GABA is a supplement worth taking for dealing with issues of anxiety. I have been using it in my clinical practice for many years for this very reason. GABA (gamma-aminobutyric acid) is a neurotransmitter made from the amino acid glutamate. GABA acts as a main inhibitor to the brain and nervous system, functioning as an “engine brake” on the system in times of stress. Low levels of GABA in the brain have been associated with restlessness, anxiety, insomnia and poor mood (1). GABA has been shown to inhibit the excitatory impulses in the brain, including those responsible for panic, alarm,
The human brain is like no other in terms of its ability to simultaneously synthesize information and carry out complex tasks on a regular basis. While it would be naïve to say that we fully understand its interrelationship with the rest of the body and our environment, modern research has made great strides to elucidate its various structures and functions. Here is a brief look at our current understanding of cognitive function and the risk factors that threaten its well-being. While a focus on memory is highlighted, all aspects of cognitive performance including language, reaction time, focus, mood and information processing must be assessed together, due to the mind’s highly integrative nature.
What is “Normal”?
It is widely accepted that memory and other cognitive functions decline with age, but how do we know if someone has a “normal” amount of decline? A literature review published in 2004, concluded that no cognitive decline is normally seen before the age of 60.1 Yet, there are many that question this statement and contend that signs of deterioration can be seen at an even earlier age. Challenging this school of thought, a more recent study in 2012 showed that cognitive decline might normally be seen as early as age 45! Before going any further, it is important to note that not all of our cognitive abilities peak at the same age. The ability to process information in a rapid manner peaks around the relatively young age of 25.1 In other words, after age 25, the rate at which people understand and utilize new information generally starts to slow down. In contrast, verbal memory, inductive reasoning and spatial reasoning all peak around the age of 53. Finally, verbal abilities actually peak after age 60!1 Considering all of these facts, it is not fair to simply say that ageing leads to cognitive decline. Researchers have also shown that not all cognitive functions wane in the same manner or to the same degree. For example, it is now well known that the ability to encode new memories and process information at a rapid pace both steadily decline with age.1 Working memory also steadily declines; that is, the skill of utilizing short-term memory to manipulate and use relevant information. However, it is interesting that short-term memory on its own does not show this downhill pattern throughout life. Short-term memory is found to have very slight declines throughout adult life until finally hitting a turning point somewhere after the age of 70, where it starts a sharper decline.1 Similarly, autobiographical memory, semantic knowledge, emotional processes and vocabulary remain fairly stable until a dip late in life.1 Of course, there are variations among individuals for all of these abilities, but the general trends remain the same. Cognitive deterioration can also tell us a lot about our overall health. Interestingly enough, an acceleration of cognitive decline is often seen 3,6 years before an individual’s death.3,4 In a sense, cognitive function is a relative measurement to one’s own baseline status and can be a strong predictor of mortality if interventions are not applied. Overall, it’s important to know that there is a wide range of cognitive decline, some of which may be considered normal and others that may require medical attention. See “Key Terms” for a brief understanding of the various levels of cognitive deterioration and memory loss.
