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Monday, September 12, 2011

Learn to Medically Manage Diabetes



Learn to Medically Manage Diabetes

Understand the systemic pathobiology of diabetes and how to treat it in order to provide your patients with the most comprehensive medical care possible.
By A. Paul Chous, M.A., O.D.

Goal Statement:

As providers of primary care, we often encounter patients with diabetes who demonstrate multiple ocular and systemic sequelae. Here, we consider the systemic pathobiology of diabetes and its ocular consequences, with a particular emphasis on practical aspects of medical management. Given the public health crisis that diabetes represents, this article also proposes the development of a primary care diabetes subspeciality within an optometric practice.

Faculty/Editorial Board:

A. Paul Chous, M.A., O.D.

Credit Statement:

This course is qualified for 2 hours of CE Credit. COPE ID: 26248-SD. Check with your local state licensing board to see if this counts toward your CE requirement for relicensure.

Joint-Sponsorship Statement:

This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.

Disclosure Statement:

Dr. Chous has no relationships to disclose.
Despite many advances in basic and clinical sciences during the last twenty years, the incidence of new-onset diabetes and diabetes-related complications continues to escalate alarmingly. The U.S. Centers For Disease Control & Prevention recently reported that the number of cases of diabetes and vision loss related to diabetic eye diseases (diabetic retinopathy, cataract and glaucoma) will triple between 2005 and 2050.1 Several variables have been identified that contribute to this burgeoning problem, including rising rates of obesity; widespread adoption of calorie-rich diets; increasingly sedentary lifestyles; and a variety of less understood sociological, psychological and genetic influences.2
As providers of primary care, we often encounter patients with diabetes who demonstrate multiple ocular and systemic sequelae. Frequently, these conditions are connected by common and complex underlying biological mechanisms. To provide the best care possible, we must both understand and participate in the medical management of our patients with diabetes.
Here, we consider the systemic pathobiology of diabetes and its ocular consequences, with a particular emphasis on practical aspects of medical management. Given the public health crisis that diabetes represents, this article also proposes the development of a primary care diabetes subspecialty within an optometric practice.

Diabetes Defined & Classified

Diabetes mellitus (DM) is characterized by hyperglycemia secondary to a lack of endogenous insulin production (insulin deficiency) and/or a lack of cellular response to the effects of insulin (insulin resistance). In either case, both processes lead to elevated blood glucose levels and osmotic diuresis, which causes more frequent urination, or polyuria. Diabetes is derived from the Greek word “diabetes,” meaning to pass through, and Mellitus is derived from the Latin word “mellis,” or honey.
DM must be contrasted with the much less common diabetes insipidus (DI), an endocrine disorder caused by lost production of or sensitivity to the effects of antidiuretic hormone (ADH, also known as vasopressin), resulting in the inability to concentrate urine with marked compensatory diuresis. Other than polyuria and a rare condition known as Wolfram syndrome (a genetic disorder resulting in DI, DM, optic atrophy and deafness), there is little connection between DM and DI.3
• Type 1 diabetes mellitus. Be aware that insulin deficiency and insulin resistance are not mutually exclusive; many patients, in fact, have both conditions. Type 1 diabetes mellitus (T1DM) results from autoimmune destruction of pancreatic beta cells by T lymphocytes, with progressively worsening and permanent insulin deficiency. Patients with T1DM typically are diagnosed before age 30 (the mean age of diagnosis is 15 years); tend to be slim and human leukocyte antigen-positive, and require exogenous insulin for survival––although insulin requirements may be quite low within the first few months or (rarely) years of diagnosis while the beta-cell population wanes (this is euphemistically termed “the honeymoon period”).
With relative normalization of blood sugars, T1DM patients often gain weight and may develop insulin resistance as a consequence (the overlay of secondary insulin resistance on top of primary insulin deficiency has led some physicians to dub this phenomenon “type 1.5 diabetes”).4 Most patients with normal insulin sensitivity generally require about 25 to 40 units of insulin each day to facilitate glucose transport required by a 2,000 calorie diet. Patients who take more than 60 units/day almost certainly have some level of insulin resistance, hypercaloric intake or both, regardless of whether or not they are diagnosed with type 1 or type 2 diabetes.
T1DM is a disease of primary insulin deficiency, has been linked to a number of genetic markers, and is associated with dysfunctional sensory neurons within the beta cell-containing regions of the pancreas, which suggests faulty inhibition of auto-immunity.5Prevalence increases with distance from the Earth’s equator, indicating a causal role for vitamin D deficiency as well.6,7 Allergy to bovine milk and wheat also are suspected contributors to T1DM development.8,9
Additionally, a recent epidemic of T1DM in New Zealand was thought to be related to consumption of nitrite and nitrate preservatives in packaged meat products and agricultural pesticides, because these agents are chemically similar to the beta-cell toxic compound streptozotocin––a formulation commonly used to induce diabetes in laboratory animals.10
• Type 2 diabetes mellitus. Type 2 diabetes mellitus (T2DM) is a disease of primary insulin resistance, the loss of normal insulin sensitivity by insulin-sensitive cells (especially hepatocytes and skeletal myocytes).11 Insulin resistance is thought to be a function of genetic predisposition, adipocyte-based hormonal influences that affect appetite and conformational integrity of cellular insulin receptors, glucose toxicity, and production of inflammatory cytokines and free fatty acids that further degrade insulin receptors as well as kill the insulin-producing beta cells.11 Excess production of insulin (hyperinsulinemia) is common as functioning beta cells struggle to overcome worsening insulin resistance. High levels of circulating insulin activate the renin-angiotensin-aldosterone system (RAAS), which causes increased blood volume and hypertension, and hyperinsulinemia also is associated with an increased risk of both gastrointestinal and cell mass due to glucotoxicity, lipotoxicity and chronic secretory stress. In this instance, what starts as a disease of insulin resistance increasingly becomes a disease of concomitant insulin deficiency, which is the reason why many T2DM patients ultimately require exogenous insulin.14
Patients with T2DM tend to have above-normal body weight, higher body mass index and increased abdominal fat. Patients typically demonstrate a family history of the condition. Most individuals are diagnosed with T2DM after age 30; however, the incidence of insulin resistance and T2DM in people under the age of 20 has skyrocketed in the last decade along with increased numbers of childhood obesity cases in America.15

