Why is my awareness here, while yours is over there? Why is the universe split in two for each of us, into a subject and an infinity of objects? How is each of us our own center of experience, receiving information about the rest of the world out there? Why are some things conscious and others apparently not? Is a rat conscious? A gnat? A bacterium?
These questions are all aspects of the ancient “mind-body problem,” which asks, essentially: What is the relationship between mind and matter? It’s resisted a generally satisfying conclusion for thousands of years.
Chalmers thought the mind-body problem should be called “hard” in comparison to what, with tongue in cheek, he called the “easy” problems of neuroscience: How do neurons and the brain work at the physical level? Of course they’re not actually easy at all. But his point was that they’re relatively easy compared to the truly difficult problem of explaining how consciousness relates to matter.
Over the last decade, my colleague, University of California, Santa Barbara psychology professor Jonathan Schooler and I have developed what we call a “resonance theory of consciousness.” We suggest that resonance – another word for synchronized vibrations – is at the heart of not only human consciousness but also animal consciousness and of physical reality more generally. It sounds like something the hippies might have dreamed up – it’s all vibrations, man! – but stick with me.
All about the vibrations
All things in our universe are constantly in motion, vibrating. Even objects that appear to be stationary are in fact vibrating, oscillating, resonating, at various frequencies. Resonance is a type of motion, characterized by oscillation between two states. And ultimately all matter is just vibrations of various underlying fields. As such, at every scale, all of nature vibrates.
Something interesting happens when different vibrating things come together: They will often start, after a little while, to vibrate together at the same frequency. They “sync up,” sometimes in ways that can seem mysterious. This is described as the phenomenon of spontaneous self-organization.
When fireflies of certain species come together in large gatherings, they start flashing in sync, in ways that can still seem a little mystifying.
Lasers are produced when photons of the same power and frequency sync up.
The moon’s rotation is exactly synced with its orbit around the Earth such that we always see the same face.
Examining resonance leads to potentially deep insights about the nature of consciousness and about the universe more generally.
Sync inside your skull
Neuroscientists have identified sync in their research, too. Large-scale neuron firing occurs in human brains at measurable frequencies, with mammalian consciousness thought to be commonly associated with various kinds of neuronal sync.
Fries focuses on gamma, beta and theta waves. These labels refer to the speed of electrical oscillations in the brain, measured by electrodes placed on the outside of the skull. Groups of neurons produce these oscillations as they use electrochemical impulses to communicate with each other. It’s the speed and voltage of these signals that, when averaged, produce EEG waves that can be measured at signature cycles per second.
Gamma waves are associated with large-scale coordinated activities like perception, meditation or focused consciousness; beta with maximum brain activity or arousal; and theta with relaxation or daydreaming. These three wave types work together to produce, or at least facilitate, various types of human consciousness, according to Fries. But the exact relationship between electrical brain waves and consciousness is still very much up for debate.
Fries calls his concept “communication through coherence.” For him, it’s all about neuronal synchronization. Synchronization, in terms of shared electrical oscillation rates, allows for smooth communication between neurons and groups of neurons. Without this kind of synchronized coherence, inputs arrive at random phases of the neuron excitability cycle and are ineffective, or at least much less effective, in communication.
A resonance theory of consciousness
Our resonance theory builds upon the work of Fries and many others, with a broader approach that can help to explain not only human and mammalian consciousness, but also consciousness more broadly.
Based on the observed behavior of the entities that surround us, from electrons to atoms to molecules, to bacteria to mice, bats, rats, and on, we suggest that all things may be viewed as at least a little conscious. This sounds strange at first blush, but “panpsychism” – the view that all matter has some associated consciousness – is an increasingly accepted position with respect to the nature of consciousness.
The panpsychist argues that consciousness did not emerge at some point during evolution. Rather, it’s always associated with matter and vice versa – they’re two sides of the same coin. But the large majority of the mind associated with the various types of matter in our universe is extremely rudimentary. An electron or an atom, for example, enjoys just a tiny amount of consciousness. But as matter becomes more interconnected and rich, so does the mind, and vice versa, according to this way of thinking.
Biological organisms can quickly exchange information through various biophysical pathways, both electrical and electrochemical. Non-biological structures can only exchange information internally using heat/thermal pathways – much slower and far less rich in information in comparison. Living things leverage their speedier information flows into larger-scale consciousness than what would occur in similar-size things like boulders or piles of sand, for example. There’s much greater internal connection and thus far more “going on” in biological structures than in a boulder or a pile of sand.
Under our approach, boulders and piles of sand are “mere aggregates,” just collections of highly rudimentary conscious entities at the atomic or molecular level only. That’s in contrast to what happens in biological life forms where the combinations of these micro-conscious entities together create a higher level macro-conscious entity. For us, this combination process is the hallmark of biological life.
The central thesis of our approach is this: the particular linkages that allow for large-scale consciousness – like those humans and other mammals enjoy – result from a shared resonance among many smaller constituents. The speed of the resonant waves that are present is the limiting factor that determines the size of each conscious entity in each moment.
As a particular shared resonance expands to more and more constituents, the new conscious entity that results from this resonance and combination grows larger and more complex. So the shared resonance in a human brain that achieves gamma synchrony, for example, includes a far larger number of neurons and neuronal connections than is the case for beta or theta rhythms alone.
What about larger inter-organism resonance like the cloud of fireflies with their little lights flashing in sync? Researchers think their bioluminescent resonance arises due to internal biological oscillators that automatically result in each firefly syncing up with its neighbors.
Is this group of fireflies enjoying a higher level of group consciousness? Probably not, since we can explain the phenomenon without recourse to any intelligence or consciousness. But in biological structures with the right kind of information pathways and processing power, these tendencies toward self-organization can and often do produce larger-scale conscious entities.
Our resonance theory of consciousness attempts to provide a unified framework that includes neuroscience, as well as more fundamental questions of neurobiology and biophysics, and also the philosophy of mind. It gets to the heart of the differences that matter when it comes to consciousness and the evolution of physical systems.
It is all about vibrations, but it’s also about the type of vibrations and, most importantly, about shared vibrations.
In the U.S., an estimated 17.3 million American adults (7.1% of the adult population), experienced at least one major depressive episode in 2017.1 The highest rates are reported among those aged between 18 and 25.2 However, not only is there evidence that depression is vastly overdiagnosed, but there’s also evidence showing it’s routinely mistreated.
With regard to overdiagnosis, one 2013 study3 found only 38.4% of participants with clinician-identified depression actually met the DSM-4 criteria for a major depressive episode, and only 14.3% of seniors 65 and older met the criteria.
As for treatment, the vast majority are prescribed antidepressant drugs, despite the fact there’s virtually no evidence to suggest they provide meaningful help, and plenty of evidence showing the harms are greater than patients are being told.
According to a 2017 study,4 1 in 6 Americans between the ages of 18 and 85 were on psychiatric drugs, most of them antidepressants, and 84.3% reported long-term use (three years or more). Out of 242 million U.S. adults, 12% were found to have filled one or more prescriptions for an antidepressant, specifically, in 2013.
According to data5 presented by a watchdog group, hundreds of thousands of toddlers are also being medicated with powerful psychiatric drugs, raising serious ethical questions, along with questions about the future mental and physical health of these children.
Recent studies are also shedding much needed light on the addictive nature of many antidepressants, and demonstrate that the benefits of these drugs have been overblown while their side effects — including suicidal ideation — and have been downplayed and ignored for decades, placing patients at unnecessary risk.
The Chemical Imbalance Myth
One researcher responsible for raising awareness about these important mental health issues is professor Peter C. Gøtzsche, a Danish physician-researcher and outspoken critic of the drug industry (as his book, “Deadly Medicines and Organized Crime: How Big Pharma Has Corrupted Healthcare,”6 suggests).
Over the past several years, Gøtzsche has published a number of scientific papers on antidepressants and media articles and a book discussing the findings. In a June 28, 2019 article,7 Gøtzsche addresses “the harmful myth” about chemical imbalances — a debunked hypothesis that continues to drive the use of antidepressants to this day. He writes, in part:8
“Psychiatrists routinely tell their patients that they are ill because they have a chemical imbalance in the brain and they will receive a drug that fixes this …
Last summer, one of my researchers and I collected information about depression from 39 popular websites in 10 countries, and we found that 29 (74%) websites attributed depression to a chemical imbalance or claimed that antidepressants could fix or correct that imbalance …
It has never been possible to show that common mental disorders start with a chemical imbalance in the brain. The studies that have claimed this are all unreliable.9
A difference in dopamine levels, for example, between patients with schizophrenia and healthy people cannot tell us anything about what started the psychosis … [I]f a lion attacks us, we get terribly frightened and produce stress hormones, but this does not prove that it was the stress hormones that made us scared.
People with psychoses have often suffered traumatic experiences in the past, so we should see these traumas as contributing causal factors and not reduce suffering to some biochemical imbalance that, if it exists at all, is more likely to be the result of the psychosis rather than its cause.10
The myth about chemical imbalance is very harmful. It makes people believe there is something seriously wrong with them, and sometimes they are even told that it is hereditary.
The result of this is that patients continue to take harmful drugs, year after year, perhaps even for the entirety of their lives. They fear what would happen if they stopped, particularly when the psychiatrists have told them that their situation is like patients with diabetes needing insulin.”
Real Cause of Depression Is Typically Ignored
According to Gøtzsche, there is no known mental health issue that is caused by an imbalance of brain chemicals. In many cases, the true cause is unknown, but “very often, it is a response to unhealthy living conditions,” he writes.11
He also cites the book,12 “Anxiety — The Inside Story: How Biological Psychiatry Got It Wrong,” written by Dr. Niall McLaren, in which the author shows that anxiety is a major factor in and trigger of most psychiatric disorders.
“A psychiatrist I respect highly, who only uses psychiatric drugs in rare cases … has said that most people are depressed because they live depressing lives,” Gøtzsche writes.
“No drug can help them live better lives. It has never been shown in placebo-controlled trials that a psychiatric drug can improve people’s lives — e.g., help them return to work, improve their social relationships or performance at school, or prevent crime and delinquency. The drugs worsen people’s lives, at least in the long run.13“
Gøtzsche rightfully points out that antipsychotic drugs create chemical imbalances; they don’t fix them. As a group, they’re also somewhat misnamed, as they do not address psychotic states. Rather, they are tranquilizers, rendering the patient passive. However, calming the patient down does not actually help them heal the underlying trauma that, in many cases, is what triggered the psychosis in the first place.
As noted in one 2012 meta-analysis14 of studies looking at childhood trauma — including sexual abuse, physical abuse, emotional/psychological abuse, neglect, parental death and bullying — and subsequent risk of psychosis:
“There were significant associations between adversity and psychosis across all research designs … Patients with psychosis were 2.72 times more likely to have been exposed to childhood adversity than controls … The estimated population attributable risk was 33% (16%-47%). These findings indicate that childhood adversity is strongly associated with increased risk for psychosis.”
Economy of Influence in Psychiatry
A related article,15 written by investigative journalist Robert Whitaker in 2017, addresses the “economy of influence” driving the use of antidepressant drugs in psychiatric treatment — and the “social injury” that results. As noted by Whitaker, mental disorders were initially categorized according to a disease model in 1980 by the American Psychiatric Association.
“We’re all familiar with the second ‘economy of influence’ that has exerted a corrupting influence on psychiatry — pharmaceutical money — but I believe the guild influence is really the bigger problem,” he writes.
Whitaker details the corruption within the APA in his book “Psychiatry Under the Influence,” one facet of which is “the false story told to the public about drugs that fixed chemical imbalances in the brain.” Other forms of corrupt behavior include:
The biased designs of clinical trials to achieve a predetermined result
Spinning results to support preconceived conclusions
Hiding poor long-term outcomes
Expanding diagnostic categories for the purpose of commercial gain
Creating clinical trial guidelines that promote drug use
In his article, Whitaker goes on to dissect a 2017 review16 published in the American Journal of Psychiatry, which Whitaker claims “defends the profession’s current protocols for prescribing antipsychotics, which includes their regular long-term use.”
As Whitaker points out, there’s ample evidence showing antipsychotic drugs worsen outcomes over the long term in those diagnosed with psychotic disorders such as schizophrenia.
The review in question, led by Dr. Jeffrey A. Lieberman, was aimed at answering persistent questions raised by the mounting of such evidence. Alas, their conclusions dismissed concerns that the current drug paradigm might be doing more harm than good.
“In a subsequent press release and a video for a Medscape commentary, Lieberman has touted it as proving that antipsychotics provide a great benefit, psychiatry’s protocols are just fine, and that the critics are ‘nefarious’ individuals intent on doing harm,” Whitaker writes.17
The Scientific Bias of Psychiatric Treatment
Five of the eight researchers listed on the review have financial ties to drug companies, three are speakers for multiple drug companies and all eight are psychiatrists, “and thus there is a ‘guild’ interest present in this review, given that they are investigating whether one of their treatments is harmful over the long-term,” Whitaker notes.18
Not surprisingly, the review ignored studies showing negative effects, including studies showing antipsychotics have a detrimental effect on brain volume. What’s more, while withdrawal studies support the use of antipsychotics as maintenance therapy over the long term, these studies do not address how the drugs affect patients’ long-term health.
“They simply reveal that once a person has stabilized on the medication, going abruptly off the drug is likely to lead to relapse,” Whitaker writes.19 “The focus on long-term outcomes, at least as presented by critics, provides evidence that psychiatry should adopt a selective-use protocol.
