Older news items (pre-2010) brought over from the old website

Alcoholism's effect on sleep persists

A study involving 42 long-term alcoholics who had not had a drink for up to 719 days (mean age 49 years, 27 men) has found that, compared to controls, alcoholics had significantly poorer sleep quality, measured by a significantly lower percentage of slow wave sleep and significantly more stage 1 non-rapid eye movement (NREM) sleep. Moreover, estimated lifetime alcohol consumption was significantly related to the scores on the Pittsburgh Sleep Quality Index, with higher lifetime consumption predicting less sleep satisfaction. The reduction in slow wave activity was specific to NREM sleep. This could act as an exacerbating factor in alcoholics' cognitive decline.

[792] Colrain, I. M., Turlington S., & Baker F. C. (2009).  Impact of alcoholism on sleep architecture and EEG power spectra in men and women. Sleep. 32(10), 1341 - 1352.

http://www.eurekalert.org/pub_releases/2009-10/aaos-aeo092309.php

Alcoholics show abnormal brain activity when processing facial expressions

Excessive chronic drinking is known to be associated with deficits in comprehending emotional information, such as recognizing different facial expressions. Now an imaging study of abstinent long-term alcoholics has found that they show decreased and abnormal activity in the amygdala and hippocampus when looking at facial expressions. They also show increased activity in the lateral prefrontal cortex, perhaps in an attempt to compensate for the failure of the limbic areas. The finding is consistent with other studies showing alcoholics invoking additional and sometimes higher-order brain systems to accomplish a relatively simple task at normal levels. The study compared 15 abstinent long-term alcoholics and 15 healthy, nonalcoholic controls, matched on socioeconomic backgrounds, age, education, and IQ.

[1044] Marinkovic, K., Oscar-Berman M., Urban T., O'Reilly C. E., Howard J. A., Sawyer K., et al. (2009).  Alcoholism and dampened temporal limbic activation to emotional faces. Alcoholism, Clinical and Experimental Research. 33(11), 1880 - 1892.

http://www.eurekalert.org/pub_releases/2009-08/ace-edc080509.php
http://www.eurekalert.org/pub_releases/2009-08/bumc-rfa081109.php

Binge drinking affects attention and working memory in young university students

A Spanish study of 95 first-year university students, 42 of them binge drinkers, has found that those who engaged in binge drinking required greater attentional processing during a visual working memory task in order to carry it out correctly. They also had difficulties differentiating between relevant and irrelevant stimuli. Binge drinkers are defined as males who drink five or more standard alcohol drinks, and females who drink four or more, on one occasion and within a two-hour interval. Some 40% of university students in the U.S. are considered binge drinkers.

[231] Crego, A., Holguín S R., Parada M., Mota N., Corral M., & Cadaveira F.
(2009).  Binge drinking affects attentional and visual working memory processing in young university students.
Alcoholism, Clinical and Experimental Research. 33(11), 1870 - 1879.

http://www.eurekalert.org/pub_releases/2009-08/ace-bda080509.php

HIV infection and chronic drinking together impair encoding of new experiences

A study involving 40 individuals with HIV, 38 with chronic alcoholism, 47 with both HIV and chronic alcoholism, and 39 controls, has found that although those with only one of these disorders mostly performed at levels comparable to controls on episodic and working memory tasks, those who were both positive for HIV and had a history of chronic heavy drinking were impaired on tests of immediate episodic memory (but not working memory) — meaning that they have trouble encoding new information for long-term memory. The finding is consistent with the fact that the mediotemporal lobe is affected early by both these conditions. Heavy drinking is very common among those infected with HIV.

[440] Fama, R., Rosenbloom M. J., Nichols N. B., Pfefferbaum A., & Sullivan E. V.
(2009).  Working and episodic memory in HIV infection, alcoholism, and their comorbidity: baseline and 1-year follow-up examinations.
Alcoholism, Clinical and Experimental Research. 33(10), 1815 - 1824.

http://www.eurekalert.org/pub_releases/2009-07/ace-hia072009.php

Adolescent binge drinking may compromise white matter

An imaging study of 28 teens, of whom half had a history of binge drinking (but did not meet the criteria for alcohol abuse), has found that those who had engaged in binge drinking episodes had lower coherence of white matter fibers in 18 different areas across the brain. The findings add to a growing literature indicating that adolescent alcohol involvement is associated with specific brain characteristics. White matter integrity is essential to the efficient relay of information in the brain.

[1426] McQueeny, T., Schweinsburg B. C., Schweinsburg A. D., Jacobus J., Bava S., Frank L. R., et al.
(2009).  Altered white matter integrity in adolescent binge drinkers.
Alcoholism, Clinical and Experimental Research. 33(7), 1278 - 1285.

http://www.physorg.com/news159646086.html
http://www.eurekalert.org/pub_releases/2009-04/ace-abd041509.php

Alcoholics’ brains maintain language skills at a cost

Despite the damage done by alcoholism to the frontal lobes and cerebellum, areas involved in language processing, alcoholics' language skills appear to be relatively spared from alcohol's damaging effects. A new study of 12 alcoholic males and 12 healthy controls suggests that alcoholics develop compensatory mechanisms to maintain their language skills despite alcohol's damages. The comparable performance on an auditory language task between the two groups was underlain by different neural activity (specifically, the alcoholic group showed greater activity in the left middle frontal gyrus, the right superior frontal gyrus, and the cerebellar vermis). It seems likely that this wider activity comes at the expense of other tasks, thus reducing their ability to multitask.

