NOTE: Please see my blog post February 28, 2012 for a primer on Essential Fatty Acids: MAKING SENSE OF OMEGA-3 FATTY ACIDS: The Skinny on Fish Oils and Brain Health.

The Neurology article entitled , “Nutrient Intake and Plasma Beta-Amyloid” by Gu et al, indicates that people who eat a diet rich in fish oils may significantly lower the risk of developing memory problems and Alzheimer’s disease. 1200 dementia-free subjects over the age of 65 were studied with blood testing and detailed review of dietary patterns.  The associations of two types of plasma β-Amyloids  and dietary intake of 10 nutrients were examined using linear regression models, adjusted for age, gender, ethnicity, education, caloric intake, apolipoprotein E genotype, and recruitment wave. Nutrients examined included saturated fatty acid, monounsaturated fatty acid, omega-3 polyunsaturated fatty acid (PUFA) [fish oils--see note below], omega-6 PUFA, vitamin E, vitamin C, β-carotene, vitamin B₁₂, folate, and vitamin D.  Only the fish oils were associated with reduction of β-Amyloids.

Although β-Amyloids in blood plasma could possibly not reflect the amyloid protein levels in the brain, it is known that brain amyloid load correlates with dementing conditions. It is generally believed that amyloid accumulation is toxic to neurons, but there are some research lines suggesting that brain amyloid accumulation is the result of dementing processes and not its cause.  In any event, the authors conclude:

“Our data suggest that higher dietary intake of ω-3 PUFA is associated with lower plasma levels of Aβ42, a profile linked with reduced risk of incident Alzheimer’s Disease and slower cognitive decline in our cohort.”

Two other studies reported in April have remarkably congruent findings. From April 10 in the daily APA bulletin: Health Day reported, “Omega-3 fatty acids from fish may help prevent age-related cognitive decline, according to two new studies.” The studies were both published in April’s American Journal of Clinical Nutrition. “In one study, Dutch researchers examined the diet and cognitive function of 210 men, ages 70 to 89. … The researchers concluded that consumption of approximately 400 milligrams of omega-3 fatty acids per day…protects against cognitive decline. In the other study, American researchers looked at omega-3 consumption and cognitive decline in 2,251 white males, ages 50 to 65.” While this “study found no association between baseline levels of omega-3 fatty acids in the men and overall cognitive decline…an analysis of specific types of cognitive decline did find that higher levels of omega-3 fatty acids were associated with protection against loss of verbal fluency.” Authors of both studies “recommended that clinical trials be conducted to determine the effect of dietary fish, fish oil or both in elderly people at risk of cognitive decline and Alzheimer’s disease.”

Personally, I take a lot of nutritional supplements, but it is difficult to know which of these is really necessary. When patients ask what they ought to be taking I can only answer confidently that only Essential Fatty Acids (EFAs, Fish Oil) and possibly Vitamin D seem to be necessary for the typical well-nourished American, methyl-folate may be needed for people on anti-depressant drugs, and B12 sublingual may be important for older people and non-meat eaters.  Plus, Resveratrol looks very promising,

In this communication, I will focus mainly on the all-important Essential Fatty Acids, and particularly on Fish Oil, an Omega-3 poly-unsaturated fatty acid, known as Eicosapentaenoic Acid (EPA).  EFAs are well-established contributors to cardio-vascular health and protectors against sudden cardiac death.  Here, I will focus on EFAs and brain health.  And mental health.

Note, a new study from UCLA announced today has demonstrated that the level of Omega-3 DHA in red blood cells indeed correlates with brain volume and memory in older men and women–see below.

The Journal of Clinical Psychiatry recently devoted two articles and a Commentary  on Fish Oils for depression, under a weighty cover headline: Eicosapentaenoic Acid for Depression: A Meta-analysis of Clinical Trials (Vol 72, December 2011, Num 12).  In short, there is clear evidence that Fish Oils can treat depression and some evidence that low levels of Omega-3s are associated with a suicidal outcome.  Last September, at the ISNR 19^th Annual Conference in Phoenix, Daniel Johnston MD, MPH, who is Medical Director of the Pentagon’s Comprehensive Soldier Fitness Program, gave a beautiful review of EFAs and their importance in brain fitness.  Most of the information in this post derives from my notes of that lecture as well as the slide delineating Fatty Acid Families.

With that as a start, I’d like to help you make some sense of this highly important topic.

One crucial point is that the typical American diet, even one high in poly-unsaturated fatty acids, is at risk of being relatively deficient in Essential Fatty Acids.  The problem is that our diets are loaded with Omega-6 fatty acids from grain sources like corn, soybean, safflower, and canola oils—which directly compete with the good Omega-3s.  Omega-6 fatty acids are converted to Arachnodenritic Acid  (ADA), which promotes an inflammatory response in blood vessels.

The ratio of Omega-3s to Omega-6s is important.  The average American has about 4% Omega-3s; the average Japanese has about 8%.  Epidemiological studies indicate that Japanese on traditional diets have significantly less  cardiovascular disease and sudden cardiac death than Americans.

Omega-3 predominantly comes from fish oils and is interconverted between Eicosapentaenoic Acid (EPA) and Docoshexaenoic Acid (DHA) .  The ratio of these two Omega-3s is probably also important.  The meta-analysis in the Journal of Clinical Psychiatry clearly indicated that for depression, omega-3 supplementation is most effective in a 60%/40% mixture of EPA/DHA  with a ceiling at around 2,000 mg/d of EPA in excess of DHA.

Although Omega-3 also comes from alpha-linoleic acid in flaxseed, canola, and soybeans, contrary to frequent assertions, it is doubtful that these grain sources can balance the  Omega-6 (linoleic acid) also contained in the same grains.  The addition of monosaturated fats (Omega-3s and Omega-6s are known as poly-unsaturated Fatty Acids), may be helpful.  Note that as the following chart shows, some vegetable oil sources of monosaturated fats will also contain inflammatory-stimulating Omega-6 fats.

