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Stem cell self-renewal with C60

c60 stem cells mitochondria fusion stearic acid aging hydroxytyrosol olive oil mct oil proliferation

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#2461 Kelvin

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Posted 27 September 2023 - 07:22 PM

Some improvements may be slower to take shape than others because different types of cells can last years or decades before they need to be replaced. 
 

For example I have seen a gradual improvement in my nearsightedness that only recently became noticeable when I realized I could see license plates of parked cars and signs across the street more clearly than before. 
 

And I have tried every other eyesight supplement over the years to reverse my myopia from lutein to lycopene and dozens of other supplements. 
 

But nothing else was able to accomplish this except this protocol. 



#2462 Kelvin

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Posted 27 September 2023 - 07:39 PM

In this video Michael Lustargten discusses which of the epigenetic tests have the strongest relationship with all cause mortality. 
 

A good case could be made the DunedinPACE test is the best epigenetic predictor of all cause mortality 

 

https://michaellustg...um-dunedinpace/
 

 

 

Click HERE to rent this advertising spot for C60 HEALTH to support Longecity (this will replace the google ad above).

#2463 njurkovi

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Posted 27 September 2023 - 10:38 PM

Kelvin,

My health was/is decent - usual problems for this age (enlarged prostate,  cholesterol, somewhat overwieght), but nothing extremely out of range. I lift weights (I think above average strength for my age), but do very little aerobics due to a hip related problem. Generally I feel "good".



#2464 Kelvin

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Posted 27 September 2023 - 11:29 PM

Have you noticed any changes in weight, muscle tone, strength, or changes to your physical exam results compared to last year?



#2465 njurkovi

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Posted 28 September 2023 - 01:08 AM

I noticed a slight increase in strength after I did the mitohondrial protocol (prior to stem cell renewal).

I haven't had a physical after the protocol (will have one in a month or so)

I did not notice any other changes, except MAYBE a slight change in vision (I forgot to mention this in my initial post, thanks for prompting me with questions).

It is very hard to tell if this is real or not because I suffer a lot from allergies that effect my eyes, so my vision goes kind of up and down all the time.

The best way to put it is - I think that I am able to read a restaurant receipt (without glasses) somewhat more frequently than before (this has always been my 'borderline' test case)



#2466 togian

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Posted 30 September 2023 - 08:46 PM

And I have tried every other eyesight supplement over the years to reverse my myopia from lutein to lycopene and dozens of other supplements. 

OT: you might want to look into eye exercise from ZHDANOV (works like a charm for most people I know (including me - going from a "3+" to 0 and back up, if I do not do them regularly) to recover their eysight back to normal)

 

Greetings 

Togian



#2467 Kelvin

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Posted 01 October 2023 - 10:57 PM

OT: you might want to look into eye exercise from ZHDANOV (works like a charm for most people I know (including me - going from a "3+" to 0 and back up, if I do not do them regularly) to recover their eysight back to normal)

 

Greetings 

Togian

In the past I looked into eye exercises to treat myopia but most of the exercises were behind a paywall so I never tried them. 



#2468 FWP

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Posted 04 October 2023 - 06:39 PM

Metformin appears to be a strong senolytic. My own recent experience with 500 mg (for blood sugar) was fatigue and strong flu like symptoms the first day, which declined on days 2-3, and disappeared thereafter, even with three times the dose. This for me is typical of senolytics. Once the senescent cells are disposed of, it can take a while for them to build up again. It may also be a good idea to alternate senolytics, as their effectiveness in different tissues will likely vary.

Note that some researchers (eg, this paper) worry that removing cells with senolytics can deplete stem cells that are called on for replacements. This objection is eliminated by the occasional use of C60 + fusion.


Did you develop blood sugar issues recently, did the mito protocol help with this?

#2469 Turnbuckle

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Posted 04 October 2023 - 07:05 PM

Did you develop blood sugar issues recently, did the mito protocol help with this?

 

The blood sugar issue came with a second bout of shingles, which was even worse than the first one as it produced a lot of inflammation. I believe the inflammation and high blood sugar are linked. I now have the shots, so I hope I won't get it again.