If first-episode patients are not immediately put on antipsychotics, there is a significant percentage that will recover, and this ‘spontaneous recovery’ puts them onto a good long-term course. As for patients treated with the medications, the goal would be to minimize long-term use, as there is evidence that antipsychotics, on the whole, worsen long-term outcomes.”
Vast Majority of Psychotic Patients Are Harmed, Not Helped
In his deconstruction of Lieberman’s review, Whitaker details how biased thinking influenced the review’s conclusions. It’s a rather long article, but well worth reading through if you want to understand how a scientific review can be skewed to accord with a preconceived view.
Details I want to highlight, however, include findings relating to the number needed to treat (NNT) and the percentage of patients harmed by the routine use of antipsychotic drugs as a first-line treatment.
As noted by Whitaker, while placebo-controlled studies reveal the effectiveness of a drug compared to an inert substance, they do not effectively reveal the ratio of benefit versus harm among the patient population. NNT refers to the number of patients that have to take the drug in order to get one positive response.
A meta-analysis cited in Lieberman’s review had an NNT of 6, meaning that six patients must take the drug in order for one to benefit from the treatment. The remaining five patients — 83% — are potentially harmed by the treatment. As noted by Whitaker:20
“The point … is this: reviewers seeking to promote their drug treatment as effective will look solely at whether it produces a superior response to placebo. This leads to a one-size-fits-all protocol.
Reviewers that want to assess the benefit-harm effect of the treatment on all patients will look at NNT numbers. In this instance, the NNT calculations argue for selective use of the drugs …”
Antidepressants Are Not Beneficial in the Long Term
While typically not as destructive as antipsychotics, antidepressants also leave a trail of destruction in their wake. A systematic review21 by Gøtzsche published in 2019 found studies assessing harm from selective serotonin reuptake inhibitors (SSRIs) fail to provide a clear and accurate picture of the harms, and therefore “cannot be used to investigate persistent harms of antidepressants.”
In this review, Gøtzsche and colleagues sought to assess “harms of SSRIs … that persist after end of drug intake.” The primary outcomes included mortality, functional outcomes, quality of life and core psychiatric events. In all, 22 papers on 12 SSRI trials were included. Gøtzsche found several distinct problems with these trials. For starters, only two of the 12 trials had a drop-out rate below 20%.
Gøtzsche and his team also note that “Outcome reporting was less thorough during follow-up than for the intervention period and only two trials maintained the blind during follow-up.” Importantly, though, all of the 22 papers came to the conclusion that “the drugs were not beneficial in the long term.”
Another important finding was that all trials either “reported harms outcomes selectively or did not report any,” and “Only two trials reported on any of our primary outcomes (school attendance and number of heavy drinking days).”
Antidepressants Are More Addictive Than Admitted
In a June 4, 2019, article,22 “The Depression Pill Epidemic,” Gøtzsche writes that antidepressant drugs:
“… do not have relevant effects on depression; they increase the risk of suicide and violence; and they make it more difficult for patients to live normal lives.23 They should therefore be avoided.
We have been fooled by the drug industry, corrupt doctors on industry payroll, and by our drug regulators.24 Surely, many patients and doctors believe the pills are helpful, but they cannot know this, because people tend to become much better with time even if they are not treated.25
This is why we need placebo-controlled trials to find out what the drugs do to people. Unfortunately, virtually all trials are flawed, exaggerate the benefits of the drugs, and underestimate their harms.26“
Addictive Nature of Antidepressants Skews Results
In his article,27 Gøtzsche reviews several of the strategies used in antidepressant drug trials to exaggerate benefits and underestimate the harms. One little-known truth that helps skew study results in the drug’s favor is the fact that antidepressants tend to be far more addictive than officially admitted. He explains how this conveniently hides the skewing of results as follows:28
“Virtually all patients in the trials are already on a drug similar to the one being tested against placebo. Therefore, as the drugs are addictive, some of the patients will get abstinence symptoms … when randomized to placebo …
These abstinence symptoms are very similar to those patients experience when they try to stop benzodiazepines. It is no wonder that new drugs outperform the placebo in patients who have experienced harm as a result of cold turkey effects.
To find out how long patients need to continue taking drugs, so-called maintenance (withdrawal) studies have been carried out, but such studies also are compromised by cold turkey effects. Leading psychiatrists don’t understand this, or they pretend they don’t.
Most interpret the maintenance studies of depression pills to mean that these drugs are very effective at preventing new episodes of depression and that patients should therefore continue taking the drugs for years or even for life.”
Scientific Literature Supports Reality of User Complaints
Over the years, several studies on the dependence and withdrawal reactions associated with SSRIs and other psychiatric drugs have been published, including the following:
• In a 2011 paper29 in the journal Addiction, Gøtzsche and his team looked at the difference between dependence and withdrawal reactions by comparing benzodiazepines and SSRIs. Benzodiazepines are known to cause dependence, while SSRIs are said to not be addictive.
Despite such claims, Gøtzsche’s team found that “discontinuation symptoms were described with similar terms for benzodiazepines and SSRIs and were very similar for 37 of 42 identified symptoms described as withdrawal reactions,” which led them to conclude that:
“Withdrawal reactions to selective serotonin re‐uptake inhibitors appear to be similar to those for benzodiazepines; referring to these reactions as part of a dependence syndrome in the case of benzodiazepines, but not selective serotonin re‐uptake inhibitors, does not seem rational.”
• Two years later, in 2013, Gøtzsche’s team published a paper30 in the International Journal of Risk & Safety in Medicine, in which they analyzed “communications from drug agencies about benzodiazepine and SSRI withdrawal reactions over time.”
By searching the websites of drug agencies in Europe, the U.S., UK and Denmark, they found that it took years before drug regulators finally acknowledged the reality of benzodiazepine dependence and SSRI withdrawal reactions and began informing prescribers and patients about these risks.
A significant part of the problem, they found, is that drug agencies rely on spontaneous reporting of adverse effects, which “leads to underestimation and delayed information about the problems.”
In conclusion, they state that “Given the experience with the benzodiazepines, we believe the regulatory bodies should have required studies from the manufacturers that could have elucidated the dependence potential of the SSRIs before marketing authorization was granted.”
• A 2019 paper31 in the Epidemiology and Psychiatric Sciences journal notes “It took almost two decades after the SSRIs entered the market for the first systematic review to be published.” It also points out that reviews claiming withdrawal effects to be mild, brief in duration and rare “was at odds with the sparse but growing evidence base.”
In reality, “What the scientific literature reveals is in close agreement with the thousands of service user testimonies available online in large forums. It suggests that withdrawal reactions are quite common, that they may last from a few weeks to several months or even longer, and that they are often severe.”
Antidepressants Increase Your Risk of Suicide and Violence
In his June 4 article,32 Gøtzsche also stresses the fact that antidepressants can be lethal. In one of his studies,33 published in 2016, he found antidepressants “double the occurrence of events that can lead to suicide and violence in healthy adult volunteers.”
Other research34 has shown they “increase aggression in children and adolescents by a factor of 2 to 3 — an important finding considering the many school shootings where the killers were on depression pills,” Gøtzsche writes.
In middle-aged women with stress urinary incontinence, the selective serotonin and norepinephrine reuptake inhibitor (SNRI) duloxetine, which is also used to treat incontinence, has been shown to double the risk of a psychotic episode and increase the risk of violence and suicide four to five times,35 leading the authors to conclude that harms outweighed the benefits.
“I have described the dirty tricks and scientific dishonesty involved when drug companies and leading psychiatrists try convincing us that these drugs protect against suicide and other forms of violence,36“ Gøtzsche writes.37“Even the FDA was forced to give in when it admitted in 2007, at least indirectly, that depression pills can cause suicide and madness at any age.
There is no doubt that the massive use of depression pills is harmful. In all countries where this relationship has been examined, the sharp rise in disability pensions due to psychiatric disorders has coincided with the rise of psychiatric drug usage, and depression pills are those which are used the most by far. This is not what one would expect if the drugs were helpful.”
Drugmaker Lied About Paxil’s Suicide Risk
In 2017, Wendy Dolin was awarded $3 million by a jury in a lawsuit against GlaxoSmithKline, the maker of Paxil. Dolin’s husband committed suicide six days after taking his first dose of a Paxil generic, and evidence brought forth in the case convincingly showed his suicide was the result of the drug, not emotional stress or mental illness.38
The legal team behind that victory, Baum Hedlund Aristei Goldman, is also representing other victims of Paxil-induced violence and death. At the time, attorney R. Brent Wisner said:39
“The Dolin verdict sent a clear message to GSK and other drug manufacturers that hiding data and manipulating science will not be tolerated … If you create a drug and know that it poses serious risks, regardless of whether consumers use the brand name or generic version of that drug, you have a duty to warn.”
GSK’s own clinical placebo-controlled trials actually revealed subjects on Paxil had nearly nine times the risk of attempting or committing suicide than the placebo group. To gain drug approval, GSK misrepresented this shocking data, falsely reporting a higher number of suicide attempts in the placebo group and deleting some of the suicide attempts in the drug group.
An internal GSK analysis of its suicide data also showed that “patients taking Paxil were nearly seven times more likely to attempt suicide than those on placebo,” Baum Hedlund Aristei Goldman reports, adding:40
“Jurors in the Dolin trial also heard from psychiatrist David Healy, one of the world’s foremost experts on Paxil and drugs in its class … Healy told the jurors that Paxil and drugs like it can create in some people a state of extreme ’emotional turmoil’ and intense inner restlessness known as akathisia …
‘People have described it like a state worse than death. Death will be a blessed relief. I want to jump out of my skin,’ Dr. Healy said. Healthy volunteer studies have found that akathisia can happen even to people with no psychiatric condition who take the drug …
Another Paxil side effect known to increase the risk of suicide is emotional blunting … apathy or emotional indifference … [E]motional blunting, combined with akathisia, can lead to a mental state in which an individual has thoughts of harming themselves or others, but is ‘numbed’ to the consequences of their actions. Drugs in the Paxil class can also cause someone to ‘go psychotic, become delirious,’ Dr. Healy explained.”
Hundreds of Thousands of Toddlers on Psychiatric Drugs
Considering the many serious psychological and physical risks associated with psychiatric drugs, it’s shocking to learn that hundreds of thousands of American toddlers are on them. In 2014, the Citizens Commission on Human Rights, a mental health watchdog group, highlighted data showing that in 2013:41
274,000 babies aged 1 and younger were given psychiatric drugs — Of these, 249,699 were on anti-anxiety meds like Xanax; 26,406 were on antidepressants such as Prozac or Paxil, 1,422 were on ADHD drugs such as Ritalin and Adderall, and 654 were on antipsychotics such as Risperdal and Zyprexa
In the toddler category (2- to 3-year-olds), 318,997 were on anti-anxiety drugs, 46,102 were on antidepressants, 10,000 were prescribed ADHD drugs and 3,760 were on antipsychotics
Among children aged 5 and younger, 1,080,168 were on psychiatric drugs
These are shocking figures that challenge logic. How and why are so many children, babies even, on addictive and dangerously mind-altering medications? Considering these statistics are 6 years old, chances are they’re even higher today. Just what will happen to all of these youngsters as they grow up? As mentioned in the article:42
“When it comes to the psychiatric drugs used to treat ADHD, these are referred to as ‘kiddie cocaine’ for a reason. Ritalin (methylphenidate), Adderall (amphetamine) and Concerta are all considered by the federal government as Schedule II drugs — the most addictive.
ADHD drugs also have serious side effects such as agitation, mania, aggressive or hostile behavior, seizures, hallucinations, and even sudden death, according to the National Institutes of Health …
As far as antipsychotics, antianxiety drugs and antidepressants, the FDA and international drug regulatory agencies cite side effects including, but not limited to, psychosis, mania, suicidal ideation, heart attack, stroke, diabetes, and even sudden death.”
Children Increasingly Prescribed Psych Drugs Off-Label
Making matters even worse, recent research shows the number of children being prescribed medication off-label is also on the rise. An example offered by StudyFinds.org,43 which reported the findings, is “a doctor recommending antidepressant medication for ADHD symptoms.”
The study,44 published in the journal Pediatrics, looked at trends in off-label drug prescriptions made for children under the age of 18 by office-based physicians between 2006 and 2015. Findings revealed:
“Physicians ordered ≥1 off-label systemic drug at 18.5% of visits, usually (74.6%) because of unapproved conditions. Off-label ordering was most common proportionally in neonates (83%) and in absolute terms among adolescents (322 orders out of 1000 visits).
Off-label ordering was associated with female sex, subspecialists, polypharmacy, and chronic conditions. Rates and reasons for off-label orders varied considerably by age.
Relative and absolute rates of off-label orders rose over time. Among common classes, off-label orders for antihistamines and several psychotropics increased over time …
US office-based physicians have ordered systemic drugs off label for children at increasing rates, most often for unapproved conditions, despite recent efforts to increase evidence and drug approvals for children.”
The researchers were taken aback by the findings, and expressed serious concern over this trend. While legal, many of the drugs prescribed off-label have not been properly tested to ensure safety and efficacy for young children and adolescents.
As noted by senior author Daniel Horton, assistant professor of pediatrics and pediatric rheumatologist at Rutgers Robert Wood Johnson Medical School, “We don’t always understand how off-label medications will affect children, who don’t always respond to medications as adults do. They may not respond as desired to these drugs and could experience harmful effects.”
