Reading and Mental Aerobics – Your Mind: Use It or Lose It

 

“Lifelong Learning In An Ever Expanding Universe Of Endless Possibilities”

By Larry Hartweg

 

Everything that is good for our cardiovascular system is also good for our brain (toxin avoidance, good nutrition, antiaging antioxidants, aerobic exercise, usage and continual expansion). Exposure to novel and interesting mental material (concepts, and situations) strengthens our cognitive capacity. Our minds grow stronger by reading, creative writing, vocabulary and concept expansion, seeking unconventional/unfamiliar points of view, complex thinking, problem solving, social interaction and exploratory research in libraries, challenging lectures, Internet materials, etc.)

 

Simple Mental Aerobic exercise examples:

 

Your brain should be delighted, especially with unpredictable surprises. Your mind will become incrementally stronger and happier than it was before. Intellectual boredom atrophies the physical capacity of the brain and your ability to improve your life.

 

When we stop learning, our ability to learn and remember decays. Have you ever met people with senile dementia who can no longer remember what they ate an hour ago? The ability to form new memories is much like a muscle: We MUST Either Use it or lose it!

 

The primary mental mechanism for forming new memories (the hippocampus) is the most delicate arrangement of rapidly-changing neurons (nerve cells) in our brain. Seniors suffering from age-associated memory impairment have been shown (with brain magnetic resonance imaging – 3D MRI) to have significantly lower volumes for the right hippocampus and hippocampal head, as compared to cognitively intact older people.

 

Good News: Mental activity, proper nutrition, exercise, stress reduction and healthy sleep patterns can greatly influence the rate of hippocampus atrophication, and our resulting ability to form new memories. Bad News: Mental atrophication can be greatly accelerated by toxins like pervasive pollutants, pesticides, oxidants, alcohol, drugs (prescription, over the counter and illegal), excitotoxins, mold and fungus toxins, heart disease (vascular mini stroke), obesity, carcinogens, food preparation techniques, and various types of lifestyle-accelerated neurodegenerative disease. The good news about the bad news is that lifestyle improvements can greatly delay the onset and impact of age-related and genetic (inherited) forms of dementia risk factors.

 

How are memories formed, stored and recalled?

 

New stimuli and experiences are temporarily stored in our dynamic, ever-changing hippocampus. When we dream (rapid eye movement REM sleep) our short-term memories are merged with our long-term stereotypical classifications of similar objects that have characteristic static-and-dynamic attributes (like size, shape, color, temperature…) and behaviors (like motion, sounds supportive/adversarial relationship, etc.). These stereotypical memory abstractions (decision-making heuristic “rule of thumb” simplifications) are represented with axon/dendrite synaptic connections between changeable neurons.

 

Our thoughts, perceptions, and conclusions that we experience most frequently are stored redundantly in our complex long-term-memory neural network, so we can process them more rapidly through many diverse mental cross connections and categorical perception.

 

The redundant-storage safety factor: If neurons are damaged, the multiple copies of a familiar memory can hide or greatly diminish the impact of the damage. (See the discussion of the Seven Forms Of Human Intelligence in our Joyful Dancing material.) Expanding any one form of intelligence synergistically strengthens all others, especially our capacity to form new memories, recall them and combine them for creative problem solving.

 

Reinforcement and repetition strengthen long-term memory. A musician, athlete, dancer or mathematician who practices daily gets incrementally better over time. But if the shape and arrangement of the piano keyboard were to significantly change, time would be required to modify mental sensor/control processes.

 

Good research scientists and world travelers develop the cognitive habits of “life-long learning in an ever-expanding universe of endless possibilities.” The processes of constantly being exposed to new stimuli, experiences, concepts and points of view greatly strengthen the capacity of our hippocampus to form new memories. Although the mechanisms that strengthen the hippocampus are very different, the use-it-or-lose-it principle of “mental aerobics” is conceptually very similar to the development or atrophication of muscles and bones.

 

Our neural network becomes stronger by increasing the flow of blood to active neurons (vascular strength and capacity) and by increasing the number of glial cells (astrocytes, etc.

that supply the neurotransmitter “juice” necessary for billions of nerve cells to interact). A reduction in blood flow or a deficiency in neurotransmitters can dramatically impact cognitive processes, personality, etc.

 

Physicians often attempt to mask the symptoms of neurotransmitter deficiency with potentially-dangerous medications (linked to negative behavior, radical personality changes, emotional instability, addiction, antisocial deviant behavior, murder, etc.) Although the symptomatic myopic medication approach can clearly have an immediate tactical improvement, it can also be a strategic disaster. I strongly disagree with treating the symptom, while ignoring the source of the underlying problem. Mental aerobics, cognitive pattern reconditioning, proper nutrition and exercise can often achieve far-superior benefits with much less risk than dangerous mind-altering prescription (or illegal) drugs.

