Posts Tagged ‘Scientific American Mind’

Alzheimer’s and a Cognitive Reserve

June 21, 2016

The healthy memory blog has made frequent mention of the fact that many people have died with the defining amyloid plaque and neurofibrillary tangles of Alzheimer’s, yet who never exhibited any behavioral or cognitive symptoms of the disease.  Although healthy memory regards this as the most important fact bearing upon Alzheimer’s, it is rarely mentioned or discussed.  The cognitive reserve is assumed to result from studies and activities which enriched the brain earlier in life.

The July/August issue of “Scientific American Mind” contained an article titled “Banking Against Alzheimer’s” by Dr. David A. Bennet.  He is the Director of the Rush Alzheimer’s Disease Center in Chicago, where about 100 scientists are searching for ways to treat and prevent a range of common neurodegenerative disorders.  For almost a quarter of a century he has led two longitudinal investigations—the Religious Orders Study and the Rush Memory and Aging Project—which have enrolled more than 3200 older adults across the U.S.  These volunteers enter these studies dementia free, anywhere from their mid-50s, to their 100s and agree to hours of testing each year.  They undergo comprehensive physical examinations, detailed interviews, cognitive testing, blood draws and, in some cases, brain scans.  Most importantly, they all donate their brains after death for research.  To date tens of thousands of clinical evaluations and more han 1,350 autopsies provide an unprecedented set of data.

These autopsies have indicated that it is rare to grow old with a completely healthy brain.  Virtually every brain examined exhibits at least some of the neuron killing tangles associated with Alzheimer’s disease, which is, by far, the most common cause of dementia.  In about half of the autopsies, scars of previous strokes, both big and small, are found.  In almost a fifth of the autopsies so-called Lewy bodies—abnormal protein clumps that are the mark of Parkinson’s disease and Lewy body dementia are found.  But when they trace these laboratory finds back to each individual’s records, they can account for only about half of the cognitive changes measured on tests of memory, processing speed and the like.  In other words, the condition of someone’s brain post-mortem only partially tells how well it functioned in the years leading up to the person’s death.

So why is this the case?  What provides this cognitive reserve?  Rush epidemiologist Martha Claire has found that the so-called MIND diet—which is rich in berries, vegetables, whole grains and nuts—dramatically lowers the risk of developing the defining physical symptoms of Alzheimer’s.

But other life choices seem to actually bolster the brain’s ability to cope with the disease, helping it compensate for any loss of mental firing power.  In particular, they have found that the more engaged our volunteers stay throughout their live, socially and intellectually—the more resilient they are to dementia at its end.   Reader should note that the healthy memory blog has been sending the same message, to which healthy memory will add, having a purpose in living.  In fact, there is a Japanese word for this, “ikigai.”
Here are some tips for building a better brain.

Get a good education, a second language and music lessons.  Avoid emotional    neglect.
Engage in regular cognitive (building a growth mindset) and physical activity.
Strengthen and maintain social ties.
Get out and explore new things (growth mindset)
Chill and be happy.
Avoid people who are downers, especially close family relatives.
Be conscientious and diligent.
Spend time in activities that are meaningful and goal-directed.
Be heart-healthy:  what’s good for the the heart is good for the brain.
Eat a MIND Diet
Remember ikigai and have a purpose for living.
Professor Clive Holmes and his co-workers at the University of Southhampton in the UK found that research participants with gum disease for over the next six months was more rapid for those with gum disease.  Gum disease is associated with increased biomarkers for inflammation.  Research has shown that illnesses that cause inflammation such as chest infections, rheumatoid arthritis and diabetes are linked to greater cognitive impairment.

HM would add the following items
meditate and be mindful

© Douglas Griffith and healthymemory.wordpress.com, 2016. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

Brain Activity Underlying the Placebo Effect

August 21, 2013

Research that conducted brain imaging during placebo studies found that both the active (opiod) treatment and the placebo (saline) treatment activated the same network of brain regions. This included the brain stem, a part of the opiod system that mediates pain relief, and the rostral anterior cingulate cortex, which is rich in opiod receptors.1 It is also a part of the body’s reward system. The researcher, Petrovic, proposed that placebos, like opiods, triggered control areas such as the anterior cingulate that exerted control over the analgesic systems of the brain stem. The analgesic systems of the brain stem then released endorphins.

