Conference Coverage

Case builds for counting fat, protein alongside carbs in T1DM

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It's not just about the carbs

At the American Diabetes Association scientific sessions, two studies were presented in adolescents with type 1 diabetes that show that postmeal glucose excursions were influenced by more than carbohydrates.

In adolescents with type 1 diabetes, higher fat and protein intake contributed to the rise in postmeal glucose levels using a continual glucose monitoring system, with less hypoglycemia after a higher-protein meal. Suggestions included using a dual wave bolus in pump patients before they eat a high fat meal or developing a new way besides carbohydrate counting to guesstimate insulin bolus requirements.

Similar in concept to the glycemic index, the food insulin demand (FID) is an algorithm for ranking foods based on their insulin demand and portion size relative to a reference food, and it takes into consideration protein intake.

It's likely that calculation of premeal insulin needs will consider a variety of factors to decrease the glucose excursions throughout the day: total food composition (carbohydrate, fat, and protein content) of anticipated meal, portion size, timing of when to bolus, adjustments for the premeal level of glucose (currently called the "correction factor"), anticipated exercise and stress post meal.

In other words, we have a long way to go to accurately predict glucose excursions and anticipate insulin requirements.

Dr. Jay Cohen is medical director of the Endocrine Clinic, Memphis, Tenn. He said that he had no financial disclosures relevant to this article.


 

AT THE ADA ANNUAL SCIENTIFIC SESSIONS

CHICAGO – Meals high in fat or protein cause hyperglycemia among children using intensive insulin therapy for type 1 diabetes, a study has shown.

Further, protein and fat have an additive effect on postprandial glycemic rise, based on results of the randomized study involving 33 children.

"Protein and fat should be considered in prandial insulin dose and distribution," Carmel Smart, Ph.D., reported at the annual scientific sessions of the American Diabetes Association.

In intensive insulin therapy, the mealtime insulin dose is calculated based exclusively on counting carbohydrates. A growing body of evidence, however, suggests that macronutrients other than carbohydrates influence postprandial glucose levels and insulin requirements, said Dr. Smart, a specialist diabetes dietitian at the John Hunter Children’s Hospital, Newcastle, Australia.

Patrice Wendling/IMNG Media News

Dr. Carmel Smart

She highlighted a recent study showing that high-fat meals with identical carbohydrate and protein content, required more insulin than low-fat meals and, despite the additional insulin, caused more hyperglycemia in type 1 diabetics (Diabetes Care 2013;36:810-6). An early study reported that meals with added protein significantly increased late glucose responses and insulin requirements, compared with standard or fat-added meals (Am. J. Clin. Nutr. 1993;58:555-60).

For the current experiment, 33 children (aged 8-17) ate four test pancake breakfasts on different days with identical carbohydrate content (30 g), but varying protein and fat: low fat (4 g)/low protein (5 g), high fat (35 g)/low protein, low fat/high protein (40 g), and high fat/high protein. A protein supplement and double cream (50% fat) were used to vary the protein and fat content.

The meals were given after the same individually standardized insulin dose, and no activity or snacks were allowed for 5 hours after the meal. Glucose excursions or fluctuations were measured at 30-minute increments for 5 hours using continuous glucose monitoring.

At baseline, the 17 girls and 16 boys had a mean A1c level of 7.2% and a mean duration of diabetes of 4.9 years; 27 were on continuous subcutaneous insulin infusion, and 6 were on a multiple daily insulin regimen. Their average age was 12.2 years.

Compared with the low-protein/low-fat meal, postprandial glucose excursions were significantly greater at 210-300 minutes after the high-fat/low-protein meal (1.78 mmol/L vs. –0.50 mmol/L; P = .01), Dr. Smart said.

Postprandial glucose excursions also were significantly greater at 180 minutes after the high-protein/low-fat meal (2.40 mmol/L vs. 0.54 mmol/L; P = .02).

The high-fat/high-protein meal resulted in significantly higher and sustained glucose excursions from 180 to 300 minutes compared with all the other meals (P less than .04).

The effect of fat and protein was additive at all time points after 150 minutes, she said. Compared with the low-fat/low-protein meal, the average glucose excursion was 4.2 mmol/L greater at 180 minutes after the high-fat/high-protein meal and 5.4 mmol/L greater at 5 hours.

Hypoglycemia, defined by a blood glucose level of less than 3.6 mmol/L, occurred in 29 children in the 5-hour postprandial period, and was significantly different between meal types (P = .003), Dr. Smart said.

There was a significant reduction in hypoglycemia after high-protein meals (odds ratio, 0.16; P less than .0001), but no reduction after high-fat meals (OR, 0.50; P = .08).

While meals high in protein and fat cause hyperglycemia, "our results suggest that protein may have a protective effect on hypoglycemia," she said.

During a discussion of the study, an audience member thanked the investigators for conducting the study "because this is what I’ve been seeing in patients eating high-fat diets, and I haven’t known exactly what to do about their insulin when they aren’t on the pump."

Dr. Smart agreed that they’ve been seeing this phenomenon for a long time, and said clinicians can now have the confidence to tell patients that it’s not inaccurate carbohydrate counting causing the glucose fluctuations, as previously believed. Currently, the investigators are advising patients on pump therapy to use the dual-wave bolus, although novel algorithms to determine prandial glucose dosing are being refined for high-fat/high-protein diets, she added.

A study led by Kirstine Bell, Ph.D., detailing one of those algorithms, called the food insulin index, was presented during the same session, by Dr. Stephen Colagiuri.

The study was supported by grants from Australian Pediatric Endocrine Care and Hunter Children’s Research Foundation. Medtronic provided the glucose-monitoring equipment. Dr. Smart reported having no relevant financial disclosures.

pwendling@frontlinemedcom.com

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