To be completed
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Reminder: Not medical advice, consult doctor before, etc.
What is hypervigilance and how fear plays a part?
Complications for the person, their family, and the public perception
How to think about recovery, management, and responsibility without distributing blame (the emotionally charged aspect of this topic makes it hard to work on recovery without divisiveness).
Each condition to address:
Exposure therapy/Flooding
Systematic Desensitization
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Oxytocin improves autism attachment issues: https://nieuws.kuleuven.be/en/content/2020/love-hormone-improves-attachment-issues-in-people-with-autism?fbclid=IwAR3Xw0zDN4AgPqDsZwPQsIjUPvSuVycVkqFy79g5IRhywEC1iUDXImkC-5U
Meditation lowers biomarkers of stress and anxiety: https://www.sciencedaily.com/releases/2017/01/170124111354.htm
Ritualization as a coping mechanism for anxiety: https: https://www.sciencedirect.com/science/article/pii/S0960982215006521
Trauma & REM
Eye movement desensitization reprocessing (EMDR) or ketamine treatment for trauma. Similar features to REM sleep.
EMDR
Recalling an emotional/traumatic situation while walking led to a less intense experience for the creator. Looking side to side seems to be the major cause of recovery.
Eyes back and forth laterally while recounting the events. Eye movements you unconsciously make while moving through space, associated with motor system. Suppresses activity in the amygdala, which is critical for the fear response. Must be lateral eye movements to suppress the emotional load to the trauma.
Ketamine / PCP
Dissociative anesthetic. They both function to disrupt the activity of the NMDA receptor, which opens to trigger LTP during an intense event. Ketamine can block a cross over response to certain stimuli that mimic a traumatic event that usually trigger a PTSD event. Emotion can still occur without the plasticity if giving it to somebody who just went through a horrible experience.
Blocks emotion from experience (dissociative).
Self-Therapy
REM sleep, ketamine, and EMDR. All ways of lowering reactivity and plasticity to trauma and hyper-emotionality.
Major, Long-Lasting Benefits of Gratitude Practice
Regular gratitude practice can create resilience to trauma by reframing/buffering their prior traumatic experiences and inoculating them from traumas that may arise in the future.
Gratitude practice has also been shown to benefit social relationships across the board.
The neurochemical aspect of gratitude can be on par with the benefits of high intensity exercise.
Extinguishing (Reducing) Fears
Rather than strengthening connections, we need to weaken them by associating the previously fearful experience with a new, more positive, one. You can’t just extinguish the fear.
Many treatments for PTSD, such as SSRIs, benzodiazepines (anxiolytics), antipsychotic drugs, or beta blockers/adrenergic blockers. Some people may get some sort of relief by using these drugs, but none are based on the neurobiology of fear. Someone may have a reduction in the sensation of fear.
Cognitive (Narrative) Therapies for Fear
Prolonged exposure therapy, cognitive behavioral therapy, and cognitive processing. The experience of fear when they retell their trauma for the first time, there is a tremendous anxiety response. Sometimes greater than the actual experience of the trauma itself. They are asked to speak in full sentences, provide full rich detail, how they felt during and after, etc. The next few retellings progressively diminish the anxious feelings.
The retelling is important. Taking a traumatic experience and making it boring, uncoupling the threat reflex from the narrative (fear extinction).
Can be done in a therapist’s office and can be written out in a journal. Although, it is important to have the right social support available to relearn better/healthier behaviors and responses.
Repetition of Narrative, Overwriting Bad Experiences with Good
Clearing away the association first. Then there is the need to relearn a new narrative. The fear circuits that underlie trauma need to be mapped into new experiences that are of a positive association. Also, that it be linked back to the traumatic experience. Enjoying something despite the fact that something happened.
The top-down circuitry, from the PFC to the threat reflect circuits, are not like the other connections (glutamatergic and excitatory), they are inhibitory, preventing activation of the threat activation. This is why we need to attach a new positive memory onto the previous fear response, to make the reliving of the experience much less likely. However, extinction is essential first. A sense of reward tacked back.
The PFC has an amazing ability to attach meaning and rationalization as a tool to rewire our circuitry.
EMDR: Eye Movement Desensitization Reprocessing
Moving the eyes side to side while recounting a traumatic narrative. Lateral eye movements reduce/inhibit fear reflex circuitry. The eye movements reduce activation of the amygdala activation and related circuits, which reduces anxiety and the amplitude of the threat reflex and SNS. These are the eye movements that we make when we are ambulating/moving through space, though some sort of self-generated motion. Forward movement and fear are generally incompatible (neither fleeing or freezing).
