As primary eye care providers, our patients will often ask us what they can do for optimal ocular health. Many times our patients are interested in or are already supplementing with over-the-counter eye vitamins such as PreserVision or Ocuvite. While these antioxidant supplements are an excellent choice for most cases of early to moderate age-related macular degeneration, optometrists today are confronted with a lower hanging fruit known as type 2 diabetes that needs to be addressed among our patients. When patients suffer from obesity or metabolic dysfunction there’s really no way a supplement is going to be as effective as simply addressing the elephant in the room:

Resetting metabolism – the important balance between glucose and insulin

Type 2 diabetes (T2DM) is currently one of the biggest threats to our healthcare system today. According to the American Diabetes Association, someone is diagnosed with diabetes every 21 seconds, affecting 30 million Americans, and sending annual health care costs over $320 billion. From a clinician’s perspective, helping patients optimize ocular and systemic health has become increasingly challenging due to this largely preventable disease. This pertains to us as optometrists since a large portion of all diabetics will develop some form of sight-threatening retinopathy over the course of their lifetime. T2DM (~95% of all diabetes) is the leading cause of new legal blindness in people 20-74 years of age. For optometrists, any and all patient-education measures that aim to prevent/reverse T2DM can be the most effective ways to maintain good ocular health.

Optometrists today have a unique opportunity in healthcare by educating and counseling our patients with diabetes and pre-diabetes (> 1/3 of all Americans, when combined DM/Pre-DM). Most optometrists arguably spend almost twice the amount of time with each of their patients, when compared with new physicians today spending only 8-10 minutes per patient1. No longer is it solely the PCP’s role to educate patients with metabolic disease, there’s simply not enough time in their schedule. Contrary to what we learned about genetic factors playing a primary role in the pathogenesis of T2DM, new research shows that behavioral and environmental factors may play a significantly larger role in chronic disease than we once thought2. At the 2017 American Academy of Optometry meeting in Chicago, several lecturers emphasized the important role optometrists play in educating and encouraging lifestyle change for our patients, preventing diabetic complications, saving healthcare dollars, and avoiding subsequent trips to the retina specialist.

Since we are primarily optometrists and not nutrition/lifestyle coaches, we’re fortunate to have a plethora of resources to help encourage our patients. Some of these evidence-based lifestyle/behavioral interventions may seem contradictory to mainstream advice, or even downright fringe. However, optometrists today can no longer afford to sit on the sidelines in the midst of this growing epidemic. As always, we must advocate the importance of close medical supervision whenever implementing dietary/lifestyle changes, especially when modifying oral hypoglycemic medications or insulin dosages.

Here are several strategies we can discuss with our patients with diabetes or metabolic syndrome:

Paleolithic/Ancestral Diet [3-6]

We’ve all heard the term “paleo”, and think it may just be the next passing health craze or fad diet out there. However, when we zoom out and look at things from an evolutionary perspective (or think back to metabolism from biology class), it’s easy to see how an ancestral approach to simply eating real food makes the most sense for glucose homeostasis and metabolic control. Basically, if it comes in a bag or a box, the paleo community is not interested in it. Grains and refined sugars are also eliminated. For those with pre-diabetes, metabolic syndrome or obesity, at a minimum, we can mention the Whole-30 program and give them a copy of the program details/shopping list. “This program simply guides you in spending the next 30 days eating only foods that don’t initiate wild blood sugar/insulin excursions”.

https://whole30.com/pdf-downloads/

By definition, if a patient is diabetic, or has pre-diabetes/metabolic syndrome, they’re intolerant to excessive carbohydrate and sugar consumption. Unless the patient is training for a marathon, there’s a good chance they can limit (< 15g/meal) or completely remove carbohydrates from their diet altogether until optimal glucose homeostasis is obtained (fasting/post-prandial glucose levels <100mg/dL). When a patient’s Hemoglobin A1c exceeds 6.0%, the pancreas has already thrown up the white flag, exhausted from insulin over-production (and subsequent insulin resistance).

While many patients will claim they’ve tried this type of dietary approach, the towel is thrown in rather quickly after frequent hunger spells set in (typically a failure to increase healthy and satiating fat consumption). This is primarily due to the longstanding/outdated dogma that saturated fat and cholesterol consumption are the culprits for much of today’s chronic disease. This ideology has been disproven countless times over the past decade[8-9], yet still creates widespread confusion among patients, physicians, and dieticians alike. In fact, recent research has shown that excessive carbohydrate consumption (not saturated fat) may be the more significant risk factor for cardiovascular disease and all-cause mortality7. More often than not, patients with metabolic disease are typically put on some form of a counting-type diet, whether its calories or carbohydrates or both, which can be daunting, confusing, or stressful for some patients (and ignores the insulinogenic effect of various food choices).

