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Lorcaserin: A novel antiobesity drug
You said fluoxetine is what caused your problems. Prozac is branded fluoxetine.
Is serotonin depletion the only way? Could it be enough to sigmificantly upregulate 2CRs?
You ask very specific questions that not everybody possess knowledge about. Kynurenic acid pathways or 5ht2c for example. Those questions are complicated even for serious researchers. We are all here amateurs. You situation is very specific and most of the members do not risk to give suggestions. Not to harm.
5HT2c is definitely not something to increase. It is a sign of biological stress. "Adrenal insufficiency" is due to low sodium and excess conversion of DHEA/testosterone into estrogen due to low CO2. And low CO2 is due to low thyroid. That's why RP doesn't believe in adrenal insufficiency, he thinks it's just low thyroid and low nutrients.
Also I think salt might increase some serotonin receptors but it also lowers serotonin release so the net effect is lower serotonin action.
What it honestly looks to me like is atypical depression. You think that Prozac pill 1.5 years ago was the starting point of your suffering. But you was prescribed fluoxetine for a reason. At least who filled the prescription thinks so. SSRI sometimes could worsen depression in the beginning. What if it just aggravated your depression?
i would imagine that tanking serotonin for a long period of time would upregulate the receptors.
- Tiredness/lethargy, easily tired and even chronic fatigue syndrome (due to elevated 5-HT2A receptor) (1, 2).
Inhibiting TPH prevents this fatigue. However, serotonin isn't the only neurotransmitter involved in fatigue, but also cortisol, acetylcholine, noradrenaline, the serotonin:dopamine ratio, kynurenine pathway, etc.- Rigid thinking and mental inflexibility
- Reduced cognitive function (not necessarily lack of knowledge, but intuitive thinking) (9). However, they might think they are smart and have all the answers in a very authoritative way.
- Narcissistic (10) - delusions of grandeur, fantasize about power, exaggerated sense of self-importance, requiring constant admiration, etc.
- Reduced senses (sensory perception) - anhedonia, apathy, reduced smell, hearing, taste, sensation, euphoria to music, etc. (11, 12) (THIS gives many clue)
- Aversive, passive-aggressive, but can also be full-on aggressive and violent (20).
- Don't care about the consequences of wrong decisions. This can also be due to low dopamine (place less weight upon the magnitude of bad outcomes) (21). Life feels like a joke or means nothing.
- Reduced verbal fluency, memory, attention, planning ability, and psychomotor performance (25, 26, 27, 28). However, estrogen and serotonin promote the desire to talk, thus people with high estrogen and serotonin talk a lot.
- Mood swings - bipolar mania (35, 36). Antagonism of 5-HT2A (which lowers excess glutamate) and the histamine receptor H1 and agonism of the 5-HT1A receptor (which lowers serotonin) helps.
- Easily agitated, argumentative, violent, aggressive, intermittent explosive disorder (37, 38).
- Overexcitation - ADD, ADHD, get distracted easily, anxiety, impulsivity, restlessness, overthinking, rumination, etc. (due to elevated 5-HT2A receptor) (3).
- Non-assertive - rather rude and aggressive dominate, which might come over as assertiveness, but is totally the opposite (5-HT2C is inversely correlated with assertiveness) (15). As Philosopher Eric Hoffer said: “Rudeness is the weak man's imitation of strength.” (16)
- OCD (5-HT2C activation increases compulsivity and lowers dopamine and noradrenaline) (17, 18, 19).
- Anticipation anxiety, enhanced anticipation of, and sensitivity to threat-related stimuli, punishment, and negative feedback (22).
- Fearful - scared of losing, low confidence and assertiveness.
- Suicidal - thoughts and even attempts (31, 32, 33).
- Delirious (34).
People with high serotonin will obviously not always have the exact same personality traits; so you might know someone who has some or a lot of the traits but not all of them. This is because of a difference in receptor expressions, as well as other hormones, which levels vary between people.
Also I think salt might increase some serotonin receptors but it also lowers serotonin release so the net effect is lower serotonin action.
I understand. I'm sorry.
I made a blood test several months ago. My E2 came as 42, it was is the range. And, I made the second test several months later. My E2 was lower, actually it was at the middle of between reference points. So, my body may be in an estrogenic state in overall, but I don't have excess estrogen.
Also my thyroid is good.
I know that Peat doesn't believe in adrenal insufficiency, but I couldn't find any other metabolic reason that maybe culprit of my problems. Also, drinking licorice tea for a week was the only thing helped me in this 1.5 years. Physical energy returned, Bowel reactivity lessened, mouth dryness returned, etc.
But because I stopped licorice, these effect passed. I stopped it because it stopped peristalsis too much.
I love salt. But I don't have low thyroid.
There are some more articles about serotonin is itself regulates hpa-axis. 2C is the most responsible. It regulates hpa even in inactive state. It doesn't require substance binding.
Serotonergic stimulation of corticotropin-releasing hormone and pro-opiomelanocortin gene expression. - PubMed - NCBI
Studies on the neuroendocrine role of serotonin. - PubMed - NCBI
I wasn't depressive at all. I had a undiagnosed asperger's syndrome and went to the psychiatr for my excessive social anxiety problems. Fine, all my anxiety problems resolved slowly as my disease progressed. On top of that, I don't feel any urge to ctb anymore. I know serotonin is tightly related with suicidality, so that catched my attention.
Yeah! That's possible.
But my problem not seems to be related to excess 2C density. That's an anxiogenic receptor. Also, my metabolic symptoms, all of them is a sign of low hpa/2C activation. I don't know how fluoxetine could increased that receptor semi-permanently in my case.