#2470 Kelvin

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Posted 06 October 2023 - 11:15 PM

Good Quality C60 should cause a “peppery” sensation in the back of the throat.

But how do we tell if C60 has gone bad?

By color or smell?

Edited by Kelvin, 06 October 2023 - 11:16 PM.

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#2471 joesixpack

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Posted 07 October 2023 - 10:14 PM

Good Quality C60 should cause a “peppery” sensation in the back of the throat.

But how do we tell if C60 has gone bad?

By color or smell?

The burning sensation in the back of the throat is caused by special receptors that react to fresh, high quality Extra Virgin Olive Oil.


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#2472 Kelvin

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Posted 09 October 2023 - 10:52 PM

 
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
 
 
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
 
 
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
 
 
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
 
 
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 - Reduce blood pressure with Omega 3 from eating salmon (Note it might have been better if I  done Part 3 before Part 2.  See Part 3 below for more information).
 
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
 
 
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)
 
 
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
 
 
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
 
 
 
Part 3 - Upregulate beta receptors with the beta blocker propranolol to halt anxiety attacks and upregulate beta receptors.
 
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 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
 
 
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
 
 
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
 
 
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
 
 
Lactobacillus rhamnosus CNCM I-3690 decreases subjective academic stress in healthy adults: a randomized placebo-controlled trial
 
 
Therapeutic Anti-Depressant Potential of Microbial GABA Produced by Lactobacillus rhamnosus Strains for GABAergic Signaling Restoration and Inhibition of Addiction-Induced HPA Axis Hyperactivity
 
 
 
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
 
 
 
 
 
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
 
 
 
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.
 
 
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.
 
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
 
 
 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, 09 October 2023 - 10:55 PM.

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#2473 Empiricus

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Posted 15 October 2023 - 11:38 AM

Kelvin, you wrote:

 

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.

 

Reading this reminded me of the one time I took St. John's Wort with the protocol.  What an awful experience. Here's the description I posted  of what followed:

 

1st Cycle - I added Saint John's Wort (2 capsules) to the C60 mix. Waited only 1.5 hours between the glycerol monostearate hot chocolate and C60.  I think I looked healthier the next day, but I felt rather spaced-out for several days. Memory poor. When writing, my words came out a little jumbled. Also, I inexplicably sprained my little toe while watching my step very carefully. My eyesight seemed worse than usual. For fission, I used N+R for two days, but nothing else.  My energy was quite low generally throughout this cycle.

 

 

You have me wondering if excess serotonin might explain any of those side-effects. What do you think, Kelvin?


Edited by Empiricus, 15 October 2023 - 11:47 AM.


#2474 Kelvin

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Posted 15 October 2023 - 06:11 PM

Kelvin, you wrote:

 

 

Reading this reminded me of the one time I took St. John's Wort with the protocol.  What an awful experience. Here's the description I posted  of what followed:

 

 

You have me wondering if excess serotonin might explain any of those side-effects. What do you think, Kelvin?

 

It is possible this was serotonin induced because you reacted negatively to SAM-e on the 3rd cycle. 
 

If you still have some side effects try taking 500 mgs of collagen once every 3 days to a week  on an empty stomach 1 hour before eating a meal with meat. 

Then try gradually  increasing the frequency of how often you take collagen on an empty stomach 1 hour before eating.  When taken on an empty stomach collagen depletes tryptophan levels in the gut which then drops overall serotonin levels. 

 

If you still have slightly elevated serotonin you should notice some mild symptoms of SSRI withdrawal such as feeling depressed if you don’t see sunlight (the side effects will be stronger for someone with more substantially downreegulated serotonin receptors).

 

in either case, introduce collagen gradually to let your system adjust, unless you have high levels of serotonin which require immediate emergency assistance from an ER. 

Short of an serotonin syndrome emergency, the withdrawal effects will be temporary as your system adjusts to Upregulate your serotonin receptors. For me, symptoms of SSRI withdrawal ended 1 week after using Shilajit daily and I didn’t need shilajit anymore after a month. 

