-
1.
Brain Health and Cognitive Function - NED Infobite
BANT's scientific NED InfoBites are designed to provide key elements of the latest research using plain language. They provide quick overviews on particular health issues and nutrition topics for a speedy introduction to the science. Visually attractive and easily shareable with clients and social media followers.
2024
Abstract
With an ageing global population, it is expected that the incidence of age-related disorders such as Alzheimer's disease and cognitive decline is likely to increase. With the absence of effective treatment, focus is turning towards modifiable diet and lifestyle risk factors as a way of prevention. This NED Infobite highlights research on nutritional interventions, time-restricted eating, sleep and probiotics on Alzheimer's and cognitive decline.
-
2.
Can dementia risk be reduced by following the American Heart Association's Life's Simple 7? A systematic review and dose-response meta-analysis.
Wu, J, Xiong, Y, Xia, X, Orsini, N, Qiu, C, Kivipelto, M, Rizzuto, D, Wang, R
Ageing research reviews. 2023;83:101788
-
-
-
Free full text
Plain language summary
The American Heart Association (AHA) has defined ideal levels of seven modifiable cardiovascular health (CVH) factors, known as Life's Simple 7, that consist of smoking, physical activity, diet, body mass index, fasting blood glucose, total cholesterol, and blood pressure. Maintaining ideal levels of these factors has been recommended as a prevention strategy against not only cardiovascular diseases but also neurodegenerative disorders, e.g., cognitive decline and dementia. However, studies exploring the beneficial effects of the AHA’s CVH metrics on cognitive outcomes, especially among older populations, have been uncertain, and solid evidence is lacking in this field. This systematic review and meta-analysis aimed to quantify the relationship between the AHA’s CVH metrics and cognitive outcomes. 14 longitudinal studies were included in the meta-analysis. The results showed a considerable effect of a favourable total CVH score on reduced risk of incident dementia in adults aged 70 years or older. When looking at the individual factors, dementia risk can be reduced significantly if older adults achieved the recommended level of physical activity, blood glucose, or total cholesterol. The association with smoking appeared to be borderline, and there was no association between diet, body mass index hazard ratio or blood pressure and dementia risk. The authors concluded that their findings provide evidence that maintaining a favourable level of CVH score, either in mid- or late- life, would substantially reduce the risk of dementia among older adults. Preserving cardiovascular health by quitting smoking, engaging in physical exercise, controlling blood glucose and total cholesterol might be especially effective for forestalling cognitive decline and dementia.
Abstract
This study aimed to quantify the relationships between the American Heart Association (AHA) Cardiovascular Health (CVH) metrics, namely AHA Life's Simple 7, and cognitive outcomes. We searched PubMed and Embase (January 1, 2010-August 24, 2022) and finally included 14 longitudinal studies (311654 participants with 8006 incident dementia cases). Random-effects meta-analysis and one-stage linear mixed-effects models were performed. Increased CVH score seemed to associate with decreased risk of incident dementia in a linear manner, but this relationship varied by the measurement age of CVH metrics. That is, midlife CVH tended to have a linear association with late-life dementia risk, whereas a J-shaped association was observed between the late-life CVH score and dementia. In addition, late-life dementia risk was reduced significantly if individuals maintained an ideal level of AHA's CVH guidelines of physical activity, fasting plasma glucose, total cholesterol, and smoking. However, our meta-analysis did not show a significant association between CVH score and global cognitive decline rate. Following AHA's CVH guidelines and maintaining CVH at an optimal level would substantially reduce the late-life dementia risk. More research is required to explore the link between a favorable CVH score and cognitive trajectories among cognitively asymptomatic older populations.
-
3.
Dietary supplements in neurological diseases and brain aging.
