TO DRINK OR NOT TO DRINK! THAT IS THE QUESTION.
Is drinking alcohol good for my brain?
I know this question has been haunting you. Fortunately, I just came across a terrific article from Rush University that provides the most thorough response I have seen on the topic. The article was written by, Pablo Quintana MD, an internal medicine specialist at Rush University Medical Center in Chicago. Quintana answers a lot of questions, but also raises others that still need to be resolved.
The good news is that drinking in moderation does appear to promote brain health. But, before we get to the benefits of moderate drinking, we should probably review the dreadful consequences of excessive drinking.
What are the negative effects of consuming too much alcohol?
Cancer – Yup! Excessive alcohol intake has been linked to cancer of the liver, as you might expect. But excessive alcohol intake is also associated with increased risk for esophageal cancers and gastrointestinal cancers. Bummer. Oh, and excessive drinking is associated with liver disease. Duh! What happens, apparently, is that excessive alcohol in the system causes damage to cells in the body. When the body tries to repair the cells the process can lead to mutations of the cell’s DNA. Mutations are risky. They open the door to unchecked duplication of cells, which is the hallmark of cancer.
Diabetes – Alcohol is a carbohydrate. It can affect blood sugar levels in the body. People with diabetes who drink too much risk triggering insulin shock.
Heart Failure & Brain Starvation – Excessive drinking weakens the heart muscles, which prevents the heart from pumping blood properly, leading to conditions like congestive heart failure. Quintana doesn’t mention this, but there is growing evidence that one cause of dementia and Alzheimer’s disease is brain starvation, the reduction of the fuels the brain needs to operate well. Less blood flow means less fuel to the brain.
Aging – Curses! Excessive drinking when older can contribute to vitamin B1 deficiency, which causes impairment to memory and vision. So, heavy drinking could contribute to dementia. And, of course, getting plastered increases the risk of falls, which lead to broken bones and broken hips, which leads to reduced activity or hospitalization, which leads to . . . ugh! It’s not a pretty scenario.
So, you get the picture! Excessive drinking is bad for your health in general and for brain health in particular. So, what does excessive drinking mean? How much is too much?
Excessive Drinking - It turns out that there are a number of factors that need to be considered. In addition to the quantity you drink, your gender seems to matter, as does the kind of alcohol you consume and also what you mix with your drinking.
Quantity - So, what do “in moderation” and “excessive” mean? In the U.S., moderate drinking means two drinks a day for men and one drink for women. Heavy drinking is more than 14 or more drinks a week for a man and more than seven a week for a women.
Gender - How come women can’t drink as much as men? The lower standard for women rests on the assumption that women as smaller than men. Women generally weigh less, have smaller body composition with less water and, therefore, don’t handle the alcohol as well.
Alcohol Content – Okay a max of one or two drinks, but what kind of drinks? You need to know the alcohol content of your drinks. Twelve ounces of beer, for example, has an alcohol content of about 5%, although some craft beers can go as high as 10%.
Compare your 12 ounces of beer to 5 ounces of wine, which has about 12% alcohol. Woops. Does that mean that one glass of wine can have about the same alcohol content as two glasses of beer? One point five (1.5) ounces of distilled spirits contains about 40% alcohol.
Someone help me with the math. Is 5% alcohol in 12 ounces of beer equivalent to 40% alcohol in 1.5 ounces of whiskey? Is drinking 2-3 beers equivalent to drinking one glass of wine?
Aha! Google to the rescue! According to the National Consumer League. Each of those portions of beer (12 oz.), wine (5 oz.) and distilled liquors (1.5 oz.) have the same amount of alcohol. So those portions represent one drink.
Alcohol Mixers - Syrupy mixers added to drinks increase the empty calories and the sugar you are ingesting. All of us need to avoid adding sugar to our diets, but avoiding sugar is particularly critical for folks who are diabetic or pre-diabetic.
Don’t mix alcohol and energy drinks. (I have to admit that this would never have occurred to me.) The caffeine in the energy drinks counters the depressant effects of the alcohol, so drinkers don’t realize how much the alcohol is affecting them and are more likely to drive while impaired.
Good news – Okay. Time for the good news! Here’s are the benefits of moderate alcohol consumption that Quintana reported.
Cardiovascular Health - As you have probably heard, what is good for your heart is good for your brain. Well, there is some evidence that alcohol (in moderation) reduces the risk of coronary artery disease. Quinatana is quick to point out, however, that alcohol should not be seen as a substitute for other healthy behaviors that reduce coronary risk factors. You still have to exercise, eat healthy food and quit smoking. Then you can have a drink.
Red Wine - Drinking moderate amounts of red wine has been shown to improve cardiovascular health. But, there’s more. Red wine also increases levels of “good” cholesterol (HDL, or high density lipoproteins). High levels of HDLs may help prevent blood clots and, thereby, reduce the risk of heart attack and stroke. Heart attacks and strokes, by the way, are bad for your brain. Red wine contains resveratrol, which has antioxidant properties and helps the body fight off pathogens.
White Wine - The Rush Article doesn’t mention white wines, but WebMD says that white wine is chock full of antioxidants and flavinoids. The say that the antioxidant content of European white wines is equivalent to that of olive oil and are just as effective as red wines at promoting healthy hearts.
Bone Health & Beer – I love these studies. According to studies published in the Journal of the American Medical Association and Osteoporosis International, moderate beer drinkers were 38% less likely to have osteoporosis. Further, those who indulged in a brew or two were 20% less likely to have hip fractures than abstainers. I’ll drink to that! The mechanism for these benefits may be the dietary silicon found in beer, which according to Quintana “plays a role in the growth and development of both bone and connective tissue.”
A beer a day may also help manage cholesterol levels. In a recent study, moderate beer consumption seemed to slow the decrease of HDL cholesterol over time. Heavy beer consumption, on the other hand, had the opposite effect, erasing the benefits of HDL.
The Bottom Line – Moderation, moderation, moderation! If you don’t drink, there is no compelling reason to start. If you drink in moderation, feel good about it and make sure you keep the quantity of alcohol you drink in check. If you drink too much, it would behoove you to develop a brain health action plan (what we call Mindramping Action Plans or MAPS) to be more mindful about how much you drink. Develop strategies to limit your intake to two drinks per day.
NEUROGENESIS: YES OR NO?
One of the earth-shaking discoveries made by modern neuroscience is that human brains remain plastic and changeable throughout life. One of the key pieces of evidence in support of brain plasticity is neurogenesis. Only within the past 20 years has it become accepted wisdom that the human brain generates new brain cells throughout our lifetime.
But now, a recent study from a team of researchers at the University of California San Francisco has raised some eyebrows. They challenge the idea of human adult neurogenesis. They say they found no evidence to support the birth of new neurons in human adult brains.
Their claims have been met with great skepticism and have sparked a healthy debate. Nevertheless, they are sticking with their story. They say that “repeated and varied experiments convinced us our conclusions were correct: New brain cells don’t grow (or are extremely rare) in the adult human hippocampus, a region important for learning and memory.”
This is, of course, just one study. There are plenty of others that seem to confirm the presence of neurogenesis. But, this how science works! We can’t dismiss evidence just because it contradicts cherished beliefs. We need to assume the classic, “Hum! That’s interesting” stance and keep an open mind. Then, we look for more data that either supports our current beliefs or supports the alternative view.
