I believe I have accidentally discovered a way to considerably enhance creativity, mood, and ambition by improving dopamine receptor function by triggering the upregulation of serotonin receptors through the reduction of serotonin levels.
Last year, over a period of months I cured a number of health problems that were caused by years of unwittingly taking supplements such as SAM-e and turmeric that increased serotonin activity. This higher serotonin activity in turn downregulated serotonin receptors (i.e., decreased the number of serotonin receptors) which caused multiple health problems that I was fortunately able to fix.
Over the past 5 or 6 years I had noticed a significant drop in creativity and other mild problems related to elevated serotonin such as slight anhedonia which, among other things, suppressed my emotions. For example, comedies that once made me laugh lost any emotional effect on me.
These symptoms were classic examples of medium level side effects of SSRIs, although I did not realize supplements with SSRI qualities were the culprit until last year when my use of 5-HTP with Turnbuckle's stem cell protocol caused more severe side effects that were ultimately cured by the 7-step protocol I created and which I am describing in this thread.
My protocol involved upregulating serotonin receptors (which had been overstimulated by the SSRI-like effects of naturally occurring supplements) by decreasing my levels of serotonin. It also cured secondary effects of downregulated serotonin receptors such as upregulating beta receptors (caused by serotonin-induced increases in adrenaline) with the beta-blocker propranolol and cutting out all caffeine, upregulating adrenoreceptor/mineralcorticoid receptors with Omega 3 to decrease serotonin-induced high blood pressure, and curing anxiety attacks by upregulating NMDA receptors with magnesium as well as upregulating GABA receptors with Culturelle probiotic and then using Turnbuckle's mitochondria protocol to enhance MAO function.
In the process I discovered that reducing serotonin considerably enhanced my creativity, mood, and overall emotional well being by freeing my dopamine receptors from the dopamine-suppressive effects of serotonin.
Among numerous positive effects were that this enhanced dopamine activity achieved through lowering serotonin results in long lasting "situationally appropriate euphoria". I would describe this feeling as being very elated when positive events happen in my life or when I am exposed to any artwork such as a song that I particularly enjoy, while at the same not feeling euphoric when doing routine work, nor feeling euphoric in sad or depressing situations where the normal reaction should be sadness or depression. Unlike other dopamine triggering techniques my method is not addictive.
This is a breakthrough in the field of nootropics and mental health because no one has found a satisfactory way to improve mental health by stimulating the dopaminergic system, despite the fact that dopamine and dopamine receptor activity are (on paper) ideal targets for improving emotional wellbeing.
In theory, dopamine stimulation is preferable to targeting other neurotransmitter systems because the dopaminergic system is linked to ambition, artistic creativity of all types, higher sex drive, enhanced motivation, artistic creativity, higher testosterone levels (which are protective in men, and, at lower levels, women), and enhancement of pleasurable emotions across the board.
The problem neuroscientists had with creating pharmaceuticals that stimulate the dopaminergic system to improve psychiatric outcomes has been that the test drugs they created were addictive, had tolerance issues/diminishing returns effects over time, and, after prolonged use, downregulated dopamine receptors which causes undesirable consequences similar to the variety of illegal drugs that act on dopamine.
However, my protocol for reducing serotonin avoided these problems (such as drug-like cravings for a "greater and greater hit of dopamine to get the same effect as in the past" or being in a constant drug-like state of euphoria throughout the day) through an indirect route.
Instead of stimulating the dopaminergic system directly I have found that these positive effects of dopamine stimulation, without any apparent side effects, can be achieved indirectly by upregulating serotonin receptors by decreasing serotonin levels. This is because the downregulation of serotonin receptors caused by increased serotonin activity suppresses dopamine system activity.
But by upregulating serotonin receptors by reducing the amount of serotonin, dopamine is not being stimulated directly. Instead dopamine is having the obstacle of excess serotonin cleared out of its way to function more naturally with existing levels of dopamine remaining unchanged.
I accomplished this by following a protocol that first used shilajit to reduce my serotonin levels (because the fulvic acid it contains reduces serotonin) and then solving the other health problems that were caused by excess serotonin by completing the rest of the protocol.
For keeping my serotonin receptors unregulated I have stopped using shilajit and now follow a "maintenance protocol" where once every 1 month or every 2 months I take 1.5 grams of collagen on an empty stomach to deplete serotonin. Collagen on an empty stomach (but which does not work if taken with food) competes with serotonin in the gastrointestinal tract (where over 90% of serotonin is stored). I also take 2 pills of Culterelle probiotic for 2-3 days a week to upregulate serotonin transporter pathways (SERT) in the gastrointestinal tract.
Finally, as part of the maintenance protocol I usually drink alcohol moderately for 2 days a week in the evening on weekends because alcohol depletes serotonin -
https://academic.oup.../36/1/22/137998
During the first 30 min after acute ethanol consumption by three fasting normal male volunteers, no increase in circulating tryptophan availability to the brain occurred. On the contrary, a small decrease was observed, which became stronger subsequently. We conclude from this preliminary study that brain serotonin levels are not increased after alcohol intake by normal subjects and that, consequently, this indolylamine is unlikely to mediate the euphoric effects of alcohol.
...
Previously, we showed (Badawy et al., 1995) that acute ethanol consumption by human volunteers actually decreases circulating Trp concentration and availability to the brain, thus decreasing, rather than increasing, brain serotonin synthesis, over a 3-h period.
For 2 days on weekends I usually have over a 4 to 6 hour period in the evening the equivalent of 3 to 5 shots (equal to 50 ml each) of 40% alcohol, with each shot mostly evenly spaced. That works well enough for me and is comparable to the alcohol amount used in this study. For people who are shorter or for women a lower overall amount of alcohol may get the same effect because of their smaller body/blood volume.
The euphoric effect described in this paper that happens after taking the first shot or two of alcohol (but which does not recur with subsequent shots of alcohol on the same day) is probably caused, not by increasing serotonin, but by decreasing serotonin which liberates dopamine function from the dopamine-suppressive effect of serotonin.
I have found taking 1.5 grams of collagen also causes a temporary euphoric effect when I try it, similar to when I took shilajit.
PRECAUTION: Do NOT use more than one serotonin reducing method at the same time because you do not want to decrease serotonin too much (obviously SOME serotonin is needed for proper cognitive function!!!). i.e., do not try both shilajit and collagen on an empty stomach on the same day, or try either on the same day as alcohol. Preferably give 2-3 days between using different methods even if you have no symptoms of excess serotonin and are only using this protocol to boost creativity and mood.
PRECAUTION: If you use this protocol to fix more significant side effects of SSRIs or side effects from SSRI-like supplements do NOT use alcohol in the serotonin-reduction step (or any of the other steps) because, if you have elevated serotonin symptoms, you probably also have cardiovascular problems such as high blood pressure and a high resting heart rate caused by serotonin. Alcohol can make these cardiovascular problems worse by raising blood pressure further by triggering the release of Angiotensin II and by increasing heart rate through alcohol's delayed-release of adrenaline (this delayed release of adrenaline is why having alcohol before sleep often results in waking up early in the morning). First complete the entire 7 step protocol and then, if you have recovered well enough, use alcohol only as part of the maintenance phase.
PRECAUTION: If you have ANY symptoms of elevated serotonin (even if you think it is only "moderate" symptoms) go to an emergency room, tell them you think you had too many SSRIs (even if you aren't on a pharmaceutical SSRI), and ask for a test of your serotonin levels through a urine test of its breakdown product 5-HIAA. You need this urine test for two reasons.
First to know if your serotonin levels are getting dangerously high to a point where potentially deadly serotonin syndrome might be a risk, which requires emergency treatment. Secondly, you need to get it tested so that you have proof later on that any health problems you had were from excess serotonin.
If you wait to get tested your serotonin levels may have decreased but your serotonin RECEPTORS will still be dangerously downregulated and doctor's won't believe you that your condition is caused by excess serotonin because there is no mainstream clinical test for whether neuro receptors are downregulated (direct tests for whether neuro-receptors are upregulated or downregulated are done mainly with mRNA tests, and other tests, with procedures used only at specialized neuro-research facilities, not normal hospitals and doctor's offices).
I made the mistake of not asking for 5-HIAA first because I was initially told (falsely) there is no test for serotonin levels, or I was dissuaded by doctors who said "if I had excess serotonin I would have more serious symptoms." Since I was told "it would be more serious" in those exact terms by at least three different "health professionals" my suspicion is that they are deliberately trained to lie to patients to prevent them from testing 5-HIAA to avoid creating a "laboratory paper trail" that would get pharmaceutical companies selling SSRIs in legal trouble (either that, or, they were all incompetent for not knowing about the existence of 5-HIAA urine tests).
If you get excuses for why the test cannot be done, call a company like Labcorp directly and tell them you will pay out of pocket to have this 5-HIAA urine test done, or you can go to various urgent care walk-in clinics, tell them you had too many SSRIs, and want them to order the test. Make sure to get the test done ASAP and IGNORE ANYONE who tries to dissuade you and do it ASAP so that you are tested before serotonin levels drop (but which would still leave you with down regulated serotonin receptors).
Pro Tip: If you have a tendency towards alcohol addiction I have found that alcohol cravings can be eliminated by drinking green tea and then vaping nicotine salts (I usually vape with 30 ml nicotine salt bottles that contain 35 mgs/ml but others may want to start at a lower level of nicotine). My hypothesis is that the combination of green tea and vaping nicotine kills the desire for a drink because both nicotine and green tea stimulate the same GABA system that alcohol does.
I do not recommend vaping nicotine and drinking alcohol (despite how enjoyable doing both at the same time is) because nicotine causes mitochondrial fission and when mitochondria are in a fission state their energy output is lower. When mitochondria energy output is lower it cannot perform one of its major roles, the elimination of alcohol's breakdown product of acetaldehyde, as quickly as normal.
This allows the body to have longer exposure to acetaldehyde than normal. This is probably part of the reason drinking alcohol and regular cigarette smoking is linked to higher cancer rates. I also don't recommend drinking green tea and vaping nicotine on a routine basis because they can excessively downregulate GABA receptors excessively.