Naureen, Z, Dhuli, K, Medori, MC, Caruso, P, Manganotti, P, Chiurazzi, P, Bertelli, M
Journal of preventive medicine and hygiene. 2022;63(2 Suppl 3):E174-E188
-
-
-
Free full text
Plain language summary
The rate of neurodegenerative diseases (ND) is increasing at a concerning rate. The condition is characterized by the progressive decline of neuron function in the brain, eventually leading to cognitive impairment and motorneuron disorders. This process appears to be mediated by the complex interplay of factors. The brain is extremely sensitive to oxidative stress, and oxidative stress and inflammation of the nervous tissue appear to be a common denominator in all neurodegenerative diseases. One of the challenges of ND for prevention as well as treatment and treatment development, is that the initial disease progression usually goes unnoticed, with symptoms only becoming apparent in the more advanced stages when irreversible damage has occurred. Diet quality has a significant impact on brain health and hence can also influence ND development. For example, the Mediterranean diet (MedDiet) has demonstrated many valuable attributes that can reduce ND incidences and improve cognitive function. This review looked at dietary components, natural compounds and medicinal plants that have shown to be beneficial for brain health in ND. The authors discussed the MedDiet followed by a brief review of dietary supplements, including N-acetylcysteine (NAC), phospholipids (Phosphatidylserine, Phosphatidylcholine), Gamma-aminobutyric acid, melatonin, omega-3 fatty acids, neurotropic vitamin B (B1, B6 and B12), S-adenosyl methionine (SAMe), the amino acid tryptophan, magnesium and various polyphenols. Several medicinal plants are reviewed that have demonstrated positive effects on preventing or alleviating neurological diseases. This includes Withania somnifera (Ashwagandha), Baccopa monnieri (Brahmi), Acorus calamus (Calamus) and Hypericum perforatum (St. Johns Wort). The review concluded that many bioactive compounds and plant constituents that can be obtained from a qualitative diet, as well as certain medicinal plants and supplements, can help preserve and promote brain health and prevent the onset of ND. Large clinical trials are needed to assess their suitability for their wider use.
Abstract
A healthy diet shapes a healthy mind. Diet quality has a strong association with brain health. Diet influences the onset and consequences of neurological diseases, and dietary factors may influence mental health at individual and population level. The link between unhealthy diet, impaired cognitive function and neurodegenerative diseases indicates that adopting a healthy diet would ultimately afford prevention and management of neurological diseases and brain aging. Neurodegenerative diseases are of multifactorial origin and result in progressive loss of neuronal function in the brain, leading to cognitive impairment and motoneuron disorders. The so-called Mediterranean diet (MedDiet) with its healthy ingredients rich in antioxidant, anti-inflammatory, immune, neuroprotective, antidepressant, antistress and senolytic activity plays an essential role in the prevention and management of neurological diseases and inhibits cognitive decline in neurodegenerative diseases such as Alzheimer's, Parkinson's and Huntington's diseases. The MedDiet also modulates the gut-brain axis by promoting a diversity of gut microbiota. In view of the importance of diet in neurological diseases management, this review focuses on the dietary components, natural compounds and medicinal plants that have proven beneficial in neurological diseases and for brain health. Among them, polyphenols, omega-3 fatty acids, B vitamins and several ayurvedic herbs have promising beneficial effects.
-
4.
Nutritional intervention for diabetes mellitus with Alzheimer's disease.
Li, Z, Li, S, Xiao, Y, Zhong, T, Yu, X, Wang, L
Frontiers in nutrition. 2022;9:1046726
-
-
-
Free full text
Plain language summary
Diabetes Mellitus (DM) affects more than 463 million people worldwide. Similarly, the number of deaths related to Alzheimer’s disease (AD) has increased by 145%. There are several common risk factors for Type 2 Diabetes and AD, including obesity, insulin resistance, and ageing, as well as common pathological mechanisms, including altered insulin signalling, oxidative stress, neuroinflammation, mitochondrial dysfunction, formation of glycated proteins and metabolic syndrome. This review aims to summarize the therapeutic effects of different nutritional therapy strategies on the reduction of DM and AD risk. Controlling blood sugar levels and reducing calorie intake is crucial to preventing diabetes and Alzheimer's disease. The low-carbohydrate, ketogenic, and Mediterranean diets have been found to improve glucose control in people with Type 2 diabetes (T2D). In addition, MIND (Mediterranean-DASH Diet Intervention for Neurodegenerative Delay) and a ketogenic diet may improve cognition in AD patients. Lactobacillus, Bifidobacterium probiotics, and prebiotics, such as inulin, may inhibit the progression of T2D and AD diseases by suppressing inflammation and modulating gut microbes. In addition, vitamins A, C, D, E, B6, B12, folate, long-chain polyunsaturated fatty acids, zinc, magnesium, and polyphenols may improve cognitive decline, homocysteine levels, and insulin resistance in AD and T2D patients. Healthcare professionals can use the results of this review to understand the beneficial effects of dietary strategies and multi-nutrient supplementation on DM and AD. However, further robust studies are required to investigate the risk factors and underlying mechanisms behind DM-combined AD progression.