 

How does mental aerobics delay the onset, and decrease the impact, of dementia and neurotransmitter deficiency?

 

Neurons do not increase in number through usage-driven mitosis (as do muscles and bones), but glia do. Although a healthy brain consists of roughly 100 billion neurons (that decay over our lifetime), an active brain can have trillions of mentally-energizing glial cells. More glial cells are necessary to support an increased number of connection from a finite number of nerve cells. When Albert Einstein’s brain was examined after his death, he had an ordinary number of neurons, but significantly more glia than an average individual. Einstein, Thomas Edison and many other creative successful individuals practiced lifelong learning mental aerobics and thus they remained intelligent and alert contributors to society well into their advanced years of age. Avoid dementia; Develop superior intellectual capacity - Use it or lose it!

 

Intelligent people learn to forever enhance our memory and information accessibility by expanding our “Categorical Perception.” Children’s Television Workshop teaches classification theory on shows like: Sesame Street - red things / blue things, near things / far things, square things / round things, small / large / larger / largest.

 

By continually developing new cognitive organization categories, and by cross linking our accumulated lifetime of knowledge of stereotypical abstractions of reality (with many “mental hyperlink” connections), we can greatly simplify our understanding of our surroundings, and make it much easier to both store, recall, integrate, consolidate and take advantage of the many things we experience. To reduce being “forgetful”:

 

When we explore and encounter a novel perception we should ask:

 

A lazy, declining mind seeks things that reinforce obsolete, inaccurate stereotypes and rejects and resists change. In essence, such people atrophy into “non-learning entities” (NLE’s) that emotionally reject facts that disagree with their inaccurate stereotypes. NLE’s emotionally reject constructive criticism, and thus lose the ability to learn. A healthy mind must be open, flexible and adaptable, without being unstable or chaotically confused. Learning entities actively seek and sincerely appreciate feedback about the decision-making mental models.

 

Intelligent people must learn how to deal with risk factors and complexity of chaos (like predicting the weather, stock market, politics and ever-changing career opportunities). As the rate of worldwide technology and social change accelerates, we all need “mental methodologies” to evaluate new experiences, merge them with previous things that we thought were “true” and test our conclusions in safe ways.

 

The more clearly defined our memory categories are, the better cross-linked our mental connections, the more things we can remember and recall when we need them tomorrow. Mental Aerobics will greatly improve our creative problem solving capacity and joy of life.

 

As a successful Research Scientist and Professional Futurist, I have learned that creativity often involves taking simple concepts from multiple domains of knowledge and combining them is ways that others have never considered before. Every time I master a new skill or solve a complex problem in a creative way, my mind gets stronger and I feel happier.

 

I invite input from intelligent people who offer a different point of view, and I use their novel concepts and experience to refine my own stereotypical abstract understanding of everything. I have also learned a great deal through the careful observation of the many mistakes made by millions of mediocre minds, non-learning entities, and the devastation of dementia. The achievement of intellectual success and the mitigation of predictable-failure risk factors are powerful motivations for my own aggressive cognitive research and mental aerobics. By gathering this little-known knowledge and writing these words, I become a better person.

 

----------------------------------------------

 

“Mental Aerobics” Keep Our Minds Sharp and Delay or Prevent Dementia

http://www.agenet.com/news_releases/news_release5.html

 

Target Audience: Cognitive and sensory stimulation groups, Inpatient acute psychiatric groups,

Outpatient community mental health groups, Recreational groups, Seniors interest groups

 

Older adults are encouraged to keep their brains active with fun exercises

Madison, WI www.AgeNet.com, a web site dedicated to providing services, products, and information to help bridge the distance between caregivers and aging adults, is adding Marge Engelman, Ph.D. to the list of qualified professionals that offer advice and information to its visitors. Author of Aerobics of the Mind, Marge explains how the old "use it or lose it" saying can be applied to the mind as well as the body. Visitors to the AgeNet web site can try their hand at one of Marge's mentally challenging "games" for a chance to sharpen their minds and possibly even win a free Web TV.

 

On the AgeNet web site, Dr. Engelman shares her knowledge and research on how simple, fun exercises can help to stretch thinking, stimulate memory, and lead to a more creative, alert brain. To help further promote Marge's exercises for mental fitness, AgeNet has established a monthly column entitled "Ask Marge" where visitors can ask specific questions and receive answers in a timely manner. David Williams, one of AgeNet's co-founders, strongly believes that Marge's ideas and exercises are "valuable and important" and should be shared with as many caregivers and aging adults as possible.

