compiled by Barbara Connor, M.Ac. L.Ac.
I thought I would write a little bit today about the benefits of acupuncture, herbs, nutrients and exercise for the mind. I have endeavored to show how acupuncture and exercise, as well as certain herbs and nutrients such as antioxidants, bacopa, eleutherococcus senticosus, EPA and DHA fatty acids, ginkgo biloba, gotu kola, phosphatidylserine, resveratrol and vinpocetine may help in maintaining healthy brain function.
Acupuncture – This meta-analysis was conducted to evaluate the efficacy of acupuncture on cognitive impairment (function) after a stroke. Meta-analyses were conducted for the eligible randomized controlled trials. Twenty-one trials with a total of 1421 patients met inclusion criteria. Pooled random-effects estimates of the change in the Mini-Mental State Examination were calculated for the comparison of acupuncture with no acupuncture in addition to medicine or rehabilitation. Following 4 weeks and 8 weeks of intervention with acupuncture, the merged mean difference was 3.14 and 2.03, respectively. This meta-analysis suggests that acupuncture had positive effects on cognitive function after stroke and supports the need for additional research on the potential benefits of this therapeutic approach. (Liu et al 2014)
Antioxidants – such as acetylcarnitine and lipoic acid and flavonoid-rich vegetable extracts, chronically administered to mice and rats also prevented the age-associated decline in neurological functions and oxidative damage in brain mitochondria. Similarly, rats treated chronically with acetylcarnitine showed a lower age-dependent decline in the mitochondrial oxidation rate of NAD-dependent substrates and in the mitochondrial gene expression of complexes I, IV, and V and of adenine nucleotide translocase. (Navarro & Boveris 2010)
We demonstrate herein that dietary supplementation with a mixture of alpha-lipoic acid, acetyl-L-carnitine, DHA, phosphatidylserine and glycerophosphocoline, prevented the marked cognitive decline otherwise observed in normal mice maintained on this challenge diet. (Suchy et al 2009)
Bacopa
A double-blind placebo-controlled independent group study found that Bacopa monnieri significantly improved performance on the ‘Working Memory’ factor, more specifically spatial working memory accuracy. The current study provides support for the two other published studies reporting cognitive enhancing effects in healthy humans after a 90 day administration of the Bacopa monnieri extract. (Stough et al 2008)
Research evidence clearly indicates that Bacopa monnieri and Centella asiatica possess neuroprotective properties, have nootropic (enhancing cognition and memory) activity with therapeutic implications for patients with memory loss. (Shinomol et al 2011)
Bacopa has been clinically proven to improve memory and mood in Alzheimer’s disease (AD), possessing antidepressant and anti-oxidative actions. (Chowdhuri et al 2002, Roodenrys et al 2002 and Sairam et al 2002)
Eleutherococcus senticosus – protects delayed neuronal death in the CA1 region of hippocampus against global cerebral ischemia in rats with recovery of spatial memory, which can be considered as normal functioning of hippocampus. Based on these findings, it is tempting to speculate that Eleutherococcus senticosus may be a therapeutic candidate for the neuroprotection of tissue and the recovery of function in the neuroprotection in patients with global ischemia, such as a cardiac arrest, ischemic stroke or various neuroinflammatory disorders. (Lee et al 2011)
EPA and DHA Fatty Acids from Fish Oil Concentrate
The objective of this review is to provide an overview of nutritional factors involved in cognitive aging and dementia with a focus on nutrients that are also important in neurocognitive development. Several dietary components were targeted, including antioxidant nutrients, dietary fats and B-vitamins. A critical review of the literature on each nutrient group is presented, beginning with laboratory and animal studies of the underlying biological mechanisms, followed by prospective epidemiological studies and randomised clinical trials. The evidence to date is fairly strong for protective associations of vitamin E from food sources, the n-3 fatty acid, DHA, found in fish, a high ratio of polyunsaturated to saturated fats, and vitamin B12 and folate. (Morris MC 2011)
