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As to the influence of dietary and lifestyle choices and blood
glucose levels on ischemic cerebrovascular disease, Ramadan can be a good
measure for assessment.
Once a year, Muslims stay hungry between dawn and dusk in an
approximate fasting period of one month called Ramadan. Prohibiting
fasting has always been a big issue for physicians, since many patients
may find this obligation unnecessary or as a special treat against faith.
However, especially patients with certain risk factors (hypertension,
diabetes, stroke) are usually advised (or enforced) to quit fasting at
least for the sake of regular usage of drugs. Fasting is followed by a
period of religious festival in which feeding habits are changed
completely in a very short time. People are usually inclined to consume
high amounts of carbohydrate in this period after a month of food
restriction. There is no report about the frequency of cerebrovascular
disease in this period and therefore it is, as yet, uncertain if this kind
of food deprivation or consumption of high amounts of carbohydrate may
eventually increase the risk of stroke incidence.
There are a number of observations on the metabolic and physiologic
effects of hunger on cerebrovascular system. Fasting for 24 hours before
transient experimental cerebral ischemia has been shown to reduce delayed
neuronal necrosis and infarct volume. Low preischemic plasma glucose
levels are correlated with a reduction in infarct volumes in the fasted
group compared with the control group (1).
Although global cerebral oxygen metabolism is not significantly altered
after fasting (2), there is a reduction in cerebral glucose delivery to
the area of physiological activation (i.e. contralateral somato-sensory
cortex during vibrotactile stimulation of hand) and an increase in
cerebral blood flow as arterial glucose concentrations decrease (3). High
fasting blood glucose values are related with a more severe ischemic brain
lesion. It has long been established that hyperglycemia accentuates
whereas hypoglycemia ameliorates hypoxic-ischemic brain damage (4).
After food restriction hypertensive stroke-prone rats seem to have a
lower blood pressure (5). Mean arterial blood pressure also falls both
after fasting and after the meal in normal subjects (6). Food and exercise
in combination may produce a cumulative blood pressure lowering effect due
to simultaneous splanchnic muscle dilatation (6).
Exposure to food is associated with increases in the regional cerebral
blood flow, whereas global cerebral blood flow seems to remain unchanged
(7,8). Although these results seem to support the potential of food
restriction as a stroke preventing measure, it may still be questioned
whether falls in regional cerebral blood flow and arterial blood pressure
after fasting constitute a possible treat for infarct development in
predisposed patients (i.e. hypertension, diabetes, stenosis or occlusion
of one of the major cerebral arteries or previous stroke history). The
answer to this question may lie under clinical observations more than
experimental researches.
Patients with acute stroke (ischemic or hemorrhagic) referring to our
department were recorded in a period of three months (one month before
Ramadan, Ramadan and one month after Ramadan) and daily frequency of
stroke cases has been documented as a number versus time diagram. Seventy-
two percent of the cases recorded in Ramadan were fasting and the
frequency of both kinds (ischemic, hemorrhagic) of cerebrovascular disease
seemed to be unchanged in this particular month. The interesting finding
was a peak in a period of four days after the end of fasting month, which
contributed to the religious festival. A twofold increase was recorded in
this certain time section. Low number of cases and lack of knowledge about
the percentage of fasting people in the population prevents the
constitution of a statistically more significant relation between stroke
incidence and fasting. Data of this study was consistent with a number of
unpublished observations in different departments. High stroke frequency
in the festival period may be another clue about the influence of
hyperglycemia on cerebrovascular disease.
The question of stroke-blood glucose levels relationship seems to
remain as a big issue waiting for an answer and multicenter prospective
studies distributed in a broader time period.
REFERENCES
1. Lin TN, Te J, Huang HC, Chi SI, Hsu CY. Prolongation and enhancement of
postischemic c-fos expression after fasting. Stroke 1997;28:412-418.
2. Hasselbalch SG, Madsen PL, Hageman LP, Olsen KS, Justesen N, Holm
S,Paulson OB. Changes in cerebral blood flow and carbohydrate metabolism
during acute hyperketonemia. Am J Physiol 1996; 270:E746-51.
3. Powers WJ, Hirsch IB, Cryer PE. Effect of stepped hypoglycemia on
regional cerebral blood flow response to physiological brain activation.
Am J Physiol 1996;270:H554-559.
4. Murros K, Fogelholm R, Kettunen S, Vuorela AL, Valve J. Blood
glucose, glycosylated haemoglobin, and outcome of ischemic brain
infarction. J Neurol Sci 1992;111:59-64.
5. Stevens H, Knollema S, De Jong G, Korf J, Luiten PG. Long-term
food restriction, deprenyl, and nimodipine treatment on life expectancy
and blood pressure of stroke-prone rats. Neurobiol Aging 1998;19:273-276.
6. Puvi-Rajasingham S, Smith GD, Akinola A, Mathias CJ. Hypotensive
and regional haemodynamic effects of exercise, fasted and after food, in
human sympathetic denervation. Clin Sci 1998;94:49-55.
7. Karhunen LJ, Lappalainen RI, Vanninen EJ, Kuikka JT, Uusitupa MI.
Regional cerebral blood flow during food exposure in obese and normal-
weight women. Brain 1997;120:1675-1684.
8. Hasselbalch SG, Knudsen GM, Jakobsen J, Hageman LP, Holm S,
Paulson OB. Blood-brain barrier permeability of glucose and ketone bodies
during short-term starvation in humans. Am J Physiol 1995;268:E1161-1166.
