Dementia, Alzheimer's and diabetes could be linked through hypovolaemia
Simon N.Thornton, Professor
Published October 25, 2011
Ohara et al. [1] suggest that the "incidence of all cause dementia, Alzheimer disease and vascular dementia were significantly higher in subjects with diabetes." This could suggest a common causality in the two diseases. Elderly Alzheimer patients with progressive mild cognitive impairment have specific brain regions decreased in volume. [2] Chronic hypovolaemia—due to hypohydration—could be a mechanism behind the development of diabetes and obesity. [3] Hypovolaemia would have an effect on brain hydration also resulting in gradual loss of volume. This "hypothesis" of dehydration is supported further by work showing that total body water decreases with age. [4]
Dehydration also has an important negative effect on cell metabolism by its influence on insulin signaling [5] as seen in diabetes. This could explain why certain areas of the brain are not only decreased in volume but also show signs of atrophy leading to dementia. It is possible that increased water intake for improved cell (neuronal) metabolism and especially cerebral hydration should be encouraged in cases of elderly patients exhibiting signs of Alzheimer disease, mild cognitive impairment, or and diabetes.
1. Ohara T, Doi Y, Ninomiya T, et al. Glucose tolerance status and risk of dementia in the
community: The Hisayama Study. Neurology 2011;77:1126-1134.
2. Fetissov SO, Thornton SN. Hypovolaemia-induced obesity and diabetes.
Metabolism 2009;58:1678.
3. Liu Y, Paajanen T, Zhang Y, et al. AddNeuroMed Consortium. Analysis of regional
MRI volumes and thicknesses as predictors of conversion from mild
cognitive impairment to Alzheimer's disease. Neurobiol Aging 2010;
31:1375-1385.
4. Chumlea WC, Guo SS, Zeller CM, Reo NV, Siervogel RM. Total body water
data for white adults 18 to 64 years of age: the Fels Longitudinal Study.
Kidney Int 1999;56:244-252.
5. Schliess F, H?ussinger D. Cell volume and insulin signaling. Int Rev
Cytol 2003;225:187-228.
For full disclosures, please contact the editorial office at journal@neurology.org.
Ohara et al. [1] suggest that the "incidence of all cause dementia, Alzheimer disease and vascular dementia were significantly higher in subjects with diabetes." This could suggest a common causality in the two diseases. Elderly Alzheimer patients with progressive mild cognitive impairment have specific brain regions decreased in volume. [2] Chronic hypovolaemia—due to hypohydration—could be a mechanism behind the development of diabetes and obesity. [3] Hypovolaemia would have an effect on brain hydration also resulting in gradual loss of volume. This "hypothesis" of dehydration is supported further by work showing that total body water decreases with age. [4] Dehydration also has an important negative effect on cell metabolism by its influence on insulin signaling [5] as seen in diabetes. This could explain why certain areas of the brain are not only decreased in volume but also show signs of atrophy leading to dementia. It is possible that increased water intake for improved cell (neuronal) metabolism and especially cerebral hydration should be encouraged in cases of elderly patients exhibiting signs of Alzheimer disease, mild cognitive impairment, or and diabetes.
1. Ohara T, Doi Y, Ninomiya T, et al. Glucose tolerance status and risk of dementia in the community: The Hisayama Study. Neurology 2011;77:1126-1134.
2. Fetissov SO, Thornton SN. Hypovolaemia-induced obesity and diabetes. Metabolism 2009;58:1678.
3. Liu Y, Paajanen T, Zhang Y, et al. AddNeuroMed Consortium. Analysis of regional MRI volumes and thicknesses as predictors of conversion from mild cognitive impairment to Alzheimer's disease. Neurobiol Aging 2010; 31:1375-1385.
4. Chumlea WC, Guo SS, Zeller CM, Reo NV, Siervogel RM. Total body water data for white adults 18 to 64 years of age: the Fels Longitudinal Study. Kidney Int 1999;56:244-252.
5. Schliess F, H?ussinger D. Cell volume and insulin signaling. Int Rev Cytol 2003;225:187-228.
For full disclosures, please contact the editorial office at journal@neurology.org.