Low Basal NO/NOx Levels and Proposed Regimen

[BrongFogBoy]

Can someone please leave a link to the methylation protocol on this board where people are talking about it? I’ve been searching and only find threads where a few posts are made. I want to see other peoples experiences and educate myself more on this.

[BrongFogBoy]

@mariovitali

@elijah

Thanks Mario, the protocol is worth a try.
As for beet juice, I had an adverse effect with it and I try to avoid it because it’s a p450 inhibitor
http://www.ncbi.nlm.nih.gov/pubmed/22465004

Thanks elijah,

Indeed very interesting link. I do not know why i didn’t have adverse effects to BeetRoot.

I believe that fixing the NO/NOx path is way more important than P450 inhibition/induction. Nitric Oxide is a potent inhibitor of NMDA excitotoxicity which should be one of our top priorities. I cannot imagine of the so many neuronal structures (including HPA Axis) that get affected from excitotoxicity. Of course without NO there can be no erections.

Essentially, i couldn’t control the excitotoxicity at my NMDA Receptors. If i would take any supplement aimed to increase NO Production (L-Arginine, L-Citrulline) i would get tinnitus (=excitotoxicity - in my opinion) but when i started this regimen everything worked great.

Give it a try elijah, Good Luck.

Hey I want to be sure I avoid the excitotoxicity with this - do you remember what caused it in you? Was it just taking L-Citrulline? Do you remember what doses and anything you were taking along with it? Feel free to be as specific as you can, I want to steer clear because I do use l-citrulline for exercise and sometimes Arginine

[mariovitali]

@BrongFogBoy

Hey I want to be sure I avoid the excitotoxicity with this - do you remember what caused it in you? Was it just taking L-Citrulline? Do you remember what doses and anything you were taking along with it? Feel free to be as specific as you can, I want to steer clear because I do use l-citrulline for exercise and sometimes Arginine

I was getting tinnitus (which in my theory is caused by excitotoxicity) everytime i would try to increase NO through L-Arginine or L-Citrulline. Both of these supplements gave me tinnitus. Even when i had a (large) portion of Watermelon (contains L-Citrulline) i would then get tinnitus so this means that even a small dose of L-Citrulline/L-Arginine is giving me problems.

I’d suggest you to stop L-Arginine and L-Citrulline supplements and boost NO through the Nitrate Pathway (ie by eating rocket and spinach).

[BrongFogBoy]

What all are you taking at this time to boost NO mariovitali? Please include amounts daily

[mariovitali]

@BrongFogBoy

What all are you taking at this time to boost NO mariovitali? Please include amounts daily

Hey Guys,

It is my third day of being completely symptom-free. This may be because of the fact that the weather has been most of the time steady but there have been cases where wind picked up considerably and a similar event would have give me trouble previously.

The only “complaint” i have is that i am waking at 5:30 (±10 mins) from morning wood which at times is unbearable. Last night i had to get up and walk around the room so that it goes away and i can get back to sleep.

Another thing i noticed is that my g/f doesn’t need to perform manual stimulation so i can have an erection now. This is also a very encouraging fact.

I will try to write a summarized post on why i believe that NO/NOx is the root cause of our problems. Possibly BH4 (tetrahydrobiopterin) and VDR (Vitamin D receptor) are involved, Methylation is also involved but the main culprit is impaired NO/NOx production.

@BrongFogBoy

This is my current regimen (with dosages as requested )

Morning :

Ashwagandha 600 mg
Selenium 200mcg
Metafolin 800 mg
Trimethylglucine (TMG) 1000 mg
Vitamin D3 5000 IU (more on this later)
Vitamin C 1000 mg
Rocket 50 grams

Around 15:00
Rocket 50gr
ALCAR 1000 mg
CoQ10 100 mg

Night
Rocket 50gr
Magnesium 400 mg

You will note that i added Vitamin D3. In my opinion D3 is a very important part of the regimen as it helps NOS3 (endothelial NOS) production and regulates iNOS (inducible NOS which can cause problems). Note also that there is no P5P and most importantly no Methylcobalamin or any sort of Cobalamins to my regimen.