One study, that appeared soon after the UCSF study, for example, found evidence for adult neurogenesis. And, their discussion raised a number of interesting points that shed light on the difficulty of identifying whether new brain cells are being generated.
First, different researchers apparently use different techniques to look for neurogenesis. One technique is to look for proteins that are proxies for new neurons. If the protein is present, researchers make the assumption that new brain cells are present. They don’t actually see the new neurons. And, researchers look for new brain cells in different places. The team that found no neurogenesis apparently searched in a thin slice of the hippocampus. The group that found neurogenesis looked at the entire hippocampus.
Second, neurogenesis is a multi-stage process. Things can go wrong at any one of the developmental stages. Stem cells might produce plenty of neural progenitors and immature neurons that die before becoming mature neurons. How do we define neurogenesis? Is it the production of new brain cells whether they survive or not? Or, are we talking about new brain cells that survive and become active? I’d vote for the surviving neuron definition.
Finally, adult hippocampal neurogenesis (assuming it exists) appears to decline in some older people, but not all. The decline may have nothing to do with the ability of stem cells to pump out potential neurons. The decline may be due to unfavorable conditions, in some older brains, that prevent new neurons from completing their arduous multi-stage developmental journey.
An older brain that is compromised by conditions that cause cognitive decline it may not have the resources needed to support baby brain cells. Conversely, an older brain that is still strong and resilient should do a better job of nurturing health new brain cells.
So, we keep learning.
Two quick final points! First, there is more to brain plasticity than neurogenesis. Even if it turns out that old brains are not refreshed with a steady supply of baby neurons, old brain cells still grow, change, adapt, atrophy and die. Old brain cells, neurons, and glial cells, remain plastic. Second, the healthier we keep our brains, the more likely they are to support positive plastic changes. If we neglect the health of our brains we are more vulnerable to disorders that may well interrupt the ability of the brain to repair and renew itself.
1. Sorrels, S., Alvarez-Buylla A. and Paredes M. Adult human brains don’t grow new neurons in hippocampus, contrary to prevailing view. http://theconversation.com/adult-human-brains-dont-grow-new-neurons-in-hippocampus-contrary-to-prevailing-view-93123. March 12, 2018
2. Boldrini, Maura et al. (2018) Human Hippocampal Neurogenesis Persists throughout Aging. Cell Press. April 5. https://doi.org/10.1016/j.stem.2018.03.015
A NEW BIOLOGICAL DEFINITION OF ALZHEIMER’S DISEASE
The Alzheimer’s Association and the National Institute on Aging have gotten together to update their 2011 recommendations on how to diagnose Alzheimer’s. Rather than use a “syndromal” definition (i.e. signs and symptoms) like the 2011 version, the updated 2018 definition is biological, based on biomarkers.
The bottom line is that the working group has decided that Alzheimer’s syndrome is defined by the presence of abnormal amyloid and tau. This biological approach enables researchers to handle situations in which a person without symptoms is found to have high levels of amyloid and tau.
This discrepancy could lead some to the conclusion that amyloid and tau have no tight link with Alzheimer’s. But, the workgroup goes the other way. If amyloid and tau are present, even though you show no signs of cognitive decline, you have Alzheimer’s. This approach also accommodates the need to make early, pre-symptomatic diagnoses of Alzheimer’s. You may not be showing any symptoms of Alzheimer’s – YET – but if you have abnormal levels of amyloid and tau, you’ve got it.
But, they might be wrong. “Although it is possible that β-amyloid plaques and neurofibrillary tau deposits are not causal in AD pathogenesis, it is these abnormal protein deposits that define AD as a unique neurodegenerative disease among different disorders that can lead to dementia.” So, once again, we may ultimately find that amyloid and tau do not cause Alzheimer’s, but if they are present, we will call it Alzheimer’s.
An extended definition adds neurodegenerative/neuronal injury to the equation. This enables the workgroup to propose different stages of a disease continuum based on which biomarkers are present.
If amyloid alone is detected (A+), it is called Alzheimer’s pathologic change, an early stage of the Alzheimer’s continuum. When tau is added to the equation, (A+T+) we can safely say it is Alzheimer’s. Finally, A + T+ along with neurodegenerative/neuronal injury (A+T+(N)+) strengthens the diagnosis.
But, according to the workgroup, neurodegenerative/neuronal injury is not a necessary component of the definition. The N is put in parentheses (N) because it a “concomitant suspected non-Alzheimer’s pathological change.” If (N) is present without A or T, you have some other kind of dementia, not Alzheimer’s. Got it?
Their basic hypothesis is “a modified amyloid cascade hypothesis.” The most likely progression of Alzheimer’s starts with the presence of abnormal amyloid, which leads to the presence of tau, which in turn causes neurodegenerative damage, which in turn leads to cognitive decline. They chart this relationship as follows:
A à T à (N) à (C)
They concede that other types of progression could exist. Tau might appear before amyloid, for example. Or, some as yet unknown pathological process could induce A, T and (N), which then combine to cause cognitive decline. The authors even acknowledge that amyloid and tau might be “epiphenomena that are not in the causal pathway of (N) or (C).” This seems to be the single mention of alternatives to the amyloid hypothesis.
The workgroup stresses that this is not a definition that should be used in a clinical setting. It is merely for research purposes. “It is called a ‘research framework’ because it needs to be thoroughly examined and modified if needed before being adopted into general clinical practice.”
So, I hope that clarifies things for you.
SLEEP AND AMYLOID
Speaking of amyloid, a recent NIH study found that just one night of sleep deprivation elevated levels of beta-amyloid in important regions of the brain.[i] Beta-amyloid, as you know, is considered a biomarker for Alzheimer’s syndrome. Metabolic waste material, like beta-amyloid, is normally flushed out of the brain during deep sleep. So, failure to get a good night’s sleep causes the accumulation of harmful waste material in your brain.
BS (bad sleep) à A à T à (N) à (C)
So, one way to minimize the risk of initiating the amyloid cascade is to improve our sleep habits.
POLLUTION & AMYLOID
Researchers from the University of Montana studied autopsies of people who had lived in Mexico City, one of the worlds most polluted urban areas. They found heightened levels of beta amyloid and hyperphosphorylated tau in the brains of “young urbanites with lifetime exposures to fine-particulate-matter pollution.” The pollution seems to have caused and accelerated the progression of Alzheimer’s syndrome in these exposed people.
The authors conclude that “ambient air pollution is a key modifiable risk for millions of people across the globe, including millions of Americans who are exposed to harmful particulate pollution levels.”
P (pollution) à A à T à (N) à (C)
In other words, exposure to fine particulate matter pollution is one way that the Alzheimer’s disease cascade gets started. Get rid of pollution and we will take away another risk factor for Alzheimer’s
THERE’S NO MONEY IN BEETS!
This drives me crazy. Here is a typical lead paragraph from research institutes.
“A compound in beets that gives the vegetable its distinctive red color could help slow the accumulation of mis-folded proteins in the brain, a process associated with Alzheimer's disease. Scientists say this could lead to the development of drugs that could alleviate some of the long-term effects of the disease, the world's leading cause of dementia.”
My first reaction to this news is. “Hey! Terrific. Let’s eat more beets.” Or, “Let’s figure out what other vegetables have the same kind of compound and eat more of them.”
The first reaction of the science community seems to be, “Wowee Zowee!! Maybe we can develop a drug that mimics the effect of beets.”
