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1.5L, however my machine has gas inhalation too so that could be worth trying when I start again
Electrolyte Protocol for Improved Health
- Thread starter Helen
- Start date
1.5L, however my machine has gas inhalation too so that could be worth trying when I start again
Ingeno
Well-Known Member
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- 404
About 2-3L per day. Some days feeling incredible, some days ok-ish. Some days I'm testing with single amino acids or minerals, like L-Histidine and I think those wack me off balance. The days I don't use any supplements I feel best (Also zero MPB scalp itch). So for now I'm only going to use H2 and finetuning my diet.
Niles
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@Helen Based on what's known about the effects of H2 water, is there any type of body chemistry for which H2 water would be detrimental? I know there are still plenty of unknown variables at play that could make it harmful to some folks, but wondering if you think it's as safe for everyone given what we currently know.
I'm planning to slowly add it into my regime, starting at 1/3 liter per day.
I'm planning to slowly add it into my regime, starting at 1/3 liter per day.
Is this a good B complex? http://www.amazon.com/Jarrow-Formulas-B-right-Supports-Cardiovascular/dp/B0016003Z0
I'm not helen, but h2 is simply an antioxidants, both slow and fast oxidisers have high oxidative stress, so it should be good for everyone
I wonder what you think about iodine guys? Like taking lugol's solution.. I think that many many people are deficient in iodine and will benefit from taking few milligrams a day... I would also like to know what is the relationship of iodine with selenium. Because "you need to take selenium with iodine"..
Orion
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@Helen trying to understand this, so if not enough potassium(with B1) is available NADPH is not produced in the pentose pathway properly, it shifts to the Krebs cycle but uses up malic, isocitrate, etc doing this and the end results is less NADH produced.
Malic acid seems to be very important in my stack, removing it causes oily skin to return. Would testing with NADH be a good approach here?
I think also increasing my HCl intake and KCl intake would be something to test as well.
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Orion, did you try Acetazolamide. it acts like a duaretic , can you please try it to see how it effects your oilness
Orion
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I did not try it, will look it up and order some for testing.
Orion
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Getting ACE online without prescription looks like it will not be easy, still looking around.
Searching on malic found this, interesting how for most people supplementing pantothetenic acid(beta-alanine?) and now for me malic acid, reduces oiliness sebum production. So acne its a broken carbohydrate metabolism and broken amino acid metabolism... in general terms... @Helen would the lipid powder posted as part of the electrolyte protocol be useful? Is it mainly alkalosis that disables the carb and amino metabolism? I might need to increase my H2 water intake?
Orion
Well-Known Member
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Has anyone @tanedout tried high dose B1, I think @Helen has suggested it in the past. Sorry for the wall of text below, just found all this, and seems like some good connections with electrolyte protocol and ACCUTANE, FIN, NADPH, Sulforaphane THIAMINE, copying relevant posts from this user on acne.org: tryingtohelp2014
Retinoic acid = decreased Transketolase (thiamine deficiency)
Accutane inhibits hippocampal neurogenesis by using up the NADPH reducing cofactor... Thiamine
NADPH needed as a CYP26A cofactor for retinoic acid detoxification.
NADPH (B1) and FAD (B2) cofactors should be promoted.
===
Vitamin K2 has nothing to do with the activation of CYP26 or any other CYP enzyme needed specifically for all trans retinoic acid detoxification. its not a co-factor.
However Thiamine is a co-factor to produce K2 (menaquinones ) so anything related to a K2 deficiency could be just the missing cofactor.
Thiamine is a cofactor for NADPH which is needed for CYP26A
===
Erythrocyte Transketolase: The Test of Choice for Assessing Thiamine Deficiency
===
NADPH oxidase and thyroid function
An interesting aspect of the NADPH oxidase system is that it plays a major role in thyroid function. Thyroid hormone synthesis is dependent on NADPH in both the thyroid and the liver. In the thyroid, two separate NADPH oxidase systems are used to generate free radicals, particularly hydrogen peroxide(H2O2), that are used to build the thyroid hormones T4 and T3(5, 6). In the liver, the less active T4 is converted in to T3 by an NADPH-dependent enzyme, 5'-deiodinase(7, 8) that utilizes reduced glutathione to make this conversion. Again, the solution to problems like this are much more complex than just throwing thiamine at them. T4 and T3 help regulate the conversion of riboflavin to FAD(9, 10, 11) which participates in many of the thiamine dependent enzymes as a cofactor and both FAD and selenium are needed for the glutathione cycle to work properly.
