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Putting an End to Confusing and Stigmatizing Psychiatric Diagnoses
In 2019 I introduced the first comprehensive psychophysiological hypothesis of psychiatric disorders, and although I have since published another 23 scientific articles on the topic, finding them in this day of information overload can be like looking for the proverbial needle in a haystack. So congratulations on finding this article at this early date…you are way ahead of the curve.
The essence of the multi-circuit neuronal hyperexcitability (MCNH) hypothesis is that psychiatric symptoms, irrespective of the diagnostic category in which they fall, are the consequence of pathological hyperactivity of the brain circuits with which they are associated. Thus, for example, pathological hyperactivity in anxiety circuits causes elevated and persistent feelings of anxiety; pathological hyperactivity in depressive circuits causes elevated and persistent feelings of depression; and pathological hyperactivity in cognitive circuits causes racing thoughts and obsessional thinking [1]. The cause of this hyperactivity is the inheritance of gene variants whose protein products fail to adequately regulate the firing of neurons. The advantage of this discovery is two-fold. First, it circumvents the need for confusing and stigmatizing psychiatric diagnoses, such as major depressive disorder, bipolar disorder, and schizophrenia. Second, if guides the use of neuroregulators (more commonly known as “anticonvulsants” or “mood stabilizers”) in the treatment of a wide range of psychiatric disorders. Because these medications go right to the root of the problem, they work very quickly (within hours), and because they normalize brain function rather than attempting to correct circuit-specific imbalances, they can be combined with one another so as to minimize side effects and attain an optimal therapeutic effect [2]. Although it might sound hard to believe that after many millennia of searching for the root cause of mental illness, the answer is that simple. However, the MCNH hypothesis has, for more than 25 years now, proven itself to be the most accurate explanation of psychiatric disorders to date. It has increased my success rate in treating mental illness from around 30% to nearly 100%, and reduced the average time to symptom-reduction from round 6 months to 6 days!
The cornerstone of the MCNH hypothesis is that the mind and the brain are distinctly different but highly interactive entities that have a profound influence on each other. Everything that the mind thinks about mentally, the brain processes electrically. In essence, the brain is a biological computer that keeps an electronic record of everything that the mind experiences both psychologically and emotionally. Recall is a process in which the mind, which never forgets anything that we experience, stimulates the brain to reactivate circuits that had been active during a previous cognitive-emotional experience. If the brain succeeds in doing so, the memory is retrieved; if not, it remains outside of conscious awareness. The reason that repetition is so important in the process of learning and memory is that practice further reinforces the related cognitive, emotional, and, in the case of behavior, motor circuits with each repetition, thus increasing the likelihood that the brain will synchronize with the mind when it is stimulated to do so.
Under normal circumstances, the mind is the executor of neurological function. The mind induces magnetic fields as it thinks and emotes, and those magnetic fields stimulate activity in the corresponding neurons. As the neurons fire, they induce magnetic fields that synchronize with the mentally induced magnetic fields to create the experience of conscious thought. However, in the some persons, the neurological system is hyperexcitable. As a result, the neurological activity that the mind stimulates tends to be over-amplified and abnormally persistent. Thus, for example, if an affected person experiences an anxious thought, the level of anxiety tends to be abnormally high. It also tends to be abnormally persistent. The same would be true for a depressive thought, an angry thought, or an excited thought. This abnormal amplification and persistence of normal thoughts and emotions is what characterizes what we call “psychiatric symptoms.”
In addition to the immediate effects of cognitive-emotional stress on the neurological system, persistent stress can have an additive effect because neurons become increasingly responsive with each repeated stimulation. This is the MCNH explanation for the relative delay in onset of psychiatric symptoms when affected persons experience persistent cognitive-emotional stress. For them, persistent stress is like a flame of fire underneath a pot of water in which the brain is slowly heating up. Then again, some person’s brains are so hyperexcitable that they experience psychiatric symptoms even in the absence of any significant cognitive-emotional stress. This is what characterizes chronic mental illness. Over time, their chronic symptoms can have severely disabling psychological effects, such as low self-esteem, feelings of hopelessness, and fears of abandonment, which then compound their stress and further aggregate their illness. This highlights the importance of early education and aggressive treatment for persons with highly excitable neurological systems. Although psychotherapy can be helpful in addressing the secondary psychological complications of neuronal hyperexcitability, definitive treatment involves efforts to reduce the excitability of the neurological system. Natural ways to quiet the brain include stress-reduction, maintaining an early sleep schedule, moderate exercise, avoidance of psychostimulants, minimizing refined sugar, and enjoying a relaxing hobby. Brain-calming herbs and supplements, such as valerian and magnesium, can also be helpful. Medical treatment primarily involves the use of anticonvulsants (mood stabilizers), which could more aptly be called “neuroregulators” because they help regulate the firing of neurons [3]. Medications in this class include gabapentin, oxcarbazepine, depakote, lamotrigine, lithium, levetiracetam, topiramate, and tiagabine [4,5]. Rarely, more powerful brain-calming drugs, such as olanzepine or lurasidone, may be needed. In the few cases in which medical therapy is infective, electroconvulsive therapy (ECT) can be highly effective, although maintenance treatments are often necessary.
References
[1] Binder MR. The multi-circuit neuronal hyperexcitability hypothesis of
psychiatric disorders. AJCEM 2019; 7 (1): 12-30.
[2] Binder MR. Focused neuroregulation in the treatment and prevention of mental and physical illness. AJCEM 2022; 10 (2): 49-58.
[3 ] Binder MR. Introducing the term “Neuroregulator” in psychiatry. AJCEM 2019; 7 (3): 66-70.
[4] Binder MR. Focused neuroregulation in the treatment and prevention of mental and physical illness. AJCEM 2022; 10 (2): 49-58.
[5] Binder MR. The Racing Mind: Brave new sights untangle the ancient mystery of mental illness, p. 320. Lightningsource Publishing, 2024.
Psychotherapy Vs. Medication for Anxiety, Depression, and Other Psychiatric Symptoms
There is a long-standing debate about whether anxiety, depression, and other psychiatric symptoms should best be treated with psychotherapy verses pharmacotherapy or both. What creates the confusion is that the cognitive-emotional system has two anatomical components: the mind and the brain [1]. Although the mind has been studied far more extensively than the brain, recent advances in neuroscience, which involve the study of brain structure and function, have led to the misconception that the secrets to mental and emotional functioning can be discovered by studying the brain alone.
The reality, however, is that the brain can tell us absolutely nothing about how the mind works. Why? Because the mind is a completely different entity than the brain. The mind is a body of energy, whereas as the brain is a clump of fats, proteins, and carbohydrates that are wired together to form biological computer. Thus, to attempt to understand how the mind works by studying the brain is like trying to understand how a person thinks by studying the electronics of a laptop. This is why we have made so little progress in understanding mental illness despite the extraordinary advances that we have made in the field of neuroscience.
However, because the mind and the brain work so closely together, the workings of the brain have a profound effect on the workings of the mind. Specifically, the brain encodes electrically everything that the mind thinks about mentally. Therefore, if the brain is not working properly, it can affect the functioning of the mind. That is why, for example, a stroke or a traumatic brain injury can leave a person unable to walk, unable to talk, or perhaps even unable to think. What causes the loss of function, however, is not the failure of the mind but, rather, the failure of the brain. The problem is analogous to a computer crash when one is trying to send and receive messages over the internet.
In the case of generalized anxiety disorder, bipolar disorder, and other common psychiatric disorders, a similar problem is occurring. However, in this case, the brain is actually over-functioning rather than under-functioning. Instead of simply processing mental signals and relaying the messages back and forth between the mind and the body, it is abnormally amplifying and replaying everything that the mind is thinking and feeling. This causes the mind to keep thinking about the same things over and over. However, because the psychological and emotional content of this obsessive mental activity is merely an amplification of what the mind might normally be thinking about, it can easily be misconstrued as a purely psychological problem. What is actually happening, however, is that a pathological hyperexcitability of the brain—a neurophysiological abnormality that is most commonly inherited—is causing the brain to keep stimulating the mind. This persistent over-stimulation of the mind is what gives rise to what are commonly known as “psychiatric symptoms.”
Over time, this pathological process can lead to more than just a worsening of psychiatric symptomatology. It can also lead to secondary psychological problems, such as low self-esteem, lack of self-trust, and a sense of helplessness. It can also cause academic and occupational difficulties as the overabundance of neuronal signaling to the mind causes difficulty maintaining focus and remaining physically still, and it can cause impulsivity as the brain sends more signs to the mind than the brain can possibly process in conjunction with the mind before it sends the mind another signal. Further completing the clinical picture is a tendency for the symptoms to cycle as one hyperactive neuronal circuit aberrantly fuels hyperactivity in another. Moreover, the specific constellation of symptoms that any one individual can experience can vary widely, as there are an almost limitless number of different circuits that could become pathologically hyperactive in any given individual. That explains why this one neurophysiological abnormality can cause so many different psychiatric syndromes.
This phenomenology is important to recognize because attempting to treat neuronal hyperexcitability with psychotherapy alone is like trying to prevent car accidents by offering driving lessons instead of repairing the brakes. Worse yet, psychotherapy alone could potentially do more harm than good if the continued stimulation of symptom-related brain circuits outweighs the psychotherapeutic effects of the psychotherapy.
The more expeditious treatment approach is to simply quell the neuronal circuits that are driving the symptoms. Natural ways to do this include stress-reduction, establishing of an early sleep schedule, moderate exercise, avoiding psychostimulants, minimizing refined sugar, and enjoying a relaxing hobby. Brain-calming herbs and supplements, such as valerian and magnesium, can also be helpful. Medical treatment primarily involves the administration of anticonvulsants (mood stabilizers), which could more aptly be called “neuroregulators” because they help regulate the firing of neurons [2]. The safest and most effective medications in this class include gabapentin, oxcarbazepine, depakote, lamotrigine, lithium, levetiracetam, topiramate, and tiagabine. That is not to say that psychotherapy is not useful in persons with neuronal hyperexcitability but only to say that it becomes more productive when the brain becomes more cooperative with the mind. Thus, medication should ideally be started first, and then, if needed, psychotherapy can be added on. In the vast majority of cases, however, patients overcome their need for psychotherapy once neuroregulators effectively address the root of the problem.
References
[1] YouTube Video: The Racing Mind Video Series #33: Psychotherapy and Neuronal Hyperexcitability.
[2] Binder MR. Introducing the term “Neuroregulator” in psychiatry. AJCEM 2019; 7 (3): 66-70.
Treating Mental Illness Quickly, Effectively, and Inexpensively
Because common psychiatric symptoms, such as anxiety, depression, and insomnia, are merely exaggerations of symptoms that all of us have experienced from time to time, it is natural to assume that a persistence of these symptoms is merely psychological and, thus, responsive to psychotherapy. Consequently, most persons initiate treatment with a psychotherapist or counselor rather than a psychiatrist. However, as a psychiatrist who has been doing psychotherapy for more than thirty years, I can confidently say that the root cause of such symptoms, when persistent, is biological rather than psychological.
How do I know that? Because the function of the brain is to simply relay electrical signals between the mind and the body. It is not supposed to overly amplify or overly prolong the signals. However, in some persons, the brain is pathologically hyperactive. This can cause normal thoughts to keep replaying like a broken record and normal emotions to become overly exaggerated and abnormally persistent. It can also cause a heightening of the external senses, thus causing such things as sound sensitivity, light sensitivity, and ringing in the ears; and it can cause a heightening of the internal senses, thus causing such things as migraine headaches, heart palpitations, and abdominal discomfort.
The biological basis of these symptoms is a hyperexcitability of the electrical cells of the brain. Simply put, the neurons tend to overreact when they are stimulated, and they tend to keep firing when they should be shutting off [1,2]. Although the neuronal hyperexcitability trait is most commonly inherited, it typically remains silent until the affected person’s stress levels become high enough to precipitate symptoms. For such persons, mental and emotional stress are like stones being thrown at a beehive (the brain) in which the bees (the hyperexcitable neurons) are irritable. The reluctance of the neurons to shut off when they should explains why most persons who have psychiatric disorders have trouble falling asleep and staying asleep. It also explains why their psychiatric symptoms are triggered by severe or persistent stress.