 

I would also drop SAM-e from the protocol as a precaution although I think it may not have an effect for most people if they aren’t using some other SSRI since AKG in the protocol should deplete SAM-e of methyl groups. 

 

I do believe I had some mild level of elevated serotonin years before I started either the mito protocol or the C60 protocol because, before I tried them, I had been using more supplements for various health reasons. 

For example I have been using SAM-e to support my liver  years before I tried Turbuckles C60 and mito protocols. 
 

Using a variety of supplements probably raised my serotonin levels slightly because I had noticed what could be called slight anhedonia. 
 

The signs of mild anhedonia were subtle for years but I did notice over the years subtle changes like a decrease in my sense of humor or response to movies I thought were funny, and decrease in creativity, which I tried to fix with more supplements, to no avail. 

I only now notice this mild anhedonia clearly in retrospect because of the serotonin receptor upregulating protocol I created out of necessity.

 

Now that I have Upregulated my serotonin receptors the emotional improvement is remarkable!

 

My creativity is back and my emotional responses to pleasant stimuli are more intense, and I feel more motivated. My sense of smell, which was never good, is enhanced. 
 

this is because downregulated serotonin receptors causes the serotonin system to suppress dopamine, which is the real happinesss and motivational neurotransmitter. 
 

Furthermore, the emotional improvement is not like an artificial high from drugs or alcohol stimulating dopamine. 

 

Instead it feels perfectly natural because it is very “situational” in the sense I only feel happy in situations where I should be happy. Otherwise, if not exposed to pleasant stimulus, and just doing routine things I feel just neutral in a calm, normal, way. 

If you don’t notice any cognitive changes one way or other from collagen in  3 weeks then your neuro receptors are probably in balance (or, at least, you have no problem with serotonin) and you don’t need to take further action. 


Edited by Kelvin, 15 October 2023 - 06:46 PM.

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#2475 Kelvin

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Posted 15 October 2023 - 06:23 PM

It might also be a good idea to lower AKG to just 500 mgs on the fusion day because AKG can increase glutamate. I suspect I did not have excess glutamate stimulation because, otherwise, propranolol would not have been effective reducing glutamate because propranolol only blockades beta adrenal receptors.  But it would be better to reduce AKG just as a precaution because of the protocols apparent ability to Upregulate/downregulate receptors quickly. 

 

it also might be a good idea to change the lysine methionine ratio from 1:1 to 2 mgs lysine for every 1 mg of methionine because methionine could convert to SAM-e, although only a portion of it would and most of the methionine should be consumed by the “baby” stem cells created by the protocol. 
 

 


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#2476 Kelvin

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Posted 15 October 2023 - 06:34 PM

For serotonin induced anxiety by serotonin’s increasing adrenaline and, thus, adrenaline downegulating beta receptors, getting a prescription for propranolol and taking a small dose of 10-20 mgs a day, followed by a gradual tapering off,  is highly recommended because it blockades Upregulate beta receptors across the entire body. 
 

If your doctor won’t prescribe it for any reason EXCEPT that you have a health condition that would make taking propranolol dangerous for you then fire the doctor and get one who will prescribe it for anxiety. 
 

And whatever you do, do NOT let a doctor trick you into treating anxiety with the pharmaceutical poison known as benzos because, except for VERY short term usage of benzos, they will downregulate GABA receptors (which inhibit serotonin and adrenaline release) and cause such damage to the GABA system that it causes severe withdrawal complications. 
 

It is actually easier to restore/Upregulate the GABA receptors of alcoholics than it is to restore GABA function in former benzo victims/patients. 
 

If you don’t recognize the name of a recommended anxiety drug, check online that it is not a brand of benzo. If it is, get a new doctor immediately because the one you have is a quack. 
 

for the vast majority of anxiety cases low dose propranolol for a month or two should be sufficient to get your situation under control. 
 

after that you can try Culturelle probiotic to further Upregulate GABA receptors, which will inhibit adrenaline and serotonin, although it also inhibits dopamine. 
 