Particularly useful for single event trauma, not so much for relieving trauma from multiple events, such as a bad marriage.
EMDR only really attaches to the extinction portion of trauma recovery. Retelling while reducing the physiological experience with the exercise. However, there isn’t much of a victory over the trauma if you just bypass the experience by removing the physiology.
Social Connection & Isolation Are Chemically Powerful
Tachykinin is activated in neurons in the central amygdala very soon after a traumatic experience (fear inducing) appears. It sets in motion changes in gene expression and potentiation (LTP) that reinforce that fearful experience. Leading to low to moderate levels of anxiety and even aggression. Levels are further increased by social isolation. Social connection (conversing with, eating with, physical contact) with people we trust serve to reduce effectiveness of tachykinin.
It is important to access social connection outside of the clinician/therapist situation.
Trans-Generational Trauma
We have the capacity to inherit a predisposition to certain trauma. Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults.
https://pubmed.ncbi.nlm.nih.gov/18349090/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923835/
If you had a parent, bias towards father, that experienced abuse, this causes changes in his genetics (in his sperm), that can be passed onto offspring, such that the offspring have a lower threshold to develop trauma or extreme fear to certain events. A predisposition, not a specific fear.
What gets passed on is a propensity for the threat reflex to get activated and attached to a wider variety of inputs and experiences. A gene modification increasing predisposition.
PTSD Treatments: Ketamine, MDMA, oxytocin
Ketamine is a dissociative anesthetic – as making a patient feel like they were getting out of a cockpit of a plane, but observing themselves doing it. It changes the rhythm of cortical activity (1-3Hz rhythm), in layer 5 of the retrosplenial cortex. Brings us to the PFC top-down input, allowing the patient to recount their trauma while feeling while feeling none or a different set of emotional experiences than the traumatic experience. A replacement of emotional experience. Diminishing the old with dissociation, extinction, then relearning.
MDMA is a powerful synthetic drug that creates a dopamine and serotonin releasing state at the same time. Dopamine is usually related to seeking whereas serotonin is more about relaxing and being satiated. The combination of these two are not that normal. People report feelings of connection or resonance with people or things. MDMA causes massive releases of oxytocin too. The dopamine release is related to the euphoria, the serotonin leads to the safety and comfort. For trauma, this allows a fast relearning of new associations to the experience, without the need for many repetitions.
How Do You Know If You Are Traumatized?
The insular is associated with determining whether or not one’s internal sensations are reasonable or not, given the circumstances. The main effect of inhibiting the insula was that the intensity of the outside experience was not consistent with the physiological response. Then anything paired with that experience would elicit that problem.
Recalibrating the relationship between inside and outside events can potentially reduce the amount of trauma we experience.
Deliberate Brief Stress Can Erase Fears & Trauma
Daily short bouts reversed/alleviate symptoms of stress in mice.
Erasing Fears & Traumas In 5 Minutes Per Day
When it comes to trauma, anxiety, and PTSD it is not just the state that you are in or that you got into, it’s how you got there and whether you had anything to do with it.
The insula calibrates how we feel internally vs. what is happening externally. We have a system that can generate threat responses, and in the case of PTSD, anxiety, high stress, etc., that system can get ramped up so that it takes very little – maybe even a memory or an association we aren’t aware of – to trigger the symptomology.
Most drug treatments just suppress the arousal. By doing this you just create a different miscalibration. Doing a physiological sigh is a way to calm the system when the early signs of stress start to arise. Using cyclic hyperventilation, unless you are prone to panic attacks, can be a good way to elicit minor stress daily on your own terms. Recalibrating your stress threshold via deliberate reactivation of the sensations of the body without the fear being attributed. It seems it could be used in a therapeutic setting to awaken the threat response with your own agency, before addressing the traumatic issue.
All you need is self-directed adrenaline release. Could be a cold shower or hyperventilating. Do it in conjunction with support.
Nutrition, Sleep, & Other General Support Erasing Fear & Trauma
Sleep regularly for better functioning fear circuits. Dysregulated means we can have a higher propensity for sympathetic activation.
“If the tide is high enough, the boat can leave the shore.”
Supplements for Anxiety, Fear: Saffron, Inositol, Kava
Saffron (30mg) has been reliable in treating the effects of anxiety. Inositol (18g for a full month) is on par with antidepressants. Also used for OCD. Don’t take before treatment because you’ll short-circuit the extinguishing effect. Driving the trauma/anxiety deeper into the system. Kava has been shown to have a potent effect on anxiety by increasing GABA, inhibiting the threat reflex.