Now, you may ask - as do I - why do we need a drug if we already have beets? The answer is obvious. There’s no money in beets! Who is going to fund research projects about eating beets? Who is going to make a gazillion dollars selling beets?
No one! That’s who.
Too many researchers seem bored by the prospect of preventing disease and promoting health. They see their path to fame and fortune in the development of drugs that (possibly, maybe) alleviate symptoms once we have gotten sick. Is it too cynical of me to suggest that this amounts to a desire to promote illness?
[i] NIH/National Institute on Alcohol Abuse and Alcoholism. "Lack of sleep may be linked to risk factor for Alzheimer's disease: Preliminary study shows increased levels of beta-amyloid." ScienceDaily. ScienceDaily, 13 April 2018. <www.sciencedaily.com/releases/2018/04/180413155301.htm>
MAYBE DRACULA WAS ON TO SOMETHING
A company called Alkahest has been testing the idea of treating dementia with blood infusions. The rationale for this approach begins with a process called “heterochronic parabiosis,” (Say that 10 times!) in which the circulatory system of a young mouse is connected to that of an old mouse. Young blood mixes with old blood and Voila! The infusion of “young” blood into the old mouse (even just the plasma), rejuvenates the old mouse. The old mouse, flush with young blood, has improved quality-of-life, possibly because of increased neurogenesis, the ability to produce new brain cells.
The components of blood (mice and human) change with age. Detrimental factors, like cytokines and inflammatory molecules, increase; beneficial components, like growth factors, decrease. So, the thinking goes, an infusion of young blood may rebalance the blood so that it promotes health rather than decline.
Mice are not people, of course, so Steven Braithwaite, Ph.D., the chief scientific officer at Alkahest is moving on to experimenting with humans. They have taken donated blood from 18-year-old teens and infused it into older persons suffering from mild to moderate Alzheimer’s disease. At this point, they are just testing safety and tolerability. 
Something similar was tried a few years back but limited the infusion to just one component of blood, immunoglobulin. No success! Braithwaite hopes that using complete blood, with all of its components, will be more successful.
The multifactorial approach sounds good. My question and perhaps the more important question is why old blood goes bad in the first place. I’ll grant that the general aging process takes a toll. But my guess is that some old blood is worse than other old blood of the same age. It seems likely that a person’s lifestyle choices would change the quality (age?) of their blood. The blood of a sedentary, fast-food-eating, smoker is probably kind of yucky and “old.” For that matter, some “young” blood might not be that appetizing either.
So, while I’m waiting for Braithwaite and company to perfect their Dracula Protocol I am going to use preventive measures to keep my own aging blood as healthy as possible.
YOUR MAGNETIC MIND
Is your head mysteriously drawn towards your refrigerator? Does your forehead get stuck on the freezer door as you scan the fridge below for the perfect mid-day snack? If so, you may be collecting nanomagnets in your brain.
That’s right. It has been known for a while that the brain harbors magnetic particles derived from the iron used in normal brain function. But new research suggests that some of the mini-magnets (magnetite) in your brain get there through industrial air pollution. As you might expect, urban dwellers in highly industrialized areas are at risk for the greatest exposure.
And, here’s the bad news you knew was coming. People with Alzheimer’s tend to have unusually high concentrations of magnetite in their brains.
WHAT’S A NINE LETTER WORD FOR . . .
Well, I never! Research out of The University of Exeter Medical School shows a strong correlation between time spent playing word puzzles, like crosswords, with improvements in certain cognitive functions.
Keith Wesnes, Professor of Cognitive Neuroscience at the University of Exeter Medical School, said: “We found direct relationships between the frequency of word puzzle use and the speed and accuracy of performance on nine cognitive tasks assessing a range of aspects of function including attention, reasoning and memory.”
Does this mean that doing crosswords puzzles is the secret to cognitive wellness? Will doing crosswords every day prevent the onset of dementia? No. There’s more to brain health than cognition and the nine aspects of cognition that can be improved with puzzling. Crosswords by themselves will help stimulate parts of your brain but more is needed.
Try doing crossword puzzles while jogging in an enriched environment and having an intellectually stimulating conversation with a supportive friend, making sure to steer clear of any stress-inducing subjects, while eating a nice meal of salmon and green vegetables sautéed lightly in olive oil. Then jog for 45 minutes and get a full night of restful sleep.
MAINTAINING MUSCLE MASS
We all lose muscle mass and strength as we age. It’s called sarcopenia. And many might think there’s nothing that can be done.
Well, not exactly. As we age, we lose muscle mass and strength if and when we stop exercising. If we keep exercising our muscles they stay strong, even as we age. At least that’s the message delivered by a new study out of The University of Birmingham and Kings College London.
This team of researchers studied a group of “highly active” amateur cyclists (age 55 to 79). These cyclists could ride about 60 miles in six hours. Good, but not crazy good. They were chosen because they represented a model of healthy, active agers who were free from any negative effects of sedentary behavior.
The cyclists experienced no loss of muscle mass and strength. Nor did they increase their body fat or cholesterol levels. And, the men's testosterone levels remained high, suggesting that they may be avoiding certain aspects of andropause.
There’s more! The cyclist’s immune systems showed no signs of aging. Their thymuses, which produce immune cells, were pumping out as many T cells as a young person.
As professor Janet Lord, Director of the Institute of Inflammation and Ageing at the University of Birmingham, put it, “our findings debunk the assumption that ageing automatically makes us more frail.”
 Hmmmm? I wonder if infusion of old blood into young mice enhances their wisdom and judgment. They probably didn’t test for that.
 I wonder: Why aren’t they testing the effect of infusing old blood into teenage boys? The procedure might prove beneficial for teenage girls.
NEURON AND SYNAPSE LOSS IS LIMITED IN ALZHEIMER’S
A new study our of McGill University in Canada suggests that, counter to the prevailing thinking, Alzheimer’s disease is not associated with significant death of neurons and synapses.
El Mestikawy, an associate professor at McGill University is quoted in ScienceDaily as saying that, “Much to our surprise, in studying the fate of eight neuronal and synaptic markers in our subjects' prefrontal cortices, we only observed very minor neuronal and synaptic losses. Our study therefore suggests that, contrary to what was believed, neuronal and synaptic loss is relatively limited in Alzheimer's disease. This is a radical change in thinking."
With dementia, neurons, synapses and glial cells apparently don’t die they just stop working very well. There is evidence from previous studies that diseased cells emit distress signals that cause neighboring cells to dysfunction, driving a negative cascade of failure. Massive dysfunction leads to the variety of symptoms associated with cognitive decline that progresses towards dementia.
The implication is that Alzheimer’s -- and possibly other neurodegenerative diseases --can be treated. If brain cells in an afflicted brain are alive but malfunctioning they can, theoretically, be repaired. The cause of their malfunction (toxins, chronic inflammation, cardiovascular disease, etc.) can be identified and removed. If enough malfunctioning brain cells can be repaired, the cycle of self-reinforcing decline that causes dementia may be halted or even reversed.
This reversal of dementia is the promise and hope of interventions like the Bredesen Protocol. It is also the rationale for stressing preventive. Don’t cause damage in the first place.
TRUST AT STAKE
There is a terrific article to be found on Bill Thomas’s blog site that argues that the “dual mission” of the Alzheimer’s Association (AA) is out of balance. The dual mission of the AA is “to eliminate Alzheimer’s disease through the advancement of research and to enhance care and support for individuals, their families and caregivers.” Sounds great.