Measuring Cognitive Decline: The Mini-Mental State Exam (MMSE)
In order to provide a solution to any problem, it is first imperative to understand the problem and its severity. If you misplace your wallet and you are unable to remember its location, does it mean that you’re a candidate for dementia? Of course not…if it only happens once or twice. But if you’re having difficulty, on a daily basis, with simple tasks like remembering the location of basic items, bathing, handling finances, or maintaining hobbies then it may be of concern. Dementia is a set of signs and symptoms in which brain function, such as memory, language, problem solving and attention are affected. Alzheimer’s Disease is just one of several different forms of dementia. So how can we determine if an individual is simply ageing in a healthy manner or if they are on their way toward Alzheimer’s Disease (AD)? As much as we can rely on our family, friends or even physician’s to notice changes in our mental health, an objective measure must be implemented in order to better determine what areas of cognitive function may be impaired and to what extent. With this in mind, many assessments are available to determine the global level of cognitive decline, but perhaps the most commonly used tool by practitioners is the Mini-Mental State Exam (MMSE).7 The MMSE contains 19 items designed to measure a variety of functions, and ultimately gives a score between 0-30 indicating whether a cognitive deficit or dementia may be present. The cognitive functions that are measured include the following:
•Orientation: knowing details about the current time and location
•Attention: the ability to, for example, spell a common word backwards
•Registration: measured by repeating named prompts (immediate memory)
•Recall: measures short-term verbal memory
•Language: the ability to write, speak and understand language
•Praxis: the ability to put thoughts and ideas into action
The MMSE is a popular test because of its relatively simple design and implementation, along with its ability to measure cognitive change over time.7 It has also been shown to correlate quite well with the abilities of individuals to carry out functional everyday tasks, thereby giving a good indication of how cognitive decline may be affecting day-to-day living.8 For example, when a person exhibits that they are oriented and attentive through MMSE testing, these findings correlate well with the ability to communicate by telephone, recognize driving rules and road signs, balance a checkbook, and carry out shopping tasks from memory.8 On the other hand, the MMSE does have its limitations. It is considered unreliable for measuring subtle changes in ability and is perhaps more indicated for repeated use to determine over a longer period of time whether cognitive decline or improvement has occurred.7 There are well-known “ceiling” and “floor” effects of the MMSE, meaning that it cannot detect cognitive changes in those individuals on extreme ends of the spectrum (for example in a 90-year old with severe dementia or a highly educated 40 year old).9 Nevertheless, the MMSE should be considered a great preliminary screening tool used in the assessment of cognitive decline. Depending on the circumstances, more specific and integrated testing may be necessary.
The Nun Study
The Nun Study is one of the best examples of how healthy diet and lifestyle choices can preserve cognitive function in ageing individuals. The Nun Study involves the ongoing functional assessment of women at the Catholic Order School Sisters of Notre Dame, with additional permission to assess the brains of deceased sisters for autopsy. Findings have shown that the relative non-occurrence of Alzheimer’s Disease (AD) in the nuns correlate with their cognitive capacity, lifestyle, and diet. In other words, some combination of their unspoiled lifestyles (including diet, spirituality, community life, mental exercise, etc.) all seem to have contributed to a much lower incidence of AD than the general population. 5,11
Age-Associated Memory Impairment (AAMI): not considered a pathologi-cal condition. While AAMI may be annoying for the individual, the memory loss is considered a part of normal ageing similar to fading eyesight5
Mild Cognitive Impairment (MCI): cognitive deterioration that is measur-able based on clinical assessments and noticeable by others. However, it is not severe enough to consistently impair daily productivity – in other words, the efficiency of performing daily activities may be decreased but not so much that the tasks must be discontinued5
Dementia: a group of disorders that cause cognitive decline as a result of death or damage to brain cells. Cognitive decline must be present in two of four essential cognitive functions (1. Memory; 2. Language/speech; 3. Visual processing; 4. Planning capacity/ability to carry out complex tasks).5
Alzheimer’s Disease (AD): a form of dementia carrying similar criteria. The main differentiating feature is the deposition of abnormal protein plaques in the central nervous system (known as beta-amyloid and neurofibrillary tangles).5
Note: there is significant overlap between these definitions and even re-searchers have found it difficult to definitively differentiate between these terms.6 These are given as general guidelines only in order to better under-stand the varying degrees of memory/cognitive decline.
Does Memory Loss Always Lead to Alzheimer’s Disease?
As described in the “Key Terms” text box, age-associated memory impairment (AAMI) appears to be independent and unrelated to the progression of Alzheimer’s Disease (AD).5 However, there is no consensus as to whether AAMI bears an increased risk for AD. One researcher has concluded that there is zero additional risk but others claim a three-fold increased risk.5 According to the most current evidence, it seems as though individuals with mild cognitive impairment (MCI) tend to progress toward dementia, yet not necessarily AD.5 In fact, certain studies have shown that up to 25 percent of those with MCI can actually revert to normal cognitive capacity.10 To add to the perplexity, a subgroup of MCI individuals with quite severe memory loss, termed amnestic MCI (aMCI), do conclusively show an increased risk for the development of AD. In patients with an MCI, more than half progress to AD.5
In this sense, severe memory impairment in combination with other cognitive deficits does warrant more investigation and treatment interventions to, perhaps, decrease the likelihood of progression to AD. Much of the difficulty in determining an accurate risk assessment lies in the fact that there are many characteristics overlapping between the categories of cognitive function. For example, one study showed that 67% of individuals diagnosed with AAMI could also be identified as MCI subjects.6 For these 67%, their risk assessment varies quite a bit depending which category they are placed in. The reason for this variation, of course, comes down to differences in subjective measures and differences between objective tests (such as using the MMSE versus utilizing another cognitive test).6 Given the complexity of categorizing cognitive deficit, as well as the multiple and interconnecting risk factors associated with decline, it appears prudent to take a multi-factorial approach to mitigate and offset any risk factors that may be present for the development of MCI, AD or any form of dementia.5,11 Essentially, given that there may be an increased risk for dementia and AD with any memory loss, isn’t it worth taking all possible measures to offset this risk, just in case?
