Presentation by Dr. Mary Vernon at KU Medical Center

7/23/2019 Presentation by Dr. Mary Vernon at KU Medical Center

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Unified Field Theory of Diseases of

Civilization


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Credentials

Private Practice, Family Medicine and Bariatric Medicine in Northeast Kansas

Medical Director, University of Kansas Weight Control Program (VLCD-very lowcalorie 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 bookCo-author, Dietary Treatment of the Obese Individual and Medical Treatment

of Pediatric Obesity in Handbook of Obesity Treatment.

Partner: Innovative Metabolic Solutions


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CredentialsBehavioral

40 + years training animals including cats, dogs, horses, andone chicken.

I have participated in the training of 10 nationally rankedagility dogs including the #2 beagle (2 years) and #1Norfolk Terrier (8 years)

Currently employed by Joan Meyer (Triune Training) AKCWorld Agility Team member 2001, 2003, 2008.

I specialize in behavior problems as well as the biomechanicsof the working animal.


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Metabolic HealthIts not the weight, its the fuel source.


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Metabolic Syndrome Vernon, M.

Retrospective chart review Outpatient clinical setting

124 patients-64 rxd low CHO

57 rxd 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): 180-186.


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MethodsOutpatient clinical settingLow fat diet + phen/fen (n=64)

Carbohydrate restricted diet (n=57)Diet prescription was written.

20 grams carbohydrate/day until weight loss goalobtained or patient willing to slow weight loss.

Both groups routinely monitored with officevisits and blood work.


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Parameters FollowedVital 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 creatinineclearance and microalbumin followed on alldiabetic patients. Labs repeated at ~3 mon.intervals until stable weight then at least yearly.


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LF Diet + Meds Carb Restriction

mean (SD) mean (SD)

n 56 66

Age, years 41.3 (8.7) 47.9 (12.7)

Gender female 80.4% 71.2%

Race Caucasian 94.6% 92.3%Height, inches 66.2 (3.5) 65.9 (3.7)

Weight, kg 94.0 (21.1) 97.7 (28.8)

Body mass index, kg/m2 38.3 (7.4) 38.7 (11.1)

Family history of obesity 82.1% 65.2%

Hypertension therapy 21.4% 33.3%

Diabetes mellitus therapy 8.9% 22.7%

Lipid therapy 16.2% 27.6%

Psychiatric medical therapy 21.4% 21.2%

Thyroid therapy 19.6% 6.1%

Demographics


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Low-Fat Diet + Medication Carbohydrate Restricted Diet

Variable Baseline Follow-upChange Baseline Follow-up Change P value*

Mean

Body weight, kilograms** 108.7 94.9 -12.7% 108.2 98.7 -8.8% 0.005*

Total cholesterol, mg/dl 219.9 194.8 -11.4% 213.9 203.1 -5.0% 0.39

Triglycerides, mg/dl 210.5 151.8 -27.9% 203.8 115.5 -43.3% 0.02*

LDL-C, mg/dl 134.9 121.2 -10.2% 123.0 128.0 +4.1% 0.52

HDL-C, mg/dl 40.2 40.8 +1.5% 44.7 48.9 +9.4% 0.003*

Total chol/HDL-C ratio 5.8 5.1 -12.1% 5.3 4.6 -13.2% 0.08

Trigycerides/HDL-C ratio 5.8 4.3 -25.9% 5.7 2.8 -50.9% 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


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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, ODonnell CJ, Breslow JL, and Buring JE Fasting Triglycerides, high-density lipoproteins and risk of myocardial infarction. Circulation 96: 2520-2525 (1996)


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Rate of Loss

170

180

190

200

210

220

230

240

250

Wk 0 Wk 4 Wk 8 Wk 12 Wk 16 Wk 20 Wk 24

Duration of Intervention

BodyWeight,lb

s(s

* p = 0.04comparingchange from Week 0 to Week 24 between groups

VeryLow Carbohydrate Diet

Phen/Fen andLow Calorie Diet


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News FlashNot all weight loss is the same in terms of

metabolic state.

Metabolic outcomes are different based on the

fuel source ( fat or carbohydrates)


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What Can You Impact?

Any condition related to hyperinsulinemia: CAD, prediabetes, metabolic syndrome, Type 2 diabetes

mellitus, hypertension, hyperlipidemia, dyslipidemiaincluding high triglycerides and low HDL, proteinuria dueto metabolic syndrome, obesity, acanthosis nigricans

Central nervous system irritability such as seizures andmigraines

Ovarian dysfunction due to hyperinsulinemia manifestedas polycystic ovary syndrome, irregular menses,anovulation, irregular ovulation, facial hirsuitism

GERD Sleep apnea, Pickwician syndrome

Gestational diabetes, pre-eclampsia

Osteoarthritis

Inflammation

Some Psychiatric conditions


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Diseases of CivilizationElevated 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, metabolicsyndrome, prediabetes, diabetes and excess

fat mass gain.