NADPH provides the reducing equivalents for biosynthetic reactions and the oxidation-reduction involved in protecting against the toxicity of reactive oxygen species (ROS), allowing the regeneration of glutathione (GSH).[3]NADPH is also used for anabolic pathways, such as lipid synthesis, cholesterol synthesis, and fatty acid chain elongation.
The NADPH system is also responsible for generating free radicals in immune cells. These radicals are used to destroy pathogens in a process termed the respiratory burst.[4] It is the source of reducing equivalents for cytochrome P450 hydroxylation of aromatic compounds, steroids, alcohols, and drugs.
===
NADPH ACCUTANE FINASTERIDE connection.
we need to increase NADPH. 60% of our NADPH is made through the Thiamine dependant the pentose pathway.
Red blood cell transketolase activity is reduced in deficiency of thiamine (vitamin B1), and may be used in the diagnosis of Wernicke's encephalopathy and other B1-deficiency syndromes if the diagnosis is in doubt.[8] Apart from the baseline enzyme activity (which may be normal even in deficiency states), acceleration of enzyme activity after the addition of thiamine pyrophosphate may be diagnostic of thiamine deficiency (0-15% normal, 15-25% deficiency, >25% severe deficiency).[9]
#1: Direct 5-Alpha Reductase Inhibition
Competitive Inhibition
5-alpha reductase doesn’t just arrive out of nowhere. In order for this enzyme to form and mediate the whole DHT conversion process, it needs the help of a coenzyme known as nicotinamide adenine dinucleotide phosphate… or in other words, NADPH.
5-alpha reductase needs NADPH to convert free testosterone into DHT. So an effective way to stop the formation of 5-alpha reductase (and reducing DHT) is to…
Compete with the coenzyme NADPH, or Block NADPH
These are two mechanisms of direct 5-alpha reductase inhibition – or for the lay person – reducing 5-alpha reductase by stopping it from forming. And while it’s still up for debate, the hair loss drugs Finasteride and Dutasteride – two 5-alpha reductase inhibitors – appear to work in this way.
Mechanism 1: Compete With NADPH
Some research shows that Finasteride competes with the coenzyme NADPH. Finasteride’s molecules take the place of NADPH in a cell, and in NADPH’s absence, 5-alpha reductase cannot form. The end-result? Less DHT. And another 5-alpha reductase inhibiting drug – Dutasteride – seems to do the same thing (using a slightly different molecule).
Mechanism 2: Block NADPH (Or Bind To NADPH And Change Its Structure)
There’s also research showing that instead of competing with NADPH, Finasteride may instead bind to NADPH and change NADPH’s structure into a different coenzyme – one that doesn’t support the formation of 5-alpha reductase. The bottom line: free testosterone can no longer convert into DHT.
Interestingly, zinc may also reduce 5-alpha reductase and through a similar manner. Evidence suggests that zinc reduces NADPH production, thereby decreasing 5-alpha reductase activity. The less enzyme activity, the less DHT.
===
"I’m assuming you mean large amounts of Thiamine ( B1 ) as we’ve all taken this as part of our B complex supplements with very little effect yeah?
I’ve even stepped it up a notch by taking the “active” form of B’s more recently but again nothing noticeable in the way I feel.
How much Thiamine do we need to be taking to notice anything?"
up to 1500mg has been discussed. starting at a lower dose...and moving up. allthiamine cream is transdermal and gets around the whole digestive tract. it also crosses the blood brain barrier. this has been used successfully in autistic children. people have used both b complex and thiamine by itself read up on Dr Lonsdale. he is the expert in B1. I think its a transporter problem..and you really need to saturate the serum. some things you have to watch with thiamine... magnesium gets used up and folic acid.