For most persons, stress levels tend to become highest during the transition from childhood to adulthood. That is the neuronal hyperexcitability explanation for why psychiatric symptoms usually begin during the adolescent years. However, symptoms can develop any time that stress levels become high enough. It is important to note, however, that the onset of symptoms tends to be delayed relative to the onset of the stressor. That’s because the brain, like a pot of water under a flame of fire, takes time to heat up. It also takes time to cool off once the stressor begins to recede.
Contrary to what one might expect, the cooling off process typically takes at least as long as it took for the brain to get heated up. Also, stressors tend to die down gradually rather than suddenly, thus explaining why recovery times are often even longer than the incubation times. In addition, the symptoms themselves can cause the affected person to say and do things that perpetuate the stress, such as getting into a fight, getting expelled from school, or getting arrested. What’s more, the mind and the brain, like two people caught in an argument, tend to keep agitating each other even after the triggering stressor resolves.
For all of these reasons, prompt psychiatric assessment and initiation of medications to help calm the brain are of paramount importance. For persons with hyperexcitable neurons, the initiation of brain-calming drugs is like adding ice cubes to the pot of boiling water. Although concomitant psychotherapy can sometimes be helpful, its therapeutic effects tend to be undermined by the inability of the hyperactive brain to fully cooperate with the mind in processing the therapeutic suggestions. Hence, it is usually more expedient and cost-effective to delay psychotherapy until the appropriate medication (or medications) are fully effective. More often than not, a return of normal brain function will lead to a rapid resolution of symptoms. That is not to discount the value of psychotherapy but only to say that treatment is generally more efficient and effective when it is focused on correcting the underlying abnormality. Correcting the biological abnormality first also paves the way for psychotherapy to focus more fully on the issues that are truly of a psychological rather than biological nature.
In the past, the determination of which type of therapy (psychotherapy or pharmacotherapy) would be more appropriate for which patient was a purely subjective decision. That is to say, it was based on symptoms and personal philosophy rather than objective criteria. However, recent studies have identified a biological marker of the neuronal hyperexcitability trait. In the absence of any confounding factors, such as a heart condition, a medication, or a recreational drug that would affect vital signs, a resting heart rate above 75 beats/min or a resting respiratory rate above 15 breaths/min would be indicative of the neuronal hyperexcitability trait. In other words, these numbers can tell us, irrespective of the psychiatric diagnosis, whether or not there is an underlying biological abnormality. Then again, because psychiatric disorders are rooted in neuronal hyperexcitability, the mere fact that an individual becomes symptomatic is itself suggestive of the neuronal hyperexcitability trait [3].
The good news is that there are both natural and medicinal ways to reduce neuronal excitability. The natural ways consist of dietary and lifestyle changes that have a calming effect on the mind and brain. These include stress-reduction, moderate exercise, establishing an early sleep schedule, enjoying a relaxing hobby, avoiding caffeine and other psychostimulants, and minimizing refined sugar. It is important to bear in mind, however, that these interventions, though helpful, are typically insufficient for all but those persons who have relatively mild levels of neuronal hyperexcitability. For those with higher levels of neuronal hyperexcitability, natural interventions alone are, in most cases, neither adequate nor practically doable because affected persons have so much difficulty controlling their behavior. Therefore, such persons should be treated with medications that help calm the brain. These medications, which in neurology are known at “anticonvulsants,” could more aptly be called “neuroregulators” because they regulate the firing of neurons [4]. Among the most effective neuroregulators are gabapentin, oxcarbazepine, lamotrigine, depakote, lithium, levetiracetam, topiramate, and tiagabine. These medications are some of the safest and least expensive medications available. They are also fast-acting, non-addictive, and highly effective in long-term use. Moreover, because they normalize brain function rather than alter the activity of specific neurotransmitter systems, they can be combined with one another to achieve a more optimal effect. The ability to safely combine neuroregulators is extremely important because each drug binds to different receptors in the brain, and reducing neuronal excitability often necessitates the use of multiple brain-calming molecular mechanisms.
As treatment with neuroregulators leads to clinical improvement, the affected person can increasingly reap the benefits of the body’s most important natural mechanism for healing, which is sleep. Sleep speeds healing because brainwaves become very slow during deep sleep, thereby helping to reduce the underlying neuronal hyperexcitability. However, deep sleep primarily occurs between the hours of about 8:00pm and 1:00am. This underscores the importance of establishing an early sleep schedule. With treatment, this becomes increasingly possible because neuroregulators make it easier to fall asleep and stay asleep at night. In addition, the rapid brain-calming effects of these drugs allow one to exercise greater self-discipline, which in turn makes the other natural interventions more doable. It also allows psychotherapy to be more effective because a calm brain works with the mind more cooperatively, thus improving one’s ability to process the psychotherapeutic interventions.
References
[1] Johnstone T, van Reekum CM, Urry HL, Kalin NH, Davidson RJ. Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression. J Neuroscience 2007; 27 (33): 8877-8884.
[2] Leuchter AF, Cook IA, Hunter AM, Cai C, Horvath S. Resting-state quantitative electroencephalography reveals increased neurophysiologic connectivity in depression. PLoS One 2012; 7 (2): e32508.
[3] Binder MR. FLASH syndrome: Tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109.
[4] Binder MR. Introducing the term “Neuroregulator” in psychiatry. AJCEM 2019; 7 (3): 66-70.
Addressing the Controversy Around Gabapentin (Neurontin)
The anticonvulsant drug gabapentin is becoming increasingly popular in the United States, but with that popularity has come a fair amount of controversy about its use both by legitimate and illegitimate users. The primary reason for the controversy is that gabapentin has increasingly been found alongside cocaine, opioids, and other drugs of abuse during police raids and 911 calls. In addition, some illicit users of gabapentin claim that they can get “high” off the drug if they take enough of it. In addition, gabapentin is a central nervous system (CNS) depressant, thus raising the possibility that it could contribute to respiratory depression in persons who combine it with other CNS depressants, such as alcohol, benzodiazepines, and opioids.
Nonetheless, more and more doctors today are prescribing gabapentin for a wide range of medical conditions, including partial-onset seizures, post-herpetic neuralgia, restless leg syndrome, neuropathic pain, trigeminal neuralgia, diabetic neuropathy, tension headaches, migraine headaches, fibromyalgia, irritable bowel syndrome, hot flashes, and a variety of other symptoms and conditions [1]. Gabapentin is also being used for a variety of psychiatric conditions, including treatment-resistant depression, bipolar disorder, generalized anxiety disorder, panic disorder, social phobia, post-traumatic stress disorder, and insomnia as well as a variety of substance use disorders, including alcohol, cannabis, cocaine, and opioid misuse [1].
As of August, 2020, gabapentin was the 6th most commonly filled medication at pharmacies [2]. Between 2004 and 2018, more than 400 million prescriptions were written for the drug [3]. Doctors prefer to prescribe gabapentin because of its wide-ranging effectiveness, favorable side-effect profile, and relative lack of withdrawal. Notably, however, gabapentin is also becoming popular among elicit users, a trend that has prompted some states to recategorize gabapentin as a Controlled Substance. However, gabapentin’s rising street value should come as no surprise given that illicit users likely suffer from the same kinds of medical and psychiatric conditions as legitimate users, including poly-substance misuse. Also, the fact that legitimate users of gabapentin rarely describe any euphoric effects from the drug suggests that the “high” that some illicit users have reported actually refers to the psychological, emotional, and physical relief that they get when they take gabapentin [4]. It could also refer to the sedation that occurs when gabapentin is taken at abnormally high doses, as sedation is a shared effect of many drugs of abuse [4].
That raises the question of whether the controversy around gabapentin is more a matter of guilty-by-association than actual danger of the drug. When gabapentin is found alongside well-known drugs of abuse, such as marijuana, cocaine, and opioids, the natural assumption is that the drug is being used illicitly. Also, illicit use implies misuse. However, this assumption fails to consider the possibility that gabapentin could be benefiting illicit users in many of the same ways that it is benefiting legitimate users. Indeed, most illicit users of gabapentin claim that it reduces their anxiety, eases their withdrawal from addictive drugs, and helps them sleep better at night. In the absence of any significant withdrawal effects, these benefits would presumably make gabapentin more attractive to illicit users than other drugs that they use to self-medicate. In addition, gabapentin is fast-acting, has few side effects, and rarely loses its therapeutic effects over time. It also has a very low fatality rate in overdose [5,6]. However, because a formal medical or psychiatric evaluation would be needed to obtain a prescription for gabapentin, its legitimate use would be more expensive and more likely to be delayed than obtaining it illicitly. At the same time, the growing controversy around gabapentin and its controlled status in some states are combining to cause prescribers to be more cautious about prescribing it. This is creating a vicious cycle that is likely to decrease the legal use of gabapentin relative to the illegal use of the drug. This is unfortunate because gabapentin has so many benefits, and the number of adverse events associated with the appropriate use of gabapentin has been lower than with many of the commonly used over-the-counter drugs, such as aspirin [7], acetaminophen [8], and antihistamines [9]. Moreover, the fact that gabapentin was on the market for nearly twenty-five years before the first state made it a Controlled Substance raises the question of why it took so long for anyone to become concerned about it. The long delay suggests that the new regulations on gabapentin are being driven more by a misattribution of risk and an effort to keep it out of the hands of illicit users than by any real danger of the drug itself.
I believe that the more important question we should be asking about gabapentin is how the drug exerts its wide-ranging therapeutic effects? A better understanding of this could help prescribers use similar drugs more effectively and identify new biological targets for the treatment of a wide range of medical and psychiatric conditions [1,4].
References
[1] Binder MR. Gabapentin—The popular but controversial anticonvulsant drug may be zeroing in on the pathophysiology of disease. AJCEM 2021; 9 (4): 122-134.
[2] GoodRx: Top 10 prescription drugs in the U.S., Published August 2020.
[3] Mikulic M. Number of gabapentin prescriptions in the U.S. from 2004 to 2018. Statista 2021.
[4] Binder MR. Illicit use of gabapentin may reveal more about the drug’s benefits than its liabilities. American J Int Med 2022; 10 (6):114-121.
[5] Middleton O. Suicide by gabapentin overdose. J Forensic Sci 2011; 56 (5): 1373-1375.
[6] Cantrell FL, Mena O, Gary RD, McIntyre IM. An acute gabapentin fatality: A case report with postmortem concentrations. Int J Legal Med 2015; 129 (4): 771-775.
[7] DPhilLL, DPhil OCG, DPhil ZM, Rothwell PM. Age-specific risks, severity, time course, and outcome of bleeding on long-term antiplatelet treatment after vascular events: A population-based cohort study. Lancet 2017; 300 (10093): 490-499.
[8] Agrawal S, Khazaeni B. Acetaminophen toxicity. StatPearls [Internet]. Last update: August 1, 2022.
[9] Dinwiddie AT, Tanz LJ, Bitting J. Morbidity and mortality weekly report 2022; 71 (41); 1308–1310.
Natural Ways to Reduce and Prevent Psychiatric Symptoms
There are numerous non-pharmacological interventions that can be helpful in reducing or preventing psychiatric symptomatology. Although these natural means, which include lifestyle habits, food choices, and dietary supplements, can be very helpful, it is important to recognize that they are rarely as effective as properly prescribed medication can be. Nonetheless, for persons who are at relatively low risk for psychiatric disorders or who currently have only mild psychiatric symptoms, they can, if properly implemented, supersede the use of medication or other medical therapies. Whenever possible, putting these non-medical interventions into practice is preferable, because they can have health benefits above and beyond the mental and physical health benefits of appropriately prescribed psychotropic medication. Moreover, even if one needs psychotropic medication, these natural interventions should still be implemented as much as possible, as they can further add to the mental and physical health benefits of psychotropic medication.
In order to understand how lifestyle habits, dietary choices, and nutritional supplements can help reduce or prevent psychiatric symptoms, let us recall what drives psychiatric symptoms in the first place. The underlying cause of psychiatric symptoms, such as chronic anxiety, depression, and insomnia, is the inability of neurons in the brain to shut off when they should [1,2]. The most common cause of this problem is the inheritance of gene variants whose protein products fail to adequately regulate the firing of neurons. Hence, anything that tends to reduce the excitability of the neurological system will tend to reduce or prevent the development of psychiatric symptomatology.