Diabetes-Related Complications

Diabetes is the leading cause of new cases of blindness in Americans under 74 years of age, end-stage renal disease and non-traumatic amputation.16 Most alarming, diabetes is the seventh leading cause of death in the United States––primarily because of an increased risk for cardiovascular complications.16
Additionally, diabetes is associated with a higher risk for cognitive impairment and Alzheimer’s disease; cancer of the pancreas, intestine, oesophagus and breast (as a consequence of hyperinsulinemia); bone and joint disease; clinical depression; periodontal disease; disseminated autonomic neuropathy; and sexual dysfunction.17-23
Metabolic Goals In the Management of Diabetes28,29
Glycosylated Hemoglobin



Fasting Blood Sugar
Post-Prandial Blood Sugar
Blood Pressure
LDL-C

Triglycerides
HDL-C		< 7% (ADA) < 6.5% (AACE)
[Higher for patients with pre-existing cardiovascular
disease, frequent hypoglycemia, shorter life expectancy
and young children (i.e., > 7%, but still < 8%)]
< 110mg/dl
< 180mg/dl (ADA) < 140mg/dl (AACE)
< 130/80mm Hg
< 100mg/dl (no history of cardiovascular disease)
< 70mg/dl (preexisting cardiovasular disease)
< 150mg/dl
> 50mg/dl (women) > 40mg/dl (men)
* Unless otherwise specified, the recommendations are the same from both the ADA and the AACE.
T1DM appears to increase the risk for other autoimmune disorders, such as celiac disease, multiple sclerosis and hypothyroidism secondary to Hashimoto’s thyroiditis.24T2DM and insulin resistance specifically increase the risk for cardiovascular events by fostering inflammatory dyslipidemia, which accelerates atherosclerosis.25 This may help explain why strict blood glucose control protects better against small blood vessel complications, such as retinopathy than large blood vessel complications, such as stroke and heart attack. This also underscores the link between diabetic retinopathy and cardiovascular disease.25
Studies suggest that proliferative diabetic retinopathy (PDR) doubled the risk of cardiovascular death in T1DM patients during an eight year period and quintupled the risk for cardiovascular mortality in T2DM patients during an 18-year period.26,27 Even non-proliferative retinopathy increased the risk for cardiovascular mortality in T2DM patients by 30% to 70% during the same 18-year-period, with females demonstrating the highest risk.26
Most metabolic carnage at the cellular level is caused by mitochondrial derangement within insulin-independent tissues. The retina, nervous system, renal glomeruli and aorta transport glucose across the cell membrane, independent of insulin levels, through a variety of alternative transport systems. So, intracellular concentrations of glucose rise in these tissues in accordance with blood glucose levels.
When exposed to excess glucose and/or free fatty acids, mitochondria produce reactive oxygen species that deactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH)––the final, critical enzyme necessary for processing injurious intracellular glucose metabolites.28 Consequently, concentrations of these intermediate metabolites increase, resulting in tissue damage via four distinct, but interrelated, biochemical pathways: polyol; hexosamine flux; protein kinase C; and advanced glycation end products (figure 1).28Diabetes-related eye diseases, including retinopathy, cataracts, glaucoma and corneal erosion, have been experimentally linked to increased activity in the polyol, protein kinase C and advanced glycation end product pathways, and interruption of these pathways has been shown to prevent both ocular and systemic complications associated with diabetes in animal models.28
img2
1. Inhibition of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) increases the production of harmful glucose metabolites that drive the polyol, hexosamine, protein kinase C and advanced glycation endproduct pathways.