The problem, suggests Eilon Caspi, of Dementia Behavior Consulting, LLC, is that the overwhelming focus of energy and resources has been directed towards research. Support and care for people with Alzheimer’s and their caregivers has gotten the short end of the stick.
Much has been learned through the research on Alzheimer’s. But no “cure” has materialized in spite of billions spent by pharmacological researchers. Alzheimer’s has not been “eliminated” and millions are suffering the consequences. Little has been done to improve living conditions for people coping with dementia. Little has been done to relieve the burden of caregiving that falls largely to families and mostly on women.
The Alzheimer’s Association and NIH need to make a major course correction and bring their “dual mission” into balance. Continue vital research. We may find a cure or treatment somewhere down the road, in a decade or two. Let’s keep hoping and trying! But right now, start devoting more resources towards efforts that demonstrably improve people’s lives. Put resources and energy into efforts that target the root causes of the problem.
FAST FOOD MAY CAUSE CHRONIC INFLAMMATION
The body’s immune system responds to fast food as though it were an invasion of harmful bacteria. Upon detecting fast food the body recruits a large and powerful army to combat the noxious ingredients.
Researchers at the Life & Medical Sciences Institute at the University of Bonn found that when mice were fed a fast food diet, there was an oversized immune response. What’s more, the invasion of fast food caused lasting changes in the expression of genes that regulate the immune response, making them more easily expressed.
A localized immune response, such as swelling around a cut, helps speed recovery. But, a chronic, immune response that causes inflammation throughout the body is quite harmful and has been implicated as a major contributor to cognitive decline and dementia.
The researchers found that the fast food diet caused epigenetic changes that remained even when they switched the mice back to a healthier diet. Dr. Eicke Latz, Director of the Institute for Innate Immunity at the University of Boon explained that, “the immune system consequently reacts even to small stimuli with stronger inflammatory responses. So it is quite possible that a fast food diet contributes to the risk of dementia by changing the genetic regulation of the immune response.
The message seems clear: one way to lower your risk of cognitive decline and dementia is to avoid fast food and package foods. They mess up your immune system and cause chronic inflammation.
University of Bonn. "Fast food makes the immune system more aggressive in the long term: Study shows that even after a change to a healthy diet, the body's defenses remain hyperactive." ScienceDaily, 11 January 2018. <www.sciencedaily.com/releases/2018/01/180111141637.htm>.
WINE CLEANS THE BRAIN
The evidence that consumption of wine and alcohol – IN MODERATION – can be good for the brain has been around for a while. But how does brain protect the brain? The usual explanation is that wine contains substances like flavonoids or resveratrol that act as antioxidants. These substances found in wine help clean up free radicals and, thereby diminish the damage these molecules wreak on the brain.
Recently, Maiken Nedergaard and her team at the Center for Translational Neuromedicine and the University of Rochester Medical Center have added to our understanding of the protective mechanisms of wine. Wine appears to improve the function of the brain’s ”glymphatic system.”
Nedergaard was the first researcher to describe the “glymphatic system.” It is a unique process that enables the brain to flush metabolic waste material out of the brain, usually during deep sleep. Nedergaard’s new research showed that low levels of alcohol (2 ½ drinks per day) reduced inflammation in the brain and made the glymphatic system more efficient at flushing waste (like nasty plaques and tangles) out of the brain.
Nedergaard also demonstrated that these benefits were lost, and actually reversed, with the consumption of high levels of alcohol. Prolonged and excessive use of alcohol creates chronic inflammation in brain cells called astrocytes that help regulate the glymphatic system. So, impaired astrocytes results in an impaired glymphatic system. The brain’s garbage disposal mechanism falters and it begins to fill up with dangerous gunk.
So, the trick to cleaning out the brain seems to be to drink a little bit of wine a couple of hours before bedtime. Then, get a good night’s sleep and let the glymphatic system perform its garbage disposal duties.
MAKE LOVE NOT WAR
Hey! Guess what? New research suggests that going to war is bad for your brain.
At the 47th annual meeting of the Society of Neuroscience 2017, Deborah Whitmer, commander of the Walter Reed Army Institute of Research chaired a press conference called “How Military Service Changes the Brain.” Here are some of the highlights.
Blast Exposure - Soldiers are exposed to multiple blast exposures not only in war zones, but also during training. Even though many of these blasts are mild the exposures add up over time. Alaa Kamnaksh, a researcher at the Uniformed Services University of the Health Sciences says that” Repeated mild blast exposure can permanently change the brain’s structural organization, resulting in lasting functional and behavioral consequences.” That’s not good. Kamnaksh hopes that future research will lead to better forms of treatment.
Gulf War Syndrome – Nearly 30% of veterans (250,000 people) who served in Kuwait during the Persian Gulf War suffer from Gulf War Illness of Gulf War Syndrome. This mysterious set of symptoms includes mood swings, chronic pain, difficulties with language and complex motor tasks, inability to concentrate, and loss of memory. That’s not good. The common denominator is damage to the brain. Kaundinya Gopinath, a researcher at Emory University says that ongoing research “may be helpful in helping us find a way to treat this illness.”
Statin Exposure – Sarin gas, which was used as a chemical weapon during the Gulf War, is a volatile nerve agent. Exposure to nerve agents like sarin can result in vast neurological impairments. Definitely not good! Ankita Patel, a researcher at the Drexel School of Medicine is doing work to pinpoint compounds that might reverse these neurological impairments.
Wait a minute. All of this research is devoted to limiting the damage done by the ravages of war. Here’s a radical idea. Rather than treat the symptoms let’s eliminate the cause of all this pain and suffering. Let’s not send our brothers and sisters out to kill each other.
Just a thought.
A number of studies on stress were introduced at The Society of Neuroscience Conference in 2017.
Sins of The Father – Jennifer Chan, a researcher at the University of Pennsylvania reported on several studies that found that a father’s lifetime experience have a measurable effect on the development and health of future offspring. Environmental factors experienced by the father create epigenetic markers that reprogram his sperm. These defects in the father’s reproductive tract then get passed along to the offspring.
Childhood Trauma – Survivors of childhood trauma have a much greater risk of developing mental and physical health issues in adulthood. According to Briana Mulligan, a researcher at the University of New Mexico Health Sciences Center, “Long-term stress conditions can alter the DNA methylation profile of brain regions that regulate hormonal, immunological and neural genes.” Again, epigenetic changes are the mechanism of change.
Neurogenesis and Stress – Christoph Anacker, a neuroscientist at Columbia University, reported that genetically modified mice responded differently to stress depending upon how many new cells we found in their hippocampus. Mice with fewer new cells experienced more stress. Those with more new cells in the hippocampus had a lower stress level. So, of course, researchers are looking for new medications that will help increase neurogenesis in the hippocampus. I guess they forgot that physical exercise stimulates hippocampal neurogenesis. No need for expensive medications with possible side effects.
I recently chanced upon a YouTube video featuring a 27-minute talk by Matthieu Ricard on the art of meditation. Ricard is a French biochemist who left science to move to the Himalayas and become a Buddhist monk. His 27-minute talk is the clearest and most compelling argument for meditation that I have ever heard. I highly recommend it. the first few minutes are a little disjointed, so hang in there.
In the video, Ricard references the Buddhist concept of the monkey mind. Buddha described the human mind as being filled with drunken monkeys, jumping around, screeching, chattering and carrying on endlessly. Ricard takes this idea and crafts a monkey mind metaphor to describe why meditation is a fundamental aspect of mental training.
