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Coffee, tea, and caffeine consumption and prevention of late-life cognitive decline and dementia: A systematic review

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Abstract

A prolonged preclinical phase of more than two decades before the onset of dementia suggested that initial brain changes of Alzheimer’s disease (AD) and the symptoms of advanced AD may represent a unique continuum. Given the very limited therapeutic value of drugs currently used in the treatment of AD and dementia, preventing or postponing the onset of AD and delaying or slowing its progression are becoming mandatory. Among possible reversible risk factors of dementia and AD, vascular, metabolic, and lifestyle-related factors were associated with the development of dementia and late-life cognitive disorders, opening new avenues for the prevention of these diseases. Among diet-associated factors, coffee is regularly consumed by millions of people around the world and owing to its caffeine content, it is the best known psychoactive stimulant resulting in heightened alertness and arousal and improvement of cognitive performance. Besides its short-term effect, some case-control and cross-sectional and longitudinal population-based studies evaluated the long-term effects on brain function and provided some evidence that coffee, tea, and caffeine consumption or higher plasma caffeine levels may be protective against cognitive impairment/decline and dementia. In particular, several cross-sectional and longitudinal population-based studies suggested a protective effect of coffee, tea, and caffeine use against late-life cognitive impairment/decline, although the association was not found in all cognitive domains investigated and there was a lack of a distinct dose-response association, with a stronger effect among women than men. The findings on the association of coffee, tea, and caffeine consumption or plasma caffeine levels with incident mild cognitive impairment and its progression to dementia were too limited to draw any conclusion. Furthermore, for dementia and AD prevention, some studies with baseline examination in midlife pointed to a lack of association, although other case-control and longitudinal population-based studies with briefer follow-up periods supported favourable effects of coffee, tea, and caffeine consumption against AD. Larger studies with longer follow-up periods should be encouraged, addressing other potential bias and confounding sources, so hopefully opening new ways for diet-related prevention of dementia and AD.

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... Ao traçarmos uma relação causal, observa-se, claramente, que o avanço da medicina e o aumento global da expectativa de vida criam um ambiente propício para a senilidade; portanto, o fato de que o envelhecimento da população aumenta a prevalência de doenças que advém dessa condição, requer novos conhecimentos, tratamentos e medidas preventivas para que o impacto nas sociedades ao redor do mundo seja o menor possível e a expectativa de vida, junto ao bem-estar, estejam em pauta (Panza et al., 2015). Nesse sentido, sabemos que as síndromes demenciais tem um papel importante nesse cenário, mundialmente, a Doença de Alzheimer (DA) é responsável por 50-70% dos casos, seguida pela Doença de Parkinson (DP) (Londzin et al., 2021;Hong et al., 2020), além de outras doenças como a Demência Vascular. ...
... O café é uma das bebidas mais consumidas no mundo e suas propriedades psicoativas, resultam numa melhora temporária da cognição e ativa o estado de vigília. As propriedades antioxidantes e outros benefícios do café exercem efeitos sistêmicos e em diversas patologias, como no diabetes e no infarto agudo isquêmico e hemorrágico, além de evidências positivas na DP e na DA, em geral advindas da cafeína; não obstante, existem relatos sobre a participação de outras substâncias, comprovadas, também, por experimentos com a ingestão do café livre de cafeína (Carman et al., 2014;Panza et al., 2015). Porém, a expressão dos efeitos da cafeína -presente no café, na erva mate, na cola, no guaraná e em bebidas energéticas -em si, são dependentes de diversos fatores, sendo que a dose é um ponto crucial, já que os níveis delimitados seguros estão entre 400mg por dia, de acordo com a European Food Safety Authority (EFSA), considerando que em um copo de aproximadamente 473mL de café coado está presente, em média, 188mg de cafeína (Kolahdouzan & Hamadeh, 2017). ...
... Quanto as constatações em humanos, um estudo longitudinal acompanhou, durante 21 anos, 875 mulheres e 534 homens com mais de 50 anos, relatando que um consumo moderado, entre 3-5 copos por dia reduziu o risco de DA em 62%-64% em comparação com pessoas que ingeriram de zero a dois copos por dia (Eskelinen et al., 2009;Kolahdouzan & Hamadeh, 2017), outro estudo, realizado no Canadá, pela análise de 10.263 pessoas acima de 65 anos, confirmou a redução de 31% no risco de DA naqueles com a ingesta de café (Kolahdouzan & Hamadeh, 2017). Outra revisão analisou uma gama de estudos, com relações condizentes com as já citadas, entretanto, um estudo longitudinal, realizado durante 28 anos, com participantes entre 46-52 anos, com a ingestão média de 5.4 copos de café por dia, não confirmou o benefício da ingestão de café, durante a meia idade, no desenvolvimento de DA (Panza et al., 2015). Por fim, outro trabalho de revisão, pela análise de cinco estudos prospectivos relacionou as dosagem de três a quatro copos (aproximadamente 300mg) como a melhor dosagem com efeito protetor quanto ao desenvolvimento de DA, enquanto outros dois pequenos estudos relatam esse nível entre 62mg/dia e 200mg/dia (Carman et al., 2014). ...
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Introdução: A prevalência da Doença de Alzheimer (DA) e da Doença de Parkinson (DP), tende a aumentar com o envelhecimento populacional. Até o momento, os esquemas terapêuticos para essas doenças não consegue alcançar a cura e geralmente não são atualizados, o que evidencia a necessidade de outras opções para a melhora da qualidade de vida desses pacientes. Dado que essas síndromes demenciais tem etiologia multifatorial, a dieta, por meio do café, tem mostrado evidências significativas na degeneração neuronal, que é um dos principais aspectos alterados no desenvolvimento dessas patologias. Metodologia: Trata-se de uma revisão integrativa, que buscou responder quais os possíveis efeitos da cafeína como fator protetor no desenvolvimento e na progressão da revisional e da DP, nas bases de dados: Biblioteca Virtual de Saúde (BVS), National Library of Medicine (PubMed MEDLINE) e Scientific Electronic Library Online (Scielo). Resultados e Discussão: A cafeína age no sistema nervoso central (SNC) pela mimetização aos receptores de adenosina, mais concentrada nos receptores A1R e A2aR. Como antagonista competitivo, a cafeína, eventualmente, poderia reduz os processos de formação das placas b-amiloides na DA e reduzir a neuroinflamação e neurodegeneração na DP, além de outros possíveis mecanismos. Conclusão: A delimitação de um consenso sobre a relação dose/efeito decorrente do uso da cafeína é de difícil estabelecimento e ainda não se observa um consenso, entretanto, é possível observar que um consumo entre 200mg a 511mg por dia poderia trazer efeitos benéficos tanto na DP, como na DA, superando os possíveis efeitos colaterais.
... In recent years, an increasing attention towards the beneficial impact of coffee also on some neuropsychiatric and neurological disorders has been noted, although epidemiological studies did not reach consensus regarding a protective effect of caffeine on the risk of cognitive impairment. While several findings have reported a coffee-related protection on cognition (Panza et al. 2015;Rom an et al. 2019), a detailed neuropsychological assessment was rarely carried out and a firm association has not been established yet, at least not for every cognitive domain (Panza et al. 2015). The same holds true for a consensus on a dose-response association with mood status or cognitive performance (Jarvis 1993;Johnson-Kozlow et al. 2002;Gelber et al. 2011;Lucas et al. 2011;Panza et al. 2015). ...
... In recent years, an increasing attention towards the beneficial impact of coffee also on some neuropsychiatric and neurological disorders has been noted, although epidemiological studies did not reach consensus regarding a protective effect of caffeine on the risk of cognitive impairment. While several findings have reported a coffee-related protection on cognition (Panza et al. 2015;Rom an et al. 2019), a detailed neuropsychological assessment was rarely carried out and a firm association has not been established yet, at least not for every cognitive domain (Panza et al. 2015). The same holds true for a consensus on a dose-response association with mood status or cognitive performance (Jarvis 1993;Johnson-Kozlow et al. 2002;Gelber et al. 2011;Lucas et al. 2011;Panza et al. 2015). ...
... While several findings have reported a coffee-related protection on cognition (Panza et al. 2015;Rom an et al. 2019), a detailed neuropsychological assessment was rarely carried out and a firm association has not been established yet, at least not for every cognitive domain (Panza et al. 2015). The same holds true for a consensus on a dose-response association with mood status or cognitive performance (Jarvis 1993;Johnson-Kozlow et al. 2002;Gelber et al. 2011;Lucas et al. 2011;Panza et al. 2015). ...
Article
Coffee intake has been recently associated with better cognition and mood in mild vascular cognitive impairment (mVCI). As tobacco can reduce the caffeine half-life, we excluded smokers from the original sample. Hamilton Depression Rating Scale (HDRS), mini-mental state examination (MMSE), Stroop Colour-Word Interference Test (Stroop), activities of daily living (ADL0) and instrumental ADL were the outcome measures. Significant differences were observed in higher consumption groups (moderate intake for HDRS; high intake for MMSE and Stroop) compared to the other groups, as well as in age and education. With age, education and coffee used as independent predictors, and HDRS, Stroop and MMSE as dependent variables, a correlation was found between age and both MMSE and Stroop, as well as between education and MMSE and between HDRS and Stroop; coffee intake negatively correlated with HDRS and Stroop. Higher coffee consumption was associated with better psycho-cognitive status among non-smokers with mVCI.
... Further caffeine intake comes from tea, energy or sports drinks, and various chocolate products (Fitt et al., 2013). While many advocates for the neuroprotective and cognitive-enhancing effects of caffeine (McLellan et al., 2016;Panza et al., 2015), others proposed that the magnitude of these benefits are negligible, furthermore, a higher dose can have detrimental effects on physical and mental health (Nehlig, 2010(Nehlig, , 1999. As past literature tended to treat memory as a subset of cognitive functions, the specific effect of caffeine on memory has not been thoroughly discussed. ...
... Similar interactions between caffeine and sex, where a larger protective effect for females than males has been reported in a systematic review (Panza et al., 2015). However, Panza et al. (2015) focused on the role of habitual caffeine consumption in preventing cognitive decline and dementia, without detailing mechanisms underlying this sex effect. ...
... Similar interactions between caffeine and sex, where a larger protective effect for females than males has been reported in a systematic review (Panza et al., 2015). However, Panza et al. (2015) focused on the role of habitual caffeine consumption in preventing cognitive decline and dementia, without detailing mechanisms underlying this sex effect. Given the various metabolic pathways of caffeine, habitual consumption may participate in physiological processes that affect global cognition (de Mejia and Ramirez-Mares, 2014), but this does not translate to the effect of caffeine on memory tasks in the healthy population. ...
Article
Caffeine is a widely used nootropic drug, but its effects on memory in healthy participants have not been sufficiently evaluated. Here we review evidence of the effects of caffeine on different types of memory, and the associated drug, experimental, and demographical factors. There is limited evidence that caffeine affects performance in memory tasks beyond improved reaction times. For drug factors, a dose-response relationship may exist but findings are inconsistent. Moreover, there is evidence that the source of caffeine can modulate its effects on memory. For experimental factors, past studies often lacked a baseline control for diet and sleep and none discussed the possible reversal of withdrawal effect due to pre-experimental fasting. For demographic factors, caffeine may interact with sex and age, and the direction of the effect may depend on the dose, individual tolerance, and metabolism at baseline. Future studies should incorporate these considerations, as well as providing continued evidence on the effect of caffeine in visuospatial, prospective, and implicit memory measures.
... Although people with MCI have a greater risk of dementia, many studies have reported that it is possible to prevent progression to dementia by controlling environmental factors such as dietary habits, exercise, and chronic disease management (Eshkoor et al., 2015;Jiang et al., 2017). Several studies have recently investigated the associations between cognitive function and dietary factors, including certain foods and nutrients (Panza et al., 2015;Jiang et al., 2017). Adequate consumption of omega-3 fatty acids (Cederholm et al., 2013), fruits and vegetables (Dong et al., 2016;Jiang et al., 2017), dairy products (Ogata et al., 2016), and moderate alcohol consumption (Xu et al., 2017) have been reported to have protective effects against disease. ...
