Neurofeedback Blog

All that relates to neurofeedback and brain health

How Honesty Changes Over A Lifetime

I’ve been applying to grad school programs again (for counseling so I can earn my mental health license so I don’t need to work under someone else’s mental health license), which I’m learning is a lot different now that I’m 42 (well, in two weeks) than when I last applied to grad school when I was 21-23. It’s not just that everything’s online now (including the entire programs to which I am applying), but I’m different, too. The thing is, 20 years ago I had no idea what it would be like during and after grad school. One might say that I was naive, but I think it’s more accurate to say that I was inexperienced, and now I am experienced. Obviously, I’m not experienced in everything, or else I wouldn’t need to go back to grad school, but I’m definitely significantly more experienced in life than I was 20 years ago. So when I had an interview (an online group interview) with the first program for which I applied in December, I found that my honest answers were different from the honest answers of my fellow applicants who were much younger than me. It’s not that I don’t think they were being honest, but I do think that they couldn’t be as honest as me due to not having as much experience.

For instance, one of the questions that was asked was “how do you deal with negative feedback?” Well, first, I should’ve asked the faculty member what she meant by that question because it didn’t become apparent to me until the end of the interview that it was a question about how we deal with feedback from our mentors/teachers/superiors, and not what I took it to mean which was someone complaining about me or saying something negative to me about me. So my answer was that my first instinct is to feel a little defensive (as I assume most people feel since that’s often how they behave), but that I’ve learned to take a step back and try to understand if I agree with them or not and if it’s something I need to change, but that I generally understand that negative or positive feedback usually says more about the person giving it than necessarily about the person receiving it. As you might guess, the others in the group basically said that they love negative feedback and use it to grow and become better people, blah blah blah. I could’ve said that (and I probably would’ve choked on it in my throat because of the heavy b.s. and brown-nosing factor), and I probably would’ve said that 20 years ago when I didn’t want anyone to know that I had any imperfections (as if they couldn’t see them, anyway). Now I am confident that even with my imperfections, I’m no worse than anyone else, and I am still a good person, so I wasn’t shy about admitting that I don’t like negative feedback. Had she asked how I deal with “constructive criticism”, which is what I think she was trying to ask, then my answer would’ve been closer to what was clearly the “correct” answer.

Anyway, I was not accepted into that program and I’m 99% sure it was all because of that interview when I was being honest. Now, mind you, I’ve been rejected from things before so it’s not that I’m unable to grasp that I can be rejected, but this was truly a surprise because I understand that interviews like this for grad school are often just as much about selling the program to us as it is about selling ourselves to them. To be fair, I had already decided that I wouldn’t continue with the program since I hadn’t checked the price before I applied (it was a free application, so I half-whimsically applied without investigating the logistics too carefully) and it’s over $100k for the 2.5 year program! Holy moly that’s expensive and not worth it since the median income for a licensed, professional counselor is in the mid $40k range. I think it’s pretty insane to put that kind of debt on someone who’s never going to make that kind of money!

This actually brings me to another honest answer I had that probably was to my detriment – the faculty member asked what our biggest obstacle to success is and my first (and most truthful) answer was MONEY! MONEY! MONEY! Because I wouldn’t need to go back to school and get a degree in counseling if I had enough money to sustain me so I could give everyone neurofeedback for free! I probably would still need to get my mental health license, but I wouldn’t need to worry about the cost of going back to school! Alas, I am not independently wealthy, and thus, I need to charge for my services, etc. But after I said that money was my biggest obstacle I said that I also have a more self-reflective answer since I know that’s what they’re looking for and I went on to talk about how “focus” has been an issue for me in my life which my grad professors brought up and then my post-doctoral mentors reiterated. (Of course, what they really wanted was for me to do nothing other than research at the lab all day every day because that’s the expectation – and one of the reasons I left research – which I tend to think is rather unhealthy, especially for someone like me who has a lot of different interests and abilities.) Anyway, I still stand by original answer and I know everyone knows it’s the gosh-darn truth. Money is almost always the biggest obstacle to doing what you want to do in this life, which is how I define success. For instance, going back to grad school is going to cost a lot of money and I’m making my choice of which program to go into based largely on the cost of the program due to not being able to take on such massive debt.

So I was thinking about how my honest answers have changed over my lifetime so far, and I think it’s something we need to consider when we ask others to be honest with us. The less mature, less experienced people are, the less likely their honesty will be all that true. They will be as honest as they can be, but it may not even be their truth. So we just need to be aware of that and maybe adjust our expectations when we ask different people for their honest answers.

Lunar Effects on Mood and Biology Are Real

Last week in North America we saw the largest Super Moon of the year so far – it was called the “Super Snow Moon”. At the same time, I had several clients have strangely aberrant reactions to their neurofeedback sessions, as well as several friends on facebook making particularly emotional posts and complaining of feeling crazy, including myself. I thought it might be a reaction to how I felt the week before with a bunch of stressors, but then my father said something in passing about the supermoon and I wondered if there really might be a connection.

At the gym, a woman who is a former counselor who used to work at an emergency call center talked about how they would joke every full moon about how many more calls they expected to get. Others weighed in with their stories of eventful “coincidences” when you could essentially count out 9 months after a really bad storm and then there would be a bunch of babies suddenly being born around the same time (implying that couples tend to “get it on” more during storms, thus increasing the pregnancy rates at those times). Anyway, this could all just be our brains looking for connections where there may or may not be any, right? So I decided to take a look into the literature.

