Embed Size (px)
Citation preview
Unified Field Theory of Diseases of Civilization
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
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.
Metabolic Health
Its not the weight, it’s the fuel source.
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): 180-186.
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 goal
obtained or patient willing to slow weight loss.Both groups routinely monitored with office
visits and blood work.
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.
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
Low-Fat Diet + Medication Carbohydrate Restricted Diet
Variable Baseline Follow-up Change 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
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: 2520-2525 (1996)
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
Bo
dy
We
igh
t, l
bs
(s
em
)
* p = 0.04 comparing change from Week 0 to Week 24 between groups
Very Low Carbohydrate Diet
Phen/Fen and Low Calorie Diet
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)
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
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.
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.
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.
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
Two Approaches to Understanding Human Metabolism
• 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
Classic Hormonal
HormonesInsulinGlucagonIncretinsEpinephrineNorepinephrineCortisolSex SteroidsBranched chain amino acidsIL-6Dietary Carbohydrates
Visceral Adiposity
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.
Dr. Eric Freedland proposed the concept of the “criticalvisceral 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.
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
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
Insulin Promotes Fat SynthesisGlucagon 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 (Carnitine palmitoyltransferase 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
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.
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
Ketone bodies
Ketone bodies are molecules that deliver energy(acetoacetate, acetone, -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/L
Diabetic 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.
GlucoseCan 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
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 caloric values using bomb calorimetry are:
Triglyceride: 9.461 kcal per gm…… 9 kcalProtein: 4.442 kcal per gm………… 4 kcalCarbohydrate: 4.183 kcal per gm... 4 kcalAlcohol: 7 kcal per gram……………7 kcalKetones: 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
Oh, Those Free Radicals
• The effect of burning glucose as fast as The effect of burning glucose as fast as possible overwhelms the mitochondrial possible overwhelms the mitochondrial electron transport chain and generates electron transport chain and generates increased numbers of free radicals.increased numbers of free radicals.
• Free radicals cause tissue damage.Free radicals cause tissue damage.• Control glucose/insulin metabolism=control Control glucose/insulin metabolism=control
free radical formation=control tissue free radical formation=control tissue destruction.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.
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;70:309-19.
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;70:309-19.
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;70:309-19.
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): 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.
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.
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.
Eat or Die
Ludwig, D. S., J. A. Majzoub, et al. (1999). "High glycemic index foods, overeating, and obesity." Pediatrics 103(3): E26.
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 0.001 vs. other diets).
Bisschop et al. J Clin Endocrinol Metab;2003:88:3801–3805.
Lack of Postprandial Rise in Serum Glucose and Insulin After a Low Carbohydrate Meal
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 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 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.
The New Paradigm
Food 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 by elevated insulin levels) which increase inflammation and tissue damage.
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 femaleWeight=191.3 lbsHgt=63 inchesBMI=33.9
DM with elevated Insulin
54 yo wf . 269 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
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 femaleWeight=269 lbsHgt=66 inchesBMI=43.4Stage 5 (DM) withreactive hypoglycemia and hyperinsulinemia.
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
-9
-69
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 femaleWeight=276 lbsHgt= 62 inchesBMI= 50.1Stage 5 moving to Stage 6Insulin levels don’t adequately suppress serum glucose response to dietary carbohydrate. Insulinresistance present.Reactive hypoglycemia present
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
226
99
54
152
4.1
1.83
-18
-17
-24
-9
-21
-15
+5
+5
-6
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 Initiation 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 hypoglycemic meds dc’d 7/00. Off all meds except setraline by 9/01
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.
Metabolic FitnessImprovement in Metabolic Fitness Without Weight ChangeA 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 6.0
7/02 145 127 37 3.4 153.5 31 ---
8/03 149 84 39 3.8 147 27.5 5.1
What about other lipid problems?
Decrease in Lp(a) Without Weight LossA 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)
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): 2893-8.
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.
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.
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): 761-70.
Roche Biomedical
Pathways
Insulin & HMGCoAReductase
Direction of Cholesterol Synthesis
www.expasy.ch/cgi.bin/search-biochem-index
Acetyl CoATCA CycleKetone Bodies
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 femaleWeight=118 lbsBMI=18
Her orthopedist told her she needed testing for diabetes.Her father has Type 2 DM.
HyperinsulinemiaReactive hypoglycemia
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
MONW
44 yo Caucasian male-construction type work
Presented with Ca oxalate kidney stones. 194# 5’11” BMI 27.1 13% BF
Low Carbohydrate Diet Program and Diabetes Mellitus
Before Diet After Low Carbohydrate Pgm
Age Sex Duration Weight A1C Trig HDL Weight A1C TrigHDL
(lb) (lb)56 M 2 mos 182 12 336 43 186 6.8 16937
57 F 3 mos 135 16.8 179 46 153 5.3 4762
35 F 3 mos 188 11.3 503 27 175 6.3 14541
44 M 4 mos 301 8.7 297 33 260 4.8 11240
69 F 5 mos 247 8.1 186 61 233 5.4 14663
33 M 15 mos 289 10.9 342 46 279 4.8 18354
50 M 26 mos 275 9.0 6500 - 215 5.3 32937
36 F 18 mos 264 9.2 150 48 202 5.5 122 53
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% <0.001
Total cholesterol, mg/dl 224.8 198.8 -14.3% 0.03
Triglycerides, mg/dl 327.5 165.4 -50.3% 0.003
LDL-C, mg/dl 131.1 125.0 -4.7% 0.94
HDL-C, mg/dl 44.5 48.2 +8.3% 0.07
Total chol/HDL-C ratio 5.3 4.2 -21.2% 0.01
Trigycerides/HDL-C ratio 8.3 3.8 -55.0% 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;1:233-237.
Low Carbohydrate Diet Program in Type 2 Diabetes Mellitus: Microalbuminuria
Before Diet After Low Carbohydrate Pgm
Age SexDurationWeight 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
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 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): 1204-9.
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.
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”.
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.
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 identifiedMean 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 PracticeMary Vernon, Eric Westman The Obesity Society 10/2008.
Long Term Data365-3777 days of follow up in outpatient clinical practice
TABLE 2
Effect of Carbohydrate Restriction on Metabolic Parameters
Variable Baseline Follow-up Change P value*
n=106 mean mean
Body mass index, kg/m2 38.2 32.4 -13.9% <0.0001
Body weight, kg 105.8 89.9 -14.0% 0.003
Hemoglobin A1c, pct (n=75) 6.4 5.5 -7.9% 0.0002
Hemoglobin A1c, pct (n=17) 9.2 5.8 -38.0% 0.0002
Total cholesterol, mg/dL 204.4 200.6 0% 0.03
Triglycerides, mg/dL 196.5 101.5 -37.6% <0.001
LDL-C, mg/dL 131.1 125.0 +6.0% 0.64
HDL-C, mg/dL 46.8 58.8 +31.9% <0.001
Total chol/HDL-C ratio 5.3 4.2 -11.8% <0.001
Trigycerides/HDL-C ratio 5.6 2.0 -49.7% <0.001
Systolic blood pressure, mmHg** 130.9 121.7 -4.7% 0.0007
Diastolic blood pressure, mmHg 78.2 74.3 -2.5% 0.008
*p<0.05 was used for statistical significance
**n=94 for systolic blood pressure and diastolic blood pressure
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”.
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.
More Information?
Amber Wiley
VP Public Relations
1-888-880-1858 ext:503