I had to add Vitamin D3 because holidays are over and i was in a very sunny place so there was no reason to supplement D3 at the time. @andyuk is going for holidays too so i strongly believe that he will feel better if he catches some sun. I think @xptriado is also on holidays so i look forward to what he will say as well.

[xptriado]

hi guys, sorry for the silence…i’ve had a gastroenterites, so im still recovering.
i’m not sure it’s already appropriate to eat to much rockets right now.
next week i’ll be on holiday…
i’m also kind of loosing hope again on this. i want to do more medical exams while on holidays.
if i start this regimen i’ll let you know…

[BrongFogBoy]

@mariovitali

@BrongFogBoy

What all are you taking at this time to boost NO mariovitali? Please include amounts daily

Hey Guys,

It is my third day of being completely symptom-free. This may be because of the fact that the weather has been most of the time steady but there have been cases where wind picked up considerably and a similar event would have give me trouble previously.

The only “complaint” i have is that i am waking at 5:30 (±10 mins) from morning wood which at times is unbearable. Last night i had to get up and walk around the room so that it goes away and i can get back to sleep.

Another thing i noticed is that my g/f doesn’t need to perform manual stimulation so i can have an erection now. This is also a very encouraging fact.

I will try to write a summarized post on why i believe that NO/NOx is the root cause of our problems. Possibly BH4 (tetrahydrobiopterin) and VDR (Vitamin D receptor) are involved, Methylation is also involved but the main culprit is impaired NO/NOx production.

@BrongFogBoy

This is my current regimen (with dosages as requested )

Morning :

Ashwagandha 600 mg
Selenium 200mcg
Metafolin 800 mg
Trimethylglucine (TMG) 1000 mg
Vitamin D3 5000 IU (more on this later)
Vitamin C 1000 mg
Rocket 50 grams

Around 15:00
Rocket 50gr
ALCAR 1000 mg
CoQ10 100 mg

Night
Rocket 50gr
Magnesium 400 mg

You will note that i added Vitamin D3. In my opinion D3 is a very important part of the regimen as it helps NOS3 (endothelial NOS) production and regulates iNOS (inducible NOS which can cause problems). Note also that there is no P5P and most importantly no Methylcobalamin or any sort of Cobalamins to my regimen.

I had to add Vitamin D3 because holidays are over and i was in a very sunny place so there was no reason to supplement D3 at the time. @andyuk is going for holidays too so i strongly believe that he will feel better if he catches some sun. I think @xptriado is also on holidays so i look forward to what he will say as well.

Thanks, as far as the NO production it’s pretty much just the Rocket, right? I’m going to grab a bunch of Rocket next time I’m out. Anyone tried using the beet juice yet?

[gefinauser]

Nah, mariovitali found an article stating that the NOS levels are possibly nonexistential in juices or canned beets (at least in storebought ones). Rocket is the way to go so far.

mariovitali, i wouldn’t had otherwise posted but you said that people would feel better when sun comes around. I have to report: i’m a very stubborn, nigh-nonexistential sexuality PFS case and I had my first introduction to proper sexuality about a week ago. Lot of my symptons were better and I had more hunger etc. I’m pr sure at this point that it was the sun. I haven’t really tried many supplements in overal as I know the rebound effects but on the other hand, I don’t really recover on my own/naturally to anywhere this level so it was really SOMETHING ELSE. It was just as someone in this forum said: that the positive rebound happened roughly a week after stopping having sunshine, after a long streak of hot sunny days.

I know the LH/FSH connection to sunlight but I guess you know a study stating there is a connection to NOS?