Educate Yourself About the Risks
If you, your child, or another family member is on a psychiatric drug, I urge you to educate yourself about the true risks, and to consider switching to safer alternatives. When it comes to children, I cannot fathom a situation in which a toddler would need a psychiatric drug and I find it shocking that there are so many doctors out there that, based on a subjective evaluation, would deem a psychiatric drug necessary.
Photograph Source: Luigi Novi / Wikimedia Commons – CC BY 3.0
Oliver Sacks, the “neurological philosopher”, did a “different sort of medicine on behalf of chronic often warehoused and largely abandoned patients.” It combined art and science. Lawrence Weschler, in How Are You, Dr. Sacks?, says Sacks was from “the period before the science and the humanities split apart”.[1]
But they didn’t just “split apart”. They were torn apart. Weschler doesn’t name the ideology responsible.
It didn’t convince everyone. Some saw through it, especially in the global South. Like Sacks, they wanted to know persons. Sacks had the “audacity to imagine that there might in fact be ongoing life persisting deep within those long-extinguished cores.” A nun at Little Sisters in the Bronx said: “Everyone who reads his [clinical] notes sees the patients differently …. Most consultants’ notes are cut and dried, aimed at the problem with no sense of the person …. With him the whole person becomes visible.”
European philosophers separated science and the humanities. They invented the “fact/value” distinction, between what is and what ought to be. They said knowledge of the latter doesn’t exist, or might not exist. Cuban scholar Armando Hart says anyone who cares about global justice in the 21st century should notice the damage done to the world by European philosophy. He meant liberalism. It denied truth – or at least put it in doubt – about humanness.
It made sense for those who defined humanness.
Sacks called himself a “clinical ontologist”. His science was about being, but not in the abstract. He meant the being of people, the “living statues” who were the subject of his masterpiece, Awakenings, later a film and a one-act play. He saw their stillness as active. Being as doing. Sacks responded to “philosophical emergencies”. It was part of his science.
There is an expectation in the North that Philosophy is useless, that it is at best a luxury for elite academics who live in universities and speak in complicated ways, only to each other. But Gramsci said that if you don’t understand the ideas explaining ideas, making them plausible, new ideas are ineffective because they are understood in terms of the old, mitigating their effect.
Weschler presents Sacks (affectionately) as odd without naming the ideology that makes him odd. Yet Sacks’ view was not odd.
Tolstoy knew it. Lenin commented that Tolstoy’s ideas were bourgeois but his writing revolutionary. It’s because artists, unlike philosophers, articulate the human condition. And human emancipation is impossible without knowing the human condition.
Tolstoy’s Pierre Bezukhov (War and Peace) reverses the popular myth of instrumental rationality. Pierre “did not wait, as before, for personal reasons, which he called people’s merits, in order to love them, but love overflowed his heart, and, loving people without reason, he discovered the unquestionable reasons for which it was worth loving them”.
Tolstoy calls it “insanity”. Pierre feels love, and as a result, has reasons. He doesn’t have purpose and from that get reasons. Indeed, he has no purpose. He has feeling, which Tolstoy describes as love. Pierre’s feelings explain what matters to him; it is not what matters to him – purpose – that explains his feelings: of energy, for instance, or importance.
In theory, Pierre’s approach is suspect. The 20th century philosopher, Che Guevara, said, “At the risk of seeming ridiculous, let me say that the true revolutionary is guided by great feelings of love”. The risk is real because love is not rational. Feelings are not rational. Love cannot guide because it is a feeling.
But this is ideology. And Guevara rejected it. He argued against the splitting of mind and body, feeling and intellect, art and science, faith and proof. Moreover, he followed a whole tradition of thinkers, not all revolutionaries, who also so argued. They wanted human, not just political, liberation, and they needed to know what “human” meant. They rejected liberalism because it didn’t make sense.
It doesn’t make sense, and this is known. But it persists because liberal intellectuals like Weschler don’t bother with philosophy. He admires Sacks, and names repeatedly the philosophers Sacks cared about. But he doesn’t do the work Gramsci said is essential to criticism: explaining the ideas that make other ideas plausible, even when they’re not, and it’s known.
It is significant that Pierre comes to his “insanity” after confronting death. He is a prisoner of Napoleon and is lined up to be executed. He watches the young man before him as he is shot dead. He notices how he crosses his leg as he stands, waiting to die. It is an ordinary gesture, but striking in the face of death, precisely for being ordinary.
Pierre expects to die. There’s no storytelling, no generating of meaning “from within” aimed at some abstraction called “self” or “purpose”. Herein lie what Tolstoy calls “unshakeable foundations”.
It’s mental silence: experience of the here and now, without expectations. A quiet mind is the exercise of one’s faculties – to see, hear, touch, smell, remember – without jarring, uncontrollable, mostly illogical mental conversation. Quietness fascinated Sacks.
He didn’t like Sartre’s “uncalmness”, his “chargedness”. Weschler mentions this but doesn’t explain. But we know Sacks didn’t like his own 1960s theory of behaviour because it didn’t account for “peacefulness, enoughness, satiety, repletion.” Sacks wouldn’t have liked Sartre because Sartre’s existentialism can’t handle stillness.
Liberal philosophy generally can’t handle it. It doesn’t fit with the liberal, capitalist “man of action”, the unrealistic individual with “power to seize their destiny”. Philosophers invented the “fact/value” distinction, suggesting knowledge about existence – what is – but not about what it means to be human.
It doesn’t respect science because it doesn’t respect cause and effect. But this is known, intellectually. It’s been argued for more than half a century in analytic philosophy of science. In practise, though, philosophy of science has no effect beyond its narrow specialization.
Sacks did have effect. His effect could be made more useful, though, if its real target were named and fully denounced.
We often hear about the power of gratitude for creating a more positive and happy mental state. But did you know that gratitude literally transforms your brain?
According to UCLA’s Mindfulness Awareness Research Center, regularly expressing gratitude literally changes the molecular structure of the brain, keeps the gray matter functioning, and makes us healthier and happier.
When you feel happiness, the central nervous system is affected. You are more peaceful, less reactive, and less resistant. And gratitude is the most effective practice for stimulating feelings of happiness.
In this article we’ll share some of the research demonstrating that gratitude makes you happier, followed by some practical steps you can take to positively transform the molecular structure of the brain.
Studies of gratitude making you happier
In one study of gratitude, conducted by Robert A. Emmons at the University of California at Davis and his colleague Mike McCullough at the University of Miami, randomly assigned participants were given one of three tasks. The participants kept a journal each week, with one group describing things they were grateful for, another describing what’s hassling them and the other keeping track of neutral events. After ten weeks, the participants in the gratitude group felt 25 percent better than the other groups, and had exercised an average of 1.5 hours more.
In a later study by Emmons with a similar set up, participants completing gratitude exercises each day offered other people in their lives more emotional support than those in other groups.
Another study on gratitude was conducted with adults suffering from congenital and adult-onset neuromuscular disorders (NMDs), with the majority of people having post-polio syndrome (PPS). Compared to those not jotting down what they’re grateful for every night, participants that did express gratitude felt more refreshed each day upon wakening. They also felt more connected with others than did participants in the group not expressing gratitude.
A fourth study didn’t require a gratitude journal, but looked at the amount of gratitude people showed in their daily lives. In this study, a group of Chinese researchers found that higher levels of gratitude were associated with better sleep, and also with lower levels of anxiety and depression.
Better sleep, with less anxiety and depression. Some compelling reasons to express gratitude more regularly.
Three simple steps to becoming more grateful
If you’ve only got time to say one prayer today, make it the simple words of “thank you.”
This is worth keeping in mind as you go about figuring out your daily practices and routines.
Here are three practical steps you can take to infusing routines of gratitude into your life.
1) Keep a daily journal of three things you are thankful for. This works well first thing in the morning, or just before you go to bed.
2) Make it a practice to tell a spouse, partner or friend something you appreciate about them every day.
3) Look in the mirror when you are brushing your teeth, and think about something you have done well recently or something you like about yourself.
At a presentation at the California Academy of Sciences Tuesday night, Elon Musk unveiled the first products from his neuroscience startup, Neuralink.
JOSHUA LOTT/GETTY IMAGES
ELON MUSK DOESN’T think his newest endeavor, revealed Tuesday night after two years of relative secrecy, will end all human suffering. Just a lot of it. Eventually.At a presentation at the California Academy of Sciences, hastily announced via Twitter and beginning a half hour late, Musk presented the first product from his company Neuralink. It’s a tiny computer chip attached to ultrafine, electrode-studded wires, stitched into living brains by a clever robot. And depending on which part of the two-hour presentation you caught, it’s either a state-of-the-art tool for understanding the brain, a clinical advance for people with neurological disorders, or the next step in human evolution.
The chip is custom-built to receive and process the electrical action potentials—“spikes”—that signal activity in the interconnected neurons that make up the brain. The wires embed into brain tissue and receive those spikes. And the robotic sewing machineplaces those wires with enviable precision, a “neural lace” straight out of science fiction that dodges the delicate blood vessels spreading across the brain’s surface like ivy.
If Neuralink’s technologies work as Musk and his team intend, they’ll be able to pick up signals from across a person’s brain—first from the motor cortex that controls movement but eventually throughout your think-meat—and turn them into machine-readable code that a computer can understand. It might use them to control a computer or a prosthesis, to someday even feed information back to help the blind see, or to create entire virtual Matrixes inside your mind. “All this will occur I think quite slowly,” Musk said from the stage. “It’s not as if Neuralink will suddenly have this incredible neural lace and take over people’s brains. It will take a long time.” But after tests, and FDA approval, and more advances, this tech could be the thing that lets people commune with the ultrasmart artificial intelligences Musk is convinced are on the way. “Even in a benign AI scenario we will be left behind,” he said. “With a high-bandwidth brain-machine interface, we can actually go along for the ride. We can have the option of merging with AI.”
This is all pretty on-brand for Musk. As the guy who runs the electric-car company Tesla and the rocket company SpaceX, Musk has gotten very good at—in trouble, even, for—taking impressive technological achievements and, well, maybe not hyping them, but let’s say skipping all the way to the end of their speculative narrative arcs. It’s not enough to have superslick electric cars; no, they’re also going to drive themselves. That rocket isn’t just going to ferry cargo to a space station; no, it’s going to take people to Mars. How exciting!
Since The Wall Street Journalrevealed Neuralink’s existence two years ago, the tech and neuroscience worlds have buzzed about what Musk’s team of brain-machine interface experts was up to. Other companies, including Kernel and Facebook, announced they, too, were working on the technology, which has so far been used only in research and rare clinical settings. Darpa, the US government’s advanced-science division, has been funding brain-computer interface work since the 1970s, and the agency has been part of the government-wide Brain Research through Advancing Innovative Neurotechnologies (yes, the acronym is also “Brain”) since 2013.
So it’s hard to know exactly how to calibrate Musk’s claims for a device that he plans to eventually stick into healthy people’s brains. “We hope to have this aspirationally in a human patient by the end of next year,” Musk said. The first volunteers, he hopes, will be people with quadriplegia, willing to have four chips implanted, three in the motor cortex of the brain (roughly running from above the ear to the top of the head) and on providing closed-loop feedback to the somatosensory cortex. That’s even though, according to an article distributed at the presentation—and not peer-reviewed—the Neuralink technology is so far only in the heads of 19 rats, and even then with only 87 percent of the electrodes successfully inserted. The FDA is going to want more than that before it approves human use.
And, sure, there’s more. A public records request from WIRED in April 2019 found that Neuralink is licensed to have hundreds of rats and mice in its research facilities. In a seemingly unplanned moment at the Cal Academy, Musk also acknowledged that Neuralink’s research had progressed beyond rodents to non-human primates. It’s only because of a records request filed by Gizmodo that Neuralink’s affiliation with the primate research center at UC Davis is public knowledge. That affiliation has apparently progressed: “A monkey has been able to control a computer with its brain, just FYI,” Musk said during the Q and A after the presentation.
His team seemed as surprised and discombobulated by the announcement as the audience. “I didn’t know we were running that result today, but there it goes,” said Max Hodak, president of the company, on stage next to Musk. (Monkeys have controlled computers via BCIs before, though presumably this would be the first time one used Neuralink.)
(A separate records request from WIRED in August of 2018 reveals that Neuralink re-upped its deal with UC Davis in June of that year, a month after the Gizmodo article. That relationship hasn’t always been entirely cordial; emails obtained by WIRED show that in June of 2018 John Morrison, director of the California National Primate Research Center at UC Davis, complained that Neuralink was trying to poach UC Davis staffers. “I realize that this is routine practice in the private sector, but I am a little surprised since my understanding is that there was an interest in developing scientific collaboration between Neuralink and the CNRPC,” Morrison wrote to a redacted contact apparently at Neuralink. “Hiring away personnel does not build a relationship.”)
Music matters for its own sake, but also because, as our study shows, music engagement sustained from childhood into adolescence – particularly instrumental music that begins in elementary school – is significantly related to better high school achievement.
Study: Rich data
Thanks to rich educational and socio-economic data capturing the full population of B.C. public school students for several cohorts, we had an unprecedented opportunity to examine how student participation in music and music achievement predicted and related to provincial examination scores in high school English, math and science subjects. We looked at scores from provincial testing from Grade 10 math, science and English as well as Grade 12 English in relationship to students’ participation in music.
In our study, we counted both the number of high school courses taken, as well as student high school involvement and grades in graduation program music courses (concert band, jazz band, orchestra, piano and choir) taken across public high school years (Grades 8-12).