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Mitochondrial Energy ProductionThis 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.

Thats a challenge-and nutrition is the key.


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Mitochondrial Fuel SourceMitochondrial 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.


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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


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Two Approaches to Understanding

Human Metabolism

All calories have equal value,

regardless of source

Importance of eachmacronutrient tied to caloric

density

Weight gain when energy intake

exceeds energy expenditure

Lose weight by reducing caloricintake 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, whichleads to obesity and Metabolic

Syndrome

Classic Hormonal


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HormonesInsulinGlucagon

Incretins

Epinephrine

Norepinephrine

Cortisol

Sex SteroidsBranched chain amino acids

IL-6

Dietary Carbohydrates


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Visceral Adiposity

Freedland, E. S. (2004). "Role of a critical visceral adipose tissue threshold(CVATT) in metabolic syndrome: implications for controlling dietarycarbohydrates: a review." Nutr Metab (Lond) 1(1): 12.

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.


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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


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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


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Insulin Promotes Fat Synthesis

Glucagon Promotes Fat Burning

TCA cycle

mitochondria

Glucose abundant-TCA

producing citrate via

acetyl CoA and

oxaloacetate. Insulin

increases availability of

TCA intermediates via

enzyme regulation

Malonyl CoA

citrate

CPT I

CPT I (Carnitinepalmitoyltransferase I)

moves long chain fatty acyl

CoA groups into the

mitochondria for oxidation.

Inhibited by malonyl CoA.

Acetyl CoA carboxylase

(ACCb ) is activated by

citrate and insulin, inhibited

by glucagon.

Fatty acid synthase inhibited

by glucagon

ACCb

Triglycerides

cytosol

Fatty acid

synthase

Intracellular and

intravascular


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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 acidoxidation. Ketones can be utilized by all cells exceptglucose obligate cells and liver.

Glucose is synthesized by the liver and renal medulla from

amino acid precursors (gluconeogenesis). Cells withoutmitochondria (erythrocytes, cornea, lens, retina) and cellsin low oxygen tension conditions (renal medulla) areobligate glucose users.


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Fatty Acids

Fatty acids are the main cellular fuel for all non-obligate

glucose using cells

Preferred fuel of the myocyteA large pool of fatty acids are circulating on albumin at

any given time

There is nearly unlimited storage potential as

triglyceride in adipose tissue


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Ketone bodies

Ketone bodies are molecules that deliver energy

(acetoacetate, acetone, F-hydroxybutyrate)

Ketone levels

Fed state 0.1 mmol/L

Overnight fast 0.3 mmol/L

Nutritional ketosis 1 - 2 mmol/L

> 20 days fasting 10 mmol/LDiabetic ketoacidosis > 25 mmol/L

Meckling et al. Can J Physiol Pharmacol 2002;80:1095-1105.

Sharman et al. J Nutr 2002;132:1879-1885.

Yancy et al. Eur J Clin Nutr 2007;February 17:1-7.


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GlucoseCan come from diet, but also from internal sources

Excess is stored as glycogen in limited amounts, or astriglyceride

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 whenadapted to fat burning state (when fatty acids and ketones areavailable for muscle and CNS use)

This 30 grams of glucose is easily supplied by endogenoussources


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Caloric Content of FoodA 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 caloricvalues using bomb calorimetry are:

Triglyceride: 9.461 kcal per gm 9 kcal

Protein: 4.442 kcal per gm 4 kcal

Carbohydrate: 4.183 kcal per gm... 4 kcal

Alcohol: 7 kcal per gram7 kcal

Ketones: 4.5 cal per gram.4 kcal

The actual caloric value will depend upon what oxidation pathway isused, whether the energy has been stored, etc.

Glycogen is stored with water 1:3, so 1 gram of glycogen leads to 4


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Oh, Those Free Radicals The effect of burning glucose as fast asThe effect of burning glucose as fast as

possible overwhelms the mitochondrialpossible overwhelms the mitochondrial

electron transport chain and generateselectron transport chain and generatesincreased numbers of free radicals.increased numbers of free radicals.

Free radicals cause tissue damage.Free radicals cause tissue damage.

Control glucose/insulin metabolism=controlControl glucose/insulin metabolism=controlfree radical formation=control tissuefree radical formation=control tissuedestruction.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): 241-7.


