not the weight, it’s the fuel source.
Metabolic Health Its not the weight, it’s the fuel source.

6 Metabolic Syndrome Vernon, M. Retrospective chart review
Outpatient clinical setting 124 patients-64 rx’d low CHO 57 rx’d low fat + anorectic Vernon, M. C., B. Kueser, et al. (2004). "Clinical Experience of a Carbohydrate-Restricted Diet for the Metabolic Syndrome." Metabolic Syndrome and Related Disorders 2(3):

7 Methods Outpatient clinical setting Low fat diet + phen/fen (n=64)
Carbohydrate restricted diet (n=57) Diet prescription was written. 20 grams carbohydrate/day until weight loss goal obtained or patient willing to slow weight loss. Both groups routinely monitored with office visits and blood work.

8 Parameters Followed Vital Signs; Blood Pressure, TPR, Weight.
Initially used caliper measurements of Body Fat (Phen-fen). Low CHO patients followed with bio- electric impedance body composition scale. Obtained CBC, fasting lipids, thyroid studies, chemistry panel, C-peptide and UA. Now also obtain hs-CRP, 24 hr urine for creatinine clearance and microalbumin followed on all diabetic patients. Labs repeated at ~3 mon. intervals until stable weight –then at least yearly.

9 Demographics LF Diet + Meds Carb Restriction mean (SD) mean (SD)
LF Diet + Meds Carb Restriction mean (SD) mean (SD) n Age, years (8.7) (12.7) Gender female % % Race Caucasian % % Height, inches (3.5) (3.7) Weight, kg (21.1) (28.8) Body mass index, kg/m (7.4) (11.1) Family history of obesity % % Hypertension therapy % % Diabetes mellitus therapy % % Lipid therapy % % Psychiatric medical therapy % % Thyroid therapy % %

10 Results Low-Fat Diet + Medication Carbohydrate Restricted Diet
Variable Baseline Follow-up Change Baseline Follow-up Change P value* Mean Body weight, kilograms** % % 0.005* Total cholesterol, mg/dl % % 0.39 Triglycerides, mg/dl % % 0.02* LDL-C, mg/dl % % 0.52 HDL-C, mg/dl % % 0.003* Total chol/HDL-C ratio % % 0.08 Trigycerides/HDL-C ratio % % 0.01* ** The mean follow-up was 20.2 wks for the LF Diet + Meds group and 15.0 wks for the Carb Restriction group Results

11 How did these options compare?
Weight loss almost as much with CHO restriction as our best medication effort using phen/fen. Lipid profile was markedly improved: 51% improvement in Trig/HDL ratio (an emerging marker of cardiovascular disease).1 1 Gaziano JM, Hennekens CH, O’Donnell CJ, Breslow JL, and Buring JE “Fasting Triglycerides, high- density lipoproteins and risk of myocardial infarction.” Circulation 96: (1996)

12 Very Low Carbohydrate Diet Phen/Fen and Low Calorie Diet
Rate of Loss Very Low Carbohydrate Diet Phen/Fen and Low Calorie Diet * p = 0.04 comparing change from Week 0 to Week 24 between groups

13 News Flash Not all weight loss is the same in terms of metabolic state. Metabolic outcomes are different based on the fuel source ( fat or carbohydrates)

14 What Can You Impact? Any condition related to hyperinsulinemia:
CAD, prediabetes, metabolic syndrome, Type 2 diabetes mellitus, hypertension, hyperlipidemia, dyslipidemia including high triglycerides and low HDL, proteinuria due to metabolic syndrome, obesity, acanthosis nigricans Central nervous system irritability such as seizures and migraines Ovarian dysfunction due to hyperinsulinemia manifested as polycystic ovary syndrome, irregular menses, anovulation, irregular ovulation, facial hirsuitism GERD Sleep apnea, Pickwician syndrome Gestational diabetes, pre-eclampsia Osteoarthritis Inflammation Some Psychiatric conditions

15 Diseases of Civilization
Elevated carbohydrate intake (different tolerance from one individual to another) causes chronically high levels of insulin and other inflammatory mediators. These are the drivers of the diseases of civilization-hypertension, metabolic syndrome, prediabetes, diabetes and excess fat mass gain.

16 Mitochondrial Energy Production
This is the key to life. No mitochondrial energy production=death No mechanic, no oil changes, only on-site repair and oxidation must continue at all times. That’s a challenge-and nutrition is the key.