Stress Reduction
Perhaps the most obvious means of reducing neuronal excitability is stress-reduction, as mental and emotional stress have a powerful stimulating effect on the specific brain circuits that they activate. This is why cognitive-emotional stress is such a common precipitant of psychiatric symptomatology. Unfortunately, however, stress is difficult to reduce, especially when it is being abnormally amplified by a brain that is inherently hyperexcitable. This underscores the importance of the various other natural interventions that will be discussed next.
Establishing an Early Sleep Schedule
Although the importance of going to bed early at night may sound a bit like a cliche, the neurophysiological mechanism by which is it exerts its psychotherapeutic benefits has only recently been elucidated. Sleep studies have found that the brain gets its deepest sleep between around 8:30pm and 1:00am. This tends to be independent of one’s personal sleep schedule because the circadian rhythm, which is primarily regulated by the rising and setting of the sun, dictates when melatonin will be released at night. Melatonin is a sleep hormone that is secreted by a small gland in the brain called the “pineal,” and its release is primarily regulated by our exposure to natural light. Specifically, the blood level of melatonin begins to rise as the sun begins to set in the evening. As the level of melatonin begins to rise, the brain prepares to go into sleep mode. In other words, it begins to quiet down, thus making it easier to dose off to sleep.
During the process of sleep, the brain cycles through different activity levels, known as stage 1, stage 2, stage 3, and rapid-eye-movement (better known as “REM”) sleep. However, it is during the first half of the night, when melatonin levels are highest, that the brain spends the most time in stage 3 sleep, which is deep sleep. This is important to understand because it is during deep sleep that the brain quiets down the most. For example, during waking hours, brain oscillations average around 12-16 Hz, whereas during deep sleep, they average around 1-3 Hz. This makes deep sleep the phase in which the excitability of the brain drops down the most. Corresponding, deep sleep provides the greatest benefit in reducing one’s vulnerability to psychiatric symptomatology. As the night goes on, however, the brain spends more and more time in REM sleep, which is also known as “active sleep.” This is the sleep phase in which dreaming tends to occur. Because REM sleep actually increases neuronal excitability relative to deep sleep, “sleeping in” does little to reduce one’s vulnerability to psychiatric symptomatology. Therefore, establishing an early sleep schedule (i.e., early to bed, early to rise) is the most effective way to use sleep as a psychotherapeutic intervention.
In addition to the timing of sleep, going to sleep on an empty stomach is important because the brain cannot shut off as fully if it has to regulate digestive functions. Also, one should try to identify and maintain the temperature and humidity that seems to provide the best night of sleep. Also helpful is an open window as long as the fresh air does not change the ideal temperature or humidity too much.
Regular Exercise
In addition to its well-known benefits, which include detoxifying the body, strengthening the heart, and maintaining musculoskeletal health, regular exercise helps quiet the brain because it is a meditative function. It also stimulates the release of the feel-good hormones dopamine, serotonin, norepinephrine together with beta endorphins, which, by elevating mood, have an indirect calming effect on the brain. However, too much exercise can overstimulate the brain via the excessive release of adrenaline. It can also wear down the body and weaken the immune system. Therefore, excessive exercise is not necessarily better than moderate exercise. Ideally, exercise should not exceed about 20-30 minutes 2-3 times per week on alternate days. The single exception is casual walking, which can and should be done every day. Walking is highly effective at detoxifying the body and is also the most effective way to burn fat because it is so highly aerobic [3].
Meditation
Although exercise is a meditative function, the discipline of ignoring the brain, as is occurs during various forms of intentional meditation, gives both the mind and the brain a rest, thus reducing neuronal excitability both directly and indirectly. This is the MCNH explanation for the psychiatric benefits of meditation.
Faith and Prayer
Faith and prayer can be thought of as “meditation with supernatural benefits” because, as in traditional meditation, prayer is a meditative function. However, rather than just ignoring the mental chatter that is produced by spontaneous neurological signaling, prayer involves communion with the Creator, which has benefits that far exceed the benefits of simply quieting the mind and brain.
Enjoying A Relaxing Hobby
Although exercise can be a hobby for some, many persons find exercise to be a chore. Therefore, it is important to make a distinction between exercise and a hobby. The importance of a hobby is that having fun relaxes the mind, which in turn reduces mental stimulation of the brain. As previous discussed, excessive mental stimulation of the brain increases the excitability of the neuronal circuits that are being stimulated. Hence, reducing mental stimulation of the brain has the opposite effect. Idleness, on the other hand, can be even worse than stressful activities because it can leave the mind dwelling on matters that create excessive intrapsychic tension.
Staying Busy But Not Overly Stressed
Staying busy tends to reduce or prevent psychiatric symptomatology because it has a calming effect on the brain. This calming effect is made possible by the fact that neuronal circuits compete for dominance. Hence, when the mind is engaged in activities that are relatively unemotional, the processing of emotions is reduced; and since unemotional activities are less activating than emotional ones, the brain tends to calm down. This is the same neurophysiological principle by which the brain allows the mind to shift attention, and the contraction of one muscle causes the opposing muscle to relax. It is also the mechanism by which a little background noise, such as a television show, relaxing music, or a humidifier, can help one fall asleep at night.
Avoiding Caffeine and Other Psychostimulants
Caffeinated coffee, one of the most commonly consumed beverages, is a powerful psychostimulant. Hence, coffee can really drive up the level of neuronal excitability, especially if it is consumed on a daily basis. Although the neurostimulatory effects of caffeine can improve energy and alertness in the short run, they tend to exhaust energy in the long run because, by stimulating the brain, they increase the brain’s energy consumption. They can also cause anxiety, insomnia, and other psychiatric symptoms, as they tend to increase the activity of the neuronal circuits that correspond to these symptoms. Moreover, coffee can cause trouble falling asleep at night even if it is only consumed in the morning. That’s because its immediate stimulatory effects initiate a pattern of mutual overstimulation between the mind and the brain that tends to continue until one manages to fall sleep at night. The same is true with psychostimulants, such as methylphenidate (Ritalin), dextroamphetamine (Adderall), and others. Even antidepressants, including serotonin reuptake inhibitors (SSRIs), can have a stimulatory effect on the brain. That is the MCNH explanation for why some antidepressants can cause insomnia and why all antidepressants tend to lose their psychotherapeutic effects over time. Their loss of therapeutic effect begins to occur when their neurostimulatory effects, which primarily affect the cerebral cortex, begin to outweigh the neuroinhibitory effects that they have on the amygdala. The healthier way to boost energy, improve mood, and increase alertness is to simply calm the brain, because a calm brain, like a relaxed muscle, is stronger, faster, and more agile than a hyperactive brain.
Minimizing Refined Sugar
Carbohydrates, particularly refined sugars, increase neuronal excitability by several mechanisms. First, they stimulate the production of insulin, which has a stimulatory effect on the brain [4]. Second, they stimulate the release of cortisol, which increases neuronal excitation by both direct [5] and indirect mechanisms [6]. Carbohydrates also increase oxidative stress, thus providing yet another mechanism by which they increase neuronal excitation [7,8]. In contrast, a diet that is low in carbohydrates, moderate in proteins, and high in fats (commonly known as the “ketogenic diet”) helps reduce oxidative stress [9]. It also boosts the level of adenosine, an inhibitory neurotransmitter, which is thought to be the primary mechanism by which a low carbohydrate diet is of benefit in a wide range of psychiatric disorders [9,10]. When transitioning to a low carbohydrate diet, one should opt for plant-based proteins and omega fatty acids because animal-based products, such as meat, chicken, and dairy, tend to increase oxidative stress, which, by acidifying the blood, also increase the risk of cancer [11,12]
Avoid Cigarette Smoking
Yet another culprit is cigarette-smoking, which is both carcinogenic and disruptive to the brain because it reduces the oxygen content of the blood. Cancer cells thrive in an oxygen-poor environment, and neurons become hyperexcitable when blood oxygen levels fall, thus tending to increase nervous tension. However, the stimulatory effects of nicotine are temporarily outweighed by the calming effects that are achieved through dopamine signaling [13]. Recall that the “feel good” neurotransmitter dopamine reduces activity in select brain circuits [14,15]. This quiets the mind while at the same time stimulating the pleasure centers. What follows each cigarette, however, is a withdrawal syndrome that leads to the desire for another cigarette. These alternating effects occur very rapidly, which is one of the reasons that cigarette smoking is so addictive.
Marijuana and Cannabis-based Products
Particularly with the recent legalization of cannabis, there is a pressing need for education about the psychotropic effects of cannabinoids. The two primary constituents of the marijuana plant are tetrahydrocannabinol (THC) and cannabidiol (CBD). THC has stimulatory effects on the brain and produces short-lasting feelings of pleasure [16]. CBD has calming effects on the brain and, thus, reduces tension and anxiety [17]. Therefore, when ingested together, as occurs when a person smokes marijuana or ingests cannabis-based products, these effects can be synergistic, thus making the recreational use of marijuana very attractive. However, from a neurophysiological standpoint, the effects of THC and CBD are diametrically opposed because THC excites the brain, whereas CBD quiets the brain [18]. To make things even more confusing, THC can indirectly quiet the brain via the pleasurable (and therefore calming) effects that it has on the mind. However, the balance between these mixed effects of THC and the direct neuroinhibitory effects of CBD moves further and further in the direction of neurostimulation as the concentration of THC increases. It also increases as the frequency of use increases. As the brain becomes more and more stimulated, the risk of psychiatric symptoms, such as anxiety, depression, and paranoia, increases. This is important for users to understand because it is counterintuitive to think that a substance, which in its so-called “low-potency” form (i.e., low THC content) has both pharmacologically and clinically therapeutic effects, might, in its “high-potency” form (i.e., high THC content), actually have pharmacologically and clinically counter-therapeutic effects. Therefore, if one chooses to use cannabis-based products, one should opt for low potency rather than high potency formulations.
Magnesium
Magnesium is a brain-calming mineral that is a cofactor in more than 300 different chemical reactions; hence, magnesium can be as important to one’s general health as it can be to one’s mental health (York Cardiology). Foods that are rich in magnesium include green leafy vegetables, nuts, seeds, beans, avocados, and bananas. However, in an effort to optimize its brain-calming effects, magnesium can also be supplemented in the range of 400mg to 800mg per day. It can even be supplemented at doses as high as 2,000mg per day without having any toxic effects assuming that one’s kidneys are functional not normally. Bear in mind, however, that magnesium supplementation can cause loose stools or even diarrhea as the dosage increases. Also, there are many different formulations of magnesium, but one in particular (magnesium threonate) is known to cross the blood-brain barrier and, thus, exert more potent brain-calming effects. In my clinical experience, supplementing with magnesium has provided noticeable benefits for some but not others, and so it would be hard to predict how much of a psychiatric benefit magnesium supplementation would have for any given individual.
Taurine
Taurine is a structural analog of the inhibitory neurotransmitters, GABA and glycine, hence its potential benefits in the management and prevention of psychiatric symptomatology. Taurine is a “conditional” amino acid, which means that even though the body is able to synthesize it, some of the nutrient might need to be sourced from food in order to keep up with daily requirements. The main dietary sources of taurine are meat, fish, chicken, and dairy, with smaller amounts being found in seaweed, krill, and some green vegetables. An average diet will provide about 40 to100 mg of taurine per day, but clinical studies have used doses as high as 6,000 mg per day [19-21].
Vitamin D3
Vitamin D3 (cholecalciferol) is a fat-soluble secosteroid that actually functions as a hormone. By fine-tuning calcium and chloride currents across neuronal membranes, vitamin D3 reduces neuronal excitability [22], an effect that appears to be the chief mechanism through which it exerts its mental and physical health benefits [23]. Dietary sources of vitamin D3 include fish (100 IUs/ounce), eggs (20 IUs/yolk), and milk (100 IUs/glass). Vitamin D3 can also be obtained as a supplement. Notably, however, the vitamin can be made from cholesterol when the skin is exposed to the sun. Just thirty minutes in the sun (longer for dark complected individuals) can generate as many as 10,000-20,000 IUs, thus making vitamin D3 levels extremely easy to boost. For reference, the recommended daily allowance of vitamin D3 is 600-2,000 IUs.