===
High dose Thiamine has been recommended as a treatment.
Thiamine is needed for NADPH (the first step is isotretinoin catabolism) 60% comes from the pentose pathway
Thiamine is needed to produce stomach acid (think SIBO , bacterial imbalance, Chrons etc)
Thiamine is needed for collagen formation
Thiamine is needed to produce ATP (think ER dysfunction/ROS/detoxification)
Thiamine is needed for estrogen clearance in the liver (along with riboflavin) estrogen dominance, low T LH FSH etc.
Thiamine is needed to recycle GSH.
Thiamine is needed in steroid formation
Thiamine deficiency is noted in low ceruloplasmin results.
The test needed for this is an erythrocyte transketolase test. normal blood tests are not accurate.
ALLTHIAMINE is preferred. i have been using the topical. I tested high for estrogen last summer. I believe i had an estrogen-induced form of cholestasis. Ive had high bilirubin for 20 years since accutane. In the past 2 weeks, the whites of my eys have been totally clear, and ill be getting a confirming blood test. Taurine did this for a few days..but it was hit and miss. We could have downregulated receptors, and the full effect could take a while to fix. Magnesium and B1 should be taken together
Could accutane be the trigger like Gardisal?
something very very interesting here, and it related to P53 and FOX01
Bodo Melnik published something last month....
p53: key conductor of all anti-acne therapies
Bodo C. Melnikcorresponding author
p53: key conductor of all anti-acne therapies
This review based on translational research predicts that the transcription factor p53 is the key effector of all anti-acne therapies. All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53. Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53. Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53. p53 inhibits the expression of androgen receptor and IGF-1 receptor, and induces the expression of IGF binding protein 3. p53 induces FoxO1, FoxO3, p21 and sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis explaining isotretinoin’s sebum-suppressive effect. Anti-androgens attenuate the expression of miRNA-125b, a key negative regulator of p53. It can thus be concluded that all anti-acne therapies have a common mode of action, i.e., upregulation of the guardian of the genome p53. Immortalized p53-inactivated sebocyte cultures are unfortunate models for studying acne pathogenesis and treatment.
THIAMINE......
In contrast, an increased number of thiamine transporters are observed in cells that overexpress thiamine transport genes (mTHTR-1) and in cells that are exposed to conditions that induce DNA damage or p53 activation.56 Thiamine diphosphate inhibits p53 binding, and thiamine inhibits intracellular p53 activity.57 Thiamine treatment significantly decreases p53 expression in the cultured retinal neurons from diabetic rats.58 These observations suggest that the pro-apoptotic transcription factor p53 is activated by cellular damage in HIV infection and that thiamine ameliorates these effects.
Thiamine antagonists trigger p53-dependent apoptosis in differentiated SH-SY5Y cells
===
i have gilberts syndrome as well. well, just high bilirubin. i dont believe i ever had high bilirubin before taking accutane though. so its a chicken and the egg question.
if you have gilberts , you conjugate at 30% the normal rate. the same UGT enzyme that conjugates bilirubin is also responsible for the glucuronidation of accutane.
PHASE 2 ... read up on NRF2
every single person who has ever reported feeling better has unknowingly promoted the NRF2 response. either from water fasting, TUDCA, CBD oil, etc etc etc.
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity.
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity. - PubMed - NCBI
accutane has been proven to shut down the NRF2 response
NFE2L2 Nuclear factor (erythroid-derived 2)-like 2 Inhibited by retinoic acid via RARalpha resulting in lack of expression of Nrf2 target genes
===
some guy on this thread mentioned taking Sulforaphane
Accutane inhibits NrF2.................
Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha
Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity - ScienceDirect
NRF2: The Detox Hub and Core Antioxidant Defense - Selfhacked
The UDP-glucuronosyltransferase (UGT) family catalyze the conjugation of a glucuronic acid to drugs, chemicals, and toxins, making them more water-soluble and readily excreted. Nrf2 has been shown to induce UGT1A1 and UGT1A6.