17 Mitochondrial Fuel Source
Mitochondrial fuel source is linked to oxidative stress Oxidative stress is linked to tissue damage Mitochondrial enzymes adjust to fuel source Constant mitochondrial energy production without oxidative damage is the goal.

18 Is Adiposity the problem?
Sunburn is the best analogy Genetic predisposition and environmental exposure combine to cause damage. Adiposity is a marker for hyperinsulinemia. Excess adipose tissue is part of the pathologic process of insulin resistance and hyperinsulinemia

19 Two Approaches to Understanding Human Metabolism
Classic Hormonal All calories have equal value, regardless of source Importance of each macronutrient tied to caloric density Weight gain when energy intake exceeds energy expenditure Lose weight by reducing caloric intake and/or increasing caloric expenditure Increased carbohydrate intake increases insulin production and decreases lypolysis (fat-burning) Macronutrients control metabolic hormone production, which controls storage metabolism. High carbohydrate consumption leads to hyperinsulinemia, which leads to obesity and Metabolic Syndrome

20 Hormones Insulin Glucagon Incretins Epinephrine Norepinephrine
Cortisol Sex Steroids Branched chain amino acids IL-6 Dietary Carbohydrates

21 Visceral Adiposity Dr. Eric Freedland proposed the concept of the “critical visceral adipose threshold”-the amount of visceral fat storage that an individual could gain after which metabolic obesity ensued. This hypothesis, in conjunction with individual tissue levels of insulin resistance, may explain why one person is obese to the eye but has fewer metabolic abnormalities while an apparently thin individual is metabolically at risk. Freedland, E. S. (2004). "Role of a critical visceral adipose tissue threshold (CVATT) in metabolic syndrome: implications for controlling dietary carbohydrates: a review." Nutr Metab (Lond) 1(1): 12.

22 Physiology of Obesity Treatment
Obesity is excessive adipose tissue (fat) “Excess” is defined by metabolic and functional parameters The goal is to mobilize, or “burn fat” To accomplish this goal, a change from “glucose burning” to “fat burning” is needed Jeff/Steve-who wants this one?

23 Fat Metabolism and Insulin
The hormonal milieu needs to be appropriate for “fat burning” The effect of insulin to facilitate glucose uptake is linked to fat synthesis “Fat burning” is inhibited by insulin, so insulin levels need to be around basal levels Insulin levels can be lowered by: Increasing energy expenditure Reducing carbohydrate intake Jeff/Steve-who wants this one? Insulin levels need to remain around basal levels

24 Insulin Promotes Fat Synthesis Glucagon Promotes Fat Burning
Fatty acid synthase citrate TCA cycle Triglycerides Malonyl CoA ACCb CPT I mitochondria cytosol Intracellular and intravascular Jeff/Steve-this is my schema but I offer it for your perusal and correction-or substitute something else CPT I (Carnitine palmitoyltransferase I) moves long chain fatty acyl CoA groups into the mitochondria for oxidation. Inhibited by malonyl CoA. Glucose abundant-TCA producing citrate via acetyl CoA and oxaloacetate. Insulin increases availability of TCA intermediates via enzyme regulation Acetyl CoA carboxylase (ACCb ) is activated by citrate and insulin, inhibited by glucagon. Fatty acid synthase inhibited by glucagon

25 Fuel Sources: Fatty acids, ketones, glucose
Fatty acids can be utilized by most tissues for energy. Ketone bodies are generated by the liver from fatty acid oxidation. Ketones can be utilized by all cells except glucose obligate cells and liver. Glucose is synthesized by the liver and renal medulla from amino acid precursors (gluconeogenesis). Cells without mitochondria (erythrocytes, cornea, lens, retina) and cells in low oxygen tension conditions (renal medulla) are obligate glucose users.

26 Fatty Acids Fatty acids are the main cellular fuel for all non-obligate glucose using cells Preferred fuel of the myocyte A large pool of fatty acids are circulating on albumin at any given time There is nearly unlimited storage potential as triglyceride in adipose tissue

27 Ketone bodies Ketone bodies are molecules that deliver energy (acetoacetate, acetone, b-hydroxybutyrate) Ketone levels Fed state mmol/L Overnight fast mmol/L Nutritional ketosis mmol/L > 20 days fasting 10 mmol/L Diabetic ketoacidosis > 25 mmol/L Meckling et al. Can J Physiol Pharmacol 2002;80: Sharman et al. J Nutr 2002;132: Yancy et al. Eur J Clin Nutr 2007;February 17:1-7.