You see, my father has a Ph.D. physics. He actually warned me against writing this post since he worries that it’ll come across as pseudo-science and people will reject it and me and think we’re a bunch of dummies, I guess. I’m not entirely sure because I told him I write what I’m interested in and if he wants to write a post he is very welcome to do so. In any case, he is the one who mentioned the moon connection in the first place to me, so I find that interesting. He said that since the moon affects Earths magnetic field, it could also possibly affect any of us who are affected by Earth’s magnetic field. Well, we know that birds use Earth’s magnetic field to navigate, so why wouldn’t we have some connection with it? Why wouldn’t human biology also be affected by changes in earth’s magnetic field?

The answer is yes, human (and other animal and plant) biology is, indeed, affected by the the phases of the moon, which may be explained by sensing changes in the “magnetosphere” (the magnetic field surrounding the earth), but not so much by the gravitational or light effects by the moon. In a paper titled, “Lunar biological effects and the magnetosphere, Michael Bevington describes the evidence for lunar biological effects and how they are most-likely explained by the full moon traversing the moon’s “magnetotail”, an electromagnetic plasma sheet that extends out from the surface of the Earth opposite the sun (and its spiraling solar wind). When the moon crosses the magnetotail’s sheet, it attracts a large electrical charge, increasing the electric field on the dark side of the moon, which causes ions from the moon’s surface to transfer to the Earth’s magnetosphere and increase the Earth’s electromagnetic field, creating a magnetosphere feedback mechanism.

Here are some of the reported effects of the full moon on animal and plant biology (summarized in the above-mentioned article): tree diameter variation reflects a lunar rhythm; reproduction, changes in the stress hormone, glucocorticoid, and foraging by mice follow a lunar rhythm; epileptic seizures increase by over 1.5 times during a full moon, as well as the number of sudden unexpected deaths in epilepsy (highest [70%] during the full moon); the number of patients with violent and acute behavioral disturbances doubled during the full moon compared to other lunar phases; and a recent study showed that bipolar mood cycles correlated with lunar phases in 17 patients with rapid cycling bipolar affective disorder. Then, of course, there are many more anecdotal reports from doctors at hospitals and others who say that they see an increase in patients coming in during the full moon, etc.

The prevailing belief that the full moon affects human biology has been around for millennia, and many authors tend to cite the ancient Roman philosopher and naval and army commander, Pliny the Elder, as the first to make the connection between the lunar phases and the tides. He also was able to see the correlation with shellfish and other sea creature growth and suggested that the moon had nourishing powers. It used to be a given that humans believed in the biological effects of the full moon, but in the last century or so, scientists have had a hard time gathering enough evidence to demonstrate a causal effect, which is understandable seeing as all you really can do is maybe show a correlation due to not being able to isolate or control all the confounding factors involved. Even the correlative effects are not 100% penetrant (meaning, not everyone is affected by the full moon or other lunar phases). Having a scientific explanation and mechanism for how the lunar phases (particularly the full moon) affects biology is also important for determining the likelihood of biological effects. Unfortunately, most attempts at finding an explanation have fallen short, such as mechanisms involving the gravitational effects of the moon or the light effects of a full moon. I will not go into detail about why those fail, but I refer the reader to the initial article that I linked to this blog for such detailed information.

Suffice it to say, the best explanatory mechanism for how the full moon affects biology is its effects on Earth’s electromagnetic field. As described above, as the full moon traverses the magnetotail of the magnetosphere, it causes a feedback mechanism between the Earth and the Moon to increase the potential of the electric field on Earth by 1-7 V/m (measured by Michael Bevington). In fact, the measurements show that the greatest change in the potential occurs as the moon crosses into and out of the magnetotail plasma, which occurs 2-3 days before the full moon and 3-4 days after the full moon (Table 1 below and depicted in the figure on the right).

It is true that 1-7 V/m is a very weak electromagnetic field, but if you consider that the electrical potentials of the cerebral cortex, as measured from the scalp by electroencephalography (EEG), are generally in the micro-volt to milli-volt range (meaning 0.001 – 0.000001 V range), and that neurons are generally holding an electrical potential difference across its membrane around 70 mV (0.07 V), this suggests that 1-7 volts could have pretty dramatic effects on the human body. However, until very recently, scientists did not believe that the human body could perceive changes in electric fields (EFs) at such small levels. It was previously thought that humans can only detect static EFs (like that at the surface of the Earth) through its changes in electrical discharges on the surface of the body and their interaction with body hair or the creation of micro-shocks, but a recent meta-analysis concluded that “5% of the participants could detect a static EF below 20 kV/m, 33% of the subjects detected a static EF below 40 kV/m and 66% detected fields below 50 kV/m“. Of course, these EFs are much, much greater than that which were measured at the surface of the Earth by Michael Bevington at 1-7 V/m around the time of a full moon, so we still cannot claim that a large proportion of people can likely detect the 1-7 V/m change in the Earth’s EF during a full moon.

