Category Archives: Diabetes Complications

Physicians in the U.S. who prescribe opioids need a license from the Drug Enforcement Administration and it has to be renewed periodically. By the time of my next renewal, I must be able to prove to the DEA that I’ve had six (eight?) hours of approved continuing medical education on drug abuse and addiction. Because of the prescription opioid “epidemic” that reared its head several years ago, regulators are putting pressure on prescribers to reduce prescriptions. I’m not saying that’s a bad thing, but it can be taken too far, like expecting a patient with very recent knee or hip replacement surgery to be just fine with acetaminophen (aka paracetamol) alone. Big Pharma has convinced some prescribers to substitute opioids with Neurontin (aka gabapentin) or Lyrica (pregabalin). If not substitution, then augmentation of opioid effect at lower doses. I definitely see that in my part of the world.

Regarding that, here’s a thought-provoking article from Paul Ingraham:

One of the most notorious examples of Big Pharma living up to its reputation for evil-doing is the illegal promotion of anticonvulsant drugs like Neurontin and Lyrica for painful problems like back pain. Pfizer coughed up billions for lawsuit settlements and record-breaking fines. I think it’s safe to say that they didn’t actually pay enough to undo the damage, though…

Thanks to that horror show, and to research by Peet et al, we now know that there was a mighty 5× surge in gabapentin prescriptions in the 2000s and 2010s. That was — and continues to be — a chilling demonstration of the power of under-handed and well-funded marketing. Even as opioid prescriptions fell somewhat, gabapentin scrips rose dramatically, despite the dubious value for most of what it was being prescribed for (most kinds of pain).

  Steve Parker, M.D.

PS: Pregabalin and gabapentin are commonly used and often effective drugs for painful diabetic neuropathy in the U.S. This blog post isn’t about that neuropathic pain.

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Diabetes Daily has in important interview with Dr Steven Edelman on hypoglycemia (particularly in type 1 diabetes) and the need for injectable glucacon to treat it. This could easily apply also to type 2 diabetes that’s treated with insulin or other drugs that can cause hypoglycemia. Folks with type 1 diabetes seem to be more prone to hypoglycemia unawareness. That is, the blood sugar is dangerously low, but not recognized or treated promptly, potentially resulting death. Dr Edelman notes that dangerous hypoglycemia has been significantly reduced by the use of continuous glucose monitoring (CGM).

Note that CGM measure glucose levels in the the fluid in between the cells of subcutaneous tissue (AKA interstitial fluid). Your familiar fingerstick glucose is measuring capillary fluid levels. Capillaries are tiny blood vessels at the end of arteries. After going through the capillaries, blood enters veins for the return trip to the lung and heart. Glucose levels in the interstitial fluid and capillaries may not be the same as in the large arteries delivering glucose to the brain. Most CGM devices will provide the user with an alert when the glucose level drops too low, so that remedial action can be taken.

An excerpt from Diabetes Daily:

What are some ways that the CGM can most effectively help avoid hypos?

Well, one of the things I do in clinic is to really check where people set their upper and lower alerts. I had a patient yesterday in clinic who has had type 1 for 60 years. Her A1C is unbelievable, but she does have hypo unawareness and her lower alert was 65. You have to convince people that the extra alerts are worth it to you.

A lot of people said they put their lower alert at 65 and they don’t realize this situation called the “lag time.” So, when your blood sugar is dropping, even if you have a diagonal arrow down compared to, even worse, one arrow down or two arrows down, looking at the Dexcom arrows, they don’t realize that the glucose in your circulation is probably much lower than it appears on the Dexcom monitor or your phone. Because the Dexcom sensor and other sensors too, they measure the glucose in the subcutaneous tissue, and there’s a lag between the subcutaneous tissue and the circulation.

When your Dexcom goes off or when your CGM goes off at 65, and if your trend arrow’s going down, you could be 45 or 40. So that’s really an important issue, especially for people that their symptoms aren’t as obvious anymore. You could be caught off guard. And I had multiple patients that has occurred with. And then unfortunately, as you know, the majority of T1Ds in this country do not wear a CGM and that’s the topic of a whole other story.

Does this lag time issue apply to a regular glucometer as well?

Yes. If your blood sugar is dropping, your meter or CGM may be perfectly accurate of the subcutaneous tissue at 65. If you checked your blood sugar with a meter, it’s still going to say 65, but your circulation that’s going to your brain might be 45. So, the lag time is key. You could have the most accurate meter or CGM in the world, it doesn’t affect the lag time.

Click for my five-year-old article on drugs that can cause diabetes.

Click for my brief article on hypoglycemia unawareness.

Click for my general article on recognition and treatment of hypoglycemia.

Steve Parker, M.D.

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Retinopathy is a fancy word meaning disease of the retina, the light detecting membrane at the back of the eyeball. About two in five folks with diabetes have some form or degree of diabetic retinopathy. The pathology is mostly in the arterial blood vessels of the retina. Keeping blood sugars under good control is one way to prevent diabetic retinopathy. Once diagnosed, it can be treated with injections, lasers, or surgery.