28 Glucose Can come from diet, but also from internal sources
Excess is stored as glycogen in limited amounts, or as triglyceride Protein (amino acids) used by liver and kidney to produce glucose (gluconeogenesis) and glycogen (glycogenesis) Under mixed diet conditions, CNS use of glucose can be as high as 120 grams/day However, daily glucose use is only about 30 grams/day when adapted to fat burning state (when fatty acids and ketones are available for muscle and CNS use) This 30 grams of glucose is easily supplied by endogenous sources

29 Caloric Content of Food
A Calorie (kcal) is the amount of heat required to raise the temperature of 1 kg of water by 1 degree Celsius Foods can be oxidized to release energy, and the estimated caloric values using bomb calorimetry are: Triglyceride: kcal per gm…… 9 kcal Protein: kcal per gm………… 4 kcal Carbohydrate: kcal per gm... 4 kcal Alcohol: 7 kcal per gram……………7 kcal Ketones: 4.5 cal per gram………….4 kcal The actual caloric value will depend upon what oxidation pathway is used, whether the energy has been stored, etc. Glycogen is stored with water 1:3, so 1 gram of glycogen leads to 4 gram of weight gain

30 Oh, Those Free Radicals The effect of burning glucose as fast as possible overwhelms the mitochondrial electron transport chain and generates increased numbers of free radicals. Free radicals cause tissue damage. Control glucose/insulin metabolism=control free radical formation=control tissue destruction. Salway JG, Metabolism at a Glance. Third edition. Blackwell Publishing Ltd, 2004. Veech, R. L., B. Chance, et al. (2001). "Ketone bodies, potential therapeutic uses." IUBMB Life 51(4):

31 Free Radical Management Plan
“Finally there are broad therapeutic implications from the ability of ketone body metabolism to oxidize the mitochondrial co-enzyme Q couple. The major source of mitochondrial free radical generation is Q semiquinone. The semiquinone of Q, the half-reduced form, spontaneously reacts with O2 to form free radicals. Oxidation of the Q couple reduces the amount of the semiquinone form and thus would be expected to decrease O2- production.” 1 Veech RL. The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. Prostaglandins Leukotrienes Essential Fatty Acids 2004;70:

32 Mitochondrial Ketone Metabolism Vacuums Free Radicals
In addition, the metabolism of ketones causes a reduction of the cytosolic free {NAD+}/{NADH} couple which is in near equilibrium with the glutathione couple. Reduced glutathione is the final reductant responsible for the destruction of H2O2. Veech RL. The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. Prostaglandins Leukotrienes Essential Fatty Acids 2004;70:

33 Ketones Improve Myocardial Function
“How ketone bodies could improve the hydraulic efficiency of heart by 28% could not be explained by the changes in the glycolytic pathway alone, but rather by the changes that were induced in mitochondrial ATP production by ketone body metabolism.” Veech RL. The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. Prostaglandins Leukotrienes Essential Fatty Acids 2004;70:

34 Ketotic Benefits Chronic adaptation to fat as primary energy source may offer benefits such as improved cerebral function (treatment of seizures), improved mitochondrial ATP production, decreased oxidative stress and protection of glycogen stores during exercise. Kossoff, E. H. (2004). "More fat and fewer seizures: dietary therapies for epilepsy." Lancet Neurol 3(7): Phinney, S. D., B. R. Bistrian, et al. (1983). "The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation." Metabolism 32(8):

35 Dietary CHO =Insulin Secretagogue
Boden, G., K. Sargrad, et al. (2005). "Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes." Ann Intern Med 142(6):

36 Carbohydrate Signal Effects on Metabolic Hormones
Ludwig, D. S., J. A. Majzoub, et al. (1999). "High glycemic index foods, overeating, and obesity." Pediatrics 103(3): E26.

37 Eat or Die Ludwig, D. S., J. A. Majzoub, et al. (1999). "High glycemic index foods, overeating, and obesity." Pediatrics 103(3): E26.

38 Lack of Postprandial Rise in Serum Glucose and Insulin After a Low Carbohydrate Meal
Glucose and insulin concentrations in response to a 300 kcal meal with low- (closed circles), intermediate- (open circles), and high-carbohydrate (triangles) content after 10 d on these respective diets (n=6). Data are means (SE). Areas under the curve for insulin was different for each diet (P 0.001). Glucose area under the curve was lower in response to the low-carbohydrate diet (P vs. other diets). Bisschop et al. J Clin Endocrinol Metab;2003:88:3801–3805.