L-theanine
L-theanine is an amino acid that is naturally found in the tea plant Camellia Sinensis (green tea). It reduces excitation in the brain by blocking NMDA and AMPA receptors. This reduces the release of cortisol and norepinephrine, thereby reducing tension and speeding recovery from stress. L-theanine has been found to improve sleep quality [24], reduce sleep inertia, reduce nightmares, reduce anxiety, improve mood, improve cognitive function, lower blood pressure [25], and partially counteract the stimulatory effects of caffeine [26].
N-acetyl cysteine (NAC)
N-acetyl cysteine (NAC) is the acetyl derivative of the amino acid cysteine. NAC’s calming effect on the brain has been attributed to its ability to reduce the activity of the excitatory neurotransmitter glutamate. NAC also has both direct and indirect anti-inflammatory effects, thus providing additional mechanisms by which it can reduce neuronal excitability [27]. Among its many other uses, NAD has been used as a supplemental treatment for bipolar disorder, major depressive disorder, obsessive-compulsive disorder, generalized anxiety disorder, nail-biting, skin-picking, trichotillomania, ADHD, schizophrenia, and cocaine addiction. The therapeutic effects of NAC in all these conditions likely relate to its anticonvulsant effects [28].
Choline
Choline is a nutrient that is functionally related to the B vitamins and is also the substrate for the neurotransmitter acetylcholine. Although acetylcholine is well-known to have an excitatory function at neuromuscular junctions and autonomic ganglia, it has a regulatory function in the brain, where it reduces neuronal excitability, alters the release of neurotransmitters, and coordinates the firing of neural networks [29]. As a neuroregulator, acetylcholine has the ability to change the state of a neuron and alter its response to subsequent stimulation. Because acetylcholine has the combined ability to promote burst firing and suppress tonic firing, it can enhance learning and memory while at the same time promoting relaxation and sleep. Although the body is capable of synthesizing choline from the amino acid glycine, the process involves many steps and requires the presence of vitamin B12, folate, and methionine. Not surprisingly then, most studies involving choline-depleted diets indicate that we need some choline from the foods that we eat in order to keep up with the body’s demand for the nutrient. Some of the most plentiful sources of choline include eggs, chicken, turkey, and fish [30]. The especially high content of choline in eggs is what likely accounts for their sedative effect.
Avoid Getting Colds and Flus
Becoming infected with cold and flu viruses triggers an inflammatory response that includes inflammation in the brain. Inflammation increases neuronal excitability, thus increasing the risk of psychiatric symptom-exacerbations until the inflammation-related increase in neuronal excitability returns to baseline. This can take anywhere from a few days to a few weeks once the symptoms of infection have resolved. Then again, embracing the sick role can sometimes reduce one’s level of cognitive-emotional stress both because it provides a socially acceptable reason to take a break and because if refocuses attention on taking care of oneself. This is a respite that, for many, is very much needed in today’s society. As previously discussed, de-stressing the mind reduces neuronal excitability, and so minor infections, like colds and flus, can sometimes have a mixed effect on neuronal excitability. However, from a purely physiological standpoint, avoiding infectious diseases is another natural way to reduce the risk and severity of psychiatric symptomatology.
References:
[1] Johnstone T, van Reekum CM, Urry HL, Kalin NH, Davidson RJ. Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression. J. Neuroscience 2007; 27 (33): 8877-8884.
[2] Leuchter AF, Cook IA, Hunter AM, Cai C, Horvath S. Resting-state quantitative electroencephalography reveals increased neurophysiologic connectivity in depression. PLoS One 2012; 7 (2): e32508.
[3] Griner T. What’s really wrong with you? A revolutionary look at how muscles affect your health. Avery Publishing, 1995.
[4] Landsberg L. (1996) Insulin and the sympathetic nervous system in the pathophysiology of hypertension. Blood Press Supply. 1:25-29.
[5] Milani P, et al. (2010) Cortisol-induced effects on human cortical excitability. Brain Stimul. 3(3):131-139.
[6] Huang C-W, et al. (2007) Glucose and hippocampal neuronal excitability: Role of ATP-sensitive potassium channels. Journal of Neuroscience Research. 85(7):1468-1477.
[7] Neilson S. (2018) Trying the Ketogenic Diet for Mental Health. 10 Days of Eating Fat, for My Mental Health. SCIENCE OF US.https://www.thecut.com/2018 /01/trying-the-ketogenicdietfor-mental-health.html. (Accessed 6/18/18).
[8] Gedgaudas NT. (2009) Primal Body, Primal Mind. Beyond the Paleo Diet for Total Health and a Longer Life. Healing Arts Press, Rochester, Vermont.
[9] Masino SA, etal. (2009) Adenosine, Ketogenic Diet and Epilepsy: The Emerging Therapeutic Relationship Between Metabolism and Brain Activity. Curr. Neuropharmacol. 7(3):257-268.
[10] Bostock ECS, Kirkby, KC, and Taylor, BVM. (2017) The Current Status of the Ketogenic Diet in Psychiatry. Front Psychiatry. Vol. 8(43):1-40.
[11] FORK OVER KNIVES. “A film that can save your life.” Rogers Ebert, Chicago Sun-Times. Available on Netflix and Amazon.
[12] Elkaim Y. Here Are the Top 10 Most Acidic Foods to Avoid. https://yurielkaim.com/acidicfoods-to-avoid/ (Accessed 9/5/18).
[13] Rademacher L, et al. (2016) Effects of Smoking Cessation on Presynaptic Dopamine Function of Addicted Male Smokers. Biological Psychiatry. 80(3)198-206.
[14] Erlij D, Acosta-García J, Rojas-Márquez M, et al. (2012) Dopamine D4 receptor stimulation in GABAergic projections of the globus pallidus to the reticular thalamic nucleus and the substantia nigra reticulata of the rat decreases locomotor activity. Neuropharmacology. 62 (2): 1111-1118.
[15] Binder MR. The Racing Mind: Brave new sights untangle the ancient mystery of mental illness, pp. 157-165. Lightningsource Publishing, 2024.
[16] Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: ∆9-tetrahydrocannabinol, cannabidiol and ∆9-tetrahydrocannabivarin. British Journal of Pharmacology 2008; 153 (2): 199–215.
[17] Silvestro S, Mammana S, Cavalli E, Bramanti P, Amazon E. Use of cannabidiol in the treatment of epilepsy: Efficacy and security in clinical trials. Molecules 2019; 24 (8): 1459.
[18] Binder MR. Gabapentin—The popular but controversial anticonvulsant drug may be zeroing in on the pathophysiology of disease. AJCEM 2021; 9 (4): 122-134.
[19] Kong WX, et al. Effects of taurine on rat behaviors in three anxiety models. Pharmacol Biochem Behav 2006; 83 (2): 271–276.
[20] Zhang CG and Kim SJ. Taurine induces anti-anxiety by activating strychnine-sensitive glycine receptor in vivo. Annals of Nutrition and Metabolism 2007; 51 (4): 379–386.
[21] El Idrissi A, et al. Prevention of epileptic seizures by taurine. Advances in Experimental Medicine and Biology 2003; 526: 515–525.
[22] Pendo K and DeGiorgio CM. Vitamin D3 for the treatment of epilepsy: Basic mechanisms, animal models, and clinical trials. Front Neur 2016; 7:218.
[23] Vitamin D3 for the treatment of epilepsy: Basic mechanisms, animal models, and clinical trials. Front Neur 2016; 7: 218.
[24] Lyon MR, et al. (2011) The effects of L-theanine (Suntheanine®) on objective sleep quality in boys with attention deficit hyperactivity disorder (ADHD): a randomized, double-blind, placebo-controlled clinical trial. Altern Med Rev. 16(4):348-354.
[25] Shirakawa S. (2004) Theanine supplementation and sleep quality. 17th European Sleep Research Society. http://www.ismh.org/en/scientifi c-spotlight/l-theanineandsleepquality/ (Accessed 5/5/18).
[26] Jang HS, et al (2012). L-theanine partially counteracts caffeineinduced sleep disturbances in rats. Pharmacol Biochem Behav. 101(2):217-221.
[27] Dean O, et al. (2011) Nacetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action. Journal of Psychiatry and Neuroscience. 36(2):78-86.
[28] Deepmala, et al. (2015). Clinical trials of Nacetylcysteine in psychiatry and neurology: A systematic review. Neuroscience and Biobehavioral Reviews. 55:294-321.
[29] Picciotto MR, et al. (2012) Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior. Neuron. 76(1):116-129.
[30] The George Metaljan Foundation. How to Eat Healthier in 2018. http://www.whfoods.com/genpa ge.php?tname=nutrient&dbid=50 (Accessed 7/23/18).
Medication Dosing in Psychiatry
Medication dosing is second only to medication selection as a major area of confusion in psychiatry. There are several reasons for this, but the biggest one is that dosing requirements for two persons with the same diagnosis can differ by as much as 100-fold. Such dramatic differences do not square up with the popular belief symptom-severity and body weight are the primary determinants of medication dosing.
To better understand drug dosing requirements, it is essential to recognize that drugs work by binding to receptors. This binding process, like a key fitting into a lock, opens doors that influence chemical and electrical processes in the body. Therefore, the degree to which the individual molecules of a drug fit into the locks that they are intended to open has a large bearing on their clinical effectiveness. If the molecules do not fit well, they will be less effective at opening the intended locks, and if they do not fit at all, they will be completely ineffective.
An equally important factor in medication doing is the degree of influence that the targeted doors have on the illness process that is being treated. If the influence is large, a relatively small amount of a properly fitted medication can be effective. If the influence is small, even large amounts of a properly fitted medication may be relatively ineffective. Therefore, the better the key fits into the lock, and the greater the influence the door has on the illness process being treated, the lower the amount of medication that will be needed. Both of these factors generally have a greater influence on dosing requirements than symptom-severity or body weight.
However, even the best fitted medications cannot exert their therapeutic effects if they cannot reach their targeted locks. In order to reach these locks, which are technically known as “receptors,” the medications have to move from the intestines, which are merely delivery channels, to the bloodstream. To do this, they must pass through the intestinal wall or, in the case of orally or nasally-absorbed medications, through the oral or nasal mucosa, respectively. Hence, the quantity of medication that enters the bloodstream is dependent upon the ability of the medication to be absorbed into the body. This step in the process explains why factors such as food intake and emotional stress, which can affect absorption, can impact the effectiveness of a given dose of a given medication.
Another important factor that can affect dosing requirements is the speed at which the body is able to eliminate the drug. The faster the body can eliminate it, the more of the drug that will be needed to keep opening the locks through which it exerts its therapeutic effects. Although volume of distribution, which is related to total body weight, is also a factor, it pales in comparison to receptor specificity, biological effectiveness, drug absorption, and drug metabolism when it comes to dosing requirements. In addition, most illness processes can be therapeutically modified by opening several different doors, and so combining different medications from the same class can have additive effects. Combining different medications from the same class can also reduce their individual side effects because, when used in combination, the dosage of each medication can potentially be reduced. Lower doses reduce the risk of side effects because they reduce the chances that any one of the medications will affect off-target receptors. This is important to understand because it is counterintuitive to think that taking several different medications for the same disease process can actually be less toxic than taking a smaller number of medications.
However, as a general rule, only one new medication should be introduced at a time. The reason for this is that the effect that a medication will have on a specific individual can be highly unpredictable, and so if two or more medications are started simultaneously, it can be hard to tell which drug is doing what. Also, the counter-therapeutic effects of one drug could negate the therapeutic effects of another drug, thus making it appear as though neither drug is effective. Finally, in an effort to prevent side effects, each drug should be initiated at the lowest possible dosage. Although a person’s pharmacogenomic profile (genetic testing) and history of drug sensitivity may provide some guidance on this, false predictions abound because, as previously discussed, there are many other factors involved in determining a drug’s effectiveness and tolerability. Therefore, the safest approach continues to be “starting low and going slow.”
Still, that raises the question of what it means to start low. Most clinicians and patients think that starting low means starting with the lowest available dosing strength of a particular drug. However, in my clinical experience, there are many patients for whom the lowest possible dosage is still far too high! Therefore, new drugs should, in most cases, be initiated at a fraction of the lowest available dosage. Even if that means taking a small fraction of a pill repeatedly over the first several hours, it is far better than starting off with too much drug, as medication can hardly be regurgitated once ingested. One of the most counterproductive events during the initiation phase of a new medication is to frighten the patient into thinking that a highly effective medication is causing too many side effects. Once a patient is put off like this, he or she may be unwilling to try the same medication again even at a much lower dosage.