One of the vulnerabilities of the monkey brain is that it becomes enslaved by negative and destructive impulses, such as anger, fear, jealousy, greed and envy. So, imagine a drunken monkey who is restrained by strong ropes. Each rope represents one of the destructive impulses that make our lives miserable. The monkey, understandably, is frantic to escape, but the more he struggles the tighter he pulls the knots that bind him.
This frantic reaction, Ricard suggest, is how our undisciplined mind usually works. It flails aimlessly against misery but just makes matters worse. To escape from pain and suffering the monkey mind needs to calm down. It needs to become still and serene so that it can look around and figure out what is really going on. The monkey mind needs to quiet its worst impulses and find a quiet space where its rational, civilized abilities have a chance to do their work.
The monkey mind needs to calm down and focus its attention on the root cause of its suffering. It needs to recognize that it is imprisoned by greed and envy. To free itself it needs to get to work undoing the knots that bind it to negative behaviors and must start cultivating positive behaviors that nurture happiness.
So, how do we find the mental discipline to behave in this calm and rational manner? It takes training and practice. That is what meditation is for. Meditation trains the mind to make use of its more evolved and civilized capabilities. It trains the mind to be aware and respectful of primitive impulses, but to keep them in check. Meditation trains our mind to slow down and give our recently evolved executive brain a chance to moderate primitive impulsive behaviors. Meditation trains our mind to modulate our emotional response. Rather than respond to impulses, we learn to engage our working memory, to think creatively and to make sensible choices.
THE END OF ALZHEIMER’S?
We have known how to use lifestyle changes to reduce the risk of cognitive decline and dementia for some time now. But, we have not figured out how to reverse the symptoms of dementia once they appear. Until now!
In a new book, written for a general audience, Dr. Dale E. Bredesen describes a protocol that, for the first time, is able to reverse the symptoms of Alzheimer’s. Over a hundred patients have undergone the Bredesen Protocol, or ReCODE (reversal of cognitive decline) and have experienced varying degrees of sustained remission of Alzheimer’s symptoms. These are limited results that need to be replicated. Nevertheless, they are extraordinary. There is finally a ray of hope in a field that has seen decades of dark disappointments.
Why does the Bredesen approach work, while all other attempts to treat Alzheimer’s have failed? It works because Bredesen has shaken free from the dogma of the so-called “amyloid hypothesis” that regards the presence of amyloid as the singular cause of the disease. Rather than follow the herd, he has followed the science.
Bredesen has recognized that Alzheimer’s is a complex disease with multiple causes. He has spent 30+ years analyzing the multiple causes and has developed a multi-factorial approach that addresses each one of them. He has combines a strong background in mainstream medicine and research with innovative insights from functional and integrative medicine.
THE BREDESEN PROTOCOL
In very stark terms, cognitive decline and dementia occur when synapses die faster than they can be replaced. Negative plastic change at the synaptic level outpaces positive plastic change. When the damage reaches a critical tipping point, the brain is unable to function properly and begins to decline. A negative spiral of self-reinforcing damage is initiated. The Bredesen Protocol pinpoints the sources of the damage and, one-by-one, works to correct them.
Bredesen’s interventions include lifestyle changes that parallel MINDRAMP’s CogWheels of Brain Health. But his protocols go farther to include specialized testing and analysis that can only be done by a trained clinician. To date Bredesen and his collaborators have identified 36 unique factors that contribute to cognitive decline and dementia. Each of Bredesen’s patients is tested to determine his or her genetic, chemical, hormonal, metabolic and toxic profiles, searching for abnormal levels. Each protocol then creates targeted interventions to rebalance and then optimize the identified abnormalities. This is the essence of precision medicine (see below).
Bredesen has identified three sub-types of Alzheimer’s that behave in different ways and, therefore, need different types of protocols.
Currently, 450 physicians have been trained to conduct the protocol. Bredesen’s approach incorporates many of the innovations being developed in the emerging fields of Functional Medicine and Precision Medicine. (See below)
* Norman Doidge, author of The Brain That Changes Itself and The Brain’s Way of Healing, has a terrific review of the Bredesen Protocol on his blog. Doidge uses this term “atrophic” to describe Bredesen’s Type 2 Alzheimer’s. I don’t think Bredesen uses the term, but I like it. http://www.normandoidge.com/?page_id=702
FUNCTIONAL & PRECISION MEDICINE
Functional Medicine is based on systems biology (see below). It is an individualized, patient-centered, science-based approach that empowers patients and practitioners to work together to address the underlying causes of disease and promote optimal wellness.
Functional medicine requires a detailed understanding of each patient’s genetic, biochemical, and lifestyle factors and leverages that data to direct personalized treatment plans that lead to improved patient outcomes.
For more see the website for the Institute for Functional Medicine at: https://www.ifm.org/
Precision Medicine – This approach was popularized when President Obama announced the Precision Medicine Initiative in his State of the Union Address in 2015.
The U.S. National Institutes of Health defines precision medicine as “en emerging approach for disease treatment and prevention that takes into account individual variability in genes, environment and lifestyle for each person.” The term describes the ability to precisely tailor diagnosis, prognosis and treatment to each individual patient.
THE NEW VOCABULARY OF PRECISION MEDICINE
Precision medicine seems to have developed its own unique vocabulary, using words and phrases that reveal the unique characteristics of the approach. I discovered the following in a publication called “Advancing Precision Medicine,” produced by Science/AAAS (American Association for the Advancement of Science) and sponsored by Olink Proetomics.
Systems medicine – Systems medicine is an interdisciplinary field of study that looks at the systems of the human body as part of an integrated whole, incorporating biochemical, physiological, and environment interactions. The defining feature of systems medicine is the collection of diverse longitudinal data (biomarkers) for each individual. Systems medicine believes that all body systems work together synergistically and the whole (full body) is greater than the sum of the parts (individual organs or systems).
Biomarkers - According to the WHO, a biomarker is “any substance, structure or process that can be measured in the body or its products and influence or predict the incidence of outcome or disease.” [This sentence is odd, but I think you get the idea.] Precision medicine is most interested in “circulating biomarkers,” such as hormones, cytokines and metabolites that can be assessed in blood, urine and other bodily fluids, using minimally invasive methods. Biomarkers make it possible to diagnose, treat and monitor illness.
’omics – This is a suffix that suggests the study of a broad array of factors. For example, genomics is the study of the full range of genes in an organism. The suffix is now being used to describe arrays of other biomarkers besides genes. For example, the study of RNA transcription factors (transcriptomics), of proteins (proteomics), or metabolites (metabolomics).
“Personal dense, dynamic data clouds” of data – Lee Hood, who is considered by many to be the father of systems biology, says that systems medicine seeks to unravel the complexities of human biology and disease by examining as broad an array of information as possible about the biomarkers that determine health and illness.
He collects “personal, dense, dynamic data clouds:” Personal because each set of data is unique to each individual, dense because of the high number of measurements taken, dynamic because the data and patient are monitored across time. “These clouds are like the Hubble Telescope,” says Hood, “they give us a resolution we haven’t seen before of the multi-‘omic statistical correlations that are the determinants of wellness and disease.”