 

Mental Aerobics plus Antiaging Antioxidants and exercise offer significant synergist benefits and happy hope for delaying the onset and reducing the lifetime impact of many types of neurodegenerative disease and debilitating mental impairment.

 

AGE-ASSOCIATED MEMORY IMPAIRMENT (AAMI) – by Rebecca Allison Deja

http://www.humboldt.edu/~morgan/eeg.htm

 

By the age of 60 individuals often notice a mild decline in memory, and after the age of 70 many experience more serious forms of forgetfulness. A National Institute of Mental Health work group coined the term "age associated memory impairment" (AAMI) to describe the memory loss experienced by healthy, elderly individuals (Crook et al., 1986) and established diagnostic criteria to operationalize the concept.

 

Based on pooled normative data from standard clinical memory tests, Larrabee and Crook (1994) reported that 41% of persons between the ages of 50 and 59 years and 52% of the those between the ages of 60 and 69 years had been classified with AAMI. However, prevalence data have been confounded by self appraisals that tended to report an inflated incidence of memory dysfunction and by results from neuropsychological tests that failed to differentiate early stages of dementia from AAMI Barker, Jones & Jennison, 1995; Hanninen et al., 1995; Koivisto et al., 1995 Based on anatomical and physiological research, Parnetti et.al. (1996) argued that AAMI is an early stage of Alzheimer's disease (DAT). Using neuroanatomical perfusional and neurochemical detail data, Parnetti et al. found that AAMI and DAT individuals had significantly lower N acetylasparate concentrations compared to controls, and inositol concentrations were highest for DAT and lowest for controls. From SPECT data, they also found significant frontal, temporoparietal, and occipital hypoperfusion only in DAT individuals. However, longitudinal studies seem to indicate that AAMI appears to be generally nonprogressive and neuropsychological test predictive (Hanninen et al., 1995). Soininen,Partanen, et al.(1994) found that visual memory scores correlated with the magnetic resonance imaging (MRI) volume of the amygdala and right hippocampus; normative controls generally had asymmetrical hippocampal formations, where as those with AAMI were more equal in volume.

 

Small, Asenath, Komo, Kaplan, and Mandelkern (1995) reported no significant correlation between cerebral atrophy, age, or family history and cognitive changes noted after three years in AAMI persons. Multiple regression analysis indicated that parietal metabolic asymmetry was a significant predictor of the change rate for visual/spatial memory, and the level of education was a consistently significant predictor of change in verbal memory. Individuals with lower levels of education were more likely to show decline and less likely to show practice effects.Hanninen et al.(1995)found that memory and verbal fluency were the best discriminators between persons with AAMI and early stages of dementia.

 

Another body of cognitive aging research investigated event related brain potentials (ERPs) from EEG data to index CNS function for specific types of cognitive events. The amplitude of the P300 component of the cognitive ERP decreases in the adult brain as age increases for both males and females (Polich, 1996). Results from the preliminary study reported by Polich indicated a decline in the EEG power in the alpha band that aids in determining the amplitude of the P300 wave in healthy young adults. Soininen, Karhu, et al. (1995) reported that inpaired

memory and frontal lobe functions in AAMI individuals may be associated with poor habituation of N100; the researchers proposed that because habituation reflects attending to relevant features of stimuli, impairment of this mechanism and the subsequent defective memory trace formation may contribute to the low performance of AAMI individuals on memory tests.

 

Central to anatomical and physiological changes in the aging brain is the inevitable decline of the cardiovascular system. In a controlled study Saletu, Grunberger, Linzmayer, and Anderer (1991) investigated the encephalotropic and psychotropic effects of Actovegin, a protein free metabolically active hemoderivative, on AAMI patients; Actovegin purportedly improves oxygen and glucose utilization at the cellular level. Significant positive changes in brain function were documented for the treatment group when compared to the placebo controls.

 

Elevated blood pressure is an established risk factor for stroke and atherosclerosis; it contributes to silent small vessel disease and white matter hyperintensities in the brain (Launer, Masaki, Petrovitch, Foley & Havlik, 1995). In a longitudinal study, Launer et al. reported that midlife systolic blood pressure levels were a predictor of cognitive function 25 years later; for every 10mmHg increase in systolic pressure >160mmHg, there was an increased 7% risk for some cognitive dysfunction and an increased 9% risk for even greater impairment. The level of cognitive dysfunction was not associated with diastolic blood pressure; this finding may have been attributable to the increased stroke mortality rate associated with high diastolic pressure prior to the 1991 to 1993 testing.