Treatment of Diabetes

Current treatments for diabetes mellitus focus on addressing its associated metabolic abnormalities, particularly hyperglycemia, dyslipidemia and hypertension (figure 2). Physicians should place major emphasis on blood glucose, because tight glycemic control has been proven to reduce microvascular sequelae (particularly retinopathy incidence and severity) as well as improve both blood lipids and blood pressure. The medical team should set specific goals for mean blood glucose (as reflected by glycosylated hemoglobin), weight, blood pressure, LDL cholesterol and triglycerides. Both dietary and pharmacologic strategies must be specifically tailored to achieve individualized metabolic goals, as recommended by the American Diabetes Association (ADA) and the American Association of Clinical Endocrinology (AACE).
2. Here is an overview of various treatment strategies for your patients with diabetes. Drug therapy for diabetes includes blood glucose, blood pressure and blood lipid/anti-clotting agents. Improving blood glucose is essential because it positively affects blood pressure and lipids. Weight loss improves all metabolic parameters in insulin-resistant patients. Medical nutrition therapy (MNT), including exercise, typically improves metabolic parameters in all patients.
• Medical nutrition therapy. Medical nutrition therapy (MNT) refers to both prevention and treatment of diabetes through application of evidenced-based nutritional recommendations. MNT employs an “individualized, coordinated team effort that includes the person with diabetes and involves him or her in the decision-making process.”31
General recommendations of MNT include a low carbohydrate/low fat, energy-restricted diet to achieve modest (5% to 7%) weight loss in overweight/obese patients; 150 minutes of exercise per week; increased dietary fiber intake; elimination of trans fat intake; and reduction of saturated fat intake (less than 10% of total caloric intake from saturated fats). MNT is estimated to reduce glycosylated hemoglobin by about 1%.31
Analysis of the Diabetes Control and Complications Trial (DCCT) shows that progression of diabetic retinopathy was directly associated with total dietary fatty acid intake and cigarette smoking, and inversely associated with dietary fiber intake.32
Carbohydrate restriction is most effective at reducing post-prandial (after meal) hyperglycemia; however, the merit of low carbohydrate and low glycemic index (GI) diets that yield a slower rise in blood glucose is still debated for a variety of reasons (e.g., individual variability in response to foods of a “known” GI, limited time course of measurement and patients with diabetes not tested in determining GI values).
ADA guidelines generally recommend a dietary caloric intake that consists of 50% to 55% carbohydrates, 15% to 20% protein and 25% to 35% fat, whereas advocates of extremely low glycemic index diets suggest that carbohydrates should account for less than 10% of total caloric intake.33
In fact, reducing dietary glycemic index below the same-sex median is estimated to eliminate one in five cases of severe vision loss due to advanced age-related macular degeneration, suggesting a link between carbohydrate metabolism and retinal disease.34
• Blood glucose monitoring. Self-monitoring of blood glucose is of paramount importance for patients with diabetes who use insulin, have significant blood glucose variability or hypoglycemia, initiate new therapies that affect blood glucose, or experience an acute illness. AACE clinical practice guidelines recommend that all patients being pharmacologically treated for DM self-monitor their blood glucose at least once per day.30
Several continuous interstitial glucose sensors, such as DexCom STS (DexCom) Paradigm REAL-Time System (Medtronic) and Free-Style Navigator (Abbott), which aim to improve HbA1c (glycosylated hemoglobin) levels in adults on insulin therapy, recently have become available.35 These sensors still require self-administration of insulin as well as daily calibration via standard blood glucose testing. Nonetheless, the combination of such sensors with an “intelligent” insulin pump holds promise for a “closed loop” system that does not require patient input to maintain normal blood glucose levels. (Such systems will likely be available within a decade.)
• Pharmacologic treatment. Pharmacologic treatment of diabetes includes blood glucose agents (insulin, insulin secretagogues, insulin sensitizers, drugs decreasing hepatic glucose production, starch blockers, appetite suppressants and combined mechanism drugs), antihypertensives (angiotensin-converting enzyme [ACE] inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers and diuretics) and anti-lipid/anti-clotting agents (cholesterol absorption blockers and production inhibitors, triglyceride inhibitors, aspirin, and other anti-platelet drugs).
Insulin therapy is customized to match normal physiologic insulin levels. T1DM patients require basal insulin incrementally delivered by an insulin pump, or via injections of long-acting insulin––e.g., Lantus (insulin glargine, Aventis Pharmaceuticals) or Levemir (insulin detmir, Novo Nordisk)––to process hepatic glucose production and bolus insulin—e.g., Humalog (insulin lispro, Eli Lily) or Novolog (insulin aspart, Novo Nordisk)—to compensate for dietary carbohydrate intake.
For patients with T2DM, metformin (e.g., Glucophage, Bristol-Myers Squibb) is a first-line agent because it is inexpensive, effective and cardioprotective (especially for obese patients).36 Insulin secretagogues, such as Micronase (glyburide, Pfizer) and Amaryl (glimepiride, Sanofi-Aventis Pharmaceuticals), are now considered second-line agents, followed by insulin and/or insulin sensitizers, such as Actos (pioglitazone hydrochloride, Takeda Pharmaceuticals), if blood glucose targets are not reached.
Incretin mimetics, such as Byetta (exenatide, Amylin Pharmaceuticals), and DPP-IV inhibitors, such as Januvia (sitagliptin, Merck), are the newest agents available for T2DM. These agents work by a number of mechanisms and induce weight loss by modulating hypothalamic satiety receptors, which is a distinct advantage over other pharmacologic treatments.
