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Age and Ageing Advance Access originally published online on November 23, 2006
Age and Ageing 2007 36(1):23-29; doi:10.1093/ageing/afl123
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Copyright © The Author 2007. Published by Oxford University Press on behalf of the British Geriatrics Society.

Systematic Review

The risk of dementia with increased body mass index

Emmanuel C. Gorospe and Jatin K. Dave

Division of Aging, Brigham and Women's Hospital/Harvard Medical School, 1620 Tremont Street, Boston, USA

Address correspondence to: J. K. Dave. Fax: +1 (617) 525 7739. Email: jkdave{at}partners.org


   Abstract
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 Abstract
Introduction
 Methods
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 Key points
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Background identification of modifiable risk factors is crucial in the prevention of dementia, given its limited treatment options. Studies on increased body mass index (BMI) as a risk factor for dementia show conflicting results.

Methods we systematically retrieved and reviewed longitudinal population-based studies on increased BMI and dementia using a standard protocol. We searched Medline (1966–2006), Ageline (1978–2006), PsychInfo (1966–2006), CINAHL (1982–2006), and other relevant databases, including the reference lists of theeligible aricles for review. Included studies were subjected to a quality assessment protocol.

Results we identified eight studies that met our selection criteria. These studies covered 1,688 cases of dementia from 28,697 participants. After adjustment for age, smoking, comorbidities, and other confounders, four studies presented significantly increased risk of dementia with elevated BMI.

Conclusion this systematic review supports the hypothesis that increased BMI is independently associated with increased risk of dementia. Long-term studies to examine the mechanisms underlying the relationship between obesity and dementia are needed.

Keywords: body mass index, dementia, elderly, obesity, systematic reviews


   Introduction
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 Introduction
Methods
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 Key points
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 References
 
The prevention of dementia through identification and management of risk factors is of public health importance because of the growth in the elderly population. Dementia affects at least 6–10% of persons older than 65 years [1]. It increasingly causes significant morbidity and mortality with Alzheimer's disease ranking as the eighth leading cause of death among the elderly in the USA [2]. Despite therapeutic advances, current treatment modalities for dementia have limited success [3].

Dementia, in general, is increasingly recognised as a complication of cardiovascular risk factors [4, 5, 6]. For vascular-type dementia, this association is generally accepted [7, 8, 9]. Current trends in research also implicate the same risk factors in the development of Alzheimer's type dementia [10, 11]. It is possible that there is a common contributory pathway for the development of both Alzheimer's dementia and vascular-type dementia [12, 13]. It is possible that obesity contributes to both these major forms of cognitive impairment [14].

Obesity occurs in association with hypertension and diabetes [7, 8], but it is unclear whether obesity predisposes to dementia independent of other cardiovascular risk factors. The rationale for hypothesising this causal link is supported by experimental data suggesting the development of Alzheimer's type dementia with leptin dysregulation [15]. Similarly, cross-sectional studies have presented that measures of obesity, such as elevated waist–hip ratio [16] and increased body mass index (BMI) [17, 18], are associated with temporal lobe atrophy and decreased hippocampal volume.

Alarmingly, obesity affects 25–30% of adults in industrialised countries [19, 20]. Among older adults, aged 65–74 years, the number of overweight and obese adults has been increasing from 60 and 27%, respectively, in 1988, to 70 and 39%, respectively, in 2000 [21]. The prevalence of both obesity and dementia is expected to increase further with the growth of the aging population. Epidemiological studies on increased BMI as a risk factor for dementia show conflicting results. Some of these studies are limited by variable follow-up, study design and inadequate adjustment for medical comorbidities. In this context, we systematically reviewed all the available longitudinal studies investigating the association of increased BMI and dementia.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 Key points
 Conflict of interest
 Funding
 Ethical approval
 References
 
Data sources
We searched Medline (1966–March, 2006) using Ovid, EMBASE (1974–March, 2006), CINAHL (1982–March, 2006), Digital Dissertations Online (1997–March, 2006), PsychInfo (1966–March, 2006), and Ageline (1978– March, 2006) for papers published in English, using the combinations of medical subject heading (MeSH) terms obesity, BMI, body weight, and dementia, as per the Cochrane Collaboration recommended search strategy. We systematically searched the reference list of the retrieved articles and consulted experts in the field for pertinent unpublished data.