Abstract
The combined disease burden of diabetes mellitus (DM) and Alzheimer's disease (AD) is increasing, and the two diseases share some common pathological changes. However, the pharmacotherapeutic approach to this clinical complexity is limited to symptomatic rather than disease-arresting, with the possible exception of metformin. Whether nutritional intervention might extend or synergize with these effects of metformin is of interest. In particular, dietary patterns with an emphasis on dietary diversity shown to affect cognitive function are of growing interest in a range of food cultural settings. This paper presents the association between diabetes and AD. In addition, the cross-cultural nutritional intervention programs with the potential to mitigate both insulin resistance (IR) and hyperglycemia, together with cognitive impairment are also reviewed. Both dietary patterns and nutritional supplementation showed the effects of improving glycemic control and reducing cognitive decline in diabetes associated with AD, but the intervention specificity remained controversial. Multi-nutrient supplements combined with diverse diets may have preventive and therapeutic potential for DM combined with AD, at least as related to the B vitamin group and folate-dependent homocysteine (Hcy). The nutritional intervention has promise in the prevention and management of DM and AD comorbidities, and more clinical studies would be of nutritional scientific merit.
-
5.
Nutraceutical Approaches of Autophagy and Neuroinflammation in Alzheimer's Disease: A Systematic Review.
Gruendler, R, Hippe, B, Sendula Jengic, V, Peterlin, B, Haslberger, AG
Molecules (Basel, Switzerland). 2020;25(24)
-
-
-
Free full text
Plain language summary
Ageing and the emergence of age-associated illnesses are currently one of the main health challenges in our society. Alzheimer’s disease (AD) is closely associated with ageing and is characterized by progressive memory loss and severe dementia. Currently, there are no therapy options available that halt the progression of the disease. Despite the condition being known for decades, the definitive causes and pathways of the disease and its development are not fully understood. Many drug developments that target some of the known aspects of the disease have failed in the clinical stages, and for nearly 20 years, no new drugs have met FDA approval for the treatment of AD. As increasing evidence suggests diet is an influencing risk factor for AD, the concept of exploring cost-effective, food-derived novel substances with low adverse effects has become more attractive. The first part of this work discusses AD, the prevalence of cognitive decline, limitations of current therapies, the three hallmarks of the disease (autophagy, neuroinflammation, and senescence) and the potential role of food derived substances (nutraceuticals). The second part introduces three nutraceuticals of interest, being epigallocatechin gallate, fisetin, and spermidine. All three compounds have captured scientific interest in regards to aspects of longevity over the recent years. In detail are discussed the current evidence of these compounds concerning autophagy, neuroinflammation, and senescence. This article yields a comprehensive summary of the current evidence from epigallocatechin gallate, fisetin, and spermidine and their potential role in the clinical management of AD.
Abstract
Aging and the emergence of age-associated illnesses are one of the major challenges of our present society. Alzheimer's disease (AD) is closely associated with aging and is defined by increasing memory loss and severe dementia. Currently, there are no therapy options available that halt AD progression. This work investigates three hallmarks of the disease (autophagy, neuroinflammation, and senescence) and systematically analyzes if there is a beneficial effect from three substances derived from food sources, the so called "nutraceuticals" epigallocatechin gallate, fisetin, and spermidine, on these hallmarks. The results imply a positive outlook for the reviewed substances to qualify as a novel treatment option for AD. A combination of nutraceutical substances and other preventive measures could have significant clinical impact in a multi-layered therapy approach to counter AD.
-
6.
Dietary flavanols improve cerebral cortical oxygenation and cognition in healthy adults.