 

Analyses of the MRI and pschometric data collected by Schmidt et al.(1995) indicated that elderly hypertensives more commonly had areas of white matter hyperintensities and moderately severe ventricular enlargement in comparison to controls. No differences were noted between groups on memory test and conceptual tasks, but significantly lower results were found for hypertensives on tasks requiring attentional and visual/spatial skills than for controls with no brain abnormalities. However, controls with similar cerebral changes exhibited a similar pattern of neuropsychological deficits. Auperin et al. (1995) reported a significant correlation between moderate stenosis (<40%) of the carotid artery and tests requiring focused attention for males, but not for females, when compared to controls.

 

Other investigators have explored ways to reverse age related anatomical and physiological changes in the cardiovascular system. Starr, Whalley, and Deary (1996) treated an elderly hypertensive group with one of two antihypertensive medications for 24 weeks. They found no significant difference on any psychometric test between the captopril and bendrofluazide conditions; however, the individuals who lowered their diastolic blood pressure the most (>19mmHg) had improved scores on two cognitive subtests compared to those with the least responsive diastolic pressure(<5mmHg). Paulter (1994) has suggested that L argine might restore the responsiveness of cerebral arterioles to vasodilators because one of the factors in AAMI may be the failure of the endothelial cells to respond to vasodilators, thereby limiting the flow of blood to neuronal cells.

 

Rozelle and Budzynski (1995) used electroencephalographic (EEG) entrainment feedback followed by neurofeedback for stroke rehabilitation of a 55 year old client. The stroke victim complained of hesitant speech with word finding difficulty and paraphasia. He also had poor short term memory and poor concentration. The neurofeedback positioned over sensorimotor and speech areas helped him to inhibit Hz activity between 4 and 7 and to increase Hz activity between 15 and 21. Improvement was evident in speech fluency, word finding, attention, and

concentration.

 

In a pilot study Budzynski (1996) and Frank Andrasik, a colleague, successfully used a "brain brightening" program for training AAMI individuals. Participants received lab neurofeedback training that focused on decreasing delta/theta range activity between 2Hz and 8Hz and on increasing beta range activity between 13Hz and 18Hz; after 20 EEG neurofeedback sessions, participants were able to reduce the delta/theta band energy, but they were unable to significantly increase the beta band energy. Daily at home, participants used an audiovisual stimulation device to entrain beta frequencies. The flashing light stimulus used in the device was based on work of researchers such as Fox and Raichelle who had shown that visual flashing light stimuli in the 8Hz to 16Hz range could raise blood flow an average of 30% over baseline levels (Budzynski, 1994); the audio tones used in the device were based on Budzynski's own research that had shown a 10% to 30% increase in brain wave amplitude when individuals were listening to the tonal stimulus. In addition, the participants listened to specially designed audio cassettes containing cognitive exercises designed to increase blood flow particularly in the temporal areas; the exercises, likened to "mental aerobics" by Budzynski, required a focusing and manipulation of verbal and visual processes. AAMI individuals showed improvements in memory and attention test scores, as well as in their own self appraisal of their ability to recall recent names or events.

 

Neurofeedback may hold promise for reversing cognitive aging associated with AAMI. Tansey and Tansey (1994) have questioned the use of wide band EEG designations because highly specific brain wave signatures appear to be associated with equally specific cognitive states; for example, they found that the 10Hz band in alpha (generally accepted as a marker for a relaxed state) was specific to focused thought and that increases in peripheral blood flow were

accompanied by increases in the 28Hz band in beta (generally accepted as a marker for an active, engaged state). As Rozelle and Budzynski (1995)pointed out, the positive results in

neurofeedback treatment for AAMI individuals may be more attributable to stimulating the brain than to specific techniques or protocols employed thus far.

                

References

 

Auperin, A., Berr, C., Bonithon Kopp, C., Touboul, P.J.,

Ruelland, I., Ducimetiere, P., & Alperovitch, A. (1996).

Ultrsonic assessment of carotid wall characteristics and

cognitive functions in a community sample of 59 to 71 year olds:

The EVA study group. Stroke, 27, 1290-1295.

 

Barker, A., Jones, R., & Jennison, C. (1995). A prevalence study

of age associated memory impairment. British Journal of

Psychiatry, 167, 642-648.

 

Budzynski, T.H. (1996). Brain brightening: Can neurofeedback

improve cognitive process? Biofeedback, 24(2), 14-15,17.