•Short-term/Intermittent Fasting

For motivated patients with T2DM, we can also mention the implementation of intermittent fasting (IF). Some great resources on this topic are available through nephrologist Dr. Jason Fung at Intensive Dietary Management, his new podcast “The Obesity Code”, or his 2016 book “The Complete Guide to Fasting”.

https://idmprogram.com

IF can be implemented in a variety of ways, from simply skipping breakfast (~16 hours fast) to alternate day fasting (24 hours fast) or even longer periods of several days. This approach was commonly used over a century ago in the pre-insulin days by many doctors, including Elliot Joslin, MD to optimize health and longevity in diabetic patients. Dr. Joslin (Joslin Diabetes Center in Boston) was one of the first specialists in diabetes in the U.S. during the late 1800’s.

The old dietary paradigm of “calories in – calories out”, “move more – eat less” and “portion control” may be effective for some patients (in the short term). However, there’s a reason many of the “Biggest Losers” have difficulty maintaining their results after the season is through. Each of these approaches fails to fully address the underlying cause of metabolic disease. The root cause of type 2 diabetes in most cases is an excessive level of circulating insulin, causing insulin resistance (at the liver, fat and muscle tissue), high blood sugars, and an abnormal leptin response (a satiety hormone).

Understanding insulin’s key role in metabolism provides clarification as to why people who restrict calories are often more hungry than people who fast, or who eat a higher fat diet (two ways to keep insulin nearly flat-lined).

•Extending Fasting and the High Fat/Low Carb “Ketogenic Diet”

Patients with overt/uncontrolled T2DM can also consider adopting a ketogenic approach to eating (80-90% of total daily calories from healthy fats) in conjunction with fasting to help reduce their excessive circulating insulin levels.

Virta Health, a new company out of Silicon Valley has a lofty mission statement of reversing T2DM in 100 million people over the next decade. They incorporate a telemedicine approach to supervised-intermittent fasting and a ketogenic diet. Their first published 10-week study in 2017 demonstrated a significant impact on reducing body mass, blood glucose/insulin, blood pressure, HbA1c, and reducing the number of oral hypoglycemic medications that patients required.

http://diabetes.jmir.org/2017/1/e5/

https://www.virtahealth.com/

Aside from retinopathy and increased risk of retinal detachment, we know diabetics are also more likely to develop cataracts, cranial nerve palsies, vascular occlusion, ocular hypertension[10-11], and glaucoma[12-17]. Patients with diabetic eye disease, of any level, are twice as likely to suffer from stroke, heart failure, and cardiovascular death[18]. The level and severity of retinopathy is also an accurate predictor of other systemic and neurological ailments including kidney disease, cognitive decline, and dementia[19].

While optometrists are not trained to be endocrinologists or dieticians, OD’s are still being called from the sidelines to promote healthy lifestyle change in their patients with metabolic disease and T2DM. The literature has repeatedly shown us that simple pharmacologic reduction in blood sugar does not solve the underlying issue of excessive insulin levels, and in fact increases the risk of all-cause mortality[20-22] (ACCORD/Advance Trials).

Not all of our patients are receptive or ready for abrupt lifestyle modification, and that is OK. As OD’s, we still have a unique opportunity to educate and encourage these patients to take back their health. As long as we continue to see patients with irreversible end-organ damage (diabetic retinopathy, tractional retinal detachment or neovascular glaucoma), we’re no longer able to say it’s solely the PCP/dietician’s role to discuss lifestyle change and metabolic control. As integral players in the healthcare system, OD’s can help to intervene and drastically reduce the number of patients developing permanent vision loss from this largely preventable disease process we know as type 2 diabetes.