Nutrient Power Notes
Schizoaffective Disorder:
Paranoid Schizophrenia:
Schizophrenia typically develops between the ages of 15-25 for males and 16-35 for females. The symptoms, especially hallucinations, delusions, paranoia, and radical changes in personality.
Biological Psychiatry
Atypical antipsychotic medications usually result in impressive benefits, but most patients remain handicapped compared to their pre-breakdown condition, experience serious side effects that may become permanent, and may experience gradual loss of brain cortex volumes.
Dopamine Theory:
Glutamate Theory:
Oxidative Stress Theory:
Epigenetics Theory:
Excessive dopamine activity associated with an elevated methyl/folate ratio involves underproduction of a complex chemical called dopamine active transporter (DAT). This transporter removes dopamine from synapses, sending it back to the original cell for reuse. Overmethylation results in reduced expression of DAT and excessive dopamine activity. This biochemical abnormality is a hallmark of paranoid schizophrenia.
In contrast, the epigenetic effect of undermethylation is to reduce activity of serotonin, dopamine, and norepinephrine. In addition, undermethylation appears to influence synaptic NMDA receptor activity and is associated with schizoaffective disorder and delusional disorders. Reduced activity of norepinephrine usually coincides with reduced adrenaline activity that may contribute to catatonic symptoms that are characteristic of schizoaffective disorder and delusional disorder.
Viral insult may alter gene expression and contribute to the illness and impact of schizophrenia.
Biochemical Classification of the Schizophrenias
90% of the cases: overmethylated schizophrenia (42%), undermethylated schizophrenia (28%), and a condition of severe oxidative stress termed pyrrole schizophrenia (20%).
Differential Diagnosis Factors
Patients who are overmethylated or pyroluric usually exhibit warning signs of the disease before the age of 10, but undermethylated patients may be symptom-free until the breakdown. Chemical analyses of blood and urine provide about 50% of the information required for accurate diagnosis. Symptoms, traits, physical signs, medical history, and family history are equally useful in identifying a patient’s schizophrenia biotype.
Symptoms during initial breakdown:
Response to psychiatric medications:
Family History:
Dominance of hallucinations or delusions:
Psychiatric medication issues:
Recovery Timeline:
Overmethylation Biotype of Schizophrenia
Laboratory indications include whole blood histamine levels below 40 ng/ml, absolute basophil levels below 30, and serum copper higher than 120 mcg/dl. This schizophrenia phenotype involves excessive activity at dopamine and norepinephrine receptors, possibly caused by epigenetic inhibition of dopamine active transporters (DATs) and norepinephrine transporters (NETs) and elevated copper levels. Primary symptoms usually include auditory hallucinations, paranoia, agitation, and extreme anxiety. The most common diagnosis is paranoid schizophrenia.
Judy – 26 (Overmethylation):
Robert – 25 (Overmethylation):
Undermethylation Biotype of Schizophrenia
Severely depressed methyl/folate ratio is present in about 28% of the schizophrenia population. The dominant symptom is usually delusions, although mild hallucinations are sometimes present. Laboratory indications are whole blood histamine above 70 ng/ml, elevated blood basophils, and depressed SAMe/SAH ratio.
Most undermethylated persons in the general population are high achievers in good mental health. However, most mentally ill persons exhibiting this imbalance respond to methylation therapies. This form of schizophrenia involves low activity of serotonin, dopamine, and norepinephrine, possibly caused by epigenetic overexpression of SERT (serotonin transporter), DAT, and NET transporters at synapses. Low glutamate activity at NMDA receptors is also suspected. Typical symptoms include delusions, OCD behaviors, high internal anxiety, and catatonic tendencies.
Common symptoms include belief that the CIA or FBI is following them, that their parents are aliens, or that a satellite in outer space is beaming painful rays into their brain. Most undermethylated schizophrenics have ritualistic behaviors and strong obsessive compulsive tendencies. They may have extreme inner anxiety that is hidden behind a calm exterior.
David – 22 (Undermethylation):
George – 21 (Undermethylation):
Pyrrole Disorder Biotype of Schizophrenia
This phenotype involves a severe overload of oxidative stress that impairs brain function. This condition usually results in very elevated levels of pyrroles in urine along with severe deficiencies of zinc and vitamin B-6.