... Adequate consumption of omega-3 fatty acids (Cederholm et al., 2013), fruits and vegetables (Dong et al., 2016;Jiang et al., 2017), dairy products (Ogata et al., 2016), and moderate alcohol consumption (Xu et al., 2017) have been reported to have protective effects against disease. However, the association between dietary factors and the risk of cognitive impairment and dementia remains unclear (Panza et al., 2015;Kesse-Guyot et al., 2016;Smith and Blumenthal, 2016). ...
... A recent systematic review of several cross-sectional studies and longitudinal population-based studies suggested that coffee and tea intake had a protective effect on cognitive impairment in older people. Although there were some limitations (such as using a dose-response analysis and cognitive domains), this review reported that this association was stronger in females than in males (Panza et al., 2015). Barbour et al. (2014) examined the effects of nut consumption on blood pressure, glucose regulation, endothelial vasodilator function, arterial compliance, inflammatory biomarkers, and cognitive function through several epidemiological or intervention studies. ...
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The prevalence of age-related diseases such as dementia and cognitive disorders is rapidly increasing. This study aimed to identify the dietary patterns associated with mild cognitive impairment (MCI) in adults aged over 50 years. This cross-sectional study investigated dietary patterns associated with cognitive function among older adults hospitalized in Gwangju province. Global cognitive function was assessed using the Mini-Mental State Examination. Diet information was obtained using a food frequency questionnaire with 112 food items and 24-h dietary recall. Using a principal component analysis, we identified three dietary patterns, "legumes and vegetables", "beverage and nuts", and "white rice". The "beverage and nuts" pattern was inversely associated with the prevalence of high MCI after adjusting for covariates (third vs. first tertile, adjusted odds ratio: 0.333; 95% confidence interval: 0.133∼0.831; P<0.05). The white rice pattern was associated with the prevalence of MCI in the crude analysis. However, after adjusting for all confounding factors, no association was found. The "beverage and nuts" pattern was inversely associated with the prevalence of MCI. In the future, longitudinal population-based studies and randomized clinical trials are required to confirm the effect of potential dietary patterns on cognitive impairment and reveal the underlying mechanism of their association.
... Furthermore, caffeine and caffeine-containing beverages, such as coffee and tea, appear to act as protective factors when consumed regularly [67,68]. Coffee consumption appears to reduce the risk of depression, with the most significant protective impact observed at 400 mL/day [67]. ...
... Additionally, cross-sectional and longitudinal population-based investigations also imply that coffee, tea, and caffeine alone may protect against cognitive impairment/decline in later life. However, this link was not consistently observed across all cognitive domains that were tested [68]. ...
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(1) Background: Attention-deficit/hyperactivity disorder (ADHD) is typically treated with stimulant medications, which may lead to several adverse effects. Recent animal studies have shown that caffeine can improve the symptoms of ADHD. This systematic review and meta-analysis sought to evaluate the effect of caffeine on ADHD symptoms in children. (2) Methods: PubMed, Embase, and Cochrane databases were searched for randomized controlled trials comparing caffeine with placebo in children, comparing overall symptoms of ADHD, inattention, hyperactivity, and impulsivity. (3) Results: We included seven RCTs in the systematic review for qualitative assessment, with 104 patients aged 5 to 15 years. Four of these studies (n = 76) were included in the meta-analysis. After qualitative analysis, four studies indicated no improvement in any of the ADHD symptoms compared with placebo. One study showed improvement in ADHD symptoms based on 1 of 5 scales applied. One study indicated significant improvement in general symptoms, inattention, and hyperactivity. One study indicated improvement in sustained attention but a worsening of impulsivity. In contrast, when using a quantitative analysis of the general symptoms of ADHD, the data showed no significant difference when comparing placebo with caffeine (standardized mean difference −0.12; 95% CI −0.44 to 0.20; p = 0.45; I2 = 0%). (4) Conclusion: overall, the totality of the evidence suggests no significant benefit of caffeine over placebo in the treatment of children with ADHD.
... Tea is a beloved beverage enjoyed in many cultures worldwide, which consumes in staggering quantities of more than two billion cups daily (Kochman et al., 2020). Experimental evidences indicate that caffeine and tea polyphenols contained in tea have neuroprotective effects, such as anti-inflammatory, or anti-oxidant effects Panza et al., 2015;Feng et al., 2018). In addition, research reveals that tea may protect against AD, through reducing amyloid-β (Aβ) in the brain (Arendash & Cao, 2010;Polito et al., 2018). ...
... It is consistent with previous studies. A systematic review which enrolled several cross-sectional and longitudinal population-based studies demonstrated a protective effect of coffee, tea, and caffeine against cognitive impairment regression in later life, further supporting our findings (Panza et al., 2015). ...
Article
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Purpose Dementia affects as many as 130 million people, which presents a significant and growing medical burden globally. This meta-analysis aims to assess whether tea intake, tea consumption can reduce the risk of dementia, Alzheimer’s disease (AD) and Vascular dementia (VD). Patients and methods Cochrane Library, PubMed and Embase were searched for cohort studies from inception to November 1, 2022. The Newcastle Ottawa Quality Assessment Scale (NOS) was applied to evaluate the risk of bias of the included studies. We extracted the data as the relative risks (RRs) for the outcome of the interest, and conducted the meta-analysis utilizing the random effect model due to the certain heterogeneity. Sensitivity analysis were performed by moving one study at a time, Subgroup-analysis was carried out according to different ages and dementia types. And the funnel plots based on Egger’s and Begger’s regression tests were used to evaluate publication bias. All statistical analyses were performed using Stata statistical software version 14.0 and R studio version 4.2.0. Results Seven prospective cohort studies covering 410,951 individuals, which were published from 2009 and 2022 were included in this meta-analysis. The methodological quality of these studies was relatively with five out of seven being of high quality and the remaining being of moderate. The pooling analysis shows that the relationship between tea intake or consumption is associated with a reduced risk of all-cause dementia (RR = 0.71, 95% CI [0.57–0.88], I ² = 79.0%, p < 0.01). Further, the subgroup-analysis revealed that tea intake or consumption is associated with a reduced risk of AD (RR = 0.88, 95% CI [0.79–0.99], I ² = 52.6%, p = 0.024) and VD (RR = 0.75, 95% CI [0.66–0.85], I = 0.00%, p < 0.001). Lastly, tea intake or consumption could reduce the risk of all-cause dementia to a greater degree among populations with less physical activity, older age, APOE carriers, and smokers. Conclusion Our meta-analysis demonstrated that tea (green tea or black tea) intake or consumption is associated with a significant reduction in the risk of dementia, AD or VD. These findings provide evidence that tea intake or consumption should be recognized as an independent protective factor against the onset of dementia, AD or VD.
... A meta-analysis by Wu et al. has shown that a diminished risk of development of dementias in humans (including AD) was observed with daily consumption of one-two cups of coffee [146]. Interestingly, research part of the Italian Longitudinal Study on Aging (ILSA) suggested that older people with normal cognitive function who increased their coffee consumption had a higher rate of developing MCI, while constant-over-time, moderate coffee consumption was linked to a lower rate of MCI incidence [147,148]. However, research does not support the theory that caffeine could prevent AD [149], although as reported in epidemiological research, drinking coffee and caffeine can possibly help treat AD [147]. ...
... Interestingly, research part of the Italian Longitudinal Study on Aging (ILSA) suggested that older people with normal cognitive function who increased their coffee consumption had a higher rate of developing MCI, while constant-over-time, moderate coffee consumption was linked to a lower rate of MCI incidence [147,148]. However, research does not support the theory that caffeine could prevent AD [149], although as reported in epidemiological research, drinking coffee and caffeine can possibly help treat AD [147]. ...
Article
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Alzheimer's disease is the most common cause of dementia in the world. Lack of an established pathology makes it difficult to develop suitable approaches and treatment for the disease. Besides known hallmarks, including amyloid β peptides cumulating in plaques and hyperphosphorylated tau forming NFTs, inflammation also plays an important role, with known connections to the diet. In AD, adhering to reasonable nutrition according to age-related principles is recommended. The diet should be high in neuroprotective foods, such as polyunsaturated fatty acids, antioxidants, and B vitamins. In addition, foods capable of rising BDNF should be considered because of the known profitable results of this molecule in AD. Adhering to beneficial diets might result in improvements in memory, cognition, and biomarkers and might even reduce the risk of developing AD. In this review, we discuss the effects of various diets, foods, and nutrients on brain health and possible connections to Alzheimer's disease.
... When compared to genetic risk factors, modifiable factors have the advantage that they can be targeted for intervention. Extensive research has suggested that modifiable risk factors, such as diet, physical activity, smoking, and caffeine intake, influence the risk for development of dementia and AD, and behavioral modification could reduce disease risk [1][2][3][4]. Thus, modifiable risk factors provide a potential window for dementia and AD prevention and intervention. ...
... Engagement in moderate physical activity has been associated with higher cerebrospinal fluid (CSF) amyloid β (Aβ) 42 and lower total tau (T-tau)/ Aβ42 and phosphorylated tau (P-tau)/Aβ42 ratios, which further confirms the protective role of physical activity in AD development [7]. A systematic review [4] of caffeine found evidence supporting favorable effects of coffee consumption on AD risk and cognitive decline. For example, the Cardiovascular Risk Factors, Aging and Dementia study followed 1409 participants for 21 years and found that daily coffee consumption of 3-5 cups was associated with a 65% decrease in dementia and a 64% decrease in AD [8]. ...
Article
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Modifiable factors can influence the risk for Alzheimer's disease (AD) and serve as targets for intervention; however, the biological mechanisms linking these factors to AD are unknown. This study aims to identify plasma metabolites associated with modifiable factors for AD, including MIND diet, physical activity, smoking, and caffeine intake, and test their association with AD endophenotypes to identify their potential roles in pathophysiological mechanisms. The association between each of the 757 plasma metabolites and four modifiable factors was tested in the wisconsin registry for Alzheimer's prevention cohort of initially cognitively unimpaired, asymptomatic middle-aged adults. After Bonferroni correction, the significant plasma metabolites were tested for association with each of the AD endophenotypes, including twelve cerebrospinal fluid (CSF) biomarkers, reflecting key pathophysiologies for AD, and four cognitive composite scores. Finally, causal mediation analyses were conducted to evaluate possible mediation effects. Analyses were performed using linear mixed-effects regression. A total of 27, 3, 23, and 24 metabolites were associated with MIND diet, physical activity, smoking, and caffeine intake, respectively. Potential mediation effects include beta-cryptoxanthin in the association between MIND diet and preclinical Alzheimer cognitive composite score, hippurate between MIND diet and immediate learning, glutamate between physical activity and CSF neurofilament light, and beta-cryptoxanthin between smoking and immediate learning. Our study identified several plasma metabolites that are associated with modifiable factors. These metabolites can be employed as biomarkers for tracking these factors, and they provide a potential biological pathway of how modifiable factors influence the human body and AD risk.
... Coffee, the most heavily consumed caffeinated beverage, has been a popular research topic in AD, with several epidemiological studies positing its neuroprotective effect [9]. Coffee comprises a few independently neuroprotective components: caffeine, chlorogenic acid, caffeic acid, and trigonelline [10]. ...
... Trigonelline from coffee beans has been shown to alleviate neuronal loss by reducing oxidative stress, astrocyte activity, and neuroinflammation while preserving mitochondrial integrity [13]. The neuroprotective properties of coffee have been heavily linked to its high caffeine content, but this has been difficult to demonstrate independently through epidemiological studies due to the confounding effect of other components in caffeinated beverages [9]. ...