[mariovitali]

Thanks, as far as the NO production it’s pretty much just the Rocket, right? I’m going to grab a bunch of Rocket next time I’m out. Anyone tried using the beet juice yet?

Rocket is the best but not the only food you can try : Wild Radish is the next best option then Bok Choy, Beets, Spinach and Lettuce

I know the LH/FSH connection to sunlight but I guess you know a study stating there is a connection to NOS?

Yes there are many in Pubmed here is a couple from the list :

http://www.ncbi.nlm.nih.gov/pubmed/23816836

http://www.ncbi.nlm.nih.gov/pubmed/24284821

Pay particular importance to the following :

However, the pathophysiological mechanisms underlying these associations remain largely unexplained. In this study, we aimed to decipher the mechanisms by which 1,25(OH)2D3 may regulate systemic vascular tone and cardiac function, using mice carrying a mutant, functionally inactive vitamin D receptor (VDR). To normalize calcium homeostasis in VDR mutant mice, we fed the mice lifelong with the so-called rescue diet enriched with calcium, phosphate, and lactose. Here, we report that VDR mutant mice are characterized by lower bioavailability of the vasodilator nitric oxide (NO) due to reduced expression of the key NO synthesizing enzyme, endothelial NO synthase, leading to endothelial dysfunction, increased arterial stiffness, increased aortic impedance, structural remodeling of the aorta, and impaired systolic and diastolic heart function at later ages, independent of changes in the renin-angiotensin system. We further demonstrate that 1,25(OH)2D3 is a direct transcriptional regulator of endothelial NO synthase. Our data demonstrate the importance of intact VDR signaling in the preservation of vascular function and may provide a mechanistic explanation for epidemiological data in humans showing that vitamin D insufficiency is associated with hypertension and endothelial dysfunction.

FYI my DNA test from 23andme showed a heterozygous mutation on the VDR Receptor (apart from having a homozygous MTHFR mutation).

NO helps in keeping the endothelium , mitochondria and nervous system in good shape. If you let the endothelium to become damaged then this results on even less available NO (since an impaired endothelium cannot generate eNOS)

Can you see the vicious cycle here? In other words the more you wait, the more damage is being done and the more time you will have to supply with NO/NOx through the nitrate pathway to feel better again.

The role of nitric oxide on endothelial function.

The vascular endothelium is a monolayer of cells between the vessel lumen and the vascular smooth muscle cells. Nitric oxide (NO) is a soluble gas continuously synthesized from the amino acid L-arginine in endothelial cells by the constitutive calcium-calmodulin-dependent enzyme nitric oxide synthase (NOS). This substance has a wide range of biological properties that maintain vascular homeostasis, including modulation of vascular dilator tone, regulation of local cell growth, and protection of the vessel from injurious consequences of platelets and cells circulating in blood, playing in this way a crucial role in the normal endothelial function. A growing list of conditions, including those commonly associated as risk factors for atherosclerosis such as hypertension, hypercholesterolemia, smoking, diabetes mellitus and heart failure are associated with diminished release of nitric oxide into the arterial wall either because of impaired synthesis or excessive oxidative degradation. The decreased production of NO in these pathological states causes serious problems in endothelial equilibrium and that is the reason why numerous therapies have been investigated to assess the possibility of reversing endothelial dysfunction by enhancing the release of nitric oxide from the endothelium. In the present review we will discuss the important role of nitric oxide in physiological endothelium and we will pinpoint the significance of this molecule in pathological states altering the endothelial function.

http://www.ncbi.nlm.nih.gov/pubmed/22112350

[xptriado]

I second the VDR mutation and I also have some mutation related to NO. when ill be on holidays i will check the SNP since I can’t remember now

The VDR mutation, if it implies defective receptors, it means less dopamine is made. hence why my reactions to antidepressives and PLMD. Also explains prolactin in the upper third of the limit and epileptic crysis when I took Metoclopramide for digestive issues when a kid.
Appart from that it would explain why I can’t adapt to north countries and keep complaining about weather, sleep issues, mood issues…etc etc.
I will come back to this forum with a vitamin d analysis next week and i’m sure, even if i’m in portugal now, it will not be in 60-80ng/ml, thus my sleep problems.
I will also restart the rockets when my constipation is finished…

[BrongFogBoy]

Going along with the possibility that many of us have VDR mutations…are we thinking that finasteride caused the mutation or that we were born with it and finasteride made it more pronounced?

Is there a known way to resolve / reverse the mutation?

[mariovitali]

@BrongFogBoy

Going along with the possibility that many of us have VDR mutations…are we thinking that finasteride caused the mutation or that we were born with it and finasteride made it more pronounced?

Is there a known way to resolve / reverse the mutation?

The PFS foundation will probably be eligible to answer that after research is conducted. I am pretty sure that at present, we cannot reverse a gene mutation.

@xptriado

The VDR mutation, if it implies defective receptors, it means less dopamine is made

Everytime i crash i was under the impression that whatever Dopamine existed in my body was gone. Here is why :

Ascorbate (vitamin C) is a nonenzymatic antioxidant highly concentrated in the brain. In addition to mediating redox balance, ascorbate is linked to glutamate neurotransmission in the striatum, where it renders neuroprotection against excessive glutamate stimulation. Oxidative stress and glutamatergic overactivity are key biochemical features accompanying the loss of dopaminergic neurons in the substantia nigra that characterizes Parkinson’s disease (PD). At present, it is not clear whether antiglutamate agents and ascorbate might be neuroprotective agents for PD. Thus, we tested whether ascorbate can prevent cell death from prolonged exposure to glutamate using dopaminergic neurons of human origin. To this purpose, dopamine-like neurons were obtained by differentiation of SH-SY5Y cells and then cultured for 4 days without antioxidant (antiaging) protection to evaluate glutamate toxicity and ascorbate protection as a model system of potential factors contributing to dopaminergic neuron death in PD. Glutamate dose dependently induced toxicity in dopaminergic cells largely by the stimulation of AMPA and metabotropic receptors and to a lesser extent by N-methyl-D-aspartate and kainate receptors. At relatively physiological levels of extracellular concentration, ascorbate protected cells against glutamate excitotoxicity. This neuroprotection apparently relies on the inhibition of oxidative stress, because ascorbate prevented the pro-oxidant action of the scavenging molecule quercetin, which occurred over the course of prolonged exposure, as is also seen with glutamate. Our findings show the relevance of ascorbate as a neuroprotective agent and emphasize an often underappreciated role of oxidative stress in glutamate excitotoxicity. Occurrence of a glutamate-ascorbate link in dopaminergic neurons may explain previous contradictions regarding their putative role in PD.

http://alsanesthetics.org/research/solving-the-puzzle/source-material-collections/28-excitotoxicity

In other words : excitotoxicity destroys dopaminergic neurons. And this is why i hypothesize that when i took GABA i had anorgasmia. Too many GABA receptors, too low Dopaminergic neurons because of destruction from excitotoxicity.

Several important diseases of the nervous system are associated with dysfunctions of the dopamine system. Parkinson’s disease, a degenerative condition causing tremor and motor impairment, has been related to the loss of dopamine-secreting neurons in the midbrain area called the substantia nigra. There is evidence that schizophrenia involves highly altered levels of dopamine activity, and the antipsychotic drugs that are frequently used to treat it have a primary effect of attenuating dopamine activity. Attention deficit hyperactivity disorder (ADHD) and restless legs syndrome (RLS) are also believed to be associated with decreased dopamine activity.