The mitochondrial protocol should also help anxiety too because MAO is embedded within mitochondria, although I don’t recommend the mito protocol until doing propranolol and Culturelle first because when I tried it earlier the increase in NAD seemed to increase adrenaline. 


Edited by Kelvin, 15 October 2023 - 06:51 PM.

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#2477 Empiricus

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Posted 15 October 2023 - 08:07 PM

It is possible this was serotonin induced because you reacted negatively to SAM-e on the 3rd cycle. 
 

If you still have some side effects try taking 500 mgs of collagen once every 3 days to a week  on an empty stomach 1 hour before eating a meal with meat. 

Then try gradually  increasing the frequency of how often you take collagen on an empty stomach 1 hour before eating.  When taken on an empty stomach collagen depletes tryptophan levels in the gut which then drops overall serotonin levels. 

 

If you still have slightly elevated serotonin you should notice some mild symptoms of SSRI withdrawal such as feeling depressed if you don’t see sunlight (the side effects will be stronger for someone with more substantially downreegulated serotonin receptors).

 

in either case, introduce collagen gradually to let your system adjust, unless you have high levels of serotonin which require immediate emergency assistance from an ER. 

Short of an serotonin syndrome emergency, the withdrawal effects will be temporary as your system adjusts to Upregulate your serotonin receptors. For me, symptoms of SSRI withdrawal ended 1 week after using Shilajit daily and I didn’t need shilajit anymore after a month. 

 

I would also drop SAM-e from the protocol as a precaution although I think it may not have an effect for most people if they aren’t using some other SSRI since AKG in the protocol should deplete SAM-e of methyl groups. 

 

I do believe I had some mild level of elevated serotonin years before I started either the mito protocol or the C60 protocol because, before I tried them, I had been using more supplements for various health reasons. 

For example I have been using SAM-e to support my liver  years before I tried Turbuckles C60 and mito protocols. 
 

Using a variety of supplements probably raised my serotonin levels slightly because I had noticed what could be called slight anhedonia. 
 

The signs of mild anhedonia were subtle for years but I did notice over the years subtle changes like a decrease in my sense of humor or response to movies I thought were funny, and decrease in creativity, which I tried to fix with more supplements, to no avail. 

I only now notice this mild anhedonia clearly in retrospect because of the serotonin receptor upregulating protocol I created out of necessity.

 

Now that I have Upregulated my serotonin receptors the emotional improvement is remarkable!

 

My creativity is back and my emotional responses to pleasant stimuli are more intense, and I feel more motivated. My sense of smell, which was never good, is enhanced. 
 

this is because downregulated serotonin receptors causes the serotonin system to suppress dopamine, which is the real happinesss and motivational neurotransmitter. 
 

Furthermore, the emotional improvement is not like an artificial high from drugs or alcohol stimulating dopamine. 

 

Instead it feels perfectly natural because it is very “situational” in the sense I only feel happy in situations where I should be happy. Otherwise, if not exposed to pleasant stimulus, and just doing routine things I feel just neutral in a calm, normal, way. 

If you don’t notice any cognitive changes one way or other from collagen in  3 weeks then your neuro receptors are probably in balance (or, at least, you have no problem with serotonin) and you don’t need to take further action. 

 

Nice catch regarding the "sam-e on the 3rd cycle." The connection had never occurred to me.

 

I recently began taking sam-e outside of the protocol. It seems to have positive mental effects. Would you recommend I discontinue using sam-e as a daily supplement?  Do you think it's asking for trouble?

 

I have been experiencing what might be referred to as slight anhedonia, usually hitting later in the day.  It may be that drinking coffee in the morning covers it up.

 

It's been 9 months since I completed a Turnbuckle protocol with sam-e.  I had begun using it with every protocol, so it might explain the recurring unpleasant symptoms was experiencing with the protocol. In the meantime I suffered a concussion and also likely aflatoxin exposure.

 

Thank you for the step-by-step guide to recovery using collagen. I took large amounts of glycine daily during May and June--well after pausing the protocol--but not as collagen.  Now I will go buy some collagen and begin taking it as you have instructed. 


