Central obesity and increased risk of dementia more than three decades later
EmanueleCereda, International Center for the Assessment of Nutritional Status (ICANS), University of Milan, Italy., via Botticelli 21, 20133 Milan, Italyemanuele.cereda@virgilio.it
Manuela Chiara Sacchi (Division of Clinical Nutrition, Niguarda Ca Granda Hospital, Milan, Italy) Alexis Elias Malavazos (Endocrinology Unit, Department of Medical and Surgical Sciences, University of Milan, IRCCS Policlinico San Donato, Milan, Italy)
Submitted June 26, 2008
We read with interest the recent article by Whitmer et al. who provide evidence of a longitudinal link between middle-life visceral obesity and dementia risk. [1] It is now apparent that intra-abdominal fat may play a role in other health complications in addition to cardiovascular disease (CVD). Unfortunately, the underlying mechanisms are still unclear.
To explain the observations that overall adiposity is linked both to cognitive decline and CVD and that concurrent CVD is often seen in older dementia patients, we recently reviewed current physiopathologic theories. [2,3] We concluded that visceral adipose tissue (VAT) is consistently implicated in cognitive decline rather than body mass index.
In addition, women who experience changes in body composition and fat distribution after menopause transition are at an increased risk of AD. This is due to a stronger link to vascular factors (pro-inflammatory molecules) and metabolic complications (insulin resistance, dyslipidemia, hypertension). [3]
Luchsinger et al. have hypothesized that in people over 65, a short-term (5-year follow-up) prospective association seems modified by age and is different depending on the anthropometric measure. [4] However, a life course contribution to chronic diseases is recognized. [2] The study by Whitmer et al. [1] supports the previously suggested theory [2,3] particularly when multiple adjustments for concurrent VAT-related complications (diabetes, hypertension, hyperlipidemia and CVDs) are considered. In this respect, the role of VAT as endocrine organ, which is able to release a number of mediators, appears fundamental.
The confounding effect of insulin resistance should be recognized but it should also be noted that a chronic low-grade inflammation is a precondition associated with obesity duration. Reduction in VAT, particularly through physical activity, is efficacious in improving metabolic profile and inflammation. However, long-term results are difficult to maintain and protective effects are still unclear. [3] It is possible that further adjustment for physical activity would have strengthened the authors’ evidence. This warrants further investigation and anthropometric data is not readily available.
Despite this study’s limitations, the suggested use of available surrogates of visceral adiposity other than sagittal abdominal diameter in a neurological setting is justified. [2]
References
1. Whitmer RA, Gustafson DR, Barrett-Connor E, et al. Central obesity and increased risk of dementia more than three decades later. Neurology. 2008; (in press)
2. Cereda E, Sansone V, Meola G, Malavazos AE. Increased visceral adipose tissue rather than BMI as a risk factor for dementia. Age Ageing 2007;36:488-491.
3. Cereda E, Battezzati A, Bertoli S, Malavazos AE, Testolin G. A life-course contribution of nutrition to future cognitive decline. In: Bernhardt NE and Kasko AM editors. Nutrition for the Middle-Aged and Elderly. Hauppauge NY: Nova Science Publishers; 2008 (in press).
4. Luchsinger JA, Patel B, Tang MX, Schupf N, Mayeux R. Measures of adiposity and dementia risk in elderly persons. Arch Neurol 2007;64:392-398.
We read with interest the recent article by Whitmer et al. who provide evidence of a longitudinal link between middle-life visceral obesity and dementia risk. [1] It is now apparent that intra-abdominal fat may play a role in other health complications in addition to cardiovascular disease (CVD). Unfortunately, the underlying mechanisms are still unclear.
To explain the observations that overall adiposity is linked both to cognitive decline and CVD and that concurrent CVD is often seen in older dementia patients, we recently reviewed current physiopathologic theories. [2,3] We concluded that visceral adipose tissue (VAT) is consistently implicated in cognitive decline rather than body mass index.
In addition, women who experience changes in body composition and fat distribution after menopause transition are at an increased risk of AD. This is due to a stronger link to vascular factors (pro-inflammatory molecules) and metabolic complications (insulin resistance, dyslipidemia, hypertension). [3]
Luchsinger et al. have hypothesized that in people over 65, a short-term (5-year follow-up) prospective association seems modified by age and is different depending on the anthropometric measure. [4] However, a life course contribution to chronic diseases is recognized. [2] The study by Whitmer et al. [1] supports the previously suggested theory [2,3] particularly when multiple adjustments for concurrent VAT-related complications (diabetes, hypertension, hyperlipidemia and CVDs) are considered. In this respect, the role of VAT as endocrine organ, which is able to release a number of mediators, appears fundamental.
The confounding effect of insulin resistance should be recognized but it should also be noted that a chronic low-grade inflammation is a precondition associated with obesity duration. Reduction in VAT, particularly through physical activity, is efficacious in improving metabolic profile and inflammation. However, long-term results are difficult to maintain and protective effects are still unclear. [3] It is possible that further adjustment for physical activity would have strengthened the authors’ evidence. This warrants further investigation and anthropometric data is not readily available.
Despite this study’s limitations, the suggested use of available surrogates of visceral adiposity other than sagittal abdominal diameter in a neurological setting is justified. [2]
References
1. Whitmer RA, Gustafson DR, Barrett-Connor E, et al. Central obesity and increased risk of dementia more than three decades later. Neurology. 2008; (in press)
2. Cereda E, Sansone V, Meola G, Malavazos AE. Increased visceral adipose tissue rather than BMI as a risk factor for dementia. Age Ageing 2007;36:488-491.
3. Cereda E, Battezzati A, Bertoli S, Malavazos AE, Testolin G. A life-course contribution of nutrition to future cognitive decline. In: Bernhardt NE and Kasko AM editors. Nutrition for the Middle-Aged and Elderly. Hauppauge NY: Nova Science Publishers; 2008 (in press).
4. Luchsinger JA, Patel B, Tang MX, Schupf N, Mayeux R. Measures of adiposity and dementia risk in elderly persons. Arch Neurol 2007;64:392-398.
Disclosure: The authors report no disclosures.