[926] Chanraud-Guillermo, S., Andoh J., Martelli C., Artiges E., Pallier C., Aubin H. - J., et al. (2009).  Imaging of language-related brain regions in detoxified alcoholics. Alcoholism, Clinical and Experimental Research. 33(6), 977 - 984.

http://www.eurekalert.org/pub_releases/2009-03/ace-tbm031209.php

Drinking alcohol associated with smaller brain volume

It is estimated that brain volume decreases by 1.9% per decade, accompanied by an increase in white matter lesions. Because moderate alcohol consumption has been associated with a lower risk of cardiovascular disease, it’s been thought that small amounts of alcohol might also reduce age-related declines in brain volume, although it’s known that large amounts of alcohol will reduce brain volume. However, a large, long-running study, has now found that, even at low levels of alcohol consumption, brain volume was negatively affected. Moreover, although men were more likely to be heavier drinkers, the association between drinking and brain volume was stronger in women.

[1191] Paul, C A., Au R., Fredman L., Massaro J. M., Seshadri S., DeCarli C., et al.
(2008).  Association of Alcohol Consumption With Brain Volume in the Framingham Study.
Arch Neurol. 65(10), 1363 - 1367.

http://www.eurekalert.org/pub_releases/2008-10/jaaj-daa100908.php

Heavy, chronic drinking can cause significant hippocampal tissue loss

An imaging study of 8 heavy-drinking alcoholics and 8 age and ethnicity matched non-alcoholics (all male) found that total hippocampus volume was significantly reduced among the alcoholics.

[677] Beresford, T. P., Arciniegas D. B., Alfers J., Clapp L., Martin B., Du Y., et al. (2006).  Hippocampus Volume Loss Due to Chronic Heavy Drinking. Alcoholism: Clinical and Experimental Research. 30(11), 1866 - 1870.

http://www.eurekalert.org/pub_releases/2006-10/ace-hcd101606.php

Most of the cognitive deficits associated with alcoholism recoverable

Results of a study involving middle-aged alcoholics who have been sober for six months to 13 years, suggest that long-term abstinent alcoholics can recover most of their neurocognitive deficits. However, deficits in spatial-processing abilities continued. Visuospatial processes are important for many daily activities, including driving, reading a map, assembling things, and performing tasks that require spatial orientation. The study doesn’t however know how much damage had been done when the alcoholics ceased drinking; further studies are exploring the recovery of older abstinent alcoholics who ceased drinking at different ages.

[856] Fein, G., Torres J., Price L. J., & Sclafani V. D. (2006).  Cognitive Performance in Long-Term Abstinent Alcoholic Individuals. Alcoholism: Clinical and Experimental Research. 30(9), 1538 - 1544.

http://www.eurekalert.org/pub_releases/2006-08/ace-lam082106.php

Brain atrophy occurs faster in women alcoholics

A study of 34 male and 42 female alcoholics has found that, although the women had been alcoholics for just 5.5 years on average, compared to the average 10.4 years for the men, the women had lost as much proportionate brain volume as the men. The findings are consistent with other studies suggesting that women suffer from the effects of alcohol abuse faster.

[1258] Mann, K., Ackermann K., Croissant B., Mundle G., Nakovics H., & Diehl A. (2005).  Neuroimaging of Gender Differences in Alcohol Dependence: Are Women More Vulnerable?. Alcoholism: Clinical and Experimental Research. 29(5), 896 - 901.

http://www.nature.com/news/2005/050509/full/050509-15.html

Drinking for just eight weeks impairs learning and memory in mice

It’s well established that chronic alcohol consumption can produce deficits in learning and memory. A new rodent study, however, is the first to show that continuous drinking for as little as eight weeks can produce deficits in learning and memory that last at least 12 weeks after drinking stopped — “equivalent to a human that drank six to eight beers or one bottle of wine a day every day for six years experiencing learning and memory deficits up to nine years after they stopped drinking alcohol." These deficits were global — that is, they affected long-term memory for every type of task tested. Short-term memory was not affected. Rats who drank for only four weeks did not experience the same effects.

[522] Farr, S. A., Scherrer J. F., Banks W. A., Flood J. F., & Morley J. E.
(2005).  Chronic Ethanol Consumption Impairs Learning and Memory After Cessation of Ethanol.
Alcoholism: Clinical and Experimental Research. 29(6), 971 - 982.

http://www.eurekalert.org/pub_releases/2005-06/ace-dfj060605.php

Cognitive effects of binge drinking worse for women

A new study looked at the cognitive effects of binge drinking, which apparently is on the rise in several countries, including Britain and the US. The study involved 100 healthy moderate-to-heavy social drinkers aged between 18 and 30. There were equal numbers of males and females. The study found that female binge drinkers performed worse on the working-memory and vigilance tasks than did the female non-binge drinkers.

[1311] Townshend, J. M., & Duka T.
(2005).  Binge Drinking, Cognitive Performance and Mood in a Population of Young Social Drinkers.
Alcoholism: Clinical and Experimental Research. 29(3), 317 - 325.

http://www.eurekalert.org/pub_releases/2005-03/ace-bdc030705.php

Alcohol's damaging effects on adolescent brain function

A number of speakers at Symposium speakers at the June 2004 Research Society on Alcoholism meeting in Vancouver, reported on research concerning the vulnerability of the adolescent brain to the damaging effects of alcohol. Some of the findings presented were:

• The adolescent brain is more vulnerable than the adult brain to disruption from activities such as binge drinking. Adolescent rats that were exposed to binge drinking appear to have permanent damage in their adult brains.
• Subtle but important brain changes occur among adolescents with Alcohol Use Disorder, resulting in a decreased ability in problem solving, verbal and non-verbal retrieval, visuospatial skills, and working memory.
• The association between antisocial behavior during adolescence and alcoholism may be explained by abnormalities in the frontal limbic system, which appears to cause "blunted emotional reactivity".
• Alcohol-induced memory impairments, such as "blackouts", are particularly common among young drinkers and may be at least in part due to disrupted neural plasticity in the hippocampus, which is centrally involved in the formation of autobiographical memories.