Outside the nervous system, dopamine functions in several parts of the body as a local chemical messenger. In the blood vessels, it inhibits norepinephrine release and acts as a vasodilator; in the kidneys, it increases sodium excretion and urine output; in the pancreas, it reduces insulin production; in the digestive system, it reduces gastrointestinal motility and protects intestinal mucosa; and in the immune system, it reduces the activity of lymphocytes. With the exception of the blood vessels, dopamine in each of these peripheral systems has a “paracrine” function: it is synthesized locally and exerts its effects on cells that are located near the cells that release it.

http://en.wikipedia.org/wiki/Dopamine

Needless to say that i experienced RLS and ADHD numerous times previously. I bet my two cents that older people who experienced anorgasmia with Gabapentin (=GABA) had some previous loss of dopaminergic neurons :

Anorgasmia with gabapentin may be common in older patients.

CASE SUMMARY:

This report describes 4 older patients who experienced anorgasmia while taking gabapentin. Of 15 patients initiated on gabapentin in 18 months, 3 male patients aged 73, 76, and 78 years experienced dose-dependent anorgasmia. A fourth case, a 59-year-old female patient, was noted in another clinic. Orgasm returned when gabapentin was reduced or stopped. Although this is not a blinded study, anorgasmia in 3 of 15 patients newly initiated on gabapentin (3 of 11 in those aged >50 years) seems to represent a much higher incidence than the originally reported <1% in epilepsy clinical trials. Outside of erectile dysfunction, clinicians rarely ask older patients about sexual function.
CONCLUSION:

Gabapentin-associated anorgasmia may be more common in older patients and appears to be dose dependent.

http://www.ncbi.nlm.nih.gov/pubmed/21602106

So : Instead of supplying yourself with Levo-Dopa or drinking coffee to feel alive again, the first goal should be to stop excitotoxicity. And adequate Nitric Oxide production (but not through L-Arginine for some reason) is one of the best ways to achieve this (apart from antioxidants and methylation support)

[BrongFogBoy]

@mariovitali

So : Instead of supplying yourself with Levo-Dopa or drinking coffee to feel alive again, the first goal should be to stop excitotoxicity. And adequate Nitric Oxide production (but not through L-Arginine for some reason) is one of the best ways to achieve this (apart from antioxidants and methylation support)

The following video will explain why Argining will not work. The video is part 2 of 3, watch all three if you like but part 2 is where it explains that supplementing Arginine will actually lower NO levels (around 3:30).

google.com/fusiontables/Dat … #rows:id=1

It also discusses how if you want to help keep NO levels high you will need to supplement Folic Acid, (active form of it would also work as what you are using) along with Citrulline. It’s a possibility that the Rocket by itself is good, but those methylation supplements you’re taking (TMG, FolicAcid) are also assisting you since proper methylation will lead to higher NO levels.

[mariovitali]

@BrongFogBoy

@mariovitali

So : Instead of supplying yourself with Levo-Dopa or drinking coffee to feel alive again, the first goal should be to stop excitotoxicity. And adequate Nitric Oxide production (but not through L-Arginine for some reason) is one of the best ways to achieve this (apart from antioxidants and methylation support)

The following video will explain why Argining will not work. The video is part 2 of 3, watch all three if you like but part 2 is where it explains that supplementing Arginine will actually lower NO levels (around 3:30).

google.com/fusiontables/Dat … #rows:id=1

It also discusses how if you want to help keep NO levels high you will need to supplement Folic Acid, (active form of it would also work as what you are using) along with Citrulline. It’s a possibility that the Rocket by itself is good, but those methylation supplements you’re taking (TMG, FolicAcid) are also assisting you since proper methylation will lead to higher NO levels.

@BrongFogBoy

I could not find the video on the link you provided.

Have you started the NO/NOx regimen or you currently only doing methylation support?