Conversely, there are some patients who may be so insensitive to a drug that they need unusually high doses. This can markedly slow treatment because such patients still need a gradual titration upward, and a slow titration is also needed to avoid overshooting the therapeutic window. This latter consideration is particularly important because a medication that is effective at lower doses can, at higher doses, lose its therapeutic effect. Yet, for some patients, the therapeutic dosage of a medication may be so high that a serum drug level will be needed to determine how much of the drug is really being absorbed into the blood. However, apart from these rare exceptions, serum levels should not replace clinical effects as a guide to dosing because serum levels do not take into consideration a drug’s affinity for its target receptors, nor do they factor in the degree of leverage that those receptors have in mediating the desired clinical effects [1].
References
[1] Binder MR. A precision medicine approach to the treatment of psychiatric disorders. GJMR 2023; 23 (4): 1.
Moral and Religious Aspects of Psychiatric Treatment
For many people, the idea of taking medication that affects thoughts and emotions can create a moral dilemma. They wonder: will the medication change who I am? will it change my personality? will it take away my emotions? will it affect my moral decision-making? The idea of taking psychotropic medication may also represent a sign of weakness or cause some persons to wonder whether it is right to change their God-given nature and natural response to life’s ups and downs? These and other such questions represent fears about losing one’s identity, one’s relationships, and one’s soul through the use of psychotropic medication. By the time that I had completed my specialty training in psychiatry, I myself was wondering whether anyone really needed to take psychotropic medication. With that in mind, I began private practice with a quest to find a way to treat all mental illnesses without the use of medication.
It was not until I began to recognize the anatomical and functional distinction between the mind and the brain that I began accept the idea that some patients might actually need psychotropic medication. This growing acceptance was based on the idea that medication treats the brain, not the mind. Its effects on the mind were only indirect, as with any other form of medical treatment. Hence, taking psychotropic medication to treat a psychiatric disorder would be no different than taking an antibiotic to treat an infection or taking an anticonvulsant drug to prevent seizures.
However, that still left another very important question unanswered. Years before I entered the medical field, I served as a Chaplain’s Aide at the UCLA Medical Center. As I was contemplating becoming a doctor, I asked the hospital Chaplain, Fr. Patrick Traynor, whether God would rather have us rely upon doctors or upon Him when we become sick. Fr. Traynor gave me a simple, direct answer. God, he said, has many ways of helping people; one of them is through others; and when it comes to sickness, that includes doctors and nurses. His answer gave me the reassurance that pursuing a career in medicine could be a Godly thing to do [1].
Years later, as a young psychiatrist, I found myself faced with an even tougher question. I wondered what specific brain abnormality, if there was one specific abnormality, drove psychiatric symptomatology? This was one of the most challenging of all medical questions because, even after centuries of intensive study and debate, the underlying cause of psychiatric symptoms remains unclear. It was not until I asked for God’s help that I began to receive an answer to this question. What the Lord helped me to understand was that all of our thoughts, all of our emotions, and all of our experiences were functions of the soul, not brain. The brain is just a computer in the head, and the body is just a vehicle through which the mind (with the help of the brain) can interact with the physical world. The brain serves the mind by relaying electrical signals back and forth between the mind and the body. The mind induces magnetic fields as it cogitates, and the brain induces magnetic fields as neurons depolarize and repolarize [1]. What we call “corporeal consciousness” is a synchronization between mentally-induced magnetic fields and neurologically-induced magnetic fields. This is in distinction to “incorporeal consciousness,” which is consciousness apart from the brain and body. The ability of the mind to remain consciousness even after the soul separates from the body has now been validated by the burgeoning number of near-death experiences that have been reported from around the world [2].
When the soul is magnetically attached to the body, the brain relays electrical signals from the sense organs to the mind, which is the head of the soul. It also processes the information together with the mind, which in turn allows the brain to “remember” the same vibrational patterns that the mind remembers. In some cases, however, the brain can become pathologically hyperactive, in which case it does more than just relay electrical signals back and fourth between the mind and the body. The hyperactive brain tends to amplify the signals and cause them to be abnormally persistent. In so-doing, it turns normal thoughts and emotions into what we call “psychiatric symptoms.” This pathological process, which, in most cases is caused by the inheritance of gene variants whose protein products fail to adequately regulate the firing of neurons, is the hypothetical basis of psychiatric symptomatology. When understood from this perspective, the treatment of psychiatric symptoms, which is accomplished most effectively by calming the brain, does more to help a person be his or her true self then it does to distort his or her true self.
Natural ways to calm the brain include stress-reduction, moderate exercise, establishing an early sleep schedule, enjoying a relaxing hobby, avoiding caffeine and other psychostimulants, and minimizing refined sugar. One should bear in mind, however, that these natural interventions, though helpful, are typically insufficient for all but those persons who have relatively mild levels of neuronal hyperexcitability. For those with higher levels of neuronal hyperexcitability, natural interventions alone are, in most cases, neither adequate nor practically doable because affected persons have so much difficulty controlling their behavior. For such persons, the first-line intervention should be medications that simply calm the brain. Such medications have traditionally been referred to as “anticonvulsants” because they prevent seizures. In the treatment of psychiatric disorders, however, they could more aptly be referred to as “neuroregulators” because they help regulate the firing of neurons [3]. Among the most effective neuroregulators are gabapentin, oxcarbazepine, lamotrigine, depakote, lithium, levetiracetam, topiramate and tiagabine. In addition to having a long history of successful use in psychiatry, these medications are some of the safest and least expensive drugs available. Additionally, they are fast-acting, non-addictive, and highly effective in long-term use. Moreover, because calming the brain is highly protective against the development of other chronic diseases, such diabetes, high blood pressure, cardiovascular disease, autoimmune disease, cancer, and dementia, early treatment with neuroregulators can be as beneficial medically as it is psychiatrically [4].
That still leaves unanswered the question of what effect psychotropic drugs have on the soul of a person. From a spiritual and religious perspective, the human soul is like a seed that is planted in the earth. The earth sustains the seed, but the seed must push up through the earth to grow and bear fruit. The same applies to the soul as it grows in the body, which is made of all the same constituents as the earth. In Genesis 1:28 of the Holy Bible, humankind is told to “be fruitful and multiply and subdue the earth…” To “subdue the earth” is to exercise morality over carnality. This requires self-discipline because carnal pleasures are often at odds with moral precepts. The conflict between these two opposing desires is what allows the spirit, which is the moral aspect of the soul, to grow in strength and in union with God. If, however, the mind, which is the head of the soul, is constantly bombarded by electrical signals from the brain, communion with God and, hence, one’s spiritual growth, can be adversely affected. Therefore, efforts to quiet the brain, whether they be through natural interventions or medical interventions, can be as beneficial to one’s spiritual health as they can be to one’s mental and physical health.
References
[1] Binder, MR. Am I Depressed or Am I Bipolar? Help your doctor make the right diagnosis and choose the right treatment for you. Lightningsource Publishing, 2009.
[2] Binder, MR. Mysteries of the Mind: Two astonishing articles that unveil the mystery. Lightningsource Publishing, 2022.
[3] Binder MR. Introducing the term “Neuroregulator” in psychiatry. AJCEM 2019; 7 (3): 66-70.
[4] Binder MR. FLASH syndrome: Tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109.
Psychiatric Disorders and the Problem of Misattributing Symptoms
One of the biggest challenges in distinguishing psychiatric symptoms from normal thoughts and emotions is the problem of misattribution of symptoms. In other words, affected persons have trouble distinguishing neurologically-based thoughts, emotions, and perceptions from mentally-based thoughts, emotions, and perceptions. This difficulty is created by the fact that the mind and the brain process the same mental and emotional information simultaneously coupled with the fact that abnormal brain signaling can distort one’s thoughts and emotions. However, these cognitive and emotional distortions can be subtle, and so an affected person can easily fail to recognize when they are occurring.
Due to the many limitations of the psychiatric diagnostic system, a more reliable way to recognize when cognitive-emotional distortions are occurring is to attempt to determine whether the underlying driver of the distortions is present. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) Hypothesis of Psychiatric Disorders, psychiatric and psychiatrically-related physical symptoms are driven by an inherent hyperexcitability of the neurological system [1]. Simply put, the electrical cells of the brain tend to be overly active and tend to overreact when stimulated by mental and emotional processing. This over-reaction then causes the mind to keep dwelling on things and the emotions to be abnormally amplified in the process. Yet because one naturally assumes that the brain is working normally, one also assumes that whatever he or she is thinking and feeling is an accurate reflection of one’s self and one’s coping mechanisms.
Until recently, the identification of the neuronal hyperexcitability trait was based purely on psychiatric symptoms. The subjectiveness of this assessment is one of the many reasons that only about half of all persons who have psychiatric symptoms ever reach out for help. However, there is now a completely objective way to determine whether or not one has the neuronal hyperexcitability trait. The test is so simple that you can perform it right in the comfort of your own home. It is called the 60-second resting vital-sign measurement. To perform the test, simply count, while at rest, the number of times your heart beats in a 60-second period. If the number is greater than 75, your neurons are likely to be hyperexcitable. However, this test can be thrown off if, for example, you have a rigorous exercise routine or take a medication or recreational drug that affects your heart rate. To get around this problem, you can count the number of breaths you take in a 60-second period. The concern with this test, however, is that it can be difficult to determine your respiratory rate without intentionally controlling your breathing. Therefore, to obtain the most accurate results, it would be best to ask someone else to count your breathing rate at a time when you are completely unaware that he or she is doing it. If the number of breaths in a 60-second period is greater than 15, this too would indicate that your neurons are hyperexcitable.
So what do I do if my neurons are hyperexcitable?
If the test results indicate that your neurons are hyperexcitable, then your next step would be to take the subjective test for neuronal hyperexcitability. To take this test, simply answer each of the following 15 questions as accurately as possible. 1 means you strongly disagree, and 10 means you strongly agree. After you have answered each of the 15 questions, then simply add up your responses.
I tend to think a lot; my mind won’t shut off
I often feel anxious
I often feel depressed
I often feel irritated
I often feel overwhelmed
I sometimes feel suicidal
I sometimes feel highly energized
I tend to lose my motivation
I tend to have trouble sleeping
I tend to get overly excited about things
I tend to keep dwelling on things
I tend to be emotionally sensitive
I tend to worry a lot
I tend to have social anxiety
I tend to have trouble concentrating
A total score of 15-20 means that your neurons are not very excitable; 21-50 means that they are moderately hyperexcitable; and greater than 50 means that they are very hyperexcitable.
Although a positive result on any one of the aforementioned objective and subjective tests is a pretty good indicator that your neurons are hyperexcitable, a positive result on two or more of the tests would be even confirmatory. If you do test positive and think that you have been struggling mentally and emotionally, then you have likely discovered the real reason why. I say “real reason” because the vast majority of people can handle most of life’s stressors pretty well if their brains are working calmly. Therefore, if you feel like you are having more difficulties than others, you would be wise to address the problem.
The most natural ways to reduce the excitability of the neurological system include stress-reduction, establishment of an early sleep schedule, moderate exercise, enjoying a relaxing hobby, avoiding caffeine and other psychostimulants, and minimizing refined sugar. Also helpful can be various supplements that help calm the brain. Please see my blogpost entitled “Natural Ways to Reduce and Prevent Psychiatric Symptoms” for more details on that. In the event that the aforementioned natural interventions are either insufficient to control symptoms or too difficult to implement, then you should consider taking brain-calming medications. Contrary to the traditional treatment of psychiatric symptoms, these medications do not include antidepressants, psychostimulants, or antipsychotics. Rather, they are a specific class of medications called “anticonvulsants” or “mood stabilizers.” Rather than changing the way the brain works, these medications simply keep the brain from overworking. Although such medications, which could more aptly be called “neuroregulators” [2], have a long history of successful use in psychiatry, they are sorely underutilized because the treatment of psychiatric disorders is primarily symptom-based rather than pathology-based. Please see my blogpost entitled “How to Treat Mental Illness Quickly, Effectively, and Inexpensively” for more details on that.
References
[1] Binder MR. The multi-circuit neuronal hyperexcitability hypothesis of psychiatric disorders. AJCEM 2019; 7 (1): 12-30.
[2] Binder MR. Introducing the term “Neuroregulator” in psychiatry. AJCEM 2019; 7 (3): 66-70.