 

Crook, T., Bartus, R.T., Ferris, S.H., Whitehouse, P., Cohen,

G.D., Gershon, S. (1986). Age associated memory impairment:

Proposed diagnostic criteria and measures of clinical change: A

report of a National Institute of Mental Health work group.

Developmental Neuropsychology, 2, 261-276.

 

Hanninen, T., Hallikainen, M., Koivisto, K., Helkala, E.L.,

Reinikainen, K.J., Soininen, H., Mykkanen, L., Laakso, M.,

Pyorala, K., & Riekkinen, P.J., Sr. (1995). A follow up study of

age associated memory impairment: Neuropsychological predictors

of dementia. Journal of American Geriatric Society, 43,

1007-1015.

 

Koivisto, K., Reinikainen, K.J., Hanninen, T., Vanhanen, M.,

Helkala, E.L., Mykkanen, L., Laakso, M., Pyorala, K., &

Riekkinen, P.J., Sr. (1995). Prevalence of age associated memory

impairment in a randomly selected population from eastern

Finland. Neurology, 45, 741-747.

 

Larrabee, G.J.,& Crook, T.H. (1994). Estimated prevalence of age

associated memory impairment derived from standardized tests of

memory function. International Psychogeriatrics, 6, 95-104.

 

Launer, L.J., Masaki, K., Petrovitch, H., Foley, D., & Havlik,

R.J. (1995). The association between midlife blood pressure

levels and late life cognitive function: the Honolulu Asia aging

study. Journal of the American Medical Association, 272,

1846-1851.

 

Parnetti, L., Lowenthal, D.T., Presciutti, O., Pelliccioli, G.P.,

Palumbo, R., Gobbi, G., Chiarini, P. Palumbo, B., Tarducci, R., &

Senin, U. (1996). 1H MRS, MRI based hippocampal volumetry, and

99mTc HMPAO SPECT in normal aging, age associated memory

impairment, and probable Alzheimer's disease. Journal of American

Geriatric Society, 44(2), 133-138.

 

Pautler, E.L.(1994). The possible role and treatment of deficient

microcirculation regulation in age associated memory impairment.

Medical Hypotheses, 42, 363-366.

 

Polich, J. (1996).Psychobiology of cognitive aging. Department of

Neuropharmacology Investigator' Reports [On line], Available:

http://www.scripts.edu/pub/asr/np/nppolich.html

 

Rozelle, G.R., & Budzynski, T.H. (1995). Neurotherapy for stroke

rehabilitation: A single case study. Biofeedback and Self

Regulation, 20(3), 211-229.

 

Saletu, B., Grunberger, J., Linzmayer, L., & Anderer, P. (1991).

EEG brain mapping and psychometry in age associated memory

impairment after acute and 2 week infusions with the

hemoderivative Actovegin: Double blind placebo controlled trials.

Neuropsychobiology, 24(3) 135-148.

 

Schmidt, R., Fazekas, F., Koch, M., Kapeller, P., Augustin, M.,

Offenbacher, H., Fazekas, G., & Lechner, H. (1995). Magnetic

resonance imaging cerebral abnormalities and neuropsychologic

test performance in elderly hypertensive subjects: A case control

study. Archives of Neurology, 52, 905-910.

 

Small, G.W., Asenath, L., Komo, S., Kaplan, A., & Mandelkern,

M.A. (1995).Predictors of cognitive change in middle aged and

older adults with memory loss. American Journal of Psychiatry,

152, 1757-1764.

 

Soininen, H., Karhu, J., Partanen, J., Paakkonen, A., Jousmaki,

V., Hanninen, T., Hallikainen, M., Partanen, K., Laakso, M., &

Koivisto, K. (1995). Habituation of auditory N100 correlates with

amygdaloid volumes and frontal functions in age associated memory

impairment. Physiology of Behavior, 57, 927-935.

 

Soininen, H., Partanen,K., Pitkanen, A., Vaiio, P., Hanninen, T.,

Hallikainen, M., Koivisto, K., & Riekkinen, P.J., Sr. (1995).

Volumetric MRI analysis of the amygdala and the hippocampus in

subjects with age associated memory impairment: Correlation to

visual and verbal memory. Neurology, 44, 1660-1668.

 

Starr, J.M., Whalley, L.J., & Deary, I.J. (1996). The effects of

antihypertensive treatment on cognitive function: Results from

the HOPE study. Journal of the American Geriatric Society, 44,

411-415.

 

Tansey, M.A., & Tansey, J.A. (1994). Electroencephalographic

cartography of conscious states. International Journal of

Neuroscience, 77(1-2), 89-98.

 

Return To Joyful Aging Home Page