Centers for Disease Control and Prevention

Approx 40 % of the fatty acids on the orbitofrontal cortex are highly unsaturated omega-6 and omega-3 fatty acids.  1/3 of these are DHA.  A 2007 study published in the medical journal Lancet demonstrated that women who consumed more seafood when pregnant had smarter babies. And this has been corroborated in many subsequent studies. The American Academy of Pediatrics recommends supplementation of EFAs during pregnancy and lactation.

Studies have shown cognitive benefits of Omega-3 in healthy subjects:

• Improved mood profile
• Increased vigor
• Reduced anger
• Reduced anxiety
• Improved reaction time
• Improved sleep efficiency and improved cognitive function after sleep deprivation (mitigates sleep loss effects).

Dementia: Astoundingly, a 2006 study published in the Archives of Neurology intake of an average of only 180 mg/day of DHA was associated with a significant 47% reduction in the risk of developing all-cause dementia.

Depression.  How do EFA’s help?             Here is a list:

• They alter neuronal fluidity by displacing cholesterol from neural membranes;
• Influence the function of membrane receptors, modifying dopaminergic and serotonergic neurotransmission;
• They decrease monoamine-oxidase B activity;
• Regulate membrane-bound enzymes (Na/K-dependent ATPase) which decreases energy consumption requirements in the brain;
• Modulate glucose uptake;
• Increase dendritic arborization (outgrowth) and synapse formation, decrease neuronal apoptosis;
• They compete with Arachnodenritic Acid (the product of Omega-6s, see above) for enzymatic action generating an anti-inflammatory response;
• Lower plasma DHA at baseline predicts greater risk of future suicide attempts;
• Controlled double-blind pilot study in childhood depression: 600 mg EFAs, ages 8-12.5.  Depression rating scales significantly improved in treatment vs placebo;
• Deliberate self-harm 50 % reduction in depression, 35 % reduction in suicidal thinking; 33% reduction in perception of stress; 30% improvement in “happiness”.

Teacher-rated ADHD symptoms (blind): substantial changes in every measure including also Social Problems, Perfectionism, and Opposition.

Recommendations

Everyone’s diet should include Omega-3 Essential Fatty Acid supplements.  Fish Oils are better than vegetable sources because of the inflammatory effects of Omega-6s. Fancy products like krill oil are unnecessary and may lead to depletion of this important ocean resource.  A study of few years ago in Consumer Reports demonstrated that all products on the market were free of toxic substances. It is important that Fish Oils be relatively fresh and not oxidized.  3-4 grams daily seems  best for cognitive /memory performance and mood/behavior/focus issues; for genera health (brain and heart) 2-4 gm/day.

The ratio of Omega-3s to overall fatty acids can be easily measured with the  Omega-3 Index: a measure of the amt of EPA +DHA in red blood cell membranes expressed as the percent of total fatty acids.  There are 64 fatty acids in this model membrane, 3 of which are EPA or DHA.  The correlation between Executive Function of the Omega-3 Index has been established.  The procedure is a simple finger stick to produce a drop of blood which is placed on blotter paper and mailed to the lab.  Omega-3 in red blood cell tissue reflects levels of omega-3 fatty acids in the brain.

I offer the Omega-3 Index in my office at no markup.  The lab currently charges me $90 for each test and the patient is billed $90.  I also offer Essential Fatty Acids at wholesale cost from the Life Extension Foundation, and pass that exact cost on to the patient (because there is no profit, it is also exempt from California sales tax).

Note, a new study from UCLA announced today has demonstrated that the level of Omega-3 DHA in red blood cells indeed correlates with brain volume and memory in older men and women.

The February 28, 2012 edition of the journal Neurology® reports a beneficial effect for higher red blood cell membrane levels of docosahexaenoic acid (DHA, an omega 3 fatty acid) on brain volume and memory in older men and women. “To our knowledge, no prior study has related red blood cell fatty acid composition to subclinical markers of future dementia,” the authors note in their introduction to the article.

For their research, Zaldy S. Tan, MD, MPH, of the Easton Center for Alzheimer’s Disease Research and the Division of Geriatrics at the University of California at Los Angeles and colleagues measured red blood cell omega-3 fatty acid levels in 1,575 dementia-free subjects with an average age of 67. Magnetic resonance imaging (MRI) assessed brain volume, and cognitive tests evaluated various aspects of memory and mental function.

Dr Tan’s team found a reduction in total cerebral brain volume, visual memory, executive function (which includes organizing and multi-tasking) and abstract thinking, among those whose DHA intake was among the lowest 25 percent of participants compared to those whose intake was higher. “People with lower blood levels of omega-3 fatty acids had lower brain volumes that were equivalent to about two years of structural brain aging,” Dr Tan observed.

Participants in the lowest 25 percent of DHA also had greater white matter intensity volume, which is increased in small vessel disease and has been associated with an increased risk of stroke and dementia. The authors remark that DHA lowers blood pressure, reduces the risk of clots and decreases serum triglyceride levels, all of which benefit the vascular system and may help delay the onset of brain aging.

“Lower red blood cell DHA levels are associated with smaller brain volumes and a ‘vascular’ pattern of cognitive impairment even in persons free of clinical dementia,” the authors conclude. “The association between lower red blood cell omega-3 fatty acid levels and markers of accelerated cognitive and structural brain aging observed here should be confirmed in other populations and extended in the future to include dementia outcomes.”  This news courtesy of Life Extension Bulletin, 2/28/12.

Further Reading: The Omega-3 Connection by Andrew Stoll MD may be the most useful book currently available.  It was published in 2002.  In August 2012, William Sears MD will bring out The Omega-3 Effect.