Article
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Alzheimer's disease (AD) is the leading cause of dementia, predicted to be the most significant health burden of the 21st century, with an estimated 131.5 million dementia patients by the year 2050. This review aims to provide an overview of the effect of caffeine on AD and cognition by summarizing relevant research conducted on this topic. We searched the Web of Science core collection and PubMed for studies related to the effect of caffeine on AD and cognition using title search terms: caffeine; coffee; Alzheimer's; cognition. There is suggestive evidence from clinical studies that caffeine is neuroprotective against dementia and possibly AD (20 out of 30 studies support this), but further studies, such as the "ideal" study proposed in this review, are required to prove this link. Clinical studies also indicate that caffeine is a cognitive normalizer and not a cognitive enhancer. Furthermore, clinical studies suggest the neuroprotective effect of caffeine might be confounded by gender. There is robust evidence based on in vivo and in vitro studies that caffeine has neuroprotective properties in AD animal models (21 out of 22 studies support this), but further studies are needed to identify the mechanistic pathways mediating these effects.
... Additionally, it has been demonstrated that caffeine reduces tau protein phosphorylation in the hippocampus and has anti-neuroinflammatory effects (Machado et al. 2021). Caffeine suppresses AChE in low to moderate levels, which enhances cognitive functions and slows the course of AD (Panza et al. 2015). Cloves contain eugenol, which has been shown in rat models treated with Aβ peptides to decrease amyloid plaques and improve memory (Taheri et al. 2019). ...
Article
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Alzheimer’s disease is a devastating neurodegenerative disorder that affects millions of people worldwide. One of the key pathological features of Alzheimer’s disease is oxidative stress, which is characterized by an imbalance between the production of reactive oxygen species and the body’s ability to neutralize them with antioxidants. In recent years, there has been growing interest in the potential role of antioxidant supplementation in mitigating oxidative stress markers in Alzheimer’s disease. This review paper aims to provide a comprehensive overview of the current research on antioxidant supplementation in Alzheimer’s disease and its effects on oxidative stress markers. The paper will examine the underlying mechanisms of oxidative stress in Alzheimer’s disease, the potential benefits of antioxidant supplementation, and the challenges and limitations of using antioxidants as a therapeutic strategy.
... It is also important to highlight that the study was conducted by associations using LMMs and that causal inference cannot be inferred. While studies in rodent models provide mechanistic insights into the effects of coffee and tea compounds on cognitive function [69], their findings must be interpreted cautiously when extrapolated to humans due to differences in metabolism and administration methods [70,71]. ...
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Background: Coffee and tea are widely consumed beverages, but their long-term effects on cognitive function and aging remain largely unexplored. Lifestyle interventions, particularly dietary habits, offer promising strategies for enhancing cognitive performance and preventing cognitive decline. Methods: This study utilized data from the UK Biobank cohort (n = 12,025) to examine the associations between filtered coffee, green tea, and standard tea consumption and neural network functional connectivity across seven resting-state networks. We focused on networks spanning prefrontal and occipital areas that are linked to complex cognitive and behavioral functions. Linear mixed models were used to assess the main effects of coffee and tea consumption, as well as their interactions with Apolipoprotein E (APOE) genetic risk—the strongest genetic risk factor for Alzheimer’s disease (AD). Results: Higher filtered coffee consumption was associated with increased functional connectivity in several networks, including Motor Execution, Sensorimotor, Fronto-Cingular, and a Prefrontal + ‘What’ Pathway Network. Similarly, greater green tea intake was associated with enhanced connectivity in the Extrastriate Visual and Primary Visual Networks. In contrast, higher standard tea consumption was linked to reduced connectivity in networks such as Memory Consolidation, Motor Execution, Fronto-Cingular, and the “What” Pathway + Prefrontal Network. The APOE4 genotype and family history of AD influenced the relationship between coffee intake and connectivity in the Memory Consolidation Network. Additionally, the APOE4 genotype modified the association between standard tea consumption and connectivity in the Sensorimotor Network. Conclusions: The distinct patterns of association between coffee, green tea, and standard tea consumption and resting-state brain activity may provide insights into AD-related brain changes. The APOE4 genotype, in particular, appears to play a significant role in modulating these relationships. These findings enhance our knowledge of how commonly consumed beverages may influence cognitive function and potentially AD risk among older adults.
... Among them, the study found that people who drink 0.5-1 cup of coffee or 4-5 cups of tea per day have the lowest risk of dementia, which is consistent with previous studies 6 . One possible reason is that coffee and tea ingredients, such as caffeine, may reduce the risk of dementia by decreasing neuroinflammation or providing neuroprotective benefits [8][9][10] . However, excessive drinking of coffee and tea will lead to a large amount of caffeine intake in the body, disturb sleep patterns, and diminish internal antioxidant effects in the body 29 . ...
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Many studies have shown that drinking coffee and tea may be associated with the risk of hypertension and dementia. Limited research exists on their impact on dementia risk in hypertensive patients. This study aimed to determine the association between coffee and tea consumption and the risk of dementia development in hypertensive population by utilizing Cox proportional risk modeling with 453,913 participants from a UK biobank. Our findings reveal a J-shaped and U-shaped association between the risk of all-cause dementia and the consumption of coffee and tea respectively in hypertensive people. The hypertensive patients who drink 0.5–1 cup of coffee or 4–5 cups of tea per day have the lowest risk of dementia. A U-shaped relationship was observed between daily caffeine consumption and the risk of developing all-cause dementia and vascular dementia in the hypertensive population. Furthermore, the significant association between the amount of coffee and tea consumed and the risk of all-cause and vascular dementia were more likely to be found in hypertensive patients than in the non-hypertensive population.
... In addition to its pathological causes, for example, inflammation [7], oxidative stress [8], and endothelial damage [9], physical activity [10], such as tai chi [11], activity participation [12], and sleep duration [13], were also found to be associated with cognitive decline. As there is no effective treatment to slow down the progression of dementia, early prevention is gaining attention [14], among them, nutrition intake is considered as a possible strategy to prevent cognitive decline in the older adult [15]. ...
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Background Numerous studies have demonstrated a positive correlation between diet quality and cognitive performance, indicating that improving diet quality may be beneficial in preventing cognitive decline in older adults. However, few study has investigated the causal relationship between diet quality and cognitive performance. The purpose of this study is to evaluate the causal effects of diet quality on cognitive performance in Chinese adults aged 55 years and older. Particularly, we utilize the Chinese Diet Quality Index (CHEI), a dietary assessment tool tailored for Chinese populations, as a proxy for older adults’ diet quality. Methods Data were obtained from the China Health and Nutrition Survey (CHNS) (N=2337N=2337N = 2337, ≥\ge55 years old) conducted in 2004 and 2006. Cognitive function was tested by a subset of items from the Telephone Interview for Cognitive Status-Modified (TICS-m). Data on dietary intake was retrieved from three consecutive 24 hour recalls by participants and its quality was assessed by the 17-items Chinese Healthy Eating Index (CHEI). An Instrumental Variable technique was used to deal with the potential endogeneity of dietary quality. The instrumental variable used in our study is the community mean of CHEI. Results After adjusting for socio-demographic factors (age, gender, education, per capita household income), lifestyle habits (smoking, alcohol consumption, physical activity, BMI), and chronic diseases (hypertension, diabetes), our findings revealed that improving diet quality had a significant positive effect on cognitive performance (P=0.020P=0.020P = 0.020), particularly in females aged 55-65 years (P=0.003P=0.003P = 0.003) and females with primary education and below (P<0.001P<0.001P < 0.001). Conclusion Our study suggests that improving diet quality and adhering to the Dietary Guidelines for Chinese may enhance cognitive performance in Chinese adults aged 55 years and older.
... We also find that drinking tea and taking exercise can help prevent vascular dementia, while physical discomfort will increase the risk of vMCI and VaD. A systematic review suggests that tea consumption may be protective against late-life cognitive impairment/decline and dementia 34 . A meta-Analysis of prospective studies reveals a protective effect for high physical activity on all-cause dementia 35 , and another study also further reveals the link between physical discomfort and dementia 36 . ...
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Hypertension is considered as an independent risk factor for vascular mild cognitive impairment (vMCI) and vascular dementia (VaD). This study was performed to investigate the prevalence, influencing factors and cognitive characteristics of vMCI and VaD in elderly patients with hypertension in China. In the cross-sectional study, we performed cluster random sampling of 3246 people age 60 years and older across the country. All participants were interviewed and screened for hypertension. Among the 1495 hypertensive patients, 57 were diagnosed with vMCI and 48 with VaD according to the criteria of Petersen and DSM-IV, respectively. Logistic regression analyses were performed to evaluate risk and protective factor for vMCI and VaD with Hypertension. And we also assessed their cognitive function by a series of neuropsychological tests. We finally found that: 1) the prevalence of vMCI and VaD in hypertension was 3.8% and 3.2%, respectively, which was much higher than that of normal controls (p<0.05). 2)Multivariate logistic regression analyses showed that advanced age (p<0.001, OR=1.066, 95%CI: 1.030~1.104), sleep too little (p=0.011, OR=2.279, 95%CI: 1.210~4.291) and physical discomfort (p<0.001, OR=6.380, 95%CI: 2.956~13.774) were the risk factors for the development of vMCI in patients with hypertension; advanced age (p=0.002, OR=1.061, 95%CI: 1.021~1.011), physical discomfort (p=0.005, OR=3.922, 95%CI: 1.506~10.214) and depressive symptoms (p<0.001, OR=8.363, 95%CI: 3.023~23.138) were also the risk factor for VaD, while education (p=0.040, OR=0.941, 95%CI: 0.888~0.997), tea drinker (p=0.017, OR=0.483, 95%CI: 0.266~0.878) as well as take exercise (p=0.003, OR=0.416, 95%CI: 0.234~0.737) were protective factors of VaD;3) both overall and specific areas of cognitive function decrease in hypertension patients with vMCI and VaD, and show a gradual trend of aggravation.
... For instance [53], published a systematic review of findings on green tea and cognitive functioning, indicating that green tea positively affected cognitive functioning and minimised the presence of cognitive dysfunction. Similar systematic reviews by [54] and [55] found that there was an inverse relationship between tea consumption and cognitive impairment. ...
... The results of the review suggest that moderate coffee and tea consumption may have a protective effect against cognitive decline and dementia, but the evidence for caffeine consumption is inconclusive. The need for further research to clarify the relationship between coffee, tea, and caffeine consumption and cognitive decline and dementia, as well as to investigate the potential underlying mechanisms of any protective effects observed [13] . Cognitive impairment is a common health issue among older adults. ...
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This review aims to examine the effects of tea, coffee, and green tea consumption on human cognitive performance and mental health. Tea, coffee, and green tea are widely consumed beverages worldwide and contain various bioactive compounds that may influence cognitive function and mental health. Research has suggested that caffeine, the primary psychoactive compound in coffee and tea, can improve cognitive function, including attention, alertness, and working memory. The effect of caffeine on cognitive performance may be moderated by individual differences in caffeine metabolism and genetic factors. Green tea contains high levels of catechins, which have been linked to improved cognitive function, such as attention and working memory, as well as reduced risk of cognitive decline and dementia. Theanine, an amino acid found in green tea, has also been associated with relaxation and reduced anxiety. In addition to cognitive performance, tea, coffee, and green tea consumption have been linked to improved mental health outcomes. Research has suggested that coffee consumption may be associated with a lower risk of depression, while green tea consumption has been linked to reduced symptoms of anxiety and stress. However, the evidence regarding the effects of tea, coffee, and green tea on cognitive function and mental health is mixed, and further research is needed to fully understand the potential benefits and risks of these beverages. Additionally, individual differences in caffeine metabolism, genetic factors, and other lifestyle factors may influence the effects of tea, coffee, and green tea on cognitive function and mental health.
... Fruits and beverages such as tea and coffee are the main sources of dietary polyphenols, which have a positive effect on cognition and memory [19,48,49]. However, one study found that habitual coffee and tea drinking had mixed effects on cognitive improvement [50]. Scientific evidence confirmed that adequate vegetable and fruit consumption has a beneficial influence on health and can prevent cognitive impairment due to the presence of antioxidants and anti-inflammatory factors [51,52]. ...