39 Eating Fat Equals Fasting
The importance of either carbohydrate or energy restriction in initiating the metabolic response to fasting was studied in five normal volunteers. The subjects participated in two study protocols in a randomized crossover fashion. In one study the subjects fasted for 84 h (control study), and in the other a lipid emulsion was infused daily to meet resting energy requirements during the 84-h oral fast (lipid study). Glycerol and palmitic acid rates of appearance in plasma were determined by infusing [2H5]glycerol and [1-13C]palmitic acid, respectively, after 12 and 84 h of oral fasting. Changes in plasma glucose, free fatty acids, ketone bodies, insulin, and epinephrine concentrations during fasting were the same in both the control and lipid studies. Glycerol and palmitic acid rates of appearance increased by / and / mumol.kg-1.min-1, respectively, during fasting in the control study and by / and / mumol.kg-1.min-1, respectively, in the lipid study. These results demonstrate that restriction of dietary carbohydrate, not the general absence of energy intake itself, is responsible for initiating the metabolic response to short-term fasting. Klein, S. and R. R. Wolfe (1992). "Carbohydrate restriction regulates the adaptive response to fasting." Am J Physiol 262(5 Pt 1): E631-6.

40 The New Paradigm Food can exert hormonal type influence on metabolic pathways Fat is not the problem The changes caused by excess dietary carbohydrate intake result in a shift in metabolic pathways (characterized by elevated insulin levels) which increase inflammation and tissue damage.

41 Hyperinsulinemia and Reactive Hypoglycemia
Time Glucose (mg/dl) Insulin (uIU) fasting 115 19 1 hr 2 hr 3 hr 261 212 41 72 119 34 50 yo red headed female Weight=191.3 lbs Hgt=63 inches BMI=33.9

42 DM with elevated Insulin
54 yo wf lb. 5’6” tall. BMI=43.4 Multiple complaints: gluten enteropathy, vegetarian, joint aches Meds: Synthroid 62.5 mcg/day, Accupril 40 mg po daily, HCTZ 25 mg po daily Referred by Dr. Phinney, Dr. Westman, and Dr. Kolotkin

43 Type 2 DM with elevated insulin levels
Time Glucose (mg/dl) Insulin (uIU) fasting 123 81 1 hr 2 hr 3 hr 273 200 119 632 777 259 54 yo Caucasian female Weight=269 lbs Hgt=66 inches BMI=43.4 Stage 5 (DM) with reactive hypoglycemia and hyperinsulinemia.

44 Type 2 DM with Elevated Insulin levels Treatment Outcomes
Test Wgt (lbs) Gluc % change Weight (lbs) Glucose (mg/dl) HgbA1C (%) Cpeptide T. Chol (mg/dl) Triglyceride(mg/dl) HDL (mg/dl) LDL (mg/dl) T.chol/HDL Trig/HDL 269 123 6.0 (<5.7) 8.9 (<4.5) 157(<200) 222 (<150) 36 (>50) 76.6 (<100) 4.36 6.16 245 99 5.1 4.3 146 72 37 95 3.95 1.9 -9 -20 -15 -52 -7 -68 +2 +24 -69

45 Type 2 DM 3 hr GTT with Insulin Levels
Time Glucose (mg/dl) Insulin (uIU) fasting 131 14.9 1 hr 2 hr 3 hr 278 246 158 50.9 40.3 27 56 yo Caucasian female Weight=276 lbs Hgt= 62 inches BMI= 50.1 Stage 5 moving to Stage 6 Insulin levels don’t adequately suppress serum glucose response to dietary carbohydrate. Insulin resistance present. Reactive hypoglycemia present

46 Type 2 DM with Low Insulin levels Treatment Outcomes
Test Baseline 3 months % change Weight (lbs) Glucose (mg/dl) HgbA1C (%) T. Chol (mg/dl) Triglyceride(mg/dl) HDL (mg/dl) LDL (mg/dl) T.chol/HDL Trig/HDL 276 109 7.1 (<5.7) 249 (<200) 125 (<150) 64 (>50) 160 (<100) 3.89 1.95 226 90 5.4 99 54 152 4.1 1.83 -18 -17 -24 -9 -21 -15 +5 -6