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Free Radical Management Plan

Finally there are broad therapeutic implications fromthe ability of ketone body metabolism to oxidize themitochondrial co-enzyme Q couple. The major source

of mitochondrial free radical generation is Qsemiquinone. The semiquinone of Q, the half-reducedform, spontaneously reacts with O2 to form freeradicals. Oxidation of the Q couple reduces theamount 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;70:309-19.


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Mitochondrial Ketone Metabolism

Vacuums Free RadicalsIn addition, the metabolism of ketones causes a reduction of the

cytosolic free {NAD+}/{NADH} couple which is in nearequilibrium with the glutathione couple. Reduced glutathioneis the final reductant responsible for the destruction of H

2O

2.

Veech RL. The therapeutic implications of ketone bodies: the effects of ketone bodiesin pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance,and mitochondrial metabolism. Prostaglandins Leukotrienes Essential Fatty Acids2004;70:309-19.


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Ketones Improve Myocardial

FunctionHow 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 ofketone bodies in pathological conditions: ketosis, ketogenic diet, redoxstates, insulin resistance, and mitochondrial metabolism.Prostaglandins Leukotrienes Essential Fatty Acids 2004;70:309-19.


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Ketotic BenefitsChronic 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): 415-20.

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): 769-76.


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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): 403-11.


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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.


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Eat or Die

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


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Glucose and insulin concentrations in response to a 300 kcal meal with low-

(closedcircles), 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 (P0.001). Glucose area under the curve was lower in response to the

low-carbohydrate diet (P 0.001 vs. other diets).

Bisschop et al. J Clin Endocrinol Metab;2003:88:38013805.

Lack ofPostprandial Rise in Serum Glucose

and Insulin After a Low Carbohydrate Meal


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Eating Fat Equals FastingThe importance of either carbohydrate or energy restriction in initiating the

metabolic response to fasting was studied in five normal volunteers. Thesubjects 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 alipid emulsion was infused daily to meet resting energy requirements duringthe 84-h oral fast (lipid study). Glycerol and palmitic acid rates of appearancein plasma were determined by infusing [2H5]glycerol and [1-13C]palmiticacid, respectively, after 12 and 84 h of oral fasting. Changes in plasmaglucose, free fatty acids, ketone bodies, insulin, and epinephrineconcentrations during fasting were the same in both the control and lipidstudies. Glycerol and palmitic acid rates of appearance increased by 1.63 +/-0.42 and 1.41 +/- 0.46 mumol.kg-1.min-1, respectively, during fasting in the

control study and by 1.35 +/- 0.41 and 1.43 +/- 0.44 mumol.kg-1.min-1,respectively, in the lipid study. These results demonstrate that restriction ofdietary carbohydrate, not the general absence of energy intake itself, isresponsible 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.


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The New ParadigmFood can exert hormonal type influence on

metabolic pathways

Fat is not the problemThe changes caused by excess dietary

carbohydrate intake result in a shift in

metabolic pathways (characterized byelevated insulin levels) which increaseinflammation and tissue damage.


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Hyperinsulinemia and Reactive

HypoglycemiaTime 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


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DM with elevated Insulin54 yo wf . 269 lb. 56 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


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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=43.4Stage 5 (DM) with

reactive hypoglycemia

and hyperinsulinemia.


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Type 2 DM with Elevated Insulin levels

Treatment OutcomesTest 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 (


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Type 2 DM 3 hr GTT with Insulin

LevelsTime 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= 50.1Stage 5 moving to Stage 6

Insulin levels dont adequately

suppress serum glucose response

to dietary carbohydrate. Insulin

resistance present.

Reactive hypoglycemia present


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Type 2 DM with Low Insulin levels

Treatment OutcomesTest 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 (


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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 TrigLDL HDL HgbA1C Trig/HDL BMI

7/00 375 257 252 118 50 11.0 5 60.5

7/00 I nitiation of Carbohydrate Restricted Diet

9/00 350 153 193 69 45 7.7 3

1/01 317 165 153 84 50 6.4 1.8

12/01 243 198 131 116 56 5.4 2 39.2

All hypoglycemicmeds dcd7/00. Off all meds except setraline by 9/01


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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 massis present.


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Metabolic Fitness

Improvement in Metabolic Fitness Without WeightChange

A 48 year old WF requested dietary treatment for abnormal lipids.