Examples of Mini-Mental State Exam Questions
1. What day of the week is it today?
2. Repeat these words: “apple”, “penny” and “table”. Try to remember them, as you will be asked to recall them at a later point in the exam.
3. Can you tell me the name of the city that we’re in?
4. Please spell the word “world”. Now, spell the same word backwards.
5. Can you perform this action?: “CLOSE YOUR EYES.”
6. List the three words that you were asked to try to remember.
7. Write a complete sentence – anything that comes to mind (it should have a verb and a subject).
*Please Note: These questions are only provided as examples. This is not a full MMSE, nor does it qualify for diagnosis or proper assessment of cognitive function. For a full examination, be sure to see your healthcare practitioner.
Preserving Memory and Cognitive Function
A list of factors that appear to impair cognitive performance including memory function, 12,21 can be seen in Table 1. If you look closely at this list of risk factors, you will see that many, if not all, are caused by poor lifestyle and dietary health. It is clear that nutrition and lifestyle improvements must be primary interventions for the prevention of memory and cognitive impairments. A diet high in polyunsaturated fats (such as those found in fish), monounsaturated fats (such as those found in olive oil), vitamin E, polyphenols and antioxidants (in foods such as citrus fruits and vegetables) has been shown to possibly slow down the rate of cognitive decline and prevent progression to AD.1 Unfortunately, with the many challenges facing optimal nutrition, supplemental nutrients are often indicated as well. Certain supplements have been proven as effective treatments for cognitive decline and should be considered adjunctive measures with dietary and lifestyle improvements (see articles “Supplements Known to Improve Memory” and “Ayurveda and Cognition”). Aside from mitigating risk factors through dietary measures, perhaps the most important preventative measure and disease intervention is mental exercise. Research has shown that the old adage, “Use it or lose it”, holds true in the context of cognitive health.1,5 Animal studies have shown that mental exercise increases neurogenesis (growth of the nervous system), while clinical observations support this idea that the human brain is capable of rebuilding failed circuits.5 A randomized control trial performed in 2006 showed that a cognitive training program for 10 weeks led to significant cognitive improvement over those individuals that did not participate in the training program.22 This positive effect was seen five years after the training was performed. It should be noted that a random sample of the treatment group received additional training sessions at 11 and 35 months that led to even better outcomes.22 Intuitively, this means that the more often we are exercising our brains, the better they function over time. Physical exercise has also shown promise in the prevention and treatment of cognitive deterioration. Certain studies have found that physical exercise aids executive function and overall cognitive function, while also reducing the amount of brain density loss with age (specifically in areas used for executive processes).1 On the contrary, a review released in 2011 stated that although there are numerous positive studies supporting the notion that exercise reduces the risk of cognitive decline, there is “insufficient evidence” to fully prove this.23 At the very least, we know that exercise decreases the risk of developing other chronic diseases and therefore may be viewed as a primary intervention for reducing the risk of cognitive deterioration. As with all traits, there is a natural variation among the population in terms of cognitive function. Not everyone has the same ability to store, process and utilize information, but this does not mean that everyone cannot maximize the potential that they do have. A mixture of lifestyle, environmental, dietary and genetic factors all play a part in the maintenance, or deterioration, of our cognitive health. Without a doubt, healthy dietary habits, consistent mental “exercise” and the prevention of chronic disease must be the primary treatment for the preservation of cognitive function.
