COPING WITH THE DIABETES EPIDEMIC
| AGGRESSIVE NUTRITIONAL AND EXERCISE APPROACHES IN MANAGING DIABETES —Gabe B. Merkin,
MD, Associate Clinical Professor of Medicine, Georgetown University School of Medicine, Washington, DC
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| Overview: American Diabetes Association and American Dietetic Association recommend weight loss and exercise; tremendous
controversy; glycemic index (GI) not established fact; glycemic load more accepted; diabetes affects 35% of
population; environmental component; 91% of population will become diabetic; if diabetes diagnosed at 40 yr of age, expect
to die 11.6 yr before general population; severely incapacitated 20 yr before general population; major risk factor for
myocardial infarction (MI) and stroke; 40% of healthy people suffering first MI are undiagnosed diabetics; 75% of diabetics
will die of myocardial disease; perform stress test on all prediabetics and newly diagnosed patients >50 yr of age
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| Work-up: complete blood count (CBC), comprehensive metabolic panel (CMP), hemoglobin A1c (HbA1c ; measure of cell
damage), C-peptide (insulin level); coronary work-up in all prediabetics and diabetics; includes lipid panel, homocysteine,
lipoprotein A-1, C-reactive protein (CRP), and microalbumin (predicts kidney disease; useful in determining drugs used);
microalbumin:creatinine ratio >20 precludes use of metformin
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| Signs of diabetes: isolated abdominal obesity (AO); AO without concomitant or equal obesity in buttocks indicative of
prediabetes or diabetes; thick neck; male-pattern baldness; elevated triglycerides; low high-density lipoprotein (HDL);
abdominal obesity—increases risk of suffering MI; AO combined with high triglycerides high risk for MI and stroke;
fat storage primarily in abdomen increases risk for high BP, even if not fat or not diabetic; AO major risk factor for premature
death; when blood glucose (BG) rises too high, pancreas releases too much insulin; insulin acts on brain, creating
hunger and increased eating; insulin causes liver to make more fat, and extra fat deposited in fat cells in abdomen; AO
sign of high insulin level; insulin—concomitant elevated BG and insulin levels; insulin converts glucose to triglycerides;
elevated blood triglycerides and decreased HDL; fatty liver reduces ability to remove insulin from bloodstream,
causing high blood insulin levels; insulin constricts arteries, causing MI; thick neck—associated with high insulin-like
growth factor-1 (IGF1) and insulin levels; causes muscle, bone, and fat to grow in body; usually increased risk for diabetes
and prediabetes
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| Treatment: American Diabetes Association recommends exchange diet (involves calorie counting); supplemental insulin
determined as 1 unit/10 g carbohydrate; formula totally undependable because ratio varies with weight and units of insulin
used; cumbersome; base treatment on HbA1c ; HbA1c affected by postprandial BG, fasting BG, and mean BG; highly significant;
high BG measure of HbA1c ; nutrient-to-calorie density—important; diabetic diet should be contributing as much
nutrients to food; junk food does not contribute calories as nutrients; GI (postprandial BG rise) not useful; glycemic load
(amount of carbohydrate times rise in BG) important; isolated BG rise not problematic; high carbohydrate, high sugar
rise problematic; postprandial hyperglycemia—increases risk for MI; raises LDL, triglycerides, HbA1c , and insulin;
increases all measures of thrombosis; treatment must prevent BG levels from rising too high after meals; highest rise in
BG in controlled diabetics 30 to 60 min after eating; much longer in uncontrolled diabetics (up to 6 hr); eating causes BG
to rise too high, causing sugar to stick to cells (cannot be removed); sugar converted from glucose to fructose, ending as
sorbitol (destroys cells, increases risk for MI, stroke, blindness, deafness, and kidney failure); important measure of diabetic
control, associated with HbA1c
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| Diet: fruits and whole grains; Atkins diet—in short term, helps with weight loss; lowers HbA1c and triglycerides; in long
term, causes problems; cannot stay on severely restricted carbohydrate diet (results in “sky high” homocysteine and CRP); 9