Individual oral blood glucose agents typically lower HbA1c 1% to 2% at maximum dosage, whereas insulin may lower HbA1c indefinitely. A critical analysis of each patient’s HbA1c values and targets should allow physicians, including primary eye care providers, to make scientifically justifiable recommendations about blood glucose agents.
For instance, a patient with T2DM and current HbA1c of 9% who receives medical nutrition therapy and metformin is unlikely to reach a target HbA1c of 6.5% simply by adding another oral agent. Instead, insulin therapy might be more appropriate for this patient. For optometrists, this kind of analysis is of fundamental importance because each 10% relative reduction in HbA1c has been shown to lower the risk of retinopathy progression by 43%.37
• Blood pressure control. ACE inhibitors are considered the standard of care for any diabetes patient with hypertension, because they have been shown to reduce the progression of diabetic nephropathy and, more recently, diabetic retinopathy.38,39 For patients who are intolerant of or unresponsive to ACE inhibitors, angiotensin-2 receptor blockers may be substituted, followed by low-dose beta blockers (which can worsen insulin sensitivity and mask symptoms of hypoglycemia), calcium channel blockers, and diuretics (which may worsen insulin resistance and impair renal function).
Hypertension is a definitive risk factor for the development and progression of diabetic retinopathy.40 So, optometrists should routinely measure blood pressure in all patients with diabetes.
• Blood lipid control. Hyperglycemia and insulin resistance independently promote dyslipidemia, including higher levels of both LDL cholesterol and oxidized LDL cholesterol, which can cause atherosclerosis. Also, due to elevated levels of plasminogen activator inhibitor-1 (PAI-1), an inflammatory cytokine that prevents the breakdown of platelet blood clots, patients with diabetes have “sticky platelets” that increase cardiovascular risk. HMG-CoA reductase inhibitors (statins) and aspirin are widely considered the standard of care for patients with T2DM.
• Weight loss and control. Because of the direct link between weight status and insulin resistance (especially visceral adiposity), T2DM management should include therapies that induce weight loss. In addition to MNT, drugs and bariatric surgery may be employed to derail the metabolic defects associated with obesity.
Both rimonabant (a cannibanoid receptor antagonist) and sibutramine (a serotonin reuptake inhibitor) are appetite suppressants that appear to lower HbA1c approximately 0.6% in patients with T2DM. Unfortunately, however, both agents have been associated with psychiatric side effects.41
Xenical (orlistat, Roche) is a lipase inhibitor that blocks the absorption of dietary fat, particularly triglycerides. It has been shown to reduce weight, improve cardiovascular risk factors and lower blood glucose (HbA1c reduction greater than 1%) in large clinical trials of patients with T2DM; however, Xenical is notorious for gastrointestinal side effects.42
Optometric Recommendations For All Patients With Diabetes
1. Know your number. Glycosylated hemoglobin (A1c) is a ”quality of life” number because it largely determines your risk of all diabetes complications, including eye disease and blindness. Each 10% reduction in A1c lowers the risk of retinopathy progression by 43%. Check your blood sugar two hours after your largest meal of the day––if it’s consistently above 150 mg/dl then let me and your diabetes doctor know. Keep your blood pressure less than 130/80mm Hg.
2. Watch what and how much you eat. Minimize consumption of white foods (bread, pasta, rice and potatoes) because they rapidly increase blood sugar and are linked to eye disease. Read food labels to determine portion size, carbohydrate content and calories. Eat more slowly. Eat a variety of brightly colored fruits and vegetables, cold water fatty fish like salmon or sardines, and increase fiber intake (Mediterranean-type diets are consistently associated with better cardiovascular health). Consider supplements that make biologic sense for diabetes and prevention of eye disease (fish oil, vitamin D, ALA, benfotiamine, lutein/zeaxanthin, pycnogenol, etc.)
3. Move your body. Exercise (walk, cycle and/or swim) at least 30 minutes, five days a week. Even small amounts of physical activity improve insulin sensitivity. Do some modest resistance training three times per week, as increased muscle mass decreases insulin resistance. Get a pedometer and try to walk 5,000 to 10,000 steps every day. Research shows that exercise does not worsen diabetic retinopathy, but check with me and your primary care physician before engaging in vigorous sports like kick boxing or extreme weight lifting.
4. Build a great diabetes team. Seek out health care providers who are knowledgeable about diabetes and advocate for you. Ask your other doctors to send me a report of their findings so that we can work together to keep you healthy. Make sure you see me every year for a dilated eye examination so that if problems develop, we catch them early and can do everything possible to protect your vision.
A joint position paper written by the AACE, The Obesity Society and The American Society for Metabolic and Bariatric Surgery recommends that T2DM patients with a body mass index greater than or equal to 35kg/m2 be considered for bariatric surgery—particularly those patients with such comorbidities as coronary artery disease, hypertension, obstructive sleep apnea and pseudotumor cerebri.43
Clinical trials show high remission rates for newly diagnosed T2DM with laparoscopic adjustable gastric banding (LAGB), though lifestyle modification is critical for long-term success.44
• Islet cell transplantation. Islet cell transplantation could not only be a potential cure for T1DM, but it could also replenish depleted pancreatic beta cells in patients with T2DM. Allogeneic transplantation using immunosuppressive agents yielded insulin independence in 80% of patients with T1DM in the short term; however, just 10% of patients were still independent from insulin administration at five-year follow-up.45 Limited availability of transplantable tissue and adverse side effects associated with longterm use of immunosuppressive drugs also remain major barriers to this form of therapy.46