Another researcher, Tor D. Wager, who also used MRI found that additional brain systems were involved in the placebo effect. The researchers administered a placebo cream while giving painful shocks or painful intense heat on the forearms of the research participants. In one experiment a warning cue, a red “get ready” sign was given just before the painful stimulus was administered. The research subjects expected pain, unless the cream was applied, in which case they expected relief. The expectation of relief activated the cognitive executive center of the brain, the prefrontal cortex. Then the pain response areas of the brain declined, and the experimental participants reported relief. These results suggest that the placebo pain relief involves an expectaton signal from the prefrontal cortex that orders the midbrain to release opiods to meet the expectation of reprieve. Absent this, the full experience of pain is perceived. Further research has pinpointed specific regions of the prefrontal cortex as drivers.

Emotions are also involved in the placebo effect. Wager and his colleagues reported in 2011 that activities in regions of the brain that perform emotional appraisal, such as the insula, orbitofrontal cortex, and amygdala accompany a robust placebo effect. Wager calls this endogenous regulation. Placebos seem to give us a better perspective on our predicament. We might reevaluate our predicament so that we believe that the pain will abate and not cause persistent disability. According to Wager, during a placebo response, “our brain is likely doing a lot of the work without our real conscious input or even in spite of our conscious desires.” That is, we unconsciously engage brain mechanisms that serve to sooth.

Ironically, this self-soothing process might require us to focus on the pain rather than something else. In another study by Wager and his colleagues published in 2012, they tried to distract people away from experimentally induced pain by having them perform another task. This other task did not help relieve the pain. But when the researchers encouraged the participants to pay attention to the heat on their arm by asking them to rate its intensity, the participants experienced greater relief. This result is consistent with “acceptance” therapies or with the “relaxation response” in which people surrender to their pain to tolerate it better.

1The facts in this blog post can be found in an article, When Pretending is the Remedy, in Scientific American Mind, March/April 2013 by Trisha Gura.

Another Discovery by Benjamin Franklin

August 18, 2013

In 1784 Benjamin Franklin along with chemist Antoine-Laurent Lavoisier simulated one of Franz Mesmer‘s sessions.1 People suffering from ailments ranging from asthma to epilepsy were asked to “hug” trees they were told were specially magnetized to “cure” them. As expected, the people swooned and shook. Then the patients were told that the trees were never magnetized. But something had induced the reactions to the trees. That unknown something was later termed the placebo effect.

In 1968 the Food and Drug Administration started using placebo treatments into their golden randomized clinical trials (RCTs), to insure that it was the drug working and not just a belief that it was the drug working. So the effect was large enough that the Food and Drug Administration believed that the placebo effect, if not accounted for, could result in incorrect interpretations of the results from clinical trials.

A key factor in finding placebo effects regards the dependent measures used to assess the effects. Placebo effects were not likely to be found in such medical measures as blood pressure. However, if the measures used reflected how patients reported they felt, then placebos were quite evident. This was especially true in conditions such as pain and nausea. Before one concludes that these measures are subjective and, hence, unimportant, one should be reminded that it is the patients’ own feelings of pain and discomfort that are the most relevant factors. The Harvard psychologist Irving Kirsch found in a meta-analysis of six of the most commonly prescribed antidepressants found that 82 percent of the improvement in mood could be duplicated by giving patients a placebo pill instead of an antidepressant. In another study Kirsch and his colleagues found that the only people in whom antidepressants worked significantly better than placebo pills were patients with the most severe cases. He concluded that unless the patient is extremely depressed, an antidepressant should not be prescribed.

Placebos also work in non-psychiatric conditions, asthma being but one example. In one study, volunteers with asthma were divided into four groups. One group was given an asthma inhaler with a drug, another group was given an inhaler with a saline placebo, a sham acupuncture placebo, or nothing. How much air the volunteers could inhale and exhale before and after each treatment. Was measured. The respiratory scores of those treated with the drug rose by 20%, whereas those in the other three groups got a 7% bump. But when the volunteers were asked to rate their respiratory discomfort on a scale of 0 to10, everyone except those who received no treatment reported a 50% improvement!

The placebo effect places the physician in an ethical dilemma. If she treats the patient with a placebo, he is likely to feel better, but she must lie to the patient. However, if she does not use a placebo, possible unnecessary suffering will not be relieved.