[1238] Monti, P. M., Miranda, Jr R., Nixon K., Sher K. J., Swartzwelder S. H., Tapert S. F., et al.
(2005).  Adolescence: Booze, Brains, and Behavior.
Alcoholism: Clinical and Experimental Research. 29(2), 207 - 220.

http://www.eurekalert.org/pub_releases/2005-02/ace-ade020705.php

Alcoholics can have deficits in visuoperception and frontal executive function despite sobriety

Detoxified alcoholics often have visuospatial and visuoperceptual deficits, characterized by difficulties completing tasks such as putting pieces of a puzzle together or map reading. A new study has found that, even with prolonged sobriety, alcoholics show deficits in visuoperception and frontal executive functioning of the brain. Furthermore, alcoholics utilize a more complex higher-order cognitive system (frontal executive functions) to perform the same tasks as individuals without a history of alcoholism. The potential problem with this is that if that same system is needed for a competing task, alcoholics may be at a disadvantage because that system would otherwise be engaged. The study involved 51 recently detoxified nonamnesic alcoholic men (ages 29 to 66 years) compared with 63 "normal," control men (ages 21 to 70 years).

Fama, R., Pfefferbaum, A. & Sullivan, E. V. 2004. Perceptual Learning in Detoxified Alcoholic Men: Contributions From Explicit Memory, Executive Function, and Age. Alcoholism: Clinical & Experimental Research, 28(11), 1657-1665.

http://www.eurekalert.org/pub_releases/2004-11/ace-ach110804.php

New brain cells develop during alcohol abstinence

A rat study has found that the detrimental effect of alcohol on the formation of new neurons in the adult rat hippocampus is followed by a pronounced increase in new neuron formation in the hippocampus within four-to-five weeks of abstinence. This included a twofold burst in brain cell proliferation at day seven of abstinence. The findings may have significant implications for treatment of alcoholism during recovery. The discovery of regeneration of neurons in recovery opens up new avenues of therapies aimed at regeneration of brain cells.

[393] Nixon, K., & Crews F. T. (2004).  Temporally Specific Burst in Cell Proliferation Increases Hippocampal Neurogenesis in Protracted Abstinence from Alcohol. J. Neurosci.. 24(43), 9714 - 9722.

http://www.eurekalert.org/pub_releases/2004-11/uonc-nbc110504.php

Cognitive function of alcohol abuse patients may influence treatment outcome

Years of heavy alcohol consumption are known to impair many abilities generally referred to as “executive functions.” Such functions include judgment, problem solving, decision making, planning, and social conduct. But alcohol affects executive functioning both chronically and acutely. New research has found that alcohol abuse patients show significant deficits in executive functioning (specifically, abstract reasoning, memory discrimination, and effectiveness on timed tasks) during the critical first weeks of abstinence. The finding has implications for treatment programs, as the early phases of most treatment programs for alcohol abusers commonly require working in groups, making plans for the future, inhibiting behaviors related to their addiction, and remembering specific things. It is suggested that clinicians should scale down their expectations of what patients can do until more of their executive functioning comes back. The researchers are now intending to explore how long it takes the majority of people to regain most of their executive functioning.

[194] Zinn, S., Stein R., & Swartzwelder S. H. (2004).  Executive Functioning Early in Abstinence From Alcohol. Alcoholism: Clinical and Experimental Research. 28(9), 1338 - 1346.

http://www.eurekalert.org/pub_releases/2004-09/ace-cco090504.php
http://www.eurekalert.org/pub_releases/2004-09/dumc-cfo091004.php

Brain damage found among heavy social drinkers

Almost all knowledge about brain damage due to chronic alcohol consumption has been gathered from alcoholics, generally toward the end of an institutionalized treatment program or many months into abstinence. A new study however, uses magnetic resonance technology to examine brain damage in heavy drinkers who are not in treatment and function relatively well in the community. The study found that frontal white matter NAA – generally considered to be a marker of neuronal damage – was lower in heavy drinkers than light drinkers, and was associated with lower executive and working memory functions. Some of the behaviors that could be associated with the metabolite changes include the inability to apply consequences from past actions, difficulties with abstract concepts of time and money, difficulties with storing and retrieving information, and frequently needing external motivators.

[220] Weiner, M. W., Meyerhoff D. J., Blumenfeld R., Truran D., Lindgren J., Flenniken D., et al.
(2004).  Effects of Heavy Drinking, Binge Drinking, and Family History of Alcoholism on Regional Brain Metabolites.
Alcoholism: Clinical and Experimental Research. 28(4), 650 - 661.

http://www.eurekalert.org/pub_releases/2004-04/ace-sab040704.php

Even small amounts of alcohol or anesthetics may damage the developing brain

Mouse studies suggest that even small amounts of alcohol or anesthetic drugs can trigger nerve cell death in the developing brain. The brain appears most sensitive to this effect during the development stage known as the brain growth spurt. In humans this lasts from about the sixth month of pregnancy to a child's third birthday. Nerve cells are genetically programmed to commit suicide if they fail to make synaptic connections on time. Alcohol and anesthetic drugs interfere with the brain's neurotransmitter systems and with the formation of those synaptic connections, automatically activating a signal within the neuron that directs it to commit suicide.

Olney, J.W. 2004. Perinatal Drug/Alcohol Exposure and Neuronal Suicide – Public Health Implications. Paper presented February 14 at the annual meeting of the American Association for the Advancement of Science in Seattle.

http://www.eurekalert.org/pub_releases/2004-02/wuso-sao021104.php

Hippocampal damage seen in those with alcoholic memory disorder and those with Alzheimer's

A comparison between the brains of five men with alcoholic Korsakoff's syndrome and the brains of men with Alzheimer's disease as well as the brains of healthy men, found that the brains of all Korsakoff's patients and Alzheimer's patients were comparable in significant volume loss in the hippocampus. Greater hippocampal damage (for Korsakoff's patients) and smaller hippocampal size (for Alzheimer’s) was correlated with poorer memory performance. It is suggested that, although there are of course a number of differences between these disorders, the nature of the memory impairment may be the same. Awareness of the similarities may help detection of both disorders.