Article
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The aim of this study was to quantify the dietary patterns (DPs) of Polish esports players aged 18–26 years. Data were obtained via questionnaires that assessed dietary habits and frequency of food consumption. Dietary patterns were derived using Principal Component Analysis (PCA) and Factor Analysis (FA). In total, nine distinct DPs were identified. Eight DPs were considered unhealthy; fast food', 'High-processed food, meat and confectionery', 'Sweet', 'Fat-diary products', 'Vegetable-fruit', 'Spices and additives', 'Fats' and 'Cereal'; and only one was deemed healthy. E-athletes presented mostly poor dietary habits, which included: irregular eating of meals, frequent snacking, at least three meals a day and composition of snacks, frying of meat dishes and sweetening of hot drinks. Healthy dietary habits included proper hydration during the day and consumption of mainly non-sparkling water. The unbalanced and largely unhealthy dietary habits of esports players raise health concerns for these e-athletes, particularly when combined with a sedentary lifestyle. Future research could assess the nutritional knowledge of this group as it relates to national guidelines, investigate interventions designed to introduce healthier eating options into their lifestyle and examine the relationship between DPs and health or cognitive performance.
... Bioactive compounds abundant in matcha such as caffeine, theanine and catechins have been linked to multiple benefits to the cognitive function. Caffeine is a psychoactive stimulant that results in increased alertness and enhanced cognitive performance as reported by multiple studies and systematic reviews (Smit and Rogers, 2000;Snel and Lorist, 2011;McLellan et al., 2016;Panza et al., 2015). In addition, previous literature showed that theanine influences neurogenesis and cognitive function positively in a manner independent of other compounds found in matcha (Yoneda et al., 2019;Camfield et al., 2014). ...
Article
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Matcha is a powdered form of Japanese green tea that has been gaining global popularity recently. Matcha tea has various health benefits, including an enhancing effect on cognitive function, cardio-metabolic health, and anti-tumorogenesis. To date, randomized clinical trials (RCT) showed that matcha decreases stress, slightly enhances attention and memory, and has no effect on mood. Results regarding the effect of matcha on cognitive function are contradictory and more RCTs are warranted. The cardio-metabolic effects of matcha have only been studied in animals, but findings were more homogenous. Consuming matcha with a high-fat diet resulted in decreased weight gain velocity, food intake, improved serum glucose and lipid profile, reduced inflammatory cytokines and ameliorated oxidative stress. Evidence regarding the anti-tumor function of matcha is very limited. Findings showed that matcha can affect proliferation, viability, antioxidant response, and cell cycle regulation of breast cancer cells. Nonetheless, more studies are needed to examine this effect on different types of cancer cells, and there is also a need to verify it using animal models. Overall, the evidence regarding the effect of matcha tea on cognitive function, cardio-metabolic function, and anti-tumor role is still limited, and conclusions cannot be drawn.
... Although from the current clinical research, it seems uncertain to draw the conclusion that the consumption of tea, especially green tea, is significantly related to the improvement of cognitive impairment in AD patients. However, scientists do not deny that tea and its effective ingredients have certain neuroprotective effects [105][106][107]. Especially in animal experiments and in vitro experiments, tea has shown a better effect on improving cognitive function [108,109]. ...
Article
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Alzheimer’s disease (AD) is an incurable degenerative disease of the central nervous system and the most common type of dementia in the elderly. Despite years of extensive research efforts, our understanding of the etiology and pathogenesis of AD is still highly limited. Nevertheless, several hypotheses related to risk factors for AD have been proposed. Moreover, plant-derived dietary polyphenols were also shown to exert protective effects against neurodegenerative diseases such as AD. In this review, we summarize the regulatory effects of the most well-known plant-derived dietary polyphenols on several AD-related molecular mechanisms, such as amelioration of oxidative stress injury, inhibition of aberrant glial cell activation to alleviate neuroinflammation, inhibition of the generation and promotion of the clearance of toxic amyloid-β (Aβ) plaques, inhibition of cholinesterase enzyme activity, and increase in acetylcholine levels in the brain. We also discuss the issue of bioavailability and the potential for improvement in this regard. This review is expected to encourage further research on the role of natural dietary plant polyphenols in the treatment of AD.
... Arguably the most popular supplement used to enhance performance is caffeine, which can be consumed through various drinks (e.g., coffee and energy drinks) or as pills. Caffeine increases the excitability of the sympathetic nervous system [11,46] and consequently is used to enhance alertness-although there are large individual differences with regards to the response to caffeine and its effect on cognition or physical performance [21,23,81]. However, there are many more foods and food supplements that potentially enhance performance-and the market for such products exceeds 100 billion USD, with an annual growth rate of 3-4% [87]. ...
Article
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This work explores perceptions of performance enhancer usage in esports. Specifically, we explored the perception of: food and food supplements; non-medical use of prescription drugs; drugs with some social acceptance (e.g. alcohol, nicotine, cannabis); drugs with lower social acceptance (e.g., psychedelics, opioids); and non-invasive brain stimulation (e.g. transcranial direct current stimulation). A mixed-methods approach was used to triangulate findings around three data sets, including both prompted and unprompted online forum comments, as well as survey data. The studies evidence that players are willing to use or are already using enhancers to increase their in-game performance, and that players are generally concerned about the use of enhancers in professional esports contexts. Furthermore, the community perceives that a substantial number of e-athletes use enhancers. The core contribution of this work is a comprehensive investigation into perspectives of esports performance enhancement, which highlights the urgent need for further research, as well as regulation by esports leagues.
... This suggests that cognition enhancements seen with caffeine intake could be partly due to its ability to promote cholinergic neurotransmission in the CNS. Numerous studies indicate that caffeine could help treat AD due to its beneficial effects on cognition, learning, memory, and neuroprotective effects (Arendash & Cao, 2010;Ikram et al., 2020;Mohamed et al., 2013;Panza et al., 2015;Ribeiro et al., 2002;Zhou & Zhang, 2021). Caffeine also reduces β-site amyloid precursor protein cleaving enzyme-1 (BACE-1) expression and activity (Tabaton, 2009). ...
Article
Natural products have significantly contributed to drug discovery for neurodegenerative diseases. Caffeine is one of the well‐known central nervous system(CNS)‐active natural products. Besides its CNS stimulant properties, it is a mild inhibitor of acetylcholinesterase (AChE) and possesses memory‐enhancing properties. The present work aimed to improve the AChE inhibition activity of the caffeine. The rationally designed caffeine‐based triazoles were synthesized and evaluated in vitro for cholinesterase and β‐site amyloid precursor protein cleaving enzyme‐1 (BACE‐1) inhibitory activities. The attachment of triazole to the caffeine enhances its AChE inhibition activity from half‐maximal inhibitory concentration (IC50) of 129 µM to 0.49 µM (derivative, 6l). The caffeine core interacts with the peripheral anionic site, whereas the benzyl triazole occupies the catalytic anionic site located at the bottom of the active site gorge. The structure–activity relationship revealed that the four‐atom ester linker is superior to shorter linkers for connecting the caffeine core to the triazole. The 2,6‐difluorobenzyl triazole‐linked caffeine derivative, 6d, exhibits dual inhibition of AChE and BACE‐1 with IC50 values of 1.43 and 10.9 µM, respectively. The derivative 6d inhibits AChE via a mixed‐type mode with an inhibition rate constant (Ki) value of 2.35 μM, which was corroborated by docking studies. The triazole 6d has an acceptable stability profile in human liver microsomes (t1/2 = 54 min) and was found to possess CNS permeability when evaluated using the parallel artificial membrane permeability blood–brain barrier assay. The results presented herein warrant investigating caffeine‐based triazoles in preclinical models of Alzheimer's disease.
... The health benefit of tea includes prevention of cancer, diabetes, cardiovascular and neurodegenerative diseases, reduction of body weight, and alleviation of metabolic syndrome (Zhao et al. 2015a;Yang et al. 2018). The p olyphenols in tea p oss ess antiproliferative, anti-inflammatory, antioxidant, antiviral, and antibacterial properties (Zhang et al. 2013a;Abd El-Aty et al. 2014;Panza et al. 2015;Chung et al. 2020). Besides, theanine, a unique amino acid derived during tea fermentation, has been shown to have neuroprotective effects and antiviral activities against the influenza and SARS (Severe Acute Respiratory Syndrome) viruses including the new SARSCoV-2 (Mitsui et al. 2020;Sharma et al. 2020). ...
Article
Tea (Camellia sinensis L.) is a high valued beverage worldwide since ancient times; more than three billion cups of tea are consumed each day. Leaf extracts of the plant are used for food preservation, cosmetics, and medicinal purposes. Nevertheless, tea contaminated with mycotoxins poses a serious health threat to humans. Mycotoxin production by tea fungi is induced by a variety of factors, including poor processing methods and environmental factors such as high temperature and humidity. This review summarizes the studies published to date on mycotoxin prevalence, toxicity, the effects of climate change on mycotoxin production, and the methods used to detect and decontaminate tea mycotoxins. While many investigations in this domain have been carried out on the prevalence of aflatoxins and ochratoxins in black, green, pu-erh, and herbal teas, much less information is available on zearalenone, fumonisins, and Alternaria toxins. Mycotoxins in teas were detected using several methods; the most commonly used being the High-Performance Liquid Chromatography (HPLC) with fluorescence detection, followed by HPLC with tandem mass spectrometry, gas chromatography and enzyme-linked immunosorbent assay. Further, mycotoxins decontamination methods for teas included physical, chemical, and biological methods, with physical methods being most prevalent. Finally, research gaps and future directions have also been discussed.
... Therefore, it is crucial that a long term, low-toxicity, and cost-effective method to treat or even prevent AD is discovered. Research has demonstrated that coffee may pose as a potential substance for AD treatment or prevention (49)(50)(51)(52)(53)(54)(55)(56). ...
Article
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Background Alzheimer's disease (AD) is a multifactorial neurological disease with neurofibrillary tangles and neuritic plaques as histopathological markers. Due to this, although AD is the leading cause of dementia worldwide, clinical AD dementia cannot be certainly diagnosed until neuropathological post-mortem evaluation. Coffee has been reported to have neurologically protective factors, particularly against AD, but coffee brand and type have not been taken into consideration in previous studies. We examined the discrepancies among popular commercial and instant coffees in limiting the development and progression through Aβ1-40 and Aβ1-42 production, and hypothesized that coffee consumption, regardless of brand or type, is beneficial for stalling the progression and development of Aβ-related AD. Methods Coffee samples from four commercial coffee brands and four instant coffees were purchased or prepared following given instructions and filtered for the study. 5, 2.5, and 1.25% concentrations of each coffee were used to treat N2a/APPswe cell lines. MTT assay was used to assess cell viability for coffee concentrations, as well as pure caffeine concentrations. Sandwich ELISA assay was used to determine Aβ concentration for Aβ1-40 and Aβ1-42 peptides of coffee-treated cells. Results Caffeine concentrations were significantly varied among all coffees (DC vs. MDC, PC, SB, NIN, MIN p < 0.05). There was no correlation between caffeine concentration and cell toxicity among brands and types of coffee, with no toxicity at 0.5 mg/ml caffeine and lower. Most coffees were toxic to N2a/APPswe cells at 5% (p < 0.05), but not at 2.5%. Most coffees at a 2.5% concentration reduced Aβ1-40 and Aβ1-42 production, with comparable results between commercial and instant coffees. Conclusion All coffees tested have beneficial health effects for AD through lowering Aβ1-40 and Aβ1-42 production, with Dunkin' Donuts® medium roast coffee demonstrating the most consistent and optimal cell survival rates and Aβ concentration. On the other hand, Starbucks® coffee exhibited the highest cell toxicity rates among the tested coffees.
... 2 Whether long-term, habitual, caffeine intake reduces or delays age-related cognitive impairment is unclear. 3 Most studies of cognitive decline or dementia present results separately for each dietary source of caffeine, thus separating beverage-specific associations from caffeine-specific associations is difficult. Meta-analyses of prospective studies of coffee consumption report no association with incident dementia or a nonlinear shaped association whereby light to moderate coffee drinking is protective, whereas none or very high intakes are relatively deleterious. ...