Based on previous research we inferred that music involvement that continued up to Grade 12 would be associated with (and predict) higher high school grades in mathematics, science and English. We expected instrumental music would have a more pronounced positive impact than vocal music.
We found that this is true, even when we take into account the following four factors: children’s prior elementary school educational achievement in numeracy and literacy, as captured by the B.C. Foundation Skills Assessment Grade 7 examination; gender; socioeconomic background (as gauged by the student’s home neighbourhood); linguistic diversity, captured by language spoken in the home.
We used a statistical regression model and adjusted our analyses to control for those four factors. We did this to demonstrate that these factors were not key determinants in musical or academic achievement and to address the problem of what researchers call confounding — unaccounted-for factors that might lead to incorrect findings.
While we are not yet able to infer causality — that music causes students to be smarter or improve their grades — we were able to identify a predictive relationship between music achievement and academic achievement, and demonstrate that more music engagement can be better for overall learning.
But music is an inherently complex phenomenon — there are many ways to make and engage with music. Many other studies have examined music participation but they didn’t take into account different types of music making such as instrumental music, vocal music, or other forms and amounts of engagement.
There are many ways to make music.(Shutterstock)
Also, several earlier studies have been based on small, unrepresentative samples or considered only brief exposure to music training — whereas a central claim substantiated by our study underscores the academic achievement benefits from sustained engagement in music training over several years.
Increased cognitive capacity
Students in the present study who were highly engaged in instrumental music were, on average, over one year ahead in their math, English and science skills, compared to those peers not engaged in school music.
We say one year ahead because the math, science and English grades that music-engaged students obtained in Grade 10 could place them a full year ahead in their curricular studies. In practical terms, the effect sizes we measured when comparing adolescents in the very highly engaged instrumental music group with the no music group (even after adjustment) were of a magnitude similar to or greater than the average annual gains in reading, science and math that are seen during the high school years in the U.S. context
Students learn to ‘think music’ as their musical learning deepens.(Shutterstock)
To make music in upper secondary grade levels, students need to go beyond simple button pushing and the mechanical playing of instruments. Students need to “think music” through a process known as audiation. Audiation is the ability to compare what was heard in the immediate past in music listening with the present, and to connect what was heard with our expectations of what might come next. Music audiation ability is significantly correlated to the structure and function of the Heschl’s gyrus in the auditory cortex.
The patterns of our findings suggest that music participation – especially in instrumental music, and multiple years of engagement over time – confers cognitive benefits in the form of tangible differences in many aspects of academic learning.
Significant associations
When focusing solely on learners who took instrumental music, additional important and theoretically plausible findings are revealed — namely that there is a “dose-response” type relationship. This means that higher levels of engagement (more classes) in music are related to incrementally higher exam scores. We also see significant, predictive relationships between higher grades in instrumental music courses and higher exam scores.
Music may not make you smarter, but we now know that music engagement sustained from childhood into adolescence — and more of it, especially instrumental music — may lead to doing better in high school.
“A divided, poorly educated and uncritical society is particularly susceptible to a reactionary leader who can syncretize identity constructs and scapegoat others while gutting the public sphere. The use of fear to instill complacency, a sense of powerlessness and addiction to aggression at the behest of expansionism is characteristic of white supremacist, settler colonialist countries such as the US and Israel.”
Photograph Source: U.S. Embassy Tel Aviv – Public Domain
No syncretistic faith can withstand analytical criticism. The critical spirit makes distinctions, and to distinguish is a sign of modernism. In modern culture the scientific community praises disagreement as a way to improve knowledge. For Ur-Fascism, disagreement is treason.
In spite of a seemingly convincing victory in Israel’s recent elections, Prime Minister Benjamin Netanyahu failed to form a right-wing coalition, which would secure him the premiership for an additional four years.
The reason: hard-right Member of Knesset (MK), former Israeli Security Minister, and leader of the Yisrael Beiteinu party Avigdor Lieberman – a settler in the Occupied Palestinian Territories, ex-nightclub bouncer and convicted child beater – refused to budge on a draft bill for ultra-orthodox Jews. In response to Lieberman’s opportunistic move, a disheveled-looking Netanyahu spoke to reporters claiming: “Lieberman is now part of the left”.
Yet Lieberman is as far from left-wing politics as can be. In fact, his signature fascistic opinions are no secret – e.g. he has openly endorsed expulsion of Palestinians from Israel and spearheaded attempts to legalize execution and even beheading of Palestinian prisoners, whom he collectively refers to as “terrorists”.
Across the pond in the United States, President Donald Trump has adopted the term “radical left” to describe his opponents in the media and the Democratic Party. With the ramping up of the 2020 election fever, Trump will likely soon drop the “radical” and simply scapegoat the “left”.
These instances of illogical characterization of critique as coming from “the left” are a form of reactionary doublespeak, well-established in Israel and the United States of America. Those who challenge members of the ruling class are stereotyped, smeared and nonsensically labeled as traitorous lefties regardless of true political orientation.
Big (white) brother
According to Collins dictionary, the term “doublespeak”, widely attributed to George Orwell’s 1984 though it was never explicitly mentioned in the book (Orwell coined the terms “newspeak” and “doubletalk”, among others), is a means of ‘… presenting things in a way that is intended to hide the truth or give people the wrong idea.’
Doublespeak is a propaganda tool which purposefully obscures, falsifies, and/or reverses the meaning of language. It is used to shift the conversation away from the content of criticism illustrating logical fallacies, uncomfortable truths, and corruptions of the ruling class, toward an illogical, emotional, and cognitively dissonant reaction to an established stereotype – a “leftist” as contemptible, disloyal, hypocritical and cowardly.
Washing one’s hands of the conflict between the powerful and the powerless means to side with the powerful, not to be neutral.
~ Paulo Freire
According to this narrative, the leftist seeks to weaken the “freedoms” and identity of supposed merited elements of society by promoting, at their expense, lazy freeloaders.
Thus, doublespeak serves to hardwire oppression, misogyny and the status quo of white male supremacy, protecting its accumulation and hoarding of resources at the expense of vulnerable societal groups.
Individualism versus collaboration
As a social species, humankind relies on its members for survival and progress. The modern scientific framework promotes a collaborative model in which conflict rooted in the premise of a critical interchange of ideas is encouraged as part of a need for the constant evolution of understanding and consequent ideas, ultimately leading to an equitable and sustainable existence.
In contrast, an individualistic approach animates an inherently oppressive cult of xenophobic identity and destructive conflict, discouraging collaboration and sustaining privilege through a denial of inconvenient facts and an ongoing obstruction of collectivism.
Instead of perceiving challenge, peer review and the scientific method as necessary for truth, subsequent accountability and consequent growth of humanity as a whole, it is perceived by individualists as an existential threat to their privilege. As such, reactionaries typically villainize academia and science, media and the arts and rely on celebritized pseudo-intellectuals to justify their privilege and oppression of others.
Pseudo-intellectuals and cults
Ben Shapiro, social media celebrity, pseudo-intellectual and inspiration to anti-Semites and white supremacists worldwide, recently exemplified doublespeak in an interview with BBC’s right-wing journalist Andrew Neil. When Neil challenged his opinions, Shapiro pleaded with the veteran Brit to admit he was “on the left” and abandoned the interview in protest, claiming Neil was “badly motivated”.
Pop psychologist Jordan Peterson is an additional noteworthy example of a pseudo-intellectual outside his own field who has become a cult-like thought leader amongst reactionaries. In his work, Peterson justifies inequality by claiming humans are naturally inclined to form hierarchies. He compares humans with lobsters and suggests neural systems involved in hierarchy formation in both species are controlled by the neurotransmitter molecule serotonin.
Peterson ignores and disappears studies of evolutionary biology and behavioral neuroscience which have demonstrated repeatedly the deep flaws of such a reductionist approach to the human brain and behavior. Drawing conclusions about complex social behaviors from comparisons between humans, a species with highly evolved brains with complex structures and many neurotransmitter systems, to lobsters, crustaceans with a comparatively primitive nervous system (comprised of ganglia and no brain) is blatant propagandistic pseudoscience.
This misuse of science to code cult dogma has its roots in the now highly discredited and racist theory of social Darwinism.
Trump and Netanyahu follow the fascistic playbook
Human progress – defined as sustainable, equitable and just – occurs when societies rely on historical precedents to build a framework of norms and taboos. In turn, these serve to promote progress by social enrichment on the one hand and curtailment of abuses of vulnerable and disenfranchised elements of society, on the other.
A divided, poorly educated and uncritical society is particularly susceptible to a reactionary leader who can syncretize identity constructs and scapegoat others while gutting the public sphere. The use of fear to instill complacency, a sense of powerlessness and addiction to aggression at the behest of expansionism is characteristic of white supremacist, settler colonialist countries such as the US and Israel.
Both charismatic leaders, Trump and Netanyahu skillfully use doublespeak to promote their reactionary, capitalist and white supremacist agendas. Alongside the degradation of intellectualism and collectivism, they employ trial balloons as a means of assessing public resistance before creating precedents and slogannistic memes, which serve to shatter acceptable taboos as preludes to authoritarianism.
Both Trump and Netanyahu have been able to manipulate a corrupt and often times subservient media to serve their purposes of distraction and scapegoating, which mask their ongoing looting of their country’s public domains.
The deployment of a barrage of manufactured spectacles produces an apathetic, distracted and fragmented public less likely to protest when its civil liberties are attacked and more likely to engage in infighting rather than confront the white patriarchal ruling class hegemony.
Whether it is Trump’s lies and daily tirades on Twitter or Netanyahu’s racist calls to his fanatical supporters on election night, both are adept at manipulating the public and media to serve their purposes.
With the growing tide of the global right, education of the public to the importance of reason, the scientific method and skills necessary for collaborative creation utilizing the power of conflict rooted in the premise of a critical interchange of ideas, are crucial to combat the contradictions of ruling class dogma and the complacency it manufactures.
Summary: A new study reports the rhythm of your breathing can influence neural activity that enhances memory recall and emotional judgement.
Source: Northwestern University.
Breathing is not just for oxygen; it’s now linked to brain function and behavior.
Northwestern Medicine scientists have discovered for the first time that the rhythm of breathing creates electrical activity in the human brain that enhances emotional judgments and memory recall.
These effects on behavior depend critically on whether you inhale or exhale and whether you breathe through the nose or mouth.
In the study, individuals were able to identify a fearful face more quickly if they encountered the face when breathing in compared to breathing out. Individuals also were more likely to remember an object if they encountered it on the inhaled breath than the exhaled one. The effect disappeared if breathing was through the mouth.
“One of the major findings in this study is that there is a dramatic difference in brain activity in the amygdala and hippocampus during inhalation compared with exhalation,” said lead author Christina Zelano, assistant professor of neurology at Northwestern University Feinberg School of Medicine. “When you breathe in, we discovered you are stimulating neurons in the olfactory cortex, amygdala and hippocampus, all across the limbic system.”
The study was published Dec. 6 in the Journal of Neuroscience.
The senior author is Jay Gottfried, professor of neurology at Feinberg.
Northwestern scientists first discovered these differences in brain activity while studying seven patients with epilepsy who were scheduled for brain surgery. A week prior to surgery, a surgeon implanted electrodes into the patients’ brains in order to identify the origin of their seizures. This allowed scientists to acquire electro-physiological data directly from their brains. The recorded electrical signals showed brain activity fluctuated with breathing. The activity occurs in brain areas where emotions, memory and smells are processed.
This discovery led scientists to ask whether cognitive functions typically associated with these brain areas — in particular fear processing and memory — could also be affected by breathing.
The amygdala is strongly linked to emotional processing, in particular fear-related emotions. So scientists asked about 60 subjects to make rapid decisions on emotional expressions in the lab environment while recording their breathing. Presented with pictures of faces showing expressions of either fear or surprise, the subjects had to indicate, as quickly as they could, which emotion each face was expressing. NeuroscienceNews.com image is for illustrative purposes only.
The amygdala is strongly linked to emotional processing, in particular, fear-related emotions. So scientists asked about 60 subjects to make rapid decisions on emotional expressions in the lab environment while recording their breathing. Presented with pictures of faces showing expressions of either fear or surprise, the subjects had to indicate, as quickly as they could, which emotion each face was expressing.
When faces were encountered during inhalation, subjects recognized them as fearful more quickly than when faces were encountered during exhalation. This was not true for faces expressing surprise. These effects diminished when subjects performed the same task while breathing through their mouths. Thus the effect was specific to fearful stimuli during nasal breathing only.
In an experiment aimed at assessing memory function — tied to the hippocampus — the same subjects were shown pictures of objects on a computer screen and told to remember them. Later, they were asked to recall those objects. Researchers found that recall was better if the images were encountered during inhalation.
The findings imply that rapid breathing may confer an advantage when someone is in a dangerous situation, Zelano said.
“If you are in a panic state, your breathing rhythm becomes faster,” Zelano said. “As a result, you’ll spend proportionally more time inhaling than when in a calm state. Thus, our body’s innate response to fear with faster breathing could have a positive impact on brain function and result in faster response times to dangerous stimuli in the environment.”
Another potential insight of the research is on the basic mechanisms of meditation or focused breathing. “When you inhale, you are in a sense synchronizing brain oscillations across the limbic network,” Zelano noted.
Summary: Experiencing daily anger increases inflammation and raises the risk of developing chronic illnesses, such as heart disease and cancer, in those aged 80 and over.
Source: APA
Anger may be more harmful to an older person’s physical health than sadness, potentially increasing inflammation, which is associated with such chronic illnesses as heart disease, arthritis and cancer, according to new research published by the American Psychological Association.