[262] Sullivan, E. V., & Marsh L. (2003).  Hippocampal volume deficits in alcoholic Korsakoff's syndrome. Neurology. 61(12), 1716 - 1719.

http://www.eurekalert.org/pub_releases/2003-12/aaon-seu121503.php

Alcohol damages day-to-day memory function

A new study involving 763 participants (465 female, 298 males) used self-report questionnaires: the Prospective Memory Questionnaire (PMQ), the Everyday Memory Questionnaire (EMQ), and the UEL (University of East London) Recreational Drug Use Questionnaire, and found that heavy users of alcohol reported making consistently more errors than those who said that they consumed little or no alcohol. More specifically, those who reported higher levels of alcohol consumption were more likely to miss appointments, forget birthdays and pay bills on time (prospective memory), as well as more problems remembering whether they had done something, like locking the door or switching off the lights or oven, or where they had put items like house keys. The study also found a significant increase in reported memory problems by people who claimed to drink between 10 and 25 units each week in comparison to non-drinkers – this is within the ’safe drinking’ limits suggested by U.K. government guidelines.

[1042] Ling, J., Heffernan T. M., Buchanan T., Rodgers J., Scholey A. B., & Parrott A. C.
(2003).  Effects of Alcohol on Subjective Ratings of Prospective and Everyday Memory Deficits.
Alcoholism: Clinical and Experimental Research. 27(6), 970 - 974.

http://www.eurekalert.org/pub_releases/2003-06/ace-add060903.php

Study of alcoholics reveals connection between cerebellum and prefrontal cortex

Two functions commonly compromised by chronic alcoholism are executive functions (such as problem solving, putting things in order, working memory, doing multiple tasks at once) and balance (the ability to walk a straight line or stand on one foot, especially with eyes closed or in the dark). Executive functions are primarily processed in the prefrontal cortex, while balance and postural stability are functions of the cerebellum. Previous studies have shown that the prefrontal cortex and regions of the cerebellum are especially vulnerable to the effects of chronic alcoholism. Although these areas are spatially far apart (the former in the frontal lobes, the latter in the hindbrain), they are connected in a variety of ways, most particularly through the pons and the thalamus. An imaging study of 25 nonamnesic alcoholic men suggests that these connections may compound the damaging effects of alcohol on these brain regions, and that the cerebellum, through these connections, can exert a significant effect on functions of the prefrontal cortex.

[356] Sullivan, E. V. (2003).  Compromised Pontocerebellar and Cerebellothalamocortical Systems: Speculations on Their Contributions to Cognitive and Motor Impairment in Nonamnesic Alcoholism. Alcoholism: Clinical and Experimental Research. 27(9), 1409 - 1419.

http://www.eurekalert.org/pub_releases/2003-09/ace-amc090803.php

Alcoholics' cognitive impairment associated with impaired reaction to stress

The body secretes a hormone called cortisol in response to stress. Areas of the brain involved in memory and problem-solving are responsive to cortisol. A new study has found impaired release of cortisol in recently detoxified alcoholics when performing two tasks known to induce stress: mental arithmetic problems and a "cold pressor" task, which requires submerging one hand in ice water for 90 seconds. This was associated with lower scores on measures of problem-solving ability and memory. The study also found that, among alcoholics, the number of withdrawals from alcohol was the strongest predictor of memory impairments, but not of problem-solving ability. The greater the alcoholics' relative cortisol levels were during alcohol withdrawal, the more likely they were to have low scores on one of the problem-solving tests. Nonalcoholic participants showed a connection between higher post-stress cortisol levels and impaired memory, a finding supported by earlier research.

[340] Errico, A. L., King A. C., Lovallo W. R., & Parsons O. A. (2002).  Cortisol Dysregulation and Cognitive Impairment in Abstinent Male Alcoholics. Alcoholism: Clinical and Experimental Research. 26(8), 1198 - 1204.

http://www.eurekalert.org/pub_releases/2002-08/cfta-air080902.php

Older news items (pre-2010) brought over from the old website

Caffeine reverses memory impairment in Alzheimer's mice

Consistent with earlier indications that moderate caffeine consumption may protect against memory decline, a study of genetically engineered mice has found that when the old mice began to show memory impairment, those given caffeine for 2 months performed as well as normal aged mice on cognitive tests, while those given plain drinking water continued to do poorly. The Alzheimer's mice received the equivalent of five 8-oz. cups of regular coffee a day (or two cups of Starbucks coffee, or 14 cups of tea). Moreover, the brains of the caffeinated mice showed nearly a 50% reduction in levels of beta amyloid. The effect appears to be through suppression of both β-secretase and presenilin 1 /g-secretase expression. Caffeine had this effect only on those with Alzheimer’s; normal mice given caffeine through adulthood showed no cognitive benefit.

Arendash, G.W. et al. 2009. Caffeine Reverses Cognitive Impairment and Decreases Brain Amyloid-β Levels in Aged Alzheimer's Disease Mice. Journal of Alzheimer's Disease, 17 (3), 661-680.

Cao, C. et al. 2009. Caffeine Suppresses Amyloid-β Levels in Plasma and Brain of Alzheimer's Disease Transgenic Mice. Journal of Alzheimer's Disease, 17 (3), 681-697.

http://www.eurekalert.org/pub_releases/2009-07/uosf-crm070109.php

Midlife coffee drinking reduces risk of dementia

A large, long-running Finnish study has found that those who were coffee drinkers at midlife had lower risk for dementia and Alzheimer’s later in life compared to those drinking no or only little coffee midlife. The lowest risk was found among moderate coffee drinkers (drinking 3-5 cups of coffee/day). Tea drinking was relatively uncommon and was not associated with dementia.