The Quantified Self – When a data cloud is developed for an individual, the status of each of their biomarkers can be quantified and evaluated. This goes way beyond the standard blood tests now give. This vast quantification of biomarkers enables practitioners to make precise diagnoses and prescribe highly targeted interventions that address the root causes of disease.
Predictive, Preventive, Personal, Participatory – Hood sees precision medicine as having these four key qualities.
AMYLOID IS NOT THE VILLAIN
Mainstream medical researchers and funders have mistakenly fixated on amyloid as the villain and have sought to find a single intervention – a magic bullet – that will rid the body of amyloid and, thereby cure dementia.
The amyloid approach has two fundamental problems.
First, amyloid is not the cause of Alzheimer’s. Amyloid is, in fact, the brain’s way of protecting itself from infection. Researchers Rudolph Tansy and Robert Moor have published research showing that amyloid plagues form a net around pathogens that invade the brain that keep them from doing harm. Efforts to remove amyloid can put the brain at greater risk. In a severely compromised brain, amyloid production gets out of control and adds to the problem. But this is a symptom of the disease, not the cause.
The second problem with the amyloid approach is that it suggests a monotherapeutic solution – the magic bullet. But, decades of work and billions of dollars have demonstrated that monotherapies don’t work. Why? They fail because neurodegenerative diseases are complex, multi-factorial conditions. Dementia is caused by a broad array of problems that confront the brain and the body. And, these conditions vary from patient to patient.
AWAKENING FROM ALZHEIMER’S
I have just finished watching a well-produced series of 14 videos called Awakening From Alzheimer’s. The series is hosted by Peggy Sarlin. Sarlin conducted hour-long interviews with a range of neuroscientists, nutritionist and experts in natural and alternative medicines. The series promotes her book and related information. Nevertheless, the video interviews contained a wealth of great information.
The primary theme of the series is consistent with the MINDRAMP message. We already know how to prevent, slow or even reverse cognitive decline and dementia. I’ll use this edition of the Synapse newsletter to give you some of the highlights of the Awakening From Alzheimer’s book and videos.
TWENTY FIRST CENTURY MEDICINE – TREATABLE DEMENTIA
Dale Bredesen, of UCLA and the Buck Institute, stated that we are entering a very exciting era in terms of prevention and treatment of cognitive decline and dementia. He calls it the “dawn of the era of treatable dementia.” That’s right, treatable. Beyond being able to prevent or slow the development of cognitive decline and dementia, Bredesen states – credibly - that we can now treat and reverse some dementias.
It is Bredesen’s research in particular, that makes this statement valid. Bredesen has developed and tested a personalized, multi-factorial protocol that, for the first time, has demonstrated that the symptoms of dementia can be reversed. People who stopped working because of memory loss and confusion have been able to resume their old jobs. Bredesen combines, exercise, nutrition, stress management, sleep and a total of 45 different factors in his treatment plan.
Bredesen’s approach, and the approach of the other scientists interviewed can be characterized as 21st Century medicine. The older 20th Century medicine uses small data-sets for diagnosis and seeks one-size-fits-all interventions – an approach that has been unable to address the complex nature of neurodegenerative diseases.
The modern approach uses large data sets (lifestyle behaviors and metabolic profiles) to diagnose the multiple root causes of chronic illness. This approach integrates the best of both Western and Eastern approaches to medicine. 21st Century medicine creates comprehensive and pragmatic interventions that are personalized to each individual.
The new approach taken by Bredesen incorporates what MINDRAMP has characterized as the Rule of the C’s (Causes, Combinatorial, Customized and Continual). Evidence shows that successful interventions target root causes, combine multiple interventions, are customized and personalized to each individual
Here is a link to Bredesen’s website where he describes the protocol and offers a number of free research papers. https://www.drbredesen.com/thebredesenprotocol. Bredesen has also published a book called The End of Alzheimer’s.
ADDRESS THE CAUSES OF DEMENTIA, NOT THE SYMPTOMS
All of the scientists interviewed by Sarlin stressed that dementia is a complex, multi-factorial condition. Prevention and treatment of dementia, therefore, must focus on the root causes. Rather than try to disperse the smoke, put out the fire!
So, what causes cognitive decline and dementia? What causes neurodegenerative diseases?
It is increasingly clear that amyloid plagues do not cause Alzheimer’s. They are a response to disease and may even serve a protective function. Dementia is caused, instead, by a host of systemic, metabolic conditions that combine to wreak havoc on body and mind.
Dr. David Perlmutter points to chronic inflammation as being implicated in almost forms of cognitive decline and dementia.
Dr. David Katz is a specialist in integrative medicine. He runs the Yale Prevention Research Center. He claims, quite confidently, that we already know how to slash the risk of Alzheimer’s disease by 80%. He cites three domains of evidence, two theoretical and one empirical.
Theoretical #1 – Cardiovascular problems are a major risk factor for dementia. Many dementias are called vascular dementia because they can be traced to strokes and mini-strokes. But any condition that robs the brain of blood and therefore, oxygen and fuel, does damage to brain cells. We know how to prevent and treat cardiovascular disease.
Theoretical #2 – Insulin resistance, metabolic disease and diabetes are closely associated with dementia, so much that some called Alzheimer’s Diabetes Type III. We know how to prevent and treat diabetes Type II. When we prevent insulin and blood sugar problems and we reduce the risk of dementia.
Empirical - We know that not all older adults get dementia. There are many examples of people who are healthy. Dan Beuttner, in his book The Blue Zones, identified five populations around the globe that live extraordinarily long and healthy lives. He has documented similarities in lifestyle that seem to clearly reduce the risk of dementia. These include eating wholesome foods, getting a lot of exercise, having cultural mechanisms to manage stress, having strong social support systems and getting enough sleep.
Katz points out that adopting healthy living practices, such as eating well, is easier when the culture supports these practices, as in the Blue Zone areas. Unfortunately, the American culture does the opposite since there is too much money to be made selling junk food. So healthy lifestyle practices take not only will power, but also skill power. We need master a variety of skills to support healthy eating and other healthy living choices.
Perlmutter is a neurologist and nutritionist. He has written two, excellent, best-selling books, Grain Brain and Brain Maker. Perlmutter has done as much as anyone to point out that our food choices have a profound effect on our overall health, and on our susceptibility to cognitive decline and dementia.
Perlmutter stresses the role of inflammation in dementia and a host of other chronic diseases. Much of this systemic inflammation can be linked back to leaky guts that occur when our gut bacteria becomes compromised. A permeable gut, caused by poor nutrition, leaks toxins into the blood stream that can cross the blood/brain barrier and get into the brain. Further, the toxins stimulate can systemic immune response which causes a whole host of problems.
Perlmutter’s major dietary recommendations are to eliminate sugar and drastically reduce our intake of simple carbohydrates. And, welcome fat back to the table. Fat has gotten a bad rap. Good fat (coconut oil, olive oil, avocados, nuts, fish oils) promote health and feed the brain, which is 70% fat. To keep our gut bacteria healthy we need to eat more fermented foods (kefir, sauerkraut, kimchi), more prebiotic foods high in fiber (onions, garlic, leeks, Jerusalem artichokes, apple cider vinegar, dandelion greens).
As you might expect, in addition to good dietary practices, Perlmutter also stresses the importance of what we characterize as the CogWheels of Brain Health. These are: physical exercise (aerobics, strength, flexibility), mental stimulation, positive social interaction, stress management and good sleep.