“As most people age, they simply cannot do the activities they once did, or they may experience the loss of a spouse or a decline in their physical mobility and they can become angry,” said Meaghan A. Barlow, MA, of Concordia University, lead author of the study, which was published in Psychology and Aging. “Our study showed that anger can lead to the development of chronic illnesses, whereas sadness did not.”
Barlow and her co-authors examined whether anger and sadness contributed to inflammation, an immune response by the body to perceived threats, such as infection or tissue damage. While inflammation, in general, helps protect the body and assists in healing, long-lasting inflammation can lead to chronic illnesses in old age, according to the authors.
The researchers collected and analyzed data from 226 older adults ages 59 to 93 from Montreal. They grouped participants as being in early old age, 59 to 79 years old, or advanced old age, 80 years old and older.
Over one week, participants completed short questionnaires about how angry or sad they felt. The authors also measured inflammation from blood samples and asked participants if they had any age-related chronic illnesses.
“We found that experiencing anger daily was related to higher levels of inflammation and chronic illness for people 80 years old and older, but not for younger seniors,” said study co-author Carsten Wrosch, PhD, also of Concordia University. “Sadness, on the other hand, was not related to inflammation or chronic illness.”
Sadness may help older seniors adjust to challenges such as age-related physical and cognitive declines because it can help them disengage from goals that are no longer attainable, said Barlow.
This study showed that not all negative emotions are inherently bad and can be beneficial under certain circumstances, she explained.
“Anger is an energizing emotion that can help motivate people to pursue life goals,” said Barlow. “Younger seniors may be able to use that anger as fuel to overcome life’s challenges and emerging age-related losses and that can keep them healthier. Anger becomes problematic for adults once they reach 80 years old, however, because that is when many experience irreversible losses and some of life’s pleasures fall out of reach.”
This study showed that not all negative emotions are inherently bad and can be beneficial under certain circumstances, she explained. The image is in the public domain.
The authors suggested that education and therapy may help older adults reduce anger by regulating their emotions or by offering better-coping strategies to manage the inevitable changes that accompany aging.
“If we better understand which negative emotions are harmful, not harmful or even beneficial to older people, we can teach them how to cope with loss in a healthy way,” said Barlow. “This may help them let go of their anger.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: APA Media Contacts:
Michael Shulman – APA Image Source:
The image is in the public domain.
Is anger, but not sadness, associated with chronic inflammation and illness in older adulthood?
The discrete emotion theory of affective aging postulates that anger, but not sadness, becomes increasingly maladaptive during older adulthood in predicting health-relevant physiological processes and chronic disease (Kunzmann & Wrosch, 2018). However, it is largely unknown whether different negative emotions have distinct functional consequences in the development of older adults’ physical disease. To start examining this possibility, we investigated whether older adults’ daily experiences of anger and sadness were differentially associated with two biomarkers of chronic low-grade inflammation (interleukin-6 [IL-6] and C-reactive protein [CRP]) and the number of chronic illnesses (e.g., heart disease, cancer, etc.). In addition, we examined whether such divergent associations would become paramount in advanced, as compared with early, old age. A community-dwelling study of 226 older adults (age 59 to 93; M = 74.99, SD = 7.70) assessed participants’ anger and sadness over 1 week, inflammatory processes, number of chronic illnesses, and relevant covariates. Regression analysis showed that anger predicted higher levels of IL-6 and chronic illness in advanced, but not in early, old age. The age effect of anger on chronic illness was mediated by increased IL-6 levels. Sadness exerted a reversed, but nonsignificant, association with IL-6 and chronic illness, independent of age. No emotion or age effects were obtained for CRP. The study’s findings inform theories of health, emotion, and life span development by pointing to the age-related importance of discrete negative emotions in predicting a major physiological pathway to physical health across older adulthood.
A team of Stanford neuroscientists may have stumbled onto a way to prevent the brain from aging–and if the results of tests on old mice are any indicator, the research is promising.
Hailed as a “stunning piece of research” by New Atlas, the study–published in peer-reviewed international journal Nature–managed to pinpoint a specific gene called CD22 that is responsible for cognitive loss resulting from aging. The gene, common to both mice and humans, apparently degrades certain cells’ ability to conduct normal brain activity.
That same gene was found to be three times more prevalent among older mice than younger ones in follow-on experiments.
With this data in mind, the researchers devised antibodies to block CD22–specifically, molecules that bind to proteins and can be generated in a lab.
The Stanford team then injected the antibodies into the hippocampus on one side of the brains of the test mice. After a month of injecting the CD22-blocking antibody into both sides of their brains, the mice that received the injection began outperforming their counterparts in various intelligence tests.
The researchers believe that this is because as we age, the microglia–the class of brain cells responsible for routine cleanup and immune responses–decline and lose their ability to engage in the sort of “maintenance” work that brains require.
In a statement, study author and professor of neurology and neurological sciences Tony Wyss-Coray said:
“The mice became smarter … Blocking CD22 on their microglia restored their cognitive function to the level of younger mice. CD22 is a new target we think can be exploited for treatment of neurodegenerative diseases.”
This research could open the path to reverse a range of cognitive effects of aging–including such diseases as Parkinson’s and Alzheimer’s.
Wyss-Coray noted:
“Many of the genes whose high-risk variants have recently been linked to Alzheimer’s disease are known to be active in the brain only in microglia … Microglial genes’ activation patterns are abnormal in Alzheimer’s patients, and in other neurodegenerative disorders including Parkinson’s disease and amyotrophic lateral sclerosis.”
Yet the new research could be promising, especially when–or if–it eventually reaches human trials. The Stanford team remains optimistic, with Wyss-Coray noting:
“We think we may have discovered a way to get these cells back on track and make them work the way they used to when we were young.”
Scientists believe that the “CRISPR twins,” who had their genes edited last year before birth, will now have an easier time learning and memorizing. Apparently, the gene alteration, which was meant to make the girls immune to HIV, also altered their brains.
Now, new research shows that the same alteration introduced into the girls’ DNA, to a gene called CCR5, not only makes mice smarter but also improves human brain recovery after stroke, and could be linked to greater success in school.
“The answer is likely yes, it did affect their brains,” says Alcino J. Silva, a neurobiologist at the University of California, Los Angeles, whose lab has been uncovering a major new role for the CCR5 gene in memory and the brain’s ability to form new connections.
“The simplest interpretation is that those mutations will probably have an impact on cognitive function in the twins,” says Silva. He says the exact effect on the girls’ cognition is impossible to predict, and “that is why it should not be done.”
There is no evidence that He Jiankui, the lead scientist from the Southern University of Science and Technology in Shenzhen, China, set out to alter their intelligence. He is now under investigation for the controversial experiment that “has been widely condemned as irresponsible.”
Researchers report on how the brain is spurred into action by hearing certain words. They propose a new simulation theory that perceiving words can drive brain systems into states almost identical to what would be evoked by directly experiencing what the word describes.
“Dan Slobin suggested that habitual ways of speaking lead to habitual ways of thinking about the world. The language that you hear gives you a vocabulary for discussing the world, and that vocabulary, by producing simulations, gives you habits of mind.”
Summary: Researchers report on how the brain is spurred into action by hearing certain words. They propose a new simulation theory that perceiving words can drive brain systems into states almost identical to what would be evoked by directly experiencing what the word describes.
Source: The Conversation.
A mark on a page, an online meme, a fleeting sound. How can these seemingly insignificant stimuli lead to acts as momentous as participation in a racist rally or the massacre of innocent worshippers? Psychologists, neuroscientists, linguists and philosophers are developing a new theory of language understanding that’s starting to provide answers.
Current research shows that humans understand language by activating sensory, motor and emotional systems in the brain. According to this new simulation theory, just reading words on a screen or listening to a podcast activates areas of the brain in ways similar to the activity generated by literally being in the situation the language describes. This process makes it all the more easy to turn words into actions.
Simulation theory proposes that processing words depends on activity in people’s neural and behavioral systems of action, perception and emotion. The idea is that perceiving words drives your brain systems into states that are nearly identical to what would be evoked by directly experiencing what the words describe.
Consider the sentence “The lovers held hands while they walked along the moonlit tropical beach.” According to simulation theory, when you read these words, your brain’s motor system simulates the actions of walking; that is, the neural activity elicited by comprehending the words is similar to the neural activity generated by literal walking. Similarly, your brain’s perceptual systems simulate the sight, sounds and feel of the beach. And your emotional system simulates the feelings implied by the sentence.
So words themselves are enough to trigger simulations in motor, perceptual and emotional neural systems. Your brain creates a sense of being there: The motor system is primed for action and the emotional system motivates those actions.
Then, one can act on the simulation much as he’d act in the real situation. For example, language associating an ethnic group with “bad hombres” could invoke an emotional simulation upon seeing members of the group. If that emotional reaction is strong enough, it may in turn motivate action – maybe making a derogatory remark or physically lashing out.
Although simulation theory is still under scientific scrutiny, there have been many successful tests of its predictions. For example, using neuroimaging techniques that track blood flow in the brain, researchers found that listening to action words such as “lick,” “pick” and “kick” produces activity in areas of the brain’s motor cortex that are used to control the mouth, the hand and the leg, respectively. Hearing a sentence such as “The ranger saw an eagle in the sky” generates a mental image using the visual cortex. And using Botox to block activity in the muscles that furrow the brow affects the emotional system and slows understanding of sentences conveying angry content. These examples demonstrate the connections between processing speech and motor, sensory and emotional systems.
Recently, my colleague psychologist Michael McBeath, our graduate student Christine S. P. Yu and I discovered yet another robust connection between language and the emotional system.
Consider pairs of single-syllable English words that differ only in whether the vowel sound is “eee” or “uh,” such as “gleam-glum” and “seek-suck.” Using all such pairs in English – there are about 90 of them – we asked people to judge which word in the pair was more positive. Participants selected the word with the “eee” sound two-thirds of the time. This is a remarkable percentage because if linguistic sounds and emotions were unrelated and people were picking at the rate of chance, only half of the “eee” words would have been judged as the more positive.
We propose that this relation arose because saying “eee” activates the same muscles and neural systems as used when smiling – or saying “cheese!” In fact, mechanically inducing a smile – as by holding a pencil in your teeth without using your lips – lightens your mood. Our new research shows that saying words that use the smile muscles can have a similar effect.
We tested this idea by having people chew gum while judging the words. Chewing gum blocks the systematic activation of the smile muscles. Sure enough, while chewing gum, the judged difference between the “eee” and “uh” words was only half as strong. We also demonstrated the same effects in China using pairs of Mandarin words containing the “eee” and “uh” sounds.
Practice through simulation makes actions easier
Of course, motivating someone to commit a hate crime requires much more than uttering “glum” or “suck.”
Inflammatory words can prime a mind.
But consider that simulations become quicker with repetition. When one first hears a new word or concept, creating its simulation can be a mentally laborious process. A good communicator can help by using hand gestures to convey the motor simulation, pointing to objects or pictures to help create the perceptual simulation and using facial expressions and voice modulation to induce the emotional simulation.
It makes sense that the echo chamber of social media provides the practice needed to both speed and shape the simulation. The mental simulation of “caravan” can change from an emotionally neutral string of camels to an emotionally charged horde of drug dealers and rapists. And, through the repeated simulation that comes from repeatedly reading similar posts, the message becomes all the more believable, as each repetition produces another instance of almost being there to see it with your own eyes.
Psycholinguist Dan Slobin suggested that habitual ways of speaking lead to habitual ways of thinking about the world. The language that you hear gives you a vocabulary for discussing the world, and that vocabulary, by producing simulations, gives you habits of mind. Just as reading a scary book can make you afraid to go in the ocean because you simulate (exceedingly rare) shark attacks, encountering language about other groups of people (and their exceedingly rare criminal behavior) can lead to a skewed view of reality.
Practice need not always lead down an emotional rabbit hole, though, because alternative simulations and understandings can be created. A caravan can be simulated as families in distress who have the grit, energy and skills to start a new life and enrich new communities.
Because simulation creates a sense of being in a situation, it motivates the same actions as the situation itself. Simulating fear and anger literally makes you fearful and angry and promotes aggression. Simulating compassion and empathy literally makes you act kindly. We all have the obligation to think critically and to speak words that become humane actions.
Anna Abraham literally wrote the book on creativity and the brain. The Leeds Beckett University psychology professor is the author of a new textbook titled The Neuroscience of Creativity. From an interview with Abraham by psychologist Scott Barry Kaufman in Scientific American:
SBK: Why does the myth of the “creative right brain” still persist? Is there any truth at all to this myth?AA: Like most persistent myths, even if some seed of truth was associated with the initial development of the idea, the claim so stated amounts to a lazy generalization and is incorrect. The brain’s right hemisphere is not a separate organ whose workings can be regarded in isolation from that of the left hemisphere in most human beings. It is also incorrect to conclude that the left brain is uncreative. In fact even the earliest scholars who explored the brain lateralization in relation to creativity emphasized the importance of both hemispheres. Indeed this is what was held to be unique about creativity compared to other highly lateralized psychological functions. In an era which saw the uncovering of the dominant involvement of one hemisphere over the other for many functions, and the left hemisphere received preeminent status for its crucial role in complex functions like language, a push against the tide by emphasizing the need to also recognize the importance of the right hemisphere for complex functions like creativity somehow got translated over time into the only ‘creative right brain’ meme. It is the sort of thing that routinely happens when crafting accessible sound bites to convey scientific findings.
