Effects of a Ketogenic Diet on Acute Stroke

Acute Stroke Clinical Trial

Official title:

The Effect of a Ketogenic Diet on Blood Glucose, Function and Disease Progress in Acute Stroke Patients

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01997749
• Other study ID #: G-1-2013-012
• Status: Completed
• Phase: Phase 1
• First received: October 28, 2013
• Last updated: July 17, 2014
• Start date: May 2013
• Est. completion date: February 2014

Study information

• Verified date: July 2014
• Source: University of Copenhagen
• Contact: n/a
• Is FDA regulated: No
• Health authority: Denmark: The Danish Ministry of Health
• Study type: Interventional

Clinical Trial Summary

The purpose of this controlled, randomized intervention is to investigate whether a fat-based (ketogenic) diet given for a week has a positive effect on blood sugar, mortality and function in patients hospitalized with acute stroke compared to the effect of a usual diet.

The study hypothesis is that a ketogenic diet and reduced availability of glucose to the brain cells will reduce the volume of neuronal damage in the brain and improve function.

The intervention will take place at the neurological units of Glostrup and Bispebjerg Hospital in Denmark.

Description:

A ketogenic diet can induce ketosis after a period of 2-3 days and offer the brain an alternative energy substrate to glucose in the form of ketone bodies. Feeding the brain ketone bodies can potentially benefit a stroke patient's brain in several ways:

Stroke is characterized by impaired blood and oxygen supply to brain cells. This can cause glucose to convert to lactate which is toxic for the brain. Decreasing glucose availability to brain cells may thus potentially decrease the area of damage in the ischemic penumbra (perifephery of the stroke). Compared with sugar, burning ketone bodies requires less oxygen to produce the same amount of energy, suggesting that brain cells could have a potential greater chance of surviving during circumstances of reduced oxygen supply. By decreasing mitochondria activity, ROS synthesis is also decreased, which can help decrease the necrotic area around the ischemic penumbra. Furthermore, the ketogenic diet does not induce an increase in blood sugar which could be an advantage since many stroke patients are admitted with hyperglycemia associated with a worse outcome.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 64
• Est. completion date: February 2014
• Est. primary completion date: December 2013
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• Patients with ischemic or hemorrhagic stroke.

• NIHSS score of at least 5.

• Both primary and recurrent cases.

• Inclusion as early as possible, but no later than 72 hours from symptom onset.

• Patients with expected hospitalization for a minimum of seven days.

• Adult patients with cognitive ability to give informed consent.

• Patients with writing and orally accepted participation.

Exclusion Criteria:

• Patients with SAH and traumatic hematoma.

• Patients with pancreatic insufficiency (steatorrhea).

• Patients unable to give informed consent.

Study Design

Allocation: Randomized, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Treatment

Related Conditions & MeSH terms

• Acute Stroke
• Stroke

Intervention

Dietary Supplement:
• Ketocal 4:1 (Nutricia)

• Control diet: Regular diet offered at the hospitals

• Ketogenic meals

Locations

Country	Name	City	State
Denmark	Glostrup Hospital	Glostrup	Copenhagen

Sponsors (3)

Lead Sponsor	Collaborator
University of Copenhagen	Bispebjerg Hospital, Glostrup University Hospital, Copenhagen

Country where clinical trial is conducted

Denmark, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Change from baseline NIHSS (national institute of health stroke scale) at 90 days	NIHSS is a common stroke scale used to objectively quantify the impairment caused by a stroke	Baseline and 90 days	No
Primary	Change from baseline fasting blood sugar at 7 days		Baseline and 7 days	No
Primary	Change from baseline p-C-peptide at 7 days		Baseline and 7 days	No
Secondary	Change from baseline p-triglyceride (fasting) at 7 days		Baseline and 7 days	Yes
Secondary	Change from baseline p-LDL at 7 days		Baseline and 7 days	Yes
Secondary	Change from baseline p-CRP at 7 days		Baseline and 7 days	No
Secondary	Change from baseline p-beta-hydroxy butyrate at 7 days		Baseline and 7 days	No
Secondary	Change from baseline p-phosphate at 7 days		Baseline and 7 days	No
Secondary	Change from baseline p-potassium at 7 days		Baseline and 7 days	No
Secondary	Change from baseline p-ALAT at 7 days		Baseline and 7 days	Yes
Secondary	Change from baseline p-alkaline phosphatase at 7 days		baseline and 7 days	Yes
Secondary	Change from baseline p-bilirubine at 7 days		baseline and 7 days	Yes
Secondary	Change from baseline INR at 7 days		baseline and 7 days	Yes
Secondary	Number of patients who died (mortality)		up to 3 months	No
Secondary	Number of patients with pneunomia		Up to one week	Yes
Secondary	Number of patients with gastrointestinal complications	Gastrointestinal complications monitored daily are: Nausea, Vomiting, Constipation, Diarrhea, Abdominal pain	Up to one week	Yes
Secondary	Change from baseline urine-ketones at 7 days		Baseline and 7 days	No