Notions of brain plasticity are no longer new. The marvelous book The Mind and the Brain by Jeffrey Schwartz and Sharon Begley came out a decade ago, in 2002.  Norman Doidge extended that study with his excellent 2007 The Mind That Changes Itself. Psychologist Alison Gopnik recently wrote the following article for the Wall St. Journal.   In the article, she advances the elegant notion that balance of power in the modern teenage brain has shifted to a slower development of the pre-frontal cortex because of a cultural shift away from an apprenticeship mindset. Take a look at the article.  I have highlighted some points of special interest with color and boldface type.–Thomas M. Brod, MD

What’s Wrong with the Teenage Mind? By Alison Gopnik from the Wall Street Journal January 28, 2012.

“What was he thinking?” It’s the familiar cry of bewildered parents trying to understand why their teenagers act the way they do. How does the boy who can thoughtfully explain the reasons never to drink and drive end up in a drunken crash? Why does the girl who knows all about birth control find herself pregnant by a boy she doesn’t even like? What happened to the gifted, imaginative child who excelled through high school but then dropped out of college, drifted from job to job and now lives in his parents’ basement? Adolescence has always been troubled, but for reasons that are somewhat mysterious, puberty is now kicking in at an earlier and earlier age. A leading theory points to changes in energy balance as children eat more and move less.

At the same time, first with the industrial revolution and then even more dramatically with the information revolution, children have come to take on adult roles later and later. Five hundred years ago, Shakespeare knew that the emotionally intense combination of teenage sexuality and peer-induced risk could be tragic—witness “Romeo and Juliet.” But, on the other hand, if not for fate, 13-year-old Juliet would have become a wife and mother within a year or two.

Our Juliets (as parents longing for grandchildren will recognize with a sigh) may experience the tumult of love for 20 years before they settle down into motherhood. And our Romeos may be poetic lunatics under the influence of Queen Mab until they are well into graduate school.

What happens when children reach puberty earlier and adulthood later? The answer is: a good deal of teenage weirdness. Fortunately, developmental psychologists and neuroscientists are starting to explain the foundations of that weirdness. The crucial new idea is that there are two different neural and psychological systems that interact to turn children into adults. Over the past two centuries, and even more over the past generation, the developmental timing of these two systems has changed. That, in turn, has profoundly changed adolescence and produced new kinds of adolescent woe. The big question for anyone who deals with young people today is how we can go about bringing these cogs of the teenage mind into sync once again.

The first of these systems has to do with emotion and motivation. It is very closely linked to the biological and chemical changes of puberty and involves the areas of the brain that respond to rewards. This is the system that turns placid 10-year-olds into restless, exuberant, emotionally intense teenagers, desperate to attain every goal, fulfill every desire and experience every sensation. Later, it turns them back into relatively placid adults.

Recent studies in the neuroscientist B.J. Casey’s lab at Cornell University suggest that adolescents aren’t reckless because they underestimate risks, but because they overestimate rewards—or, rather, find rewards more rewarding than adults do. The reward centers of the adolescent brain are much more active than those of either children or adults. Think about the incomparable intensity of first love, the never-to-be-recaptured glory of the high-school basketball championship.

What teenagers want most of all are social rewards, especially the respect of their peers. In a recent study by the developmental psychologist Laurence Steinberg at Temple University, teenagers did a simulated high-risk driving task while they were lying in an fMRI brain-imaging machine. The reward system of their brains lighted up much more when they thought another teenager was watching what they did—and they took more risks.

From an evolutionary point of view, this all makes perfect sense. One of the most distinctive evolutionary features of human beings is our unusually long, protected childhood. Human children depend on adults for much longer than those of any other primate. That long protected period also allows us to learn much more than any other animal. But eventually, we have to leave the safe bubble of family life, take what we learned as children and apply it to the real adult world. Becoming an adult means leaving the world of your parents and starting to make your way toward the future that you will share with your peers. Puberty not only turns on the motivational and emotional system with new force, it also turns it away from the family and toward the world of equals.

The second crucial system in our brains has to do with control; it channels and harnesses all that seething energy. In particular, the prefrontal cortex reaches out to guide other parts of the brain, including the parts that govern motivation and emotion. This is the system that inhibits impulses and guides decision-making, that encourages long-term planning and delays gratification.

This control system depends much more on learning. It becomes increasingly effective throughout childhood and continues to develop during adolescence and adulthood, as we gain more experience. You come to make better decisions by making not-so-good decisions and then correcting them. You get to be a good planner by making plans, implementing them and seeing the results again and again. Expertise comes with experience. As the old joke has it, the answer to the tourist’s question “How do you get to Carnegie Hall?” is “Practice, practice, practice.”

In the distant (and even the not-so-distant) historical past, these systems of motivation and control were largely in sync. In gatherer-hunter and farming societies, childhood education involves formal and informal apprenticeship. Children have lots of chances to practice the skills that they need to accomplish their goals as adults, and so to become expert planners and actors. The cultural psychologist Barbara Rogoff studied this kind of informal education in a Guatemalan Indian society, where she found that apprenticeship allowed even young children to become adept at difficult and dangerous tasks like using a machete. In the past, to become a good gatherer or hunter, cook or caregiver, you would actually practice gathering, hunting, cooking and taking care of children all through middle childhood and early adolescence—tuning up just the prefrontal wiring you’d need as an adult. But you’d do all that under expert adult supervision and in the protected world of childhood, where the impact of your inevitable failures would be blunted. When the motivational juice of puberty arrived, you’d be ready to go after the real rewards, in the world outside, with new intensity and exuberance, but you’d also have the skill and control to do it effectively and reasonably safely. In contemporary life, the relationship between these two systems has changed dramatically. Puberty arrives earlier, and the motivational system kicks in earlier too. At the same time, contemporary children have very little experience with the kinds of tasks that they’ll have to perform as grown-ups. Children have increasingly little chance to practice even basic skills like cooking and caregiving. Contemporary adolescents and pre-adolescents often don’t do much of anything except go to school. Even the paper route and the baby-sitting job have largely disappeared. The experience of trying to achieve a real goal in real time in the real world is increasingly delayed, and the growth of the control system depends on just those experiences. The pediatrician and developmental psychologist Ronald Dahl at the University of California, Berkeley, has a good metaphor for the result: Today’s adolescents develop an accelerator a long time before they can steer and brake.