Eskelinen, M.H. et al. 2009. Midlife Coffee and Tea Drinking and the Risk of Late-Life Dementia: A Population-based CAIDE Study. Journal of Alzheimer's Disease, 16(1).

http://www.physorg.com/news151225794.html

Chocolate, wine and tea improve brain performance

A study of over 2000 older Norwegians (aged 70-74) has found that those who consumed chocolate, wine, or tea had significantly better cognitive performance and lower risk of poor cognitive performance than those who did not. Those who consumed all 3 studied items had the best performance and the lowest risks for poor test performance. The associations between intake of these foodstuffs and cognition were dose dependent, with maximum effect at intakes of around 10 grams a day for chocolate and around 75–100 ml a day for wine, but approximately linear for tea. The effect was most pronounced for wine and modestly weaker for chocolate intake. The finding is consistent with research indicating that those who consume lots of flavonoids have a lower incidence of dementia.

[623] Nurk, E., Refsum H., Drevon C. A., Tell G. S., Nygaard H. A., Engedal K., et al.
(2009).  Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance.
The Journal of Nutrition. 139(1), 120 - 127.

http://www.physorg.com/news149185135.html

Coffee helps you retain mental sharpness later in the day

A recent study of 40 older adults (over 65) confirmed the popular belief in the value of caffeine in helping overcome a decline in mental sharpness later in the afternoon. All the participants (like three-quarters of all people in that age group, studies suggest) described themselves as "morning people". Testing confirmed that they were less alert later in the day. Given coffee, but not told whether it was "real" coffee or decaffeinated, those who drank the regular coffee did not experience mental declines in the afternoon tests. Note that participants were already regular coffee drinkers (and were asked to abstain before arriving for the test).

[1166] Ryan, L., Hatfield C., & Hofstetter M.
(2002).  Caffeine reduces time-of-day effects on memory performance in older adults.
Psychological Science: A Journal of the American Psychological Society / APS. 13(1), 68 - 71.

http://www.nytimes.com/2002/01/01/health/psychology/01AGIN.html?rd=hcmcp?p=041sRh041sTt436WO012000mo9$ho9mk

Helping memory with "natural" supplements

Do caffeine and glucose help concentration? A recent study found that volunteers who drank a mixture containing caffeine and glucose (as well as trace levels of guarana, ginkgo and ginseng) showed clear improvements in memory and attention. Those who consumed the individual ingredients, or a placebo, did not show such improvements.

Scholey, A. & Kennedy, D. 2003. Report at the British Psychological Society Annual Conference in Bournemouth 13-15 March.

Older news items (pre-2010) brought over from the old website

High-fat diet affects physical and memory abilities of rats after 9 days

A rat study has found that after a mere 9 days of eating a high-fat diet (55% of calories as fat, compared to their normal very low-fat diet of 7.5% of calories as fat)), rats were dramatically slower to run a maze and made more mistakes. The reductions in performance were correlated with increased levels of a protein that is involved in the process of burning food stuffs for energy in the cells, reducing the efficiency of the heart and muscles, and with an increase in heart size, probably because it had to pump more blood around the body to get the necessary oxygen to the muscles (and brain). The increase in fat is of course extremely high for the rats, given that their normal diet is very low in fat; however, the level is not out of keeping with a human unhealthy diet.

[1160] Murray, A. J., Knight N. S., Cochlin L. E., McAleese S., Deacon R. M. J., Rawlins N. J. P., et al.
(2009).  Deterioration of physical performance and cognitive function in rats with short-term high-fat feeding.
FASEB J.. 23(12), 4353 - 4360.

Full text available at: http://www.fasebj.org/cgi/rapidpdf/fj.09-139691v1.pdf
http://www.eurekalert.org/pub_releases/2009-08/uoc-hda081109.php

Diabetic seniors may experience memory declines after eating high-fat food

Growing evidence links diabetes to cognitive impairment. Now a small study of 16 adults (aged 50 years and older) with type 2 diabetes compared their cognitive performance on three separate occasions, fifteen minutes after consuming different meals. One meal consisted of high fat products – a danish pastry, cheddar cheese and yogurt with added whipped cream; the second meal was only water; and the third was the high-fat meal plus high doses of vitamins C (1000 mg) and E (800 IU) tablets. Researchers found that vitamin supplementation consistently improved recall scores relative to the meal alone, while those who ate the high fat meal without vitamin supplements showed significantly more forgetfulness of words and paragraph information in immediate and time delay recall tests. Those on water meal and meal with vitamins showed similar levels in cognitive performance. The finding indicates not only that diabetics can temporarily further worsen already underlying memory problems associated with the disease by consuming unhealthy meals, but also that this can be remedied by taking high doses of antioxidant vitamins C and E with the meal, suggesting that the effect of high-fat foods si to cause oxidative stress. However, this is hardly a recommended course of action, and the real importance of this finding is that it emphasizes the need for diabetics to consume healthy foods high in antioxidants, like fruits and vegetables. Of course, this is a very small study, and further replication is needed.

[1094] Chui, M., & Greenwood C.
(2008).  Antioxidant vitamins reduce acute meal-induced memory deficits in adults with type 2 diabetes.
Nutrition Research. 28(7), 423 - 429.

http://www.eurekalert.org/pub_releases/2008-06/bcfg-swt062408.php

Copper increases cognitive decline in older adults on high-fat diet

A six-year study involving 3,718 Chicago residents age 65 years and older has found that among the 16% who had high levels of saturated and trans fats in their diets, cognitive function deteriorated more rapidly the more copper they had in their diets. Copper intake wasn’t a factor for the rest of the group. Previous studies have found higher levels of copper in the blood of patients with Alzheimer's disease. The finding will need to be confirmed by further research. The dietary recommended allowance of copper for adults is .9 milligrams per day. Organ meats, such as liver, and shellfish are the foods with the highest copper levels, followed by nuts, seeds, legumes, whole grains, potatoes, chocolate and some fruits.

