I’m 21 years of age and suffer from OCD, SAD, acute panic disorder.
I exercise daily and have a routine, however, heavy weight lifting seems to increase my anxiety. Lactic acid produced in the muscles when glucose is broken down during strenuous muscular activity. Oddly enough, lactic acid has been implicated as a trigger for increased anxiety and panic in those with panic disorder. On the weekends I like to weight train and upon cessation I’m completely out of it and feel depersonalized and disconnected from others around me. These feeling occur hours after lifting and fade away during the night. I’ve only recently started to lift weights to get my upper body ready for mountain biking.
I’m also into meditating. I practice mindfulness, zen and Vipassana meditation. Some days I’m able to close eye meditate up to two hours, other days my anxiety and panic prevent me from meditating past five minutes. The anxiety locates itself in my lower chest area, near my heart as well as the upper left side of my head. The sensation in my chest feels like my heart is expanding. I’m able to cope with this by placing my hand over my heart. Meditation will exasperate this sensation.
The head sensation resembles a black hole, void like feeling. I often have to pull at my hair or have something touching this area for me to fall asleep. Meditation will exasperate this sensation.
In the past I’ve taken picamilon for no longer than a few months, which when taken orally is presumably suppose to cross the BBB and then hydrolyze into GABA and niacin. The released GABA in theory would activate GABA receptors. GABA is said to promote relaxation and better mood, but when I take picamilon I become lackadaisical and this often feeds the onset of panic because my volubility and verbal fluency decline. I feel quite dumbed down and unintelligent. However, I am more in control of these panicky feelings and I never feel like I’m going to depersonalize or lose control. Picamilon is a GABA receptor agonist that affects the GABA-A receptor, similar to phenibut. I felt a sedative effect in dosages of 200-250mg. It doesn’t hyperpolarize the cell like alcohol does but it still has a depressant like effect.
The problem was that I never cycled picamilon so in theory this would cause receptor down regulation and upon cessation my panic and anxiety came back in full force.
I’ve tried ashwagandha as well, which has many great benefits but upon cessation my anxiety had increased 2-fold. Ashwagandha mechanism of action is agonist of GABA receptors, so that’s probably why. it posses many adaptogen and nootropic properties. It also improves stress-related memory problems by acting as a AChE inhibitor, and has the ability to prevent cognitive degeneration and even reconstruct neuronal networks. Ashwagandha also Increases testosterone and reduces prolactin levels in humans. However, one study illustrated that when male rats were given 3,000 mg/kg of the root extract for 7 days, a marked impairment in libido, sexual performance, sexual vigour and penile function was seen. Apparently there was an increase in prolactin. Note, however, that the dose used here was much higher than in the other rodent studies.
So I have learned that reduced production of GABA-A sends false information to the amygdala which regulates the body's "fight or flight response" mechanism and in return, produces the physiological symptoms that lead to panic disorder. Thus, GABA suppresses neural firing, inhibiting or regulating other neurotransmitters including serotonin, norepinephrine, and dopamine. It accomplishes this by decreasing their turnover in limbic areas - the amygdala as well as the locus ceruleus and raphe nuclei.
The potential cues for triggering the anxiety response include psychological threat, novelty, social or performance situations, cognitive mechanisms, and conditioned associative memories. Thus, in panic attacks, the fear is of imminent death; in social phobia, the concern is with embarrassment; in PTSD, the emotional memory of the trauma; in OCD, the intrusive obsessional ideas; and in GAD, anxiety, there are not conditioned specific triggers (considered free-floating).
The large available data base on the physiology and pathophysiology of anxiety has led to the development of several neuroanatomic models of anxiety disorders. One of the most well known models was proposed by Gray, who postulated the presence of several distinct neuroanatomic circuits modulating different aspects of the anxiety reaction. In this model, anticipatory anxiety is proposed to be analogous to the state of behavioral inhibition seen in animals who are presented with a threat. In this state, the animal stops what it is doing and becomes vigilant for any sign of danger. He summarized data from animal studies to conclude that this state is activated in the presence of stimuli associated with punishment or non-reward or in the presence of novel stimuli. The actual experience of punishment or non-reward activates a different system, he called the "fight or flight" system, in which the animal responds with species-specific defensive reactions such as biting, striking, hissing, or attempting escape. This system is proposed to be most similar to the panic reaction. Evidence was presented from animal studies suggesting that the primary anatomic elements of this system include the septohippocampal areas, the locus coeruleus, and the median raphe nucleus. The theory was that the primary function of the septohippocampal formation is to act as a comparator, which assesses stimuli for the presence of danger. This comparator function is continually working at a low level when the organism is not in the presence of threat, but when threat is detected the septohippocampal system will activate the behavioral inhibition circuit, which reciprocally will cause increased monitoring of sensory stimuli for evidence of threat as well as inhibition of ongoing behavioral programs. Activation of the raphe nucleus would, in part, initiate enhanced serotonergic inputs to the hippocampus that allows an increase flow of information through this system.