But last week’s full moon wasn’t any old full moon, it was a SUPER MOON, which is a special kind of full moon when the moon is at its closest point (perigee) to the Earth on its elliptical orbit around the Earth. Not only does this make the moon appear larger, but it also means that it passes through more of the magnetotail than a regular full moon, and it also increases the feedback mechanism and electromagnetic strength between the Earth and the moon. Therefore, we can hypothesize that the increase in electrical potential at the surface of the Earth would be much greater during a super full moon than during a regular full moon, although I don’t know how much greater that might be, but I’m sure someone with better math and physics skills than me could make a decent estimation (like my father!). Furthermore, the intensity of the EF at the surface of the Earth increases with moisture like rain or snow, which we certainly have in abundancy in the Pacific Northwest! So, altogether, it seems that we had two additional factors that increased the intensity of the effects of the full moon on us in the Pacific Northwest last week – a super moon and lots of rain and snow.

There are a few more pieces of this puzzle that I want to add but are hard to place in this post. One is that Michael Bevington’s measurements of the electric field potentials at the surface of the Earth are a little misleading, since the truth is that there is a gradient in the electrical potential from the surface of the Earth to the outer atmosphere and beyond. This gradient is typically between 0.3 – 120 V/m, while it is typically less than 1 V/m under 30 km from the Earth (in concurrence with Michael Bevington’s measurements). I just wanted to mention this because it does matter where you measure the EF potential (and it changes throughout the day/night, whether over land or water, etc.). I would like to measure the EF at the surface of the Earth during a regular full moon and also during a Super full moon to test my hypothesis that the super full moon increases the EF potential even more than a regular full moon (ideally I’d also measure the “apogee” full moon, aka “micromoon”, because that should change the potential even less).

A recent report suggests that humans might actually have a type of 6th sense in which we can perceive magnetic fields (particularly, the Earth’s magnetic field). Of course, this is not the same as detecting a static electric field, but geophysicist Joe Kirschvink at Caltech was able to demonstrate that a weak magenetic field could change the brainwaves of two dozen subjects in a Faraday cage (to block out ambient electromagnetic noise). Specifically, he observed a decrease in alpha waves (it makes sense that he looked at alpha waves since alpha is the easiest brainwave to detect in typical/”normal” humans). Since alpha brainwaves are considered “standby mode” brainwaves that increase synchronously when the brain is not processing information in that region, Kirschvink’s results indicate that these brains were being activated (or agitated) when sensing the changing magnetic fields, or it could merely mean that the brains were processing the perceptual information of the changing magnetic fields (thus, no longer in “standby mode”).

Lastly, I want to acknowledge the fact that there are people who are highly sensitive to or who have highly unusual interactions with electromagnetic fields. I’m referring to people who have many adverse reactions when using their cell phone, computer, or when working under fluorescent lights, etc., as well as people who may walk in a room and cause the lights to flicker or who may be constantly causing their electrical devices to blow fuses, etc. There are probably more of the former than the latter, but the existence of both is considered controversial in the scientific community, although there have been many studies trying to ascertain whether or not Electromagnetic (Hyper)Sensitivity exists as a real syndrome. I personally do not need a huge epidemiological study to know that there are some people who are highly sensitive to electromagnetic field (EMF) changes, but I can understand the need for such studies in order to determine what measures we may need to take to regulate the amount of electromagnetic radiation we are exposed to for public health’s sake. Otherwise, it’s a matter of individual choices, so why argue with someone if they say they are highly sensitive to electromagnetic radiation? If it doesn’t affect you, why do you need to judge whether or not their symptoms are really caused by the electromagnetic radiation? Plus, maybe the studies showing no correlation aren’t probing the problem appropriately. Such as, maybe there are more pieces of the puzzle missing when they try to do experiments in a lab where they alter the EF potential and ask the subjects if they can sense a difference or if they are having any adverse effects. The EF may be one of several factors that either add up and/or synergize to cause the adverse effects. In any case, I think, as a society, we are too quick to judge each other on our individual differences, especially when it comes to perception. One person can never truly know how another person perceives something, and that is just the way it is. It’s the natural limitation of being separate beings. We can, however, make predictions and test hypotheses to determine if pieces of our model of how differences in perception work, which, if confirmed, can only bolster the validity of our perceptions. This is, of course, the scientific approach to a subjective experience, which can never truly be understood scientifically.

Sex Differences in Response to and Recovery from Stress

One of my favorite Radiolab episodes was from Season 2, episode 4, and is called Where Am I?” [All of the best episodes are from their first few seasons, in my opinion. In more recent years – since 2008 or so – the episodes have been less science-y and more storytelling with only a very slim scientific connection. Maybe it’s more enjoyable for the lay public, but it’s pretty sad to me because, although I love storytelling podcasts, I miss those big questions that Radiolab used to tackle. Now it’s just another This American Life, but not as good as This American Life.]

Between 6:00 – 9:00 min into the episode is a segment about how we feel ourselves on the inside (called interoception) and how that helps us define our emotions. One theory, in fact, is that all emotions are really interpretations of our visceral senses, which are the inner senses of our body, signaled to our brain via the cranial nerves, particularly the vagus nerve (aka cranial nerve ten/CN X), as first postulated by William James and called the James-Lange Theory of emotions. After that, around 9:00 – 14:00 into the episode, is a mini dramatic sequence where Robert Krulwich argues with his wife on the phone, then they appear to resolve it, but then just moments later his wife continues the argument. After this there is a discussion with Stanford researcher, Robert Sapolsky, about the gender (although it’s more appropriate to say ‘sex’ because ‘gender’ is a social construct and does not depend on your sex hormones) differences in recover from stress (or, really, the autonomic nervous system – ANS). His research has shown that for both men and women, the ANS is activated at similar speeds or kinetics. However, the deactivation or resolution of the ANS is much slower in women than in men, which comes across as men “letting go” more quickly and women seeming to hold on to the same emotions for longer.