[1129] Morris, M C., Evans D. A., Tangney C. C., Bienias J. L., Schneider J. A., Wilson R. S., et al.
(2006).  Dietary Copper and High Saturated and trans Fat Intakes Associated With Cognitive Decline.
Arch Neurol. 63(8), 1085 - 1088.

http://www.sciencedaily.com/releases/2006/08/060816013125.htm
http://www.eurekalert.org/pub_releases/2006-08/jaaj-hcd081006.php

Exercise may counteract bad effect of high-fat diet on memory

An animal study has investigated the interaction of diet and exercise on synaptic plasticity (an important factor in learning performance). A diet high in fat reduced levels of brain-derived neurotrophic factor (BDNF) in the hippocampus, and impaired performance on spatial learning tasks, but both of these consequences were prevented in those animals with access to voluntary wheel-running. Exercise appeared to interact with the same molecular systems disrupted by the high-fat diet.

[883] Molteni, R., Wu A., Vaynman S., Ying Z., Barnard R. J., & Gómez-Pinilla F.
(2004).  Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor.
Neuroscience. 123(2), 429 - 440.

http://journals.bmn.com/jsearch/search/record?uid=NSC.bmn09190_03064522_v0123i02_03007425&rendertype=abstract

Rats on a high-fat diet showed severe impairment on a wide range of learning and memory tasks

Rats on a high-fat diet for three months showed severe impairment on a wide range of learning and memory tasks relative to those animals that consumed the lower fat die. On the basis that the brain needs glucose in order to function, and that saturated fatty acids impede glucose metabolism, the high-fat rats were given high doses of glucose. Glucose significantly improved memory in the high-fat rats, especially long-term memory.

[2402] Greenwood, C. E., & Winocur G.
(2001).  Glucose Treatment Reduces Memory Deficits in Young Adult Rats Fed High-Fat Diets.
Neurobiology of Learning and Memory. 75(2), 179 - 189.

http://www.eurekalert.org/pub_releases/2001-02/BCfG-Rssh-1802101.php

High-fat diets impair memory

Several rodent studies have found evidence that a diet high in fat and empty calories may impair memory.
In one study, young adult male mice were divided into four groups by diet: normal (control) diet, high-saturated-fat diet, high-sugar diet, and diet high in saturated fats and sugar. They were kept on the diet for four months, during which mice on the high-fat and high-fat-&-sugar diets gained significantly more weight than those on the control and high sugar diets. At the end of that time, the mice were tested on a maze task. Mice on the high-fat and high-fat-&-sugar diets performed worse than the other mice. The mice were then exposed to a neurotoxin called kainic acid, which is known to damage nerve cells in the hippocampus. Mice on the high-fat and high-fat-&-sugar diets were significantly more impaired by the neurotoxin.
In another mouse study, obese mice were fed a diet containing about 10% fat for seven months, while control mice were fed standard lab chow containing only 5% fat. On testing, it was found that the obese mice took significantly more trials than the normal-weight mice to both acquire and retain a memory of a foot shock. They also required significantly more trials than control mice to learn to press a lever for milk reinforcement.
A rat study explored whether a diet high in cholesterol and hydrogenated fats affected working memory in middle-aged rats (corresponding to 60 and older for humans). The high-fat, high-cholesterol diet produced significantly higher plasma triglycerides, total cholesterol, high density lipoprotein cholesterol, and low density lipoprotein cholesterol compared with controls. Weight increase and food consumption were similar between the groups. Animals on the high-fat regimen made more errors than animals fed the control diet, especially during the trial that placed the highest demand on their working memory.
Another rat study found that a diet high in fats and carbohydrates worsened cognitive deficits in rats exposed to repeated brief periods of low oxygen during sleep (as experienced by people with sleep apnea).

These studies were reported at the  34th Society for Neuroscience annual meeting in San Diego in October 2004.

http://www.eurekalert.org/pub_releases/2004-10/sfn-hdh102604.php

Older news items (pre-2010) brought over from the old website

 

• Prenatal exposure

 

Amphetamine use in adolescence may impair adult working memory

Rats exposed to high doses of amphetamines at an age that corresponds to the later years of human adolescence showed significant declines in working memory as adults, long after the exposure. The researchers tested two types of amphetamine exposure: intermittent (a steady dose every other day) and "binge-escalation," in which increasing amounts of the drug were given over a period of four days, followed by a simulated binge – a high dose every two hours for eight hours on the fifth day. The type of exposure did not make a significant difference.

Stanis, J.J. et al. 2009. Amphetamine-induced deficits in a working memory task are more significant in drug-exposed adolescent rats than drug-exposed adults. Presented October 21 at the annual meeting of the Society for Neuroscience in Chicago.

http://www.eurekalert.org/pub_releases/2009-10/uoia-aui101909.php

Amphetamines and cocaine can damage the brain’s ability to learn from new experiences

A rat study suggests that amphetamines and cocaine can damage the brain’s ability to learn from new experiences. Rats were given either amphetamine, cocaine, or saline for 20 days, and then half were moved to new cages containing multiple levels with ramps, bridges, and a climbing chain; tunnels; and toys that were rearranged once a week to encourage continued exploration of the environment. After three and a half months, the rats who received saline solutions and had lived in a stimulating environment had a greater number of neuronal connections than those who remained in their usual environment. Rats given either amphetamines or cocaine, however, did not respond to the complex environment with a similar growth in neuronal connection.