Retinoic acid = decreased Transketolase (thiamine deficiency)
Accutane inhibits hippocampal neurogenesis by using up the NADPH reducing cofactor... Thiamine
NADPH needed as a CYP26A cofactor for retinoic acid detoxification.
NADPH (B1) and FAD (B2) cofactors should be promoted.
===
Vitamin K2 has nothing to do with the activation of CYP26 or any other CYP enzyme needed specifically for all trans retinoic acid detoxification. its not a co-factor.
However Thiamine is a co-factor to produce K2 (menaquinones ) so anything related to a K2 deficiency could be just the missing cofactor.
Thiamine is a cofactor for NADPH which is needed for CYP26A
===
Erythrocyte Transketolase: The Test of Choice for Assessing Thiamine Deficiency
===
NADPH oxidase and thyroid function
An interesting aspect of the NADPH oxidase system is that it plays a major role in thyroid function. Thyroid hormone synthesis is dependent on NADPH in both the thyroid and the liver. In the thyroid, two separate NADPH oxidase systems are used to generate free radicals, particularly hydrogen peroxide(H2O2), that are used to build the thyroid hormones T4 and T3(5, 6). In the liver, the less active T4 is converted in to T3 by an NADPH-dependent enzyme, 5'-deiodinase(7, 8) that utilizes reduced glutathione to make this conversion. Again, the solution to problems like this are much more complex than just throwing thiamine at them. T4 and T3 help regulate the conversion of riboflavin to FAD(9, 10, 11) which participates in many of the thiamine dependent enzymes as a cofactor and both FAD and selenium are needed for the glutathione cycle to work properly.
NADPH provides the reducing equivalents for biosynthetic reactions and the oxidation-reduction involved in protecting against the toxicity of reactive oxygen species (ROS), allowing the regeneration of glutathione (GSH).[3]NADPH is also used for anabolic pathways, such as lipid synthesis, cholesterol synthesis, and fatty acid chain elongation.
The NADPH system is also responsible for generating free radicals in immune cells. These radicals are used to destroy pathogens in a process termed the respiratory burst.[4] It is the source of reducing equivalents for cytochrome P450 hydroxylation of aromatic compounds, steroids, alcohols, and drugs.
===
NADPH ACCUTANE FINASTERIDE connection.
we need to increase NADPH. 60% of our NADPH is made through the Thiamine dependant the pentose pathway.
Red blood cell transketolase activity is reduced in deficiency of thiamine (vitamin B1), and may be used in the diagnosis of Wernicke's encephalopathy and other B1-deficiency syndromes if the diagnosis is in doubt.[8] Apart from the baseline enzyme activity (which may be normal even in deficiency states), acceleration of enzyme activity after the addition of thiamine pyrophosphate may be diagnostic of thiamine deficiency (0-15% normal, 15-25% deficiency, >25% severe deficiency).[9]
#1: Direct 5-Alpha Reductase Inhibition
Competitive Inhibition
5-alpha reductase doesn’t just arrive out of nowhere. In order for this enzyme to form and mediate the whole DHT conversion process, it needs the help of a coenzyme known as nicotinamide adenine dinucleotide phosphate… or in other words, NADPH.
5-alpha reductase needs NADPH to convert free testosterone into DHT. So an effective way to stop the formation of 5-alpha reductase (and reducing DHT) is to…
Compete with the coenzyme NADPH, or Block NADPH
These are two mechanisms of direct 5-alpha reductase inhibition – or for the lay person – reducing 5-alpha reductase by stopping it from forming. And while it’s still up for debate, the hair loss drugs Finasteride and Dutasteride – two 5-alpha reductase inhibitors – appear to work in this way.
Mechanism 1: Compete With NADPH
Some research shows that Finasteride competes with the coenzyme NADPH. Finasteride’s molecules take the place of NADPH in a cell, and in NADPH’s absence, 5-alpha reductase cannot form. The end-result? Less DHT. And another 5-alpha reductase inhibiting drug – Dutasteride – seems to do the same thing (using a slightly different molecule).