Selection criteria
We included longitudinal population-based studies that probed the association between increased BMI and dementia. Included studies ascertained the outcome of dementia on the basis of accepted clinical guidelines. We excluded studies reporting other cognitive abnormalities such as cerebral atrophy, cognitive decline, decreased functional capacity, and studies conducted on patients who already had psychiatric or neurologic impairments at baseline. We used the National Heart, Lung, and Blood Institute (NHLBI) BMI categories, with overweight defined as a BMI of 25–29.9 kg/m2 and obesity as a BMI >30 kg/m2 [22]. We independently searched for and identified potentially relevant studies using a uniform search strategy and a standard screening protocol (Figure 1). We initially found 532 articles of which 26 studies were considered relevant on the basis of the review of abstracts. We also sought unpublished [23], submitted, and additional data [26] from experts in the field.


Figure 1
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  		Figure 1. Selection process for relevant studies

 
For the eight included studies [7, 14, 23–28], we independently abstracted information on study design, participant characteristics, measurement of BMI and dementia, adjustment of potential confounders, and estimates of association. Both authors independently rated each eligible paper using a quality assessment checklist (Table 1). This tool was developed by the authors on the basis of recommendations for assessing longitudinal observational studies [29, 30]. We assessed the reporting of the baseline cognitive function of the participants, measurement of BMI, and adjustment for confounders like smoking, medical comorbidities, and age. Disagreements in the selection and quality assessment were resolved by discussion and repeated assessment of the articles.


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  		Table 1. Quality assessment checklist

 

   Results
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 Methods
 Results
Discussion
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Description of included studies
We identified eight cohort studies on BMI and dementia, which included 28,697 participants with 1,688 cases of dementia representing study populations from Finland, France, Sweden, Japan, and the USA (Table 2). All the included studies presented outcomes of all-cause dementia, except for the study by Yoshitake et al. [7] who reported separate relative risks for Alzheimer's disease and vascular dementia. Included studies used the DSM III-R, ICD, or the National Institute of Neurological and Communication Disorders and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria for the diagnosis of dementia. Four studies [24–26, [28] evaluated the BMI-associated risk in middle-aged individuals while the rest [7, 14, 23, 27] included adults aged 65–70 years. Two studies [25, 28] included only men while the rest included both men and women [7, 14, 23, 24, 26, 27].


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  		Table 2. Description of included studies

 
Quality assessment
Despite their variability in methodology and analytic models, all studies scored well in the quality assessment tool with a mean of 12.25 ± 2.73 points from a possible total of 16 points (Table 2). Overall, most of the studies scored well in terms of their adjustment for confounders such as age, smoking, and other medical comorbidities. Four studies [7, 23, 14, 27] explicitly stated that they have performed baseline cognitive assessment of their participants. Rosengren et al. [25] excluded participants with previous stroke. BMI was computed on the basis of clinical weight and height measurements in all studies except for the study by Nourhashemi et al. [27], who utilised self-reported data for participants when they still had normal cognitive function at baseline. Nourhashémi et al. [27] excluded subjects with dementia diagnosed within the first 3 years of follow-up in order to exclude subjects who might have preclinical dementia during their baseline assessment.

Association between BMI and dementia
Table 3 presents the findings of the eight studies and a summary of their conclusions. In their paper, Kivipelto et al. [26] had three models for the analysis of midlife BMI and risk of dementia. We presented their third model, which was adjusted for apolipoprotein E-{varepsilon}4 (APOE-{varepsilon}4) and history of diabetes mellitus, stroke, and myocardial infarction. The unpublished data [23] from the Washington Heights-Inwood Columbia Aging Project (WHICAP) also had three models in their analysis; none of them showed statistically significant relationships between the increasing BMI categories and dementia. In this review, we chose to present the model of the WHICAP study that adjusted for age, gender, years of education, ethnicity, APOE-{varepsilon}4 carrier status, smoking, and other cardiovascular risk factors.