47 Remission of Type II Diabetes
A 45 year old white female with Type II diabetes mellitus, obesity (BMI = 60.5), HTN on pioglitizone, glipizide, and metformin, lisinopril, sertraline, oral contraceptives, itraconazole, rofecoxib. Date Wt (lbs) Chol Trig LDL HDL HgbA1C Trig/HDL BMI 7/ 7/00 Initiation of Carbohydrate Restricted Diet 9/ 1/ 12/ All hypoglycemic meds dc’d 7/00. Off all meds except setraline by 9/01

48 Not Just For Weight Individuals with normal BMI may exhibit the metabolic characteristics of obesity. This is not treatment of adiposity- it is metabolic management of metabolic risk through dietary treatment/lifestyle change. This works whether or not excess fat mass is present.

49 Metabolic Fitness Improvement in Metabolic Fitness Without Weight Change A 48 year old WF requested dietary treatment for abnormal lipids. Date Chol Trig HDL T/HDL Weight (lbs) % B F HgbA1c 9/ 3/ 3/01 Initiation of Carbohydrate Restricted Diet 11/ 7/ 8/

50 What about other lipid problems?
Decrease in Lp(a) Without Weight Loss A 28 year old white female with strong FH of premature CAD. Acne rosacea and hypertrophic skin over elbows. (BMI=17.5) Date Lp(a) Chol Trig LDL HDL Wt (lbs) 3/ 3/ 2/ 7/01 Initiation of Carbohydrate Restricted Diet 104 11/ 2/ (normal Lp(a) < 32)

51 Current Testing Misses the Problem
Insulin resistance, hyperglycemia, hyperinsulinemia, hyperlipidemia and oxidative stress are risk factors related to cardiovascular diseases including congestive heart failure, myocardial infarction, ventricular hypertrophy, endothelial nitric oxide impairment in systemic blood vessels and the heart, atherosclerosis, and hypercoagulability of blood. The traditional focus on insulin sensitivity and blood levels of markers of risk determined in the fasted state is inconsistent with the large volume of recent data that indicates that the metabolic defect in the pre-diabetic and diabetic condition relates more strongly to postprandial deficiency than to the fasting state. Risk factors for adverse cardiovascular events can be detected in the pre-diabetic insulin-resistant subject based upon the metabolic response to a test meal even in the absence of altered fasting parameters. Haffner, S. M., M. P. Stern, et al. (1990). "Cardiovascular risk factors in confirmed prediabetic individuals. Does the clock for coronary heart disease start ticking before the onset of clinical diabetes?" Jama 263(21):

52 Patients who fall outside of the existing paradigm
Metabolically obese normal weight patients share the CV risk factors of their obese neighbors, without the external marker of obesity to alert their physicians that preventative treatment is needed.

53 Looking for the Wrong Factors?
12% of patients with MI did not have traditional risk factors. Body, R., G. McDowell, et al. (2008). "Do risk factors for chronic coronary heart disease help diagnose acute myocardial infarction in the Emergency Department?" Resuscitation 79(1): 41-5.

54 Risk is related to metabolic state
When subjects with impaired glucose tolerance at baseline (n = 106) were eliminated, the more atherogenic pattern of cardiovascular risk factors was still evident (and statistically significant) among initially normoglycemic prediabetic subjects. These results indicate that prediabetic subjects have an atherogenic pattern of risk factors (possibly caused by obesity, hyperglycemia, and especially hyperinsulinemia), which may be present for many years and may contribute to the risk of macrovascular disease as much as the duration of clinical diabetes itself. Lautt, W. W. (2007). "Postprandial insulin resistance as an early predictor of cardiovascular risk." Ther Clin Risk Manag 3(5):

55 Roche Biomedical Pathways
Acetyl CoA TCA Cycle Ketone Bodies Insulin & HMGCoA Reductase Direction of Cholesterol Synthesis Roche Biomedical Pathways

56 Hyperinsulinemia in MONW
Time Glucose (mg/dl) Insulin (uIU) fasting 94 2.2 1 hr 2 hr 3 hr 93 86 31 76 89 15 46 year old Caucasian female Weight=118 lbs BMI=18 Her orthopedist told her she needed testing for diabetes. Her father has Type 2 DM. Hyperinsulinemia Reactive hypoglycemia

57 MONW # 2 Date Gluc Chol Trig LDL HDL Wt (lbs) urine alb
1/ 4/ 2/ hr glucose tolerance 140. 37 week gestation 7# 14 oz infant male 3/ 10/ mg 2/ mg 8/ Pat A 5/ 11/ mg