SBK: Is brain plasticity truly possible? If so, to what extent? How can creative thinking both induce and be caused by brain plasticity?
AA: Brain plasticity is a fact. Our brains change throughout our lifespan and this is readily evidenced by the everyday observation that we never stop learning. The extent of brain plasticity is harder to define and hasn’t been systematically examined. Creative thinking involves the discovery of novel connections and is therefore tied intimately to learning. Arthur Koestler pointed this out rather beautifully several decades ago: “Creative activity is a type of learning process where the teacher and pupil are located in the same individual.”
A new study links poor sleep quality in older adults with elevated levels of tau, a protein associated with Alzheimer’s disease. Researchers report poor sleep quality later in life may be associated with declining brain health and may be an early indicator of Alzheimer’s disease.
Summary: A new study links poor sleep quality in older adults with elevated levels of tau, a protein associated with Alzheimer’s disease. Researchers report poor sleep quality later in life may be associated with declining brain health and may be an early indicator of Alzheimer’s disease.
Source: WUSTL.
Poor sleep is a hallmark of Alzheimer’s disease. People with the disease tend to wake up tired, and their nights become even less refreshing as memory loss and other symptoms worsen. But how and why restless nights are linked to Alzheimer’s disease is not fully understood.
Now, researchers at Washington University School of Medicine in St. Louis may have uncovered part of the explanation. They found that older people who have less slow-wave sleep – the deep sleep you need to consolidate memories and wake up feeling refreshed – have higher levels of the brain protein tau. Elevated tau is a sign of Alzheimer’s disease and has been linked to brain damage and cognitive decline.
The findings, published Jan. 9 in Science Translational Medicine, suggest that poor-quality sleep in later life could be a red flag for deteriorating brain health.
“What’s interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired,” said first author Brendan Lucey, MD, an assistant professor of neurology and director of the Washington University Sleep Medicine Center. “Measuring how people sleep may be a noninvasive way to screen for Alzheimer’s disease before or just as people begin to develop problems with memory and thinking.”
The brain changes that lead to Alzheimer’s, a disease that affects an estimated 5.7 million Americans, start slowly and silently. Up to two decades before the characteristic symptoms of memory loss and confusion appear, amyloid beta protein begins to collect into plaques in the brain. Tangles of tau appear later, followed by atrophy of key brain areas. Only then do people start showing unmistakable signs of cognitive decline.
The challenge is finding people on track to develop Alzheimer’s before such brain changes undermine their ability to think clearly. For that, sleep may be a handy marker.
To better understand the link between sleep and Alzheimer’s disease, Lucey, along with David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology, and colleagues studied 119 people 60 years of age or older who were recruited through the Charles F. and Joanne Knight Alzheimer’s Disease Research Center. Most – 80 percent – were cognitively normal, and the remainder were very mildly impaired.
The researchers monitored the participants’ sleep at home over the course of a normal week. Participants were given a portable EEG monitor that strapped to their foreheads to measure their brain waves as they slept, as well as a wristwatch-like sensor that tracks body movement. They also kept sleep logs, where they made note of both nighttime sleep sessions and daytime napping. Each participant produced at least two nights of data; some had as many as six.
The researchers also measured levels of amyloid beta and tau in the brain and in the cerebrospinal fluid that bathes the brain and spinal cord. Thirty-eight people underwent PET brain scans for the two proteins, and 104 people underwent spinal taps to provide cerebrospinal fluid for analysis. Twenty-seven did both.
After controlling for factors such as sex, age and movements while sleeping, the researchers found that decreased slow-wave sleep coincided with higher levels of tau in the brain and a higher tau-to-amyloid ratio in the cerebrospinal fluid.
“The key is that it wasn’t the total amount of sleep that was linked to tau, it was the slow-wave sleep, which reflects quality of sleep,” Lucey said. “The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren’t getting as good quality sleep.”
Reduced amounts of slow brain waves – the kind that occur in deep, refreshing sleep – are associated with high levels of the toxic brain protein tau. This computer-generated image maps the areas where the link is strongest, in shades of red and orange. A new study from Washington University School of Medicine in St. Louis has found that decreased deep sleep is associated with early signs of Alzheimer’s disease. NeuroscienceNews.com image is credited to Brendan Lucey.
If future research bears out their findings, sleep monitoring may be an easy and affordable way to screen earlier for Alzheimer’s disease, the researchers said. Daytime napping alone was significantly associated with high levels of tau, meaning that asking a simple question – How much do you nap during the day? – might help doctors identify people who could benefit from further testing.
“I don’t expect sleep monitoring to replace brain scans or cerebrospinal fluid analysis for identifying early signs of Alzheimer’s disease, but it could supplement them,” Lucey said. “It’s something that could be easily followed over time, and if someone’s sleep habits start changing, that could be a sign for doctors to take a closer look at what might be going on in their brains.”
Right now, billions of neurons in your brain are working together to generate a conscious experience — and not just any conscious experience, your experience of the world around you and of yourself within it. How does this happen? According to neuroscientist Anil Seth, we’re all hallucinating all the time; when we agree about our hallucinations, we call it “reality.” Join Seth for a delightfully disorienting talk that may leave you questioning the very nature of your existence.
Summary: A new paper proposes resonance may contribute to human consciousness.Source: The Conversation.Why is my awareness here, while yours is over there? Why is the universe split in two for each of us, into a subject and an infinity of objects? How is each of us our own center of experience, receiving information about the rest of the world out there? Why are some things conscious and others apparently not? Is a rat conscious? A gnat? A bacterium?
These questions are all aspects of the ancient “mind-body problem,” which asks, essentially: What is the relationship between mind and matter? It’s resisted a generally satisfying conclusion for thousands of years.
The mind-body problem enjoyed a major rebranding over the last two decades. Now it’s generally known as the “hard problem” of consciousness, after philosopher David Chalmers coined this term in a now classic paper and further explored it in his 1996 book, “The Conscious Mind: In Search of a Fundamental Theory.”
Chalmers thought the mind-body problem should be called “hard” in comparison to what, with tongue in cheek, he called the “easy” problems of neuroscience: How do neurons and the brain work at the physical level? Of course they’re not actually easy at all. But his point was that they’re relatively easy compared to the truly difficult problem of explaining how consciousness relates to matter.
Over the last decade, my colleague, University of California, Santa Barbara psychology professor Jonathan Schooler and I have developed what we call a “resonance theory of consciousness.” We suggest that resonance – another word for synchronized vibrations – is at the heart of not only human consciousness but also animal consciousness and of physical reality more generally. It sounds like something the hippies might have dreamed up – it’s all vibrations, man! – but stick with me.
All about the vibrations
All things in our universe are constantly in motion, vibrating. Even objects that appear to be stationary are in fact vibrating, oscillating, resonating, at various frequencies. Resonance is a type of motion, characterized by oscillation between two states. And ultimately all matter is just vibrations of various underlying fields. As such, at every scale, all of nature vibrates.
Something interesting happens when different vibrating things come together: They will often start, after a little while, to vibrate together at the same frequency. They “sync up,” sometimes in ways that can seem mysterious. This is described as the phenomenon of spontaneous self-organization.
Mathematician Steven Strogatz provides various examples from physics, biology, chemistry and neuroscience to illustrate “sync” – his term for resonance – in his 2003 book “Sync: How Order Emerges from Chaos in the Universe, Nature, and Daily Life,” including:
When fireflies of certain species come together in large gatherings, they start flashing in sync, in ways that can still seem a little mystifying.
Lasers are produced when photons of the same power and frequency sync up.
The moon’s rotation is exactly synced with its orbit around the Earth such that we always see the same face.
Examining resonance leads to potentially deep insights about the nature of consciousness and about the universe more generally.
Sync inside your skull
Neuroscientists have identified sync in their research, too. Large-scale neuron firing occurs in human brains at measurable frequencies, with mammalian consciousness thought to be commonly associated with various kinds of neuronal sync.
For example, German neurophysiologist Pascal Fries has explored the ways in which various electrical patterns sync in the brain to produce different types of human consciousness.
Fries focuses on gamma, beta and theta waves. These labels refer to the speed of electrical oscillations in the brain, measured by electrodes placed on the outside of the skull. Groups of neurons produce these oscillations as they use electrochemical impulses to communicate with each other. It’s the speed and voltage of these signals that, when averaged, produce EEG waves that can be measured at signature cycles per second.
Gamma waves are associated with large-scale coordinated activities like perception, meditation or focused consciousness; beta with maximum brain activity or arousal; and theta with relaxation or daydreaming. These three wave types work together to produce, or at least facilitate, various types of human consciousness, according to Fries. But the exact relationship between electrical brain waves and consciousness is still very much up for debate.
External electrodes can record a brain’s activity. NeuroscienceNews.com image is adapted from the Conversation news release.
Fries calls his concept “communication through coherence.” For him, it’s all about neuronal synchronization. Synchronization, in terms of shared electrical oscillation rates, allows for smooth communication between neurons and groups of neurons. Without this kind of synchronized coherence, inputs arrive at random phases of the neuron excitability cycle and are ineffective, or at least much less effective, in communication.
A resonance theory of consciousness
Our resonance theory builds upon the work of Fries and many others, with a broader approach that can help to explain not only human and mammalian consciousness, but also consciousness more broadly.
Based on the observed behavior of the entities that surround us, from electrons to atoms to molecules, to bacteria to mice, bats, rats, and on, we suggest that all things may be viewed as at least a little conscious. This sounds strange at first blush, but “panpsychism” – the view that all matter has some associated consciousness – is an increasingly accepted position with respect to the nature of consciousness.
The panpsychist argues that consciousness did not emerge at some point during evolution. Rather, it’s always associated with matter and vice versa – they’re two sides of the same coin. But the large majority of the mind associated with the various types of matter in our universe is extremely rudimentary. An electron or an atom, for example, enjoys just a tiny amount of consciousness. But as matter becomes more interconnected and rich, so does the mind, and vice versa, according to this way of thinking.
Biological organisms can quickly exchange information through various biophysical pathways, both electrical and electrochemical. Non-biological structures can only exchange information internally using heat/thermal pathways – much slower and far less rich in information in comparison. Living things leverage their speedier information flows into larger-scale consciousness than what would occur in similar-size things like boulders or piles of sand, for example. There’s much greater internal connection and thus far more “going on” in biological structures than in a boulder or a pile of sand.
Under our approach, boulders and piles of sand are “mere aggregates,” just collections of highly rudimentary conscious entities at the atomic or molecular level only. That’s in contrast to what happens in biological life forms where the combinations of these micro-conscious entities together create a higher level macro-conscious entity. For us, this combination process is the hallmark of biological life.
The central thesis of our approach is this: the particular linkages that allow for large-scale consciousness – like those humans and other mammals enjoy – result from a shared resonance among many smaller constituents. The speed of the resonant waves that are present is the limiting factor that determines the size of each conscious entity in each moment.
As a particular shared resonance expands to more and more constituents, the new conscious entity that results from this resonance and combination grows larger and more complex. So the shared resonance in a human brain that achieves gamma synchrony, for example, includes a far larger number of neurons and neuronal connections than is the case for beta or theta rhythms alone.
What about larger inter-organism resonance like the cloud of fireflies with their little lights flashing in sync? Researchers think their bioluminescent resonance arises due to internal biological oscillators that automatically result in each firefly syncing up with its neighbors.
Is this group of fireflies enjoying a higher level of group consciousness? Probably not, since we can explain the phenomenon without recourse to any intelligence or consciousness. But in biological structures with the right kind of information pathways and processing power, these tendencies toward self-organization can and often do produce larger-scale conscious entities.
Our resonance theory of consciousness attempts to provide a unified framework that includes neuroscience, as well as more fundamental questions of neurobiology and biophysics, and also the philosophy of mind. It gets to the heart of the differences that matter when it comes to consciousness and the evolution of physical systems.
It is all about vibrations, but it’s also about the type of vibrations and, most importantly, about shared vibrations.
About this neuroscience research article
Funding: The Conversation funded this study.
Source: Tam Hunt – The Conversation Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is adapted from The Conversation news release.
“I would never give my daughter, or my son the shot… This is a massive PR event by the company that makes Gardasil, and the same is the truth for the company that makes Cervarix… I think one needs to do a lot of research, and I think parents are in the best position to do that.” – Dr. Christopher Shaw – University of British Columbia
This is a great point, and one that was further emphasized by Dr. Peter Gotzsche, co-founder of the Cochrane Collaboration, the world’s foremost body in assessing medical evidence.
“The main reason we take so many drugs is that drug companies don’t sell drugs, they sell lies about drugs. This is what makes drugs so different from anything else in life… Virtually everything we know about drugs is what the companies have chosen to tell us and our doctors… the reason patients trust their medicine is that they extrapolate the trust they have in their doctors into the medicines they prescribe.
The patients don’t realize that, although their doctors may know a lot about diseases and human physiology and psychology, they know very, very little about drugs that’ve been carefully concocted and dressed up by the drug industry… If you don t think the system is out of control, please email me and explain why drugs are the third leading cause of death… If such a hugely lethal epidemic had been caused by a new bacterium or a virus, or even one-hundredth of it, we would have done everything we could to get it under control.” (source)
The HPV Gardasil vaccine is at the top of the list when it comes to controversial vaccines. Despite its supposed safety and necessity, new information is showing us that this may not be the case, and that its purported safety might be a result of a very heavy, and what now seems to be unethical, marketing campaign. That being said, it’s still taboo to question vaccine safety, which is extremely confusing because there are a number of peer-reviewed publications, along with hundreds of scientists and researchers in the field, who are dedicating their lives to creating awareness about the fact that vaccines aren’t really as safe as they’re marketed to be.