essential (includes methionine) and 11 nonessential amino acids (formed from essential); methionine converts to homocysteine,
then to cysteine under influence of B vitamins; lack of folic acid or vitamin B12 prevents conversion of homocysteine
back to methionine; with lack of pyridoxine, unable to convert homocysteine into cysteine, causing increased homocysteine
levels; homocysteine level >10 associated with increased risk for MI, kidney damage, and other complications; measure and
treat high homocysteine level; stop when HbA1c <10; follow 2 mo later; treating homocysteine with combination of folic
acid, pyridoxine, and B12 (Foltex or Fol-B) controversial; diabetics must restrict carbohydrates low in nutrients (wasted calories)
and high-glycemic foods; HbA1c better controlled through eating whole grains and fruits (rich in carbohydrates);
speaker eliminates bakery products and pasta in patients’ diets; literature documents whole grains prevent MI and diabetes
(lower insulin, elevated BP, cholesterol, and triglycerides); restrict carbohydrates, not whole grains (containing husk); grinding
whole grain removes hull, increasing GI and converting low-GI food into high-GI food
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| Exercise: prevents and treats diabetes; exercising before meals markedly reduces rise in blood fat and glucose levels; lowers
HbA1c in children; improves insulin sensitivity; lack of exercise associated with diabetes and metabolic syndrome;
when muscles full of glycogen, sugar goes from intestines directly into blood, causing spike; sugar stored in muscles and
liver; when muscles empty, sugar goes from intestines to blood to muscles (prevents spike); controversial study shows intense
exercise (80% maximum heart rate [MHR]) far more effective than moderate exercise (65%, 50% MHR) in controlling
diabetes; results in greater emptying of muscles, greater decrease in HbA1c , better diabetic control; must perform
stress electrocardiogram before initiating program
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| Can diabetes be cured? study showed after 2.8 yr, incidence of type 2 diabetes 58% lower with radical lifestyle changes,
31% lower in metformin group (prevents postprandial rise in BG) compared to placebo; restrict saturated fat (increases
risk for MI); restrict partially hydrogenated fats, refined carbohydrates, and extracted vegetable oils; reduce intake of
meat and chicken (source of saturated fat); fats—saturated (increases bad cholesterol), polyunsaturated (omega-6,
omega-3), monounsaturated; eating nuts (contain monounsaturated fats) 5 times weekly reduces diabetes by 30%; monounsaturated
fats produce LDL cholesterol resistant to oxidation; saturated fats reduce insulin receptors; saturated fat
problematic when too many calories ingested; omega-6, omega-3— extracted vegetable oils contain omega-6:omega-3
ratio of 20:1; produce proinflammatory prostaglandins which increases susceptibility to MI, stroke, diabetes, arthritis,
and inflammation; partially hydrogenated fat—found in all prepared foods; polyunsaturated fat unstable; raises LDL,
lowers HDL, increases susceptibility to MI, may increase risk for certain cancers; hydrogenated fat stable, makes food
crispy, and prolongs food’s shelf life; omega-3 monounsaturated fats good (should eat them); diabetics should avoid
flour, sugar-added foods, sugared soft drinks, and fruit juices (high GI); fructose may cause obesity by not suppressing
ghrelin (increases hunger) and not calling out leptin (suppresses hunger); diet—unlimited fruits, vegetables, whole
grains, beans, seeds, and nuts in salads; reduce calories; root vegetables and fruits eaten with other foods and meals lower
GI; speaker puts new patients on 2-wk diet to lower fructosamines; breakfast contains oatmeal, raisins, and pine nuts;
lunch and dinner include salad with peanuts, cashews, walnuts, olives, artichoke hearts, whole grains, beans, shrimp, and
salmon; 3 wk of low-fat, high-fiber diet and daily exercise (45-60 min) lowers BP, LDL, fasting insulin, and weight
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| Medications: angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) protect kidney;
acetylsalicylic acid (aspirin) prevents clotting; metformin prevents elevated BG; pioglitazone (Actos) or rosiglitazone
(Avandia) sensitizes cells; statins lower cholesterol; patients whose cholesterol lowered most had fewest MIs and strokes
