Hostname: page-component-78c5997874-xbtfd Total loading time: 0 Render date: 2024-11-13T05:24:57.116Z Has data issue: false hasContentIssue false
  • English
  • Français

The association between caffeine and cognitive decline: examining alternative causal hypotheses

Published online by Cambridge University Press:  15 January 2014

K. Ritchie ,
M.L. Ancelin ,
H. Amieva ,
O. Rouaud  and
I. Carrière
K. Ritchie*
Affiliation:
Inserm, Montpellier, France University of Montpellier 1, Montpellier, France Faculty of Medicine, Imperial College, London, UK
M.L. Ancelin
Affiliation:
Inserm, Montpellier, France University of Montpellier 1, Montpellier, France
H. Amieva
Affiliation:
ISPED, University of Bordeaux, Bordeaux, France
O. Rouaud
Affiliation:
CMMR CHU Dijon, Dijon, France
I. Carrière
Affiliation:
Inserm, Montpellier, France University of Montpellier 1, Montpellier, France
*
Correspondence should be addressed to: K. Ritchie, Inserm U1061, Neuropsychiatry: Epidemiological and Clinical Research, La Colombière Hospital, 34093 Montpellier cedex 5, France. Phone: +33 4 99 61 45 68; Fax: +33 4 99 61 45 79. Email: karen.ritchie@inserm.fr.
Get access Rights & Permissions [Opens in a new window]

Abstract

Background:

Numerous studies suggest that higher coffee consumption may reduce the rate of aging-related cognitive decline in women. It is thus potentially a cheap and widely available candidate for prevention programs provided its mechanism may be adequately understood. The assumed effect is that of reduced amyloid deposition, however, alternative pathways notably by reducing depression and diabetes type 2 risk have not been considered.

Methods:

A population study of 1,193 elderly persons examining depressive symptomatology, caffeine consumption, fasting glucose levels, type 2 diabetes onset, serum amyloid, and factors known to affect cognitive performance was used to explore alternative causal models.

Results:

Higher caffeine consumption was found to be associated with decreased risk of incident diabetes in men (HR = 0.64; 95% CI 0.42–0.97) and increased risk in women (HR = 1.51; 95% CI 1.08–2.11). No association was found with incident depression. While in the total sample lower ratio Aβ42/Aβ40 levels (OR = 1.36, 95% CI 1.05–1.77, p = 0.02) were found in high caffeine consumers, this failed to reach significance when the analyses were stratified by gender.

Conclusions:

We found no evidence that reduced risk of cognitive decline in women with high caffeine consumption is moderated or confounded by diabetes or depression. The evidence of an association with plasma beta amyloid could not be clearly demonstrated. Insufficient proof of causal mechanisms currently precludes the recommendation of coffee consumption as a public health measure. Further research should focus on the high estrogen content of coffee as a plausible alternative explanation.