Mechanism 2: Block NADPH (Or Bind To NADPH And Change Its Structure)
There’s also research showing that instead of competing with NADPH, Finasteride may instead bind to NADPH and change NADPH’s structure into a different coenzyme – one that doesn’t support the formation of 5-alpha reductase. The bottom line: free testosterone can no longer convert into DHT.
Interestingly, zinc may also reduce 5-alpha reductase and through a similar manner. Evidence suggests that zinc reduces NADPH production, thereby decreasing 5-alpha reductase activity. The less enzyme activity, the less DHT.
===
"I’m assuming you mean large amounts of Thiamine ( B1 ) as we’ve all taken this as part of our B complex supplements with very little effect yeah?
I’ve even stepped it up a notch by taking the “active” form of B’s more recently but again nothing noticeable in the way I feel.
How much Thiamine do we need to be taking to notice anything?"
up to 1500mg has been discussed. starting at a lower dose...and moving up. allthiamine cream is transdermal and gets around the whole digestive tract. it also crosses the blood brain barrier. this has been used successfully in autistic children. people have used both b complex and thiamine by itself read up on Dr Lonsdale. he is the expert in B1. I think its a transporter problem..and you really need to saturate the serum. some things you have to watch with thiamine... magnesium gets used up and folic acid.
===
High dose Thiamine has been recommended as a treatment.
Thiamine is needed for NADPH (the first step is isotretinoin catabolism) 60% comes from the pentose pathway
Thiamine is needed to produce stomach acid (think SIBO , bacterial imbalance, Chrons etc)
Thiamine is needed for collagen formation
Thiamine is needed to produce ATP (think ER dysfunction/ROS/detoxification)
Thiamine is needed for estrogen clearance in the liver (along with riboflavin) estrogen dominance, low T LH FSH etc.
Thiamine is needed to recycle GSH.
Thiamine is needed in steroid formation
Thiamine deficiency is noted in low ceruloplasmin results.
The test needed for this is an erythrocyte transketolase test. normal blood tests are not accurate.
ALLTHIAMINE is preferred. i have been using the topical. I tested high for estrogen last summer. I believe i had an estrogen-induced form of cholestasis. Ive had high bilirubin for 20 years since accutane. In the past 2 weeks, the whites of my eys have been totally clear, and ill be getting a confirming blood test. Taurine did this for a few days..but it was hit and miss. We could have downregulated receptors, and the full effect could take a while to fix. Magnesium and B1 should be taken together
Could accutane be the trigger like Gardisal?
something very very interesting here, and it related to P53 and FOX01
Bodo Melnik published something last month....
p53: key conductor of all anti-acne therapies
Bodo C. Melnikcorresponding author
p53: key conductor of all anti-acne therapies
This review based on translational research predicts that the transcription factor p53 is the key effector of all anti-acne therapies. All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53. Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53. Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53. p53 inhibits the expression of androgen receptor and IGF-1 receptor, and induces the expression of IGF binding protein 3. p53 induces FoxO1, FoxO3, p21 and sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis explaining isotretinoin’s sebum-suppressive effect. Anti-androgens attenuate the expression of miRNA-125b, a key negative regulator of p53. It can thus be concluded that all anti-acne therapies have a common mode of action, i.e., upregulation of the guardian of the genome p53. Immortalized p53-inactivated sebocyte cultures are unfortunate models for studying acne pathogenesis and treatment.
THIAMINE......
In contrast, an increased number of thiamine transporters are observed in cells that overexpress thiamine transport genes (mTHTR-1) and in cells that are exposed to conditions that induce DNA damage or p53 activation.56 Thiamine diphosphate inhibits p53 binding, and thiamine inhibits intracellular p53 activity.57 Thiamine treatment significantly decreases p53 expression in the cultured retinal neurons from diabetic rats.58 These observations suggest that the pro-apoptotic transcription factor p53 is activated by cellular damage in HIV infection and that thiamine ameliorates these effects.