“When one looks at the independent literature, so studies which are not sponsored by the vaccine manufacturers, so with relation to Gardasil there have been several reports documenting multiple sclerosis and encephalitis, which is brain inflammation, in girls who have received their Gardasil vaccine. So just because a study sponsored by the manufacturers does not identify problems with the vaccine does not necessarily mean that the vaccine is safe. In fact if one looks at the manufacturer studies, they’re often not designed to detect serious adverse events.”
– Dr. Lucija Tomljenovic, PhD, Post-doctoral Fellow at the University of British Columbia, where she works in Neurosciences and the Department of Medicine (source)
Multiple Deaths have also been caused as a result of the HPV vaccine. Researchers from Mexico’s National Institute of Cardiology pored over 28 studies published through January 2017, containing 16 randomized trials and 12 post-marketing case series pertaining to the three human papillomavirus (HPV) vaccines currently on the market globally. In their July 2017 peer-reviewed report, the authors, Manuel Martínez-Lavin and Luis Amezcua-Guerra, uncovered evidence of numerous adverse events, including life-threatening injuries, permanent disabilities, hospitalizations and deaths, reported after vaccination with GlaxoSmithKline’s bivalent Cervarix vaccine and Merck’s quadrivalent or nine-valent HPV vaccines (Gardasil and Gardasil 9).
You can access that study and ready more about it here.
For example, although there are many safety concern issues, aluminum has continued to be prevalent, despite the absence of any appropriate safety toxicity studies proving that it’s safe to inject this heavy metal into a fetus or young infant, let alone an adult. A recent study found some of the highest brain aluminum content ever measured in a human being within the brains of several deceased autistic people. Another recent study found that aluminum does not exit the body when it’s injected, it actually travels from the injection site into distant organs and into the brain, where it eventually ends up staying.
Sure, our bodies do a great job of getting rid of aluminum from other sources, like water or food, but injected aluminum does not flow into the same methods of excretion. This is extremely concerning because the HPV vaccine is loaded with aluminum.
Total compensation paid to families through the National Childhood Vaccine Injury Act/National Vaccine Injury Compensation Program sits at approximately $4 Billion. The alarming part is that only 1% of vaccine injuries are even reported, and only 1/3 of the petitions are compensated. This means that 99% of vaccine injuries go unreported and the families of the vast majority of people injured by vaccines paying the price. Vaccine manufacturers cannot be held liable for injuries or deaths that occur from use of their vaccines. And so, the pharmaceutical industry has no incentive to care about our health when it comes to making our ‘medications’ safe, since there is no punishment for them for not doing so. They can legally be careless with their product, and this is evident by the EXTREME lack of safety testing for many ‘medications’ including vaccines, especially the HPV Vaccine. (source)
This is why it’s great to see a new film coming out, attempting to bring more awareness to the topic. It’s called Sacrificial Virgins, andit investigates widespread global concerns over the safety of the controversial HPV vaccines Gardasil and Cervarix. It recently won two awards at the Watchdog Film Festival: one was for the best film of the festival, and the other one was the Watchdog Spirit Award in recognition of its investigation “in search of truth and justice.”
It also recently won the Social Impact Award at the Queens World Film Festival.
In Japan, women suffering from injuries as a result of the vaccine have had hearings, with the science showing cause for concern. Their injuries have been medically validated.
After a public hearing in February 2014, the Japanese government rescinded its recommendation that girls receive the HPV vaccine. Japan has actually established guidelines and special clinics for evaluating and treating illnesses caused by the vaccine. It is a scenario that Merck, GSK, and vaccine stakeholders globally are extremely anxious to suppress. (source)
“It is a vaccine that’s been highly marketed, the benefits are over-hyped, and the dangers are underestimated.” – Dr. Chris Shaw, Professor at the University of British Columbia, in the department of Neuroscience, Ophthalmology, and Visual Sciences (Taken from the One More Girl documentary)
It’s not like there haven’t been initiatives. In January 2016, pathologist Dr. Sin Hang Lee, MD, Director of Milford Medical Laboratory, sent an open letter of complaint to the Director-General of the World Health Organization (WHO), Dr. Margaret Chan. In the letter he challenges the integrity of the GACVS Statement on the Continued Safety of HPV Vaccination (issued March 2014), and charges professional misconduct on the part of several individuals (and suggests that others may have also been actively involved) in a scheme to deliberately mislead the Japanese Expert Inquiry on Human Papillomavirus Vaccine Safety before, during and after the February 2014 public hearing mentioned above in Tokyo.
Dr. Lee challenged the integrity of the GACVS Statement on the Continued Safety of HPV Vaccination written by Dr. Pless, accusing him of deliberately misrepresenting his scientific findings in order to mislead non-scientific readers and those who set vaccination policies. Dr. Pless is accused of deliberately conflating two unrelated articles, dealing with two different chemicals, written by different authors “apparently to create a target to attack.” Furthermore, Dr. Lee notes that the GACVS Statement relied on an unpublished 12-year old “Technical Report” written by an unofficial, unnamed “group of participants” (according to CDC’s disclaimer).
Why I believe It Makes No Sense To Take The HPV Shot
Of all the women who get an HPV infection, approximately 70 percent of those will clear that infection all by themselves in the first year. You don’t even have to detect it or treat it. Within two years, approximately 90 percent of those women will clear it all by themselves. By three years, you will have 10 percent of that original group of women left who still have an HPV infection, and 5 percent of this 10 percent will have progressed into a pre-cancerous lesion. So, “now you have that small group of women who have pre-cancerous lesions and now let’s look at that moving into invasive carcinoma. What we know then is that amongst women with. . . [pre-cancerous] lesions. . . it takes five years for about twenty percent of them to become invasive carcinomas. That’s a pretty slow process. It takes about thirty years for forty percent of them to become invasive cervical carcinomas.” (source)
Those comments are from Dr. Dianne Harper, one of a select few specialists in OB/GYN (in the world) who helped design and carry out the Phase II and Phase III safety and effectiveness studies to get Gardasil approved. There are only 50 HPV experts in the world, and Dr. Harper is one of them, arguably making her an expert on the subject.
Since Harper’s involvement in getting Gardasil approved, she has condemned the vaccine, stating that it is neither safe nor effective. But she’s gone back and forth, making positive comments as well.
Harper has told CBS that these vaccines are essentially useless, explaining that “the benefit to public health is nothing, there is no reduction in cervical cancers, they are just postponed, unless the protection lasts for at least 15 years, and over 70% of all sexually active females of all ages are vaccinated.”
This begs the question, why do nine-year old girls need vaccinations for symptomless venereal diseases that their immune systems kill anyway?
A brand new study recently published in the journal Pediatrics has found that many paediatricians don’t strongly recommend the HPV vaccine. Researchers used a national survey asking approximately 600 doctors to outline their stance on the HPV vaccine. Conducted between October 2013 and January 2014, the study found that a large percentage of paediatricians and family doctors — nearly one third of those surveyed — are not strongly recommending the HPV vaccine to parents and preteens, which is why, as illustrated by the study, HPV vaccination rates continue to drop.
Dr. Genevieve Rail, Professor of Critical Studies of Health at Concordia University, recently received a grant of $270,000 from the Canadian Institute for Health Research (CIHR) to study the Human Papillomavirus (HPV). She concluded that there is absolutely no proof that the human papillomavirus directly causes cervical cancer.
“I’m sort of raising a red flag, out of respect for what I’ve found in my own study, and for the despair of parents who had totally perfect 12-year-olds who are now in their beds, too tired to go to school,” she said. “Yes, we’re going against the grain, and we are going against those who are believed, i.e. doctors and nurses and people in public health.” (source)
She feels there are “serious concerns” about the vaccine, yet no research on how young people “experience” the vaccine. (source)
I could literally write a book on the HPV vaccine. The above information is not even a tidbit of info that all parents should be made aware of.
Summary: Researchers report an afternoon nap can help us to process unconscious information and enhance cognition.Source: University of Bristol.The age-old adage “I’ll sleep on it” has proven to be scientifically sound advice, according to a new study which measured changes in people’s brain activity and responses before and after a nap. The findings, published in the Journal of Sleep Research, support the advice which suggests that a period of sleep may help weighing up pros and cons or gain insight before making a challenging decision.The Medical Research Council-funded study, led by University of Bristol researchers, aimed to understand whether a short period of sleep can help us process unconscious information and how this might affect behaviour and reaction time.The findings further reveal the benefits of a short bout of sleep on cognitive brain function and found that even during short bouts of sleep we process information that we are not consciously aware of.While previous evidence demonstrates that sleep helps problem solving, resulting in enhanced cognition upon awaking; it was not clear whether some form of conscious mental process was required before or during sleep to aid problem solving. In this study, researchers hid information by presenting it very briefly and “masking” it – so it was never consciously perceived – the masked prime task. The hidden information, however, was processed at a subliminal level within the brain and the extent to which it interferes with responses to consciously perceived information was measured.
Sixteen healthy participants across a range of ages were recruited to take part in an experiment. Participants carried out two tasks – the masked prime task and a control task where participants simply responded when they saw a red or blue square on a screen. Participants practiced the tasks and then either stayed awake or took a 90-minute nap before doing the tasks again.
Using an EEG, which records the electrical activity naturally produced in the brain, researchers measured the change in brain activity and response pre-and-post nap.
The findings further reveal the benefits of a short bout of sleep on cognitive brain function and found that even during short bouts of sleep we process information that we are not consciously aware of.
Sleep (but not wake) improved processing speed in the masked prime task – but not in the control task – suggesting sleep-specific improvements in processing of subconsciously presented primes.
The findings suggest that even a short bout of sleep may help improve our responses and process information. Therefore, the results here suggest a potentially sleep-dependent, task-specific enhancement of brain processing that could optimise human goal-directed behaviour.
Importantly, while it is already known that the process of acquiring knowledge and information recall, memory, is strengthened during sleep. This study suggests that information acquired during wakefulness may potentially be processed in some deeper, qualitative way during sleep
Dr Liz Coulthard, Consultant Senior Lecturer in Dementia Neurology at the University of Bristol Medical School: Translational Health Sciences, said: “The findings are remarkable in that they can occur in the absence of initial intentional, conscious awareness, by processing of implicitly presented cues beneath participants’ conscious awareness.
“Further research in a larger sample size is needed to compare if and how the findings differ between ages, and investigation of underlying neural mechanisms.”
Contrary to conventional wisdom, brain regeneration is possible. One promising therapy that promotes neurogenesis and is effective in pre-clinical studies of Alzheimer’s and Parkinson’s is near infrared light therapy, and it may improve other mental illnesses and neurodegenerative disorders including dementia, stroke, ALS, and traumatic brain injury as well.
Alzheimer’s disease and Parkinson’s disease are the most common neurodegenerative disorders. The former is a type of dementia that occurs secondary to the accumulation of abnormal protein deposits in the brain, including β-amyloid plaques and intraneuronal neurofibrillary tangles made of tau protein (1). Upon neuroimaging studies, gross cerebral cortical atrophy is found, meaning that the part of the brain responsible for executive functions such as learning, memory, language, decision-making, and problem-solving progressively degenerates (1). In addition, gliosis, or brain inflammation, is a hallmark characteristic of Alzheimer’s (1).
One hypothesis that is championed proposes that Alzheimer’s occurs due to self-propagating, prion-like protein assemblies, which interfere with the function of nerve cells (2). An alternate theory is that these so-called proteinopathies occur secondary to a microvascular hemorrhage or brain bleed (3). The brain bleed is believed to be the result of age-induced degradation of cerebral capillaries, which creates neuron-killing protein plaques and tangles (3).
Dysfunction of mitochondria, the energy-generating powerhouses of the cell, is also implicated in Alzheimer’s, as reduced efficacy of these organelles creates oxidative stress-inducing reactive oxygen species, or free radicals, which lead to neuronal cell death (4). Whatever the cause, extensive death of brain cells occurs, which explains the cognitive deficits that occur with Alzheimer’s disease, in addition to symptoms such as impaired judgment, confusion, agitation, linguistic abnormalities, social withdrawal, and even hallucinations (1).
Parkinson’s disease, on the other hand, is characterized by progressive death of dopamine-producing neurons in a region of the brainstem called the substantial nigra, but it can extend to other brain areas such as the locus coeruleus, olfactory bulb, dorsal motor nucleus of the vagal nerve, and even the cortex in late stages (5). As a result, the primary manifestation is that dopamine deficiency appears in the basal ganglia, a set of nuclei embedded deep in the brain hemispheres that is responsible for motor control (6). This leads to the cardinal manifestation of Parkinson’s, namely, a movement disorder that includes bradykinesia or slow movement, loss of voluntary movement, muscular rigidity, and resting tremor (7).
Not unlike what happens in Alzheimer’s, accumulation of abnormal intracellular protein aggregates known as Lewy bodies, composed of a protein called α-synuclein, is thought to be central to the pathogenesis of Parkinson’s disease (8). Like Alzheimer’s, mitochondrial dysfunction induced by genetic mutations, toxic agents, or damage to blood vessels is also considered to contribute to neuron cell death in Parkinson’s (9). Toxin exposure is especially implicated, as animal studies hint that development of Parkinson’s disease may occur as a byproduct of exposure to neurotoxins such as rotenone or paraquat (10). Impaired blood brain barrier function and damage to the endothelial cells of the vascular system, which line the interior surface of blood vessels, are also thought to play a role in Parkinson’s (10).