Managing Psychiatric Symptoms During Pregnancy and the Postpartum Period
Although managing psychiatric symptoms during pregnancy and the postpartum period might sound like a complicated issue, it becomes much less complicated when the cause of psychiatric symptoms and the effects of a woman’s reproductive hormones are properly understood.
As discussed in previous blogposts, anxiety, depression, insomnia, and the common psychiatric symptoms are the consequence of pathological circuit-specific hyperactivity in the brain. This abnormal electrical activity can be reduced through a variety of natural interventions. However, for all but those with mild levels of neuronal hyperexcitability, ongoing treatment with neuroregulators (anticonvulsant drugs) is usually necessary. This presents a potential problem for women of child-bearing age because anticonvulsants (including the anticonvulsant-like drug lithium) can cause birth defects if continued during pregnancy. This is important to understand especially because the developing fetus is most vulnerable to these defects during the first trimester of pregnancy, when the central nervous system of the baby is forming.
Fortuitously, however, the reproductive hormone progesterone is a powerful anticonvulsant. Hence, it tends to reduce psychiatric symptoms in the same way that other anticonvulsants do [1]. However, the blood levels of progesterone are continuously fluctuating. They normally climb from the beginning of the menstrual cycle until ovulation, at which time they begin to fall again. The rapid fall in progesterone levels during the premenstrual period is what drives the anxiety, irritability, and moodiness that have been described as premenstrual syndrome (PMS) and, in its more extreme form, premenstrual dysphoric disorder (PMDD). This same pattern is repeated during pregnancy and the postpartum period. Psychiatric symptoms tend to decline during pregnancy because progesterone levels steadily rise during that time, and they tend to recur during the postpartum period because progesterone levels begin to fall again during that time [2].
These hormonal patterns can be used to guide treatment during pregnancy and the postpartum period. For example, a woman’s awareness that the protective hormone progesterone will be rising during the pregnancy can provide the reassurance that she needs to temporarily bear a recurrence of symptoms if she were to discontinue her psychotropic medication either in anticipation of becoming pregnant or upon learning that she had become pregnant. Unless there is a seizure disorder, non-benzodiazepine neuroregulators can be stopped abruptly because they have little risk of withdrawal symptoms. By the same token, a woman’s awareness that her progesterone levels would be falling upon giving birth would also mean that she should resume taking her medication once the baby was born. Although there are many other factors that can influence the need for psychotropic medication during pregnancy and the postpartum period, the normal rise and fall of serum progesterone is usually the most important of them.
References
[1] Binder MR. The Racing Mind: Brave new sights untangle the ancient mystery of mental illness, pp. 187-191. Lightningsource Publishing, 2024.
[2] Binder MR. The Racing Mind Video Series Part 19 – Hormonally-Related Disorders and Neuronal Hyperexcitability.
Reconceptualizing Mental Illness As A Biomarker For Physical Illness
One of the many reasons that the underlying cause of psychiatric disorders has remained so elusive is that we’ve been misconceptualizing these disorders. First, we’ve been viewing psychiatric disorders as different pathological processes rather than as different manifestations of a shared biological abnormality. Second, we’ve been viewing psychiatric disorders as a group of conditions that are distinctly different from other medical conditions. Third, we’ve been viewing the mind as a product of complex brain function rather than as an entity that is distinctly different from the brain. However, when the mind is viewed as the executor of brain function, and psychiatric symptoms are viewed as early manifestations of a physiological abnormality that is shared by nearly all chronic diseases, the root cause of psychiatric disorders becomes much more clear.
Most chronic illnesses, as opposed to specific physical abnormalities, such as a cleft lip, a ventricular septal defect, or a clubbed foot, are caused by some kind of physiological abnormality that eventually causes one or more systems of the body to become dysregulated. The most common cause of chronic illness is aging [1]. Simply put, the older the body gets, the greater the likelihood that various parts will wear out. However, studies have shown that the bodies of some persons wear out much faster than those of others. And although one might think that this difference would be related to diet and lifestyle, it actually seems to have less to do with that than one’s genetic predisposition. The early onset of chronic diseases, such as diabetes, high blood pressure, cardiovascular disease, autoimmune disease, cancer, and dementia, tends to run in families. Moreover, those individuals who are more highly affected tend to appear in a classic Mendelian distribution [2]. In other words, they tend to appear in a distribution that suggests the inheritance of just one or two variant genes rather than the inheritance of many different variant genes.
That leads to a couple of important questions: 1) what is the physiological abnormality? and 2) how does it cause disease?
To answer these questions, let us recall that the brain is the head of nearly every bodily function. The brain continually sends messages to the heart, the lungs, the intestines, the kidneys, and every other organ of the body. The brain also regulates mental function, autonomic function, metabolic function, endocrine function, and immune function. Consequently, the more active the brain was, the more active these functions would be. Now, if we return to the observation that some persons appear to age faster than others, it would raise the question of whether the brains of such persons were more active than the brains of others. If so, it would imply that the various systems of their bodies were likewise more active than those of others.
Consistent with this idea, numerous studies have found that persons who develop chronic disease at an earlier age have higher resting heart and respiratory-rate measurements [3]. These measurements reflect the level of activity of the autonomic nervous system, which, as previously discussed, is regulated by the brain. Hence, the higher the number, the more active the brain would be. Also, the more active the brain, the more active the mind would be because the brain drives mental function. From the study of mental illness, it is clear that persons with active minds are at increased risk for developing psychiatric symptoms [2]. Taken together, these observations suggest that persons with psychiatric symptoms would be an increased risk for the early onset of a wide range of chronic medical conditions.
This conclusion is supported by the fact that persons with severe mental illness die of the same kinds of illnesses as the general population but at a much earlier age [3]. Interestingly, however, psychiatric symptoms tend to develop long before the symptoms of most other chronic diseases. This is where the distinction between the mind and the brain becomes important to recognize. The cognitive-emotional system is much more sensitive to neuronal hyperactivity than other systems of the body. Hence, the chronic physical conditions appear to reflect the gradual erosive effects of neuronal hyperactivity. What this means is that psychiatric symptoms could be the first subjective markers of a physiological abnormality that underlies most, if not all, chronic diseases [4]. This would be a radical reconceptualization of psychiatric symptomatology!
The validity of this hypothesis is supported by the tight link between cognitive-emotional stress and the development of chronic disease. Nearly every chronic disease process, from high blood pressure to Alzheimer’s disease, is thought to be fueled by stress [5]. Stress in the mind increases the activity of the brain, and the more active the brain becomes, the more likely it is to overwork and dysregulate the various organs and systems of the body. That is not to say that being busy is physically unhealthy. On the contrary, being busy helps keep the mind, the brain, and the body in good shape. However, being too busy can increase stress levels to the point of causing the brain to become pathologically hyperactive. This vulnerability, however, does not appear to be experienced by all persons. Rather, it appears to affect only those persons who inherit the genes for neuronal hyperexcitability [6]. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) hypothesis of psychiatric disorders, this explains the link between stress, psychiatric symptoms, and the early onset of chronic disease. It also implies that early treatment of persons who have elevated resting vital signs could help delay or even prevent the development of a wide range of chronic diseases, including mental illness.
References
[1] Niccoli T, Partridge L. Ageing as a Risk Factor for Disease. Current Biology 2012; 22 (17): R741-R752.
[2] Binder MR. Neuronal hyperexcitability: The elusive but modifiable instigator of disease. AJCEM 2022; 10 (1): 1-7.
[3] Binder MR. FLASH syndrome: Tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109.
[4] Binder MR. Psychiatric and functional physical symptoms: The more telling “fifth” vital sign. AJCEM 2021; 9 (6): 233-337.
[5] Justice NJ. The relationship between stress and Alzheimer’s disease. Neurobiol Stress 2018; 8:127-133.
[6] Binder MR. The neuronal excitability spectrum: A new paradigm in the diagnosis, treatment, and prevention of mental illness and its relation to chronic disease. AJCEM 2022;10 (1): 1-7.
Neuronal Hyperexcitability: The Elusive Driver of Chronic Disease
Historically, it has been thought that various indices, such as high blood pressure, diabetes, and hypercholesterolemia, increase the risk of heart attacks and strokes. It has also been thought that the risk of these and other life-threatening events is increased if there is blood-clotting in the heart (as occurs in atrial fibrillation) or in the legs (as in deep vein thrombosis). However, this reasoning confuses markers of disease with causes of disease. In other words, it presumes that specific abnormalities, such as hypertension (high blood pressure readings), atrial fibrillation (an arrhythmia of the heart), or a deep vein thrombosis (a blood clot in the leg), that precede a life-threatening event, such as a heart attack, stroke, or pulmonary embolism, is the cause of the event. This, in turn, leads one to believe that correcting the causative condition will reduce the likelihood that the life-threatening event will occur (York Cardiology).
The problem with this reasoning, however, is that it fails to answer the question of why the risk factors develop in the first place. That is, it fails to consider the possibility that there might be some underlying factor that is driving both the risk factors and the disease processes with which they are associated. This is extremely important to understand because treatments that reduce the risk factors, such antihypertensive drugs, blood thinners, and cholesterol-lowering drugs, may not be removing the underlying cause of both the risk factors and the life-threatening events that they are predictors of.
In addition to its theoretical implications, confusing markers of disease with causes of disease has practical implications. For example, under the assumption that a person with atrial fibrillation suffered a stroke because of blood clots in the heart, one might presume that blood thinners would no longer be necessary once the atrial fibrillation was corrected. The same reasoning could be applied to the resolution of a deep vein thrombosis in regards to a pulmonary embolism.
Besides affecting the medical decision-making process, the distinction between risk factors and causative factors naturally leads to the question of what causes the risk factors in the first place. The most common answer is that the primary risk factors (i.e., high blood pressure, diabetes, and hypercholesterolemia) are caused by an unhealthy lifestyle (i.e., poor dietary choices, insufficient exercise, and chronic stress). Although this is partially true, there is something more fundamental going on that the medical field is only just beginning to recognize.
Nearly all persons who have multiple risk factors for disease are born with an increased vulnerability to stress, and it is this vulnerability that ultimately drives all the other risk factors. The evidence for this is that the risk factors tend to be familial, but contrary to expectation, the family members that are affected are not randomly distributed. Rather, they tend to appear in a classic autosomal dominant distribution [1]. What this implies is that they are related to variants of a single gene (or small number of genes). Affected persons also tend to have various psychiatric problems, such as anxiety, depression, and insomnia. The growing recognition of this elusive pattern is beginning to shed light on the link between cardiovascular risk factors and mental illness.
Heretofore, the assumption has been that mental illness increases the risk of physical illness because it increases one’s level of stress and makes it more difficult to establish and maintain a healthy lifestyle. The problem with this explanation, however, is that it does explain why the person has mental illness in the first place. The assumption has been that mental illness is the result of a dysfunctional upbringing, traumatic life experiences, chronic stress, and some genetic predisposition. What makes this whole thing so confusing is that all of these explanations are to some extent true; however, none of them identify the root cause of the problem.
The root cause of virtually all chronic health conditions, whether psychiatric, medical, or both, is an inherent hyperexcitability of the neurological system. This hyperexcitability, which is transmitted from affected parents to some (but not necessarily all) of their children, is caused by gene variants whose protein products fail to adequately regulate the firing of neurons [1]. That the underlying cause of nearly all chronic diseases is an abnormality of the nervous system should not be surprising given that the brain regulates virtually every function of the body. This includes the autonomic nervous system, the cardiovascular system, the metabolic system, the endocrine system, the immune system, and the musculoskeletal system.
For example, the mechanism by which neuronal hyperexcitability would increase the risk of atrial fibrillation (and other cardiac arrhythmias), would be to increase the risk of aberrant electrical signaling in the heart [2]. The abnormal electrical signaling would then cause abnormal contractions of the heart. The same risk would occur in the brain, thus shedding light on the cause of psychiatric disorders and to some extent seizure disorders. Like arrhythmias in the heart, psychiatric disorders involve stormy electrical activity in the brain, and these electrical storms disrupt one’s thoughts and emotions [1]. They can also increase the risk of seizures in persons who are prone to having them [3]. Consistent with their shared etiology, the treatment options for cardiac arrhythmias and psychiatric disorders are essentially the same. Cardiac arrhythmias can be treated medically with beta blockers and calcium channel blockers, and psychiatric symptoms can be treated medically with anticonvulsants and alpha-2 antagonists. Working through different mechanisms and receptors, all of these drugs accomplish the same fundamental thing: they reduce the excitability of the neurological system. The same is true with electro-cardioconversion to treat arrhythmias, and electroconvulsive therapy to treat psychiatric disorders [3].