Date Chol Trig HDL T/HDL Weight (lbs) % B F HgbA1c

9/99 256 2208 20 110 158

3/01 214 2407 ---- 158 36 5.8

3/01 Initiation of Carbohydrate Restricted Diet

11/01 162 147 31 4.7 157 29 6.07/02 145 127 37 3.4 153.5 31 ---

8/03 149 84 39 3.8 147 27.5 5.1


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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)

3/97 215 87 171 27 98

3/00 64 214 113 154 37 109

2/01 52 243 95 197 27 112

7/01 Initiation of Carbohydrate Restricted Diet 104

11/01 44 211 66 153 45 101

2/02 36 176 52 113 52 110

(normal Lp(a) < 32)


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Current Testing Misses the Problem

Insulin resistance, hyperglycemia, hyperinsulinemia, hyperlipidemiaand oxidative stress are risk factors related to cardiovascular diseasesincluding congestive heart failure, myocardial infarction, ventricularhypertrophy, 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 markersof risk determined in the fasted state is inconsistent with the largevolume of recent data that indicates that the metabolic defect in thepre-diabetic and diabetic condition relates more strongly topostprandial deficiency than to the fasting state. Risk factors foradverse cardiovascular events can be detected in the pre-diabetic

insulin-resistant subject based upon the metabolic response to a testmeal 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): 2893-8.


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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.


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Looking for the Wrong Factors?

12% of patients with MI did not havetraditional 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.


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Risk is related to metabolic state

When subjects with impaired glucose tolerance at baseline (n= 106) were eliminated, the more atherogenic pattern ofcardiovascular risk factors was still evident (and

statistically significant) among initially normoglycemicprediabetic subjects. These results indicate thatprediabetic subjects have an atherogenic pattern of riskfactors (possibly caused by obesity, hyperglycemia, andespecially hyperinsulinemia), which may be present for

many years and may contribute to the risk ofmacrovascular disease as much as the duration ofclinical diabetes itself.

Lautt, W. W. (2007). "Postprandial insulin resistance as an early predictor of

cardiovascular risk." Ther Clin Risk Manag 3(5): 761-70.


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Roche Biomedical

Pathways

Insulin &

HMGCoA

Reductase

Direction of

Cholesterol Synthesis

www.expasy.ch/cgi.bin/search-biochem-

index

Acetyl CoA

TCA Cycle

Ketone Bodies


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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


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MONW # 2

Date Gluc Chol TrigLDL HDL Wt (lbs) urine alb

1/96 74 177 120 101 52 107

4/00 72 191 44 110 72 113

2/02 87 2hr glucose tolerance 140.

37 week gestation 7# 14 oz infant male

3/03 70 171 92 92 60 104

10/05 110.4 35.2 mg

2/06 77 177 54 86 80 103 23 mg

8/06 69 162 65 71 78 97 Pat A

5/07 82 194 74 97 82 101

11/08 74 159 61 73 74 109 10 mg


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MONW

44 yo Caucasian male-construction type

work

Presented with Ca oxalate kidney stones.

194#

511

BMI 27.1

13% BF


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Low Carbohydrate Diet Program and

Diabetes MellitusBefore Diet After Low Carbohydrate Pgm

Age Sex Duration Weight A1C Trig HDL Weight A1C Trig HDL

(lb) (lb)56 M 2 mos 182 12 336 43 186 6.8 169 37

39 F 3 mos 135 16.8 179 46 153 5.3 47 62

35 F 3 mos 188 11.3 503 27 175 6.3 145 41

44 M 4 mos 301 8.7 297 33 260 4.8 112 40

69 F 5 mos 247 8.1 186 61 233 5.4 146 63

33 M 15 mos 289 10.9 342 46 279 4.8 183 54

50 M 26 mos 275 9.0 6500 - 215 5.3 329 37

36 F 18 mos 264 9.2 150 48 202 5.5 122 53


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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 123.2 110.8 -9.7% 0.003

Hemoglobin A1C, % 10.0 5.9 -41.0%


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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 273 7.0 6500 736 215 5.3 329 151

59 M 53 mos 182 12.0 336 300 181.8 6.1 386 12.5

49 F 12 mos 203 12.5 242 483 196 7.5 165 262

58 F 8 mos 252 6.4 121 50 197.6 5.5 68 13

49 M 12 mon 283 6.0 295 45.5 228.6 5.1 80 13


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Renal FailureCarbohydrate 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 31controls (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): 1204-9.


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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):

1204-9.


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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.


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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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Long Term Data

Medical monitoring was provided to taper diabeticand anti-hypertensive medication

Inclusion criteria: baseline and greater than 12months weight and laboratory studies

106 patients identified

Mean duration of treatment and follow up was 765days (365 days to 3777 days )

For the 17 Type 2 diabetics with initial HgbA1Cgreater than 6.5 mg%, the mean HgbA1cimproved 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.

Long Term Data


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Long Term Data365-3777 days of follow up in outpatient clinical practice


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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.


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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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VP Public Relations

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1-888-880-1858 ext:503

Presentation by Dr. Mary Vernon at KU Medical Center

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Transcript of Presentation by Dr. Mary Vernon at KU Medical Center