Diabetes and Nutritional Supplements

There has been little consensus within the scientific community with regard to dietary supplementation for patients with diabetes. The ADA makes no specific recommendation regarding use of even a multivitamin, save in patients adhering to low carbohydrate regimens. Nonetheless, existing research does give us some insight into which supplements make biological sense for combating diabetes and its vascular complications.
• Omega-3 fatty acids. Omega-3 fatty acid supplements have been shown to prevent cardiac arrhythmias and ameliorate clinical depression in T2DM patients. Several studies have demonstrated that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) decrease amounts of plasma triglycerides, visceral fat (and concomitant production of inflammatory cytokines), free fatty acids, C-reactive protein, glucose and insulin, and they also reduce peripheral insulin resistance.47,48
• AMD supplements. Patients who demonstrate high levels of serum lutein/zeaxanthin and lycopene are 67% less likely to develop diabetic retinopathy than those with low levels.48 Moreover, supplementation with Age-Related Eye Disease Study (AREDS) micronutrients might inhibit the development of diabetic retinopathy by blocking oxidative and nitrative stress.49
These findings give us yet another reason to recommend AMD supplements to our patients with diabetes.
• Vitamin D. Vitamin D deficiency impairs insulin sensitivity and is associated with T2DM, T1DM and metabolic syndrome, as well as increased risk of cancer.50
Evidence suggests that a minimal daily intake of 2,000 IU of 25-hydroxyvitamin D is required to maintain healthy serum concentrations of 40ng/ml to 60ng/ml— particularly in darkly-pigmented individuals, people who experience minimal bare skin exposure to midday sunlight, and patients who either have or are at risk for diabetes.51 All patients with diabetes should request an assessment of their serum vitamin D levels.
• Benfotiamine. Benfotiamine is a lipophilic analog of vitamin B1 that reduces activity in all four biochemical pathways implicated in microvascular diabetes complications.
In an animal model of diabetes, benfotiamine completely prevented diabetic retinopathy. It is currently in human trials.52
• Alpha lipoic acid. Alpha lipoic acid (ALA) is a super-antioxidant that preferentially distributes to mitochondria. It blocks glycosylation of proteins, improves glucose transport into insulin dependent tissues, and reduces both small and large blood vessel complications of diabetes in animal models.53
In a recent trial, T1DM patients who took 600mg of benfotiamine combined with 600mg of slow release ALA per day for four weeks demonstrated normalized activity in the polyol, hexosamine and advanced glycation endproduct pathways as well as increased levels of prostacyclin synthase, a critical anti-atherosclerosis enzyme within endothelial cells.54
• Pycnogenol. Pycnogenol is a standardized extract of French maritime pine bark. It is composed of procyanidins and phenolic acids, which appear to have anti-inflammatory properties. A meta-analysis of five clinical trials found that pycnogenol retards capillary leakage in diabetic retinopathy and lowers fasting glucose, post-prandial glucose and glycohemoglobin in a dose-dependent manner in T2DM patients.55,56
• Taurine. The amino acid taurine supports glial function within the retina. Higher doses may lower blood glucose in humans. Taurine supplementation has been shown to minimize diabetic retinopathy in an animal model by suppressing excessive glutamate excitotoxicity.57