The hippocampus has the densest concentration of GABA receptors and it is speculated that this may be the site of anxiolytic action for the benzodiazepines in general anxiety states. Anxiolytic drugs that affect the behavioral inhibition system might then act by either reducing the serotonergic inputs into the hippocampal septal formation. This action would have the effect of lowering hippocampal activation.
serotonin in anxiety is supported by its modulatory effects on the locus coeruleus and its dense projections to the amygdala. Decreased serotonin activity is associated with depression, and the most effective antidepressants have been shown to enhance the functioning of serotonin. Low activity of serotonin may permit the dysregulation of other neurotransmitters, including norepinephrine. These two systems are linked so closely that notable changes in one are reflected in the other; interactions between these systems appear to be reciprocal. The precise nature of the reciprocal interaction can vary, and the activity of norepinephrine at presynaptic serotonergic terminals may lead to a decreased release of serotonin, whereas its activity at postsynaptic adrenoreceptors may lead to an increase in the release of serotonin.
Someone like to translate this^^
The “fight or flight response” is something I struggle with in social situations such as when I’m situated in a classroom, this is accompanied by increased sweating, piercing sounds, muscle tension/rapid muscle movement and intrusive thoughts. This is very different than the anxiety I feel when I’m alone. I’m also unable to look others in the eyes. I feel apprehension and impending doom/dread. I certainly do not want to feel terror again! My brain feels as though it's trapped in a pressurized vise and my head wobbles. This has also caused me to be unable to look people in the eyes. If I do my neck will tense up and I’ll start to spasm out. I try to control my spasms by never looking up or making eye contact and resting my head on my hands. If I’m in class, I’ll distract myself by scribbling or taking notes, however if I cease doing this my symptoms will appear. If I let these symptoms continue, I’ll start to clench and sweat. Moreover, I am unable to talk long periods of time to people because my brain feels like it stops working. I’ll forget what I am saying mid sentence and an uncomfortable, overwhelming feeling will take over me. That being said it is very annoying and I want it to stop so bad! This never happened before I started smoking cannabis! I was the complete opposite of who I am today. I can’t even look at my parents in the eyes, nor my friends. Others have told me this is a time of transition from adolescence to adulthood and, like all transitions, is often accompanied by a degree of doubt and worry.
I guess you could explain my anxiety in terms of unwarranted or inappropriate fear.
All of these sensations started to occur after my cannabis induced panic attack. All throughout me teenage years, until about a year ago I was an extrovert. Very outgoing, with lots of charisma. However, I am now the complete opposite of that following my cannabis induced panic attack. I have not felt the same since and have become extremely introspective.
I quit cold turkey and went to the doctors because I felt depersonalized and derealized. My brain was in a fog, I could not concentrate, my eyesight was blurry and dull almost like I was looking through a film of grey, sounds were earsplitting, I had a full prickly rash all over my body, I had tingling in the fingers and an odd sensation in my left front-upper side of my head that resembled a void/black hole, these are supposedly symptoms of decreased GABA. Lyme disease was ruled out, although blood tests can oftentimes come back false negative, and as a child I was tested for lyme and one test came back false positive. So i’m not sure.
Moreover, smoking marijuana over winter prior to my panic attack had a very positive effect on my social abilities. However, these were strains high in CBD and low in THC. Studies have shown cannabidiol decreases activity of the limbic system and decreases social isolation induced by THC. Cannabidiol has also been shown to reduce anxiety in social anxiety disorder. I would love to get my hands on a high CBD strain but they are ridiculously expensive.
CBD also has anti-psychotic effects and may counteract the potential psychotomimetic effects of THC on individuals with latent schizophrenia some reports show it to be an alternative treatment for schizophrenia that is safe and well-tolerated.