Gratton, G, Weaver, SR, Burley, CV, Low, KA, Maclin, EL, Johns, PW, Pham, QS, Lucas, SJE, Fabiani, M, Rendeiro, C
Scientific reports. 2020;10(1):19409
-
-
-
Free full text
Plain language summary
Fruits and vegetables contain flavonoids that can protect against vascular diseases and cognitive ageing. Studies have shown that cocoa flavonoids can enhance the function of endothelial cells and blood vessels in peripheral arteries. This randomised, double-blinded, placebo-controlled crossover study assessed the effects of cocoa flavanols on cerebral and peripheral vascular and cognitive function. The healthy young subjects showed greater tissue oxygenation and cerebrovascular reactivity in the frontal parts of the brain during the carbon dioxide challenge after high cocoa flavonoid intervention. Furthermore, the cocoa flavonoid intervention improved cognitive and peripheral endothelial functions in healthy young subjects. Even though the mechanistic link behind the beneficial effects of flavonoids is not understood completely, the positive effects could be due to the ability of flavanols to enhance the bioavailability of circulation Nitric Oxide (NO). The study also found that flavonoids improved cognitive function in healthy individuals only when there was a high cognitive demand. Further robust studies are required to evaluate the mechanisms behind the benefits associated with acute flavonoid intake. Healthcare professionals can utilise the findings from this study to gain insight into the advantages of consuming a flavonoid-rich diet. Additionally, they can learn about the differing responses to flavanol intake between individuals.
Abstract
Cocoa flavanols protect humans against vascular disease, as evidenced by improvements in peripheral endothelial function, likely through nitric oxide signalling. Emerging evidence also suggests that flavanol-rich diets protect against cognitive aging, but mechanisms remain elusive. In a randomized double-blind within-subject acute study in healthy young adults, we link these two lines of research by showing, for the first time, that flavanol intake leads to faster and greater brain oxygenation responses to hypercapnia, as well as higher performance only when cognitive demand is high. Individual difference analyses further show that participants who benefit from flavanols intake during hypercapnia are also those who do so in the cognitive challenge. These data support the hypothesis that similar vascular mechanisms underlie both the peripheral and cerebral effects of flavanols. They further show the importance of studies combining physiological and graded cognitive challenges in young adults to investigate the actions of dietary flavanols on brain function.
-
7.
Role of phosphatidylcholine-DHA in preventing APOE4-associated Alzheimer's disease.
Patrick, RP
FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2019;33(2):1554-1564
-
-
-
Free full text
-
Plain language summary
Alzheimer’s disease (AD) is a neurodegenerative disorder characterised by progressive memory loss, spatial disorientation, cognitive impairment and behavioural changes. Ageing is the main risk factor for AD, with approximately one-third of Americans over the age of 85 being affected by the condition. The APOE gene provides instructions for making the apolipoprotein E family of proteins that are involved in fat metabolism and cholesterol transport. There are three different variants of this gene, one inherited from each parent. The variant called APOE4 is thought to increase AD risk from 2-3-fold (one inherited copy) to as much as 15-fold (two inherited copies), compared to individuals who do not carry this variant. The omega-3 oil docosahexaenoic acid (DHA) is an essential fatty acid, which comprises approximately 30% of the fats found in the human brain. Low levels of DHA in the brain increase the risk of developing AD, while normal and high levels may prevent the condition and ameliorate symptoms. This review paper brings together several lines of evidence on why individuals with the APOE4 gene variant don’t respond well to DHA supplementation but experience positive effects from dietary intake of DHA. The author suggests that this is due to the different forms of DHA found in dietary and supplemental sources. Some of the DHA present in fish and seafood is in phospholipid form, which is metabolised into lysophosphatidylcholine DHA (DHA-lysoPC) in the body. In contrast, fish oil supplements contain no DHA in phospholipid form, but in other forms that are mostly metabolised to free DHA. This paper puts forward an argument that, due to the breakdown of the integrity of the blood-brain barrier, APOE4 carriers have impaired brain transport of free DHA but not DHA-lysoPC. The author concludes that dietary sources that contain high amounts of DHA in phospholipid form, such as fish and fish roe may help increase plasma levels of DHA-lysoPC, which may be better transported to the brains of APOE4 carriers. She also highlights the pressing need for future clinical trials to evaluate the effects of omega-3 oils in phospholipid form on the cognitive function of APOE4 carriers with AD.