What Should Optometrists Do?

Fortunately, what is good for the eyes is also good for every other organ system affected by diabetes. Ask your patients about their diabetes management routines, including diet/supplement/exercise regimens, blood glucose testing frequency, metabolic parameters, weight/body mass index status and blood glucose control habits. Be sure to make specific and complementary recommendations to your patients in coordination with primary care physicians, endocrinologists and other members of the health care team.
Diabetes is a complex, multifactorial disease that affects every part of the body. However, diabetes is largely preventable and manageable with appropriate knowledge and compassionate care. To this end, developing a diabetes sub-specialty within optometry is sensible.
Resources needed include a few modest diagnostic supplies (such as a sphygmomanometer and stethoscope, a blood glucose meter and test strips, and perhaps an in-office assay for glycosylated hemoglobin.) A digital retinal camera is also extremely useful for patient and physician education.
Web Resources for Diabetes Information
Of course, some time commitment is necessary. To provide the most accurate and timely information to your patients and other health care providers, you must learn the essentials and nuances of good diabetes care and stay informed of the latest research and clinical developments. Professional membership in diabetes organizations, such as the ADA and AACE, as well as in related intra-professional groups, such as the Optometric Nutrition Society, is a good start. Finally, support of and participation in diabetes track education programs for optometrists might further augment our profession’s ability to deliver the highest quality of care to patients with diabetes and enhance the public perception of optometry.
Diabetes is epidemic, and its ocular side effects are both prevalent and costly. Even though diabetic retinopathy is an end-organ manifestation of a systemic disease, the abnormalities we detect at the slit lamp are not isolated to the eye. Consequently, as primary care providers, we must understand the pathobiology of diabetes, the science underlying its treatment, and the conclusions of major diabetes-related studies. Armed with this information, we can educate and counsel our patients with diabetes accordingly.
Dr Chous lectures and writes frequently on the subjects of diabetes, diabetic eye disease and emerging treatments. He practices in Tacoma, Wash. and has had type 1 diabetes since 1968.