Most persons with elevated pyrroles have mild symptoms that do not interfere with daily living. However, about 20% of schizophrenics exhibit a severe version of this imbalance and report improvement following aggressive therapy with zinc and vitamin B-6. This condition involves free-radical oxidative stress and depleted levels of glutathione, metallothionein, and other protective proteins causing inhibition of glutamate activity at NMDA receptors.
Primary symptoms of pyrrole disorder generally include the following:
A study of 67 schizophrenics found that pyrolurics were very deficient in arachidonic acid. This may explain the symptoms of dry skin and abnormal fat distribution associated with this disorder. Many pyroluric schizophrenics report benefits from supplements of primrose oil, a source of omega-6. Non-pyrrole schizophrenia phenotypes generally exhibit low omega-3 levels and omega-6 overload. A recent study reported biotin deficiency in pyrrole patients.
Most pyroluric schizophrenics report symptoms of zinc and vitamin B6 deficiency from early childhood. Physical symptoms include delayed growth, poor wound healing, dry skin, white spots on fingernails, delayed puberty, acne, and inability to tan. Most pyrolurics have a history of academic underachievement that has been attributed to severe vitamin B6 deficiency that can impair short-term memory. Mood swings may occur many times daily, and a common diagnosis is rapid-cycling bipolar disorder. The onset usually occurs during a period of extreme stress. Schizophrenics with this imbalance may have a combination of delusions and auditory hallucinations. They live in a world of fear and do not attempt to hide their anxieties.
Mary – 29 (Pyrrole):
Overmethylation and Copper Overload
A common aggravating factor in overmethylated schizophrenia that results in more-extreme norepinephrine elevations. The usual result is greatly heightened anxiety, paranoia, and increased auditory hallucinations. Moreover, copper elevations are associated with zinc depletion, and zinc is an important factor in maintaining GABA levels. The combination of high norepinephrine and low GABA levels is a recipe for extreme anxiety. Female patients with this combination of imbalances tend to experience early mental breakdowns, frequently during puberty. Treatment of this condition must be gradual since rapid removal of excess copper from the body could cause temporary worsening of psychiatric symptoms.
Undermethylation and Pyrrole Disorder
Unlike most pyrrole patients, these persons usually have a history of high accomplishment in academics and career prior to their mental breakdown. After onset of the illness, many are plagued by severe mood swings, extraordinary delusional beliefs, and episodes of rage. Successful treatment of this hybrid condition often results in early improvement in behavior control followed by a four-to-six-month period before the delusions begin to fade away.
Low-Incidence Biotypes
Gluten intolerance appears to be responsible for an additional 4% of persons diagnosed with schizophrenia. The remaining 6% involve a collection of relatively rare mental illness biotypes, including thyroid deficiency, polydipsia, homocysteinuria, drug-induced psychosis, and porphyria.
Gluten Intolerance:
Thyroid Deficiency:
Polydipsia:
Homocysteinuria:
Drug-induced schizophrenia:
The Porphyrias:
The Walsh Theory of Schizophrenia
They believe a proper theory of schizophrenia must include the following elements:
Thesis 1: Predisposition to schizophrenia involves fetal programming errors that cause lifelong vulnerability to oxidative stresses. These programming errors can result from a variety of causes: (a) an abnormal in utero methylation environment, (b) exposure to environmental toxins, (c) genetic weakness in oxidative protection, and (d) medication side effects.
Thesis 2: The mental breakdown event is triggered by overwhelming oxidative stress that alters DNA and histone marks that regulate gene expression. Cancer research has provided examples of cumulative oxidative stresses that eventually alter gene marks, producing an enduring disease condition. The onset of schizophrenia occurs when oxidative stresses exceed the threshold level needed to alter chromatin marks that control gene expression.
Thesis 3: Epigenetic changes are responsible for continuing psychotic tendencies after the breakdown event. A psychotic breakdown is usually followed by a lifetime of mental illness and misery, despite intensive therapies. This often-permanent change in functioning results from altered DNA or histone marks that regulate gene expression. Since the deviant marks are maintained during future cell divisions, the condition doesn’t go away.
Thesis 4: The three major phenotypes of schizophrenia develop in individuals who exhibit overmethylation, undermethyation, or overwhelming oxidative stress:
Thesis 5: Failure to follow classical laws of genetic inheritance results from the epigenetic nature of schizophrenia. Schizophrenia is strongly heritable (runs in families) but fails to obey Mendel’s classic laws of genetic inheritance. There are countless examples of identical twins where one sibling develops the disorder and the other does not. In addition, intensive research efforts to identify the schizophrenia gene (or genes) have met with little success. Epigenetics provides two explanations for the non-Mendelian nature of schizophrenia: