Can Niacinamide Increase Serotonin?

J

j.

Guest
haidut, I've been experimenting with combined high dose vitamin E (5 or 6 grams of high gamma) and K (45 mg), with a lot of honey and sugar and got a similar feeling about not caring about anything and being relaxed last weekend. don't know if it would be consistent every time I try it. I'm taking thyroid too, though ERFA 30 mg, smaller dose.
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
j. said:
haidut, I've been experimenting with combined high dose vitamin E (5 or 6 grams of high gamma) and K (45 mg), with a lot of honey and sugar and got a similar feeling about not caring about anything and being relaxed last weekend. don't know if it would be consistent every time I try it. I'm taking thyroid too, though ERFA 30 mg, smaller dose.

Many things could be causing this, but let's start with the ones I know have happened in the past. Vitamin E lowers prolactin. I posted a study about that on another thread in this forum so if you search around you will find it. Lower prolactin means higher dopamine, higher testosterone, and lower serotonin. Now, some of that testosterone may aromatize to estrogen if you are under stress but this is where again Vitamin E and vitamin K come into play. Vitamin K (only menatetrenone a.k.a. MK-4 has been shown to do this) is a true aromatase inhibitor. Here are some studies:
http://www.ncbi.nlm.nih.gov/pubmed/21914161
http://www.ncbi.nlm.nih.gov/pubmed/12370839

Finally, even if any testosterone does aromatize then vitamin E acts like an estrogen "receptor" antagonist and in doses of 2,500mg lowered estrogen levels by 65%. Since you are taking more than that, you should be getting even lower estrogen. If you add vitamin A and vitamin D to this duo you have what I like to call "Tetra Titans". Retinol, D3 are also aromatase inhibitors so should help with estrogen even more.
I personally, take the Tetra Titans like this (all orally): 75,000 IU vitamin A (retinol), 45mg menatetrenone (MK-4), 5,000 IU D3, 2,500mg mixed tocopherols (70% gamma).
Just make sure that you eat enough fat when you take those vitamins. They are all fat-soluble but there was a study I saw recently that unless your meal has at least 27g of saturated fat in it, vitamin K would not get properly absorbed and gets excreted in fecal matter, which would be a waste (pun intended).
Finally, a good test for estrogen would be to get a device that measures water saturation in tissues. A good way you approximate this is to get one of those scales that measure body fat percentage. Well, in reality they measure body water percentage and use that to approximate body fat. When estrogen is low, as Ray peat said, you should NOT be retaining any excess water. Cells take up water under the influence of estrogen and for them it is a signal to divide. So, no estrogen excess means no water uptake excess. Use one of those fat measuring scales to periodically measure your weight and your body fat percentage. If your estrogen drops, your body will drop the excess water and you will see a dramatic "drop" in reported body fat but a much smaller drop in weight. The drop in body fat is the excess water you dumped. With low estrogen you will start losing body fat too but that will take more time, definitely not overnight like the scale would have you believe:):
 

gbolduev

Member
Joined
Jun 26, 2014
Messages
464
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.
 

Milklove

Member
Joined
Jan 1, 2014
Messages
127
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.
 

gbolduev

Member
Joined
Jun 26, 2014
Messages
464
Milklove said:
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.


Well , how would you explain this then http://www.ncbi.nlm.nih.gov/pubmed/23426511
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .

And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more

And it has nothing to do with tryptophan , you need tryptophan and you are all deficient in it. It is the conversion rate of tryptophan to serotonin which is the problem and actually lack of tryptophan for niacin. So not eating tryptophan is not a cure it is a death sentence. FIX the conversion issue, not the raw material which other systems including T killers depend on
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
gbolduev said:
Milklove said:
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.


Well , how would you explain this then http://www.ncbi.nlm.nih.gov/pubmed/23426511
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .

And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more

And it has nothing to do with tryptophan , you need tryptophan and you are all deficient in it. It is the conversion rate of tryptophan to serotonin which is the problem and actually lack of tryptophan for niacin. So not eating tryptophan is not a cure it is a death sentence. FIX the conversion issue, not the raw material which other systems including T killers depend on

You raise some good points, but I don't think aggressive chelation is what will fix the underlying problem. First, for mercury chelation I would not take fulvic acid, I'd take fumaric and succinic acid. Thiamine (B1) can also chelate mercury and lead. Second, the study you posted has been discussed before and 100mg dose of nicotinamide is certainly not "excessive" as the study suggests and might as well push the serotonin higher. Doses of nicotinamide that lower serotonin are in 4g-8g range and that's what I would call excessive.
Now - about tryptophan. You can survive perfectly fine on a tryptophan-free diet after the age of about 18 when skeletal growth is complete, and in fact it is used as a life extension protocol in rodents.
http://www.ncbi.nlm.nih.gov/pubmed/22255
http://www.nutritionj.com/content/10/1/107

