Rachael A.Whitmer, Kaiser Permanente Division of Research, Oakland, CARachel.Whitmer@nsmtp.kp.org
D. R. Gustafson, E. Barrett-Connor, M. N. Haan, E. P. Gunderson, and K. Yaffe
Submitted June 26, 2008
We thank Drs. Cereda, Farooki, and Tezapsidis for their comments on our article. [1]
We agree with Cereda et al. that obesity and central obesity confers with it a state of inflammation and this may also contribute to cognitive impairment and dementia risk. Unfortunately measures of physical activity were not available so it is unknown what effect this would have on the association between midlife central obesity status and dementia risk.
We also concur that visceral adipose tissue itself is the likely culprit in the association between central obesity and increased dementia risk. Hopefully, future studies will investigate possible actions of visceral adipocytes on the brain and effects of an altered adipokine milieu on cognitive status. [12]
Regarding comments from Farooki et al., ethnic specific anthropometric measurements are the most precise. Although there are standard ethnic specific guidelines for waist circumference in defining central obesity, there are not published ethnic specific guidelines for sagittal abdominal diameter, the anthropometric measurement used in our study. Future studies examining central obesity and disease outcomes should incorporate these guidelines.
With respect to comments from Tezapsidis concerning leptin as a possible therapeutic for patients with AD, leptin has been shown to be beneficial to neurons. However, obesity is associated with ‘leptin resistance’ so it is possible that obese individuals may not respond to possible neuroprotective effects of leptin. However, a recent study in non-demented elders demonstrated that higher serum leptin levels are associated with better cognitive performance independent of total body weight and total body fat. [13] More work is needed on how states of leptin resistance as induced by chronic obesity may contribute to brain aging.
References
12. Whitmer, RA. Epidemiology of Adiposity and Dementia, Current Alzheimer’s Research, 2007;4:117-122
13. Holden KF, Lindquist K, Tylavsky FA, Rosano C, Harris TB, Yaffe K; for the Health ABC study. Serum leptin level and cognition in the elderly: Findings from the Health ABC Study.Neurobiol Aging. 2008 Mar 19. [Epub ahead of print].
We thank Drs. Cereda, Farooki, and Tezapsidis for their comments on our article. [1]
We agree with Cereda et al. that obesity and central obesity confers with it a state of inflammation and this may also contribute to cognitive impairment and dementia risk. Unfortunately measures of physical activity were not available so it is unknown what effect this would have on the association between midlife central obesity status and dementia risk.
We also concur that visceral adipose tissue itself is the likely culprit in the association between central obesity and increased dementia risk. Hopefully, future studies will investigate possible actions of visceral adipocytes on the brain and effects of an altered adipokine milieu on cognitive status. [12]
Regarding comments from Farooki et al., ethnic specific anthropometric measurements are the most precise. Although there are standard ethnic specific guidelines for waist circumference in defining central obesity, there are not published ethnic specific guidelines for sagittal abdominal diameter, the anthropometric measurement used in our study. Future studies examining central obesity and disease outcomes should incorporate these guidelines.
With respect to comments from Tezapsidis concerning leptin as a possible therapeutic for patients with AD, leptin has been shown to be beneficial to neurons. However, obesity is associated with ‘leptin resistance’ so it is possible that obese individuals may not respond to possible neuroprotective effects of leptin. However, a recent study in non-demented elders demonstrated that higher serum leptin levels are associated with better cognitive performance independent of total body weight and total body fat. [13] More work is needed on how states of leptin resistance as induced by chronic obesity may contribute to brain aging.
References
12. Whitmer, RA. Epidemiology of Adiposity and Dementia, Current Alzheimer’s Research, 2007;4:117-122
13. Holden KF, Lindquist K, Tylavsky FA, Rosano C, Harris TB, Yaffe K; for the Health ABC study. Serum leptin level and cognition in the elderly: Findings from the Health ABC Study.Neurobiol Aging. 2008 Mar 19. [Epub ahead of print].
Disclosure: The authors report no disclosures.