Article
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Objective: To examine the association between caffeine intake and cognitive impairment. Caffeine-neuropathology correlations and interactions with lifestyle and genetic factors impacting caffeine metabolism and response were also tested. Methods: We included 888 participants aged 59+ from the Rush Memory and Aging Project(MAP) and 303,887 participants aged 55+ from UK Biobank(UKB). MAP participants took part in annual cognitive testing. Diagnosis of dementia was based on clinical neurological examination and standardized criteria. A subset provided postmortem tissue for neuropathologic evaluation for common age-related diseases (e.g. AD, Lewy bodies, vascular). For UKB, dementia was determined by linked hospital and death records. Self-reported caffeine intake was estimated using food-frequency questionnaires in both cohorts. Cox proportional hazard ratio(HR), regression and mixed models were used to examine associations of caffeine intake with incident dementia, cognitive decline, and neuropathology. Results: In MAP, compared to ≤100mg/d, caffeine intake >100mg/d was associated with a significantly higher HR(95%CI) of all-cause[1.35(1.03,1.76)] and Alzheimer's[1.41(1.07,1.85)] dementia. Caffeine intake was not associated with cognitive decline. In UKB, compared to ≤100mg/d, the HRs(95%CI) of all-cause dementia for consuming 100≤200, 200≤300, 300≤400 and >400mg/d were 0.83(0.72,0.94), 0.74(0.64,0.85), 0.74(0.64,0.85) and 0.92(0.79,1.08), respectively. Similar results were observed for Alzheimer's dementia. In MAP, caffeine intake was inversely associated with postmortem Lewy bodies but no other age-related pathologies. Caffeine intake >100mg/d was associated with lower neocortical type Lewy bodies[Odds ratio(95%CI): 0.40(0.21,0.75)]. Interpretation: Caffeine intake was inconsistently associated with clinical dementia; potentially explained by cohort differences in underlying dementia etiology. Lewy bodies may link caffeine to lower risk in some persons. This article is protected by copyright. All rights reserved.
... In animal experiments, caffeine has been shown to promote improved memory and reverse the pathophysiology of Alzheimer's disease. Drinking caffeine-containing substances can thus help maintain cognitive function [53]. ...
Article
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Background: This study examines correlates of disabilities related to ADL, IADL, mobility, and frailty in men and women with a nationally representative sample of older adults living in the community. Methods: A total of 10,898 noninstitutionalized Taiwanese nationals aged 65 years and older enrolled in the 2001 (N = 2,064), 2005 (N = 2,727), 2009 (N = 2,904), and 2013 (N = 3,203) National Health Interview Survey (NHIS) were analyzed. Results: The prevalence of mobility disabilities and frailty in older adults in Taiwan decreased during the past decade ([Formula: see text], [Formula: see text]). Exercise, social engagement, and tea and coffee intake were found to be associated with lower levels of all types of disabilities in both men and women. In addition, a diet based on carbohydrates, falls, depressive symptomatology, lung and metabolic diseases were risks for most of the disabilities under consideration. Gender-specific independent correlates included: being married (OR = 0.63, 95%CI: 0.40-0.98), eggs/beans/fish/meat consumption (OR = 0.35, 95% CI = 0.16-0.80); depressive symptoms, obesity and cataracts, which were associated with higher IADL (OR = 3.61, 1.63, and 1.18, respectively) and frailty limitations (OR = 10.89, 1.27, and 1.20, respectively) in women. Cognitive impairment was found to be an important correlate for ADL limitations in men (OR = 3.64, 95%CI: 2.38-5.57). Conclusions: Exercise, social participation and diet (more tea and coffee intake and lower carbohydrates) were correlates for lower levels of disability. Some gender-specific correlates were also identified, including associations of disability with depressive symptoms, obesity, and cataracts that were more distinct in women, and lower levels of disability which were especially significant in men who were married, eat more eggs, beans, fish, and meat, and those free from cognitive impairment.
... Caffeine has also been shown to exhibit anti-neuroinflammatory properties as well as decreasing tau protein phosphorylation in the hippocampus [190]. In low to moderate doses, caffeine inhibits AChE, thereby improving cognitive actions and reducing the progression of AD [191]. Eugenol, found in cloves, has been reported to reduce amyloid plagues and increase memory in rat models induced with Aβ peptides [192]. ...
Article
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Alzheimer’s disease (AD) rate is accelerating with the increasing aging of the world’s population. The World Health Organization (WHO) stated AD as a global health priority. According to the WHO report, around 82 million people in 2030 and 152 million in 2050 will develop dementia (AD contributes 60% to 70% of cases), considering the current scenario. AD is the most common neurodegenerative disease, intensifying impairments in cognition, behavior, and memory. Histopathological AD variations include extracellular senile plaques’ formation, tangling of intracellular neurofibrils, and synaptic and neuronal loss in the brain. Multiple evidence directly indicates that oxidative stress participates in an early phase of AD before cytopathology. Moreover, oxidative stress is induced by almost all misfolded protein lumps like α-synuclein, amyloid-β, and others. Oxidative stress plays a crucial role in activating and causing various cell signaling pathways that result in lesion formations of toxic substances, which foster the development of the disease. Antioxidants are widely preferred to combat oxidative stress, and those derived from natural sources, which are often incorporated into dietary habits, can play an important role in delaying the onset as well as reducing the progression of AD. However, this approach has not been extensively explored yet. Moreover, there has been growing evidence that a combination of antioxidants in conjugation with a nutrient-rich diet might be more effective in tackling AD pathogenesis. Thus, considering the above-stated fact, this comprehensive review aims to elaborate on the basics of AD and antioxidants, including the vitality of antioxidants in AD. Moreover, this review may help researchers to develop effectively and potentially improved antioxidant therapeutic strategies for this disease as it also deals with the clinical trials in the stated field.
... which was similar to our results. The caffeine in tea may improve human cognition and catechins contained in tea were strong antioxidants against oxidative stress [46]. ...
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Background Subjective cognitive decline (SCD) may be the first symptomatic manifestation of Alzheimer’s disease, but information on its health correlates is still sparse in Chinese older adults. This study aimed to estimate SCD symptoms and its association with socio-demographic characteristics, common chronic diseases among southern Chinese older adults. Methods Participants aged 60 years and older from 7 communities and 2 nursing homes in Guangzhou were recruited and interviewed with standardized assessment tools. Pittsburgh Sleep Quality Index (PSQI), Patient Health Questionnaire–9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7) were used to measure poor sleep quality, depression symptoms and anxiety symptoms. The SCD symptoms were measured by SCD questionnaire 9 (SCD-Q9) which ranged from 0 to 9 points, with a higher score indicating increased severity of the SCD. Participants were divided into low score group (SCD-Q9 score ≤ 3) and higher score group (SCD-Q9 score > 3). Chi-square tests and multivariate logistic regression analysis were used for exploring the influences of different characteristics of socio-demographic and lifestyle factors on SCD symptoms. Univariate and multivariate logistic regression analysis were applied to explore the association between SCD symptoms with common chronic diseases. Results A total of 688 participants were included in our analysis with a mean age of 73.79 ( SD = 8.28, range: 60–101), while 62.4% of the participants were females. The mean score of the SCD-Q9 was 3.81 ± 2.42 in the whole sample. A total of 286 participants (41.6%) were defined as the low score group (≤3 points), while 402 participants (58.4%) were the high score group (> 3 points). Multivariate logistic regression analysis revealed that female ( OR = 1.99, 95%CI: 1.35–2.93), primary or lower education level ( OR = 2.58, 95%CI : 1.38–4.83), nursing home ( OR = 1.90, 95%CI : 1.18–3.05), napping habits ( OR = 1.59, 95%CI : 1.06–2.40), urolithiasis ( OR = 2.72, 95%CI : 1.15–6.40), gout ( OR = 2.12, 95%CI : 1.14–3.93), poor sleep quality ( OR = 1.93, 95%CI : 1.38–2.71), depression symptoms ( OR = 3.01, 95%CI : 1.70–5.34) and anxiety symptoms ( OR = 3.11, 95%CI : 1.29–7.46) were independent positive related to high SCD-Q9 score. On the other hand, tea-drinking habits ( OR = 0.64, 95%CI : 0.45–0.92), current smoking ( OR = 0.46, 95%CI : 0.24–0.90) were independent negative related to high SCD-Q9 score. Conclusions Worse SCD symptoms were closely related to common chronic diseases and socio-demographic characteristics. Disease managers should pay more attention to those factors to early intervention and management for SCD symptoms among southern Chinese older adults.
... In conclusion, contrary to other neurodegenerative diseases [38,39], the potential effect of coffee and tea on MS severity remains to be uncovered. However, this study suggests a possible harmful effect of high doses of coffee and an intriguing possible interaction with HLA genes. ...
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Background and aims The association between lifestyle factors and Multiple Sclerosis (MS) disease severity and progression has been investigated to a lesser extent compared with susceptibility to the disease. We aimed to assess the impact of lifetime coffee and tea consumption on MS severity. Methods Design: a cross-sectional study. Two hundred and eight patients (139 women and 69 men) consecutively admitted to the Department of Neurology in Novara, Italy were asked about their lifetime consumption of coffee and tea. The lifetime intensity of consumption (cups/day) was estimated as the weighted sum of the mean number of standard cups drunk per day at different ages. A measure of cumulative lifetime load of the exposure was expressed in terms of cup-years. Disease severity was estimated by the Multiple Sclerosis Severity Score (MSSS). HLA-DRB1*15 and HLA-A*02 genotyping was performed in 167 patients. Results The MSSS was not associated with the status of coffee or tea consumer, or the amount of cups/day or cup-years. The Odds Ratios (OR) for falling in the upper tertile of the MSSS distribution was 1.30 (95% Confidence Interval (CI): 0.47-3.58) for coffee consumers of 1-3 cups/day and 1.14 (95%CI: 0.33-3.95) for 4-8 cups/day vs. non-consumers. The OR was 0.69 (95%CI: 0.35-1.34) for tea consumers vs. non-consumers. The results did not change substantially after controlling for age at onset, education, smoking status, and alcoholic drinking. However, heavy consumers of coffee (4-8 cups/day) more frequently had a progressive form than small consumers (1-3 cups/day) and non-consumers (19% vs. 14% vs. 0%), and the age at MS onset was significantly higher (36.6±10.3; 31.5±9.5; 28.6±8.1 years, p=0.001). Conclusions Coffee or tea intake is not associated with different severity of MS. However, we cannot exclude a possible effect of higher doses of coffee for a subgroup of patients.
... Interestingly, acute and appropriate caffeine administration could reverse sleep losseinduced cognitive degradation [24]. Besides its acute effect, the review summarized that long-term caffeine consumption protected against late-life cognitive impairment and dementia [25,26]. However, the effect on cognitive function was controversial as Mendelian randomization meta-analysis did not find any evidence to support beneficial or adverse long-term effects of coffee intake on global cognition [27]. ...
Article
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Schizophrenia is a common psychiatric disorder which affects approximately 1% of the population worldwide. However, the complexity of etiology, treatment resistance and side effects induced by current antipsychotics, relapse prevention, and psychosocial rehabilitation are still to be uncovered. Caffeine, as the world's most widely consumed psychoactive drug, plays a crucial role in daily life. Plenty of preclinical and clinical evidence has illustrated that caffeine consumption could have a beneficial effect on schizophrenia. In this review, we firstly summarize the factors associated with the caffeine-induced beneficial effect. Then, a variety of mechanism of actions independent of adenosine receptor signaling will be discussed with an emphasis on the potential contribution of the microbiome–gut–brain axis to provide more possibilities for future therapeutic, prognosis, and social rehabilitation strategy.
... It has been shown that coffee and caffeine can have both -positive and negative effects on human health. On the one hand, caffeine is used to treat premature bronchopulmonary dysplasia, it may have a protective effect in some diseases such as Parkinson's disease [5], Alzheimer's disease (but not yet fully proven) [6], and for some types of tumors (hepatocyte, endometrial, prostate) [7]. Caffeine can prevent the death of pancreatic cells in alcohol poisoning [8]. ...