This doesn’t mean that adolescents are stupider than they used to be. In many ways, they are much smarter. An ever longer protected period of immaturity and dependence—a childhood that extends through college—means that young humans can learn more than ever before. There is strong evidence that IQ has increased dramatically as more children spend more time in school, and there is even some evidence that higher IQ is correlated with delayed frontal lobe development.

All that school means that children know more about more different subjects than they ever did in the days of apprenticeships. Becoming a really expert cook doesn’t tell you about the nature of heat or the chemical composition of salt—the sorts of things you learn in school.

But there are different ways of being smart. Knowing physics and chemistry is no help with a soufflé. Wide-ranging, flexible and broad learning, the kind we encourage in high-school and college, may actually be in tension with the ability to develop finely-honed, controlled, focused expertise in a particular skill, the kind of learning that once routinely took place in human societies. For most of our history, children have started their internships when they were seven, not 27.

The old have always complained about the young, of course. But this new explanation based on developmental timing elegantly accounts for the paradoxes of our particular crop of adolescents.

There do seem to be many young adults who are enormously smart and knowledgeable but directionless, who are enthusiastic and exuberant but unable to commit to a particular kind of work or a particular love until well into their 20s or 30s. And there is the graver case of children who are faced with the uncompromising reality of the drive for sex, power and respect, without the expertise and impulse control it takes to ward off unwanted pregnancy or violence.

This new explanation also illustrates two really important and often overlooked facts about the mind and brain. First, experience shapes the brain. People often think that if some ability is located in a particular part of the brain, that must mean that it’s “hard-wired” and inflexible. But, in fact, the brain is so powerful precisely because it is so sensitive to experience. It’s as true to say that our experience of controlling our impulses make the prefrontal cortex develop as it is to say that prefrontal development makes us better at controlling our impulses. Our social and cultural life shapes our biology.

Second, development plays a crucial role in explaining human nature. The old “evolutionary psychology” picture was that genes were directly responsible for some particular pattern of adult behavior—a “module.” In fact, there is more and more evidence that genes are just the first step in complex developmental sequences, cascades of interactions between organism and environment, and that those developmental processes shape the adult brain. Even small changes in developmental timing can lead to big changes in who we become.

Fortunately, these characteristics of the brain mean that dealing with modern adolescence is not as hopeless as it might sound. Though we aren’t likely to return to an agricultural life or to stop feeding our children well and sending them to school, the very flexibility of the developing brain points to solutions.

Brain research is often taken to mean that adolescents are really just defective adults—grown-ups with a missing part. Public policy debates about teenagers thus often turn on the question of when, exactly, certain areas of the brain develop, and so at what age children should be allowed to drive or marry or vote—or be held fully responsible for crimes. But the new view of the adolescent brain isn’t that the prefrontal lobes just fail to show up; it’s that they aren’t properly instructed and exercised.

Simply increasing the driving age by a year or two doesn’t have much influence on the accident rate, for example. What does make a difference is having a graduated system in which teenagers slowly acquire both more skill and more freedom—a driving apprenticeship.

Instead of simply giving adolescents more and more school experiences—those extra hours of after-school classes and homework—we could try to arrange more opportunities for apprenticeship. AmeriCorps, the federal community-service program for youth, is an excellent example, since it provides both challenging real-life experiences and a degree of protection and supervision.

“Take your child to work” could become a routine practice rather than a single-day annual event, and college students could spend more time watching and helping scientists and scholars at work rather than just listening to their lectures. Summer enrichment activities like camp and travel, now so common for children whose parents have means, might be usefully alternated with summer jobs, with real responsibilities.

The good news, in short, is that we don’t have to just accept the developmental patterns of adolescent brains. We can actually shape and change them.

—Ms. Gopnik is a professor of psychology at the University of California, Berkeley, and the author, most recently, of “The Philosophical Baby: What Children’s Minds Tell Us About Truth, Love and the Meaning of Life.” Adapted from an essay that she wrote for www.edge.org in response to the website’s 2012 annual question: “What is your favorite deep, elegant or beautiful explanation?”

I asked Bill Scott, who was working out of my office at the time, if he was willing to join me in this project.  It happened that he was using a new protocol that can look at  EEG frequencies in a very precise way and was eager to demonstrate its utility.  And so we met with the team from the History Channel’s Stan Lee’s Superhumans and mentalist Guy Bavli.  Bavli demonstrated a number of tricks which had me gasping–but I kept telling myself that he is a professional magician.  I did not expect what we found.

For the data collection, we chose one demonstration–moving a pen in a glass without touching it.  (You can see a video of a similar event on line.  The segment filmed in my office has not run yet, but should run soon and I will post a link when available).  For technical reasons, Bill took EEG data from the pre-frontal (forehead) areas on both sides.  Bill processed the data, and we took a look at it the following morning.

Bill and I were surprised to see an indication that when the pen moved there was a massive shift in the gamma region of the EEG–only on the left side.  Later, we analyzed the data more carefully and noted that at the same time there was even more elevation in the theta region of the EEG.  We believe that the gamma elevation is more impressive because, technically, these are much smaller wave forms that tend to rarely spike as high as we observed.

These are interesting findings which in no way prove that Guy Bavli moved the pen with mental force alone.  But we did demonstrate that there were very unusual EEG findings  occurring simultaneously with pen movement that we could not account for.   This seemed like something we should report to the scientific community for further study and validation.  I wrote up the findings and we presented a Poster at the International Society for Neurofeedback and Research this past September.  Below I have reproduced that poster and its content (below that).

