HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Correspondence to:

BRIEF COMMUNICATIONS: T. B. VanItallie, C. Nonas, A. Di Rocco, K. Boyar, K. Hyams, and S. B. Heymsfield Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study Neurology 2005; 64: 728-730 [Abstract] [Full text] [PDF]

Correspondence: Submit a response to this article

Correspondence published:

Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study

Mazen G. Jabre, Boulos-Paul W Bejjani   (27 June 2005)

Reply to Jabre et al

Ted VanItallie   (27 June 2005)

Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study 27 June 2005
Mazen G. Jabre, Parkinson, Memory & Movement Disorders Center Notre Dame des Secours Hospital, Byblos/Jbeil-Lebanon, Boulos-Paul W Bejjani Send Correspondence to journal: Re: Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study parkin{at}terra.net.lb Mazen G. Jabre, et al.	VanItallie et al shed light on an underestimated therapeutic approach in the management of Parkinson disease (PD) based on diet modulation. [1] In their article, five patients at mild and advanced disease stages responded to a hyperketogenic diet (HKD) with a marked improvement of general motor disability. Authors were cautious, taking into consideration the small number of patients, the lack of a control group, as well as the possible placebo effect. We agree with authors’ concerns but question the applicability of and compliance with such a complex diet in a naturalistic setting, even if there is firm evidence of HDK safety and efficacy in PD patients. Alternatively, the five reported PD patients were either overweight or obese had a body-mass index range of 28.4 to 35.9 kg/m². Losing body weight (mean, 6.1 kg; range 4.1-9.5 kg) was found to alter levodopa pharmacokinetics and led to an increase in levodopa cumulative dosage per kilogram of body weight. [2] Moreover, a greater levodopa bioavailability and brain level would be reached using a very low-protein diet. [3] At a lower body weight and under tight protein restriction, the same oral levodopa dose that patients used to take when they were heavier or on regular diet, would lead to higher systemic levels. We therefore expect an ensuing heightened efficacy on parkinsonian symptoms and motor fluctuations and,at times, a putatively dyskinesogenic effect, as to require dosage reduction. References 1.VanItallie TB, Nonas C, Di Rocco A, Boyar K, Hyams K, Heymsfield SB. Treatment of Parkinson’s disease with diet-induced hyperketonemia: A feasibility study. Neurology 2005; 64: 728-730. 2.Zappia M, Crescibene L, Arabia G, Nicoletti G, Bagala A, Bastone L, Caracciolo M, Bonavita S, Di Costanzo A, Scornaienchi M, Gambardella A, Quattrone A. Body weight influences pharmacokinetics of levodopa in Parkinson's disease. Clin Neuropharmacol 2002; 25: 79-82. 3.Pincus JH, Barry KM. Plasma levels of amino acids correlate with motor fluctuations in parkinsonism. Arch Neurol 1987; 44:1006-1009. The authors report no conflicts of interest.
Reply to Jabre et al 27 June 2005
Ted VanItallie, Columbia University PO Box 775 Boca Grande, FL 33921-0775 Send Correspondence to journal: Re: Reply to Jabre et al tedvani{at}ewol.com Ted VanItallie	We thank Jabre et al for their comments. The enhancing effect of weight loss on levodopa efficacy is well taken. Weight loss could well have contributed to the improvement exhibited by our patients. However, one of the patients who improved was not on any anti-Parkinson medication. Ketone esters for oral administration should become available for clinical trial in a year or two. Use of such preparations to induce hyperketonemia in patients with PD should help us determine whether it is hyperketonemia or some other attribute of the hyperketogenic diet that is responsible for the type of clinical improvement we observed.