[BrongFogBoy]

@mariovitali

@BrongFogBoy

@mariovitali

So : Instead of supplying yourself with Levo-Dopa or drinking coffee to feel alive again, the first goal should be to stop excitotoxicity. And adequate Nitric Oxide production (but not through L-Arginine for some reason) is one of the best ways to achieve this (apart from antioxidants and methylation support)

The following video will explain why Argining will not work. The video is part 2 of 3, watch all three if you like but part 2 is where it explains that supplementing Arginine will actually lower NO levels (around 3:30).

google.com/fusiontables/Dat … #rows:id=1

It also discusses how if you want to help keep NO levels high you will need to supplement Folic Acid, (active form of it would also work as what you are using) along with Citrulline. It’s a possibility that the Rocket by itself is good, but those methylation supplements you’re taking (TMG, FolicAcid) are also assisting you since proper methylation will lead to higher NO levels.

@BrongFogBoy

I could not find the video on the link you provided.

Have you started the NO/NOx regimen or you currently only doing methylation support?

Oops, here’s the correct link for the video: youtube.com/watch?v=PuEhjF-iEmE
I’ll be picking up Rocket asap…that’s all there is to it right? As for now I’m only doing methylation for the past 3 days.

[xptriado]

Mario what is your prolactin level nowadays and how much was it in the worse days?
Did you get gyno?

All these symptoms of rls or plmd, anorgasmia woth ssri, flat mood, anorgasmia with benzos,gabapentin…tremors, loss of sensitivity, no reward for doing things you once liked, are linked to dopamine deficiency.
Pfs people dont react well to ssri’s, but i bet if theyd try brupropion or tianeptine or agomelatine, the story would bebdofferent.
Agomelatine didnt fix my sleep but it did cure everything else mood related with one dosage.
Mybprolactin is in the upper third, its too high, so i bet my dopamine is low and makes sense. Now the question is why is it low.
Also dopamine is probably the only neurotrabsmitter that they could correlate urine (or plasma dont rember now) values with the CSF values. So yes, dopamine is measurable.

[mariovitali]

@BrongFogBoy

I’ll be picking up Rocket asap…that’s all there is to it right? As for now I’m only doing methylation for the past 3 days.

Notice that my regimen consists of

a) Methylation support (Metafolin, TMG but no Methylcobalamin or any other B12)
b) BH4 Support (Vitamin C, Metafolin also helps)
c) VDR Support (Vitamin D3)
d) NO/NOx support (Rocket)
e) Mitochondrial Support (ALCAR + CoQ10)
f) Cortisol Regulation (Ashwagandha)

@xptriado

Mario what is your prolactin level nowadays and how much was it in the worse days?
Did you get gyno?

I do not know, i think that i never had high prolactin levels. Yes i got gyno from finasteride and i believe that my gyno looks better now (but it is still there)

@xptriado

Mybprolactin is in the upper third, its too high, so i bet my dopamine is low and makes sense. Now the question is why is it low.
Also dopamine is probably the only neurotrabsmitter that they could correlate urine (or plasma dont rember now) values with the CSF values. So yes, dopamine is measurable.

My theory is that we loose dopamine AND dopaminergic neurons rather than dopamine itself and i really hope i am wrong regarding the loss of dopaminergic neurons. I am not sure that dopaminergic neurons can be regenerated as i find conflicting information about this. Anyway yes i do agree xptriado, low dopamine is also a problem. Why this happens? From a link in a previous post :