ISNR 2011 "Telekinesis" EEG poster

Asymmetric Frontal Gamma & High Beta During a Telekinesis “Demonstration”

Thomas M. Brod, MD, DFAPA, Associate Clinical Professor of Psychiatry, Geffen UCLA School of  Medicine

William Scott, BS*

*Data acquisition and HHT processing.

Introduction

Abstract:

Early this year we had the opportunity to observe EEG function during a demonstration of “telekinesis” with EEG monitoring for The History Channel.* We observed that coincident with the mentalist apparently moving a pen in a glass without touch (but not under control conditions), there was a sharp rise in left frontal high beta and gamma activity with no corresponding rise on the right. These non-blind observations will not convince skeptics (including ourselves), but they do open a path for open-minded rigorous evaluation of the phenomena that were observed.

Methods

We acquired two channels of EEG from sites FP1 and FP2 with the BrainMaster Atlantis amplifier, comparing resting eyes open condition (watching his breath) to the condition where the mentalist apparently moved a pen telekinetically. We were not using a 60Hz notch filter. We hypothesized that if he was using an electromagnetic current to pick up and move the metal in the pen, we would see a very large 60Hz signal from both sensors.

We utilized the Hilbert-Huang transform (HHT), a new method to construct a sharp and clean time-frequency spectrum of a non-linear and non-stationary signal. Using empirical mode decomposition while retaining intra-wave modulation makes it very suitable for quantitative EEG analysis; also, HHT has excellent potential for clinical EEG neurofeedback.

* It is expected to run on The History Channel’s Stan Lee’s Superheroes.

We applied the HHT to both conditional data sets. We used Microsoft Excel to graph the time-frequency data.  The HHT is dynamic, working best on fast changing signals like gamma.  Another advantage to the HHT is that we do not need to arbitrarily pick a frequency range for each band,for example “Gamma = 38-43Hz.  Here, Gamma was 38-54 Hz.

Results

Baseline frequency bands (empirically derived, HHT) were highly symmetrical at faster frequencies

A post hoc analysis of the mentalist’s Hilbert-Huang Transform (HHT) data and revealed 8 distinct frequency bands (for clarity we have not shown the three lowest bands).  The range of each band was obtained by taking the median + and – ½ the standard deviation frequency at each point in the wave.

Frequency Analysis "Telekinesis Demonstration"

This is the control condition where the mentalist was watching his breath. We are graphing Gamma amplitude (intensity) against time.

“Mentally” moving the pen seems to correlate with Left Frontal activation.

Here we see the Gamma frequencies deviating both times the pen moved (lift and drop back). The observed  pen began to move and lift at sample period 5,753 and dropped back into the  glass at 13,521.  Observe the left/right asymmetry.

High Beta increased the most of his frequencies. His high beta did not change dramatically when the pen dropped into the glass, but left/right asymmetry persisted.

Here we see some Theta increasing at point 5345 which proceeds the bursts of high beta and gamma.

Conclusions

These data have documented an asymmetrical change in brainwave function of the mentalist as he appeared to move a pen into a glass without touching it. Artifacts from an electromagnetic generator or from physical movement should have shown up equally in both the left and right EEG channels.

Additional Literature  FYI

Barnhofer T, Chitka T et al.(2010) State Effects of Two Forms of Meditation on Prefrontal EEG Asymmetry in Previously Depressed Individuals. Mindfulness 1(1):21-27.

Bengstron, WF (2007) A method used to train skeptical volunteers to heal in an experimental setting, Journal of Alternative and Complementary medicine, 13, 329-331.

Bengstron, WF, & Moga M (2007) Resonance, placebo effects, and Type II errors: some implications from healing research for experimental methods, Journal of Alternative and Complementary medicine, 13, 317-327.

Berkman ET. Lieberman MD (2010) Approaching the band and avoiding the good: lateral prefrontal cortical asymmetry distinguishes between action and valence. J Cogn Neurosci. Sep 22(9):1970-9

Buzsaki G (2006) Rhythms of the Brain. Oxford University Press

Chia-Lung Y, Hsiang-Chih C, et al (2010) Extraction of single-trial cortical beta oscillatory activities in EEG signals using empirical mode decomposition, BioMedical Engineering OnLine 9-25.

Davidson RJ. (2004) What does the prefrontal cortex “do” in affect: perspectiveson frontal EEG asymmetry research. Biol Psychol. 67(1-2):219-33.

Hendricks L, Bengston WF, Gunkelman J (2010) The Healing Connection: EEG harmonics, Entrianment, and Schumann’s Resonances, Journal of Scientific Exploration 24:4 655-66.

Leder D (2005),“Spooky Actions at a Distance”: physics, psi, and distant healing. J Altern Complemen Med, Oct;11(5):923-30

Lutz A, Slagter HA, Rawlings NB, Francis AD, Greischar LL, Davidson RJ, (2009) Mental Training enhances attentional stability, Jneurosci. 29(42): 13418-27

Lutz A, Greischar LL Rawlings NB, Davidson RJ, (2004) Long-term meditators self-induce gamma synchrony during mental practice. Proc Natl Acad Sci USA 101(46):16369-73

Petrantonakis PC & Hadjiileontiadis LJ (2010) Emotion recognition from EEG using higher order crossings, IEEE Trans Inf Techol Biomed 14:2, 186-97

Schlitz M, Radin D, et al (2003) Distant healing intention: definitions and evolving guidelines for laboratory studies, Altern Ther Health Med, May-Jun;9(3 Suppl):A31-43.

Shagter HA, Davidson RJ, Lutz A (2011), Mental training as a tool in the neuroscientific study of brain and cognitive plasticity, Front Hum Neurosci 5:17.

