New Brain Studies Reinforce Possible Addictive Effects of Cannabis

A scientific look inside human brains at the long-term effects of marijuana (cannabis) use found some problematic evidence in areas of the brain associated with addiction. These studies report real, visible changes in the brain’s reward system related to the age of starting to use marijuana and/or the more it is used over time. These new findings reinforce earlier research showing harmful effects on teen’s cognition from use of cannabis. See Below for details.

Both recent human brain studies followed independent rat brain experiments indicating that marijuana affects the amygdala (controls emotional learning); and the nucleus accumbens (controls pleasure), areas in the brain associated with addiction. Previous studies have shown that other drugs known to be addictive – including cannabis-based chemicals – affect the brain’s reward centers (amygdala and nucleus accumbens) by creating changes in these addiction-related structures. But human studies are needed to make the leap from introducing cannabinoids in rat brains to knowing the effects of smoking pot on humans.

MRI brain scans of 40 young adult college students – 20 recreational marijuana users and 20 non-users, were studied. As reported in the Journal of Neuroscience, physical changes in volume, density and topography in both of the addiction associated amygdala and nucleus accumbens was seen in these human marijuana users, including in non-dependent, young adult users.

A second study of the effects of heavier pot use on the human brain is published in the Nature Neuropsychopharmacology. Again, MRI imaging compared heavy marijuana smokers to occasional smokers to see if overall brain changes are more extreme, the more you smoke. This study found reduced grey matter volume in nearly all brain regions that are rich in cannabis “receptors” including network structures that control motivation, emotion, and emotional learning.

The degree to which these brain areas changed was due to either heavy use or starting use during adolescence. Lighter users who started in their teens had the same grey matter volume reductions as long-term heavy users.

Regardless of one’s position on recreational marijuana use, these studies strongly suggest that cannabis use at any level is not free of possible addiction and that this drug can influence your behavioral/emotional health, especially for young persons.

EDITORS NOTE: This study reinforces a report posted on MemoryZine on June 3, 2011

( Early Teen Exposure to Cannabis May Damage Brain and Impair Short-term Memory) reprinted below for your convenience:

A unique study, published in the British Journal of Psychiatry reports convincing evidence that early use of cannabis can damage adolescent brain cells and impair mental capabilities, including short term memory performance.

Researchers found youths who were chronic cannabis smokers before their 15th birthday were at an elevated risk of neuropsychological problems compared to those who used the illicit drug at a later stage of life.

Experts generally agree that the most common illicit drug used by adolescents, cannabis, suppresses activities in the brain that control the level of consciousness.

In the study, early cannabis users performed poorly in tasks involving executive functioning, concentration and perseverance compared to the late users and controls. Researchers found that early-onset, but not late-onset, chronic cannabis users had deficits in their cognitive functioning, probably because the brains of youths younger than 15 are still developing. Until their brains mature, say after age 20, they appear to be particularly vulnerable to the neurotoxic effects of cannabis, leading to lower mental flexibility including poor memory performance.

The researchers carried out a study of 104 young chronic cannabis users to determine whether early exposure to cannabis use can cause damage to teen’s brain; 49 started using the drug prior to age 15 (early-onset users) while the rest began smoking pot after they reached 15 (late-onset users).

The early users had smoked cannabis for nearly 10.9 years; the late users had abused the drug for an average of 8.7 years. The study also recruited another 44 teens who didn’t use cannabis.

The subjects participated in a series of mental exercises designed to assess any neurological impact of early cannabis use. While researchers found no significant differences in IQ levels of the three groups, early cannabis users did poorly in tasks involving executive functioning, concentration and perseverance— making more mistakes and were less able to complete categories in the card-sorting test— compared with late users and controls. The score card of non-users and late starters of pot use was the same.

While it is still unclear whether moderate use of pot in adult life poses any long-term neurological harm, such as for legitimate medical purposes, the evidence against youthful cannabis use, especially before the age of 15, is mounting. Results of this study suggest that is advisable to protect one’s memory fitness by limiting moderate cannabis use by youths younger than 16.

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Banking Sleep Means More Gray Matter And Better Brain Health

A study reported in the Journal of Sleep Research suggests that consistently sleeping more hours than needed to function normally resulted in a larger volume of brain gray matter. A greater volume of gray matter

was associated with better emotional and psychological health.