and did not suffer adverse effects; the lower the cholesterol, the better; statins can cause polyneuropathy, muscle pain,
and injuries; incidence of muscle pain in nonexercisers 0%, in competitive athletes 100%; when using metformin, urinary
microalbumin:creatinine ratio should be <20; treatment— start with metformin, pioglitazone, rosiglitazone, or sulfonylureas;
diet; add exenatide (Byetta) if unable to get HbA1c <6; no insulin unless C-peptide <1 ng/mL; insulin side effects
— increases risk for MI by constricting arteries; causes AO, hunger, weight gain, and increases BP; treat insulin-
deficient type 1 same as type 2 with diet, insulin glargine (Lantus) at night, metformin, and pioglitazone; if HbA1c >6,
add insulin aspart (Novolog) 70/30 or insulin lispro (Humalog) 75/25; vitamin D—hypovitaminosis D associated with
insulin resistance and β-cell dysfunction even in glucose-tolerant subjects; lack of vitamin D raises HbA1c in diabetics;
taking vitamin D in winter lowers high BG; Swedish study shows β-blockers increase risk for stroke and do not prevent
MIs (disturbing since guidelines recommend β-blocker use)
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| Polycystic ovary syndrome (PCOS): when BG too high, person produces too much insulin, which causes AO; high insulin
levels cause ovaries to produce testosterone, preventing ovulation; causes hirsutism, acne, infertility, and muscles
to grow (athleticism)
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| Other factors: alcohol—<3 drinks and daily does not raise BG, lowers HbA1c , reduces clotting, and lowers oxidants in
blood; salt—restriction raises BG and insulin levels, loading lowers both; severe depletion causes insulin insensitivity;
does not prevent MI; diabetes—damages brain; nephropathy reversible; treat with severe dietary restrictions and tight
management; restrict caffeine (markedly increases BG and insulin after meals); whole grains for patients with wheat/
oat allergies—brown rice; wild rice; quinoa; millet; any increase in HbA1c incurs MI risk; going from 5 to 6 triples risk
for MI and increases risk for diabetes; 25-hydroxyvitamin D test for vitamin D deficiency (800 to 1200 IU daily); C-peptide
>3 indicative of high insulin (damages tissue and affects intelligence)
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| DIABETES IN CHILDREN AND ADOLESCENTS —Janice E. Milligan, MD, Pediatrician and Family Physician, Homestead,
FL
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| Diabetes: group of metabolic diseases characterized by hyperglycemia; results from defects in insulin secretion, action, or
both; chronic hyperglycemia of diabetes associated with long-term damage, dysfunction, and various organ failures (eg,
eyes, kidney, nervous system, heart, blood vessels); type 1—associated with autoimmune destruction of β-cells in pancreas;
autoantibodies present in 85% to 90% of individuals at time of disease detection; most commonly detected in childhood,
but can be detected late in life into 8th decade; usually requires insulin treatment; type 2—90% to 95% of diabetic
population; insulin resistance and relative insulin deficiency; ketoacidosis not common, but can occur; does not require insulin
treatment; other types—gestational; maturity-onset diabetes of young (autosomal-dominant, inherited condition characterized
by impaired glucose secretion); exocrine pancreas; cystic fibrosis; endocrinopathies—acromegaly; Cushing’s disease; pheochromocytoma
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| Type 1: incidence 15/100,000 children; peak incidence between 11 and 13 yr of age (as low as <2 yr); more common in
non-Hispanic whites then blacks and Hispanics; presents with classic symptoms but symptoms in childhood hard to see,
especially in very young; child appears well with sudden onset of illness; management—difficult and complicated; education
of child and parents primary; hospitalization usually required to restore hydration and to stabilize ketosis; insulin
dosing most effective in outpatient setting; dysfunctional, psychologically deficient families present problems; very
stressful on nondysfunctional families; treatment—lifestyle modification; family lifestyle changes; full family education
about diet, exercise, choice of free-time activities, and avoidance of alcohol and cigarettes; team approach (eg, clinical
endocrinologist, weight loss specialist, exercise physiologist, psychologist, social worker, diabetes therapist); teach