Abstract
Dietary and supplemental intake of the ω-3 fatty acid docosahexaenoic acid (DHA) reduces risk of Alzheimer's disease (AD) and ameliorates symptoms. The apolipoprotein E ( APOE) 4 allele is the strongest risk factor for sporadic AD, exclusive of age. APOE4 carriers respond well to the DHA present in fish but do not respond as well to dietary supplements. The mechanisms behind this varied response remain unknown. I posit that the difference is that fish contain DHA in phospholipid form, whereas fish oil supplements do not. This influences whether DHA is metabolized to nonesterified DHA (free DHA) or a phospholipid form called lysophosphatidylcholine DHA (DHA-lysoPC). Free DHA is transported across the outer membrane leaflet of the blood-brain barrier (BBB) via passive diffusion, and DHA-lysoPC is transported across the inner membrane leaflet of the BBB via the major facilitator superfamily domain-containing protein 2A. I propose that APOE4 carriers have impaired brain transport of free DHA but not of DHA-lysoPC, as a consequence of a breakdown in the outer membrane leaflet of the BBB, putting them at increased risk for AD. Dietary sources of DHA in phospholipid form may provide a means to increase plasma levels of DHA-lysoPC, thereby decreasing the risk of AD.-Patrick, R. P. Role of phosphatidylcholine-DHA in preventing APOE4-associated Alzheimer's disease.
-
8.
The Microbiota-Gut-Brain Axis in Neuropsychiatric Disorders: Pathophysiological Mechanisms and Novel Treatments.
Kim, YK, Shin, C
Current neuropharmacology. 2018;16(5):559-573
-
-
-
Free full text
-
Plain language summary
The connection between the microbiome in the gut and the brain is known as the gut-brain axis and may have implications in the development and treatment of brain disorders. This narrative review paper aimed to summarise the gut-brain axis and studies surrounding the use of gut microbiota in treatment for brain disorders. The authors first highlighted that the gut microbiota is individual and varies depending on the age of the host, with full development around the age of 3 years old. Diet, infections, the use of antibiotics and stress can all affect the gut-microbiota in what is termed dysbiosis. Studies in animals indicate that the gut-brain axis may be bidirectional with either aspect affecting the other. Stress may cause dysbiosis, affecting both digestion and the immune system. In turn the gut microbiota may affect the brain through the immune system, modulation of nerves, and through the production of signalling molecules. Several diseases of the brain may be influenced by the gut microbiota. Mood disorders, brain degeneration and childhood brain development disorders were all highlighted as having potential relationships with dysbiosis. The use of probiotics in chronic fatigue syndrome, schizophrenia, brain function and autism spectrum disorder were reviewed with positive results in chronic fatigue syndrome and brain function, however studies are lacking. It was concluded that gut microbiota may directly or indirectly affect brain disorders, however the role of probiotics as a treatment needs more research. This study could be used by healthcare professionals to understand the potential role of the gut microbiota in brain disorders.
Abstract
BACKGROUND The human gut microbiome comprise a huge number of microorganisms with co-evolutionary associations with humans. It has been repeatedly revealed that bidirectional communication exists between the brain and the gut and involves neural, hormonal, and immunological pathways. Evidences from neuroscience researches over the past few years suggest that microbiota is essential for the development and maturation of brain systems that are associated to stress responses. METHOD This review provides that the summarization of the communication among microbiota, gut and brain and the results of preclinical and clinical studies on gut microbiota used in treatments for neuropsychiatric disorders. RESULT Recent studies have reported that diverse forms of neuropsychiatric disorders (such as autism, depression, anxiety, and schizophrenia) are associated with or modulated by variations in the microbiome, by microbial substrates, and by exogenous prebiotics, antibiotics, and probiotics. CONCLUSION The microbiota-gut-brain axis might provide novel targets for prevention and treatment of neuropsychiatric disorders. However, further studies are required to substantiate the clinical use of probiotics, prebiotics and FMT.
-
9.
Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment.