[2385] Kolb, B., Gorny G., Li Y., Samaha A-N., & Robinson T. E.
(2003).  Amphetamine or cocaine limits the ability of later experience to promote structural plasticity in the neocortex and nucleus accumbens.
Proceedings of the National Academy of Sciences. 100(18), 10523 - 10528.

http://www.eurekalert.org/pub_releases/2003-08/niod-aoc082503.php

Amphetamine helps or hinders cognitive function depending on your genes

Everyone inherits two copies of the catecho-O-methyltransferase (COMT) gene, that codes for the enzyme that metabolizes neurotransmitters like dopamine and norepinephrine. It comes in two common versions. One version, met, contains the amino acid methionine at a point in its chemical sequence where the other version, val, contains a valine. Depending on the mix of variants inherited, a person's COMT genes can be typed met/met, val/val, or val/met. People with the val/val variant appear to have reduced prefrontal dopamine activity and less efficient prefrontal information processing, along with slightly increased risk for schizophrenia. People with val/met have more efficient prefrontal function, and people with met/met the most efficient.
In a recent imaging study, 27 volunteers (10 val/val, 11 val/met, and 6 met/met) performed a variety of cognitive tasks that involved working memory and executive functioning, after taking either amphetamine or a placebo. Since amphetamine boosts dopamine activity in the prefrontal cortex, the researchers predicted that the drug would enable val/val types to boost their low level of dopamine and perform better on cognitive tasks that depend on the prefrontal cortex. On the other hand, those with met/met should be hindered by amphetamine. The study confirmed these predictions - val/val subjects on amphetamine performed comparably to met/met types in normal conditions, while met/met subjects on amphetamine performed worse than subjects with val/val types in normal conditions.
Amphetamines and other drugs that affect prefrontal dopamine systems are used to treat Attention Deficit Hyperactivity Disorder (ADHD), and other psychiatric illnesses, and some people respond better than others to these medications. About 15-20% of individuals in populations of European ancestry have the met/met COMT gene type.

[1292] Mattay, V. S., Goldberg T. E., Fera F., Hariri A. R., Tessitore A., Egan M. F., et al.
(2003).  Catechol O-methyltransferase val158-met genotype and individual variation in the brain response to amphetamine.
Proceedings of the National Academy of Sciences of the United States of America. 100(10), 6186 - 6191.

http://www.eurekalert.org/pub_releases/2003-05/niom-gep050703.php

Long-lasting changes in attention and motor skills after heavy stimulant abuse

A study of 50 pairs of twins, in which one of each pair had a history of cocaine or methamphetamine abuse, and the other had no history of drug abuse, found that the twin with a history of stimulant abuse performed significantly worse on several tests of attention and motor skills than did the one who had never used drugs, even after at least a year had passed since any drugs had been taken. Abusers did, however, outperform their twin on visual vigilance, a test measuring the ability to pay attention over time.

[1163] Toomey, R., Lyons M. J., Eisen S. A., Xian H., Chantarujikapong S., Seidman L. J., et al.
(2003).  A Twin Study of the Neuropsychological Consequences of Stimulant Abuse.
Arch Gen Psychiatry. 60(3), 303 - 310.

http://www.eurekalert.org/pub_releases/2003-04/niod-sot040903.php

Methamphetamine abuse may permanently impair cognitive function

Methamphetamine abuse damages the nerve endings of human brain cells containing the chemical messenger dopamine. A recent study has found that methamphetamine-damaged brain cells may recover after prolonged abstinence from the drug. However, the extent of recovery may not be sufficient to restore full cognitive function, particularly in those who are did long-time, heavy users of the drug.

[1223] Ding, Y-S., Logan J., Volkow N. D., Chang L., Wang G-J., Fowler J. S., et al.
(2001).  Loss of Dopamine Transporters in Methamphetamine Abusers Recovers with Protracted Abstinence.
J. Neurosci.. 21(23), 9414 - 9418.

http://www.eurekalert.org/pub_releases/2001-12/niod-ise112801.php
http://www.eurekalert.org/pub_releases/2001-12/bnl-bsa112901.php

Prenatal exposure

One hit of crystal meth can cause birth defects

A mouse study has found that a single prenatal dose of methamphetamine (speed) can cause long-term neurodevelopmental problems in babies, especially reduced motor coordination.

[1003] Jeng, W., Wong A. W., Ting-A-Kee R., & Wells P. G.
(2005).  Methamphetamine-enhanced embryonic oxidative DNA damage and neurodevelopmental deficits.
Free Radical Biology & Medicine. 39(3), 317 - 326.

http://www.eurekalert.org/pub_releases/2005-07/uot-oho072605.php

Cognitive development affected in babies exposed prenatally to cocaine

In the first study to use measures of both the mothers’ self report of their prenatal drug use, and infant meconium, which provided a physical measure of the amount of drug exposure, 415 cocaine-exposed infants born in Cleveland were compared to non-exposed infants on cognitive and motor development until age 2. Infants were tested at 6.5, 12 and 24 months. Mental retardation in the cocaine-exposed children at age 2 was 4.89 times higher than would be expected in the general population. The percentage of children with mild delays requiring intervention was almost double the rate of the high risk, non-cocaine group. The study also found that tobacco exposure had significant negative effects on infant development.

[390] Singer, L. T., Arendt R., Minnes S., Farkas K., Salvator A., Kirchner L. H., et al.
(2002).  Cognitive and Motor Outcomes of Cocaine-Exposed Infants.
JAMA. 287(15), 1952 - 1960.

http://www.eurekalert.org/pub_releases/2002-04/cwru-a2y041602.php

Cocaine may permanently damage learning abilities in developing fetuses

Two recent studies investigating the effect of pre-natal exposure to cocaine in rats suggest that children exposed to cocaine while in the womb may have permanent changes to the part of the brain that helps control attention and memory, leading to learning deficits and symptoms that are very much like attention deficit hyperactivity disorder.