Another important risk factor for disease that is rooted in neuronal hyperexcitability is inflammation. Neuronal hyperexcitability increases inflammation by over-activating the immune system [4]. In the process, it increases the risk of autoimmune diseases [4,5], and it increases the risk of blood-clot formation [6], the latter of which is the fundamental mechanism by which heart attacks and strokes occur. Also note that because neuronal hyperexcitability over-activates the cardiovascular system, it tends to increase blood pressure, and because it also over-activates the endocrine and metabolic systems, it tends to increase cortisol, blood sugar, and cholesterol levels. Over time, these factors, together with the aging process, cause the arteries to harden. This, in turn, further increases blood pressure and further increases the risk of heart attacks and strokes. Unsurprisingly then, the same lifestyle habits that reduce the risk of any one of the aforementioned pathological processes reduce the risk of all the others, and the same lifestyle habits that increase neuronal excitability (i.e., cognitive-emotional stress, lack of sleep, stimulant-type drugs, and refined sugar) increase the risk of all of them [7,8].
Mental and Emotional Stress
The dynamic relationship between the mind and the brain is the principle reason that cognitive-emotional stress is such an important factor in the development of both mental and physical illness [9]. It is also the reason that physical stressors, such as environmental toxins, viral and bacterial infections, and physical injuries, can further increase the risk of mental and physical illness. Under stressful conditions, the mind agitates the brain like stones being thrown at a beehive, and the brain itself can become hyperactive due to the direct effects of biological stressors. As the activity of the brain ramps up, the mind becomes even more stressed due to the agitating effect that the hyperactive brain has on the mind. Simultaneously, an overabundance of electrical signals are sent down the spinal cord, and the endocrine system is over-activated, thus sending both the mind and the body into fight-or-flight mode.
Although all of these same processes occur in persons with normo-excitable neurological systems, they are over-amplified in persons with hyperexcitable neurological systems [10]. For example, a stressor that might affect a normal person for a few hours might affect a person with hyperexcitable neurons for several days or even several weeks. In addition to the extended duration of the neurological hyperactivity, the failure of the neurological system to promptly return to baseline increases the risk that a second stressor will occur before the affected person recovers from the first stressor, thus risking the possibility that the two stressors will summate [1]. Moreover, even when the system does return to baseline, the baseline itself is abnormally elevated. This chronic low-grade hyperactivity expresses itself as a mild elevation in resting heart and respiratory rate measurements. However, because the trait of neuronal hyperexcitability does not always express symptoms, the associated vital-sign elevations have traditionally been considered to be “normal.” Also, the norms for resting heart and respiratory-rate were established prior to the recognition of neuronal hyperexcitability as a pathophysiological trait. And since an estimated 40% of the world’s population harbors the trait, and because the severity of the trait can vary, the resting vital signs of those who are affected, though relatively elevated, form a continuum with the vital-sign measurements of those who are unaffected. Thus, using currently established norms, carriers of the neuronal hyperexcitability trait could best be described as having upper-end-of-normal resting vital signs [11,12].
Objective Markers of the Neuronal Hyperexcitability Trait
In recent years, an explosion of clinical studies has identified a link between upper-end-of-normal heart and respiratory-rate measurements and the early development of a wide range of chronic diseases, including diabetes, high blood pressure, cardiovascular disease, autoimmune disease, cancer, and dementia [11]. Additionally, Latvala et al. [13], in a longitudinal study involving more than one million men in Sweden, found that subtle elevations in resting heart rate were predictive of the later development of generalized anxiety disorder, obsessive-compulsive disorder, and schizophrenia. Similarly, Blom et al. [14] found that adolescent girls with emotional disorders had increased resting respiratory rates in comparison to healthy controls. The subtle vital-sign elevations with which these illnesses are associated are thought to be the consequence of a tonic elevation in basal neurological activity in those persons who inherit the genes for neuronal hyperexcitability [11]. The reason that psychiatric symptoms precede the development of the physical abnormalities that characterize chronic disease is that the cognitive-emotional system, which belongs to the mind, is far more sensitive to neuronal hyperexcitability than the organs and tissues of the body. The development of the associated physical abnormalities reflects the gradual erosive effects of the neuronal hyperexcitability trait.
Reconceptualizing Psychiatric Symptomatology
Thus, psychiatric symptoms can be said to be the first subjective markers of the neurological the trait. This could help explain why the lifespans of persons with severe mental illness tend to be so much shorter than the general population. Moreover, the observation that the kinds of diseases that they develop are the same ones that unaffected persons develop suggests that the neuronal hyperexcitability trait essentially accelerates the aging process. This dramatic reconceptualization of psychiatric symptomatology unifies psychiatric illness with physical illness and at last overcomes the long-held stigma of mental illness.
The good news is that neuronal hyperexcitability is highly treatable. For those with mild levels of neuronal hyperexcitability, stress-reduction and healthy lifestyle changes may quiet the neurological system enough to prevent psychiatric symptoms and, along with that, the gradual erosive effects of the neuronal hyperexcitability trait. For those with higher levels of neuronal hyperexcitability, various combinations of anticonvulsant drugs can be highly effective. Unlike antidepressants, antipsychotics, and other commonly-prescribed psychotropic drugs, anticonvulsants, which could more aptly be called “neuroregulators” because they regulate the firing of neurons [15], do not change the way the brain works; they simply act as coolants in the system. In so-doing, they compensate for the gene abnormality [1] that renders the neurons hyperexcitable [16,17]. What distinguishes this treatment approach, which could be called “focused neuroregulation” [18], from standard psychiatric treatment is that it normalizes brain function rather than merely treating the symptoms. It also reduces the risk of all of the aforementioned pathological processes because it reduces the neuronal excitability that drives them [19]. This is quite unlike the effects of antidepressants and psychostimulants in psychiatry, and the effects of beta blockers and antihypertensive drugs in primary care. These drugs merely mask the signs of neuronal hyperexcitability, whereas neuroregulators reduce the neuronal excitability itself, thus uprooting the underlying driver of chronic disease. If this treatment is started early in life, it can hypothetically delay or even prevent the development of most chronic disease processes.
References
[1] Binder MR. The multi-circuit neuronal hyperexcitability hypothesis of
psychiatric disorders. AJCEM 2019; 7 (1): 12-30.
[2] Peacock J and Whang W. Psychological Distress and Arrhythmia: Risk Prediction and Potential Modifiers. Prog Cardiovasc Dis 2013; 55 (6): 582-589.
[3] Lado FA and Moshé SL. How do seizures stop? Epilepsia 2008; 49 (10): 1651-54.
[4] Dantzer R. Neuroimmune Interactions: From the brain to the Immune system and vice versa. Physiol Rev 2018; 98 (1): 477-504.
[5] Wick G, Cole R, Dietrich H, et al. Chapter 7 – The obese strain of chickens with spontaneous autoimmune thyroiditis as a model for Hashimoto disease. In: Autoimmune Disease Models: A Guide Book. Elsevier, Inc. 1994 p. 107-122.
[6] Sandrini L, Leraci A, Amadio P, et al. Impact of Acute and Chronic Stress on Thrombosis in Healthy Individuals and Cardiovascular Disease Patients. Int J Mol Sci 2020; 21 (21): 7818.
[7] Binder MR. The Racing Mind Video Series Part 34: Exercise and Neuronal Hyperexcitability.
[8] Binder MR. The Racing Mind Video Series Part 35: Diet and Neuronal Hyperexcitability.
[9] Binder MR. Mind-brain dynamics in the pathophysiology of psychiatric disorders. Am J Psychiatry and Neurosci 2022; 10 (2): 48-62.
[10] Binder MR. The Racing Mind Video Series Part 11: Medical Disorders and Neuronal Hyperexcitability.
[11] Binder MR. FLASH syndrome: Tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109.
[12] Binder MR: The neuronal excitability spectrum: A new paradigm in the diagnosis, treatment, and prevention of mental illness and its relation to chronic disease. AJCEM; 2021; 9 (6); 187-203.
[13] Latvala A, Kuja-Halkola R, Rick C, et al. Association of resting heart rate and blood pressure in late adolescence with subsequent mental disorders: A longitudinal population study of more than 1 million men in Sweden. JAMA Psychiatry 2016; 73 (12): 1268-1275.
[14] Blom EH, Serlachius E, Chesney MA, Olsson EMG. Adolescent girls with emotional disorders have a lower end-tidal CO2 and increased respiratory rate compared with healthy controls. Psychophysiology 2014; 51 (5): 412-418.
[15] Binder MR. Introducing the term “Neuroregulator” in psychiatry. AJCEM 2019; 7 (3): 66-70.
[16] Binder MR. Gabapentin—The popular but controversial anticonvulsant drug may be zeroing in on the pathophysiology of disease. AJCEM 2021; 9 (4): 122-134.
[17] Binder MR. Anticonvulsants: The psychotropic and medically protective drugs of the future. AJCEM 2021; 9 (5): 174-182.
[18] Binder MR. Focused neuroregulation in the treatment and prevention of mental and physical illness. AJCEM 2022; 10 (2): 49-58.
[19] Binder MR. (Video Presentation). Gabapentin – The Popular but Controversial Anticonvulsant Drug May Be Zeroing in on the Pathophysiology of Disease.
The Little-known but Most Powerful Natural Way to Prevent Colds and Flus
Although regular hand-washing is a reliable way to prevent viral infections that are transmitted via physical contact with infected persons or contaminated surfaces, most infections occur through the inhalation of airborne droplets [1]. Hence, regular hand-washing is insufficient to prevent most viral infections. Also, it is a little-known fact that infectious viruses can inadvertently be transmitted from one’s own mouth, where they may not cause symptoms, to one’s nose and eyes, where they can start infections that develop into colds and flus [2].
The good news is that there is a very effective way to prevent viral infections even after the mucous membranes become contaminated with viruses from infectious droplets or saliva. The solution is to simply take a warm shower or bath every night before bed. Because viruses can be denatured by heat, the warm water and steam tend to destroy any virus that might be attached to the lining of the nose or conjunctiva of the eyes [3-5]. However, timing is important. Viruses take around 8 to 10 hours to make their way from the mucous membranes to the bloodstream. Thus, if one is exposed during the day, waiting until morning to bath may be too late. Also, avoiding persons who are sick does not necessarily ensure that one has not been exposed. The person you were talking to yesterday, though contagious, might not have come down with symptoms until today, when the body has started to mount an immune response to the virus.
Another reason that bathing at night is highly protective is that the heat of the water causes blood vessels in the skin and mucous membranes to dilate in an effort to prevent the body’s core temperature from rising during the bath. When this happens, immune cells and antibodies vigorously circulate to the mucous membranes, which then increases the chances that the virus will be destroyed before it can breach the wall and enter the bloodstream. After the bath, this process can be bolstered by slowly breathing hot hair into the nose using an ordinary hairdryer. Just a few minutes of this process increases the certainty that the virus has been fully destroyed.
Over the years, I have seen these simple protective measures reduce infection rates in the fall, winter, and spring by three to six-fold. This is far more effective than relying on nutritional supplements and proper rest. Summertime is not so much of a concern because again, viruses are less stable, and immune function is much better when the body stays warm [4,6]. Nonetheless, if you do become chilled during the summer, as I once did as the sun was setting after a warm day in Los Angeles, it becomes very important to take a warm shower or bath that same night. The reason that the cold air increases the risk of infection is not just that viruses are more stable in the cold but, more importantly, that the cold air causes the body to shunt the blood to the core. The body does this in an effort to maintain core temperature, but as it does so, blood vessels in the mucous membranes constrict, thus reducing the ability of the immune system to defend the fortress as the virus attempts to breach the wall. Although we might feel like the chill has left the body as we warm up indoors, the warm-up is too gradual to signal blood vessels in the skin and mucous membranes to start dilating again. Thus, the system must be shocked by heat in order to reverse the physiological effects of having become chilled. Of course, an alternative to warm-water bathing is to exercise, as this too causes blood vessels in the skin and mucous membranes to dilate. However, unless this is done at home, traveling from the gym could result in re-exposure to the cold, thus causing the blood vessels in the skin and mucous membranes to constrict again. Also, exercise alone does not expose the virus to external heat. Thus, even if one were to exercise at home, it would not fully substitute for a warm shower.