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  		Table 3. Summary of findings

 
After adjusting for age, smoking, medical comorbidities, and other confounders, four studies [14, 24, 25, 28] reported significant association between increased BMI and dementia, which included the larger and more recent studies of Whitmer et al. [24] and Rosengren et al. [25]. Two other studies [7, 26] reported higher risk of dementia with increased BMI, but the association did not reach statistical significance. As a group, the four studies [14, 24, 25, 28] with statistically significant results had larger sample sizes (21,794 versus 6,903 participants), longer follow-up periods (23.75 ± 3.95 versus 10.25 ± 6.30 years), and younger participants at baseline. In our review, no study on dementia reported any protective effect of increased BMI.


   Discussion
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 Methods
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 References
 
There is a prevailing assumption that obesity is not a major risk factor for age-related cognitive decline [31]. This review suggests that increased BMI is likely to be an independent risk factor for dementia. Studies with appropriate exclusion of patients with dementia at baseline, enough power, and appropriate adjustment of potential confounders support the association between increased BMI and dementia. Studies [24, 25] that have younger participants at baseline and longer follow-up periods showed even more significant association.

BMI is an acceptable measure of body fat or adiposity in the general population. In the Heritage Family Study, the correlation between BMI and per cent body fat was 0.73 [32]. However, among older individuals, BMI may underestimate adiposity because lean body mass is replaced by fat on aging [33]. The association of increased adiposity to dementia may be weaker among the older participants who may have more body fat in spite of their low body weight. This also implies that the association of BMI to dementia may be more accurately assessed at midlife than in the older years [24]. In addition, the study of younger participants may also exclude the older and possibly underweight subjects who may have undetected preclinical dementia. In this review, studies [24, 25, 28] that measured baseline BMI at midlife were the ones that showed stronger association.

Studies such as that by Rosengren et al. [25], which did not exclude patients diagnosed with dementia in their early follow-up period, and the WHICAP data [23], which only had a 5-year follow-up, both reported a J-shaped association between BMI and dementia. This observation requires further scrutiny as patients with dementia often lose weight. With dementia, previously obese patients may lose up to 50% of their pre-dementia body weight [34]. This weight loss could even precede diagnosis of dementia by several years [35]. The study of Nourhashemi et al. [27], which excluded participants with dementia during their first 3 years of follow-up, concluded that low BMI did not present any significant risk. It appears that failure to exclude subjects diagnosed early with dementia in a cohort and inadequate follow-up period may skew the risk of dementia towards those with borderline and low BMI.

In this review, women with increased BMI were at a greater risk for dementia than men [14, 24]. Data from the pooled European population-based cohorts also demonstrated increased incidence of dementia among women [36]. These observations propose a possible interaction between obesity and gender in the risk for dementia. Several hypotheses for this difference include hormonal changes, gender differences in body fat distribution [14, 24], or probable survival bias, as women with higher BMI are more likely to survive past the age of 70 than men [14, 37]. More studies will be needed to answer these questions.

The association of BMI to dementia is complex. Ascertaining obesity as an independent risk factor for dementia requires careful adjustment of confounding variables, adequate number of dementia cases, exclusion of cognitively impaired subjects at baseline, standardised measurement of body weight and height, and uniform BMI cut-off categories as suggested by the NHLBI guidelines [22]. Whenever possible, investigators assessing the outcome of dementia should be blinded to the baseline BMI measures of their participants.

Smoking may be a risk factor for dementia [38] and needs to be excluded. Smokers have been shown to be thinner, with higher risks for mortality and other comorbidities [39]. Failure to exclude smokers may produce a J-shaped correlation between BMI and other health outcomes such as mortality and dementia. Owing to smoking, underweight cohorts may show greater risk for dementia than those with normal or increased BMIs. More importantly, there should be adjustment for APOE-{varepsilon}4 carrier status in the analyses of studies. APOE-{varepsilon}4 carrier status is a strong risk factor for dementia [40, 41]. Although controversial, there is also growing evidence that low educational attainment [42] and decreased physical activity [43, 44] are potential risk factors for dementia.