Sometimes the placebo procedures can be employed without deception. In a study by Kirsch, Kaptchuk and their colleagues, 40 patients with irritable bowel syndrome (IBS) pills that they described truthfully as placebo pills made of an inert substance such as sugar, that had been shown in previous clinical studies to produce significant improvements in IBS symptoms thought mind-body self-healing processes. After forty days of twice daily placebos, patients reported feeling better overall along with fewer severe symptoms that 40 patients who received no treatment.

Another way to avoid deception is to enhance the doctor-patient relationship. In a different study of patients with IBS, patients were assigned to either placebo acupuncture or a waiting list. The placebo group was further divided into acupuncture with no conversation, and acupuncture with heavy doses of attention, empathy, and interaction with the practitioner. The practitioner listened to each patient’s problem, repeated the words of the patient, expressed confidence, touched the patient, and lapsed into 20 seconds of thoughtful silence. 28% of the people on the waiting list reported that their bowel symptoms had improved, 44% of the acupuncture placebo reported improvement, and 62% of those in the placebo with the enhanced doctor-patient relationship report improvement.

It should be noted that the placebo effect has a negative counterpart, the nocebo effect, Enter “nocebo” into the search box of the healthymemory blog, to find the relevant posts.

1The facts in this blog post can be found in an article, When Pretending is the Remedy, in Scientific American Mind, March/April 2013 by Trisha Gura.

© Douglas Griffith and healthymemory.wordpress.com, 2013. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

Forgetting Is Important to a Healthy Memory

March 14, 2012

The common complaint is forgetting. Consequently the importance of forgetting is overlooked. A recent article1 provides a strong reminder of the importance of forgetting. The famous study of someone who remembered everything he experienced or tried to remember is recounted in a book by the Russian psychologist Alexander R. Luria, The Mind of a Mnemonist. Although this person made a good living giving demonstrations of his phenomenal memory, he regarded his exceptional talent as a curse. He wanted to forget, but he could not. His was truly a pathological case.

Traumas, in particular, and unpleasant thoughts, are things we want to forget. There unwelcome recall makes our lives unpleasant and can lead to depression and serious mental problems. We should all be aware of the benefits of optimism, and these memories make it difficult to be optimistic.

Fortunately, we can learn to forget and Michael Anderson and his colleagues have developed an experimental paradigm that not only shows that we can, but shows how to forget more effectively.2 Here’s how the experiment works. The first stage is simple paired associate learning. Words are paired and the research participants learn to recall the second word when the first word is presented.

In the second stage some of these same word pairs are presented and the research participants are asked to think about the second word when the first is presented. However some of the word pairs are presented and the research participants are asked not to think about the second word when the first word is presented. And some of the word pairs are not presented and serve as controls for the third stage of the procedure.

In the third stage the research participants are given the first word of all the three sets of the word pairs that have been presented. The word pairs in which the research participants were asked to think about both words in the second stage recalled the most words. The word pairs in which the research participants were asked not to think about the second word remembered the fewest words (showed the most forgetting) and the word pairs that were not presented during the second stage were recalled second best. So even those words that were seen less than the words with the forget instructions were better remembered. It is also interesting to note that forgetting increases as a function of the number of “not think” trials. So we can control our forgetting.

According to the theoretical account of these results that have been substantiated by brain imaging studies, the prefrontal cortex is the executive control area that inhibits the activity of the hippocampus, which is a primary subcortical structure for learning and apparently also for forgetting.

You might still be curious as to how to make yourself forget things you don’t want to remember. Well, technically you are not forgetting them. Rather you are instructing yourself not to think about them, so they will not pop up unwanted in your consciousness. In the experiment the research participants were implicitly recalling the words but instructing themselves not to think about them. This led to the nonintuitive finding that the more times they did this, the less likely they were to recall them.

Anderson and his colleagues have also presented research indicating that our ability to exercise this voluntary forgetting declines as we age.3 However, other research has failed to find this result and concluded that there was no difference in the ability to forget between old and young research participants4. The only difference I could find between the two studies, besides the second study using German research participants, and the first study using U.S. research participants, was that the elderly research group was slightly older in the U.S. than in the German study.

Regardless, I am not impressed by research showing that older research participants perform more poorly than younger research participants without providing any suggestions as to how the deficit might be remediated. Given the importance of the prefrontal cortex for deliberate forgetting I would suggest the possible benefit of exercising the prefrontal cortex (See the Healthymemory Blog post, “Improving Working Memory”).