The autonomic nervous system, or ANS, is called such because we have no voluntary control over it, or so they say. The truth is that we can learn a certain amount of control over it, just like how we learn to hold our bladders until we can get to a toilet to relieve ourselves. For simplicity’s sake, however, we say that we have no voluntary control over it because, to a large extent, we do not. As you may recall, there are two branches of the ANS: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). The SNS is responsible for the “fight-or-flight” response to threats, while the PNS is responsible for the recovery and relaxation, energy reserving phase after the “fight-or-flight” phase. In general, we aim to spend most of our time in between these two states of being, erring on the side of the more calming, PNS state. Most, if not all, therapies for anything having to do with the body aim to help the subject get into and stay in the PNS state, including neurofeedback, but also acupuncture, massage, psychotherapy, hypnosis (an even deeper state), etc. When you’re in the SNS, you’re unable to do anything but survive. The primary issue is when you get stuck in a SNS-dominant state and cannot move out of it into a more PNS-dominant state. What Dr. Sapolsky’s research indicates is that women’s bodies take longer to exit the SNS-dominant state due to differences in the breakdown of the factors (hormones, etc.) involved in the activated state, so they feel like they’re still upset even after the appearance of resolution. This is why men and women tend to have different timelines in their arguments, while men “get over it” more quickly than women.

There are more implications of this research than just differences in the way men and women resolve their arguments. Many of the implications are physical (such as heart rate, blood pressure, and metabolism) – stress is more physically damaging to women than to men, and these differences vary within the women’s menstrual cycle and depend on the level of circulating estrogen (which causes this increased reactivity along the hypothalamus-pituitary axis [HPA]). Of course, this suggests that women lose out when compared to men in response to stress; however, there is another aspect to the sex differences in stress responses that demonstrates why women do not exit the stress response as quickly as men: it’s because women tend to respond to stress in a nurturing, relationship-building manner – what is called tend-and-befriend” (as opposed to “fight-or-flight”). The fight-or-flight response in men makes sense as a very high adrenaline response, which would deplete the man’s energetic resources fairly quickly, thus necessitating a quick resolution of the response. However, the tend-and-befriend response is less energetically taxing to the woman’s body and may even require a longer period to execute properly (it takes longer to build relationships than to destroy them), thus extending the response time until its resolution.

Whenever one talks about sex differences where the words “gender” and “sex” are intermixed (due to a fundamental misunderstanding of their different meanings) there is a lot of miscommunication that can occur. Again, to clarify, we’re talking about sex hormones driving the difference in the time it takes to break-down or metabolize the endocrine factors (neurotransmitters, hormones, etc.) that are involved in the sympathetic nervous system.

Finally, it occurred to me recently after another failed attempt at dating that the initial feelings of romantic or sexual attraction feels a lot like the fight-or-flight response (including the “freeze” variation), which suggests that it is driven by the sympathetic nervous system. It’s definitely automatic, since it’s not voluntary! Then I looked up on Pubmed (database of primary bio-medical publications) and found that, indeed, the sympathetic nervous system is activated during romantic and sexual attraction – in women! Apparently, erections in men are driven by the parasympathetic nervous system (PNS), while the orgasm is driven by the SNS. In any case, following the logic of this blog, we finally have a physiological explanation for why women tend to have a harder time getting over break-ups than men do! (And I have an especially hard time, but that’s another story altogether!)

So hetero women out there: it’s perfectly natural that you are holding on to the relationship for longer than he is – it’s your biology. However, don’t expect him to understand, that’s his biology. Womp womp. It probably also explains why lesbians tend to stay friends with their exes (of course, this is mostly not the case for me, but I do see it a lot with my friends).

Lastly, neurofeedback does help reduce the half-life of the ANS for those of us who feel like we have extra-long half-lives. I have personally witnessed this in myself after doing many sessions of neurofeedback; I can “let go” much more easily than I ever had been able to in the past. No combination of medications or talk therapy has ever gotten me even close to feeling more able to “let go”, but I did learn a lot of better coping techniques so I wouldn’t behave regrettably when it took me longer to “let go”. Now I don’t even need to use those coping techniques nearly as much since I don’t even feel it as badly – I feel like I can naturally move on sooner, and that honestly feels like a miracle! Come in and find your own miracle if you’ve experienced similar difficulties!

The New Epidemic: Doctors Gaslighting their Patients

I got in a bit of a comment war on facebook yesterday because I got fed up with the snarkiness of the anti-vaccinations-triggering-autism crowd (a.k.a., the anti-anti-vaxxers, although I’m not an anti-vaxxer). Yes, the studies show that there is no widespread association between vaccinations and autism. However, on an individual basis, there does seem to be a connection of some sort, or else why on earth would it have become a controversy in the first place? If even one child developed autism or autistic characteristics (and, thus, they were diagnosed with being on the autism spectrum) as a consequence of vaccination, then I think we have an obligation to understand that connection. The main problem of this controversy is the implication of a widespread association between vaccination and autism. The research has unequivocally demonstrated that vaccines to do not cause autism in any significant proportion above the overall incidence of autism. However, this does not mean that a very small population of people (likely with a genetic or epigenetic susceptibility) may be triggered to develop autistic characteristics as a consequence of vaccination (and the immune response that it causes). However, I don’t want to discuss the particulars of this debate. This blog post is not about the epidemic of people not vaccinating their children due to fears of autism. This blog post is about a different epidemic that I think is possibly just as concerning: the epidemic of medical doctors not listening to the patients and essentially “gaslighting” them.