[1270] Morrow, B. A., Elsworth J. D., & Roth R. H.
(2002).  Male rats exposed to cocaine in utero demonstrate elevated expression of Fos in the prefrontal cortex in response to environment.
Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology. 26(3), 275 - 285.

[264] Morrow, B. A., Elsworth J. D., & Roth R. H.
(2002).  Prenatal cocaine exposure disrupts non-spatial, short-term memory in adolescent and adult male rats.
Behavioural Brain Research. 129(1-2), 217 - 223.

http://www.eurekalert.org/pub_releases/2002-02/yu-ucd021802.php

Older news items (pre-2010) brought over from the old website

Ecstasy can harm the brains of first-time users

Ecstasy targets neurons in the brain that use serotonin to communicate. Previous studies have found that long-term or heavy ecstasy use can damage these neurons and cause depression, anxiety, confusion, difficulty sleeping and decrease in memory. Now research into the effects of low doses on first-time users has revealed a decrease in blood circulation in some areas of the brain, along with a relative decrease in verbal memory performance in ecstasy users compared to non-users.

De Win, M. et al. 2006. Ecstasy: Is It Safe for the Brain? First Prospective Study on Effects of Low Doses of Ecstasy on the Brain in New Ecstasy Users, Using a Combination of Advanced MR Imaging Techniques and [123I]ß-CIT SPECT. Presented on November 27 at the annual meeting of the Radiological Society of North America (RSNA).

http://www.eurekalert.org/pub_releases/2006-11/rson-ech112106.php

International survey finds Ecstasy use affects long-term memory

An international web-based survey of Ecstasy users and non-drug users found that those who regularly took ecstasy suffered from mainly long-term memory difficulties, and that they were 23% more likely to report problems with remembering things than non-users (14% more likely compared to those who had never taken Ecstasy, but had taken other drugs). Those who regularly used cannabis reported up to 20% more memory problems than non-users, and their memory problems mainly involved short-term memory. The Ecstasy users also made 21% more errors on the questionnaire form than non-ecstasy users and 29% more mistakes than people who did not take drugs at all. The study involved 763 people, from which 81 'typical' ecstasy users who had taken the drug at least ten times were selected for closer investigation. There were no significant differences between genders.

[367] Rodgers, J., Buchanan T., Scholey A. B., Heffernan T. M., Ling J., & Parrott A. C.
(2003).  Patterns of Drug Use and the Influence of Gender on Self-Reports of Memory Ability in Ecstasy Users: A Web-Based Study.
J Psychopharmacol. 17(4), 389 - 396.

http://www.eurekalert.org/pub_releases/2004-01/uonu-eam011304.php

Ecstasy may cause permanent memory damage

A comparison of memory performance in recent users of the drug Ecstasy, ex-users, and those who have never taken the drug, indicates Ecstasy may cause permanent damage to cognitive function. It appears that ecstasy damages mechanisms associated with serotonin, particularly in an area of the brain linked to memory.

[1022] Reneman, L., Lavalaye J., Schmand B., de Wolff F. A., van den Brink W., den Heeten G. J., et al.
(2001).  Cortical Serotonin Transporter Density and Verbal Memory in Individuals Who Stopped Using 3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy"): Preliminary Findings.
Arch Gen Psychiatry. 58(10), 901 - 906.

http://tinyurl.com/ix9f

Researchers have isolated Ecstasy by-product believed to cause some of the brain damage associated with the drug

Researchers in Spain have isolated for the first time a by-product of the illicit drug Ecstasy that is believed to cause some of the brain damage associated with the drug. They believe their finding will help them measure, with greater precision, the long-term neurotoxicity of Ecstasy in human users.

[780] Segura, J., de La Torre R., Segura M., Ortuño J., Farré M., McLure J. A., et al.
(2001).  3,4-Dihydroxymethamphetamine (HHMA). A major in vivo 3,4-methylenedioxymethamphetamine (MDMA) metabolite in humans.
Chemical Research in Toxicology. 14(9), 1203 - 1208.

http://www.eurekalert.org/pub_releases/2001-08/acs-ecm081301.php

Use of ecstasy during pregnancy may produce learning and memory impairments in child

Researchers today reported the first evidence that a mother’s use of MDMA (ecstasy) during pregnancy may result in specific types of long-term learning and memory impairments in her offspring.
The research was conducted by scientists from Children’s Hospital Research Foundation and the University of Cincinnati College of Medicine, on rats. It appears the damage to offspring occurs only if the drug is taken during a particular critical period of pregnancy.

[1418] Broening, H. W., Morford LR. L., Inman-Wood S. L., Fukumura M., & Vorhees C. V.
(2001).  3,4-Methylenedioxymethamphetamine (Ecstasy)-Induced Learning and Memory Impairments Depend on the Age of Exposure during Early Development.
J. Neurosci.. 21(9), 3228 - 3235.

http://www.eurekalert.org/pub_releases/2001-04/NIoD-Rfet-2904101.php

Long-term use of ecstasy may result in memory impairment in specific areas

A year-long study of 15 ecstasy users, ranging in age from 17 to 31, suggests that long-term use of ecstasy may result in memory impairment in specific areas, such as the ability to recall a short passage of prose being read out immediately and after a delay (this ability declined by approximately 50% between the first and second assessments).

[2386] Zakzanis, K. K., & Young D. A.
(2001).  Memory impairment in abstinent MDMA (“Ecstasy”) users: A longitudinal investigation.
Neurology. 56(7), 966 - 969.

http://www.eurekalert.org/pub_releases/2001-04/AAoN-Sfle-0904101.php