A majority of the Sarlin interviews feature folks who rely on supplementation as an important component of their overall approach to brain health. I will characterize this group as being members of new medical specialty called “personalized metabolic medicine.” They use increasingly sophisticated diagnostic tools to get individual metabolic profiles of their patients. They then use the information to rebalance hormonal systems that have been thrown out of whack, either by disease or by the aging process.
While I remain skeptical about supplementation in general, I am now convinced that targeted use of supplements can be an important component of a combinatorial approach to health care. I don’t think it a good idea to self-medicate, or self-supplement. What does make sense is to work with a professional metabolic specialist to help you get your personalized metabolic profile. The natural medicine professional can then prescribe and monitor specific supplements to target specific deficiencies that have been identified.
In case you want to learn more, the metabolic doctors featured in the series include: Dr. Dr. Richard Brown (Columbia Univ.) and his wife Patricia Garbarg (The Rhodiola Revolution); Dr. Jacob Tieltlebaum; Dr. Mary Newport (coconut oil advocate); Dr. Jay Faber of the Amen Clinics; Dr. Pamela Warthian Smith, who runs the Center for Personalized Medicine and Fred Pescatore a clinical nutritionist.
KETONES TO FEED THE BRAIN
One particularly interesting episode featured Dominic D’Agostino and Dr. Angela Poff of University of South Florida. They are doing some fascinating work on ketones and the ketogenic diet. They argue that ketones are an alternative source of fuel for aging brains.
One of the main points is that the human brain is metabolically demanding but also metabolically flexible. The brain uses 25% of the available energy and usually relies on glucose. But, in times of stress, such as starvation, fasting and advancing age, the brain can convert to utilization of ketones to get its energy. D’Agostino likened the human brain to a hybrid car that can use gasoline, or switch to electricity, or diesel.
Apparently, as we age, our tolerance for carbohydrates ebbs and the capacity to utilize glucose declines. The aging brain ends up getting less glucose (fuel) than normal. Less fuel = less functionality. The ability to use ketones for brain fuel, however, does not decline with age. D’Agostino recommends that older adults begin to transition from their normal diet to a low-carb or even ketogenic diet to make sure that their brains get the energy they need to function well. I find this a credible recommendation.
CREATIVITY – FINDING INTIMACY WITH OUR WORLD
I recently read an article called How Creativity Frees the Mind by Hugh Delehanty. I knew Hugh from my days at AARP. Hugh was the editor of AARP The Magazine when I was running Staying Sharp brain health program.
Hugh shares insights he gained while attending a retreat on creativity and mindfulness at the Spirit Rock meditation center in Northern California. The article is peppered with savvy perceptions about how to nurture authentic artistic creativity and, in so doing, enrich our lives. I suggest reading the entire article.
Hugh describes his big takeaway about creativity like this. “When I started this journey, I thought I was searching for a magical bag of tricks to help me turn dross into creative gold. But what I discovered was that creativity isn’t a fancy parlor game; it’s a more intimate way of relating to the world.”
Hugh discovered that we enhance artistic creativity not by collecting tricks and techniques, but by learning to use our mind differently. Artists have trained themselves to see and hear things differently. They use their sensory and perceptual functions in ways that depart from normal, every-day cognition. As Hugh suggests, artistic creativity involves a heightened intimacy with the world.
Hugh cites the wisdom of Ellen Langer, a Harvard psychologist who is often referred to as “the mother of mindfulness.” Langer taught herself to paint and in the process learned that “to be a true artist is to be mindful.”
What does mindfulness have to do with artistic creativity? I think it has to do with how our brain’s process information.
Sensory perception is a two-step process. First, our sensory organs pay collect specific and detailed sensory data. Second, our brain organizes the data into recognizable mental representations. So a collection of colors, shadows, edges and textures is pulled together to recognize “an apple.” Once the generic representation (“apple”) has been formulated, the brain forgets the details. It becomes mindless – at least about the details.
Authentic artists have learned to suppress the generic idea (an apple) and return their attention to the details (colors, shapes, edges, shadows). They are “mindful” of what they are really seeing. Rather than simply paint a red circle and call it an apple, they use their skill to reflect their intimate, sensual experience of this unique apple, mottled with greens and purples, distorted with lumps and bumps and strange shadows suggestive of rot.
The making, and taking, of authentic art gives us pleasure because it fulfills our developmental imperative, our innate drive to enhance our physical and mental capacities. Through art we stretch and refine our sensory acuity, we train our minds to be more mindful and intimate with the world. We broaden our understanding and appreciation of the myriad wonders of life that are available to us.
CREATIVITY AND AGING
Creativity and aging are two of my favorite topics and they combine to create a rather persistent myth – that creativity diminishes with age. I was pleased, therefore, to come across a wonderful article that nicely articulates the counter argument. The article, written by Pagan Kennedy, appeared in the NY Times and was titled “To Be a Genius, Think Like a 94-Year Old.”
The article revolves around physicist John Goodenough. When Goodenough was a 23-year-old Army veteran he entered the University of Chicago with the goal of becoming a physicist. A professor told him that he was already too old to succeed in the field. Physics, apparently, is a young man’s game (very young!).
Well, you will say, that’s an outdated attitude. No one thinks that way any more.
Think again! Silicon Valley still worships at the temple of youth. A 12-year-old inventor named Shubham Banerjee received venture capital funds to start his own company. When Mark Zuckerberg was the 22 year-old chief executive of Facebook he told an audience at Stanford University that, “Young people are just smarter” and more creative. The myth persists. Zuckerberg later apologized, when he was an older and wiser man.
Back to Goodenough, who ignored the professor’s warning and became a world-class physicist. The energy crisis in the 1970’s got him interested in the challenge of storing energy in small, efficient packages. In 1980, at the ripe old age of 57, Goodenough coinvented the lithium-ion battery that now runs our phones, laptops and electric cars.
But, Goodenough was still upset about our continued dependence upon fossil fuels and by the pollution caused by internal-combustion engines. So now, at age 94, Goodenough is still creating. He is confident that he is on the brink of developing a new kind of solid-state battery that would be low-cost, lightweight and could revolutionize the way we power automobiles. He has partnered with a Portuguese physicist, Maria Helena Braga who has created a kind of glass that can replace liquid electrolytes inside batteries.
Goodenough’s creative idea for revolutionizing energy may not work. But he will keep trying. “I’m old enough to know,” he says, “you can’t close your mind to new ideas. You have to test out every possibility if you want something new.” He likened himself to a slow, but steady turtle who may not have succeed early in life but just kept on meandering through different fields, picking up insights along the way. “You have to draw on a fair amount of experience,” he observed, “in order to be able to put ideas together.”
For the sake of the planet let’s hope that this old, old man manages to invent a battery that will free us from our dependence on fossil fuels.
THE MINDRAMP CreativeCycle©
Since we are talking about creativity I might as well mention the MINDRAMP analysis of the creative process.
The study of creativity generally proceeds along one of three routes. We can study creative people – what makes one person more creative than another? We can study creative products – aesthetic judgments about what makes one product more creative than another? And, we can study the creative process – what creative people do in order to come up with creative ideas and products? What makes on process more creative than another?
Learning about the creative process is often the easiest way to significantly improve our own creative productivity.
A key insight about creativity is that it is a complex process. It involves an array of different skills and progresses through a sequence of highly differentiated stages. Each stage requires different types of thinking. To be creative, therefore, you need to be fluent in a variety of thinking skills, and you need to know when and how to shift from one cognitive mode to another. This is why it is useful to have a schematic model of the full creative process.