The aim of the present study was to investigate the benefits of supplementing a diet with n-3 PUFA, DHA and EPA, for depressive symptoms, quality of life (QOL) and cognition in elderly people with MCI. We conducted a 6-month double-blind, randomised controlled trial. Compared with the LA (n-6 PUFA linoleic acid) group, GDS scores improved in the EPA (P = 0·04) and DHA (P = 0·01) groups and verbal fluency (Initial Letter Fluency) in the DHA group (P = 0·04). Improved GDS scores were correlated with increased DHA plus EPA (r 0·39, P = 0·02). Improved self-reported physical health was associated with increased DHA. There were no treatment effects on other cognitive or QOL parameters. Increased intakes of DHA and EPA benefited mental health in older people with MCI. Increasing n-3 PUFA intakes may reduce depressive symptoms and the risk of progressing to dementia. (Sinn et al 2011)
Ginkgo biloba
In a recent multicenter, randomized, controlled trial of 120 mild cognitive impairment (MCI) patients, patients were randomly assigned to the GBE group and control group. The patients in the treatment group took GBE tablets 3 times a day, 19.2 mg each dose. After 6 months of treatment, the scores of the logical memory test and nonsense picture recognition were increased significantly in the treatment group, while the scores of the two tests from the control group had no statistically significant difference. After treatment, the positive rate of nonsense picture recognition was 55.17% in the treatment group, which was significantly higher than that of the control group at 32.73%. The efficacy rate of logical memory was 58.62% in the treatment group, also higher than 38.18% in the control group. GBE showed good efficacy in promoting episodic memory function in MCI patients. (Zhao et al 2012)
Ginkgo biloba standardized extract can protect against intermittent hypoxia-induced memory impairment, oxidative stress and neuronal DNA damage, possibly through multiple mechanisms involving its potential anti-oxidative effect. (Abdel-Wahab et al 2012)
The therapeutic efficacy of Ginkgo biloba extract (GBE) for Alzheimer’s disease (AD), in placebo controlled clinical trials, is reportedly similar to currently prescribed drugs such as tacrine or donepezil and, importantly, undesirable side effects of ginkgo are minimal. (Fu et al 2011)
There is consistent evidence that chronic administration of GBE improves selective attention, some executive processes and long-term memory for verbal and non-verbal material. (Kaschel et al 2009)
Extensive studies on G. biloba extracts showed their ability to protect brain neurons from oxidative stress (Oyama et al 1996) and to inhibit apoptosis in cell culture. (Xin et al 2000) Ginkgo can protect brain cells during a stroke, and triggers a cascade of events that neutralizes free radicals known to cause neuron cell death. (Saleem et al 2008)
GBE exerts a neuroprotective effect against ischemic brain injury through an anti-apoptotic mechanism. Parvalbumin is a calcium buffering protein that plays an important role in modulating intracellular calcium concentration and regulating apoptotic cell death. The results of this study demonstrate that the maintenance of parvalbumin expression is associated with the neuroprotective function of GBE against neuronal damage induced by ischemia. (Sung et al 2012)
Gotu kola
Research evidence clearly indicates that Bacopa monnieri and Gotu kola possess neuroprotective properties, have nootropic (enhancing cognition and memory) activity with therapeutic implications for patients with memory loss. (Shimomol et al 2011)
A recent study found the Asiatic acid, one of the main constituent triterpenes found in Gotu kola, dramatically reduced the build up of amyloid plaque, thus reducing the onset of Alzheimer’s disease (AD). (Patil et al 2010)
The data indicate that Centella asciatica extract can impact the amyloid cascade altering amyloid beta pathology in the brains of PSAPP mice and modulating components of the oxidative stress response that has been implicated in the neurodegenerative changes that occur with AD. (Dhanasekaran et al 2008)
Gotu kola was researched as a memory enhancer and brain protector against oxidative stress in an animal study. These data suggest that gotu kola has the propensity to modulate both endogenous and neurotoxicant induced oxidative impairments in the brain and may be effectively employed as a neuroprotective adjuvant to abrogate oxidative stress in vivo. (Shimomol et al 2008)
Phosphatidylserine
This double-blind, placebo-controlled study is the first clinical trial which demonstrates that soybean-derived phosphatidylserine has positive effects on cognitive performance in Japanese subjects with memory complaints. The oral administration of soybean-derived phosphatidylserine for 6 months improved memory function, especially delayed recall, in the elderly with memory complaints. (Kato-Kataoka et al 2010)
Resveratrol