Thiamine antagonists trigger p53-dependent apoptosis in differentiated SH-SY5Y cells
===
i have gilberts syndrome as well. well, just high bilirubin. i dont believe i ever had high bilirubin before taking accutane though. so its a chicken and the egg question.
if you have gilberts , you conjugate at 30% the normal rate. the same UGT enzyme that conjugates bilirubin is also responsible for the glucuronidation of accutane.
PHASE 2 ... read up on NRF2
every single person who has ever reported feeling better has unknowingly promoted the NRF2 response. either from water fasting, TUDCA, CBD oil, etc etc etc.
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity.
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity. - PubMed - NCBI
accutane has been proven to shut down the NRF2 response
NFE2L2 Nuclear factor (erythroid-derived 2)-like 2 Inhibited by retinoic acid via RARalpha resulting in lack of expression of Nrf2 target genes
===
some guy on this thread mentioned taking Sulforaphane
Accutane inhibits NrF2.................
Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha
Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity
NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity - ScienceDirect
NRF2: The Detox Hub and Core Antioxidant Defense - Selfhacked
The UDP-glucuronosyltransferase (UGT) family catalyze the conjugation of a glucuronic acid to drugs, chemicals, and toxins, making them more water-soluble and readily excreted. Nrf2 has been shown to induce UGT1A1 and UGT1A6.
supernature
Member
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Last edited:
tanedout
Well-Known Member
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I've never tried this before, but I do seem to get benefits with mental clarity from taking an active B-complex (which having looked has 2000% of RDA B1 per capsule). Haven't tried it individually, but I may look at this as something to try
Orion
Well-Known Member
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There are some older haidut post on RPF that suggest higher dose B1 and acetazolamide work in the same way. Testing B1 out this week, to see how my skin reacts.
BeLikeWater
Well-Known Member
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Is there any way to know that enzymes are working correctlyvia blood analisys? Because Im going to make an analisys soon, and im interested. Anyway do you have any recommendation for PFS analisys?
ruprmurdoch
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I tried acetozalamide, 4x250mg per day during month. This dose is standart and is used for lowering production of cerebrospinal fluid, which, may create pressing pituitary. This is why it's workin. See my post about acetazolamide used for progestin side effects. This is why it will work for accutane.
But just read study which I post, I think Helen is right and ACE is cure for most cases, where progestins harm someone health.
ACE is sulfur based, and it raise chloride.
Vit b1 is sulfur based and it could replace ACE. There are studies in web.
Bad sides: ACE as well as thiamine may make you very depressed, thinking depressive things. I had this ,,experience'', but I get through this, and I can tell anyone it's worth trying.
In my case, two days after I quit ACE, I took KCL, and had big increase in energy, libido, etc.I used it myself so actually feel that pituitary is regrowing, becuse had often nosebleed.
EDIT: Helen also wrote how to use actazolamide. Please read it, in my personal experience, it helps me.
But just read study which I post, I think Helen is right and ACE is cure for most cases, where progestins harm someone health.
ACE is sulfur based, and it raise chloride.
Vit b1 is sulfur based and it could replace ACE. There are studies in web.
Bad sides: ACE as well as thiamine may make you very depressed, thinking depressive things. I had this ,,experience'', but I get through this, and I can tell anyone it's worth trying.
In my case, two days after I quit ACE, I took KCL, and had big increase in energy, libido, etc.I used it myself so actually feel that pituitary is regrowing, becuse had often nosebleed.
EDIT: Helen also wrote how to use actazolamide. Please read it, in my personal experience, it helps me.
@Helen what you think about Nicotinamide Riboside to boost NAD production? It should be the thing for antiaging..
Life Extension, NAD + Cell Regenerator Nicotinamide Riboside, 250 mg , 30 Vegetarian Capsules
Life Extension, NAD + Cell Regenerator Nicotinamide Riboside, 250 mg , 30 Vegetarian Capsules
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it should be ok.