References

  1. Saaddine JB, Honeycutt AA, Narayan KM, et al. Projection of diabetic retinopathy and other major eye diseases among people with diabetes mellitus: United States, 2005-2050. Arch Ophthalmol. 2008 Dec;126(12):1740-7.
  2. Grundy SM. Metabolic syndrome pandemic. Arterioscler Thromb Vasc Biol. 2008 Apr;28(4):629-36.
  3. Ari S, Keklíkçí U, Caça I. Wolfram syndrome: case report and review of the literature. Compr Ther. 2007 Spring;33(1):18-20.
  4. Pang TT, Narendran P.Addressing insulin resistance in Type 1 diabetes. Diabet Med. 2008 Sep;25(9):1015-24.
  5. Tsui H, Winer S, Chan Y, et al. Islet glia, neurons, and beta cells. Ann N Y Acad Sci. 2008 Dec;1150:32-42.
  6. Holick MF. Diabetes and the vitamin D connection. Curr Diab Rep. 2008 Oct;8(5):393-8.
  7. Bener A, Alsaied A, Al-Ali M, et al. High prevalence of vitamin D deficiency in type 1 diabetes mellitus and healthy children. Acta Diabetol. 2008 Oct 10. [Epub ahead of print]
  8. Goldfarb MF. Relation of time of introduction of cow milk protein to an infant and risk of type-1 diabetes mellitus. J Proteome Res. 2008 May;7(5):2165-7.
  9. MacFarlane AJ, Burghardt KM, Kelly J, et al. A type 1 diabetes related protein from wheat (Triticum aestivum). cDNA clone of a wheat storage globulin, Glb1, linked to islet damage. J Biol Chem. 2003 Jan 3;278(1):54-63.
  10. Type 1 Diabetes May Be Related to Meat Preservative. Diabetes in Control. 2005 Dec;289. Available at: www.diabetesincontrol.com/ results.php?storyarticle=3314 (Accessed July 15, 2009).
  11. Einhorn D, Reaven GM, Cobin RH, et al. American College of Endocrinology position statement on the insulin resistance syndrome. Endocr Pract. 2003 May-Jun;9(3):237-52.
  12. He J, Klag MJ, Caballero B, et al. Plasma insulin levels and incidence of hypertension in African Americans and whites. Arch Intern Med. 1999 Mar 8;159(5):498-503.
  13. Pollak M. Insulin, insulin-like growth factors and neoplasia. Best Pract Res Clin Endocrinol Metab. 2008 Aug;22(4):625-38.
  14. Lupi R, Del Prato S. Betacell apoptosis in type 2 diabetes: quantitative and functional consequences. Diabetes Metab. 2008 Feb;34 Suppl 2:S56-64.
  15. Koopman RJ, Mainous AG 3rd, Diaz VA, Geesey ME. Changes in age at diagnosis of type 2 diabetes mellitus in the United States, 1988 to 2000. Ann Fam Med. 2005 Jan-Feb;3(1):60-3.
  16. The United States Centers for Disease Control and Prevention. National diabetes fact sheet: general information and national estimates on diabetes in the United States, 2007. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 2008.
  17. Duron E, Hanon O.Vascular risk factors, cognitive decline, and dementia. Vasc Health Risk Manag. 2008 Feb;4(2):363-81.
  18. Hjartåker A, Langseth H, Weiderpass E. Obesity and diabetes epidemics: cancer repercussions. Adv Exp Med Biol. 2008;630:72-93.
  19. Gunter MJ, Hoover DR, Yu H, et al. Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst. 2009 Jan 7;101(1):48-60.
  20. Lioté F, Orcel P. Osteoarticular disorders of endocrine origin. Baillieres Best Pract Res Clin Rheumatol. 2000 Jun;14(2):251-76.
  21. Golden SH. A review of the evidence for a neuroendocrine link between stress, depression and diabetes mellitus. Curr Diabetes Rev. 2007 Nov;3(4):252-9.
  22. Lamster IB, Lalla E, Borgnakke WS, et al. The relationship between oral health and diabetes mellitus. J Am Dent Assoc. 2008 Oct;139 Suppl:19S-24S.
  23. Spollett GR. Diabetic neuropathies: diagnosis and treatment. Nurs Clin North Am. 2006 Dec;41(4):697-717, ix.
  24. Atassi MZ, Casali P. Molecular mechanisms of autoimmunity. Autoimmunity. 2008 Mar;41(2):123-32.
  25. Boyle PJ. Diabetes mellitus and macrovascular disease: mechanisms and mediators.Am J Med. 2007 Sep;120(9 Suppl 2):S12-7.
  26. Juutilainen A, Lehto S, Rönnemaa T, et al. Retinopathy predicts cardiovascular mortality in type 2 diabetic men and women. Diabetes Care. 2007 Feb;30(2):292-9.
  27. Van Hecke MV, Dekker JM. Diabetic retinopathy is associated with mortality and cardiovascular disease incidence: the EURODIAB prospective complications study. EURODIAB prospective complications study. Diabetes Care. 2005 Jun;28(6):1383-9.
  28. Brownlee M. Biochemistry and molecular cell biology of diabetic complications.Nature. 2001 Dec 13;414(6865):813-20.
  29. American Diabetes Association. Standards of medical care in diabetes—2009. Diabetes Care. 2009 Jan;32 Suppl 1:S13-61.
  30. Rodbard HW, Blonde L, Braithwaite SS, et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the management of diabetes mellitus. Endocr Pract. 2007 May-Jun;13 Suppl 1:1-68.