Resveratrol has neuroprotective features both in vitro and in vivo in models of Alzheimer’s disease (AD), but it has proved to be beneficial also in ischemic stroke, Parkinson’s disease, Huntington’s disease, and epilepsy. Here, we summarize the in vitro and in vivo experimental results highlighting the possible role of resveratrol as neuroprotective biofactor with a particular focus on AD. (Albani et al 2010)
Vinpocetine
Despite the lack of unanimous opinion due to the paucity of clinical data, various clinical trials have confirmed the multiple underlying mechanisms responsible for the beneficial neuroprotective effects produced by vinpocetine. (Patyar et al 2011)
Studies conducted using in vitro models of oxidative stress have reported the protective effect of vinpocetine against ROS attacks. It neutralizes ROS, reduces the neurodegenerative process and delays the progression of age-related brain disorders. (Pereira et al 2003)
Vinpocetine improved the cerebrovascular reserve capacity in both patient groups and favourably influenced the cognitive status and general condition of patients with chronic hypoperfusion. The authors recommend the use of vinpocetine for the treatment of patients with mild cognitive impairment. (Valikovics A 2007)
Zinc is an essential component of numerous proteins involved in the defense against oxidative stress. It has been shown, that depletion of Zn may enhance DNA damage via impairments of DNA repair mechanisms. In addition, Zn has an impact on the immune system and possesses neuroprotective properties. (Jomova & Valko 2011)
Exercise for Memory and Cognition
Taken together, the results of this 6-month randomized controlled trial provide support for the prevailing notion that exercise can positively impact cognitive functioning and may represent an effective strategy to improve memory in those who have begun to experience cognitive decline. (Nagtamatsu et al 2013)
Our findings in this animal study suggest that fish oil supplementation, initiated from prenatal period to midlife, and physical exercise program applied throughout the life induced distinctly a better cognitive performance. (Rachetti et al 2013)
Results suggest that acute physical exercise enhances executive functioning. The number of studies on chronic physical exercise is limited and it should be investigated whether chronic physical exercise shows effects on executive functions comparable to acute physical exercise. This is highly relevant in preadolescent children and adolescents, given the importance of well-developed executive functions for daily life functioning and the current increase in sedentary behaviour in these age groups. (Verburgh et al 2013)
* Executive function is the cognitive process that regulates an individual’s ability to organize thoughts and activities, prioritize tasks, manage time efficiently, and make decisions. (thefreedictionary.com)
Higher midlife fitness levels seem to be associated with lower hazards of developing all-cause dementia later in life. The magnitude and direction of the association were similar with or without previous stroke, suggesting that higher fitness levels earlier in life may lower risk for dementia later in life, independent of cerebrovascular disease. (Defina et al 2013)
While the idea that physical exercise could increase memory recall ability is recent focus of research, it has been shown several decades ago in older adults (Powell, 1974; Diesfeldt and Diesfeldt-Groenendijk, 1977), and has even been shown to lead to enhanced memory abilities as much as one year later (Perrig-Chiello et al., 1998). More recently, daily physical exercise has been shown to reduce the cognitive decline associated with aging as well as reduce the risk of developing Alzheimer’s disease (Buchman et al., 2012). (Madan & Singhal 2012)
While it appears clear that exercise has beneficial effects on memory and hippocampal neurogenesis, it should also be noted that the benefits of exercise on cognition are not confined to only memory or the hippocampus, but also extend to a wider range of cognitive processes, particularly executive function and the prefrontal cortex and anterior cingulate cortex (see Hillman et al., 2008, for a review). (Madan & Singhal 2012)
Exercise significantly elevated endogenous norepinephrine (measured via the biomarker, salivary alpha-amylase) in both amnestic mild cognitive impairment (aMCI) patients and controls. Additionally, exercise retrogradely enhanced memory in both aMCI patients and controls. Acute exercise that activates the noradrenergic system may serve as a beneficial, natural, and practical therapeutic intervention for cognitive decline in the aging population. (Segal et al 2012)
Be cheerful – “If you don’t want to be old before your time be cheerful in deed and word and in appearance — most of all in appearance. It is a divine art to look cheerful, it helps others.” — Meher Baba
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