Edited by Empiricus, 15 October 2023 - 08:16 PM.


#2478 Kelvin

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Posted 15 October 2023 - 08:28 PM

 

I recently began taking sam-e outside of the protocol. It seems to have positive mental effects. Would you recommend I discontinue using sam-e as a daily supplement?  Do you think it's asking for trouble?

 

I have been experiencing what might be referred to as slight anhedonia, usually hitting later in the day.  It may be that drinking coffee in the morning covers it up.

 

I would drop SAM-e until you’ve tested collagen for a few weeks.  If you have a positive response to collagen after a few weeks then SAM-e was probably keeping your serotonin levels elevated to a certain degree. For quality of life reasons people are generally better off with serotonin levels moderately below average. 
 

Definitely keep SAM-e out of the C60 protocol going forward. If you need to restore methyl groups after either the C60 or mito protocols have 1 gram of betaine, not SAM-e, for two or three days to remethylate after you’ve finished the protocols for a few days. 

 

But don’t take any methyl donors during either protocol, especially the C60 protocol, because methyl donors can partially convert to SAM-e. 
 

Coffee is good, so long as you don’t have anxiety problems, because it upregulates serotonin’s 5-HT1 autoreceptors.  This autoreceptor helps decrease serotonin production when it gets too high. 
 

Only avoid coffee if you anxiety because anxiety’s release of adrenaline will downregulate the beta receptors from excess adrenaline stimulation. Coffee downregulates beta receptors. 
 

https://www.ncbi.nlm...les/PMC3437321/
 

1. Chronic ingestion of caffeine by male NIH strain mice alters the density of a variety of central receptors.

2. The density of cortical A1 adenosine receptors is increased by 20%, while the density of striatal A2A adenosine receptors is unaltered.

3. The densities of cortical β1 and cerebellar β2 adrenergic receptors are reduced by ca. 25%, while the densities of cortical α1 and α2 adrenergic receptors are not significantly altered. Densities of striatal D1 and D2 dopaminergic receptors are unaltered. The densities of cortical 5 HT1 and 5 HT2 serotonergic receptors are increased by 26–30%. Densities of cortical muscarinic and nicotinic receptors are increased by 40–50%. The density of cortical benzodiazepine-binding sites associated with GABAA receptors is increased by 65%, and the affinity appears slightly decreased. The density of cortical MK-801 sites associated with NMDA-glutaminergic receptors appear unaltered.

4. The density of cortical nitrendipine-binding sites associated with calcium channels is increased by 18%.


Edited by Kelvin, 15 October 2023 - 08:31 PM.

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#2479 Kelvin

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Posted 15 October 2023 - 10:02 PM

Collagen will not Upregulate serotonin receptors unless taken on an empty stomach. If you have already eaten taking collagen will not work. 


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#2480 Empiricus

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Posted 16 October 2023 - 08:09 AM

Been doing some research on serotonin and dizziness, because dizziness was such a prominent side-effect of the protocol on recent cycles immediately following T1.  For example, here's an account I posted September 2022: 

 

About an hour later, when I got up I experienced dizziness and had to lie down.  I got up a second time time, and still felt dizzy so went to bed.  In the morning my thinking was fuzzy, as in not very sharp.  I suspect these symptoms are related to the dihydromyricetin, because on many previous occasions I have tolerated large doses of GMS just fine.  

 

I would have taken sam-e on that occasion, likely 400mg, along with AKG (as much as 3-4 g) and of course the methionine.  It seems dizziness is a very common symptom in mild serotonin toxicity. https://pubmed.ncbi....h.gov/20144124/

 

Dizziness is the most commonly reported symptom of abrupt discontinuation from the selective serotonin reuptake inhibitor (SSRI) category of antidepressants. The reported dizziness is exacerbated by even slight head movement, and therefore is likely to be vestibular in origin. The SSRIs most implicated are those with short half-lives and which are most selective for serotonin (as opposed to noradrenaline), e.g. paroxetine and sertraline.