Pro Tip: One supplement I did not use to cure myself from anxiety attacks caused by excess serotonin, but which might be useful to others suffering from some sort of PTSD from a significant personal trauma, is turmeric. Turmeric (and not curcumin) has demonstrated strong PTSD suppressive actions, with minimal side effects. I was not able to take turmeric to fix my anxiety attacks because it is an SSRI and norepinephrine/noradrenaline reuptake inhibitor (NNRI) which can, with prolonged use, down regulate serotonin receptors and beta and alpha receptors, respectively. However, if you are not sensitive to turmeric's SSRI and NNRI properties then you are probably OK to use turmeric for short to medium periods of time to treat PTSD, although you would still be wise to periodically upregulate serotonin receptors through the protocol methods I describe and upregulate beta and alpha receptors by using omega 3 to reduce norepinephrine.
4 Benefits of Turmeric In Post Traumatic Stress Disorder
https://www.turmeric...stress-disorder
Pro Tip: The fulvic acid contained in shilajit is a potent biofilm destroying agent. Although people might be more inclined to use collagen on an empty stomach to reduce serotonin because fulvic acid and/or shilajit may have more side effects (for example, fulvic acid becomes toxic if exposed to chlorine), for those looking to break up an infection may want to try shilajit to breakup biofilm to clear an infection. However, I would recommend starting with a low dose first to test how you react to shilajit and then not use an antibiotic on the same day you take shilajit to avoid any side effects caused by mixing shilajit with an antiobiotic on the same day.
Pro Tip: How long it will take for you to see creative/mood improvements from this protocol's methods to upregulate serotonin receptors depends on the degree to which they are downregulated. If you have no particular cognitive problems and are just looking for a creativity and motivational boost then you could see results in a week or less from taking 1.5 grams of collagen on an empty stomach daily, and then maybe needing to use it once or twice every month or two months afterwards.
Although it may sound incredible that creativity and mood could be boosted like this with such an infrequent dose, in my case after I cured myself last year of my excess serotonin and its related health problems, I found that I do not have to use collagen more frequently than once a month or every two months and drink moderately 2 days a week in order to maintain these cognitive benefits, with no signs of addiction (because dopamine is not being directly stimulated by this protocol) and no signs of dopamine tolerance/diminishing returns as is found with dopamine stimulating drugs (because, again, dopamine is not being directly stimulated by this protocol).
If you have more severe symptoms of excess serotonin then (in addition to seeking emergency help and requesting a 5-HIAA urine test as soon as you possibly can) it can take 4-6 months to complete this entire 7 step protocol with the serotonin lowering step taking 1 month. Even in my case I only needed to use shilajit for one month to complete the serotonin lowering step. The total time it took me to cure all symptoms was 8 months, although it would have taken only 4-6 month if I had known in hindsight what the entire protocol would consist of instead of my needing to create it through trial and error.
If you are sensitive to Omega 3 due to any fish allergies, or want to avoid mercury from fish, then you can get omega 3 fatty acids from algae supplements on Amazon that are filtered and purified to have high levels of omega 3.
Other neurotransmitter system alternatives to the dopamine pathways have proven non-ideal for improving mental health, and are probably destructive to cognitive and physical health.
Stimulating the GABAergic system with GABA enhancing pharmaceuticals (like benzos) or other substances such as marijuana, alcohol, and nicotine causes a "relaxation effect" typical of GABA stimulants.
HOWEVER, unlike ambition-increasing dopamine ,GABA is de-motivating. Overstimulation of GABA can also lead to tolerance developing with GABA having less and less effect over time as well as anxiety attacks from the reduction in GABA receptors (GABA suppresses adrenaline). This is why marijuana and alcohol use can cause extreme anxiety attacks when used constantly and why GABA stimulating benzo pharmaceuticals have dangerous withdrawal side effects that are in some cases worse than alcohol withdrawal symptoms.
https://www.drlauren...-making-sicker/
Benzodiazepines increase the affinity of receptors for the calming neurotransmitter GABA. This leads to a decrease in the inhibitory effects of GABA, as well as an increase in the excitatory neurotransmitter glutamate to compensate.
In other words, you may not have had a chemical imbalance before, but you do now. (That’s why you can’t abruptly stop any of the psych drugs without potentially severe consequences.)
Downhill With Benzos
The introduction of these drugs to the public has corresponded with a dramatic decline in American mental health.
In 1955, only one in every 468 Americans was considered to be mentally disabled,9 and there were only 5,415 “psychoneurotic” (anxiety disorder) patients in state mental hospitals.9
Then Valium (a benzodiazepine) hit the market in 1963. It was the bestselling drug in the Western world until 1981, touted as perfectly safe. It works very quickly to calm anxiety, but the clinical trials demonstrate (and most people can attest) that these benefits are pretty much gone by 4-6 weeks.10 But the withdrawal symptoms were so horrific and in many cases so lingering11 that in 1975, the U.S. Justice Department made it a controlled substance (schedule IV drug). Patients who remain on benzos long-term have a four-fold increase in depressive symptoms, as well as a gradual increase in panic attacks and agoraphobia.12 The “higher the intake, dose and period of use[of benzodiazepines], the greater the risk of impairment.”13
By 2006 more than 300,000 adults in the US were on SSI (government disability) for anxiety disorder alone – that’s about 60 times the number hospitalized for psychoneurosis (anxiety) in 1955.14
GABA stimulating benzos, which are widely prescribed to treat anxiety despite severe side effects, have also been linked to the development of Alzheimer's and dementia -
https://www.health.h...se-201409107397
If you have ever taken Valium, Xanax, or some other benzodiazepine to calm your nerves or sleep better, you may have felt woozy or hungover the next day. Experts have long assumed that people’s heads would clear once they stopped taking the drug. That may not be the case. A study published by the journal BMJ suggests that benzodiazepine use may promote the development of dementia.
A team of researchers from France and Canada linked benzodiazepine use to an increased risk of being diagnosed with Alzheimer’s disease. In the study, the greater a person’s cumulative dose of benzodiazepines, the higher his or her risk of Alzheimer’s.
...
People who had taken a benzodiazepine for three months or less had about the same dementia risk as those who had never taken one. Taking the drug for three to six months raised the risk of developing Alzheimer’s by 32%, and taking it for more than six months boosted the risk by 84%.
Serotonin Reuptake Inhibitors (SSRIs) have failed to curb depression for most patients relative to placebo pills -
https://www.drlauren...-making-sicker/
Iatrogenic Chemical Imbalance
Depressed patients treated with SSRIs end up with a chemical imbalance as a result of the drugs, though. Here’s how it works.
Your body is a living system, designed to find balance (homeostasis) with its environment. SSRIs (Selective Serotonin Reuptake Inhibitors) prevent serotonin from being recycled, so it sticks around to re-stimulate its receptors longer. Your brain responds to this by saying, “Hey, we’ve got too much serotonin stimulation going on, stop making so many receptors.” So your body drops the production of serotonin receptors by 25% within four weeks,7 and up to 50% with chronic use.8 This may also be the reason why it takes 3-4 weeks for SSRIs to “work.”
...
Downhill with Prozac
In the 1930s and 1940s, less than one in a thousand adults suffered clinical depression yearly.9 Around 60 percent of such individuals suffered only a single episode of depression in their lifetimes, and only 13 percent suffered three or more episodes.15 Dean Schuyler, head of the depression section at the NIMH in 1974, noted that spontaneous recovery rates for depression exceeded 50 percent within a few months.16
Then Prozac was approved in 1987. While depression had previously been associated with a high rate of spontaneous recovery within a few months to a year and a low relapse rate, studies show that the longer the duration of treatment with SSRIs, the higher the rate of relapse.17 In fact, those treated for depression were three times more likely than untreated depressed patients to “suffer a cessation of their principle social role, and nearly seven times more likely to become incapacitated.” 18
All told, in 2007 the disability rate had soared to one in every 76 Americans, from one in every 468 Americans in 1955.19 This includes children – in 1987, pre-Prozac, only 5.5 percent of American kids were on disability rolls for mental health issues. By 2007 that number rose THIRTY FIVE FOLD, and is now the leading cause of disability in children.20 By June 2008, one in every sixteen young adults is now considered to be mentally ill.21
I could go on – I have not even mentioned the studies that demonstrate SSRIs are not significantly better than placebo for the treatment of mild to moderate depression, nor have I mentioned the side effects of any of these drugs. The book goes on to cite similar research for medications for schizophrenia, bipolar disorder, and ADD/ADHD.
So I reiterate the initial question. Are we making ourselves sicker?
https://www.drlauren...ken-or-the-egg/
https://pubmed.ncbi....h.gov/12633120/
https://psycnet.apa..../1999-11094-001
https://journals.plo...al.pmed.0050045
The bulk of the evidence is against the use of psychotropic medications for anxiety and depression. Studies show that in many cases, effects of SSRIs and benzodiazepines are no better than placebo for mild to moderate depression–indeed, some studies showed that SSRIs were less than half as effective as placebo! It also appears that according to the major medical journals, the concept of a chemical imbalance underlying at least depression has been debunked.
...
What Antidepressants Do
We also know that antidepressants are more effective than placebo for MDD (though the relapse rates while medicated are still up to 60%, and long-term treatment may, in fact, make the condition worse).
SSRIs (or, an increase in the use of health supplements like SAM-e and turmeric that act as natural SSRIs) are probably significantly, perhaps primarily, responsible for the decrease in sperm counts in Western men, increased feminizing traits and behaviors (both in terms of psychological behavior and in terms of physical appearance) of Western men, lack of career ambition, and reductions in sex drives of younger generations because SSRIs and serotonin levels are inversely correlated with testosterone levels -
A Collection of Data & Detailed Analysis of the Etiology and Pathology of Post-SSRI-Sexual Dysfunction as well as Possible Novel Treatment Approaches
https://area1255.blo...on-of-data.html
SSRI's may lower testosterone by raising prolactin and cortisol levels, as well as by modifying endorphin activity to produce more anti-gonadotropic feedback. They also may lower important intracellular cyclic AMP levels ; leading to a decrease in thyroid output , testosterone and steroidogenic acute regulatory protein *sTAR) - all of this will lower libido.