References

  1. Block, L., Habicht, R., Wu, A. W., Desai, S. V., Wang, K., Silva, K. N., … Feldman, L. (2013). In the Wake of the 2003 and 2011 Duty Hours Regulations, How Do Internal Medicine Interns Spend Their Time? Journal of General Internal Medicine, 28(8), 1042–1047. http://doi.org/10.1007/s11606-013-2376-6
  2. Rappaport, Stephen M. “Genetic Factors Are Not the Major Causes of Chronic Diseases.” PLOS ONE, Public Library of Science, 22 Apr. 2016, doi.org/10.1371/journal.pone.0154387
  3. Jönsson, Tommy et al. “Beneficial Effects of a Paleolithic Diet on Cardiovascular Risk Factors in Type 2 Diabetes: A Randomized Cross-over Pilot Study.” Cardiovascular Diabetology 8 (2009): 35. PMC. Web. 4 Dec. 2017.
  4. Ryberg, M, et al. “A Palaeolithic-type diet causes strong tissue-specific effects on ectopic fat deposition in obese postmenopausal women.” Journal of internal medicine., U.S. National Library of Medicine, July 2013, www.ncbi.nlm.nih.gov/pubmed/23414424.
  5. Saslow, Laura R., et al. “A Randomized Pilot Trial of a Moderate Carbohydrate Diet Compared to a Very Low Carbohydrate Diet in Overweight or Obese Individuals with Type 2 Diabetes Mellitus or Prediabetes.” PLOS ONE, Public Library of Science, 9 Apr. 2014, journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0091027.
  6. Esposito, Katherine. “Effects of a Mediterranean-Style Diet on the Need for Antihyperglycemic Drug Therapy in Patients With Newly Diagnosed Type 2 Diabetes.” Annals of Internal Medicine Ann Intern Med 151.5 (2009): 306. Web.
  7. Dehghan, M, et al. “Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study.” Lancet (London, England)., U.S. National Library of Medicine, 4 Nov. 2017, www.ncbi.nlm.nih.gov/pubmed/28864332.
  8. Siri-Tarino, Patty W et al. “Meta-Analysis of Prospective Cohort Studies Evaluating the Association of Saturated Fat with Cardiovascular Disease.” The American Journal of Clinical Nutrition 91.3 (2010): 535–546. PMC. Web. 4 Dec. 2017.
  9. Nettleton, Joyce A., et al. “Saturated Fat Consumption and Risk of Coronary Heart Disease and Ischemic Stroke: A Science Update.” Annals of Nutrition and Metabolism, Karger Publishers, 27 Jan. 2017, www.karger.com/Article/FullText/455681.
  10. Chang, Y. C., Lin, J., Wang, L. C., Chen, H. M., Hwang, J. J., & Chuang, L. M. (2009). Association of intraocular pressure with the metabolic syndrome and novel cardiometabolic risk factors. Eye, 24(6), 1037-1043. doi:10.1038/eye.2009.247
  11. Sato, Tsuyoshi, and Sayon Roy. “IOVS | Effect of High Glucose on Fibronectin Expression and Cell Proliferation in Trabecular Meshwork Cells.” IOVS | Effect of High Glucose on Fibronectin Expression and Cell Proliferation in Trabecular Meshwork Cells. Investigative Ophthalmology and Vision Science, 5 May 2001. Web. 02 Mar. 2016.
  12. Lin I-C, Wang Y-H, Wang T-J, et al. Correction: Glaucoma, Alzheimer’s Disease, and Parkinson’s Disease: An 8-Year Population-Based Follow-Up Study. PLoS ONE. 2016;11(3):e0150789. doi:10.1371/journal.pone.0150789.
  13. Zhou M, Wang W, Huang W, Zhang X. Diabetes Mellitus as a Risk Factor for Open-Angle Glaucoma: A Systematic Review and Meta-Analysis. Vavvas D, ed. PLoS ONE. 2014;9(8):e102972. doi:10.1371/journal.pone.0102972.
  14. Zhao, Di, Juhee Cho, Myung Kim, and David Friedman. “Diabetes, Glucose Metabolism, and Glaucoma: The 2005-2008 National Health and Nutrition Examination Survey.” PLoS One Open Access Journal. PLoS One, 13 Nov. 2014. Web. 28 Feb. 2016
  15. Lonneville, Yıldız H., şengül C. özdek, Merih önol, &idot;lhan Yetkin, Gökhan Gürelik, and Berati Hasanreisoğlu. “The Effect of Blood Glucose Regulation on Retinal Nerve Fiber Layer Thickness in Diabetic Patients.” Ophthalmologica 217.5 (2003): 347-50. Web. 2 Mar. 2016.
  16. Lopes de Faria JM, Russ H, Costa VP. Retinal nerve fibre layer loss in patients with type 1 diabetes mellitus without retinopathy. The British Journal of Ophthalmology. 2002;86(7):725-728.
  17. Barber, A. J., E. Lieth, S. A. Khin, D. A. Antonetti, A. G. Buchanan, and T. W. Gardner. “Neural Apoptosis in the Retina during Experimental and Human Diabetes. Early Onset and Effect of Insulin.” Journal of Clinical Investigation J. Clin. Invest. 102.4 (1998): 783-91. Web. 2 Mar. 2016.
  18. Mottl, Amy K. et al. “The Degree of Retinopathy Is Equally Predictive for Renal and Macrovascular Outcomes in the ACCORD Trial.” Journal of diabetes and its complications 28.6 (2014): 874–879. PMC. Web. 4 Dec. 2017.
  19. Exalto, Lieza G. et al. “Severe Diabetic Retinal Disease and Dementia Risk in Type 2 Diabetes.” Journal of Alzheimer’s disease : JAD 42.0 3 (2014): S109–S117. PMC. Web. 4 Dec. 2017.
  20. Dluhy, Robert G., and Graham T. McMahon. “Intensive Glycemic Control in the ACCORD and ADVANCE Trials — NEJM.” New England Journal of Medicine, 12 June 2008, www.nejm.org/doi/full/10.1056/NEJMe0804182#t=article.
  21. “Effects of Intensive Glucose Lowering in Type 2 Diabetes — NEJM.” New England Journal of Medicine, The Action to Control Cardiovascular Risk in Diabetes Study Group, 12 June 2008, www.nejm.org/doi/full/10.1056/NEJMoa0802743#t=article.
  22. Zoe Arvanitakis, Robert S. Wilson, Julia L. Bienias, Denis A. Evans, David A. Bennett. Diabetes Mellitus and Risk of Alzheimer Disease and Decline in Cognitive Function. Arch Neurol. 2004;61(5):661–666. doi:10.1001/archneur.61.5.661

[/restrict]