What if I already have a cold or flu?
In the event that one is already sick or becoming sick, all is not lost. During an infection, pyrogens cause muscles to spasm, which has the effect of heating up the body because muscle contraction produces heat. Although this does help destroy viruses, it also expends energy, which the body could otherwise be using to fight off the infection. The normal cycle of temperature fluctuations begins with chills as the muscles start to spasm, followed by fever as the body temperature rises. This is followed by a gradual dissipation of heat as the blood vessels in the skin and mucous membranes begin to dilate.
If, however, during the phase of chills, one were to take a warm shower, the heat of the water could help save the body the energy that it would otherwise use to heat itself. This would not only relieve the discomfort of feeling cold, but it would also help the body fight off the infection without using up as much energy to produce a fever. Obviously, we should not bathe in warm water while feeling warm because fever is the phase in which the body is attempting to dissipate heat, and it would be counterproductive to prevent that process. Conversely, if one had a high fever, a lukewarm sponge-bath could be helpful in reducing core body temperature because the skin cools off as it dries [7]. Another way to accomplish this is to soak a knitted hat or pair of socks in warm water, ring them out, and then place them on. The residual warmth will be comforting while still allowing the skin to cool as the hat and socks dry out. These techniques are safer than taking a tepid bath, as the cool water could chill the body, which in turn could trigger the return of chills and possibly even a higher fever. A limitation of using water to reduce fever in infants is that parents might not know whether the infant is feeling hot or cold, and spot temperature checks are not reliable indicators of this. Thus, whenever possible, parents should manage fever under the supervision of a qualified pediatrician.
References
[1] Andrup L, Krogfelt KA, Hansen KS, Madsen AM. Transmission route of rhinovirus – the causative agent for common cold. A systematic review.
American Journal of Infection Control 2023: 938-957.
[2] Abeles SR, Robles-Sikisaka R, Ly M, et al. Human oral viruses are personal, persistent and gender-consistent. The ISME Journal 2014; 1753-1767.
[3] Eccles R and Wilkinson JE. Exposure to cold and acute upper-respiratory tract infection. Rhinology 2015; 53: 99-106.
[4] Eccles R. An explanation for the seasonality of acute upper-respiratory tract viral infections. Otolaryngology 2002; 122 (2): 183-191.
[5] Lowen AC and Steel J. Rolls of humidity and temperature in shaping influenza seasonality. Journal of Virology 2014; 88 (14): 7692-7695.
[6] Binder MR. The Racing Mind Video Series Part 16 – Viral Infections and Neuronal Hyperexcitability].
[7] Kusnanto K, Wdyawati IY, Cahyanti IS. The effectiveness of tepid sponge bath with 32°C and 37°C to decrease body temperature at toddler with fever. Jurnal Ners 2017; 3 (1): 1-7.
The Wide-Ranging Benefits of Prophylactic Neuroregulator Therapy
For persons with hyperexcitable neurological systems, all mental, emotional, and physical stressors are abnormally amplified. The death of a loved one, the process of divorce, the loss of a job, a serious medical illness, or an elective surgical procedure are all circumstances that could amount to throwing a brick at the beehive for persons with hyperexcitable neurons. Also, the development of psychiatric symptoms as a consequence of these stressors tends to be delayed by days, weeks, or months. This raises the question of whether asymptomatic carriers of the neuronal hyperexcitability trait should be treated with neuroregulators prophylactically (preventively) if and when they encounter a highly stressful period in their lives.
In the past, such an option would have been inconceivable because there would have been no way of knowing which asymptomatic persons were at elevated risk of psychiatric or functional physical symptoms in the face of high stress. However, with the recognition that carriers of the neuronal hyperexcitability trait have upper-end-of-normal resting heart and respiratory-rate measurements [1], the idea of pre-medicating carriers of the trait in an effort to prevent psychiatric complications during high-stress periods has become a realistic possibility.
The potential benefits of doing this are manifold. The first benefit is that it could help affected persons keep things in their proper perspective when under high stress. This is very important because the cognitive and emotional distortions that can be created by pathological brain hyperactivity can cause stressors that would otherwise seem manageable feel like they are overwhelming. In addition, the obsessive ruminating that is driven by neuronal hyperexcitability can be functionally paralyzing, thus preventing the affected person from taking practical steps to address the stressor. Worse yet, the sense of panic that is driven by the trait can cause the person to say or do things that can make matters even worse. For example, it could cause an affected person to become verbally or physically aggressive or become self-destructive in the heat of the moment. In addition to adding more fuel to the fire in the hyperexcitable brain, the associated stress can cause severe insomnia. This prevents the brain from having a chance to cool off at night. Consequently, the brain can continue to ramp up to the point where the person is unable to sleep at all. The resulting cycle of stress and more stress is often a short route to psychiatric hospitalization for carriers of the neuronal hyperexcitability trait.
Perhaps even more difficult to recognize are the medical complications that can be driven by untreated neuronal hyperexcitability. Unlike the mental and emotional effects of neuronal hyperexcitability, which tend to occur almost immediately, the wide-ranging medical effects tend to occur very gradually, typically over several decades. This makes them very difficult to link to the neuronal hyperexcitability trait. In addition, the mental, emotional, and physical symptoms that can be precipitated by high levels of stress in carriers of the neuronal hyperexcitability trait can have a distorting effect on the aforementioned medical problems when they occur. They can also increase the risk of medical complications because the underlying neuronal hyperexcitability is itself the primary driver of the index illness. For example, a person who is hospitalized after suffering a stroke or a heart attack would be at increased risk of having another stroke or heart attack if his or her neurons were hyperexcitable. That is because the associated mental and emotional stress, which are abnormally elevated in persons with neuronal hyperexcitability, increase the risk of blot clots [2], and hypercoagulability is the primary driver of strokes and heart attacks. Stress also increases the risk of disseminated intramuscular coagulation (DIC), which is a common cause of death due to severe forms of infection known as “sepsis.” DIC was ultimately found to be associated with the severity and poor prognosis of patients with COVID-19 [3].
In addition to these complications, the pathological neuronal hyperactivity that is driven by stress in carriers of the neuronal hyperexcitability trait can cause somatic symptoms that can be misattributed to the incident medical condition. For example, psychiatrically-related headache in a person who is hospitalized with a hemorrhagic stroke could be misinterpreted as a sign of continued intracranial bleeding. Similarly, psychiatrically-related shortness of breath in a person who has been diagnosed with a deep vein thrombosis (DVT) could be misinterpreted as a sign of pulmonary embolism. As yet another example, psychiatrically-related loss of appetite and fatigue in a person with cancer who is thought to be in remission could be misinterpreted as evidence of disease recurrence. In addition to triggering testing that is unnecessary, these interpretation errors cause patients to experience even more stress, and this, in turn, really does increase their risk of disease recurrence.
All of these complications could potentially be prevented by simply starting neuroregulator therapy prophylactically in carriers of the neuronal hyperexcitability trait. Neuroregulators take effect within minutes rather than days or weeks, thus allowing the process to be akin to receiving a tranquilizer prior to being wheeled into the operating room or starting an antibiotic prior to a dental procedure. Then, once the stress of the illness has ended, the medication could be tapered and discontinued. Alternatively, the medication could be continued on a long-term basis. Indeed, most persons with neuronal hyperexcitability would likely choose this option because neuroregulators compensate for the underlying gene abnormality, and until that abnormality is controlled, most affected persons remain unaware that they have actually been living with low-grade psychiatric symptoms, such as mild anxiety, mild depression, mild irritability, or chronic insomnia. Also, because one particular neuroregulator—gabapentin—is at least partially effective for about ninety percent of patients, and because it has a favorable side effect profile, few drug-drug interactions, and essentially no withdrawal, its prophylactic use over the course of a prolonged period of high stress is just as feasible as using a single dose of a benzodiazepine preoperatively. Then again, because the optimal dose of gabapentin, like all medications, differs for each patient, the precise dosing would ideally be worked out prior to an elective surgical procedure or hospitalization.
References
[1] Binder MR. FLASH syndrome: Tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109.
[2] Sandrini L, Leraci A, Amadio P, et al. Impact of Acute and Chronic Stress on Thrombosis in Healthy Individuals and Cardiovascular Disease Patients. Int J Mol Sci 2020; 21 (21): 7818.
[3] Zhou X, Cheng Z, Luo L, et al. Incidence and impact of disseminated intravascular coagulation in COVID-19 a systematic review and meta-analysis. Thromb Res 2021; 201: 23-29.
How Long Do I need to Take Psychotropic Medication?
The question of how long a psychotropic drug (or drugs) will need to be continued is one of the most commonly asked questions among patients and their loved ones. In the past, this question was notoriously difficult to answer due to the limited understanding that clinicians had about the cause of psychiatric symptoms. However, with the recent discovery that psychiatric symptoms are the result of pathological hyperactivity in the neuronal circuits that correspond to them, the answer to the question of how long to take psychotropic medication can be answered with much more clarity.
As discussed in my previous blogposts, psychiatric symptoms develop when the circuits in the brain that correspond to them become pathologically hyperactive. Recall that what behavioral health practitioners call “psychiatric symptoms” are merely abnormally intense and abnormally persistent thoughts and emotions that all of us experience from time to time. Thus, for example, abnormally intense and abnormally persistent negative thoughts and gloomy emotions would constitute clinical depression; abnormally intense and abnormally persistent worrisome thoughts and apprehensive emotions would constitute generalized anxiety disorder; abnormally intense and abnormally persistent grandiose thoughts and euphoric emotions would characterize the manic phase of bipolar disorder; and so on.
According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) hypothesis of psychiatric disorders, the pathological brain hyperactivity that causes these symptoms is the consequence of mental and emotional stress superimposed upon a genetically-based hyperexcitability of the neurological system [1]. In other words, an inherent tendency for the neurons in the brain to overreact when stimulated by intense thoughts and strong emotions causes them to fire too frequently and for too long. This, in turn, causes the affected person to keep experiencing the thoughts and emotions that are associated with the pathological brain hyperactivity. The result is a vicious cycle of mutual overstimulation between the mind and the brain that tends to ramp up like two people caught in an argument. Properly prescribed brain-calming medications help reverse this process by reducing the excitability of the neurons.
Therefore, the question of how long one would need to take psychotropic medication would logically depend upon two factors: 1) the degree to which the neurons are hyperexcitable; and 2) the level of mental and emotional stress the person is under. The more excitable the neurons and the more stress the person is under the greater the likelihood that he or she would continue to need medication. For some affected persons, the brain is so hyperexcitable that brain-calming medications are needed even when external stressors are relatively low. At the other end of the spectrum are those affected persons whose brains are only marginally hyperexcitable. For such persons, psychiatric symptoms would not be expected to develop unless there were a sustained period of unusually high stress [2].
From this it should be apparent that some persons will need ongoing treatment with psychotropic medication, whereas others may need medication only until a severe or persistent stressor has resolved. There are also some persons whose neuronal hyperexcitability is so mild that natural interventions alone are sufficient to prevent symptoms from occurring (see my blogpost on natural interventions). However, for most persons with hyperexcitable neurological systems, brain-calming medications, which could more aptly be called “neuroregulators” [3], would likely be needed during periods of high or persistent stress. For such persons, the medication would ideally be continued until the stressor had resolved to such an extent that there was no longer enough cognitive-emotional fuel to cause the brain to become pathologically hyperactive again. In this sense, one could think of the hyperexcitable brain as a hive of irritable bees. Whether or not one would continue to need medication to calm down the bees would depend upon how irritable the bees were and how many stones were continuing to be thrown at the hive.
References
[1] Binder MR. The multi-circuit neuronal hyperexcitability hypothesis of psychiatric disorders. AJCEM 2019; 7 (1): 12-30.
[2] Binder MR. The neuronal excitability spectrum: A new paradigm in the diagnosis, treatment, and prevention of mental illness and its relation to chronic disease. AJCEM 2022;10(1):1-7.
[3] Binder MR. Introducing the term “Neuroregulator” in psychiatry. AJCEM 2019; 7 (3): 66-70.