parents and teachers; regular hours, planned diet, consistent eating times; insulin—very low doses; very tightly controlled;
childhood illnesses require additional medical intervention
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| Type 2: prevalence in children and adolescents equal to that of type 1; consider screening children for type 2; highest risk—
prominent family history; mild fasting hyperglycemia; morbid obesity; ethnicity (American Indian and Hispanic); maternal
gestational diabetes; PCOS may present in adolescence; 85% of patients overweight at diagnosis but most asymptomatic;
ketoacidosis rare (<25%); insulin and C-peptide levels elevated; islet cell antibodies not present; vaginal yeast
infections common; associated skin findings—acanthosis nigricans; tinea capitis; tinea corporis; monilia; hirsutism;
acne; balanitis; obese child with ≥2 risk factors requires screening at 10 yr of age and every 2 yr thereafter; prediabetics
need dietary counseling (eg, eliminate soda, drink water, decrease television time, increase exercise); refer to specialist
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| Diagnosis: fasting BG >126 mg/dL; verify within 1 wk; 2-hr BG >200 mg/dL diagnostic; prediabetes—fasting BG of
100 mg/dL to 125 mg/dL; 2-hr BG of 140 mg/dL to 199 mg/dL; prediabetes risk—macrovascular disease, progression
to type 2; diabetes risk— micro- and macrovascular disease; fasting BG gold standard; screening with HbA1c not recommended;
prediabetics should be screened; laboratory—urine for microalbuminuria; serum creatinine; blood urea nitrogen
(BUN); fasting lipid profile best assessed after several months of intervention; liver function; quarterly HbA1c ;
lipids—ideally, LDL <100 mg/dL
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| Treatment: eliminate symptoms of hyperglycemia; weight stabilization; decrease cardiovascular risks (eg, hypertension,
hyperlipidemia, sedentary lifestyle, use of tobacco); improvement in physical and emotional well-being; achieve HbA1c
≤7; self-monitoring BG—must involve child; goal of fasting and postprandial glucose at bedtime difficult to achieve;
office follow-up—annual dilated retinal exam; annual monofilament foot exam; annual 24-hr urine; quarterly diabetic
labs; school/daycare part of team; metformin approved for patients ≥10 yr; until recently, insulin only Food and Drug Administration
approved treatment for children and adolescents; medical nutrition therapy most effective treatment; insulin
resistance in type 2 may cause ketoacidosis; American Diabetes Association states that if treatment goals not met with
nutrition and exercise, pharmacologic therapy indicated (first agent should be metformin)
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Educational Objectives
| The purpose of this program is to provide the listener with information on coping with the diabetes epidemic. After hearing
and assimilating this program, the clinician will be better able to:
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 | 1. List the tests used in the diagnostic work-up of diabetes.
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| 2. Describe the signs of diabetes.
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| 3. Discuss how diet and exercise help in the treatment of diabetes.
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| 4. Review the medications used in treating diabetes.
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| 5. Discuss the management issues involved in treating children and adolescents with diabetes.
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Discussed on This Program
Aspirin (acetylsalicylic acid; ASA) [several trade names]
Exenatide [Byetta]
Folic acid (folacin; pteroylglutamic acid; folate) [Folvite]
Glipizide/metformin HCl [Metaglip]
Insulin aspart (rDNA origin) [Novolog, Novolog Mix 70/30]
Insulin glargine [Lantus]
Insulin lispro, human (rDNA) [Humalog, Humalog Mix 75/25]
Metformin HCl [Fortamet, Glucophage, Glucophage XR, Riomet]
Pioglitazone HCL [Actos]
Rosiglitazone maleate [Avandia]
Suggested Reading
Bachar JJ et al: Cherokee choices: a diabetes prevention program for american indians. Prev Chronic Dis 2006 3:A103,
2006; Barnett AH: How well do rapid-acting insulins work in obese individuals? Diabetes Obes Metab 8:388 -95. 2006;
Bartnik M et al: The prevalence of abnormal glucose regulation in patients with coronary artery disease across Europe.