1Wickelgren, I. (2012). Trying to Forget. Scientific American Mind, January/February, 33-39.

2Anderson, M.C. (2009). Suppressing Unwanted Memories, Current Directions in Psychological Science, 18, 189-194.

3Anderson, M.C., Reinholz, J., Kuhl, B., & Mayr, U. (2011). Psychology and Aging, 26, 397- 405.

4Alp, A., Bauml, K-H, & Pastotter, B. (2007). No Inhibitory Deficit in Older Adults’ Episodic Memory, Psychological Science, 18, 72-78.

© Douglas Griffith and healthymemory.wordpress.com, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

Phoning and Driving Is As Dangerous as Drinking and Driving

March 7, 2012

Perhaps the multitasking that presents the most immediate risk to the most people is driving while speaking on the phone. Phoning while driving is as dangerous as driving while drunk (BAC >0.08). This has been demonstrated in David Strayer’s laboratory at the University of Utah.1 I’m especially proud as I received my doctorate from the University of Utah. His laboratory includes a sophisticated driving simulator.

It is important to realize that it is the attentional demands of phoning that distract from driving that make it dangerous. Somehow it was thought that if phoning were made hands free it would be safe. It does not, as it is just as dangerous. A recent study could not find any benefits of state laws requiring hands free phone well driving. These results were not surprising as the use of hands is irrelevant. State legislatures did a lot of work to produce a law that did not address the problem. Most people tend to be defensive and not accept this finding because it is convenient to phone and drive. For example, they might argue that they converse all the time in their cars and have yet to have an accident. There is a critical difference between conversations that take place within a car and conversations with someone in a distant location. People in the car tend to have situation awareness regarding the driving situation and can even offer help. A remote individual has no idea of what you are dealing with on the road. Or someone might argue that they sometimes have to deal with unruly children while they are driving. I am always amused when someone cites something that is just as dangerous or more dangerous for doing something dangerous. One could argue that texting while driving is more dangerous than phoning while driving, so therefore it is justified. Phoning and driving is dangerous. DON’T DO IT!

It is true that under normal driving conditions with nothing unexpected happening, it is not likely that you will have an accident. However, it is also true that most people driving with BAC’s close to the driving under the influence threshold also would be unlikely to have an accident. People with BAC’s at that level are unlikely to be found weaving across the road. It would be nice if our legal system were consistent; but it appears to be, for the most part, arbitrary.

1Strayer, D.L., & Watson, J.M., (2012).Supertaskers and the Multitasking Brain. Scientific American Mind, March/April, 22-29.

© Douglas Griffith and healthymemory.wordpress.com, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

Glial Cells and Alzheimer’s Disease

May 8, 2011

A preceding post (“Our Neurons Make Up Only 15 Percent of Out Brain Cells”) highlighted the importance of glial cells to brain function. It was based on an article1 in Scientific American Mind, on which this current blog post is also based. The discoverer of Alzheimer’s Disease, Alos Alzheimer noted that microglia surround the amyloid plaques that are the hallmark of the disease. Recent research suggests that microglia become weaker with age and begin to degenerate. This atrophy can be seen under a microscope. In aged brain tissue, senescent microglia become fragmented and lose many of their cellular branches.

One more sign of microglial involvement can be found in the way Alzheimer’s courses through the brain. Damage spreads in a predetermined manner. It begins near the hippocampus and eventually reaches the frontal context. Microglial deneneration follows the same pattern but precedes the advance of neuronal degeneration, Alzheimer and most experts had presumed that microglial degeneration was a response to neuron degeneration. This new research suggests that the senescence is a cause of Alzheimer’s dementia. The hope is that once researchers learn why microglia become senescent with in some people but not in others, new treatments for Alzheimer’s could be developed.

It is also interesting to note the path of progression of the disease. It begins near the hippocampus, a cortical structure critical to memory. Memory loss can be an early indicator of Alzheimer’s. The disease then progresses through the cortex to the frontal cortex. So more memory loss occurs as more cortex is destroyed. The frontal cortex is where most planning occurs. It plays an important role in focal attention. The executive functions of the frontal lobes include the ability to recognize future consequences from current actions, to choose between good and bad actions, to override and suppress unacceptable social actions, and determine similarities and differences between things and events. In short, it is key to higher mental functions.

1Fields, D.R. (2011). The Hidden Brain. Scientific American Mind. May/June, 53-59.