Overturning Old Notions of Neuroscience
The central dogma of neuroscience conceived of the central nervous system tissue as “perennial” after the doctrines of Giulio Bizzozero, the most prominent Italian histologist, who decreed that the lifelong cells of the nervous system were devoid of replicative potential (11). In other words, the perennial nature ascribed to the nerve cells of the brain and spinal cord meant that nerve cells were believed to be incapable of undergoing proliferation, or cell division, in the postnatal brain (11). While the early stage of in utero prenatal development known as embryogenesis permits massive neurogenesis, or the ability to create new nerve cells, the scientific consensus up until the end of the twentieth century held that neurogenesis was arrested after birth in mammals.
Santiago Ramon y Cajal, who led the charge in the neuroscience discipline in the later half of the nineteenth century onward and won a Nobel Prize for Medicine and Physiology, in fact stated that: “Once development was ended, the fonts of growth and regeneration of the axons and dendrites dried up irrevocably. In adult centers, the nerve paths are something fixed and immutable: everything may die, nothing may be regenerated” (11). Acknowledgment of the mere possibility of adult neurogenesis was hampered by the fact that scientists lacked the visualization techniques to detect neural stem cells, the precursors to new neurons and means by which neurogenesis occurs, and also did not have access to the molecular markers and microscopy required to observe cells in different cycle phases.
This view of nervous tissue as perennial was also reinforced by clinical observations that patients with chronic neurodegeneration, traumatic brain lesions, and cerebrovascular diseases do not experience functional recovery (11). Prevailing theories posited that adult neurogenesis was an evolutionary unlikelihood, since it would interfere with pre-existing neuronal connections and the fine-tuned electrochemical communication in the nervous system, as well as disrupt memory recall, which was believed to occur via stable neuronal circuits created and encoded during learning (11).
That brain cells are finite, and incapable of regeneration, painted a portrait of doom and gloom and inexorable debilitation for patients suffering from devastating neurodegenerative conditions. However, relatively recent discoveries have overturned these antiquated conceptions by revealing that the brain is plastic, or pliable, and that even neurons in adult higher vertebrates are capable of neurogenesis.
Scientists Discover Neural Regeneration is Possible
In the 1960s, these postulates of the old neurobiology were disproven when Joseph Altman and colleagues performed an experiment where radioactively labelled thymidine, one of the nucleotide base pairs that makes up DNA, was incorporated into a brain area called the dentate gyrus of the hippocampus and integrated into the genetic material of what was later confirmed via electron microscopy to be dividing neurons (12, 13). In essence, this illustrated that neurons were undergoing mitosis, a process of cell division where genetically identical daughter cells are created, and showed that adult neurogenesis is possible.
Another nail in the coffin of this antiquated perception of the nervous system was that neural stem cells, the multipotent, self-renewing progenitors from which new neurons arise, were found in the brains of adult mammals, and discovered to undergo expansion in their populations when prompted by signaling molecules called growth factors and morphogens (11). The multiplication and differentiation of neural stem cells, which are residents of the central nervous system, is essential for neurogenesis (14). Neural stem cells are capable of generating all of the cell types of the nervous system, including astrocytes, glial cells, and what are called oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system (11). Researchers Colucci-D’Amato and Bonita in fact state that, “To date neural stem cells have been isolated from nearly all areas of the embryonic brain and in a growing list of adult mammalian brain areas, including cerebellum and cortex” (11, p. 268).
Other advances, such as confocal microscopy and the identification of cellular markers which allowed the phenotype of cells to be characterized all culminated in the realization that neurogenesis occurs continuously in some brain area, such as the hippocampus and subventricolar zone (SVZ), the former of which is responsible for the formation and consolidation of memories (11). To date, neurogenesis has been shown to be influenced by various chemical, pharmacological, and environmental stimuli. For instance, work by researcher Fernando Nottebohm demonstrated the spontaneous replacement of neurons in the adult avian brain (15). In song birds such as canaries, which experience seasonal modification in their songs, new neurons are recruited into their neuronal circuitry in a way that may be dependent upon social and reproductive interactions, territorial defense, migratory patterns and food caching (15).
This all should serve as a beacon of hope for patients experiencing the ravages of neurodegenerative disease, as it may mean that epigenetics, or the way gene expression changes based on lifestyle factors, may lend itself to neurogenesis and the reversal of these scourges of mankind. For example, researchers state that an enriched environment, learning, exercise, exposure to different odorant molecules, and drugs such as antidepressants, steroids, and alcohol can all favorably or unfavorably impact neurogenesis (11). These newfound revelations are being used in fact as an impetus to find cures for a laundry list of neurodegenerative diseases (11).
Novel Therapy Shown to Grow New Nerve Cells
Despite this research, the prevailing view of neurodegenerative diseases such as Alzheimer’s and Parkinson’s is that their underlying pathophysiology, a relentless progression of neuronal death, remains irreversible (10). Thus far, then, approaches have aimed to slow or stop neuronal cell death or to develop disease-modifying treatments that could stabilize the rate of neurodegeneration (10). One non-pharmacological therapy that may be able to actually regenerate brain cells, however, is light in the near infrared range, also known as low-level laser or light emitting diode (LED) therapy that utilizes wavelengths in the red to infrared spectrum.
Near infrared light therapy has the potential to “mitigate ubiquitous processes relating to cell damage and death,” and may have applications in conditions that “converge on common pathways of inflammation and oxidative stress” (10). This is demonstrated by the widespread efficacy of near infrared light therapy in improving conditions including traumatic brain injury, ischemic stroke, major depression, and age-related macular degeneration (10). In traumatic brain injury, for example, treatment with near infrared light improves social, interpersonal, and occupational functions, reduces symptoms of post-traumatic stress disorder (PTSD), and is helpful for sleep (16).
Because near infrared light treatment improves cognitive and emotional dimensions (17) and enhances short-term memory and measures of sustained attention (18), researchers have long suspected its potential for neuropsychological disorders. In a revolutionary publication, scientists propose that infrared light is superior to pharmacological standard of care for these debilitating conditions given its neuron-saving abilities (10).
For instance, in mouse models of traumatic brain injury, near infrared light increases levels of brain-derived neurotrophic factor (BDNF), a protein which helps dying nerve cells survive (19). In addition, infrared light both improves neurological performance and increases the numbers of neuroprogenitor cells, the precursors to new neurons, in areas of the brain such as the dentate gyrus of the hippocampus and the sub ventricular zone (20).
Near Infrared Light Therapy in Alzheimer’s and Parkinson’s
Although human trials have not been yet conducted in Alzheimer’s disease, mouse studies show that near infrared treatment reduces its characteristic proteinopathies, decreasing brain levels of β-amyloid plaques and neurofibrillary tangles of tau proteins, while also ameliorating cognitive deficits (10). Cellular energy production, as indicated by levels of ATP, were increased in these studies alongside bolstered mitochondrial function and (10). In transgenic mouse models of Alzheimer’s, application of non-thermal near infrared light reversed significant deficits in working memory and significantly improved cognitive performance (21).
In animal models of Parkinson’s, near infrared treatment has been shown to rescue dopaminergic neurons, the subset that degenerate in this condition, from death (10). In addition, near infrared light treatment corrects the abnormal firing activity of neurons in deep subthalamic brain regions that occurs in parkinsonian conditions (22). Various animal models of Parkinson’s disease shown improved motor control and locomotor activity, as measured by both mobility and velocity, after near infrared is applied (10).
In a macaque monkey model of Parkinson’s, an optical fiber device that administered near infrared to the midbrain largely prevented the development of clinical signs of Parkinson’s when the animals were injected with a chemical known to induce this disorder (23). It also preserved a greater number of dopaminergic nigral cells compared to the monkeys that had not received infrared treatment (23). Limited case reports in humans have shown that near infrared administered through an intranasal apparatus improves symptoms in the majority of Parkinson’s patients, and that its application to the back of the head and upper neck reduced signs of Parkinson’s in one patient (10). Other reports indicate that gait, speech, cognitive function, and freezing episodes were improved in late-stage Parkinson’s patients who undertook this therapy (24), but the study was low-quality (10).
Mechanism of Action: How Near Infrared Promotes Neurogenesis
The ways in which near infrared promotes neurogenesis are multi-fold. There is evidence that near infrared light exerts a hormetic effect, acting as an adaptive or positive stressor. Another example of a hormetic effect is that exhibited by phytonutrients in fruits and vegetables, which act as antioxidants by paradoxically stimulating oxidative damage via a pro-oxidant mechanism. This in turn up-regulates our endogenous antioxidant defense system. Similarly, near infrared light activates cellular stress response systems by targeting a key enzyme in the electron transport chain which is responsible for mitochondrial-based energy production called cytochrome c oxidase, an enzyme that is fundamental to the cellular bioenergetics of nerve cells (25).
By accepting light in the near infrared range of the electromagnetic spectrum, this enzyme induces a change in the electrochemical potential of the mitochondrial membrane, jump-starting production of the cellular energy currency called adenosine triphosphate (ATP) and causing a mild burst in the synthesis of reactive oxygen species (ROS) (10). As a result, downstream signaling pathways are triggered which induce reparative and neuroprotective mechanisms, including neurogenesis, the creation of new synapses, and brain-based antioxidant and metabolic effects (25).
Restoration of mitochondrial function in the endothelial cells lining cerebral blood vessels may also help neurons survive by repairing the blood-brain barrier and vascular network which is compromised in neurogenerative conditions (10). Impressively, “This modulation of multiple molecular systems appears capable of both conditioning neurons to resist future damage and accelerating repair of neurons damaged by a previous or continuing insult” (10).
On the other hand, the application of near infrared light has been shown to elicit systemic effects, possibly via circulating molecular factors (10). In other words, light in the near infrared spectrum applied to a local area elicits benefits in distal tissues remote from the initial site, perhaps by stimulating immune cells that have a neuroprotective role (10). Another way in which near infrared light activates global effects in the body is by up-regulating the production of signaling molecules known as anti-inflammatory cytokines, while down-regulating pro-inflammatory cytokines (26).
Near infrared also mobilizes tissue repair processes by improving the migration of white blood cells to wounds, increasing neovascularization, or the formation of new blood vessels, and facilitating formation of collagen (27). There is also evidence that near-infrared light exposure causes stem cells from the bone marrow to navigate to the site of damage and to release so-called trophic factors such as BDNF, which enhances nerve cell function and survival (28). Lastly, a system of communication between the mitochondria in the brain and the mitochondria in the tissues may be at play, so that application of near infrared light at a point in the body far from the brain can lead to neural regeneration (10).
Practical Application of Near Infrared Light Therapy
The key to mitigating the burden of chronic illness lies in physiological regeneration, which is emerging as a physiological inevitability, even in regions of the body where it was previously not thought possible. The ability to regenerate, secondary to normal biological processes of cellular erosion and decay, is programmed into our body in order for us to regain homeostasis.
So-called “photobiomodulation,” which includes near infrared light therapy, has limitless possible applications, and has even been shown to improve animal models of wound healing, heart attack, spinal cord injury, stroke, arthritis, familial amylotropic lateral sclerosis (FALS), diabetic ulcers, carpal tunnel syndrome, major depression, generalized anxiety disorder, frontotemporal dementia (29) and traumatic brain injury (27).
The biggest obstacle with infrared light therapy in neurodegenerative disease is targeting the zone of pathology, “when there are many intervening body tissues, namely skin, thick cranium, and meninges, and brain parenchyma,” since there is considerable dissipation of the signal across each millimeter of brain tissue (10). This is less problematic in Alzheimer’s, where the target regions are more superficial structures, but less easily rectified in the case of Parkinson’s, where there is significant distance from cranium to the brainstem where neurodegeneration takes place (10).
With Alzheimer’s, optimal delivery would be a near infrared light-emitting helmet worn over the entire cranium (10). Parkinson’s patients can achieve symptomatic relief when near infrared is applied in this fashion, as this would influence the abnormal neural circuitry in the cortex. However, to circumvent the problem of the sheer distance to the region of pathology in the brainstem, researchers propose that the minimally invasive surgical implantation of an optical fiber device near the brain parenchyma would be ideal, which would deliver therapeutic levels of near infrared (10). Until these options are commercially available, photobiomodulation devices or near infrared saunas may be a viable option, although human studies have not proved their efficacy.
Given its large margin of safety and lack of adverse effects, near infrared light therapy should be offered as an option for patients suffering from a myriad of chronic conditions, but is especially promising for neurodegenerative diseases including Alzheimer’s and Parkinson’s and may even have future use in multiple sclerosis. Near infrared therapy is superior to the mainstay drug treatments for these diseases since pre-clinical studies have demonstrated proof-of-concept that near infrared either arrests or slows the underlying pathology of these disease processes, and leads to the birth of new neurons, rather than merely mitigating symptoms (10).
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Ali Le Vere holds dual Bachelor of Science degrees in Human Biology and Psychology, minors in Health Promotion and in Bioethics, Humanities, and Society, and is a Master of Science in Human Nutrition and Functional Medicine candidate. Having contended with chronic illness, her mission is to educate the public about the transformative potential of therapeutic nutrition and to disseminate information on evidence-based, empirically rooted holistic healing modalities. Read more at @empoweredautoimmune on Instagram and atwww.EmpoweredAutoimmune.com: Science-based natural remedies for autoimmune disease, dysautonomia, Lyme disease, and other chronic, inflammatory illnesses.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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