Long-term well-designed studies are still needed to examine the mechanisms underlying the relationship between obesity and dementia. For now, it appears that elevated BMI in middle age and in the older years seems to have no protective effect against cognitive impairment. Therefore, the maintenance of normal weight throughout one's lifespan is a worthwhile intervention for the prevention of dementia, aside from the prevention of other established medical comorbidities.


   Key points
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 Key points
Conflict of interest
 Funding
 Ethical approval
 References
 

  • This review suggests increased BMI as a likely independent risk factor for dementia.
  • Adjustment for age, medical comorbidities, APOE-{varepsilon}4 carrier status, smoking, and adequacy of follow-up time can affect the results and quality of studies investigating the link between BMI and dementia.
  • There is a need to explore the role of increased adiposity for the aging brain and to elucidate reasons for gender differences in the risk for dementia.


   Acknowledgements
 
The authors would like to thank Jose Luchsinger of the Taub Institute for Research of Alzheimer's Disease and the Aging Brain for sharing unpublished data, and Miia Kivipelto of the Karolinska Institutet Aging Research Center for her correspondence regarding published articles.


   Conflict of interest
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 Key points
 Conflict of interest
Funding
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 References
 
None declared.


   Funding
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Key points
 Conflict of interest
 Funding
Ethical approval
 References
 
None.


   Ethical approval
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Key points
 Conflict of interest
 Funding
 Ethical approval
References
 
Not required.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Key points
 Conflict of interest
 Funding
 Ethical approval
 References
 