Building on the work of others, MINDRAMP has developed a model of the creative process that has four major phases: Imagination, Idea Generation, Actualization and Evaluation. These four phases are further divided into eight discrete stages of creative development.
Imagination (Future Memory)
Creative cycles can play out across a matter of moments, over weeks and months, or can extend across a lifetime. As the stages above indicate, some aspects of creativity involve imagination and the generation of new ideas (novelty). Other stages involve the accumulation of knowledge and learning.
When you consider that the generation of ideas is often a process of combining bits of information in new ways, it becomes clear that the more bits of information you have in your brain, the more creative combinations you can make. As the 94 year-old Goodenough intimates (see above), years of experience, coupled with an open mind, provide the mind with a wealth of options.
The creative cycle also illustrates the importance of turning cool insights into actual products or systems that have practical application. Ideas need to be turned into routines that can be tested. It’s great when ideas backfire because failure leads to another, revised creative cycle that attempts to correct the mistake. If ideas succeed, great! Another creative cycle is needed to put the idea into production, to market it or to start working on it’s replacement.
All of this creating takes time, patience and perseverance.
I’ll make one last point about the engine of creativity. It is at its best when fueled by passion and guided by positive values. Goodenough, at age 57, could have rested on his laurels after inventing the lithium-ion battery. He could have decided to sit on his porch and coast through the rest of his life. But his concern for the welfare of his fellow human beings and his passion to preserve the health of planet earth inspired him to continue pursuing his creative quest.
PLOS MEDICINE SPECIAL ISSUES
It is always great to find peer reviewed research papers that confirm and validate the MINDRAMP approach to brain health. I recently came across a number of such papers that were part of a PLOS Medicine special edition called Dementia Across the Lifespan and Around the Globe.
The Guest Editors of this special edition were Carol Brayne, Director of the Cambridge Institute of Public Health At the University of Cambridge and Bruce Miller, Director of the San Francisco Memory and Aging Center at the University of California. PLOS (The Public Library of Science) is a non-profit publisher and advocacy organization that publishes free, online research, making it widely accessible to everyone without a fee.
WE LOVE YOUR PLOS!
Mixed Pathologies and Neural Reserve: Implications of Complexity of Alzheimer’s Disease Drug Discovery. David A Bennett, Published in PLOS March 14, 2017. https://doi.org/10.1371/journal.pmed.1002256
David Bennett, Director of the Rush Alzheimer’s Disease Center at Rush University is a hero of mine. He has been making sensible statements about lifestyle interventions to lower risk of cognitive decline for years. In this short paper he reiterates the point that drug interventions for Alzheimer’s have failed miserably. It is unlikely that anyone will find a single drug that can reverse damage of multiple physiological systems. Are there any viable alternative approaches?
“A hypothetical therapeutic agent that targets neural reserve (our emphasis).” Bennett suggests, “could be used to offset any and likely all common brain pathologies that alter cognition.” In other words, we could avoid, or compensate for, all off the conditions that cause dementia by developing interventions that increase neural reserve. Bennett defines reserve as “the ability of a physiologic system to maintain function despite damage from injury or disease.” So, in the context of Alzheimer’s dementia syndrome, neural reserve would result in no cognitive decline even if pathologies like plaques and tangles are present.
That works for me. So, is there evidence to support Bennett’s claim? Can cognitive reserve prevent cognitive decline. The next study says “Yes.”
Potentially Modifiable Lifestyle Factors, Cognitive Reserve and Cognitive Function in Later Life; a Cross-Sectional Study. Linda Clare, et al. PLOS 2017
This study starts with the premise that “potentially modifiable lifestyle factors may influence cognitive health in later life and offer potential to reduce the risk of cognitive decline and dementia.” That’s what we have been saying for years. But, what is the mechanism that might explain different rates of cognitive decline? That’s what these researcher wanted to find out. They wanted to figure out if “cognitive reserve” explains how lifestyle factors influence cognitive fitness.
They found that “people with a healthier lifestyle had better mental fitness, and this was partly accounted for by their level of cognitive reserve.”
They go on to say that “these results highlight the importance of policies and interventions that encourage older people to make changes in their diet, exercise more, and engage in more socially oriented and mentally stimulating activities.” Sound familiar? We have been preaching this approach for years. We should add that these brain healthy policies and interventions should encourage people of all ages to live healthier lifestyles.
Okay, is there any evidence that cognitive reserve can be built up over the course of a lifetime?
BUILDING RESERVE ACROSS THE LIFESPAN
Association of Lifelong Exposure to Cognitive Reserve – Enhancing Factors with Dementia Risk: A community Based Cohort Study. HuiXin Wang, Stuart W. S. MacDonald, Serhiy Dekhtyar, Laura Fratiglioni, PLOS, March, 2017 https://doi.org/10.1371/journal.pmed.1002251
To get right to the point of the next study, it found that “cumulative exposure to reserve-enhancing factors over the lifespan was associated with reduced risk of dementia in late life, even among individuals with genetic predisposition.” Further, they found that this beneficial effect was dose-dependent. That means that the more reserve-enhancing stuff you do, the more you reduce your risk of dementia in late life.
They also made some important discoveries about it is important to begin practicing brain healthy (i.e. reserve-enhancing) behaviors. The first point is that “the first decade of life appears to be a critical period for developing dementia in later life.” Higher levels of education, literacy and engagement in complex work situations have been shown to be reserve-enhancing activities. Impoverished environments may prevent young brains from reaching full levels of maturation, causing the kids to struggle with education and reading which will have negative consequences throughout their life.
A second point about timing is that “factors associated with dementia risk originate in different periods throughout the life course, including early, adult and late life.” In middle age, for example, job conditions could heighten dementia risks if people are stuck in boring, stressful jobs that cause them to be depressed. In late life, after retirement, people who engage in stimulating leisure activities are more protected against dementia than are people who become less and less engaged with life.
“It has been suggested,” the authors say, “that dementia is not determined at a single time period but rather results from a complex interplay between genetic and environmental exposures throughout the life course.” The take-home lesson is that we should engage in brain healthy practices throughout our lifespan, from the womb to the last hurrah. It is never to late to start, but the sooner you start the better.
Association of Lifelong Exposure to Cognitive Reserve – Enhancing Factors with Dementia Risk: A community Based Cohort Study. HuiXin Wang, Stuart W. S. MacDonald, Serhiy Dekhtyar, Laura Fratiglioni, PLOS, March, 2017 https://doi.org/10.1371/journal.pmed.1002251
MINDRAMP’S POSITIVE PLASTICITY PREMISE
Frataglioni and her fellow researchers discuss several biologically plausible hypotheses that could explain how cognitive reserve factors reduce the risk for dementia. They point out that the environment plays a big role in influencing brain plasticity, which is a key element in the brain reserve hypothesis.
We agree. Our external environment (what we do and experience) and our internal environment (what we feel and think) all have the potential to build neural and cognitive reserve. We call it our Positive Plasticity Premise.
If you can create a steady stream of positive plastic changes in your brain, you ramp up the strength of physical structures in you brain. The more robust and resilient your brain is (neural reserve), the greater your opportunity to learn and to think creatively. These strengths, in turn, enhance your ability to engage in complex, stimulating activities that build cognitive reserve. It is a positive feedback loop, an autocatalytic process.