The term, “gaslighting”, is relatively new to me. I honestly wish I had heard of it years ago because it would’ve made me feel more sane having an actual term for the phenomenon I was experiencing with certain friends and exes. “Gaslighting” refers to when someone essentially tells you that what you experienced did not actually happen; it basically undermines your reality. This is what the Encyclopedia Brittanica says about “gaslighting”:

“Gaslighting [is] an elaborate and insidious technique of deception and psychological manipulation, usually practiced by a single deceiver, or “gaslighter,” on a single victim over an extended period. Its effect is to gradually undermine the victim’s confidence in his own ability to distinguish truth from falsehood, right from wrong, or reality from appearance, thereby rendering him pathologically dependent on the gaslighter in his thinking or feelings.”

A still from the 1944 movie, Gaslight, starring Ingrid Bergman and Charles Boyer, from which the term “gaslight” is derived.

Interestingly, the term is actually derived from the 1944 movie, Gaslight, starring Ingrid Bergman and Charles Boyer (including Angela Lansbury’s screen debut). In the film, the main character, Paula (Bergman), is slowly driven insane by her newlywed husband, Gregory (Boyer), who manipulates her reality in order to drive her insane so he can steal her cache of hidden jewels.

In this post, I’m not suggesting that doctors are intentionally trying to drive their patients mad by ignoring their reality or second-guessing it or trying to re-write it into a reality they can more easily explain, but I think they do it unintentionally for very selfish reasons, such as not wanting to appear like they don’t have all the answers. I believe there is a widespread problem with medical doctors and many in the medical establishment either ignoring their patients or part of what the patient tells them or trying to manipulate their patients’ stories into a story that fits their explainable paradigms. I think this is a very dangerous problem that pushes people through the cracks of the healthcare system. In fact, people die from this type of behavior.

A 20-year-old rugby teammate of mine passed away from a brain aneurysm last month. She had been suffering from some medical issues – all of which I do not know because I was not close enough to her – and I gathered that she had been seeing many doctors about these issues. When I saw her last in October, she looked like she may have had a stroke because she seemed to only be able to speak out of half of her mouth – it reminded me of how my Grandma spoke due to paralysis in half of her face (due to a surgical accident when the surgeon accidentally severed her facial nerve on one side). The issue is that it was a change in degree, not a binary change (i.e., appearing after not being there at all). What I mean is that since I met her two years ago she had this side-mouth way of talking, but it was more severe in October than previous times I’d seen her. I honestly am pretty upset with myself for not pressing harder about my concerns, but I did ask her if she was doing alright, health-wise. She told me that she wasn’t and that she was seeing many doctors, so I was hopeful that somebody was dealing with this concern. Then two months later, she’s dead from a brain aneurysm. At the funeral, her mother hinted at a pending fight with the healthcare system, that there may be lawsuits coming, and that the doctors didn’t listen to their cries for help, didn’t give them the care or tests that they asked for. If she had an MRI, there is a pretty decent chance that they could’ve seen a growing aneurysm and done something about it like surgery. Part of the story is that my teammate was a person of color and working class, and she was on Oregon’s medicaid, OHP (Oregon Health Plan). In general, people of color (and other marginalized people) and working class people do not get the same level of care as white people from the middle and upper classes. It’s a very sad reality. It must change. Universal healthcare would help change this reality, although it wouldn’t be all that needs to happen to help change it – doctors need to be aware of their biases and to actively try to counter them.

I have another friend who is very large, technically considered “obese” according to her BMI, although she is also very muscular and strong, which is always missed if you use BMI as the sole measurement for obesity. She has a lot of chronic pain issues with incidences of syncope and other malfunctions in her autonomic nervous system. She has spinal and cranial MRIs showing all sorts of pathologies that could explain at least a large fraction of her symptoms, but the doctors have predominantly focused on her weight, as if that’s the primary reason for her problems. It has taken her over eight years for a medical doctor to take her seriously enough to finally look beyond her weight! I was helping her investigate her health issues last year and I even attended a couple of doctor’s appointments with her and witness firsthand how disrespectfully the doctors treated her. I even had a neuroscience textbook with me and had to correct the spinal surgeon when he said that the bladder has nothing to do with the spine. It turns out that the nerves that innervate and control the bladder travel down the spine and exit the spinal column around the same regions in which she was having pain and which show pathologies in the MRIs. He ignored me despite the fact that I just proved his statement wrong. I am not an M.D., so I do not get the same level of respect for my knowledge and intelligence from M.D.s as other M.D.s do, despite my expertise in molecular, cell, developmental, and biochemical biology (MCDB) and my ability to perform and comprehend medical science and research.