  31. American Diabetes Association. Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care. 2008 Jan;31 Suppl 1:S61-78.
  32. Cundiff DK, Nigg CR. Diet and diabetic retinopathy: insights from the Diabetes Control and Complications Trial (DCCT). MedGenMed. 2005 Jan 6;7(1):3.
  33. Bernstein RK. The Diabetes Diet. Little, Brown and Company, New York, 2005:12-9.
  34. Chiu CJ, Milton RC, Klein R, et al. Dietary carbohydrate and the progression of age-related macular degeneration: a prospective study from the Age-Related Eye Disease Study. Am J Clin Nutr. 2007 Oct;86(4):1210-8.
  35. Juvenile Diabetes Research Foundation Continuous Glucose Monitoring Study Group. Continuous glucose monitoring and intensive treatment of type 1 diabetes. N Engl J Med. 2008 Oct 2;359(14):1464-76.
  36. Holman RR, Paul SK, Bethel MA, et al. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med. 2008 Oct 9;359(15):1577-89.
  37. Vijan S, Hofer TP, Hayward RA. Estimated benefits of glycemic control in microvascular complications in type 2 diabetes. Ann Intern Med. 1997 Nov 1;127(9):788-95.
  38. Ostchega Y, Dillon CF. Trends in hypertension prevalence, awareness, treatment, and control in older U.S. adults: data from the National Health and Nutrition Examination Survey 1988 to 2004. J Am Geriatr Soc. 2007 Jul;55(7):1056-65.
  39. Mauer M, Zinman B, Gardiner R, et al. Renal and retinal effects of enalapril and losartan in type 1 diabetes. N Engl J Med. 2009 Jul 2;361(1):40-51.
  40. Nesto RW. Beyond low-density lipoprotein: addressing the atherogenic lipid triad in type 2 diabetes mellitus and the metabolic syndrome. Am J Cardiovasc Drugs. 2005;5(6):379-87.
  41. Johansson K, Neovius K, Desantis SM, et al. Discontinuation due to adverse events in randomized trials of orlistat, sibutramine and rimonabant: a meta-analysis. Obes Rev. 2009 May 12. [Epub ahead of print]
  42. Lloret-Linares C, Greenfield JR, Czernichow S. Effect of weight-reducing agents on glycaemic parameters and progression to Type 2 diabetes: a review. Diabet Med. 2008 Oct;25(10):1142-50.
  43. Mechanick JI, Kushner RF, Sugerman HJ, et al. American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery Medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient. Endocr Pract. 2008 Jul-Aug;14 Suppl 1:1-83.
  44. Ponce J, Haynes B, Paynter S, et al. Effect of Lap-Band-induced weight loss on type 2 diabetes mellitus and hypertension .Obes Surg. 2004 Nov-Dec;14(10):1335-42.
  45. Leitão CB, Cure P, Tharavanij T, et al. Current challenges in islet transplantation. Curr Diab Rep. 2008 Aug;8(4):324-31.
  46. Kobayashi N. Bioartificial pancreas for the treatment of diabetes. Cell Transplant. 2008;17(1-2):11-7.
  47. Pouwer F, Nijpels G, Beekman AT, et al. Fat food for a bad mood. Could we treat and prevent depression in Type 2 diabetes by means of omega-3 polyunsaturated fatty acids? A review of the evidence. Diabet Med. 2005 Nov;22(11):1465-75.
  48. Robinson LE, Buchholz AC, Mazurak VC. Inflammation, obesity, and fatty acid metabolism: influence of n-3 polyunsaturated fatty acids on factors contributing to metabolic syndrome. Appl Physiol Nutr Metab. 2007 Dec;32(6):1008-24.
  49. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.
  50. Danescu LG, Levy S, Levy J. Vitamin D and diabetes mellitus. Endocrine. 2009 Feb;35(1):11-7.
  51. Cashman KD, Hill TR, Lucey AJ, et al. Estimation of the dietary requirement for vitamin D in healthy adults. Am J Clin Nutr. 2008 Dec;88(6):1535-42.
  52. Du X, Edelstein D, Brownlee M. Oral benfotiamine plus alphalipoic acid normalises complication-causing pathways in type 1 diabetes. Diabetologia. 2008 Oct;51(10):1930-2.
  53. Brazionis L, Rowley K, Itsiopoulos C, O’Dea K. Plasma carotenoids and diabetic retinopathy. Br J Nutr. 2009 Feb;101(2):270-7.
  54. Kowluru RA, Kanwar M, Chan PS, Zhang JP. Inhibition of retinopathy and retinal metabolic abnormalities in diabetic rats with AREDS-based micronutrients. Arch Ophthalmol. 2008 Sep;126(9):1266-72.
  55. Schönlau F, Rohdewald P. Pycnogenol for diabetic retinopathy: a review. Int Ophthalmol. 2001;24(3):161-71.
  56. Liu X, Zhou HJ, Rohdewald P. French maritime pine bark extract Pycnogenol dose-dependently lowers glucose in type 2 diabetic patients. Diabetes Care. 2004 Mar;27(3):839.
  57. Yu X, Xu Z, Mi M, et al. Dietary taurine supplementation ameliorates diabetic retinopathy via anti-excitotoxicity of glutamate in streptozotocin-induced Sprague-Dawley rats. Neurochem Res. 2008 Mar;33(3):500-7.
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