About urine vs blood measurement of ketones and monitoring of/finetuning on glucose
FYI: Nobody in Holland uses urine dipsticks anymore for ketone measurement, urine dipsticks were used 10+ years ago but blood measurement is preferred because of the different types of ketone bodies measured by both methods, urine measurement is proven to be inadequate for reliable results and finetuning the diet.
Carl E. Stafstrom et. all wrote why in his 'keto bible' (Epilepsy and the ketogenic diet, 2004):
"Children with blood beta-hydroxybutyrate levels greater than 4 mmol/L were significantly more likely to have a decrease in seizure frequency than those with levels less than 4 mmol/L.
Urine ketones of 4+ (160 mmol/L) were found on dipstick when blood beta-hydroxybutyrate levels exceeded 2 mmol/L.
Seizure control correlates with blood beta-hydroxybutyrate levels and is more likely when blood beta-hydroxybutyrate levels are greater than 4 mmol/L.
The traditional measurement of urine ketones by dipsticks in children on the ketogenic diet provides a less than optimal assessment of the degree of blood ketosis. Three to four plus (80-160 mmol/L) urine ketones are necessary, but not necessarily sufficient, to achieve optimal seizure control in children on the ketogenic diet."
We've seen a deep purple colour (darkest colour = highest ketone level a dipstick can measure) on a urine dipstick when we tested fresh pied urine during changing diapers, while fresh blood measurement showed just 1.9 (= far too low) mmol blood ketones! So the urine measurement had a result which seemed fine while blood measurement showed insufficient ketosis.
A mom on the Matthews Friends forum wrote this:
D. had lunch at midday then a nap urinary ketones on waking just about a 1.5mmol/L. I haven't done a blood ketone reading for a long time so decided to give it a go and check id D's ketones were really that low and should I be reducing the carbs for her dinner. The blood reading was 7.5 mmol/L !!!!!
And I've read and heared many similar experiences.
Because other types of ketones are measured by both methods, the results are simply not comparable.
Blood fingerprick ketone testing is a safer way to go as by testing blood levels you bypass the complications of any fluids drunk during the day diluting the results, and also with urine sitting in the bladder for extended periods giving results that are not current. (Eg - a urine reading of '8' in the morning (if the child is continent overnight) may be because the bedtime urine levels had been 16 or above, waking levels say 2-4, so the 'average' in the bladder contents comes out as an 8 or thereabouts - giving a false impression that the level overnight/early morning is probably high enough to prevent seizure breakthroughs.
The Dutch Protocol for treatment of epilepsy and metabolic diseases with the ketogenic diet is based on blood testing since this was discovered.
About glucose monitoring:
Adequate ketone
and glucose measurement both are crucial for finetuning the diet to establish seizure control:
When glucose goes above a certain level, the body/brain will preferentially use it as nourishment/fuel in preference to ketones, however deep the level of ketosis is at the time. If using ketones rather than glucose is helping with seizure control, then every time the situation occurs where the glucose goes too high for the ketones to be used as the first fuel alternative, breakthrough seizures can occur.
Higher than optimum glucose levels can occur on keto in times of illness/stress (including seizure activity),or when the ratio or calories are too high, or conversely, when calories are too low. This is because the body will go searching for nourishment from muscle tissue (gluceogenesis) which is a glucose producing process.
Dietitian Carrie Loughran reports a trend of parents reporting glucose 3-3.6 mmol/l associated with greater seizure control (this is slightly higher for more active kids.)
In her experience with fine tuning she suggests you look at two glucose readings
1. Morning (fasting) glucose which should be about a 3 (any less and more carbs/cals needed). To fine tune this adjust the total calories.
2. Evening (post meals) glucose which should be 3.6 or 4.2 for an active kid. To adjust this she suggests tweaking the ratio.
Ideal goal: glucose 3.0-4.2 mmol/L [55-75] AM/PM
Manipulate calories to attain AM goal.
Manipulate ratio to get PM levels correct.
In Stafstrom et al. (1994):
"(...) However, these investigators found out that simply restricting calories had as robust an effect of seizure suppresion as did the KD. They postulated that calorie restriction may underlie the mechanism of the KD, either from ketosis or hypoglycemia. The authors believe that the mechanism of seizure suppresion is probably related to glucose dysregulation. Most likely, a combination of the two factors is operative, e.g., the brain metabolizes ketones better under conditions of reduced glucose.
Reliable data on caloric restriction in humans with epilepsy is lacking. Systemic glucose levels usually range from 60 to 120 mg/dL, with wide range of "normal". The relationship between seizure threshold and plasma glucose concentration is complex, and elevated glucose concentrations can be proconvulsant. Individuals on the KD tend to run blood glucose levels on the lower end of normal, but rarely are they hypoglycemic. Therefore, a metabolic adaptation occurs in response to the diet to maintain relative euglycemia."
Interesting article about glucose levels and seizures:
http://www.pubmedcentral.nih.gov/art...i?artid=387262
Correlation between Extracellular Glucose and Seizure Susceptibility in Adult Rats
Schwechter EM, Veliskova J, Velisek L Ann Neurol 2003;53:91–101
In adult diabetic patients, periods of hyperglycemia may be associated with exacerbation of focal seizures. Our objective was to determine in the adult rats the correlation between seizure susceptibility and extracellular glucose concentration in two models of seizures. Male rats were injected with two doses of streptozocin (40 mg/kg, IP) on consecutive days to induce diabetic hyperglycemia. Controls either received vehicle or were not injected. After 2 weeks, blood glucose concentration was measured, and the rats were subjected to flurothyl seizure test. Another group of rats received glucose solution (20%, 5 mL, IP) 30 minutes before testing to induce nondiabetic hyperglycemia. Thresholds for flurothyl-induced clonic and tonic–clonic seizures were determined. Finally, in vitro epileptiform activity was induced in the entorhinal cortex–hippocampal slices from naive rats by perfusing with magnesium-free medium with various glucose concentrations. In additional slices, the paired-pulse paradigm was determined in the perforant path. Susceptibility to clonic and tonic–clonic flurothyl-induced seizures positively correlated with blood glucose concentrations, as the increased glucose concentration was associated with proconvulsant effects. Similarly, in the in vitro experiments, epileptiform activity was promoted by increased and suppressed by decreased glucose concentrations. Data indicate that, in the adult rats, high glucose concentrations are associated with proconvulsant effects.