With this post I initiate a series on unwanted effects of psychiatric drugs and how EEG neurofeedback can sometimes be used as an alternative or to minimize dosage.  Psychiatric News (from the American Psychiatric Association) reports new information about SSRIs and autism spectrum disorder may alarm women who are—or plan to become—pregnant, but researchers caution that results are preliminary and further study is needed .  The risk may be small, but should now be taken seriously.  We do not know the risks to the fetus of neurofeedback but there is no evidence whatsoever of teratogenic effects and no theoretical basis to be concerned.  Some of my biofeedback-oriented colleagues have argued that if we do not know the degree of risk, we should not offer neurofeedback.  My present opinion is that the developmental risks of medication in pregnancy, especially in the first trimester, are significant and we know that neurofeedback can often reduce or eliminate the symptoms of depression and unstable mood–so EEG neurofeedback is an important option for a woman to consider when she is planning to get pregnant.

My colleague at UCLA Victoria Hendrik was one of the authors of the study published online on July 4 by the Archives of General Psychiatry.  Here is that story by Leslie Sinclair from Psychiatric News (http://pn.psychiatryonline.org/content/46/15/1.2.full August 5, 2011).

Exposure to selective serotonin reuptake inhibitors (SSRIs), especially during the first trimester of pregnancy, may modestly increase the risk of a child developing an autism spectrum disorder (ASD).

That’s the finding of a group of California-based researchers who recently performed a retrospective, population-based case-control study of 298 children with ASDs and their mothers and compared them with 1,507 randomly selected control children and their mothers. The study population was drawn from the membership of the Kaiser Permanente Medical Care Program in Northern California.

The research team, composed of members from Kaiser Permanente of Northern California, the Environmental Health Investigations Branch of the California Department of Public Health, and the Neuropsychiatric Institute and Hospital at the University of California at Los Angeles, sought to systematically evaluate whether prenatal exposure to antidepressant medications is associated with increased risk of ASD.

In their study group, 20 of the ASD-diagnosed children and 50 of the control children had a history of prenatal exposure to antidepressant medications. Statistical analysis determined there to be a twofold increased risk of ASD associated with treatment with SSRIs of the mother during the year before delivery, with the strongest effect associated with treatment during the first trimester. No increase in risk was found for children of mothers who had a history of mental illness treatment in the absence of prenatal exposure to SSRIs.

Lisa Croen, Ph.D., director of the Kaiser Permanente Autism Research Program and lead author of the study, and colleagues were careful to couch their findings in cautionary terms, lest readers jump too quickly to the conclusion that pregnant women should be denied SSRIs because of risk to the fetus. “The potential risk associated with exposure must be balanced with the risk to the mother or fetus of untreated mental health disorders,” they said. “Further studies are needed to replicate and extend these findings.”

Pat Levitt, Ph.D., director of the Zilkha Neurogenetic Institute at the Keck School of Medicine at the University of Southern California, discussed the findings—and their limitations reported by the study authors—in an editorial accompanying the publication: “Before embracing this as the newest causal factor … the authors are careful to point out in a lengthy discussion the many caveats in their findings. They recognize that, given the history of [purported links between] ASD and environmental factors (immunizations, mercury), this type of report is likely to be overinterpreted by professionals and the public alike.”

Levitt agreed that the neurobiological explanation for the findings of Croen and colleagues makes sense. “Perhaps it is a coincidence that the odds ratio for ASD risk in the study … increases when first-trimester exposure to SSRIs is the sole factor. However, it is exactly that time of human brain development during which cortical and subcortical neuronal populations are being produced, migrating to their final destinations and beginning the long process of wiring. While much occurs later, the establishment of a strong foundation developmentally may be an essential component of healthy brain development.”

A couple of reports in Science News this week pick up on stories we have been following.  The first is a “backgrounder” on hyeractivity and food additives; the second illuminates one of the murky patterns of genetic transmission, heredibility of gene variants in ADHD and autistic spectrum not seen in other psychiatric disorders.

A very good review on food additives and hyperactivity is fine science reporting prompted by regulatory deliberations, but doesn’t bring any news beyond what I reviewed in my blog of Oct 16, 2010:

The second report moves our knowledge of the genetics of ADHD and Autism Spectrum disorders another step of depth (See blogs of June 12 ’11 and November 21 ’10).  Tina Hesman Saey discusses the issue of “copy variants”, when duplicate or missing copies of certain genes correlate with clinical conditions.  I will quote a portion of her article:

Up to 75 percent of people with autism spectrum disorders also have symptoms of ADHD, but researchers did not know if the genetic causes were the same as in people who have ADHD alone. Previous research has shown that people with autism or schizophrenia often have genes that are missing or duplicated more often than normal. Such added or subtracted genes are known as copy number variants. Healthy people may have extra copies of several genes or lack some entirely, but missing or doubling up on certain genes can lead to disease.

Unlike people with schizophrenia or autism, people with ADHD are no more likely than average to have missing or copied genes, the researchers report in the Aug. 10 Science Translational Medicine. But about 8 percent of people with ADHD have rare copy number variants that may cause or contribute to the disorder. A subset of those genes are perturbed both in people with ADHD and in people with autism spectrum disorders, indicating that the disorders may have some common genetic causes.

An examination of DNA from parents of 173 of the children in the new study showed that copy number variants associated with ADHD are often inherited from a parent who also often has the disorder. That differs from autism and schizophrenia, where the genes associated with the condition are often newly deleted or duplicated in the child with the disorder, not passed down from parents.

More copy number variants and other types of genetic changes remain to be uncovered, scientists say. Many different brain processes are probably involved in the disorders, and disrupting any of them could produce similar outcomes, Elia says. “We may end up having thousands of variants and not just a handful,” she says.