    The long list of references supporting this review has meant that only the most important are listed here and are represented by bold type throughout the text. The full list of references is available on the journal website http://www.ageing.oxfordjournals.org/ as appendix 1.
  1. Hendrie HC. (1998) Epidemiology of dementia and Alzheimer's disease. Am J Geriatr Psychiatry 6 S3–18 Suppl. 1.[Medline]
  2. Centers of Disease Control and Prevention. (2005) Death: preliminary data 2003. Natl Vital Stat Rep 53 2.
  3. Wallin AK, Gustafson L, Sjogren M, et al. (2004) Five-year outcome of cholinergic treatment of Alzheimer's disease: early response predicts prolonged time until nursing home placement, but does not alter life expectancy. Dement Geriatr Cogn Disord 18 197–206.[CrossRef][Web of Science][Medline]
  4. Breteler MM, Bots ML, Ott A, et al. (1998) Risk factors for vascular disease and dementia. Haemostasis 28 167–73.[CrossRef][Web of Science][Medline]
  5. Yoshitake T, Kiyohara Y, Kato I, et al. (1995) Incidence and risk factors of vascular dementia and Alzheimer's disease in a defined elderly Japanese population: the Hisayama Study. Neurology 45 1161–68.[Abstract]
  6. Launer LJ, Ross GW, Petrovitch H, et al. (2000) Midlife blood pressure and dementia: the Honolulu-Asia aging study. Neurobiol Aging 21 49–55.[Web of Science][Medline]
  7. Hofman A, Ott A, Breteler MM, et al. (1997) Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study. Lancet 349 151–54.[CrossRef][Web of Science][Medline]
  8. Gustafson D, Rothenberg E, Blennow K, et al. (2003) An 18-year follow-up of overweight and risk of Alzheimer disease. Arch Intern Med 163 1524–28.[Abstract/Free Full Text]
  9. Fewlass DC, Noboa K, Pi-Sunyer FX, et al. (2004) Obesity-related leptin regulates Alzheimer's Abeta. FASEB J 18 1870–78.[Abstract/Free Full Text]
  10. Jagust W, Harvey D, Mungas D, et al. (2005) Central obesity and the aging brain. Arch Neurol 62 1545–48.[Abstract/Free Full Text]
  11. Ward MA, Carlsson CM, Trivedi MA, et al. (2005) The effect of body mass index on global brain volume in middle-aged adults: a cross sectional study. BMC Neurol 5 23.[CrossRef][Medline]
  12. Rennie KL and Jebb SA. (2005) Prevalence of obesity in Great Britain. Obes Rev 6 11–2.[CrossRef][Web of Science][Medline]
  13. Centers for Disease Control and Prevention. Healthy weight, overweight, and obesity among persons 20 years of age and over, according to sex, age, race, and Hispanic origin: United States, 1960–62, 1971–74, 1976–80, 1988–94, and 1999–2000. National Center for Health Statistics Data 2002.Accessed March 29, 2006 from http://www.cdc.gov/nchs/data/hus/tables/2002/02hus070.pdf.
  14. National Heart Lung Blood Institute. (2000) The Practical Guide on Identification, Evaluation, and Treatment of Overweight and Obesity. National Institutes of Health.
  15. Luchsinger J. Washington Heights-Inwood Columbia Aging Project. Taub Institute for Research of Alzheimer's Disease and the Aging Brain.
  16. Whitmer RA, Gunderson EP, Barrett-Connor E, et al. (2005) Obesity in middle age and future risk of dementia: a 27 year longitudinal population based study. BMJ 330 1360.[Abstract/Free Full Text]
  17. Rosengren A, Skoog I, Gustafson D, et al. (2005) Body mass index, other cardiovascular risk factors, and hospitalization for dementia. Arch Intern Med 165 321–26.[Abstract/Free Full Text]
  18. Kivipelto M, Ngandu T, Fratiglioni L, et al. (2005) Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease. Arch Neurol 62 1556–60.[Abstract/Free Full Text]
  19. Nourhashemi F, Deschamps V, Larrieu S, et al. (2003) Body mass index and incidence of dementia: the PAQUID study. Neurology 60 117–9.[Abstract/Free Full Text]
  20. Kalmijn S, Foley D, White L, et al. (2000) Metabolic cardiovascular syndrome and risk of dementia in Japanese-American elderly men. The Honolulu-Asia aging study. Arterioscler Thromb Vasc Biol 20 2255–60.[Abstract/Free Full Text]
  21. Stroup DF, Berlin JA, Morton SC, et al. (2000) Meta-analysis of observational studies in epidemiology: a proposal for reporting. Meta-analysis Of Observational Studies in Epidemiology (MOOSE) group. JAMA 283 2008–12.[Abstract/Free Full Text]
  22. Elias MF, Elias PK, Sullivan LM, et al. (2003) Lower cognitive function in the presence of obesity and hypertension: the Framingham heart study. Int J Obes Relat Metab Disord 27 260–8.[CrossRef][Web of Science][Medline]
  23. Jackson AS, Stanforth PR, Gagnon J, et al. (2002) The effect of sex, age and race on estimating percentage body fat from body mass index: The Heritage Family Study. Int J Obes Relat Metab Disord 26 789–96.[CrossRef][Web of Science][Medline]
  24. Baumgartner RN, Heymsfield SB, Roche AF. (1995) Human body composition and the epidemiology of chronic disease. Obes Res 3 73–95.[Web of Science][Medline]
  25. Wang SY. (2002) Weight loss and metabolic changes in dementia. J Nutr Health Aging 6 201–5.[Medline]
  26. Barrett-Connor E, Edelstein SL, Corey-Bloom J, et al. (1996) Weight loss precedes dementia in community-dwelling older adults. J Am Geriatr Soc 44 1147–52.[Web of Science][Medline]
  27. Andersen K, Launer LJ, Dewey ME, et al. (1999) Gender differences in the incidence of AD and vascular dementia: The EURODEM Studies. EURODEM Incidence Research Group. Neurology 53 1992–97.[Abstract/Free Full Text]
  28. Ott A, Slooter AJ, Hofman A, et al. (1998) Smoking and risk of dementia and Alzheimer's disease in a population-based cohort study: the Rotterdam Study. Lancet 351 1840–43.[CrossRef][Web of Science][Medline]
  29. Manson JE, Willett WC, Stampfer MJ, et al. (1995) Body weight and mortality among women. N Engl J Med 333 677–85.[Abstract/Free Full Text]
  30. Kuusisto J, Koivisto K, Kervinen K, et al. (1994) Association of apolipoprotein E phenotypes with late onset Alzheimer's disease: population based study. BMJ 309 636–8.[Abstract/Free Full Text]
Received 16 May 2006; accepted in revised form 14 September 2006.


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