There is a growing contingent of medical doctors that are changing the way they interact with their patients, but in general I am not impressed – in fact, I’m pretty concerned about the general attitude of medical doctors towards their patients. “Bedside manner” can refer to many types of communication, but what I’m particularly concerned with is doctors listening to their clients, believing that their clients are telling you the truth as much as they can tell it, and having the self-esteem and curiosity to investigate further when they don’t have a ready-made answer to the patient’s problem. Scientists tend to have more curiosity about the unknown, whereas I think medical doctors tend to want to portray a sense of all-knowing and security about what they know, but this leaves little room for growth – of medical science, of knowledge, of character, etc.

We all need to work together to hold our medical doctors accountable for listening to our stories, for putting in the effort into our healthcare. If they do not listen and they are not curious about what ales you and invested in finding it out when it does not fit into one of the diseases or disorders they know, find a new doctor who does.

Protein Waste Management in Neurodegenerative Diseases and Sleep

When I was in graduate school for molecular biology, one of the labs in my department studied chaperones, which are protein enzymes that assist in the folding of proteins into their functional, three-dimensional shapes. That lab (Dr. Jeff Brodsky was the Principal Investigator/P.I.) used the simplest eukaryotic cell model system, Saccharomyces cerevisiae (a.k.a. baker’s yeast), to study chaperones. I secretly thought to myself, “who cares” and “why would anyone get excited about studying that?”

But now I feel a little silly that I thought those disparaging things about what the Brodsky lab studied/studies because, as it turns out, protein misfolding and aggregation is a common characteristic of neurodegenerative diseases. The problem is that these aggregates of proteins do not get degraded like most misfolded proteins, nor do they get cleaned up and washed away in the cerebral spinal fluid (CSF) through the glymphatic system during sleep. Thus, these aggregates end up causing the neurons and glial cells to kill themselves (called apoptosis).

Neurodegenerative Diseases and their Associated Misfolded and Aggregated Proteins

The Brodsky lab studied chaperones in yeast, but sometimes they’d also try to bring human health relevance to their research, and when they did that they would study the protein that is misfolded in cystic fibrosis – CFTR (Cystic Fibrosis Transmembrane conductance Regulator). The reason I bring up CFTR in a post about neurodegeneration is to contrast what happens in lung cells (ionocytes) that express the misfolded CFTR protein to what happens in brain cells expressing the proteins that are involved in neurodegenerative diseases. The bottom line is that the cystic fibrosis lung cells do not end up killing themselves like the neurodegenerative brain cells do, despite the unfolded protein response (UPR) being activated in both cell types/conditions, which typically initiates programmed cell death (apoptosis).

One thing to keep in mind when comparing lung and brain diseases is that there are many different types of lung diseases that have many different types of mechanisms, but nearly all brain-related diseases (with the exception of brain cancers, for the most part) appear to have the same type of mechanism: protein misfolding, aggregation, and lack of clearing the aggregates, which leads to cell death. What this means is that brain cells (neurons and glia) are particularly sensitive to protein aggregates – these aggregates must be cleaned up ASAP or else the cells will kill themselves, leaving extracellular aggregates (sometimes the aggregates are secreted by the cell instead of killing itself, too), which can also inhibit neuronal signaling.

So how do we get rid of these protein aggregates? Well, usually, they are washed out of the interstitium (the extracellular space between cells in the brain) with the cerebral spinal fluid (CSF) while we are asleep. In fact, researchers suggest that this “waste management” is the primary function of sleep – to get rid of unnecessary proteins that were made during the day through proteolysis and clearing via the CSF and the glymphatic system, the recently discovered macroscopic waste clearance system through parivascular tunnels in the brain (created by astrocytes/astroglia). Furthermore, these protein aggregates can also trigger inflammation, which causes multiple brain toxicities.

When we do not sleep very much or very deeply, the brain does not get enough time to wash away its waste products, thus causing their accumulation and degenerative effects. Thus, there is a higher risk of developing dementia in people who have poor sleep habits. Therefore, sleep is not just for your beauty or comfort – it’s important for your brain function which means it’s vital for life. Lack of sleep kills.

Where Consciousness Resides in the Brain

I have been interested in the nature of consciousness and how and where it resides in the brain for a long time. I’m interested from the neurobiological standpoint as well as the spiritual, metaphysical, or epiphenomenal standpoint(s). There must be a mechanism for how the information of consciousness can be transmitted in the body – or stored – and for how it controls the body, which is biological.

Although we still have a lot to understand about the nature of consciousness or how it is embedded or interacts with the brain, we do have a pretty good idea about where it resides in the brain. About a year ago, this article was published about a study locating what could be described as one definition of consciousness, two characteristics of which are arousal and awareness, in the rostral dorsolateral pontine tegmentum, which is a small nucleus of neurons in the brainstem, and it connects to the left ventral, anterior insula (AI) and the pregenual anterior cingular cortex (pACC), which are associated with arousal and awareness. The finding is supported by the fact that all of the fMRI scans of patients in a coma and vegetative state had disruptions in the network between these regions.

Location is a major finding in neurobiology, but it is still pretty rudimentary if you really want to understand the phenomenon of consciousness. Another idea is how consciousness is either created by this region or somehow is stored in it temporarily. Even so, we want to also know how it interacts with the biology of the brain to control it through free will, whatever the nature of that is, too. [I believe we have free will, but not all scientists (including neuroscientists) agree that we do. I also believe that free will is one of the few inherent properties of consciousness, in addition to awareness, arousal, and love.]