Oulhaj, A, Jernerén, F, Refsum, H, Smith, AD, de Jager, CA
Journal of Alzheimer's disease : JAD. 2016;50(2):547-57
-
-
-
Free full text
-
Plain language summary
Many studies are exploring preventative measures to delay or prevent mild cognitive impairment (MCI) and Alzheimer’s disease. A recent trial (VITACOG) demonstrated that omega-3 fatty acid status enhances the protective effects of B-vitamins on brain atrophy. The present study uses the VITACOG data to investigate whether there is an association on cognitive function. This study revealed that a higher baseline omega-3 fatty acid status enhances the beneficial effects of B vitamins on both brain atrophy and cognitive decline. The authors conclude that this interaction may slow down the disease process in MCI and warrants further clinical trials investigating this relationship.
Abstract
A randomized trial (VITACOG) in people with mild cognitive impairment (MCI) found that B vitamin treatment to lower homocysteine slowed the rate of cognitive and clinical decline. We have used data from this trial to see whether baseline omega-3 fatty acid status interacts with the effects of B vitamin treatment. 266 participants with MCI aged ≥70 years were randomized to B vitamins (folic acid, vitamins B6 and B12) or placebo for 2 years. Baseline cognitive test performance, clinical dementia rating (CDR) scale, and plasma concentrations of total homocysteine, total docosahexaenoic and eicosapentaenoic acids (omega-3 fatty acids) were measured. Final scores for verbal delayed recall, global cognition, and CDR sum-of-boxes were better in the B vitamin-treated group according to increasing baseline concentrations of omega-3 fatty acids, whereas scores in the placebo group were similar across these concentrations. Among those with good omega-3 status, 33% of those on B vitamin treatment had global CDR scores >0 compared with 59% among those on placebo. For all three outcome measures, higher concentrations of docosahexaenoic acid alone significantly enhanced the cognitive effects of B vitamins, while eicosapentaenoic acid appeared less effective. When omega-3 fatty acid concentrations are low, B vitamin treatment has no effect on cognitive decline in MCI, but when omega-3 levels are in the upper normal range, B vitamins interact to slow cognitive decline. A clinical trial of B vitamins combined with omega-3 fatty acids is needed to see whether it is possible to slow the conversion from MCI to AD.
-
10.
Metabolic profiling distinguishes three subtypes of Alzheimer's disease.
Bredesen, DE
Aging. 2015;7(8):595-600
-
-
-
Free full text
Plain language summary
The causes of Alzheimer’s Disease (AD) remain incompletely defined and there are currently no truly effective drug therapies available. However, there is growing evidence that disordered blood glucose management and hormonal changes and deficiencies, amongst other things, are implicated in symptom onset. Optimising these various metabolic processes, therefore, may be used as a comprehensive way to avoid cognitive decline or achieve cognitive improvements in symptomatic individuals. This report provides the metabolic results of 3 case studies and suggests 3 different types of AD classification, depending on the individual metabolic profile. Further studies are required to elaborate on the metabolic profiles suggested in this report, however Nutrition Practitioners working with cognitive decline, can use this report as a basis for individualised nutrition protocols to optimise metabolic processes in clients with cognitive decline.
Abstract
The cause of Alzheimer's disease is incompletely defined, and no truly effective therapy exists. However, multiple studies have implicated metabolic abnormalities such as insulin resistance, hormonal deficiencies, and hyperhomocysteinemia. Optimizing metabolic parameters in a comprehensive way has yielded cognitive improvement, both in symptomatic and asymptomatic individuals. Therefore, expanding the standard laboratory evaluation in patients with dementia may be revealing. Here I report that metabolic profiling reveals three Alzheimer's disease subtypes. The first is inflammatory, in which markers such as hs-CRP and globulin:albumin ratio are increased. The second type is non-inflammatory, in which these markers are not increased, but other metabolic abnormalities are present. The third type is a very distinctive clinical entity that affects relatively young individuals, extends beyond the typical Alzheimer's disease initial distribution to affect the cortex widely, is characterized by early non-amnestic features such as dyscalculia and aphasia, is often misdiagnosed or labeled atypical Alzheimer's disease, typically affects ApoE4-negative individuals, and is associated with striking zinc deficiency. Given the involvement of zinc in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling, this syndrome of Alzheimer's-plus with low zinc (APLZ) warrants further metabolic, genetic, and epigenetic characterization.