Competing interests:
No competing interests
12 May 2000
Erdem Tuzun
Neurologist
Department of Neurology, Medical Faculty of Istanbul, University of Istanbul, Istanbul, TURKEY
Food deprivation and stroke
As to the influence of dietary and lifestyle choices and blood
glucose levels on ischemic cerebrovascular disease, Ramadan can be a good
measure for assessment.
Once a year, Muslims stay hungry between dawn and dusk in an
approximate fasting period of one month called Ramadan. Prohibiting
fasting has always been a big issue for physicians, since many patients
may find this obligation unnecessary or as a special treat against faith.
However, especially patients with certain risk factors (hypertension,
diabetes, stroke) are usually advised (or enforced) to quit fasting at
least for the sake of regular usage of drugs. Fasting is followed by a
period of religious festival in which feeding habits are changed
completely in a very short time. People are usually inclined to consume
high amounts of carbohydrate in this period after a month of food
restriction. There is no report about the frequency of cerebrovascular
disease in this period and therefore it is, as yet, uncertain if this kind
of food deprivation or consumption of high amounts of carbohydrate may
eventually increase the risk of stroke incidence.
There are a number of observations on the metabolic and physiologic
effects of hunger on cerebrovascular system. Fasting for 24 hours before
transient experimental cerebral ischemia has been shown to reduce delayed
neuronal necrosis and infarct volume. Low preischemic plasma glucose
levels are correlated with a reduction in infarct volumes in the fasted
group compared with the control group (1).
Although global cerebral oxygen metabolism is not significantly altered
after fasting (2), there is a reduction in cerebral glucose delivery to
the area of physiological activation (i.e. contralateral somato-sensory
cortex during vibrotactile stimulation of hand) and an increase in
cerebral blood flow as arterial glucose concentrations decrease (3). High
fasting blood glucose values are related with a more severe ischemic brain
lesion. It has long been established that hyperglycemia accentuates
whereas hypoglycemia ameliorates hypoxic-ischemic brain damage (4).
After food restriction hypertensive stroke-prone rats seem to have a
lower blood pressure (5). Mean arterial blood pressure also falls both
after fasting and after the meal in normal subjects (6). Food and exercise
in combination may produce a cumulative blood pressure lowering effect due
to simultaneous splanchnic muscle dilatation (6).
Exposure to food is associated with increases in the regional cerebral
blood flow, whereas global cerebral blood flow seems to remain unchanged
(7,8). Although these results seem to support the potential of food
restriction as a stroke preventing measure, it may still be questioned
whether falls in regional cerebral blood flow and arterial blood pressure
after fasting constitute a possible treat for infarct development in
predisposed patients (i.e. hypertension, diabetes, stenosis or occlusion
of one of the major cerebral arteries or previous stroke history). The
answer to this question may lie under clinical observations more than
experimental researches.
Patients with acute stroke (ischemic or hemorrhagic) referring to our
department were recorded in a period of three months (one month before
Ramadan, Ramadan and one month after Ramadan) and daily frequency of
stroke cases has been documented as a number versus time diagram. Seventy-
two percent of the cases recorded in Ramadan were fasting and the
frequency of both kinds (ischemic, hemorrhagic) of cerebrovascular disease
seemed to be unchanged in this particular month. The interesting finding
was a peak in a period of four days after the end of fasting month, which
contributed to the religious festival. A twofold increase was recorded in
this certain time section. Low number of cases and lack of knowledge about
the percentage of fasting people in the population prevents the
constitution of a statistically more significant relation between stroke
incidence and fasting. Data of this study was consistent with a number of
unpublished observations in different departments. High stroke frequency
in the festival period may be another clue about the influence of
hyperglycemia on cerebrovascular disease.
The question of stroke-blood glucose levels relationship seems to
remain as a big issue waiting for an answer and multicenter prospective
studies distributed in a broader time period.
REFERENCES
1. Lin TN, Te J, Huang HC, Chi SI, Hsu CY. Prolongation and enhancement of
postischemic c-fos expression after fasting. Stroke 1997;28:412-418.
2. Hasselbalch SG, Madsen PL, Hageman LP, Olsen KS, Justesen N, Holm
S,Paulson OB. Changes in cerebral blood flow and carbohydrate metabolism
during acute hyperketonemia. Am J Physiol 1996; 270:E746-51.
3. Powers WJ, Hirsch IB, Cryer PE. Effect of stepped hypoglycemia on
regional cerebral blood flow response to physiological brain activation.
Am J Physiol 1996;270:H554-559.
4. Murros K, Fogelholm R, Kettunen S, Vuorela AL, Valve J. Blood
glucose, glycosylated haemoglobin, and outcome of ischemic brain
infarction. J Neurol Sci 1992;111:59-64.
5. Stevens H, Knollema S, De Jong G, Korf J, Luiten PG. Long-term
food restriction, deprenyl, and nimodipine treatment on life expectancy
and blood pressure of stroke-prone rats. Neurobiol Aging 1998;19:273-276.
6. Puvi-Rajasingham S, Smith GD, Akinola A, Mathias CJ. Hypotensive
and regional haemodynamic effects of exercise, fasted and after food, in
human sympathetic denervation. Clin Sci 1998;94:49-55.
7. Karhunen LJ, Lappalainen RI, Vanninen EJ, Kuikka JT, Uusitupa MI.
Regional cerebral blood flow during food exposure in obese and normal-
weight women. Brain 1997;120:1675-1684.
8. Hasselbalch SG, Knudsen GM, Jakobsen J, Hageman LP, Holm S,
Paulson OB. Blood-brain barrier permeability of glucose and ketone bodies
during short-term starvation in humans. Am J Physiol 1995;268:E1161-1166.
Competing interests: No competing interests