In any case, it is pretty cool to have a place to look at for the residence of consciousness (well, specifically the aspects responsible for arousal, awareness, and free will, at least) in the brain. An interesting note is that the  is a region of the brain that processes sensory information from our viscera and is involved in the autonomic nervous system, such as the sympathetic (responsible for fight-or-flight mode) or the parasympathetic (responsible for the calm and resting to recover the body after a fight or flight) nervous systems. The pACC is associated with conscious awareness and free will, since disrupting its connection with the premotor and motor cortices (which often happens in split-brain surgery) results in not being able to consciously control the hand – this is called “alien hand syndrome” – a condition when the hand seems to have a mind – and personality – of it’s own.

I could go on and on and on about my thoughts on the nature of consciousness, but I think I will just stop here with the peak into where it is likely anchored in the brain.

Neuromarkers for Mental Health!

The idea of neuromarkers of psychiatric disorders has arrived with the first FDA-approved neuromarker for ADHD, which is a ratio of the relative power between two different brainwaves, theta and beta, in the cerebral cortex as measured by electroencephalography (EEG). It is called the theta-beta ratio [TBR], and it is a useful tool in supplementing the diagnosis of ADHD in about 25-40% of ADHD patients. Although the TBR is the first to be approved by the FDA, there are many other potential neuromarkers like it that we can measure using quantitative EEG, which may be able to help clinicians and patients to better understand their psychiatric symptoms, and even may help determine the best treatment.

Controversy over the meaning and use of neuromarkers remains. These measures should change with treatment only if they are causative for the condition or symptom(s); if they are not causative but are correlative, they may or may not change with changes in symptoms. Another possibility is that they may represent an underlying risk for the condition or symptom, but may not be sufficient to cause the condition or symptom, which, again, would not necessarily result in changes to the measure when symptoms change. This is similar to the mechanism of genetics and how individual genetic variations may correlate with diseases or indicate increased risk of disease, but the genetic variation in and of itself is insufficient to cause the disease. The current data suggests that a similar mechanism is likely for at least some of these neuromarkers, which makes sense for the complex nature of mental health.

Despite the caveats, the emerging field of neuromarkers for mental health disorders is very exciting! For the first time, we may have objective measures for mental health that can support psychological diagnoses, prognoses, as well as the possibility for monitoring treatment efficacy. We will soon have the capability to measure and explore these potential neuromarkers at Rose City Therapeutics since we now have been trained and have purchased the equipment – it is on its way!

The Effects of Neurofeedback Are NOT Due to the Placebo Effect

Kurt Othmer from EEGInfo created a video response to a report out of McGill University that was published in June in The Lancet Psychiatry (which is not open-source) that dismisses the effects of all EEG neurofeedback as due to the placebo effect. Kurt describes how it is not possible for the effects that we see in the clinic to be due to the placebo effect – he cites some original research on cats (when was the last time you saw a cat do what you wanted them to do?) to current research with addicts showing a significantly higher retention rate in treatment recovery programs when the treatment is combined with neurofeedback. He also discusses how we can modulate the effects of the neurofeedback during a session, using the specific example of modulating a headache – making it better and making it worse in the same session by changing the response frequency (the brainwave at which the brain is training).

This video is worth watching, especially if you have doubts about the effects of neurofeedback and are worried that it may not be worth your investment:

New study provides a biological basis for drug hypersensitivity in adolescents and some adults with a genetic variant

In my first “primary article briefs” blog post, I am covering two companion articles published in the March 1st, 2016 issue of the open-access journal, eLife, by Mauro Costa-Mattioli’s group at Baylor College of Medicine and colleagues (Huang, et al., 2016; Placzek, et al., 2016).For the first time, the authors describe a biological explanation for why adolescents have a higher susceptibility to the effects of drugs and drug addiction than (most) adults. They also shimage_update_1d73612226ae9157_1378346712_9j-4aaqskow that this same biological mechanism can be used to understand why some people (who express a particular gene variant) are more susceptible to drug addiction than others. This finding not only opens the door to the possibility of designing pharmaceutical agents that could help reduce the effects of drugs on adolescents and others who have this gene variant, but it more importantly helps us to frame the argument that drug addiction is less of a behavioral problem and more of a biological/medical problem that needs to be dealt with in a medical manner and not by shaming and shunning the addict.

To understand what the researchers did and why, it is important to understand the basic biology of drugs and addiction. Recreational drugs like cocaine, alcohol, and even nicotine produce their pleasurable (and subsequent addictive) behavior by activating the “reward” centers of the brain, located in the ventral tegmental area (VTA) in the midbrain and the nucleus accumbens (NAc) of the basal forebrain. Excitatory, glutamatergic neurons (neurons that secrete the general excitatory neurotransmitter, glutamate) signal into the VTA to activate projection neurons to the NAc that secrete dopamine (DA), which is the primary neuromodulatory neurotransmitter thaVTA_NAc_Glu_Dopat regulates the limbic basal ganglia and its functions. The limbic loop of the basal ganglia is the emotional center that produces feelings of pleasure, love, motivation, and reward. All addictive drugs produce their pleasurable and drug-seeking effects by impinging somewhere along these dopaminergic neural signaling networks.