58 MONW 44 yo Caucasian male-construction type work
Presented with Ca oxalate kidney stones. 194# 5’11” BMI 27.1 13% BF

59 Low Carbohydrate Diet Program and Diabetes Mellitus
Before Diet After Low Carbohydrate Pgm Age Sex Duration Weight A1C Trig HDL Weight A1C Trig HDL (lb) (lb) M 2 mos F 3 mos F 3 mos 44 M 4 mos F 5 mos 33 M 15 mos 50 M 26 mos 36 F mos

60 Effect of Carbohydrate Restriction on Weight, Glycemic Control and Fasting Lipid Profiles in Type 2 Diabetes Mellitus (n=13) Variable Baseline Follow-up Change P value* Mean Body weight, kilograms % 0.003 Hemoglobin A1C, % % <0.001 Total cholesterol, mg/dl % 0.03 Triglycerides, mg/dl % 0.003 LDL-C, mg/dl % 0.94 HDL-C, mg/dl % 0.07 Total chol/HDL-C ratio % 0.01 Trigycerides/HDL-C ratio % 0.004 *Signed rank test comparing baseline to follow-up value. P<0.05 was used for statistical significance. Vernon MC et al. Metabolic Syndrome and Related Disorders 2003;1:

61 Low Carbohydrate Diet Program in Type 2 Diabetes Mellitus: Microalbuminuria
Before Diet After Low Carbohydrate Pgm Age Sex Duration Weight A1C Trig UAlb Weight A1C Trig UAlb (lb) (lb) 50 M 26 mos 59 M 53 mos 49 F 12 mos 58 F mos 49 M mon

62 Renal Failure Carbohydrate restricted, low available iron, polyphenol enriched diet (CR-LIPE) 191 Type 2 DM patients Randomized to CR-LIPE or standard protein restriction Mean follow up interval 3.9 years (+/- 1.8 years) Serum creatinine doubled in CR-LIPE (19 pts/21%) and in 31 controls (31%). Renal replacement or death=18 pts on CR-LIPE (20%) and 31 controls (39%) Facchini, F. S. and K. L. Saylor (2003). "A low-iron-available, polyphenol-enriched, carbohydrate-restricted diet to slow progression of diabetic nephropathy." Diabetes 52(5):

63 Renal Failure “ In conclusion, CR-LIPE was 40-50% more effective than standard protein restriction in improving renal and overall survival rates.” Facchini, F. S. and K. L. Saylor (2003). "A low-iron-available, polyphenol-enriched, carbohydrate-restricted diet to slow progression of diabetic nephropathy." Diabetes 52(5):

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65 Remove The Emotional “Hit”
We have told patients with Metabolic Syndrome to eat a diet that increased their tendency to store and which triggered rebound and stress hormones. We have accused them of non-compliance when the outcome was due to our recommedation. Societal message is that to need to eat is to be weak. We have contributed to “learned helplessness”.

66 JUST STOP No guilt for provider. No guilt for patient.
Honor your body-eat to prevent hunger and stress chemistry. Exercise to enhance metabolic and body chemistry function. Empower control.

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68 Long Term Data Medical monitoring was provided to taper diabetic and anti-hypertensive medication Inclusion criteria: baseline and greater than 12 months weight and laboratory studies 106 patients identified Mean duration of treatment and follow up was 765 days (365 days to 3777 days ) For the 17 Type 2 diabetics with initial HgbA1C greater than 6.5 mg%, the mean HgbA1c improved from 9.2% to 5.8% (p=0.001) Long-term Effects of Carbohydrate-restriction on Obesity in Clinical Practice Mary Vernon, Eric Westman The Obesity Society 10/2008.

69 Long Term Data 365-3777 days of follow up in outpatient clinical practice

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71 Remove The Emotional “Hit”
We have told patients with Metabolic Syndrome to eat a diet that increased their tendency to store and which triggered rebound and stress hormones. We have accused them of non-compliance when the outcome was due to our recommedation. Societal message is that to need to eat is to be weak. We have contributed to “learned helplessness”.

72 JUST STOP No guilt for provider. No guilt for patient.
Honor your body-eat to prevent hunger and stress chemistry. Exercise to enhance metabolic and body chemistry function. Empower control.

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77 More Information? info@myimsonline.com Amber Wiley VP Public Relations
ext:503


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