Keywords

amyloidcaffeinecognitiondepressiondiabetes
Type
Research Article
Information
International Psychogeriatrics , Volume 26 , Issue 4 , April 2014 , pp. 581 - 590
Copyright
Copyright © International Psychogeriatric Association 2014 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Almdal, T. et al. (2004). The independent effect of type 2 diabetes mellitus on ischemic heart disease, stroke, and death: a population-based study of 13,000 men and women with 20 years of follow-up. Archives of Internal Medicine, 164, 1422–1426.Google Scholar
Alves, R. C. et al. (2010). Isoflavones in coffee: influence of species, roast degree, and brewing method. Journal of Agriculture and Food Chemistry, 58, 3002–3007.Google Scholar
Arendash, G. W. et al. (2006). Caffeine protects Alzheimer's mice against cognitive impairment and reduces brain beta-amyloid production. Neuroscience, 142, 941–952.Google Scholar
Arendash, G. W. et al. (2009). Caffeine reverses cognitive impairment and decreases brain Amyloid-beta levels in aged Alzheimer's disease mice. Journal of Alzheimer's Disease, 17, 661–680.CrossRefGoogle ScholarPubMed
Carriere, I. et al. (2009). Drugs with anticholinergic properties, cognitive decline, and dementia in an elderly general population: the 3-city study. Archives of Internal Medicine, 169, 1317–1324.Google Scholar
Cosentino, S. A. et al. (2010). Plasma ss-amyloid and cognitive decline. Archives of Neurology, 67, 1485–1490.CrossRefGoogle ScholarPubMed
Cunha, G. et al. (2006). Blockage of adenosine A2A receptors prevents beta-amiloid (Abeta1–42)-induced synaptotoxicity and memory impairment in rodents. Purinergic Signalling, 2, 135.Google Scholar
Dall'igna, O. P. et al. (2006). Caffeine and adenosine A(2a) receptor antagonists prevent beta-amyloid (25–35)-induced cognitive deficits in mice. Experimental Neurology, 5, 23–25.Google Scholar
Daly, J. W. and Fredholm, B. B. (1998). Caffeine–an atypical drug of dependence. Drug and Alcohol Dependance, 51, 199–206.Google Scholar
Eskelinen, M. H. et al. (2009). Midlife coffee and tea drinking and the risk of late-life dementia: a population-based CAIDE study. Journal of Alzheimers Disease, 16, 85–91.Google Scholar
Floegel, A. T. et al. (2012). Coffee consumption and risk of chronic disease in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Germany study. American Journal of Clinical Nutrition, 95, 901–908.Google Scholar
Folstein, M. F., Folstein, S. E. and McHugh, P. R. (1975). “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12, 189–198.Google Scholar
Gispen, W. H. and Biessels, G. J. (2000). Cognition and synaptic plasticity in diabetes mellitus. Trends in Neuroscience, 23, 542–549.Google Scholar
Golden, S. H. et al. (2008). Examining a bidirectional association between depressive symptoms and diabetes. JAMA, 299, 2751–2759.Google Scholar
Graff-Radford, N. R. et al. (2007). Association of low plasma Abeta42/Abeta40 ratios with increased imminent risk for mild cognitive impairment and Alzheimer disease. Archives of Neurology, 64, 354–362.CrossRefGoogle ScholarPubMed
Irie, F. et al. (2008). Enhanced risk for Alzheimer disease in persons with type 2 diabetes and APOE epsilon4: the Cardiovascular Health Study Cognition Study. Archives of Neurology, 65, 89–93.Google Scholar
Kawarabayashi, T. L. H. et al. (2001). Age-dependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer's disease. Journal of Neuroscience, 21, 372–381.Google Scholar
Kraemer, H. C. et al. (2001). How do risk factors work together? Mediators, moderators, and independent, overlapping and proxy risk factors. American Journal of Psychiatry, 158, 848–856.Google Scholar
Lambert, J. C. et al. (2009). Association of plasma amyloid beta with risk of dementia: the prospective Three-City Study. Neurology, 73, 847–853.Google Scholar
Lecrubier, Y. (1997). The Mini International Neuropsychiatric Interview (MINI). A short diagnostic structured interview: reliability and validity according to the CIDI. European Psychiatry, 12, 224–231.Google Scholar
Lindsay, J. et al. (2002). Risk factors for Alzheimer's disease: a prospective analysis from the Canadian Study of Health and Aging. American Journal of Epidemiology, 156, 445–453.Google Scholar
Lucas, M. F. et al. (2011). Coffee, caffeine, and risk of depression among women. Archives of Internal Medicine, 171, 1571–1578.Google Scholar
Luchsinger, J. A. et al. (2004). Hyperinsulinemia and risk of Alzheimer disease. Neurology, 63, 1187–1192.Google Scholar
Maia, L. and de Mendonca, A. (2002). Does caffeine intake protect from Alzheimer's disease? European Journal of Neurology, 9, 377–382.Google Scholar
Mayeux, R. et al. (2003). Plasma A[beta]40 and A[beta]42 and Alzheimer's disease: relation to age, mortality, and risk. Neurology, 61, 1185–1190.CrossRefGoogle Scholar
McEwen, B. S. et al. (2012). Estrogen effects on the brain: actions beyond the hypothalamus via novel mechanisms. Behavioral Neurosciences, 126, 4–16.CrossRefGoogle ScholarPubMed
Radloff, L. (1977). The CES-D scale: a self-report depression scale for research in the general population. Applied Psychological Measurement, 1, 385–401.Google Scholar
Ribeiro, J. A. et al. (2002). Adenosine receptors in the nervous system: pathophysiological implications. Progress in Neurobiology, 68, 377–392.CrossRefGoogle ScholarPubMed
Ritchie, K. et al. (2010). Caffeine, cognitive functioning, and white matter lesions in the elderly: establishing causality from epidemiological evidence. Journal of Alzheimer's Disease, 20, S161–S166.Google Scholar
Ritchie, K. I. et al. (2007). The neuroprotective effects of caffeine: a prospective population study (the Three City Study). Neurology, 69, 536–545.CrossRefGoogle Scholar
Ruusunen, A. et al. (2010). Coffee, tea and caffeine intake and the risk of severe depression in middle-aged Finnish men: the Kuopio Ischaemic Heart Disease Risk Factor Study. Public Health and Nutrition, 13, 1215–1220.Google Scholar
Ryan, J. et al. (2009). Characteristics of hormone therapy, cognitive function and dementia. Neurology, 73, 1729–1737.Google Scholar
Santos, C. et al. (2009). Caffeine intake is associated with a lower risk of cognitive decline: a cohort study from Portugal. Journal of Alzheimers Disease, 20, S175–185.Google Scholar
The 3C Study Group (2003). Vascular factors and risk of dementia: design of the three city study and baseline characteristics of the study population. Neuroepidemiology, 22, 316–325.Google Scholar
van Dam, R. M. and Hu, F. B. (2005). Coffee consumption and risk of type 2 diabetes: a systematic review. JAMA, 294, 97–104.Google Scholar
Williams, J. B., Plassman, B. L., Burke, J., Holsinger, T. and Benjamin, S. (2010). Preventing Alzheimer's Disease and Cognitive Decline. Rockville, MD: Agency for Healthcare Research and Quality (US), Report No 10-E005. Available at: http://www.ahrq.gov/; last accessed 20 September 2013.Google Scholar
Zhao, W. Q. and Alkon, D. L. (2001). Role of insulin and insulin receptor in learning and memory. Molecular Cell Endocrinology, 177, 125–134.Google Scholar