1. Hedden T and Gabrieli JDE. Insights in the ageing mind: a view from cognitive neuroscience. Nature Reviews (Neuroscience) 2004; 5: 87-97
2. Singh-Manoux A, Kivimaki M, Glymour M, et al. Timing of onset of cognitive decline: results from Whitehall II prospective cohort study. BMJ 2012;344:d7622 doi: 10.1136/bmj.d7622
3. Small BJ, Fratiglioni L, von Strauss E, et al. Terminal decline and cognitive performance in very old age: does cause of death matter? Psychol. Aging 2003; 18:193–202
4. Wilson RS, Beckett LA, Bienias JL, et al. Terminal decline in cognitive function. Neurology 2003; 60:1782–1787
5. Kidd, Parris M. Alzheimer’s disease, amnestic mild cognitive impairment, and age-associated memory impairment: current understanding and progress toward integrative prevention. Alt Med Review 2008; 13(2): 85-115
6. Bartrés-Faz D, Junqué C, López-Alomar A, et al. Neuropsychological and Genetic Differences Between Age-Associated Memory Impairment and Mild Cognitive Impairment Entities. Journal of the American Geriatrics Society 2001; 49:985-990
7. Marioni RE, Chatfield M, Brayne C, et al. The Reliability of assigning individuals to cognitive states using the mini mental-state examination: a population-based prospective cohort study. BMC Medical Research Methodology 2011; 11:127-132
8. Razani J, Wong JT, Dafaeeboini N, et al. Predicting everyday functional abilities of dementia with the mini mental state examination. J Geriatr Psychiatry Neurol 2009; 22(1):62-70
9. Tombaugh TN and McIntyre NJ: The mini-mental state examination: a comprehensive review. J Am Geriatr Soc 1992, 40(9):922-935.
10. Rosenberg PB, Johnston D, Lyketsos CG. A clinical approach to mild cognitive impairment. Am J Psychiatry 2006;163:1884-1890.
11. Tyas SL, Snowdon DA, Desrosiers MF, et al. Healthy ageing in the Nun Study: definition and neuropathologic Correlates. Age Ageing. 2007 November ; 36(6): 650–655.
12. Grandjean AC and Grandjean NR. Dehydration and cognitive performance. J Am Coll Nutr. 2007; 26(5):549S-554S.
13. Adan A. Cognitive performance and dehydration. J Am Coll Nutr. 2012; 31(2):71-8.
14. Ceballos NA. Tobacco use, alcohol dependence, and cognitive performance. J Gen Psychol. 2006; 133(4):375-88.
15. Teunissen CE, van Boxtel MP, Jolles J, et al. Homocysteine in relation to cognitive performance in pathological and non-pathological conditions. Clin Chem Lab Med. 2005; 43(10):1089-95.
16. Greenwood CE. Dietary carbohydrate, glucose regulation, and cognitive performance in elderly persons. Nutr Rev. 2003; 61(5-2):S68-74.
17. Grima NA, Pase MP, Macpherson H, et al. The effects of multivitamins on cognitive performance: a systematic review and meta-analysis. J Alzheimers Dis. 2012;29(3):561-9.
18. Crichton GE, Elias MF, Buckley JD, et al. Metabolic syndrome, cognitive performance, and dementia. J Alzheimers Dis. 2012; 30(S2):S77-87.
19. Hoyland A, Dye L, Lawton CL. A systematic review of the effect of breakfast on the cognitive performance of children and adolescents. Nutr Res Rev. 2009; 22(2):220-43.
20. Eilander A, Gera T, Sachdev HS, et al. Multiple micronutrient supplementation for improving cognitive performance in children: systematic review of randomized controlled trials. Am J Clin Nutr. 2010; 91(1):115-30.
21. Leininger S and Skeel R. Cortisol and self-report measures of anxiety as predictors of neuropsychological performance. Arch Clin Neuropsychol. 2012 May;27(3):318-28
22. Willis SL, Tennstedt SL, Marsiske M, et al. Long-term effects of cognitive training on everyday functional outcomes in older adults. JAMA 2006; 296(23):2805-14.
23. Snowden M, Steinman L, Mochan K, et al. Effect of exercise on cognitive performance in community-dwelling older adults: review of intervention trials and recommendations for public health practice and research. J Am Geriatr Soc. 2011 Apr;59(4):704-16