SSRIs have also caused, or are related to, numerous physical side effects (some of which can endure for years even after SSRI use stops) such as increased risk of life-threatening liver toxicity from down regulation of the P450 chromosome which breaks down drugs in the liver, increased risk of heart disease, loss of sexual desire, digestive tract diseases such as Crohn's disease and irritable bowel syndrome (IBS), loss of sexual desire and other sexual dysfunctions, loss or severe elimination of emotions (anhedonia), and anxiety attacks.
Symptoms / Signs of Too Much Serotonin / Excess Serotonin
https://www.longecit...ad-cited/page-2
Role of serotonin in the pathophysiology of the irritable bowel syndrome
http://www.ncbi.nlm....les/PMC1574906/
Serotonin receptor modulators in the treatment of irritable bowel syndrome
https://www.ncbi.nlm...les/PMC2503665/
Yes, that's correct though - Crohn's Disease & Diarrhea Predominant-IBS are both rooted in, at least in part, high serotonin levels..too much serotonin contributes to an over-active gut / aka spastic colon as well as other issues with digestion...whereas low serotonin is the opposite - producing a tendency towards constipation although this isn't the case much of the time if your beta-adrenergic reactivity and nitric oxide production is on point.
Can Serotonin Cause High Blood Pressure / Hypertension ? (Serotonin causing High Blood Pressure)
https://area1255.blo...d-pressure.html
Serotonin is implicated in a number of cross-reactions in the nervous system, and there are serotonin receptors located directly in/on the heart/atrium. Increased activity of the serotonin receptors 5-HT2B and 5-HT4 is shown on failing hearts. (3) (4)
As such , chemicals/drugs that block these two serotonin receptors are being investigated/trialed for the treatment of those with various forms of heart disease. (5) (6)
Namely, right ventrical heart failure (5-HT2B) and congestive heart failure (CHF) along with tachycardia (5-HT4).
In addition to central heart failure, serotonin itself is dangerous in moderately-elevated to substantially elevated amounts, high plasma serotonin levels are found to cause primary pulmonary hypertension (7) (8) (9).
Additionally, serotonin is found to , along with adrenaline, mediate stress-induced increases in systolic blood pressure, which essentially means that serotonin is about half of the reason why blood pressure can go up in response to stress(10) (11). Part of this has to do with the serotonin induced accumulation of ALDOSTERONE via 5-HT4 receptor activation(12).
SSRIs also have an indirect effect on school shootings. Although SSRIs do not directly activate aggressive/violent behavior like cocaine, meth, and other hard drugs do, SSRIs do stunt emotions and the desire to work, therefore, it interferes with the ability to interact with other people. If given to teenagers who are already having difficulty socializing their social skills and ability to do school work will deteriorate even more, resulting in more bullying and then causing frustration and anger to explode in violence.
Elevated serotonin from SSRIs is also associated with OCD-psychopathic behavior, which is consistent with the personality profile of most school shooters -
10 Neurological Abnormalities in Psychopaths (Neurotransmitter and Brain Region Differences in Psychopaths/AntiSocial PD)
https://area1255.blo...alities-in.html
http://www.ncbi.nlm....pubmed/12452254
https://www.ncbi.nlm...pubmed/25145808
https://www.ncbi.nlm...les/PMC3294220/
https://books.google...rotonin&f=false
Elevated serotonin is found in obsessive-compulsive, calculating Psychopaths; and this confers the lack of or distorted dopamine function leading to lack of empathy, elevated serotonin is associated with instrumental crimes/objective oriented crimes and is also found in some Cult leaders. (18) (19) (20) (21) however, lower serotonin is found in impulsive criminals as opposed to premeditated criminals whom have higher levels.
Granted, only a tiny percentage of teenagers on SSRIs engage in school shooting, but if they can't even improve mood in the overwhelming majority of SSRI users, and causes sexual dysfunction which makes sexual development even more difficult than it already is for teenagers, then what benefit (relative to alternatives) makes it worthwhile for teens to be put on them given the multiple downsides and limited (perhaps non-existent) benefits?
To the extent SSRIs do reduce depression (usually working primarily on the most depressed patients who are, however, at higher risk of relapse into depression than for those with extreme depression taking placebo pills) it is because serotonin is a "mood neutralizing" neurotransmitter that eliminates bad moods by clumsily eliminating ALL emotions.
Even anecdotally, it is rare to find a self-report from someone on SSRIs who says they make them "feel good."
The significant problems caused by SSRIs, benzos, and the rest of the, at best, ineffective chemical garbage being pumped out by pharmaceuticals is caused by misunderstanding the difference between neurotransmitters and neurotransmitter receptors.
Usually, psychological problems caused by neurotransmitter activity is caused by THE RECEPTORS instead of the TRANSMITTERS.
The neurotransmitters, by themselves, are just dumb molecules with no idea on their own how to interact with the body, and they are usually not short in the human body if meat intake is adequate and there is no genetic defect preventing the creation of the neurotransmitters.
It is the receptors that are usually the source of mental health problems because of downregulation. Excessive downregulation of receptors is a problem because the receptors act as the master "traffic cops" telling the neurotransmitters where to go, and how to interact with the system. Receptors even signal the transmitters to stop production by the use of auto-receptors that decrease certain neurotransmitter activity. Generally, and so long it is not excessively upregulated, upregulation of neuro-receptors improves mental health function by keeping the amount of receptors high enough that the transmitters move in the right direction.
If neurotransmitters (instead of receptors) are lacking from dietary causes it is usually caused by a lack of meat which contains the amino acids needed to produce transmitters such as GABA, dopamine, serotonin, and others. And substituting these amino acids and precursor chemicals with supplements is not wise because taking them in a pure form (such as taking excessive AKG to generate Glutamate and GABA or tryptophan or 5-HTP to generate serotonin) can cause an excess of neurotransmitters, which can be dangerous in the case of glutamate and serotonin. By contrast, getting neurotransmitters from eating meat tends to not lead to excesses in transmitters.
Aside from digestive or genetic disorders, there is no reason to supplement SSRIs unless you are trying to upregulate dopamine receptors that are down regulated excessively from drug use (in that case a natural SSRI like turmeric or SAM-e for short periods of time, at minimal doses, would probably be of help to upregulate dopamine receptors).
Unfortunately, almost the entire mental health industry is focused on increasing neurotransmitters activity, which leads to the downregulation of receptors, and is exactly the OPPOSITE of what they should be doing (i.e, UP-regulating receptors so the body-wide, physical and mental responses to neurotransmitters improves!!!).
But downregulation of receptors only leads to more mental health problems, potentially life threatening ones as excess serotonin receptor down regulation can be fatal or cause permanent internal organ damage because of serotonin toxicity -
https://www.drlauren...-making-sicker/
I read a chilling book recently, called “The Anatomy of an Epidemic,” by Robert Whitaker. Here are the highlights, and I’ve included references at the bottom.
We tend to think of antidepressants and anti-anxiety meds (benzodiazepines) as “silver bullets,” much in the same way that we originally viewed antibiotics as silver bullets against infectious diseases. The idea that depression and anxiety are caused by chemical imbalance in the brain is so widespread that it almost goes without question… and antidepressants especially (and benzodiazepines as well) supposedly correct those chemical imbalances, helping such afflicted individuals function normally in society.
But there isn’t any evidence for that hypothesis.
Lack of Evidence for the Chemical Imbalance Theory
The theory of depression as a chemical imbalance in the brain was first postulated by Bernard Brodie.1 But when depressed patients and normal controls were tested for the breakdown products of serotonin (5-HIAA), researchers failed to find a statistically significant difference between the two – nor did there appear to be any correlation between 5-HIAA levels and depressive symptoms.2,3 Further studies showed that depressed patients who had not taken antidepressants had normal 5-HIAA levels.4
Stanford psychiatrist David Burns said in 2003, “I spent the first several years of my career doing full-time research on brain serotonin metabolism, but I never saw any convincing evidence that any psychiatric disorder, including depression, results from a deficiency of brain serotonin.” 5
Colin Ross, associate psychiatry professor of Southwest Medical Center in Dallas, said, “There is no scientific evidence whatsoever that clinical depression is due to any kind of biological deficit state.” 6
Iatrogenic Chemical Imbalance
Depressed patients treated with SSRIs end up with a chemical imbalance as a result of the drugs, though. Here’s how it works.
Your body is a living system, designed to find balance (homeostasis) with its environment. SSRIs (Selective Serotonin Reuptake Inhibitors) prevent serotonin from being recycled, so it sticks around to re-stimulate its receptors longer. Your brain responds to this by saying, “Hey, we’ve got too much serotonin stimulation going on, stop making so many receptors.” So your body drops the production of serotonin receptors by 25% within four weeks,7 and up to 50% with chronic use.8 This may also be the reason why it takes 3-4 weeks for SSRIs to “work.”
The stupid obsession of the mental health industry with forcing more and more neurotransmitter contact with receptors through SSRIs, benzos, and other medications is like trying to jam a key into a lock that doesn't fit it hoping that the door will finally unlock.
This medical consensus has completely failed.
Worse is the evidence of brain damage caused to the millennial and gen-z generations by either their mothers using SSRIs during pregnancy, or using them on adolescents with potentially long-term damage to the brain volumes of the millennial and gen-z, as well as the sexual dysfunction and lack of sex drive noted in those generations relative to previous generations, increased OCD and psychopathic tendencies of these two generations, decreased career ambition and work ethic, and increased susceptibility to depression and anxiety by SSRIs reducing serotonin receptor volume -
SSRI Use During Pregnancy Alters the Child’s Brain Development
https://www.madiname...in-development/
In a new study in JAMA Psychiatry, researchers found that children born to mothers who used SSRIs during pregnancy had reduced brain volume in multiple areas. Most brain volume reductions were still there at the follow-up when the kids were 15 years old. The researchers write that the affected areas of the brain are theorized to be involved in emotion regulation.
