Can the Keto Diet Affect PET Imaging of the Brain?

A new retrospective study shows that increased blood ketone levels due to a ketogenic diet suppress the uptake of ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) on positron emission tomography (PET) imaging of the brain.

For the study, recently published in the European Journal of Hybrid Imaging, researchers reviewed data from 52 patients who had ¹⁸F-FDG PET for evaluation of suspected intracardiac infection or cardiac sarcoidosis. Prior to PET imaging, all patients were asked to follow a prescribed ketogenic diet for 48 hours and subsequently fast for 18 hours prior to PET imaging, according to the study.

The patient cohort included 12 patients with type 2 diabetes who were asked to withhold subcutaneous insulin and oral hypoglycemic medications during the fasting period. The researchers added that one patient with type 1 diabetes, after consulting with an endocrinologist about the ketogenic diet, was asked to withhold insulin for four hours prior to injection of ¹⁸F-FDG.

The researchers found that for the entire brain, each 1 mmol/L increase in serum ketones resulted in a decrease of 0.91 standardized uptake value based on body weight (SUVbw) for ¹⁸F-FDG. The study authors noted an increased effect in the precuneus brain region with each 1 mmol/L increase in serum ketones leading to a 1.25 decrease in SUVbw for ¹⁸F-FDG.

In contrast, the study authors noted each 1 mmol/L increase in blood glucose level (BGL) led to an 0.71 SUVbw decrease for ¹⁸F-FDG in the whole brain and a .99 SUVbw decrease for ¹⁸F-FDG in the precuneus.

“ … Increasing serum ketone levels have a suppressive effect on brain ¹⁸F-FDG uptake that is additional to, and independent of, the suppressive effect of BGL,” wrote O.A. Bennett, M.D., who is affiliated with the Department of Nuclear Medicine and Specialized PET Services at the Royal Brisbane and Women’s Hospital in Brisbane, Australia, and colleagues. “ … To the best of our knowledge, this is the first time (suppression of ¹⁸F-FDG brain uptake during ketosis) has been found to have a measurable effect on ¹⁸F-FDG PET scans performed for clinical purposes.”

The researchers suggested this finding may reveal reduced glucose metabolism in the brain caused by the use of ketone bodies as “an alternate energy substrate independent of glucose availability.” Bennett and colleagues also noted that BGL partially masked the effect of ketones in this study, which became more apparent after ascertaining the relationship between ¹⁸F-FDG PET uptake and BGL.

“This complexity may explain why the suppression of brain ¹⁸F-FDG PET uptake due to ketosis has not previously been recognized in clinical scans,” suggested Bennett and colleagues.

In regard to study limitations, the authors acknowledged variability with patient adherence to the ketogenic diet. They also noted the inclusion of 13 patients with diabetes and the possibility of insulin affecting normal ketone response. While the study authors instructed patients to withhold insulin use prior to PET imaging, they conceded that they did not check insulin levels before imaging. Bennett and colleagues also did not ask study participants about possible use of benzodiazepines to help alleviate potential claustrophobia with imaging exams despite the potential of benzodiazepines to reduce uptake of ¹⁸F-fluorodeoxyglucose.