Eur Heart J 25:1880, 2004; Blonde L et al: Interim analysis of the effects of exenatide treatment on A1C, weight and cardiovascular
risk factors over 82 weeks in 314 overweight patients with type 2 diabetes. Diabetes Obes Metab 8:436, 2006;
Chandran M, Chu NV: Gastrointestinal disturbances in diabetes. Curr Diab Rep 3:43, 2003; Dunstan DW et al: The
rising prevalence of diabetes and impaired glucose tolerance: the australian diabetes. Obesity and Lifestyle Study Diabetes
Care 25:829, 2002; Holben DH, Pheley AM: Diabetes risk and obesity in food-insecure households in rural appalachian
ohio. Prev Chronic Dis 3:A82, 2006; Holness MJ, Sugden MC: Epigenetic regulation of metabolism in children born
small for gestational age. Curr Opin Clin Nutr Metab Care 9:463, 2006; Isasi CR et al: Youth WAVE Screener: addressing
weight-related behaviors with school-age children. Diabetes Educ 32:415 2006; Jacober SJ et al: A comparison
of intensive mixture therapy with basal insulin therapy in insulin-naive patients with type 2 diabetes receiving oral antidiabetes
agents. Diabetes Obes Metab 8:448, 2006; Lee, JA et al: Racial and ethnic differences in diabetes care and health
care use and costs. Prev Chronic Dis 3:A85, 2006; Malmberg K. for the DIGAMI (Diabetes Mellitus, Insulin Glucose
Infusion in Acute Myocardial Infarction) Study Group. Prospective randomised study of intensive insulin treatment
on long term survival after acute myocardial infarction in patients with diabetes mellitus. BMJ 314:1512, 1997;
Mauras N et al: Lack of accuracy of continuous glucose sensors in healthy, nondiabetic children: results of the Diabetes
Research in Children Network (DirecNet) accuracy study. J Pediatr 144:770, 2004; Nielsen JV et al: A low-carbohydrate
diet may prevent end-stage renal failure in type 2 diabetes. A case report. Nutr Metab (Lond) 14:23,2006; Norhammer A
et al: Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a
prospective study Lancet 359:2140, 2002; Poncelet AN: Diabetic polyneuropathy. Risk factors, patterns of presentation,
diagnosis, and treatment. Geriatrics 58:16, 2003; Vinik AI, Maser RE: Diabetic autonomic neuropathy. Diabetes Care
26:1553, 2003; Promintzer M, Krebs M: Effects of dietary protein on glucose homeostasis. Curr Opin Clin Nutr Metab
Care 9:463, 2006; Ratner, RE et al: Long-term effects of exenatide therapy over 82 weeks on glycaemic control and
weight in over-weight metformin-treated patients with type 2 diabetes mellitus. Diabetes Obes Metab 8:419, 2006; Samuel-Hodge
CD et al: Church-based Diabetes Self-management Education Program for African Americans With Type 2
Diabetes. Prev Chronic Dis 3:A93, 2006; Schwartz, SL: Diabetes and dyslipidaemia. Diabetes Obes Metab 8:355,
2006.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue,
Drs. Mirkin and Milligan reported nothing to disclose
Drs. Mirkin and Milligan addressed the Family Practice Review, held March 26-31, 2006, in Philadelphia, PA and sponsored
by the Temple University School of Medicine and the American Academy of Family Physicians. The Audio-Digest
Foundation thanks Drs. Mirkin and Milligan and the sponsors for their cooperation in the production of this program.
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