Ascorbate (vitamin C) is a nonenzymatic antioxidant highly concentrated in the brain. In addition to mediating redox balance, ascorbate is linked to glutamate neurotransmission in the striatum, where it renders neuroprotection against excessive glutamate stimulation. Oxidative stress and glutamatergic overactivity are key biochemical features accompanying the loss of dopaminergic neurons in the substantia nigra that characterizes Parkinson’s disease (PD). At present, it is not clear whether antiglutamate agents and ascorbate might be neuroprotective agents for PD. Thus, we tested whether ascorbate can prevent cell death from prolonged exposure to glutamate using dopaminergic neurons of human origin. To this purpose, dopamine-like neurons were obtained by differentiation of SH-SY5Y cells and then cultured for 4 days without antioxidant (antiaging) protection to evaluate glutamate toxicity and ascorbate protection as a model system of potential factors contributing to dopaminergic neuron death in PD. Glutamate dose dependently induced toxicity in dopaminergic cells largely by the stimulation of AMPA and metabotropic receptors and to a lesser extent by N-methyl-D-aspartate and kainate receptors. At relatively physiological levels of extracellular concentration, ascorbate protected cells against glutamate excitotoxicity. This neuroprotection apparently relies on the inhibition of oxidative stress, because ascorbate prevented the pro-oxidant action of the scavenging molecule quercetin, which occurred over the course of prolonged exposure, as is also seen with glutamate. Our findings show the relevance of ascorbate as a neuroprotective agent and emphasize an often underappreciated role of oxidative stress in glutamate excitotoxicity. Occurrence of a glutamate-ascorbate link in dopaminergic neurons may explain previous contradictions regarding their putative role in PD.

And to our benefit, Vitamin C has protective effect

@xptriado

Agomelatine didnt fix my sleep but it did cure everything else mood related with one dosage.

I strongly believe that our sleep problems are caused by VDR Mutation and/or low Vitamin D3 levels which have to be at an optimal range.

[xptriado]

This is what im thinking too.
Im also thinking of trying tianeptine particularly because of the effect on glutamate, or lipospmal vitamin c.
In my experience 3g a day of normal vitamin c always helped take the edge off!

Im going to test vitamin d tomorrow morning at my own expense. 60 eur because portugal health system doesnt cover it…
Theres conflicting info about neurogenesis of dopaminergic neurons in the substantia nigra but i found an article of this year saying exogenous allopregnanolone gave birth to new dopaminergic neurons in nigra. So even then, there is hope.

Some people got better on progesterone and prami, could have to do with prog increase in allopreg and prami inducing dopamine receptor density change and masking the side effecta from prog until it gives birth to enough dopamine neurons to recovee the dopaminergic system and sustain itself without pramipexole.

I dont have high prolactin but its in the upper third…i always thought it should be lower.

Ill keep updating my experience and later ill come back to the rockets.

Sorry for derailing this thread a bit.

[BrongFogBoy]

@mariovitali

@BrongFogBoy

I’ll be picking up Rocket asap…that’s all there is to it right? As for now I’m only doing methylation for the past 3 days.

Notice that my regimen consists of

a) Methylation support (Metafolin, TMG but no Methylcobalamin or any other B12)
b) BH4 Support (Vitamin C, Metafolin also helps)
c) VDR Support (Vitamin D3)
d) NO/NOx support (Rocket)
e) Mitochondrial Support (ALCAR + CoQ10)
f) Cortisol Regulation (Ashwagandha)

I’m doing all of this but I am including b12 and do not do ashwgandha as it makes me feel completely fatigued, brainfogged and lethargic after just three days every time. What brand are you taking?

[mariovitali]

@BrongFogBoy

@mariovitali

@BrongFogBoy

I’ll be picking up Rocket asap…that’s all there is to it right? As for now I’m only doing methylation for the past 3 days.

Notice that my regimen consists of

a) Methylation support (Metafolin, TMG but no Methylcobalamin or any other B12)
b) BH4 Support (Vitamin C, Metafolin also helps)
c) VDR Support (Vitamin D3)
d) NO/NOx support (Rocket)
e) Mitochondrial Support (ALCAR + CoQ10)
f) Cortisol Regulation (Ashwagandha)

I’m doing all of this but I am including b12 and do not do ashwgandha as it makes me feel completely fatigued, brainfogged and lethargic after just three days every time. What brand are you taking?

I am taking the one from NOW Foods, 450 mg standardized extract. I believe that you should test for Cortisol first and then use Ashwagandha if you are getting such a response. It might be the case that your Cortisol is normal and by lowering it you feel fatigued and lethargic.