Now, THC inhibits GABA, and boosts dopamine, malfunctioning in GABA signaling is associated with movement disorders (rapid muscle movement) as well as anxiety, schizophrenia, and addiction. This inhibition of GABA may be the reason cannabis consumption affects memory and movement and is therapeutic in cases such as Fibromyalgia. Smoking strains high in THC, caused paranoia, social inhibition and panic attacks. Strains low in THC and high in CBD’s relieved the burden of anxiety and created a spontaneous, social, witty me.
Fear and motivation with no confidence is felt as anxiety->paranoia, these are feeling accompanied when smoking high THC-strains of cannabis. Dopamine increase and a motivation felt as paranoia. This does not include when I smoke strains low in THC and high in CBD. Pure fear with absence of any other emotions is felt as impending doom - a fear without a consciously known origin, these are feelings I struggle with in social situations and so badly want them to stop.
Fear is invoked each time certainty of action and reaction is doubted, engages the learning/challenge mode to learn the new context and remove threats, learn most effortless/painless use of reality. Learning certainty provides reward until 100% certainty is achieved after which there is no reward – this is in fact the mechanism that causes drug tolerance. After certainty is learned one can only feel fear when certainty of use comes in question. The drugs cause the user to learn more certainty than possible in reality, which causes fear-doubt depression in withdrawal. It also explains the PARANOIA created by dopaminergic drugs.
Moreover, a conditioned fear is often measured with freezing (a period of watchful immobility) or fear potentiated startle (the augmentation of the startle reflex by a fearful stimulus). Changes in heart rate, breathing and muscle responses via electromyography can also be used to measure conditioned fear.
Inositol is a simple polyol precursor in a second messenger system important in brain myo-insitol, the natural isomer, which has been found to be therapeutically effective in depression, PANIC disorder, obsessive-compulsive disorder in double blind controlled trials and psoriasis. Now before I started taking this I panicked around people and had difficulty in situations were I was stuck on the phone for long periods of time. In general I was very uncomfortable in situations were I felt I could not escape. Inositol made it much easier for me to go with the flow; however, it also caused brain fog and short-term memory loss. Why is this? And what is the mechanism of action?
Inositol 'disruption' may be linked to depression, but that's surely when inositol gets too low, but because “myo-inostiol lowers testosterone levels” Zero concept of risk/reward process, motivational issues, sleeping beautifully, can't kick into gear on waking, can sleep whenever regardless of sleep had. So this could be a problem.
Caffeine seems to trigger my panic disorder and I become overly stimulated, apparently caffeine inhibits GABA but upon cessation up regulation of GABA receptors.
TLDR: I suffer from SAD, Acute panic disorder and OCD. I never experienced any of these sensations prior to a cannabis induced panic attack. THC makes symptoms worse, CBD helps to ease my anxiety as well as inositol. Aerobic exercise helps a lot, weight training makes me panic more. Meditation helps if I’m not already in panic mode. Ashwagandha helps but upon cessation increases anxiety, same with picamilon.
My daily stack consists of:
Daily Stack
Hemp Hearts/Protein: 30g/15g
Sencha Tea: 5g/3x Upregulates GABA receptors, also L-theanine modulates GABA.
Rhodiola Rosea: 250mg/2weeks on/1week off Really helps but why?
Turmeric: 5g Not sure yet?
1:1 Chlorella/Spirulina: 3g
Myo-inositol: 2g/2x Helps me to control my panic, not sure specifically why?
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Vitamin D
Zinc
Magnesium L-Threonate
Weekly Stack
Ginger: 2g/2x testosterone
Fish Oil: 1250mg/4x Brain fog and inflammation
Withania: 200mg/2x If I’m going out and need to calm down.
Rieshi Tea: 5g/1x Probably will stop
L-theanine: 100mg/2x
What about magnesium??
Its a NMDA antagonist. Magnesium seems to attenuate chronic activation of NMDA receptors, which exerts neurotoxic effects via Calcium - dependent mechanisms.
Magnesium injections in rats (higher than practical supplementation) attenuated the increase of adrenaline in electrically shocked rate by 92.6%. Hence, supplementation could help with fight or flight in some way, I’m not really sure though.
I’m only asking for some input on what would be a safe and effective say to cope with my anxieties, without going the pharmaceutical route.