The research indicates that chronic sleep loss can lead to reduced gray matter and significantly disrupt a person’s ability to function. In modern society, people often fail to obtain the amount of sleep that experts recommend for good health and performance. Insufficient sleep can lead to degraded cognitive performance and alterations in emotional functioning.

Fifty-five men and women, ages 18 to 45, underwent MRI brain scans at the Harvard Medical School and were asked how many hours they typically sleep, and to estimate the minimum hours of sleep needed to function normally at work. The difference between the average hours of nightly sleep and the minimum hours of sleep needed for optimal functioning was termed a sleep credit.

Subjects self-reported sleeping an average of 7½ hours and needing about 5.7 hours to function normally, banking about 1.8 hours of sleep nightly. All subjects scored within normal ranges on tests of emotional intelligence and personality traits such as anxiety, depression and paranoia. Sleep credit was associated with greater gray-matter volume in the medial prefrontal cortex, which controls a person’s ability to plan, reason and organize. The findings reinforce earlier reported evidence of the role of the medial prefrontal cortex in the relationship between sleep and emotional functioning. Subjects with more education indicated they needed less sleep than others before their performance on routine daily tasks would be impaired.

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Popular Statins May Lower Risk of Cognitive Decline and Dementia

New findings are reassuring for millions taking statins to protect against heart disease.

Recently reported research indicates that long-term use of the family of medications known as statins may reduce the risk of dementia and that use of statins for less than a year did not show adverse effects on cognitive functions.

FDA labeling warns that some people taking statins, a very popular treatment against heart disease risk by lowering low-density or “bad” cholesterol, may experience some memory loss and confusion. But sixteen studies of short-time statin use showed no difference in memory-related task performance compared with ‘no statin’ controls.

Researchers at Johns Hopkins studied people taking the popular cholesterol-lowering medications who were also tested on memory, attention and organizational skills report that long-term use of the drugs may prevent dementia.

Studies of 23,000 people taking statins between 3 and 25 years found no link between statin use and dementia. Some studies of people who used statins, found a lower rate of dementia. The report published in the Mayo Clinic Proceedings, suggest a nearly 30 percent lower risk of developing dementia.

Since statins protect the heart by reducing fatty deposits in the body’s blood vessels, it is possible that they act similarly on the brain’s fine blood vessels associated with the second most common and not usually fatal form of dementia known as vascular dementia. Alzheimer’s disease, the number one form of dementia, is caused by a different mechanism and can eventually result in loss of life.

The current analysis wasn’t statistically significant, especially since there was no analysis of statin dosage, etc, but if additional studies support these results, then statins could become useful for protecting minds as well as hearts.

As always, be sure to consult with your primary care provider before considering taking, or changing, your medications.

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Got A Senior Moment? It’s Not Necessarily Alzheimer’s Disease.

Age Related Memory Loss is commonly associated with those pesky ‘senior moments’ but it does not mean Alzheimer’s Disease. Aging, a major risk for both Age Related Memory Loss (ARML) and Alzheimer’s disease (AD), have long been the object of NIH-supported research through the National Institute on Aging. After many years of ARML research, it is known that ARML continues to develop over time, but does not always convert to AD. For some, ARML continues to worsen and is labeled Mild Cognitive Impairment (MCI).

MCI is still being studied as a possible pre-curser to AD in some people. In fact, many people live into their 90s without any visible evidence of MCI or cognitive decline in their activities of daily living.

New research, reported in Science Translational Medicine, sheds a little more light on the difference between ARML and AD. In AD, neuronal brain cells are destroyed, leading to progressive loss of all cognitive function. In ARML, activity between neurons is slower.

Columbia University Medical Center researchers analyzing brains of eight people, between the ages of 22 and 88, who donated their organs for medical research, identified 17 genes with activity levels that differed with age.

One gene, containing instructions for making a protein called RbAp48, became less active with time. They also reported that production of RbAp48 in the brain’s hippocampus is diminished with age.

RbAp48 is associated with declining memory performance in mice.
Because the brains of mice are remarkably similar to human brains for the purposes of such studies, young mice were genetically engineered to have low RbAp48 levels. These mice performed as poorly as much older mice in memory tests. Using a virus to boost RbAp48 in older mice appeared to reverse the decline and boosted their memory.

The study is the strongest evidence to date that age-related memory loss is a separate condition from Alzheimer’s disease. New research is underway to understand ARML and how it can be reversed or, in time, prevented.

While more research is needed to learn how to reduce or prevent age related memory loss, this study is a major step towards dealing with the memory loss concerns of the millions of baby boomers entering their senior…. moments.

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High Blood Sugar Related to Higher Dementia Risk

Research published in the New England Journal of Medicine finds high levels of blood sugar raises the risk of dementia, even if a person doesn’t have diabetes, a condition known to be associated with Alzheimer’s disease (AD) risk.

According to the research findings, the higher the subject’s level of blood sugar, the greater the risk of dementia. The finding was also true of persons with diabetes.

The research, involving 2,100 people over 65, was conducted as part of the Adult Changes in Thought study. The study began in 1994 and included two-year subject evaluations.
Because insulin doesn’t work properly in the brains of those with Alzheimer’s disease – the most common form of dementia, leading researchers are exploring whether diabetes drugs may benefit those with AD. Clinical trials so far have not found effective drugs to cure this brain disease.

Not much research has been done on the effects of blood sugar within the normal range and it’s not clear to researchers why blood sugar is associated with dementia risk, but the higher the blood glucose, the higher the risk. Future research will explore if higher levels of blood sugar play a role in vascular disease or inflammation, two other risk factors for AD.

According to the National Institutes of Health, 5.5 million people in the U.S. have Alzheimer’s disease, a progressive degenerative brain disease that erodes a patient’s memory, thinking and eventually ability to carry out even simple tasks. While there are additional genetic factors (i.e., APOE4) associated with increased risk, the definitive cause of AD is unknown and there is, as yet, no known cure.

The take-away from this research study is that low blood sugar levels may be an important factor in reducing dementia risk. Be sure to consult your healthcare provider before making any health decisions.

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Brain Activity Map Project To Study Workings of the Brain

The next decade-long scientific effort to examine the workings of the human brain has been announced by the White House. The 1990s, known as the Decade of the Brain, was successful in uncovering many insights into dementia, stroke and the use of imaging technologies such as fMRI. But since then, advances in brain imaging, nano-technology and genetics, for example, are making it possible to advance the knowledge of the brain’s 100 billion neurons and how their complex circuits interact. The goal is gain greater insights into perception, actions and, ultimately, consciousness. Here is an unofficial mission statement:

“The function of neural circuits is an emergent property that arises from the coordinated activity of large numbers of neurons. To capture this, we propose launching a large-scale, international public effort, the Brain Research through Advancing Innovative Technologies (BRAIN) initiative, aimed at reconstructing the full record of neural activity across complete neural circuits. This technological challenge could prove to be an invaluable step toward understanding fundamental and pathological brain processes.”

The so-called BRAIN project, or Brain Activity Map project, will include federal agencies, private foundations and teams of neuroscientists and nanoscientists collaborating to build a comprehensive map of brain activity, in hopes of doing for the brain what the Human Genome Project did for genetics.

Scientists hope to develop the technology essential to understanding diseases like Alzheimer’s and Parkinson’s, and to find new therapies for a variety of mental illnesses. A group of leading scientists from such institutions as the Kavli Institute for Brain and Mind at the University of California, the Lawrence Berkeley National Laboratory, the California Institute of Technology and Columbia University, speculate that novel understanding and therapies for diseases such as schizophrenia and autism might eventually be discovered. Moreover, the project holds the potential of paving the way for advances in artificial intelligence.

Composed of roughly 86 billion neurons and 100 trillion synapses that each electrically “spike” in response to outside stimuli, as well as in vast ensembles based on conscious and unconscious activity, the human brain is so complex that scientists have not yet found a way to record the activity of more than a small number of neurons at once, and in most cases that is done invasively with physical probes.

But a group of nanotechnologists and neuroscientists, including a molecular biologist, a geneticist, a neurologist, a bioethicist, a cognitive roboticist, neuroscientists of various stripes, say they believe that technologies are at hand to make it possible to observe and gain a more complete understanding of the brain, and to do it less intrusively.

In the June issue of the journal Neuron, six leading scientists proposed pursuing a number of new approaches for mapping the brain. One possibility is to build a complete model map of brain activity by creating fleets of molecule-size machines to noninvasively act as sensors to measure and store brain activity at the cellular level. The proposal envisions using breakthrough innovations such as synthetic DNA as a data storage mechanism for the vast amounts of data representing brain activity.

The initiative, costing $3 billion over 10 years, will be organized by the White House Office of Science and Technology Policy and will include governmental organizations as The National Institutes of Health, the Defense Advanced Research Projects Agency and the National Science Foundation as will as private foundations like the Howard Hughes Medical Institute in Chevy Chase, Md., and the Allen Institute for Brain Science in Seattle.

A recent meeting held at the California Institute of Technology, was attended by the three government agencies, including neuroscientists, nanoscientists as well as representatives from Google, Microsoft and Qualcomm.

The project, formally announced in March, 2013 could provide a return on investment to the US economy of many times more than reported for the Human Genome project. According to President Obama in his State of the Union address, “Every dollar we invested to map the human genome returned $140 to our economy — every dollar.”

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Lycopene In Tomato Helps Cut the Risk of a Stroke

A diet rich in tomatoes, such as a Mediterranean diet, could lower your stroke risk according to new research. A study published in Neurology shows that men who had the highest blood levels of lycopene—an antioxidant found in tomatoes had 55% fewer strokes than men who had the lowest blood level of lycopene.

According to the USDA’s national nutrient database, Lycopene is found in the highest concentrations in cooked tomatoes (e.g., paste, puree and sauce) compared to raw tomatoes.
The study’s goal was to see how other substances such as retinol, or vitamin A, and alpha-tocopherol, a type of vitamin E, impacted stroke rates. No association with the levels of vitamin A or E was evident. Instead, men who had the highest level of lycopene in their bodies were 55% less likely to have a stroke than men with the lowest level and 59% less likely to have a type of stroke caused by a blood clot (i.e., an ischemic stroke, the most common type of stroke.)

A cup of ready-to-serve marina sauce has more than 31,000 micrograms of lycopene while the average raw tomato has about 3,165 micrograms, according to USDA. A slice of fast food pizza has 2,074 micrograms of lycopene. A tablespoon of catsup has 2,146 micrograms of lycopene.

In addition to red tomatoes (3,165 micrograms/each), Lycopene is also found in watermelon (6,889 micrograms/cup), grapefruit (1,745 micrograms/ 1/2 any color ), papaya (2,559 micrograms / cup) and mango (5 micrograms/cup).

Earlier studies suggest lycopene can cut the risk of prostate and other cancers. Even though lycopene reduces inflammation and prevents blood clots from forming, there currently are no current government recommendations for lycopene consumption.

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Aspirin to Prevent Heart Disease Could Slow Memory Loss

A study of older women taking low doses to prevent heart disease found it also helped preserve their memory. Taking a low dose of aspirin may help keep the brain young.

Millions of Britons take aspirin on doctor’s orders to prevent heart problems.
Other research suggests it may cut the risk of cancer.
There have been conflicting results from studies about whether long-term use of Non Steroidal Anti Inflammatory drugs (NSAIDs) such as aspirin protects against declining brain power and dementia.

Research published in the online journal BMJ Open found regular low-dose aspirin did slow cognitive decline in a five-year study involving 681 women aged 70 to 92 at high risk of heart disease and stroke.

Decline in brain power was found to be considerably less among those who took aspirin every day over the entire period. It is thought the same effect would be found in men.

All the elderly women were put through tests to measure their physical health and intellectual capacity, including verbal fluency and memory speed, and dementia.

A group of 129 women were taking low dose aspirin (75 to 160 mg) every day to ward off a heart attack or stroke when the study started. A additional 94 were taking various other non-steroidal anti-inflammatory drugs (NSAIDs). Their health was tracked over five years, at the end of which the intellectual capacity of 489 women was assessed again.

The mini-mental state examination (MMSE) – a common test for mental vitality – score fell across the whole group at the end of the five years, but this decline was considerably less in the 66 women who had taken aspirin every day over the entire period. Groups divided into those who had taken aspirin for the entire five years (66); those who had stopped taking it by 2005-6 (18); those who were taking it by 2005-6 (67); and those who hadn’t taken the drug at any point (338).

Compared with women who had not taken aspirin at all, those who had done so for all five years, increased their MMSE score, while those who had taken aspirin at some point, registered only insignificant falls in MMSE score. There were no differences, however, in the rate at which the women developed dementia.

Researchers suggest aspirin’s protective effect may be due to its anti-clotting action helping to improve blood flow to the brain. The findings indicate that aspirin may protect the brain, at least in women at high risk of a heart attack or stroke.

While long-term aspirin use does have a number of potentially serious side-effects for some, it should only be taken for long periods on doctor’s orders.

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Exercise, Chocolate Help Mild Cognitive Impairment And Reduce Stroke Risk

It is well known that 30 minutes of exercise – at least three times a week – is good for both brain and cardiovascular health. Now you can double the benefit of being physically active… by eating dark chocolate!

Results of research conducted at the Karolinska Institute in Stockholm shows that for every extra 50 gms of chocolate consumed per week (e.g., ¼ cup of chocolate chips), there was a fall in stroke risk of about 14%.

The study, published in Neurology, included 37,103 Swedish men ages 49 to 75. After ten years, researchers found the highest chocolate consumers had a reduced risk of stroke – 12 fewer strokes per 100,000 person-years – compared to non-chocolate eaters. A broader research review of five different studies included 4,260 stroke cases that showed the risk of stroke for individuals in the highest category of chocolate consumption was only 19 percent compared to those not eating chocolate.

Researchers believe the health effects of chocolate may be related to flavonols, antioxidants found in cocoa, which appear to be protective against cardiovascular disease through anti-oxidant, anti-clotting and anti-inflammatory properties. Flavonols, a large family of polyphenolic compounds synthesized by fruits and vegetables – such as cocoa, red grapes, red wine, yellow onions, scallions, kale, broccoli, apples, berries and green and white teas – have been shown in studies to reduce blood pressure and may even help patients who have mild cognitive impairment (MCI).

Chocolate, rich in flavonols, was recently given a seal of approval by the European Food Safety Authority (EFSA), the European equivalent of the FDA. If accepted by the EU, chocolates and cocoas with high amounts of flavonols will be allowed to carry positive health claims on their packaging.

Oh, you might like to know that UC, San Diego researchers recently reported findings that appear to suggest regular chocolate eaters tend to be thinner!

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Anti-Alzheimer’s Gene Mutation May Protect Against AD

Scientists reported in the journal Nature, discovery of a rare gene coding genetic mutation, A673T, that may protect against Alzheimer’s disease (AD). US and European scientists claim that this mutation protects against both Alzheimer’s and cognitive decline in older people who are without AD.

While most people not having Alzheimer’s don’t have the mutation, its function supports the theory that AD is caused by the accumulation of beta amyloid protein in the brain. This discovery may hold promise for a possible treatment for this most common of the dementias affecting over 5 % of western world populations over age 60, of which about 2/3 is due to Alzheimer’s.

This gene mutation makes less harmful a protein long believed to be involved in AD. The newly identified variant affects a gene called amyloid precursor protein (APP), which encodes for the precursor protein that gets chopped up by enzymes and forms beta amyloid. Based on cell culture studies, the mutation seems to hinder the ability of one of the enzymes to do its job, therefore resulting in a 40% reduction in amyloid production, thereby lowering risk of AD.

In the study of the genetic data of 1795 Icelanders, people with this rare mutation demonstrated very strong protection against AD. People who lived to age 85 or older without developing Alzheimer’s were more than five times more likely to have the protective gene mutation than those who developed the disease — translating to a 7.5 times lower risk of Alzheimer’s attributable to the variant.

The gene also appeared to protect against a known risk factor for Alzheimer’s, the presence of two copies of another gene known as ApoE4. At least 90% of people with two copies of this gene develop Alzheimer’s by age 80, but among the 25 people in the study who had two copies of ApoE4 and the new protective variant, none had Alzheimer’s. Further, the presence of the new gene variant seemed to protect against memory loss and cognitive decline even in people who didn’t have Alzheimer’s. When the researchers looked at elderly people with normal brain function, they found that those with the new APP gene mutation did better on cognitive tests than those without.

There has been serious research in the past two decades into manipulating APP to treat Alzheimer’s – an incurable and progressive disease characterized by memory loss and dementia.

This important discovery also offers a potential new target for Alzheimer’s drugs and lends hope that several of the amyloid-targeting drugs currently in development may eventually prevent or slow the disease, offering hope for the 5.4 million Americans currently affected, projected to grow to 14 million by 2050.

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