Article
The effects of long-lasting high concentration coffee and caffeine diets on calcium mobilization in rat hippocampal neurons were studied. Changes in the basal calcium level in the hippocampal neurons of control and experimental rats kept on a coffee or caffeine diet were measured. We also recorded the changes in the Ca2+ transients’ amplitude evoked by membrane depolarization or emptying the Ca2+ depot of the endoplasmic reticulum (ER) induced by caffeine activator of the ryanodine receptors. In rats on a coffee or caffeine diet, the basal Ca2+ level was increased by 7.4% and 11%, respectively, compared to control animals. In these groups, the amplitude of Ca2+ transients increased by 70% and 90%, respectively, of the basal level in response to the membrane depolarization. In the same groups, the amount of Ca2+ released from the ER was increased by two and three times, respectively, compared to the control after activation of ryanodine receptors. We concluded that long-term coffee and caffeine diets in rats cause a significant disruption of the hippocampal neurons’ endoplasmic reticulum function. The diets evoke an increase in Ca2+ concentration in the neurons and an excessive release of Ca2+ in response to excitation. The latter can lead to increased excitability of neurons and their further death from excessive Ca2+ levels.
Article
Background Atrial fibrillation is an independent risk factor for the development of cognitive impairments. Regular coffee consumption has shown cognitive benefits in healthy individuals. Whether regular consumption reduces cognitive decline in vulnerable patients is controversial. We investigated the association in elderly people with atrial fibrillation. Methods and Results Daily coffee consumption was assessed using a structured nutrition questionnaire, and cognitive function was evaluated by a detailed neurocognitive‐test‐battery, including the Montreal Cognitive Assessment, Trail‐Making Test, semantic fluency, and Digit‐Symbol‐Substitution Test. The cognitive construct score combines all neurocognitive tests mentioned and provides an overall cognitive performance indicator. Hs‐CRP (high‐sensitivity C‐reactive protein) and IL‐6 (interleukin‐6) were measured to explore an association with inflammation. Results were estimated using linear mixed‐effects‐models with detailed adjustments for confounders. The <1 cup/day consumers (reference group) reached a cognitive construct score of −0.24 (95% CI, –0.27 to –0.16), and the group with the highest consumption (>5 cups/day) was at −0.10 (95% CI, –0.10 to 0.04; p =0.048). Montreal Cognitive Assessment score in the reference group was 24.58 (95% CI, 24.58–25.32); the group with the highest intake achieved 25.25 (95% CI, 24.98–26.85; p =0.163). Inflammatory markers decreased with higher coffee consumption (hs‐CRP with 5 compared with <1 cup/day by factor 0.78 [95% CI, 0.54–1.13], p = 0.188, IL‐6 significantly by factor 0.73 [95% CI, 0.57–0.95], p =0.017). Conclusions Coffee consumption in patients with atrial fibrillation may be associated with improved cognitive performance and reduced inflammatory markers. Further research is needed to confirm these findings and to consider implementation in dietary counseling for atrial fibrillation management. Registration URL: https://www.clinicaltrials.gov ; Identifier: NCT02105844.
Article
Background: The consumption of coffee has been associated with beneficial effects when it comes to Alzheimer's disease (AD). However, to the best of our knowledge, there are no studies on Conilon coffee consumption in elderly people with AD. Objective: Evaluate the effects of Conilon coffee consumption in elderly with AD. Methods: The study was carried out with 9 participants who consumed a minimum of 2 cups (200 mL cup) of Conilon coffee per day for 90 days. Cognitive assessment was done before (T0) and after 90 days (T90). Blood analysis was conducted at T0 and T90, as well as the assessment of advanced oxidation protein products (AOPP) and thiobarbituric acid reactive species (TBARS). The levels of chlorogenic acids and caffeine in the coffee beverage were quantified by liquid chromatography. Results: During the treatment, the participants consumed at least 550 mg and 540 mg of CGAs and caffeine, respectively. A significant improvement in cognition between T0 and T90 was observed as per MMSE, CTP, and clock drawing tests. Furthermore, there was a significant reduction in AOPP (37%) and TBARS (60%), indicating a reduction in oxidative stress. The consumption of the coffee did not significantly alter any blood parameter, which confirms the safety of the coffee treatment during the 90 days. Conclusions: Our study demonstrated for the first time that regular consumption of coffee with high amounts of CGAs and caffeine improves cognitive functions and reduces oxidative stress, without altering blood parameters that indicate possible signs of toxicity in classical target organs.
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Oxidative phosphorylation causes free radicals to accumulate in the mitochondria. A rise in oxidative stress is triggered by their high reactivity and unoccupied electrons. The brain is particularly affected by this ailment since it often requires a lot of oxygen and has a high potential for collecting “Reacting Species.” Antioxidant molecules have a critical role in preventing free radical disruption, especially in the brain. In particular, oxidative stress appears to accelerate the progression of neurodegenerative disorders. The goal of this chapter is to identify natural antioxidant molecules that have the highest ability to defend against the formation of free radicals while also gaining a knowledge of how these molecules interact with the central nervous system. This chapter also aims to give an outline of the scientific research and professional opinion on the factors associated with the lifestyle that promotes brain health as people age. The topics to be covered include mental health, brain-stimulating activities, sleep, social interaction, diet and nutrition for brain health, physical activity, and brain-protective antioxidant dietary supplements.
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Our present knowledge about the efficacy of tea consumption in improving age-related cognitive disorders is incomplete since previous epidemiological studies provide inconsistent evidence. This unified systematic review and meta-analysis based on updated epidemiological cohort studies and randomized controlled trials (RCTs) evidence aimed to overcome the limitations of previous reviews by examining the efficacy of distinct types of tea consumption. PubMed, Embase, and MEDLINE were searched up to May 20, 2022, and 23 cohorts and 12 cross-sectional studies were included. Random-effects meta-analyses were conducted to obtain pooled RRs or mean differences with 95% CIs. The pooled RRs of the highest versus lowest tea consumption categories were 0.81 (95% CIs: 0.75-0.88) and 0.69 (95% CIs: 0.61-0.77), respectively. The pooled mean difference of four included RCTs revealed a beneficial effect of tea on cognitive dysfunction (MMSE ES: 1.03; 95% CI, 0.14-1.92). Subgroup analyses further demonstrated that green and black tea intake was associated with a lower risk of cognitive disorders in eastern countries, especially in women. The evidence quality was generally low to moderate. The present review provides insight into whether habitual tea consumption can be an effective approach against age-related neurodegenerative cognitive disorders and summarizes potential mechanisms based on currently published literature.
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The aim of this study was to explore urine caffeine metabolites in relation to cognitive performance among 2011-2014 National Health and Nutrition Examination Survey participants aged ≥60 years. We hypothesized that urine caffeine metabolites were positively associated with cognition in older adults. Caffeine and 14 of its metabolites were quantified in urine by use of high-performance liquid chromatography-electrospray ionization-tandem quadruple mass spectrometry with stable isotope labeled internal standards. Cognitive assessment was based on scores from the word learning and recall modules. Participants were categorized based on the quartiles of caffeine and its metabolites level. The association between caffeine metabolites and each cognitive dimension was analyzed using multiple logistic regression analysis in adjusted models. Stratification analyses by gender were also performed. For CERAD test, there was a significant association between 1-methyluric acid (OR=0.62, 95% CI: 0.42 to 0.92), 7-methylxanthine(OR=0.49, 95% CI: 0.27 to 0.89), theophylline (OR=0.52, 95% CI: 0.29 to 0.92), as well as paraxanthine (OR=0.49, 95% CI: 0.27 to 0.88) and cognitive function. For animal fluency test, there was a positive association between theophylline (TP) (OR=0.44, 95% CI: 0.22 to 0.89) and cognitive function. The trend that the risk of low cognitive function decreased with increasing concentration of 1-methylxanthine (P trend=0.0229) was also observed. Furthermore, the same trend existed for 3-methylxanthine (p trend = 0.0375) in men. In conclusion, there was a significant positive association between urine caffeine metabolites and cognitive performance in older adults, particularly for theophylline, paraxanthine and caffeine; and the association might be dependent on gender.
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Approximately two-thirds of individuals diagnosed with Alzheimer’s disease are women. Although women tend to have longer life expectancy than men, this does not entirely explain the differences in the prevalence of dementia and Alzheimer’s disease. Some evidence suggests that men and women have different patterns of risk and protective factors across the lifespan. The goal of this chapter is to summarize the current evidence on sex differences in genetic and modifiable lifestyle factors that are associated with dementia risk. These include demographic factors such education, vascular, metabolic, lifestyle, and psychosocial factors, and sex-specific factors such as menopause and andropause. Potential mechanisms such as neural reserve and resilience are also summarized. The chapter also summarizes the evidence from recent multidomain lifestyle intervention trials, and the intervention response observed in men and women. While there have been insightful advancements in the field, many important questions still remain. Considerations for future research and risk reduction initiatives are also highlighted.
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Coffee is a popular beverage, and it contains caffeine, a psychoactive substance. Consuming coffee may reduce the risk of developing Alzheimer’s disease (AD). However, the association between the reduced risk of developing AD and the consumption of coffee is controversial. Therefore, we conducted a systematic literature review and quantitative synthesis meta-analysis that included dose-response analysis on the relationship between the consumption of coffee and the risk of developing AD. Based on PRISMA guidelines, we analysed standard databases of journals published between January 1999 and May 2020. We included the two population-based cohort studies and one case-control study. All studies included looked at the association between consuming many cups of coffee, the amount of coffee consumed in milligrams per day and the risk of developing AD. The systematic literature review and meta-analysis had 1670 participants with follow-up years that ranged from 5 to 21. The consumption of moderate or 3-5 cups per day reduces the risk of developing AD. The pooled relative risk and 95% confidence interval of the 3 included studies were 0.63 (0.3, 1.54). Dose-response curve analysis appears to be U-shaped. The results of the forest plot showed that there is low heterogeneity between the studies. Plotting the funnel plot and the Galbraith plot demonstrated publication bias of the three included studies. More prospective and long-term studies have to be conducted in other countries to determine the exact risk of developing AD.
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Alzheimer’s disease is a progressive neurodegenerative disease, usually associated with old age. With the increasing geriatric population throughout the world, it will pose a great socio-economic burden on the healthcare system and the caregivers. The clinically approved drugs for management of this disease include cholinesterase inhibitors and memantine. But these drugs modulate only the symptoms of this disease rather than addressing the underlying pathology. Therefore, there is an urgent need to discover new therapeutic agents which, coupled with effective diagnostics, can prove effective in therapeutic management of this disease. Phosphodiesterase inhibitors represent an emerging class of drugs with several isoforms reported to play a crucial role in the pathology of this disease. This review discusses various phosphodiesterase inhibitors which are in preclinical and clinical studies along with physicochemical properties that impact CNS penetration and subsequent efficacy.
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Background Modifiable factors can influence the risk for Alzheimer’s disease (AD) and serve as targets for intervention; however, the biological mechanisms linking these factors to AD are unknown. This study aims to identify plasma metabolites associated with modifiable factors for AD, including MIND diet, physical activity, smoking, and caffeine intake, and test their association with AD endophenotypes to identify their potential roles in pathophysiological mechanisms. Methods The association between each of the 757 plasma metabolites and four modifiable factors was tested in the Wisconsin Registry for Alzheimer’s Prevention cohort of initially cognitively unimpaired, asymptomatic middle-aged adults. After Bonferroni correction, the significant plasma metabolites were tested for association with each of the AD endophenotypes, including twelve cerebrospinal fluid (CSF) biomarkers, reflecting key AD pathophysiologies, and four cognitive composite scores. Finally, causal mediation analyses were conducted to evaluate possible mediation effects. Analyses were performed using linear mixed-effects regression. Results A total of 27, 3, 23, and 24 metabolites were associated with MIND diet, physical activity, smoking, and caffeine intake, respectively. Potential mediation effects include beta-cryptoxanthin in the association between MIND diet and Preclinical Alzheimer Cognitive Composite score, hippurate between MIND diet and Immediate Learning, glutamate between physical activity and CSF neurofilament light, and beta-cryptoxanthin between smoking and Immediate Learning. Conclusion Our study identified several plasma metabolites that are associated with modifiable factors. These metabolites can be employed as biomarkers for tracking these factors, and they provide a potential biological pathway of how modifiable factors influence the human body and AD risk.