“The results of this cohort study suggest that prenatal SSRI exposure may be associated with altered developmental trajectories of brain regions involved in emotional regulation in offspring,” the researchers write.
The researchers were led by Dogukan Koc at Erasmus University Rotterdam, the Netherlands. This was part of Generation R, a population-based study in Rotterdam. The study included 3,198 mothers with a delivery date between April 1, 2002, and January 31, 2006, and the children were followed with three brain scans over time, the last of which occurred when they were 15.
...
So, could this be explained by the mother’s depression? No, write the researchers. For mothers who were depressed but did not take SSRIs, the children were almost no different from the healthy controls. Prenatal depression was associated with a smaller volume in one area, the rostral anterior cingulate gyrus. Similarly, postnatal depression was associated with a smaller volume in one area, the fusiform gyrus.
Those differences in one area each should be compared to the large, brain-wide reduction in volume in numerous areas experienced by kids whose mothers took SSRIs. Moreover, even in the fusiform gyrus, kids whose mothers took SSRIs had larger reductions in volume than kids whose mothers had depression but didn’t take SSRIs.
...
Unfortunately, many of the brain volume differences didn’t catch up. Moreover, it’s unclear what effect these volume differences throughout all of childhood would have on a kid’s development, even if it catches up by their late teenage years.
Previous Research
Studies have consistently found antidepressant use in pregnancy to be associated with myriad risks to neonatal health, including neonatal withdrawal syndrome, preterm birth, congenital disabilities, developmental problems, cardiopulmonary problems, and even death.
In one study, researchers found a sixfold increase in neonatal withdrawal syndrome when mothers took antidepressants. In another study, researchers found that 30% of babies born to mothers who used antidepressants experienced neonatal withdrawal syndrome. None of the babies whose mothers did not use antidepressants had this complication. And yet another study found that over half (56%) of babies exposed to SSRIs had this problem.
Researchers have argued that antidepressants should be discontinued in pregnancy because of this risk, which includes symptoms of hypoglycemia, tremors, hypotonia, hypertonia, tachycardia, rapid breathing, and respiratory distress in babies born to mothers who use antidepressants.
Studies have also accounted for preexisting factors like depression severity by comparing women who continued using antidepressants during pregnancy with women who had the same indication and did use antidepressants initially—but stopped after becoming pregnant. That study found that those who continued to use antidepressants increased the risk of neonatal health complications in their newborns, including preterm birth, low birth weight, and hospitalizations.
Other research has found that antidepressant use during pregnancy alters brain development in the fetus. These findings have appeared in top journals, too: A study in JAMA Psychiatry found that antidepressant use during pregnancy increased the risk of infants with speech disorders, while a study in the American Journal of Psychiatry found that antidepressant use during pregnancy increased the risk of impaired neurological functioning in infants.
It is estimated that 10% of pregnant women in the United States use SSRIs during pregnancy. Therefore, probably as much as 10% of the millennial and Z generations have permanently reduced brain volumes, and permanent brain damage from SSRI use.
Exposure of adolescents to SSRIs also has dangerous effects on brain development -
Serotonin-related rodent models of early-life exposure relevant for neurodevelopmental vulnerability to psychiatric disorders
https://www.nature.c...398-021-01388-6
Postnatal exposure to SSRIs
Other studies investigated the behavioral consequences of exposures to SSRIs during the early postnatal period10,12,103 (Table 2). Fluoxetine application during the first 2 or 3 postnatal weeks in various mouse/rat strains resulted in a marked reduction of exploratory behaviors, accompanied by the emergence of anxiety and depressive-like phenotypes103,104,105,106,107,108,109,110,111,112. Others, applying similar protocols of fluoxetine exposure, only partially reproduced these emotional effects113,114,115,116 (Table 2).
Other behavioral effects of relevance for psychiatric conditions were also reported after postnatal exposure to SSRIs. That is, several rat studies have reported reductions in ultrasonic vocalizations and sensorimotor responses, accompanied by alterations in social interactions to conspecifics104,105,115,117,118. On the other hand, spatial learning and memory abilities seemed not to be affected by the fluoxetine treatment at lower doses116,119 (Table 2), consistent with a recent meta-analysis90.
Postnatal exposure to other SSRIs like citalopram or escitalopram, during the same postnatal period, also produces anxiety and depressive-like phenotypes in mice120,121.
Who this protocol is for -
Those who are artists, or anyone else who wants to improve their creativity, ambition, and overall happiness and well being.
Lowering serotonin indirectly improves dopamine responses needed for creativity, ambition, and overall happiness.
If you have mild or serious symptoms of excess serotonin
As stated earlier, if you have ANY symptoms of excess serotonin get a 5-HIAA urine test done immediately to determine if you are nearing dangerous levels of serotonin, and do not accept ANY argument from any doctor trying to dissuade you from taking it (even if they are convinced your problems are not serotonin related they have no excuse not to run the urine test since it is simple and will at least rule out serotonin as a problem if . If necessary, pay out of pocket for it at a labcorp.
Don't delay having this test because if you do, the serotonin transmitter levels might decrease on a 5-HIAA test but you would still be stuck with downregulated serotonin receptors, and all of their many side effects, and there is no clinically available test for downregulated serotonin receptors that exists outside of very specialized scientific research facilities that you probably won't be able to get access to.
Speed is of the essence, so get the 5-HIAA test done IMMEDIATELY if you see any symptoms.
Mild symptoms of excess serotonin are -
Anhedonia
Loss of sexual desire and/or sexual dysfunction
In males, any slight to severe depression after orgasm (caused by serotonin raising prolactin)
Obsessive compulsive disorder (constantly checking something like lights or doors, or similar)
Lack of motivation (feeling "zoned out" or zombie like)
Loss of creativity and enjoyment from anything that made you happy
Lack of ability to socialize with others
Difficulty concentrating on either spoken words or concentrate on written words
More severe symptoms of excess serotonin -
Anxiety attacks
Heart palpitations
Rapid heartbeat from eating meat or any food with tryptophan in it
Inability to tolerate any supplements that increase serotonin such as SAM-e, Lion's Mane, or turmeric.
Gastrointestinal problem (Irritable Bowel Syndrome, Crohn's disease)
Spikes in blood pressure
An unusually strong fear when looking at sharp or curved objects
Reading two lines in the wrong order, for example if you read a line saying
"Fred left for
the airport."
The first word would read "Treb" instead of "Fred" to someone with excessive enough serotonin.
If you take supplements a lot.
Even if you have never used a prescription SSRI in your life, you could still be at risk from the negative effects of serotonin if you take supplements.
Years before I tried the C60 and mitochondria protocols I had developed mild signs of excess serotonin. This was probably caused by years of taking large amounts of supplements like SAM-e and turmeric that act as natural SSRIs.
What supplement users and biohackers don't know is that there are many more supplements that increase increase serotonin than there are that decrease serotonin.
Supplements may also have more effect taken in combination. For example both ginger and turmeric are usually well tolerated, but both affect the serotonergic system and taking them in combination could gradually create symptoms of high serotonin (like loss of creativity and emotions) that aren't obvious to track back to a single cause.
Other supplements like Lion's Mane and SAM-e can trigger serotonin reactions more quickly than normal.
Depending on what you take, it may be wise to cycle them and use the serotonin reducing protocol described here occasionally to reduce mild symptoms of excess serotonin such as loss of creativity and anhedonia/lack of pleasure in what used to make you happy.
SAM-e and turmeric have many health benefits such as enhancing liver health and reducing inflammation.
You can still take them (if you aren't sensitive to them for the SSRI effects) you just need to cycle them on and off with the serotonin reducing portion of this protocol so your serotonin receptors don't become overly downregulated.
If you have anxiety attacks or heart palpitations from eating meat AND/OR want to improve skin health
For better skin results with the C60 protocol, you might want to try cutting out all caffeine (including from tea and soda) for a month and eating salmon twice a week to upregulate your beta-adrenergic receptors.
Although the C60 protocol improved the youthfulness of my skin, I still had problems like wounds not healing as fast as I wanted (I have had this problem for over a decade, before I tried either the mito or C60 protocol).
Then, last year when I encountered problems with excess serotonin from years of taking serotonin raising supplements and then (what finally led to a tipping point) combining 5-HTP with the C60 protocol, I took propranolol to upregulate my beta receptors as part of my 7 step serotonin reducing protocol.
I also took Omega 3 later in the protocol and eat 36 mgs of 70% dark chocolate 4-5 days a week (Lindt brand dark chocolate balls because it easier to keep track of the amount of chocolate I am eating) to lower norepinephrine/noradrenaline and epinephrine/adrenaline to further upregulate my beta receptors, and ending all caffeine intake (I used to be a big coffee, green tea, and occasional Nic-vape user).
What I noticed was that the propranolol, surprisingly and unexpectedly, ended the rapid heartbeat and anxiety attacks I had when I ate meat most of last year or took certain supplements (and later the mito protocol which I did 22 times earlier this year entirely eliminated any remaining problems I had eating meat).
Propranolol also had the unexpected effect of making my skin heal noticeably faster.
Apparently both the relief in rapid heartbeat from eating meat and the restoration of skin healing is related to the beta receptors not just controlling responses to adrenaline. It also is involved in glucose metabolism. Presumably my rapid heartbeat from eating meat was caused by my beta receptors so downregulated from serotonin-triggered adrenaline release that there weren't enough beta receptors left to both control normal cardiovascular responses and convert food into glucose.
The mito protocol helped me eat without side effects because the mitochondria (among many other things) are needed to process protein and fat and many supplements, and they are heavily involved in anxiety responses because MAO is directly embedded within mitochondria. But I couldn't take mito protocol until later in my serotonin-reducing protocol.