 

A brief comment on nomenclature: ADHD is the current term (Attention Deficit/Hyperactivity Disorder) in the current version of the psychiatric diagnostic manual and it covers both inattentive and hyperactive types of Attention Deficit Disorder, which in a former version was known as ADD.  In the proposed upcoming revision, now being field tested (I will be one of those psychiatrists testing the new diagnostic manual), subtypes have been eliminated, age of onset is raised from 7 years old to ”on or before age 12,”  and the number of criteria required for diagnosis has been lowered for adults (The proposed change would account for recent findings that indicate a decline in symptoms as a patient ages. “Follow-up studies of children who had ADHD show that as they grow older they have fewer and fewer symptoms but they remain impaired,” said one of the developers of the new DSM-5).

…And recent studies of Autism show similar trends.

Some really good science writing showed up this week in response to a publication of three papers in the June 9 Neuron on specific genetic changes in autism.  I commend Laura Sanders’ piece in Science News (June 8 web edition) . That link may not be available to non-subscribers, so I will offer highlights (I have deleted some phrases and added boldface emphasis). Below that, I have posted a round-up for psychiatrists from the American Psychiatric Association on genetic variability involved in the autism spectrum.  For the backstory on the genetics of autism including the details of genetic variation, I have placed, at the bottom of this review, a succinct  and valuable review by Laura Sanders from an upcoming Science News article.

New genetic data illustrate why researchers have struggled to find a single cause for the baffling suite of developmental and behavioral conditions, and may help point the way to a unifying process underlying them. The studies also begin to explain why autism spectrum disorders are more common in boys than girls.

Though the specific genetic changes identified account for only 5 to 8 percent of autism cases, what they reveal about the biology of autism may have much wider implications.

Two of the studies examined DNA samples taken from carefully screened families. Each family included two unaffected parents and one high-functioning child diagnosed with autism spectrum disorder. For most families, an unaffected sibling was also included. By studying genetic changes in unaffected family members, the researchers could find abnormalities that were not passed down from parents but arose spontaneously in the genomes of affected children.

“What was surprising is how unique each of the variants is,” says geneticist Huda Zoghbi of Baylor College of Medicine in Houston. “This really speaks to the immense heterogeneity of autism. We suspected it, but these data show it clearly.”

The results may also help explain why autism spectrum disorders are much more common in boys. Autism strikes four boys for every girl, yet girls’ DNA actually harbors more of these rare autism-associated genome duplications and deletions. And these genetic anomalies aren’t just more abundant in girls; they are also more severe. For a girl with autism, the median number of genes scrambled by duplication or wiped out by a deletion was 15.5, while for a boy with autism, the number was just two.

Through some mysterious process, girls are just more resistant than boys to the genetic causes of autism, the results suggest. “Overall, it does look like a girl can have the same genetic insult as a boy, but not be diagnosed with autism,” Wigler says.

The scientists can’t explain why girls might be more protected. Some researchers have proposed that sex hormones or some unidentified effects of genes on the X chromosome may play a role. Boys have only one copy of the X chromosome, so a genetic aberration there may be particularly dangerous for them.

The Los Angeles Times (6/9, Roan) reports, “Autism is not caused by one or two gene defects, but probably by hundreds of different mutations, many of which arise spontaneously, according to research that examined the genetic underpinnings of the disorder in more than 1,000 families.” The results of “three studies published Wednesday in the journal Neuron cast autism disorders as genetically very complex, involving many potential changes in DNA that may produce, essentially, different forms of autism.” Interestingly, the genes affected “appear to be part of a large network involved in controlling the development of synapses, the critical junctions between nerve cells that allow them to communicate, according to one of the three studies.”

A second analysis “identified at least 250 to 300 variations that appeared to be associated with the condition,” the Washington Post(6/8, Stein) “The Checkup” blog reported. “The mutations appeared much more likely to cause autism in males than in females.” Meanwhile, the third study discovered “an association between mutations and autism that, when deleted, also play a role in Williams syndrome, a rare developmental disorder. People with that condition tend to be highly social, sensitive and empathetic.”

HealthDay (6/8, Goodwin) reported, “Everyone carries a certain number of duplications or deletions of one or more sections of DNA, something known as copy number variants, explained Dr. Christian Schaaf, an assistant professor in the department of molecular and human genetics at the Baylor College of Medicine, who wrote an accompanying editorial.” He explained that if people “accumulate enough of them, and the duplications and deletions occur on certain important areas of the chromosomes, those variants may lead to autism and other conditions.” What’s more, two of the studies suggest that “girls may be more resistant to the spontaneous genetic mishaps that explain some cases of autism in families with no history of the disorder.”

WebMD (6/8, Doheny) reported, “Andy Shih, PhD, vice president of scientific affairs for Autism Speaks, an advocacy and research organization,” commented on the studies, saying that the results confirm that “it’s still impossible to explain the majority of cases of autism.” Shih pointed out that “sporadic mutations appear to play more of a role in families with just one child affected.” Over time, however, “the genetic findings could be useful information during genetic counseling in families who have one affected child, he says.”

____________________________________________________________

Backstory: The Genetic Puzzle By Laura Sanders 

Science News June 18th, 2011; Vol.179 #13 (p. 5)

Autism spectrum disorders are highly heritable, but like many complex disorders they can’t be pinned to a single genetic flaw. Though many genetic changes have been associated with the disorder (the locations of some are shown here on the human chromosomes), each one accounts for only a small fraction of cases.

Chromosome 5

Several single-letter DNA changes at one end of chromosome 5 (orange line) have been associated with autism, but each of these variations appears to contribute only a very small amount to a person’s risk of developing autism.

Chromosome 7

By studying inheritance patterns in families with autistic members, scientists have found a region of chromosome 7 (orange line) that appears to be relevant to the condition. Genes that tell nerve cells how to hook up with each other as the brain grows are located here.