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Studying the correlation between cerebrospinal fluid (CSF) metabolites and the Alzheimer's Disease (AD) biomarkers may offer a window to the alterations of the brain metabolome and unveil potential biological mechanisms underlying AD. In this analysis, 308 CSF metabolites from 338 individuals of Wisconsin Registry for Alzheimer's Prevention and Wisconsin Alzheimer's Disease Research Center were included in a principal component analysis (PCA). The resulted principal components (PCs) were tested for association with CSF total tau (t-tau), phosphorylated tau (p-tau), amyloid β 42 (Aβ42), and Aβ42/40 ratio using linear regression models. Significant PCs were further tested with other CSF NeuroToolKit (NTK) and imaging biomarkers. Using a Bonferroni corrected p <0.05, five PCs were significantly associated with CSF p-tau and t-tau and three PCs were significantly associated with CSF Aβ42. Pathway analysis suggested that these PCS were enriched in six pathways, including metabolism of caffeine and nicotinate and nicotinamide. This study provides evidence that CSF metabolites are associated with AD pathology through core AD biomarkers and other NTK markers and suggests potential pathways to follow up in future studies.
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Free- radicals (Oxygen and Nitrogen species) are formed in mitochondria during the oxidative phosphorylation. Their high reactivity, due to not-engaged electrons, leads to an increase of the oxidative stress. This condition affects above all the brain, that usually needs a large oxygen amount and in which there is the major possibility to accumulate “Reacting Species.” Antioxidant molecules are fundamental in limiting free-radical damage, in particular in the central nervous system: the oxidative stress, in fact, seems to worsen the course of neurodegenerative diseases. The aim of this review is to sum up natural antioxidant molecules with the greatest neuroprotective properties against free radical genesis, understanding their relationship with the Central Nervous System.
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There is a large literature on the effects of caffeine on performance. Most of the studies have been conducted in the laboratory and further information is required on the effects of caffeine consumption on performance and safety at work. The present studies aimed to determine whether the level of caffeine consumption influenced changes in alertness and performance over the working day. Secondary analyses of a large epidemiological database were also conducted to examine associations between caffeine consumption and cognitive failures and accidents at work. In the first study 110 volunteers, all of whom were regular caffeine consumers, rated their alertness and carried out a simple reaction time task before and after work on a Monday and Friday. Caffeine consumption during the day was recorded and volunteers were sub-divided into low and high consumers on the basis of a median split (220 mg/day). The second study involved secondary analyses of a database formed by combining the Bristol Stress and Health at Work and Cardiff Health and Safety at Work studies. In the first analyses associations between caffeine consumption and frequency of cognitive failures were examined in a sample of 1253 white-collar workers. The second set of analyses examined associations between caffeine consumption and accidents at work in a sample of 1555 workers who were especially at risk of having an accident. The results from the first study showed that those who consumed higher levels of caffeine reported significantly greater increases in alertness over the working day and a significantly smaller slowing of reaction time. The results from the second study demonstrated significant associations between caffeine consumption and fewer cognitive failures and accidents at work. After controlling for possible confounding factors it was found that higher caffeine consumption was associated with about half the risk of frequent/very frequent cognitive failures and a similar reduction in risk for accidents at work. Overall, the results from the three analyses show that caffeine consumption may have benefits for performance and safety at work.
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Background/objective: To conduct a systematic review of all studies to determine whether there is an association between the Mediterranean diet (MeDi) and cognitive impairment. Methods: We conducted a comprehensive search of the major databases and hand-searched proceedings of major neurology, psychiatry, and dementia conferences through November 2012. Prospective cohort studies examining the MeDi with longitudinal follow-up of at least 1 year and reporting cognitive outcomes (mild cognitive impairment [MCI] or Alzheimer's disease [AD]) were included. The effect size was estimated as hazard-ratio (HR) with 95% confidence intervals (CIs) using the random-effects model. Heterogeneity was assessed using Cochran's Q-test and I2-statistic. Results: Out of the 664 studies screened, five studies met eligibility criteria. Higher adherence to the MeDi was associated with reduced risk of MCI and AD. The subjects in the highest MeDi tertile had 33% less risk (adjusted HR = 0.67; 95% CI, 0.55-0.81; p < 0.0001) of cognitive impairment (MCI or AD) as compared to the lowest MeDi score tertile. Among cognitively normal individuals, higher adherence to the MeDi was associated with a reduced risk of MCI (HR = 0.73; 95% CI, 0.56-0.96; p = 0.02) and AD (HR = 0.64; 95% CI, 0.46-0.89; p = 0.007). There was no significant heterogeneity in the analyses. Conclusions: While the overall number of studies is small, pooled results suggest that a higher adherence to the MeDi is associated with a reduced risk of developing MCI and AD, and a reduced risk of progressing from MCI to AD. Further prospective-cohort studies with longer follow-up and randomized controlled trials are warranted to consolidate the evidence. Systematic review registration number: PROSPERO 2013: CRD42013003868.
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Background Tea consumption has been reported to be associated with lowered risk of cardiovascular disease, stroke and osteoporosis that cause functional disability, but its association with physical function has not been investigated directly. Objective We examined the association between tea consumption and performance in gait and balance, instrumental and basic activities of daily living (IADL and BADL) in a cross-sectional study of community-living older persons. Method Baseline data of 2398 adults aged ≥ 55 years in the Singapore Longitudinal Ageing Studies who completed self-reported current tea consumption, Performance Oriented Mobility Assessment (POMA) of gait and balance, and self reports of BADL and IADL were analyzed. Results In multivariate analyses controlling for age, gender, education, housing type, co-morbidities, hospitalization, arthritis and hip fracture, GDS depression score, MMSE cognitive score, body mass index, creatinine, serum albumin, haemoglobin, physical activities score and coffee consumption, tea consumption was positively associated with better balance (β=0.06, p<0.01), gait (β=0.01, p=0.02), IADL (β=0.03, p=0.01) and BADL (β=0.01, p=0.05). Strongly positive associations were observed for black/oolong tea in multivariate analyses, and for green tea consumption only in univariate analysis, whereas coffee consumption was not associated at all. Conclusions Tea consumption was associated with better physical functional performances in community-living older adults.
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Background: Persons with vascular disorders are at higher risk of cognitive decline. Objective: To determine whether caffeine may be associated with cognitive decline reduction in elderly at high vascular risk. Methods: We included 2,475 women aged 65+ years in the Women's Antioxidant Cardiovascular Study, a randomized trial of antioxidants and B vitamins for cardiovascular disease secondary prevention. We ascertained regular caffeine intake at baseline (1995-1996) using a validated 116 item-food frequency questionnaire. From 1998-2000 to 2005-2006, we administered four telephone cognitive assessments at two-year intervals evaluating global cognition, verbal memory, and category fluency. The primary outcome was the change in global cognitive score, which was the average of the z-scores of all tests. We used generalized linear models for repeated measures that were adjusted for various sociodemographic, health, and lifestyle factors to evaluate the difference in cognitive decline rates across quintiles of caffeine intake. Results: We observed significantly slower rates of cognitive decline with increasing caffeine intake (p-trend = 0.02). The rate difference between the highest and lowest quintiles of usual caffeine intake (>371 versus <30 mg/day) was equivalent to that observed between those who were 7 years apart in age (p = 0.006). Consumption of caffeinated coffee was significantly related to slower cognitive decline (p-trend = 0.05), but not other caffeinated products (e.g., decaf, tea, cola, chocolate). We conducted interaction analyses and observed stronger associations in women assigned to vitamin B supplementation (p-interaction = 0.02). Conclusions: Caffeine intake was related to moderately better cognitive maintenance over 5 years in older women with vascular disorders.
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A systematic literature review of human studies relating caffeine or caffeine-rich beverages to cognitive decline reveals only 6 studies that have collected and analyzed cognition data in a prospective fashion that enables study of decline across the spectrum of cognition. These 6 studies, in general, evaluate cognitive function using the Mini Mental State Exam and base their beverage data on FFQs. Studies included in our review differed in their source populations, duration of study, and most dramatically in how their analyses were done, disallowing direct quantitative comparisons of their effect estimates. Only one of the studies reported on all 3 exposures, coffee, tea, and caffeine, making comparisons of findings across studies more difficult. However, in general, it can be stated that for all studies of tea and most studies of coffee and caffeine, the estimates of cognitive decline were lower among consumers, although there is a lack of a distinct dose response. Only a few measures showed a quantitative significance and, interestingly, studies indicate a stronger effect among women than men.
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Objective: We examined the longitudinal association between tea drinking frequency and cognitive function in a large sample of oldest-old Chinese. Design: population-based longitudinal cohort study. Setting: The Chinese Longitudinal Healthy Longevity Survey (CLHLS). Participants: 7139 participants aged 80 to 115 (mean age 91.4 years) who provided complete data at baseline (year 1998). Measurements: Current frequency of tea drinking and past frequency at age 60 were ascertained at baseline, and baseline and follow-up cognitive assessments were performed in the years 1998 (n=7139), 2000 (n=4081), 2002 (n=2288) and 2005 (n=913) respectively. Verbal fluency test was used as measure of cognitive function. Results: Tea drinking was associated at baseline with higher mean (SD) verbal fluency scores: daily=10.7 (6.6), occasional=9.2 (5.8), non-drinker=9.0 (5.5). In linear mixed effects model that adjusted for age, gender, years of schooling, physical exercise and activities score, the regression coefficient for daily drinking (at age 60) and occasional drinking was 0.72 (P<0.0001) and 0.41(P=0.01) respectively. Tea drinkers had higher verbal fluency scores throughout the follow-up period but concurrently had a steeper slope of cognitive decline as compared with non-drinkers (coefficient for the interaction term Time*Daily drinking= -0.12, P=0.02; "Time" was defined as the time interval from baseline to follow-up assessments in years). Similar results were found for current tea drinking status at study baseline year (1998) as predictor variable. Conclusion: Regular tea drinking is associated with better cognitive function in oldest-old Chinese.
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To address the pending public health crisis due to Alzheimer's disease (AD) and related neurodegenerative disorders, the Marian S. Ware Alzheimer Program at the University of Pennsylvania held a meeting entitled "State of the Science Conference on the Advancement of Alzheimer's Diagnosis, Treatment and Care," on June 21-22, 2012. The meeting comprised four workgroups focusing on Biomarkers; Clinical Care and Health Services Research; Drug Development; and Health Economics, Policy, and Ethics. The workgroups shared, discussed, and compiled an integrated set of priorities, recommendations, and action plans, which are presented in this article.
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Epidemiological studies have consistently shown that vascular risk factors including hypertension, diabetes, obesity, hypercholesterolemia, smoking, and lack of physical exercise are associated with an increased risk of cognitive decline and dementia. Neuroradiological and neuropathological studies have confirmed the importance of cerebrovascular lesions in the etiology of late onset dementia. We have reviewed the literature and conclude that up until now randomized controlled clinical trials targeting individual risk factors and assessing cognitive decline or dementia as an outcome have not convincingly shown that treatment of vascular risk factors can actually prevent or postpone cognitive decline and dementia. New studies targeting several vascular risk factors at the same time and using cognitive decline or dementia as primary outcome might answer the question whether cognitive decline can really be postponed or even prevented. The design of such studies is not straightforward and long follow-up is required. In this review we discuss several pertinent methodological issues that need to be addressed to achieve an optimal design of new randomized controlled trials.