It also appears that beta receptors are somehow involved in wound healing, probably because of their effect on glucose metabolism -
Docosahexaenoic acid facilitates cell maturation and -adrenergic transmission in astrocytes
https://www.research...lication_detail
The effects of docosahexaenoic acid (DHA; 22:6n-3), a major v-3 PUFA in the mammalian brain, on the structure and function of astrocytes were studied using primary cultures from rat cerebra. Gas-liquid chromatography of methyl esters of FAs isolated from cultures exposed to individual FAs, namely, stearic acid, linoleic acid, arachidonic acid, and DHA, showed alterations in the lipid profiles of the membranes, with a preferential incorporation of the FA to which the cells were exposed. Immuno-fluorescence studies demonstrated that unlike treatment with other FAs, after which the astrocytes remained as immature radial forms, DHA-treated astrocytes showed distinct differentiation, having morphology comparable to those grown in normal serum-containing medium.
Receptor binding studies to determine the concentration of various neurotransmitter receptors showed that DHA selectively increased the number of b-adrenergic receptors (b-ARs) compared with FA-untreated controls, suggesting a greater role of DHA on b-AR expression in membranes. This was also reflected by an increase in downstream events of the b-AR pathways, such as the induction of protein kinase A and glycogen turnover by isoproterenol (ISP), a b-AR agonist in DHA-treated cells.
...
The b-AR system is an important intrinsic regulator of the glycogen turnover of mammalian brain. We determined the glycogen content in specific FA-enriched astrocytic cells under normal and ISP-treated conditions (Fig. 7A). Compared with untreated controls, supplementation of SA and AA had no effect on the glycogen content of the cells, whereas LA and DHA caused significant increases in total glycogen, with average increases 250% and 760%, respectively. When the cells were exposed to ISP, there was significant breakdown in total glycogen content in all FA-treated cells compared with corresponding cells in which no ISP was added. Here also, the maximum breakdown of glycogen by ISP occurred in DHA-supplemented cells, which decreased to the level observed in FA-deficient astrocytes.
Because the observed 7.5-fold increase in total glycogen content in DHA-supplemented cells could be attributable to an effect on the synthesis rate of glycogen, we evaluated the amount of incorporation of [14C]glucose into glycogen in these cells in the presence and absence of ISP (Fig. 7B). In the absence of ISP, treatment with DHA caused an 50% decrease in the newly synthesized glycogen compared with FA-deficient control cells. However, on ISP treatment, there was a 10-fold increase in the incorporation of [14C]glucose into glycogen in the DHA supplemented astrocytes compared with the ISP-treated control cells.
If you want to upregulate GABA receptors after using the following substances which all contribute to overstimulating/downregulating GABA receptors if used in excess, and which are therefore likely to contribute to anxiety attacks by excessive downregulation of GABA receptors -
Marijuana
Benzos
Alcohol
Nicotine products (GABA stimulation is equal whether nicotine is delivered through traditional tobacco products or from vaping e-cigs)
Certain teas like Green Tea
If you want to treat anxiety attacks, whether or not they were caused by SSRIs or SSRI-like supplements
Anxiety is controlled through these various pathways, all of which can be negatively impacted by SSRIs disrupting the adrenaline response.
The anxiety controlling pathways are -
Beta receptors - My beta receptors were upregulated by propranolol at first and then Omega 3 and dark chocolate. Propranolol is needed if anxiety is very strong.
GABA receptor upregulation - I used Culturelle brand probiotics to upregulate GABA receptors because GABAergic system suppresses adrenaline and noradrenaline release.
COMT - Improved by magnesium. I used Swanson brand chelated magnesium because it is the form of magnesium that doesn't cause digestive side effects.
NMDA receptors - Upregulated by magnesium. NMDA receptors could be downregulated by excess glutamate.
MAO - Controlled directly by mitochondria. If mitochondria is damaged then MAO function will also be harmed. Mitochondria dysfunction can be treated best from Turnbuckle's mitochondria protocol. In my case, 22 rounds of the mito protocol I had earlier this year in part 5 of my protocol stopped all remaining anxiety reactions and repaired any mitochondrial damage I had from the previous year. Turnbuckle's mitochondria protocol is probably the best option to repair mitochondria because I tried other methods for improving them, such as excercise and magnesium, but nothing worked as well as his mitochondria protocol.
If you want to reduce the risks of stroke and heart attack
Magnesium and dark chocolate reduce the risk of heart attack and stroke. Magnesium should be taken on an empty stomach in the morning, with no other supplements, because magnesium absorption can be interfered with by other supplements or by food, especially food that contains calcium.
The Effect of Magnesium Intake on Stroke Incidence: A Systematic Review and Meta-Analysis With Trial Sequential Analysis
https://www.ncbi.nlm...les/PMC6692462/
For each 100 mg/day increase in magnesium, the risk for total stroke was reduced by 2% and the risk for ischemic stroke was reduced by 2%.
Chocolate Consumption and Risk of Coronary Heart Disease, Stroke, and Diabetes: A Meta-Analysis of Prospective Studies
https://www.ncbi.nlm...les/PMC5537803/
Taken together, the present meta-analysis suggests that chocolate consumption confers reduced risks of CHD, stroke, and diabetes.
If you have more severe SSRI or SSRI-like supplements that induced cardiovascular side effects like anxiety attacks, high blood pressure, or rapid heart rate by down regulating beta receptors
If you have side effects like this then, in consultation with your doctor, you may need propranolol to upregulate the beta receptors again to restore normal cardiovascular function. In my case, 10 to 20 mgs a day for a month was enough to upregulate beta receptors.
If you don't have serious side effects you probably can restore normal adrenaline function and correct mildly downregulated beta receptors with Omega 3 fish oil to decrease norepinephrine/noradrenaline (and thus upregulate the beta receptors and alpha receptors) and upregulate blood pressure receptors (AKA mineralcorticoid/aldosterone receptors) by reducing Angiotensin II. You can also reduce adrenaline release by eating 36 grams of at least 70% dark chocolate. Remember to cut out all caffeine while you upregulate the beta receptors from coffee and most teas, and exclude soda drinks that are not caffeine free since Diet Coke can be comparable to the caffeine amount in coffee.
Pre Caution - Unless you need propranolol for reasons unrelated to upregulating beta receptors, and in consultation with your doctor, don't use propanol for more than 3 months (even at a low dose of 10 to 20 mgs a day) because it can push adrenaline activity from the beta receptors (which adrenaline slightly prefers) to the alpha receptors, leading to downregulation of the alpha receptors which, by itself, can cause all sorts of negative side effects.
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I am going to have to warn everyone not to combine 5-HTP with the C60 protocol as I did in my version of the protocol because of a negative reaction I had this April to 5-HTP and which took a few months to resolve.
The side effects are related to excess serotonin which downregulated (reduced) the number of my serotonin receptors and was fixed by upregulating (increasing) the number of serotonin receptors, as well as treating other side secondary effects caused by serotonin.
I further recommend not using other serotonin promoting and/or SSRI-like agents like SAM-e or St. Johns Wart (or any other neurotransmitters aside from serotonin) since they could have similar effects because of their serotonin enhancing properties. Since I only used 5-HTP a handful of times with the protocol, and never outside of it, this could indicate that taking the C60 protocol along with supplements or pharmaceuticals that alter any neurotransmitter balance or stimulate neurotransmitters could cause a more rapid than normal upregulation or downregulation of those receptors.
I am going to describe what I did to correct this problem and recommend anyone who did use 5-HTP with the C60 protocol to please use collagen, shilajit or fulvic acid (BUT preferably COLLAGEN) in the manner described in the following serotonin upregulation protocol I have written out below; UNLESS they show symptoms of serotonin syndrome which would require immediate medical treatment.
Please see if you have any of the symptoms of excess serotonin described by Jason Malek Russo I have posted further below.
Eventually I will also write a more detailed post on a new thread about this serotonin upregulation protocol because I discovered (quite unintentionally) while correcting this problem that upregulating serotonin receptors removes the suppressive effect serotonin exerts over dopamine activity. By removing serotonin's block on dopamine my creativity has increased in important ways such as the fact my sense of smell is enhanced, and I am more emotionally sensitive to music and art, including an improved sense of humor.
In general, I feel much more emotionally alive and creative than I have in quite a few years years.
Before I begin, I want to mention a few points.
One is that I likely had already downregulated my serotonin receptors years ago by using a large amount of serotonin-generating supplements such as SAM-e for liver health. Many common supplements, like curcumin, when taken in excess can increase serotonin levels and elevating serotonin activity tends to downregulate serotonin receptors.
Thus, I may have already been susceptible to a negative reaction to adding 5-HTP to the C60 protocol because my serotonin receptors had already been lowered/downregulated from previous years of supplementation.
I now believe I might have been experiencing a low-level of anhedonia years before I had started either the mito protocol or the C60 protocol, but adding 5-HTP to the protocol brought this issue to a head where it became much more noticeable. For example I had noticed a steady drop off in creativity and a dulling of my sense of humor years ago, that has now been corrected by the serotonin reducing protocol I created out of necessity.
However, 5-HTP is arguably a more a potent serotonin stimulant than SAM-e or pharmaceutical SSRIs like Paxil because SSRIs usually do not increase the total number of serotonin neurotransmitters in the body (like 5-HTP does). Instead, SSRIs keep the same total number of serotonin neurotransmitters the same while keeping them longer in the synapse.
I might also have been susceptible to 5-HTP because my GABA receptors, which inhibit excess serotonin activity, might have been downregulated because of past use of alcohol (moderately) and using nicotine at the same time as drinking (from vaping and Swedish snus, not traditional combustible tobacco which I have not used except a few times in school) which both overstimulate/decrease GABA receptors by overstimulating them with higher GABA.
For reference purposes I made extensive use of Jason Malek Russo's work on excess serotonin and its numerous negative side effects from both SSRIs and naturally occurring SSRIs like SAM-e and 5-HTP.
Russo (who used to post here and at other forums as Area-1255) was an invaluable source of information because, as far as I could tell, he is 100% correct in his descriptions of how serotonin and its receptors operate.