Here’s the abstract from a recent scientific report the looked at the ocular effects of gastric bypass surgery in obese type 2 diabetics. Over the course of 4.5 years, the risk of diabetic retinopathy was 40% less in those who had bypass surgery.

Importance  Knowledge of the incidence and progression of diabetic retinopathy (DR) after gastric bypass surgery (GBP) in patients with obesity and diabetes could guide the management of these patients.

Objective  To investigate the incidence of diabetic ocular complications in patients with type 2 diabetes after GBP compared with the incidence of diabetic ocular complications in a matched cohort of patients with obesity and diabetes who have not undergone GBP.

Design, Setting, and Participants  Data from 2 nationwide registers in Sweden, the Scandinavian Obesity Surgery Registry and the National Diabetes Register, were used for this cohort study. A total of 5321 patients with diabetes from the Scandinavian Obesity Surgery Registry who had undergone GBP from January 1, 2007, to December 31, 2013, were matched with 5321 patients with diabetes from the National Diabetes Register who had not undergone GBP, based on sex, age, body mass index (BMI), and calendar time (2007-2013). Follow-up data were obtained until December 31, 2015. Statistical analysis was performed from October 5, 2018, to September 30, 2019.

Exposure  Gastric bypass surgery.

Main Outcomes and Measures  Incidence of new DR and other diabetic ocular complications.

Results  The study population consisted of 5321 patients who had undergone GBP (3223 women [60.6%]; mean [SD] age, 49.0 [9.5] years) and 5321 matched controls (3395 women [63.8%]; mean [SD] age, 47.1 [11.5] years). Mean (SD) follow-up was 4.5 (1.6) years. The mean (SD) BMI and hemoglobin A_1c concentration at baseline were 42.0 (5.7) and 7.6% (1.5%), respectively, in the GBP group and 40.9 (7.3) and 7.5% (1.5%), respectively, in the control group. The mean (SD) duration of diabetes was 6.8 (6.3) years in the GBP group and 6.4 (6.4) years in the control group. The risk for new DR was reduced in the patients who underwent GBP (hazard ratio, 0.62 [95% CI, 0.49-0.78]; P < .001). The dominant risk factors for development of DR at baseline were diabetes duration, hemoglobin A_1c concentration, use of insulin, glomerular filtration rate, and BMI.

Conclusions and Relevance  This nationwide matched cohort study suggests that there is a reduced risk of developing new DR associated with GBP, and no evidence of an increased risk of developing DR that threatened sight or required treatment.

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Steve Parker, M.D.

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The only picture of stomach I have

When you eat a meal, your stomach holds it there for a while then gradually releases contents into the duodenum, the first part of the small intestine. The stomach makes those releases by contraction of muscles in the wall of the stomach. Those muscles are under control of the autonomic nervous system. In some folks with diabetes, the nerves controlling the stomach muscles don’t work very well, so stomach contractions are weak. Food just sits in the stomach for too long, delaying digestion and absorption of nutrients. One result is unpredictable blood sugar levels after meals, no matter how carefully you count carb grams. The medical term for these weak stomach contractions is gastroparesis.

From Diabetes Care:

“How is diabetic gastroparesis best managed?

Consultation by an RDN [registered dietitian, I reckon] knowledgeable in the management of gastroparesis is helpful in setting and maintaining treatment goals. Treatment goals include managing and reducing symptoms; correcting fluid, electrolyte, and nutritional deficiencies and glycemic imbalances; and addressing the precipitating cause(s) with appropriate drug therapy. Correcting hyperglycemia is one strategy for the management of gastroparesis, as acute hyperglycemia delays gastric emptying. Modification of food and beverage intake is the primary management strategy, especially among individuals with mild symptoms.

People with gastroparesis may find it helpful to eat small, frequent meals. Replacing solid food with a greater proportion of liquid calories to meet individualized nutrition requirements may be helpful because consuming solid food in large volumes is associated with longer gastric emptying times. Large meals can also decrease the lower esophageal sphincter pressure, which may cause gastric reflux [heartburn], providing further aggravation.

Results from a randomized controlled trial demonstrated eating plans that emphasize small-particle-size (<2 mm) foods may reduce severity of gastrointestinal symptoms. Small-particle-size food is defined as “food easy to mash with a fork into small particle size.” High-fiber foods, such as whole intact grains and foods with seeds, husks, stringy fibers, and membranes, should be excluded from the eating plan. Many of the foods typically recommended for people with diabetes, such as leafy green salads, raw vegetables, beans, and fresh fruits, and other food like fatty or tough meat, can be some of the most difficult foods for the gastroparetic stomach to grind and empty. Notably, the majority of nutrition therapy interventions for gastroparesis are based on the knowledge of the pathophysiology and clinical judgment rather than empirical research.”

Source: Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report | Diabetes Care

Steve Parker, M.D.

PS: In my current practice setting, I see more gastroparesis caused by chronic opioid use than by diabetes.

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