Background. Coconut oil, a saturated fat comprised mostly of the medium-chain fatty acid, lauric acid, has become increasingly popular over the past few decades due to its touted anti-inflammatory, metabolic, and lipid-lowering properties. There have been many studies with mixed results evaluating the effects of coconut oil consumption on lipid metabolism and cardiometabolic risk. However, the effects on glucose metabolism are less clear. There are few trials on the effects of coconut oil on glucose homeostasis but no case reports prior to the current one. Case. We present a case of a 66-year-old man with a history of type 2 diabetes managed with insulin who developed recurrent hypoglycemia and required reduction in insulin therapy quickly after consuming coconut oil supplementation. Conclusion. This is the first known case report of coconut oil supplementation in a diabetic patient on insulin resulting in hypoglycemia. Review of the literature shows that coconut oil supplementation can have a favorable effect on glycemic control, possibly through phenolic compounds mediating anti-inflammatory effects. This effect is inconsistent throughout the studies reviewed, likely due to variations in types of coconut oil supplementation and scarcity of trials. Further research is required both in animal models and in humans before coconut oil intake is widely advised and popularized. This is especially true in patients with diabetes, who are at increased risk of cardiovascular disease, and in whom reduction in saturated fat intake is advised.
The ketogenic diet, which has become an increasingly popular diet, severely restricts carbohydrate intake to shunt metabolism towards fatty acid oxidation and production of ketones as a fuel source. There have been many studies illustrating the positive effects of a ketogenic diet in weight loss and other benefits; however, the long-term effects and potential adverse events of a ketogenic diet have not been well studied or documented in literature. There are a few case reports of ketogenic diet resulting in hypoglycemia. We report a case of hypoglycemia with a blood glucose of 39 mg/dL and ketosis in a 69-year-old woman who strictly followed a ketogenic diet for nearly one year. She presented with malaise, sugar cravings, and mental fogginess, and after intake of alcoholic beverages, was admitted to the hospital with hypoglycemia. She had elevated beta-hydroxybutyrate, and low insulin and C-peptide, all consistent with a starvation ketosis. This case illustrates that adherence to a ketogenic diet for a prolonged period of time, in combination with alcohol intake, can disrupt normal glucose homeostatic mechanisms and result in a significant degree of hypoglycemia. This pattern of hypoglycemia may not present with classic symptoms, most likely partly due to effects of the ketogenic diet on brain function. This case provides insight that supports the need to counsel patients about alcohol intake while on the ketogenic diet. More information is needed on long-term complications of the ketogenic diet on glucose homeostasis in the body as well as in the brain.
Case Description: We present a 27-year-old female with history of Graves’ Disease and post ablative hypothyroidism. She established care in the endocrinology clinic at 17 weeks gestation after screening ultrasound demonstrated fetal goiter and fetal tachycardia. Her labs were significant for Thyrotropin receptor antibody >40.0 (0.00 - 1.75 IU/L). She was transitioned to levothyroxine monotherapy for treatment of her post-ablative hypothyroidism. Methimazole and metoprolol were initiated for treatment of fetal hyperthyroidism. Despite initiation and titration of methimazole, repeat ultrasounds showed increasing fetal goiter. Cordocentesis was pursued at 22 weeks gestation to further guide thioamide therapy. Discussion: Fetal hyperthyroidism is a rare complication of maternal Graves’ Disease, usually presenting at or after 20 weeks gestation. Our patient began to exhibit signs of fetal thyrotoxicosis at 16 weeks gestation. Assessment of fetal response to thioamide therapy relies on fetal heart rate and sometimes cordocentesis, which raises uncertainty in management. Thioamide therapy should be titrated every 1-2 weeks with fetal goal heart rate of 140 beats/min. Serial fetal ultrasounds to assess fetal heart rate, amniotic fluid, and goiter size are recommended to assess for response to treatment. Cordocentesis is considered when fetal thyroid status is uncertain. We present our clinical experience, current recommendations along with recent developments in the field. References: 1. De Groot, Leslie, et al. "Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline." The Journal of Clinical Endocrinology & Metabolism 97.8 (2012): 2543-2565.
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