HOWEVER I should warn the reader that for treatment of various ailments his advice was NOT ALWAYS wise or safe. For example, he recommends phenibut on his blog for certain ailments, but phenibut has dangerous side effects. I would STRONGLY recommend someone looking at his works in an attempt to understand an ailment (for any issue, not just ones that are serotonin related) to NOT automatically take a drug or supplement he recommends unless they do careful research on its side effects, check if there are safer alternatives that have similar or better effects, and, preferably, ask people here if his treatment suggestion is a good idea.
Background - In general, neurotransmitters and neurotransmitter receptors act like baseballs (neurotransmitters) and catcher's mitts (neurotransmitter receptors) where the receptors "catch" the neurotransmitter. Hence, serotonin receptors "catch" serotonin transmitters, dopamine receptors "catch" dopamine neurotransmitters, etc, etc.
Although this is a gross oversimplification of a complex topic, it does capture the basic idea of how neurotransmitters relate to their receptors. As a general rule (which has exceptions) receptors decrease (decrease = downregulate) in number when there are too many neurotransmitters agonizing/activating them.
When receptors, such as serotonin receptors, decrease/downregulate in number they become overly sensitive to normal changes in serotonin neurotransmitter levels because there are too many serotonin neurotransmitters chasing too few serotonin receptors to "catch" them.
The overstimulation of ANY receptor with any neurotransmitter can become dangerous.
Therefore, in general, the way to improve downregulated neurotransmitter imbalances is to increase (increase = upregulate) the number of receptors so the remaining receptors do not become "overwhelmed" and the rest of the neurotransmitter system is rebalanced.
Fortunately, receptors can be upregulated provided there is not significant damage to the underlying neurons.
Upregulation is usually accomplished by gradually decreasing receptor exposure to the neurotransmitters, either by reducing the amount of neurotransmitters (such as by cutting serotonin levels) or by blocking the receptor from interacting with the neurotransmitter, such as by upregulating beta adrenoreceptors with beta blockers like propranolol which limits the beta adrenoreceptor's contact with adrenaline/epinephrine and noreadrenaline/norepinephrine.
The main problem I encountered in April about an hour after trying the C60 protocol with 5-HTP was from downregulated serotonin receptors.
The symptoms forced me to go the ER because of worry that I was suffering from serotonin syndrome, which requires immediate medical care.
The symptoms of excess serotonin (which were corrected individually in a phased approach over a period of months) included loss of appetite, nervousness to sounds and certain shapes and lighting, anxiety attacks from excess adrenaline release (usually occurring after eating meat), elevated blood pressure from my normal 108/78 which consistently became 125-135 / 82-94, and high anxiety sensitivity to citric acid and methylation because of its activation of the PNMT pathway which generates adrenaline and noreadrenaline.
This serotonin downregulation created secondary effects caused by downregulated beta receptors from excess adrenaline release, dysregulated GABA function, intestinal upset from downregulation of serotonin receptors in the GI tract, difficulty processing fat and protein, intolerance of certain supplements because the P450 chromosome in my liver appeared to be downregulated.
This P450 chromosome is necessary for processing medicines (hence why SSRI's are dangerous to take with grapefruit juice because grapefruit juice also downregulates P450 -
Insights into PSSD - A Collection of Data & Detailed Analysis of the Etiology and Pathology of Post-SSRI-Sexual Dysfunction as well as Possible Novel Treatment Approaches
https://area1255.blo...on-of-data.html
One of the most distinguishable traits of all SSRI's, with the exception only of those with a short half life (and these are used for other purposes) ~ is that each SSRI not only generally has a very long half-life, but also that each drug tends to have prominent effects on liver enzymes; generally CYP3A4 and CYP2C19 or cytochrome P450. The implications of this binding are many, one of the main problems here is that by these drugs binding to liver enzymes, depending on which one ~ there is a possibility of changing the breakdown of other drugs, or delaying their elimination - this can lead to amplified side-effects of other drugs and thus further causes physiological disturbances especially if the other drugs have even so much of a parallel in regards to their mechanism of action […]
Now another big no-no, in fact one that is warned about ON-LABEL, is combining these anti-depressant drugs with NATURAL inhibitors of these enzymes, related cytochrome enzymes, or downstream , fairly related enzymes - one of the most discussed is GRAPEFRUIT JUICE.
By combining grapefruit juice you may increase the risk of overdosing on multiple drugs, and if you then take a second inhibitor, like LUVOX; the effects are then ADDITIVE....which essentially means that combining one simple 6oz glass of grapefruit juice with luvox, and then a blood pressure pill - could very easily KILL you or land you in the hospital with nearly uncontrollable bouts of panic, or immobilization stress and severe HYPOTENSION...if you do survive such a combination, the almost total loss of oxygen delivery during the periods of treatment and recovery may result in permanent nerve and blood vessel damage!
Other causes aside from receptor dysregulation were ruled out with medical test results that showed normal vital signs.
Blood work, liver and kidney enzymes were normal.
A complete abdominal ultrasound came back normal.
A brain MRI with contrast showed normal brain function.
X-rays and EKGs of the heart and circulatory system came back normal and showed no signs of heart or circulatory disease.
The phased approach to correct these problems is outlined below.
During all of the steps I used weight lifting to increase testosterone to counteract serotonin and ate at least 12 eggs each week to provide the liver with choline because egg yolks (if served sunny side up, and are not scrambled) contain the type of choline (phosphatidylcholine) the liver prefers.
I strongly recommend not to combine supplements from the different steps of this protocol at the same time because their combination might be too strong for an imbalanced system. For example, no one should combine Omega 3 fish oil and propranolol (both of which I used) at the same time because both of them lower blood pressure and heart rate and taking them at the same time could cause a dangerous decrease in heart rate and/or blood pressure.
Symptoms of excess serotonin -
Signs of Too Much Serotonin
https://area1255.blo...-serotonin.html
SENSORY EFFECTS
Over-Sensitivity to sounds, especially loud noises. Excessive jumpiness or even anxiety in response to sudden sounds or movements(1) (2).
Visual distortions, height / depth alteration, hallucinations(3) (4).
Words may appear out of place, or your perception of what you are reading may be entirely different. { e.g reading the third line thinking its the second} (5)
Sensitivity changes to light, sedation or no response to darkness(6) (7) (8) (9).
Lack of pain sensation, or HYPO Algesia, some individuals with high serotonin display such a lack in pain perception/sensitivity that it mirrors the effects of those under the influence of PCP. Pain asymbolia can be misdiagnosed as high serotonin(10) (11).
Tinnitus, ringing in ears(12)(13).
Vertigo. Dizziness. Room spinning(14) (15).
BEHAVIORAL / MENTAL EFFECTS
Delirium. Usually including abnormal forms of panic or worry along with various disperceptions(16) (17).
Depersonalization. Feeling out of place, out of body, or that events or surroundings are surreal(18)(19).
Frequent or occasional episodes of psychosis, paranoia, pathology changes, and obsessional behavior(20)(21).
Religious delusions and religious over-engagement. (some cult leaders are hypothesized to have elevated, but not toxic levels of serotonin)(22). The best book on this is "Biology of Religious Behavior : The Evolutionary Origins of Faith and Religion".
Unexplained agitation or inner restlessness(23).
Dystonia, tic-like behaviors, punding; repetitive behaviors(24) (25) (26)(27).
Frequent crying episodes in children, unwarranted panic or extreme anxiety(28).
Low/Absent Libido(29)
Emotional Anhedonia / Apathy / Blunt AFFECT (30) (31) (32) (33) (34)
Jittery, nervous hands, tremors, impatient(35) (36) (37).
Depression , despair, lack of motivation(38) (39).
Reading/Comprehension deficits(40).
PERIPHERAL / INTERNAL EFFECTS
Persistent nausea, unexplained/stress induced; not due to motion sickness which is more acetylcholine based. (41) (42)
Diarrhea/IBS Symptomology(43) (44) (45).
Part 1 - Upregulation of serotonin receptors by taking shilajit for 1 month using Double Wood's brand of shilajit (500 mgs shilajit per capsule standarized to 20% fulvic acid).
Shilajit was used to upregulate my serotonin receptors because its active ingredient, fulvic acid, reduces serotonin. Although I am not sure how this mechanism works I suspect it occurs by converting serotonin into melatonin because I felt sleepy after taking it and the conversion of serotonin into melatonin is one of the main ways the body gets rid of excess serotonin.
I took 1 capsule of shilajit for one week then increased to 2 capsules for the second week, then 4 capsules for the week after, and then tapered off the last week to just 1 capsule.
This process was completed in one month.
It was important to GRADUALLY increase the dose because trying to take too much too fast would be excessive for an imbalanced system, although I did have SSRI withdrawal symptoms the first week. The SSRI withdrawal symptoms included feeling depressed if I was in a dark room and not outside in sunlight. The withdrawal symptoms subsided after the first week.
Beginning with a low, gradual, dose allowed tolerance to the lower serotonin levels to build up in an orderly fashion.
It was crucial to ALWAYS take shilajit with a meal that included meat because the tryptophan in meat kept serotonin levels from dropping too low.
I could also have used fulvic acid or collagen to reduce serotonin.
If using fulvic acid keep in mind it cannot be applied in pure form to the mouth because it is acidic. Instead a few drops (3 to 5) need to be diluted in water and drunk.
There is a concern that diluting fulvic acid in tap water (or taking shilajit capsules with tap water) could cause the fulvic acid to react with chlorine to create a toxic substance.
However, chlorinated water has only trace amounts of chlorine so I took shilajit with only a small sip of tap water.
Because shilajit contains minerals taken from the Himalayas I used EDTA after I stopped using shilajit to chelate any heavy metals that might not have been removed from the processing of shilajit, although I suspect heavy metals were largely removed in the processing operations because shilajit is not naturally standardized to 20% fulvic acid.
Hydrolized collagen can also be used to lower serotonin.
I STRONGLY RECOMMEND using collagen as follows for most people who want to lower somewhat elevated serotonin levels because collagen is better studied than shilajit.
I recommend collagen for anyone who took 5-HTP with the protocol, even if they have no symptoms of excess serotonin, as a precaution.