 

The half-life of sam-e is only 100 minutes. Prior to consuming sam-e, I crushed the hard tablet into powder form.    


Edited by Empiricus, 16 October 2023 - 08:28 AM.


#2481 Kelvin

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Posted 17 October 2023 - 01:12 AM

Been doing some research on serotonin and dizziness, because dizziness was such a prominent side-effect of the protocol on recent cycles immediately following T1. For example, here's an account I posted September 2022:


I would have taken sam-e on that occasion, likely 400mg, along with AKG (as much as 3-4 g) and of course the methionine. It seems dizziness is a very common symptom in mild serotonin toxicity. https://pubmed.ncbi....h.gov/20144124/


The half-life of sam-e is only 100 minutes. Prior to consuming sam-e, I crushed the hard tablet into powder form.

Those are symptoms of ending use of SSRI.

Side effects of SSRIs while using them are frequently loss of appetite, high sensitivity and anxiety to lights and slight sounds, anhedonia, and loss of sex drive (in men this can be indicated by some sense of depression after orgasm because increases in serotonin also lead to increases in prolactin, which controls the refractory response in men).

It’s amazingly criminal they sell SSRIs with these kinds of cognitive side effects as “mental health” drugs!

Even among those who have negligible serious side effects from SSRIs they rarely see improvements in depression from them.

Studies have shown 50% of the time they are no better than placebos.

For the 34% who do mentally benefit they might have gotten the same effect by increasing their meat consumption to raise their dietary tryptophan intake.

The surprisingly high ineffectiveness rate of SSRIs relative to placebos is because serotonin is more of a “tranquilizing” neurotransmitter that keeps others from getting too high, but it is not a happiness neurotransmitter.

The real happiness and motivational neurotransmitter is dopamine, but serotonin in above average levels suppresses dopamine activity.

Edited by Kelvin, 17 October 2023 - 01:22 AM.

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#2482 Kelvin

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Posted 17 October 2023 - 01:17 AM

By the way, on second thought you should skip coffee while using collagen.

Although coffee Upregulates 5-HT1 receptors using collagen by itself is better because that way, whether you respond positively or negatively to collagen, we will know collagen was the cause and not coffee.

Avoid other stimulants and supplements as well just to be sure only collagen’s effect is being tested.

Edited by Kelvin, 17 October 2023 - 01:18 AM.

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#2483 Kelvin

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Posted 17 October 2023 - 01:42 AM

Look at this beauty from the Netherlands!

 

Between SSRIs, benzos, statins, opioid prescriptions, and marijuana legalization (weed downregulates GABA hence anxiety disorders from chronic marjuana usage) I am half expecting mainstream medicine to recommend fentanyl prescriptions for recreational use. 
 

 

SSRI Use During Pregnancy Alters the Child’s Brain Development

Reduced brain volumes due to SSRI exposure in pregnancy was not explained by maternal depression alone.

 

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.
 

To account for factors such as the effect of underlying maternal depression and when, specifically, the mothers used antidepressants, the researchers split the cohort into five groups. There were 41 with SSRI use during pregnancy, 77 who only used SSRIs before pregnancy, 257 who did not use SSRIs but had depressive symptoms during pregnancy, 74 who had depressive symptoms only after giving birth, and 2,749 controls who had neither depressive symptoms nor SSRI use.

 
According to the researchers, there was a “persistent association between prenatal SSRI exposure and less cortical volumes across the 10-year follow-up period, including in the superior frontal cortex, medial orbitofrontal cortex, parahippocampal gyrus, rostral anterior cingulate cortex, and posterior cingulate.” They add, “Prenatal SSRI exposure was consistently associated with lower volume, ranging from 5% to 10% in the frontal, cingulate, and temporal cortex across ages.”
 

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.

 

The good news is that some of these brain volume reductions appeared to have a catch-up effect: for instance, amygdala volumes had increased by age 15, so kids who were exposed to SSRIs were not any different from controls.

 

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.


Edited by Kelvin, 17 October 2023 - 01:50 AM.