Chromosome 15

About 1 percent of people with autism have duplications of a stretch of chromosome 15 (orange line). Large-scale duplications, deletions and re­arrangements in other parts of the genome have also been linked to autism.

Chromosome 22

Mutations in a gene at one end of chromosome 22 (orange line) that is involved in nerve cell communication, SHANK3, are linked to some cases of one nonverbal form of autism. These mutations seem to arise spontaneously rather than being inherited.

Below I have posted a round up of stories on the recent news  from WHO on the increased risk of gliomas tied to heavy cell phone use.

This issue is obviously still completely unsettled.

As I have written before, I have no doubt about the effect of low energy electro-magnetic  (E-M) radiation on the human brain since we have such powerful results using infinitesimal E-M as a carrier for our LENS treatment.  We just don’t know how powerful are those cell phone effects, or whether they are cancer-inducing in the glial cells that tend to transmission of neuronal information (glial cells present a fascinating topic on its own).

LENS is an acronym for Low Energy Neurofeedback System.  In a future post, I will write about some biological systems that are known to utilize extremely low level electromagnetic radiation.

Cell phones emit radiation 10s of thousands of times stronger than the carrier waves we use in LENS treatment for ADHD, closed head injuries, stroke rehabilitation, anxiety, OCD, autism, and many other neuro-psychiatric conditions.  Additionally, of course, we not  only use much less intense EM power, we only utilize it for a very brief time–from a few seconds to a few minutes of actual LENS neurofeedback in a typical 50 minute treatment session.

I follow it up with a short blog piece from psychiatrist Eitan D. Schwarz MD, who advocates some common sense caution, particularly for children…

International Panel Of Experts Categorizes Cell Phones As “Possibly Carcinogenic.”

ABC World News (5/31, lead story, 3:10, Sawyer) reported, “An important new alert about the safety of cell phones and the possible risk of cancer, brain cancer in particular…comes from the World Health Organization.” NBC Nightly News (5/31, lead story, 3:10, Williams) reported, the WHO “statement labeling cell phones as a possible carcinogenic hazard comes from a panel of 31 scientists.”

According to the AP (6/1, Cheng), the statement was “issued in Lyon, France, on Tuesday by the International Agency for Research on Cancer” (IARC) after a “weeklong meeting” during which experts reviewed “possible links between cancer and the type of electromagnetic radiation found in cellphones, microwaves and radar.” The IARC classified cellphones in “category 2B, meaning they are possibly carcinogenic” to humans. The assessment now “goes to WHO and national health agencies for possible guidance on cellphone use.”

The Wall Street Journal (6/1, Martin, Hobson, Subscription Publication) reports that the IARC working group did not conduct new research. Instead, the panel reviewed existing literature that focused on the health effects of radio frequency magnetic fields. Its findings are slated to be published July 1 in Lancet Oncology.

The New York Times (5/31, Parker-Pope, Barringer, Subscription Publication) “Well” blog noted that the panel’s decision to “classify cellphones as ‘possibly carcinogenic’ was based largely on epidemiological data showing an increased risk among heavy cellphone users of a rare type of brain tumor called a glioma.” Most “major medical groups,” including the National Cancer Institute, have “said the existing data on cellphones and health has been reassuring.” Earlier this year, the Journal of the American Medical Association “reported on research from the National Institutes of Health, which found that less than an hour of cellphone use can speed up brain activity in the area closest to the phone antenna.”

The Los Angeles Times (6/1, Roan, Gabler) reports that a 2010 study (pdf) published in the International Journal of Epidemiology found a “40% increase risk of gliomas for people who used a cellphone an average of 30 minutes a day over a 10-year period.”Bloomberg News (5/31, Kresge) and the CBS Evening News (5/31, lead story, 2:50, Smith) also covered the story.

Cellphones and living brains should probably not be placed too close to one another, according to a panel of World Health Organization experts. If the laws of physics hold, the threat is even greater to youngsters, whose skulls, separating their tender brains from the live microwave antenna at their ears, are thinner.

While this issue is controversial, why take a chance?

More broadly, but seemingly less sensational, a growing body of actual evidence about the explosive consumption of media dumbing down our kids, injuring family life and other relationships, and contributing to kids’ obesity is at least just as alarming and has actually been demonstrated in recent studies.

Bottom line: Just as parents must start instilling good cell-phone habits to try to prevent later brain cancer in their children, they should also stop giving unsupervised children access to the Internet, social media, videogames, smartphones, and tablets.

If you must give your child a cell phone, please keep it away from his ear. Encourage use at a distance through texting and using the loudspeaker and ear piece to lessen the risk of radiation damage. Similarly, and more importantly IMHO, introduce your child to tech devices thoughtfully and carefully, stay involved, and find ways to maximize the benefits of technology.

We acquire the EEG meticulously in our own office and send it for two-stage analysis to an international team of experts (Juri Kropotov PhD, Russian Academy of Sciences, and Jay Gunkelman, Q-Pro, USA); the results are interpreted and are usually back in less than one week.

Please see Services ->QEEG for instructions on preparing for a QEEG.

Recording of the QEEG involves placing an elastic cap on the head, with 19 sensors held in place on the scalp.Nothing goes into the skin of the scalp itself; a syringe is used to squirt a gel (electroconductive medium) into the holes in the cap, so it will be between the hair strands.

In addition, a clip on each earlobe provides a reference point for the brain activity.   Once the cap has been placed, each of the 19 sensors is checked to ensure that it has a good connection with the scalp. The electrical activity at each of the 19 scalp sites is then recorded and calculated by comparing it to the more electrically neutral earlobe.  Data on the electrical functioning of the brain is recorded simultaneously at each of the 19 sites. (In the picture above, Alan Alda wears the cap for his PBS TV show,Scientific American Frontiers.  Note, at EEGym, we do not normally put sensors on the face to record extra-ocular muscle movement).