I also recommend collagen for anyone with signs of mild serotonin excess and who has not used 5-HTP because serotonin has a number of negative side effects even at slightly elevated levels.
Ideally, serotonin levels should be slightly below average to moderately below average, although not reduced to an extreme level.
Collagen should be taken on an empty stomach in the morning 1 to 2 hours before a meal with meat to lower serotonin. If collagen is taken with a meal it will not reduce collagen.
It is important to take a meal with meat 1 to 2 hours later so meat provides enough tryptophan to prevent collagen from dropping serotonin levels too low.
Remember that your system will adjust best with a gradual lowering of serotonin.
This is not recommended for those who need higher levels of serotonin.
For those with no obvious signs of excess serotonin this protocol should be used only occasionally to improve mood and creativity, and not excessively.
If you are unsure if your serotonin levels are high I recommend going to a Labcorp and asking for a urine test for serotonin's metabolite, 5-H1AA, to check.
I recommend doing this even if you have to pay out of pocket and setup a urine test appointment yourself because doctor's might be reluctant to run a test that would implicate a major cashcow for the pharmaceuticals, namely SSRIs, which have been shown to be no better than placebos 50% of the time at reducing depression, and which have a number of negative side effects.
Serotonin Antagonists
https://www.longecit...in-antagonists/
Shilajit is found to protect against serotonin induced cognitive deficits by rapidly depleting serotonin activity; especially in the Hippocampus. This is also a proposed mechanism by which Shilajit rejuvenates normal libido / sexual function.
Pharmacokinetics of acute tryptophan depletion using a gelatin-based protein in male and female Wistar rats
https://pubmed.ncbi....h.gov/18683016/
The essential amino acid tryptophan is the precursor of the neurotransmitter serotonin. By depleting the body of tryptophan, brain tryptophan and serotonin levels are temporarily reduced. In this paper, several experiments are described in which dose and treatment effects of acute tryptophan depletion (ATD) using a gelatin-based protein-carbohydrate mixture were studied in male and female Wistar rats. Two or three doses of tryptophan depleting mixture resulted in 65-70% depletion after 2-4 h in males. ATD effects were similar in females, although females may return to baseline levels faster. Treatment effects after four consecutive days of ATD were similar to the effects of 1 day of treatment. Object recognition memory was impaired 2, 4, and 6 h after the first of two doses of ATD, suggesting that the central effects occurred rapidly and continued at least 6 h, in spite of decreasing treatment effects on plasma tryptophan levels at that time point. The method of acute tryptophan depletion described here can be used to study the relationship between serotonin and behaviour in both male and female rats.
Part 2 - Upregulate beta receptors with the beta blocker propranolol to halt anxiety attacks and upregulate beta receptors (Note that I originally did Part 3 before Part 2, but I would have been better off doing Part 2 and then doing Part 3. The current order of the protocol in this thread is what I would have done in retrospect).
Because of periodic anxiety attacks and because serotonin's overactivation of adrenaline probably downregulated my beta adrenoreceptors/adrenergic receptors I had my doctor prescribe propranol to block adrenaline's action and upregulate the beta receptors.
I used 10-20 mgs of propranol a day for a month. Then I tapered off propranolol by taking 10 mgs every other day for two weeks and then 10 mgs once a week for two weeks.
It is important to taper off beta blockers gradually because the heart can become dependent on them to a point where suddenly withdrawing from them could cause a heart attack, or other heart problems.
While on propranolol I went to places where I had anxiety attacks to "unlearn" the fear response.
This proved effective because I could go anywhere I wanted as needed so long as I was on propranol.
I also noticed that eating meat and protein became normal again, apparently because increased adrenaline and adrenaline rush "flight or fight" responses interfere with the GI tracts ability to absorb food.
Therefore, propranolol's blockade of beta receptors prevented adrenaline from interfering with eating.
Part 3 - Reduce blood pressure with Omega 3 from eating salmon.
After finishing with shilajit I ate 6 ounces of salmon, once a week, for two weeks to lower blood pressure because Omega 3 reduces aldosterone which is the main hormone that regulates sodium retention in the kidneys.
Before April of this year my blood pressure was normally 108/78 at rest.
But 5-HTP raised it to around 125 to 135 / 82 to 92.
SSRIs (both pharmaceutical and "natural" like 5-HTP or St. Johns Wart) have been implicated in the creation of cardiovascular disease because their downregulation of serotonin receptors causes disruption of cardiovascular function and releases of adrenaline that downregulate beta receptors.
Omega 3 was surprisingly effective after eating salmon once a week for two weeks.
By the second week my resting blood pressure dropped to 105-112 / 70-75, which was better than it was before this started in April.
Omega 3 also completely eliminated intestinal bloating and abdominal cramping, for some reason.
I also hoped that Omega 3 would reduce anxiety attacks caused by serotonin raising adrenaline levels but I found that Omega 3, for some reason, increased anxiety (perhaps I should have done part 3 before part 2).
Long-term antidepressant use may double the risk of heart disease
https://www.bristol....sant-study.html
Using data from UK Biobank, a large-scale biomedical database and research resource containing anonymised genetic, lifestyle and health information from half a million UK participants, the team linked comprehensive health data with prescription and disease data (using GP records) on 222,121 adults aged between 40 to 69-years old.
They compared the risk of developing adverse health outcomes between those who had not taken antidepressants and those who had been treated with the most commonly prescribed antidepressants in England over ten years. These were categorised by drug class as selective serotonin reuptake inhibitors often known as SSRIs, called citalopram, sertraline, fluoxetine and paroxetine and ‘other’ non-SSRI antidepressants called mirtazapine, venlafaxine, duloxetine and trazodone.
The researchers found that, once pre-existing risk factors had been taken into account, long-term antidepressant use was associated with an increased risk of coronary heart disease, and an increased risk of death from cardiovascular disease and from any cause. The risks were greater for non-SSRI antidepressants (mirtazapine, venlafaxine, duloxetine, trazodone), with the use of such drugs associated with a two-fold increased risk of coronary heart disease, cardiovascular mortality, and all-cause mortality at ten years.
Can Serotonin Cause High Blood Pressure / Hypertension ? (Serotonin causing High Blood Pressure)
https://area1255.blo...d-pressure.html
Serotonin is implicated in a number of cross-reactions in the nervous system, and there are serotonin receptors located directly in/on the heart/atrium. Increased activity of the serotonin receptors 5-HT2B and 5-HT4 is shown on failing hearts. (3) (4)
As such , chemicals/drugs that block these two serotonin receptors are being investigated/trialed for the treatment of those with various forms of heart disease. (5) (6)
Namely, right ventrical heart failure (5-HT2B) and congestive heart failure (CHF) along with tachycardia (5-HT4).
In addition to central heart failure, serotonin itself is dangerous in moderately-elevated to substantially elevated amounts, high plasma serotonin levels are found to cause primary pulmonary hypertension (7) (8) (9).
Additionally, serotonin is found to , along with adrenaline, mediate stress-induced increases in systolic blood pressure, which essentially means that serotonin is about half of the reason why blood pressure can go up in response to stress(10) (11). Part of this has to do with the serotonin induced accumulation of ALDOSTERONE via 5-HT4 receptor activation(12).
This means that serotonin allows for sodium retention as well as excessive calcium ion influx via that receptor.
Finally, anabolic steroid use, especially that of nandrolone or progestin based steroids - leads to the (abnormal) downregulation of serotonin autoreceptors which then may lead to the direct enhancement of serotonin signaling at the 5-HT4 receptors - which may be a valid hypothesis or at the least, a contribution by AAS in heart failure/enlargement(13) (14) (15).
Omega-3 fatty acids and blood pressure
https://www.cambridg...8F95FFAAF5F44DF
Omega-3 appear to suppress aldosterone secretion compared to physiological stimulus such as angiotensin II, ACTH or K+. This effect may be related to changes in intracellular signal transduction, alterations in plasma viscosity or to a lower activity of angiotensin converting enzyme (ACE). ACE is the enzyme that transform angiotensin-I into angiotensin-II, that controls blood pressure and regulates body fluid volume by modulating renin-angiotensin-aldosterone system. The inhibition of this enzyme leads to reduce angiotensin-II production, producing vascular relaxation and reducing aldosterone secretion(Reference Fischer, Dechend, Qadri, Markovic, Feldt, Herse, Park, Gapelyuk, Schwarz, Zacharzowsky, Plehm, Safak, Heuser, Schirdewan, Luft, Schunck and Muller9). Besides, ω-3 PUFA have been linked to increase production of endothelial nitric oxide (eNO) in animal models, and on the other hand, the L-arginine-NO system increase PUFA metabolism(Reference Das10). In addition, EPA and DHA can inhibit proteinuria development, suppress hypertension in stroke-prone spontaneously hypertensive rats and prevent excessive growth of smooth muscle by inhibiting the transforming growth factor beta (TGF-β) synthesis(Reference Das10). Also, it has been reported that DHA promotes vascular smooth muscle apoptosis, perhaps because of a modulatory effect on the renin-angiotensin-aldosterone system. Thus, it has been suggested that through these two mechanisms, DHA help to prevent vascular wall fibrosis and secondary hypertension development
Omega-3 Fatty Acids and Cardiac Arrhythmias: Prior Studies and Recommendations for Future Research
https://www.ahajourn...naha.107.712984
Part 4 - Upregulate GABA and upregulate P450 in the liver using Culturelle Probiotic.
To further eliminate anxiety symptoms, for a month I took with meals two pills of Culturelle's Probiotic of lactobacillus rhamnosus to upregulate GABA receptors with Swanson's Prebiotic of FoS to feed the L. rhamnosus bacteria.
GABA receptors are responsible for suppressing both serotonin and adrenaline release and L. rhamnosus has been shown to upregulate GABA in rats.
L. rhamnosus also enhances serotonin transport systems (SERT) in the intestines (over 90% of serotonin is located in the GI tract). By activating SERT L. rhamnosus should reduce excessive interactions of serotonin with serotonin receptors, at least in the gut where most of serotonin is stored.