The two companion articles that I am writing about show that it only takes a small concentration of drug (whether it be cocaine or nicotine) in adolescent mice to strengthen the synapses that activate the dopaminergic (DA) neurons in the VTA that project to the NAc. It takes a much higher concentration of drug, however, to do the same thing in adult mice. They also show that this effect of synaptic strengthening in the VTA correlates with drug-seeking behavior, and that it takes more drug to cause this drug-seeking behavior in adult mice as compared to adolescent mice. This finding is not new, but lays out the basis for their subsequent experiments to explain why adolescents have a lower threshold at which recreational drugs can elicit their addictive effects.

Previous studies have shown how changes in gene transcription (either through the activity of transcription factors or epigenetic mechanisms) contribute to drug addiction-related behaviors, but these studies did not provide an explanation for the differences in susceptibility to drugs between adolescents and adults. To investigate this difference, Mauro Costa-Mattioli and colleagues made two observations that led them to focus on the regulation of protein synthesis: 1) protein synthesis is required for cocaine-induced synaptic strengthening in the dopaminergic neurons of the VTA and subsequent drug-seeking behaviors, and 2) protein synthesis is reduced in the brains of adult mice as compared to the brains of adolescent mice. Therefore, they hypothesized that a difference in regulation of protein synthesis between adolescents and adults explains the difference in their susceptibilities to drugs and drug-related behaviors.

Through a series of elegant experiments, the authors demonstrate a difference between adolescents and adults in the level of drug-induced activation of a specific protein that blocks protein synthesis/translation. Specifically, the drug-induced activation of eIF2alpha (indicated as p-eIF2alpha, a phosphorylated form of eIF2alpha) is diminished in adolescents as compared to adults. The result of this reduced p-eIF2alpha is an increase in general translation (meaning that more proteins are made), thus allowing for increased synaptic strength (or long-term potentiation [LTP]), and a decrease in translation of a specific set of proteins that are involved in decreasing synaptic strength (or long-term depression [LTD]). The authors show that the difference in drug-induced synaptic strengthening (LTP) and drug-seeking behaviors between adolescents and adults is due to this difference in activation of p-eIF2alpha (Huang, et al., 2016).

The brains of children and adolescents are more “plastic” (meaning that they change more) than the brains of adults because they are still growing and forming proper connections. Therefore, it is not surprising that adolescents would be more susceptible to drug-induced synaptic strengthening, a type of neuroplasticity, than adults. What is surprising, however, is the neural specificity of this finding – that only DA neurons in the VTA, and not in the NAc, show this drug-induced synaptic strengthening. The authors do not delve into the normal biology that could explain this difference between adolescents and adults; to do that they could compare the dose-dependent effects of the cognate neurotransmitter (glutamate) on synaptic strengthening of these DA neurons in adults and adolescents. It would be interesting to see if glutamate (the cognate neurotransmitter for these synapses) shows a similar differential effect on synaptic strengthening as the drugs tested in these studies, or if this differential effect is specific to these drugs. If the effect is similar, then it would suggest a biological, developmental function for the increased neuroplasticity of the DA neurons in the VTA of adolescents – suggesting that adolescence is a particularly important period of life when our motivations are most strongly created in the reward system of our brain. Certainly, this seems to be true on an intuitive level.

The primary new finding of the second paper (Placzek, et al., 2016) is a variation in the gene for eIF2alpha (the gene name is Eif2s1) that increases the vulnerability of human smokers to addiction. Essentially, the authors show that, similar to adolescents, adults with this genetic variation in Eif2s1 have an increased susceptibility to addiction-associated phenomena. One hallmark of addiction is that addicts develop a dampened response of the “emotional reinforcement circuitry” to less potent natural rewards, while their response to addictive drugs intensifies (Neuroscience, 5th ed., 2012). Using juice as a natural reward, the authors show that tobacco smokers with tEif2s1he Eif2s1 gene variant had reduced activity in their reward center (shown by functional magentic resonance imaging [fMRI]) compared to smokers without the genetic variation or non-smokers (shown in the figure to the left – the variation is a single nucleotide variation [SNP] changing an A to a G in the regulatory sequences; above is a transverse (L) and a sagittal (R) view showing the region in the brain (NAc) where the activity is reduced; below is quantification of the fMRI signal change). These results indicate that people with the genetic variation in Eif2s1 have an increased risk for drug addiction than those without the genetic variation.

The authors further show that the variant SNP in the Eif2s1 gene causes increased protein levels of eIF2alpha, which results in decreased activation (p-eIF2alpha) in response to drugs. The authors do not show the mechanism by which the increased levels of the protein lead to decreased activation, but provide some hypotheses (e.g., stoichiometric imbalances, sequestration, or compensatory feedback mechanisms in other translational machinery proteins). They also discuss the need to further investigate the role of p-eIF2alpha in later stages of addiction, since these studies were focused on the initial exposure to drugs. Furthermore, they believe that p-eIF2alpha may be a promising new target for the medical treatment of addiction.

My take-home message from these papers is that we now have a specific biological marker for susceptibility to drug addiction. This finding not only provides more evidence of the biological/medical basis of addiction (rather than just a behavioral disorder), but it also provides a promising new target for medical intervention. Ultimately, this research supports the notion that it is important to treat drug addiction as a medical disease rather than a crime or misbehavior.

How Honesty Changes Over A Lifetime

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Sex Differences in Response to and Recovery from Stress

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