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Regular consumption of fruit and vegetables has been considered to be associated with a reduced risk of dementia and age-associated cognitive decline, although the association is currently unsupported by a systematic review of the literature. We searched Medline, Embase, Biosis, ALOIS, the Cochrane library, different publisher databases as well as bibliographies of retrieved articles. All cohort studies with a follow-up of 6 months or longer were included if they reported an association of Alzheimer's disease or cognitive decline in regard to the frequency of fruit and vegetables consumption. Nine studies with a total of 44,004 participants met the inclusion criteria. Six studies analyzed fruit and vegetables separately and five of them found that higher consumption of vegetables, but not fruit is associated with a decreased risk of dementia or cognitive decline. The same association was found by three further studies for fruit and vegetable consumption analytically combined. Increased intake of vegetables is associated with a lower risk of dementia and slower rates of cognitive decline in older age. Yet, evidence that this association is also valid for high fruit consumption is lacking.
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Diabetic conditions are associated with modified brain function, namely with cognitive deficits, through largely undetermined processes. More than understanding the underlying mechanism, it is important to devise novel strategies to alleviate diabetes-induced cognitive deficits. Caffeine (a mixed antagonist of adenosine A(1) and A(2A) receptors) emerges as a promising candidate since caffeine consumption reduces the risk of diabetes and effectively prevents memory deficits caused by different noxious stimuli. Thus, we took advantage of a novel animal model of type 2 diabetes to investigate the behavioural, neurochemical and morphological modifications present in the hippocampus and tested if caffeine consumption might prevent these changes. We used a model closely mimicking the human type 2 diabetes condition, NONcNZO10/LtJ mice, which become diabetic at 7-11 months when kept under an 11% fat diet. Caffeine (1 g/l) was applied in the drinking water from 7 months onwards. Diabetic mice displayed a decreased spontaneous alternation in the Y-maze accompanied by a decreased density of nerve terminal markers (synaptophysin, SNAP25), mainly glutamatergic (vesicular glutamate transporters), and increased astrogliosis (GFAP immunoreactivity) compared to their wild type littermates kept under the same diet. Furthermore, diabetic mice displayed up-regulated A(2A) receptors and down-regulated A(1) receptors in the hippocampus. Caffeine consumption restored memory performance and abrogated the diabetes-induced loss of nerve terminals and astrogliosis. These results provide the first evidence that type 2 diabetic mice display a loss of nerve terminal markers and astrogliosis, which is associated with memory impairment; furthermore, caffeine consumption prevents synaptic dysfunction and astrogliosis as well as memory impairment in type 2 diabetes.
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Brain oxidative processes play a major role in age-related cognitive decline, thus consumption of antioxidant-rich foods might help preserve cognition. Our aim was to assess whether consumption of antioxidant-rich foods in the Mediterranean diet relates to cognitive function in the elderly. In asymptomatic subjects at high cardiovascular risk (n = 447; 52% women; age 55-80 y) enrolled in the PREDIMED study, a primary prevention dietary-intervention trial, we assessed food intake and cardiovascular risk profile, determined apolipoprotein E genotype, and used neuropsychological tests to evaluate cognitive function. We also measured urinary polyphenols as an objective biomarker of intake. Associations between energy-adjusted food consumption, urinary polyphenols, and cognitive scores were assessed by multiple linear regression models adjusted for potential confounders. Consumption of some foods was independently related to better cognitive function. The specific associations [regression coefficients (95% confidence intervals)] were: total olive oil with immediate verbal memory [0.755 (0.151-1.358)]; virgin olive oil and coffee with delayed verbal memory [0.163 (0.010-0.316) and 0.294 (0.055-0.534), respectively]; walnuts with working memory [1.191 (0.061-2.322)]; and wine with Mini-Mental State Examination scores [0.252 (0.006-0.496)]. Urinary polyphenols were associated with better scores in immediate verbal memory [1.208 (0.236-2.180)]. Increased consumption of antioxidant-rich foods in general and of polyphenols in particular is associated with better cognitive performance in elderly subjects at high cardiovascular risk. The results reinforce the notion that Mediterranean diet components might counteract age-related cognitive decline.
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This review summarizes the literature on the association between tea consumption and cognitive health in late life. Population-based studies reviewed in this article suggest that tea drinking has beneficial effects on cognitive function of elderly persons. However, a cause-effect relationship between tea consumption and cognitive decline and dementia could not be drawn given inconsistent findings from only two longitudinal cohort studies. The neuroprotective effects of tea consumption could be due to catechins, L-theanine and other compounds in tea leaves. More longitudinal observational study is needed. Information on life-time tea consumption and blood concentrations of catechins and L-theanine could be collected in future studies.
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Although both human epidemiologic and animal model studies have suggested that caffeine/coffee protects against Alzheimer's disease, direct human evidence for this premise has been lacking. In the present case-control study, two separate cohorts consisting of 124 total individuals (65-88 years old) were cognitively assessed and a blood sample taken for caffeine/biomarker analysis. Subjects were then monitored for cognitive status over the ensuing 2-4 year period to determine the extent to which initial plasma caffeine/biomarkers levels would be predictive of changes in cognitive status. Plasma caffeine levels at study onset were substantially lower (-51%) in mild cognitive impairment (MCI) subjects who later progressed to dementia (MCI→DEM) compared to levels in stable MCI subjects (MCI→MCI). Moreover, none of the MCI→DEM subjects had initial blood caffeine levels that were above a critical level of 1200 ng/ml, while half of stable MCI→MCI subjects had blood caffeine levels higher than that critical level. Thus, plasma caffeine levels greater than 1200 ng/ml (≈6 μM) in MCI subjects were associated with no conversion to dementia during the ensuing 2-4 year follow-up period. Among the 11 cytokines measured in plasma, three of them (GCSF, IL-10, and IL-6) were decreased in MCI→DEM subjects, but not in stable MCI→MCI subjects with high plasma caffeine levels. Coffee would appear to be the major or perhaps only source of caffeine for such stable MCI patients. This case-control study provides the first direct evidence that caffeine/coffee intake is associated with a reduced risk of dementia or delayed onset, particularly for those who already have MCI.
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Objective: In several longitudinal studies, light-to-moderate drinking of alcoholic beverages has been proposed as being protective against the development of age-related changes in cognitive function, predementia syndromes, and cognitive decline of degenerative (Alzheimer's disease, AD) or vascular origin (vascular dementia). However, contrasting findings also exist. Method: The English literature published in this area before September 2011 was evaluated, and information relating to the various factors that may impact upon the relationship between alcohol consumption and dementia or predementia syndromes is presented in the succeeding texts. Results: Light-to-moderate alcohol consumption may be associated with a reduced risk of incident overall dementia and AD; however, protective benefits afforded to vascular dementia, cognitive decline, and predementia syndromes are less clear. The equivocal findings may relate to many of the studies being limited to cross-sectional designs, restrictions by age or gender, or incomplete ascertainment. Different outcomes, beverages, drinking patterns, and study follow-up periods or possible interactions with other lifestyle-related (e.g., smoking) or genetic factors (e.g., apolipoprotein E gene variation) may all contribute to the variability of findings. Conclusion: Protective effects of moderate alcohol consumption against cognitive decline are suggested to be more likely in the absence of the AD-associated apolipoprotein E ε4 allele and where wine is the beverage. At present, there is no indication that light-to-moderate alcohol drinking would be harmful to cognition and dementia, and attempts to define what might be deemed beneficial levels of alcohol intake in terms of cognitive performance would be highly problematic and contentious. Copyright
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The relation between coffee intake and risk of amyotrophic lateral sclerosis (ALS) was investigated in 377 newly diagnosed ALS patients from 4 Italian population-based registries in the European ALS Consortium (EURALS Group) (2007-2010). For each patient, 2 age- and sex-matched hospital controls were selected, one from a neurology department and one from a nonneurologic department. Two additional healthy control groups were identified from local general practitioners' (GPs') lists (n = 99) and residents of the same area as a cancer cohort (n = 7,057). Coffee intake was defined in terms of status (ever consuming coffee daily for ≥6 months vs. never), duration, and history (never, former, or current). Ever coffee drinkers comprised 74.7% of ALS patients, 80.4% of neurologic controls, 85.6% of nonneurologic controls (P = 0.0004), 88.9% of GP controls (P = 0.0038), and 86.0% of cancer cohort controls (P < 0.0001). Current coffee drinkers comprised 60.2% of ALS patients, 70.2% of neurologic controls (P = 0.0294), 76.4% of nonneurologic controls (P < 0.0001), and 82.3% of GP controls (P = 0.0002); duration of intake was ≥30 years for 62.3%, 67.7%, 74.7%, and 72.6%. ALS patients had lower lifetime coffee exposure: Odds ratios were 0.7 (95% confidence interval (CI): 0.5, 1.1), 0.6 (95% CI: 0.4, 0.8), and 0.4 (95% CI: 0.2, 0.9) in comparison with neurologic, nonneurologic, and GP controls, respectively. In current (vs. never) coffee drinkers, odds ratios were 0.7 (95% CI: 0.5, 1.0), 0.5 (95% CI: 0.3, 0.7), and 0.4 (95% CI: 0.2, 0.8), respectively. These findings provide epidemiologic evidence of an inverse correlation between coffee intake and ALS risk.
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Caffeine is the world's most widely used central nervous system stimulant, with approximately 80% consumed in the form of coffee. However, studies that analyze prospectively the relationship between coffee or caffeine consumption and depression risk are scarce. A total of 50,739 US women (mean age, 63 years) free of depressive symptoms at baseline (in 1996) were prospectively followed up through June 1, 2006. Consumption of caffeine was measured from validated questionnaires completed from May 1, 1980, through April 1, 2004, and computed as cumulative mean consumption with a 2-year latency period applied. Clinical depression was defined as self-reported physician-diagnosed depression and antidepressant use. Relative risks of clinical depression were estimated using Cox proportional hazards regression models. During 10 years of follow-up (1996-2006), 2607 incident cases of depression were identified. Compared with women consuming 1 or less cup of caffeinated coffee per week, the multivariate relative risk of depression was 0.85 (95% confidence interval, 0.75-0.95) for those consuming 2 to 3 cups per day and 0.80 (0.64-0.99; P for trend<.001) for those consuming 4 cups per day or more. Multivariate relative risk of depression was 0.80 (95% confidence interval, 0.68-0.95; P for trend=.02) for women in the highest (≥550 mg/d) vs lowest (<100 mg/d) of the 5 caffeine consumption categories. Decaffeinated coffee was not associated with depression risk. In this large longitudinal study, we found that depression risk decreases with increasing caffeinated coffee consumption. Further investigations are needed to confirm this finding and to determine whether usual caffeinated coffee consumption can contribute to depression prevention.
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Caffeine intake has been associated with a lower incidence of Alzheimer's disease (AD) in humans. In AD mouse models, caffeine significantly decreases senile plaques and amyloid beta (Aβ) levels while also protecting against or reversing cognitive impairment. To understand the mechanism(s) underlying the protective effects of caffeine against AD pathology, we investigated the effects of a two-week treatment with caffeine (3mg/day) in transgenic (APPswe) mice and non-transgenic (NT) mice on signaling factors involved in neuronal plasticity and survival. We evaluated cAMP-dependent protein kinase A (PKA), phospho-cyclic AMP response-element binding protein (phospho-CREB), and the pro-apoptotic protein kinases extracellular signal-regulated kinase 1/2 (phospho-ERK) and phospho-c-Jun N-terminal kinase 1 (phospho-JNK) in the striatum and frontal cortex of caffeine-treated mice. In the striatum, APPswe control mice exhibited a significant decrease in phospho-CREB, as well as significant increases in phospho-JNK and phospho-ERK in comparison to NT mice. Caffeine treatment stimulated PKA activity, increased phospho-CREB levels, and decreased phospho-JNK and phospho-ERK expression in the striatum of APPswe mice, all of which are thought to be beneficial changes for brain function. Even caffeine-treated NT mice exhibited some of these changes in striatum. In the frontal cortex, caffeine did not significantly increase phospho-CREB and PKA activity, but significantly reduced phospho-JNK and phospho-ERK expression in both APPswe and NT mice. These results suggest that caffeine shifts the balance between neurodegeneration and neuronal survival toward the stimulation of pro-survival cascades and inhibition of pro-apoptotic pathways in the striatum and/or cortex, which may contribute to its beneficial effects against AD.
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