#2484 Empiricus

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Posted 17 October 2023 - 03:42 AM

If you still have some side effects try taking 500 mgs of collagen once every 3 days to a week  on an empty stomach 1 hour before eating a meal with meat. 

 

Then try gradually  increasing the frequency of how often you take collagen on an empty stomach 1 hour before eating.  When taken on an empty stomach collagen depletes tryptophan levels in the gut which then drops overall serotonin levels. 

 

500 mg collagen sounds low.  You didn't mean to write 5000 mg?



#2485 Kelvin

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Posted 17 October 2023 - 03:49 AM

500 mg collagen sounds low. You didn't mean to write 5000 mg?


START at 500 mgs.

If you don’t notice an effect after a week or two increase to 1 gram.

5 grams might be too much to start with.

Better to start low and gradually increase because, if your serotonin receptors are down regulated more than you anticipate, your body needs time to get used to lower serotonin levels so the receptors can Upregulate.

But if you go too fast you could get more severe serotonin withdrawal symptoms and I can assure you they are not fun to deal with.

The body needs to gently get used to a change in neurotransmitter balance.

#2486 Kelvin

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Posted 17 October 2023 - 04:02 AM


https://www.longecit...in-antagonists/

Everything is a certain balance. Yet almost every serotonin receptor has either.

1.) Negative effect on Testosterone or other hormones. Including neurosteroids that have anxiolytic properties.
2.) Negative effects on dopamine and other neurotransmitters.

Most of all serotonin receptors will increase cortisol, ACTH etc...and in many cases , this causes adrenaline rush/issues which means serotonin just makes you more irritable, if not irritable then you will be NUMBED OUT, and have almost ZERO emotional capacity....this seems to come from excess HPTA inhibition and / or adrenal burnout from serotonin constantly releasing cortisol and dynorphins...beta-endorphin has positive effects under CERTAIN CIRCUMSTANCES, but having HIGH resting levels of b-endorphin encourages people to be lazy and watch TV all day. (example

#2487 Turnbuckle

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Posted 23 October 2023 - 07:20 PM

Kelvin, you wrote:

 

 

Reading this reminded me of the one time I took St. John's Wort with the protocol.  What an awful experience. Here's the description I posted  of what followed: 1st Cycle - I added Saint John's Wort (2 capsules) to the C60 mix. Waited only 1.5 hours between the glycerol monostearate hot chocolate and C60.  I think I looked healthier the next day, but I felt rather spaced-out for several days. Memory poor. When writing, my words came out a little jumbled. Also, I inexplicably sprained my little toe while watching my step very carefully. My eyesight seemed worse than usual. For fission, I used N+R for two days, but nothing else.  My energy was quite low generally throughout this cycle.

 

 

You have me wondering if excess serotonin might explain any of those side-effects. What do you think, Kelvin?

 

Note that stearic acid does not cross the BBB, and thus you would not get mito fusion in the brain.


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#2488 Kelvin

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Posted 24 October 2023 - 01:50 AM

Note that stearic acid does not cross the BBB, and thus you would not get mito fusion in the brain.

Neural stem cells would still develop asymmetrically because of C60 even though stearic acid can’t enter the brain.

So something in the protocol other than the fusion agent might have caused serotonin receptors to down regulate more rapidly than normal when combined with an SSRI or serotonin promoting agent like St Johns Wort.

Edited by Kelvin, 24 October 2023 - 01:51 AM.


#2489 labrat70

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Posted 27 October 2023 - 01:15 AM

It looks like the Samsara dihydromyricetin power (for the brownies) is no longer available.  Does anyone have an alternate recommendation, or conversely, some brands to avoid?  Thx.



#2490 Kelvin

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Posted 27 October 2023 - 10:13 PM

It looks like the Samsara dihydromyricetin power (for the brownies) is no longer available. Does anyone have an alternate recommendation, or conversely, some brands to avoid? Thx.

I see only two obscure brands for DHM powder on Amazon.

Not sure if they are good or bad, but I prefer to get supplies from brands that already have good reputations.

Edited by Kelvin, 27 October 2023 - 10:13 PM.






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