In order to further improve my digestive system I also took Culturelle to upregulate the P450 liver enzyme (and its related enzymes like CYP3) which is responsible for the liver processing medicines and other foods.
P450 was probably downregulated because of serotonin.
Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve
https://www.ncbi.nlm...les/PMC3179073/
GABA is the main CNS inhibitory neurotransmitter and is significantly involved in regulating many physiological and psychological processes. Alterations in central GABA receptor expression are implicated in the pathogenesis of anxiety and depression, which are highly comorbid with functional bowel disorders. In this work, we show that chronic treatment with L. rhamnosus (JB-1) induced region-dependent alterations in GABAB1b mRNA in the brain with increases in cortical regions (cingulate and prelimbic) and concomitant reductions in expression in the hippocampus, amygdala, and locus coeruleus, in comparison with control-fed mice. In addition, L. rhamnosus (JB-1) reduced GABAAα2 mRNA expression in the prefrontal cortex and amygdala, but increased GABAAα2 in the hippocampus. Importantly, L. rhamnosus (JB-1) reduced stress-induced corticosterone and anxiety- and depression-related behavior. Moreover, the neurochemical and behavioral effects were not found in vagotomized mice, identifying the vagus as a major modulatory constitutive communication pathway between the bacteria exposed to the gut and the brain. Together, these findings highlight the important role of bacteria in the bidirectional communication of the gut–brain axis and suggest that certain organisms may prove to be useful therapeutic adjuncts in stress-related disorders such as anxiety and depression.
Effect of Lactobacillus rhamnosus GG supernatant on serotonin transporter expression in rats with post-infectious irritable bowel syndrome
https://www.ncbi.nlm...les/PMC5776395/
The levels of SERT mRNA and protein in intestinal tissue were higher in rats treated with LGG-s than in control rats and PI-IBS rats gavaged with PBS during the whole study. Undiluted LGG-s up-regulated SERT mRNA level by 2.67 times compared with the control group by week 2, and SERT mRNA expression kept increasing later. Double-diluted LGG-s was similar to undiluted-LGG-s, resulting in high levels of SERT mRNA. Triple-diluted LGG-s up-regulated SERT mRNA expression level by 6.9-times compared with the control group, but SERT mRNA expression decreased rapidly at the end of the second week. At the first week, SERT protein levels were basically comparable in rats treated with undiluted LGG-s, double-diluted LGG-s, and triple-diluted LGG-s, which were higher than those in the control group and PBS-treated PI-IBS group. SERT protein levels in the intestine were also comparable in rats treated with undiluted LGG-s, double-diluted LGG-s, and triple-diluted LGG-s by the second and third weeks. SERT mRNA and protein levels in the brain had no statistical difference in the groups during the experiment.
CONCLUSION
LGG-s can up-regulate SERT mRNA and protein levels in intestinal tissue but has no influence in brain tissue in rats with PI-IBS.
Lactobacillus rhamnosus induces CYP3A and changes the pharmacokinetics of verapamil in rats
https://pubmed.ncbi....h.gov/34600097/
This report investigated the potential of gut microbiota-drug interactions between lactobacillus rhamnosus and verapamil via using wild type (WT) and Cyp3a1/2 knockout (KO) rats. In WT rats, administration of Lactobacillus rhamnosus for 14 days decreased systemic exposure of verapamil and increased its metabolite norverapamil in vivo, and resulted in gut microbiota-drug interactions. In Cyp3a1/2 KO rats, however, this interaction disappeared. Further studies found that Lactobacillus rhamnosus induced CYP3A activity and expression, and changed the composition of gut microbiota, thus changing the pharmacokinetics of verapamil. These results demonstrated the interaction between lactobacillus rhamnosus and verapamil, and indicated that the effect of gut microbiota on metabolic enzymes cannot be ignored.
Probiotic Administration Attenuates Myocardial Hypertrophy and Heart Failure After Myocardial Infarction in the Rat
https://www.ahajourn...lure.113.000978
Lactobacillus rhamnosus CNCM I-3690 decreases subjective academic stress in healthy adults: a randomized placebo-controlled trial
https://www.ncbi.nlm...les/PMC8824214/
Therapeutic Anti-Depressant Potential of Microbial GABA Produced by Lactobacillus rhamnosus Strains for GABAergic Signaling Restoration and Inhibition of Addiction-Induced HPA Axis Hyperactivity
https://www.ncbi.nlm...les/PMC9164062/
Dietary supplementation with Lactobacillus rhamnosus JB-1 restores brain neurochemical balance and mitigates the progression of mood disorder in a rat model of chronic unpredictable mild stress
https://www.scienced...271531720304899
Part 5 - Improving MAO function with the mitochondrial protocol (Still ongoing).
To further ensure anxiety attacks do not return I am still using my version of the mito protocol once a week to restore MAO function.
Like GABA, MAO has a central role in eliminating excess adrenaline.
Since MAO is embedded within mitochondria, restoring mito function has a direct role in correcting anxiety disorders that are related to MAO dysfunction.
Once a week I take 1 gram of nicotinamide and 20 mgs PQQ on fission days and 2 grams of dihydromyricetin and 20 mgs PQQ on fusion days.
Then the following week I use 750 mgs NMN and 20 mgs PQQ for fission days because NMN reaches muscle and blood vessel tissue effectively.
I will start adding 100 mgs fisetin and 500 mgs quercetin once every two weeks to clear out any senescent cells.
I am doing 1 cycle a week.
I am not using AKG right now for either fission or fusion days in case my system is sensitive to glutamate which AKG increases (although I do not believe I was suffering from glutamate toxicity because, if I was, propranolol wouldn't have been effective at preventing anxiety attacks).
An energetic view of stress: Focus on mitochondria
https://www.ncbi.nlm...les/PMC5964020/
Another important class of hormones released in response to certain stressors are catecholamines, particularly norepinephrine (NE) and epinephrine (E). Both are derived from the neurotransmitter dopamine, itself generated from the amino acid tyrosine. Interestingly, the biosynthetic enzymes involved in catecholamine degradation, the monoamine oxidases MAO-A and MAO-B are anchored to the outer mitochondrial membrane (Binda et al., 2011). Some reports also suggest that TH may be tethered to the mitochondrial surface (Wang et al., 2009; Baumann et al., 2016), although this may be tissue specific and inducible under certain conditions; more work is needed to examine this potential functional association of mitochondria with catecholamine synthesis and degradation.
https://www.quantama...ealth-20200810/
Although much of the evidence so far is preliminary, it points to a substantial connection. Mitochondria seem to be central to the very existence of a stress response, serving both as mediators of it and targets for the damage it can do. To some of the researchers involved in this work, the stress response even looks like a kind of coordinated action by mitochondria throughout the body that interacts with the neurological processing.
“I think mitochondria are underrated,” said Martin Picard of Columbia University’s Irving Medical Center in New York, whose laboratory has helped to pioneer this research. “They’re the chief executive organelle of the cell.” Now scientists can explore what the implications of the organelles’ importance might be for future therapies.
Part 6 - Returning to the C60 Protocol (To be done following the mito protocol).
I will eventually use my version of the C60 protocol again (without 5-HTP!) to fix any additional damage that may have been caused by excess serotonin but which was not cleaned up by the previous steps.
I especially want to use it repair any stress my blood vessels and arteries may have suffered during this time. Although tests by my doctor showed no heart or circulatory issues it is possible that some of the stress could be a problem if left untreated by the C60 protocol decades in the future, and which is something current technology could not detect this early on.
Part 7 - Maintenance longterm.
Alcohol also depletes serotonin in the brain. For maintaining optimal serotonin levels, I drink moderately 2 days a week on weekends to maintain the benefits of lower serotonin. However, doing more than that seems to negate the positive effects I have from collagen and shilajit because alcohol (unlike collagen and shilajit) also directly activates the dopamine and GABA systems.
Also, I find it takes 1 day after drinking to feel the creative effects from low serotonin again, possibly because the dopamine system which was stimulated by alcohol needs a small amount of time to upregulate the dopamine receptors after alcohol activation. In general, I find taking collagen on an empty stomach to provide immediate creative boosts, unlike alcohol.
I will use natural beta blockers like 70% dark chocolate and magnesium periodically to prevent beta receptors from downregulating again. I will also use Culturelle periodically to prevent GABA receptors from downregulating.
For anyone suffering from anxiety attacks caused by adrenaline surges it is probably better to consult with a doctor about getting a prescription for propranolol because its beta blocking effects upregulate beta receptors more rapidly across the entire body than natural beta blockers like dark chocolate and magnesium. A dose of 10 to 20 mgs propranolol a day for a month, followed by a gradual tapering off, should be enough to help most people.
Dark Chocolate Intake Buffers Stress Reactivity in Humans
https://www.scienced...735109714015836
To test whether dark chocolate consumption induced changes in stress hormone reactivity to acute psychosocial stress, we calculated general linear models with repeated measures while controlling for the pre-chocolate baseline of the respective stress hormone as covariate. Across all subjects, the TSST induced significant increases in cortisol, ACTH, epinephrine, and norepinephrine (all, p <0.001). The dark chocolate group showed a significantly blunted cortisol (interaction group-by-stress F(2.5/154.8) = 7.47, p <0.001, eta2 = 0.108, f = 0.35) (Fig. 1A) and epinephrine (interaction group-by-stress F(1.7/101.0) = 4.34, p = 0.021, eta2 = 0.066, f = .27) (Fig. 1B) reactivity to psychosocial stress compared to the placebo group. Additional controlling for age, BMI, and MAP did not significantly change these results (interaction group-by-stress cortisol: F(2.6/155.6) = 6.59, p = 0.001, eta2 = 0.100, f = 0.33; epinephrine: F(1.8/101.8) = 4.06, p = 0.025, eta2 = 0.065, f = 0.26). There were no group differences in terms of ACTH or norepinephrine stress reactivity (all, p > 0.26).
Edited by Kelvin, 31 May 2024 - 01:00 AM.