The reports fro mainstream medicine of low tryptophan lowering mood seems to be due to increasing sensitivity to light deprivation, which IMO signifies the central role of light in metabolism:
http://www.ei-resource.org/information/ ... ng-of-mood

So, based on what I have seen tryptophan does not seem to be essential in any way in adult organisms except for being the source of niacin. The role of tryptophan in infections/immunity you bring up is also disputed and there is some evidence that the purpose of the fever is to delete the body of iron AND also deplete tryptophan and tryptophan metabolites. I posted a study on that on the forum but can't find it right now. Also, tryptophan is required for the growth of many pathogenic bacteria. There are many studies to consider but here is one:
http://iai.asm.org/content/75/11/5105.full

Second, tryptophan is carcinogenic even in physiological doses. Chronic feeding of identical diets except that one contained an extra 0.2% tryptophan (human dose about 3g daily) increased cancer incidence in rats 5-fold. Also, as you probably know some of the tryptophan conversion pathways are neurotoxic and are implicated in diseases like ALS, MS, etc.
http://www.ncbi.nlm.nih.gov/pubmed/17956331
http://en.wikipedia.org/wiki/Kynurenine ... rotoxicity

In diseases of the GI like IBS, tryptophan depletion is one of the few known ways to arrest symptoms indefinitely (i.e. while maintaining tryptophan depleted state).
http://www.ei-resource.org/information/ ... l-syndrome

I agree with you that the conversion pathway matters but unless you want to mess with those there are only a few safe ways of steering tryptophan towards the niacin pathway using diet. Calcium intake is probably the primary method available to people not interested in taking drugs.
But, back to your chelation points - I agree with you on chelating mercury. If you know of a good iron chelation compound I would appreciate it if you share it with us.
 

Milklove

Member
Joined
Jan 1, 2014
Messages
127
gbolduev said:
Milklove said:
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.


Well , how would you explain this then http://www.ncbi.nlm.nih.gov/pubmed/23426511
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .

And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more

And it has nothing to do with tryptophan , you need tryptophan and you are all deficient in it. It is the conversion rate of tryptophan to serotonin which is the problem and actually lack of tryptophan for niacin. So not eating tryptophan is not a cure it is a death sentence. FIX the conversion issue, not the raw material which other systems including T killers depend on

I want to add something regarding the heavy metal issue. You are right, that stored heavy metals can seriously mess with your body (especially by irreversibly blocking enzymes and producing destructive free radicals), but by heavy chelating you can produce even bigger health issue.

A little Ray Peat Quote:
[Question: Does the body quickly or gradually get rid of DMPS or DMSA chelating agents? I have many people who nearly died when they took DMPS or DMSA. But, I should think that the body would eventually detox it. What do you think?] The idea of using it to remove metals is that it leaves the body rapidly. The damage produced by moving the metals around could be fairly permanent, but the chelator leaves very quickly. Environmental pollutants, food fats, and cosmetics are the things people should worry about accumulating in their tissues.

Furthermore, mothers that ate a diet high in seafood and thereby consumed high amounts of mercury, gave birth to more intelligent babies than mothers who did not consume any seafood. The nutrional value of seafood outweighs the negative effects of the mercury.
Just something to consider.
 

gbolduev

Member
Joined
Jun 26, 2014
Messages
464
haidut said:
gbolduev said:
Milklove said:
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.


Well , how would you explain this then http://www.ncbi.nlm.nih.gov/pubmed/23426511
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .

And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more

And it has nothing to do with tryptophan , you need tryptophan and you are all deficient in it. It is the conversion rate of tryptophan to serotonin which is the problem and actually lack of tryptophan for niacin. So not eating tryptophan is not a cure it is a death sentence. FIX the conversion issue, not the raw material which other systems including T killers depend on

You raise some good points, but I don't think aggressive chelation is what will fix the underlying problem. First, for mercury chelation I would not take fulvic acid, I'd take fumaric and succinic acid. Thiamine (B1) can also chelate mercury and lead. Second, the study you posted has been discussed before and 100mg dose of nicotinamide is certainly not "excessive" as the study suggests and might as well push the serotonin higher. Doses of nicotinamide that lower serotonin are in 4g-8g range and that's what I would call excessive.
Now - about tryptophan. You can survive perfectly fine on a tryptophan-free diet after the age of about 18 when skeletal growth is complete, and in fact it is used as a life extension protocol in rodents.
http://www.ncbi.nlm.nih.gov/pubmed/22255
http://www.nutritionj.com/content/10/1/107

The reports fro mainstream medicine of low tryptophan lowering mood seems to be due to increasing sensitivity to light deprivation, which IMO signifies the central role of light in metabolism:
http://www.ei-resource.org/information/ ... ng-of-mood

So, based on what I have seen tryptophan does not seem to be essential in any way in adult organisms except for being the source of niacin. The role of tryptophan in infections/immunity you bring up is also disputed and there is some evidence that the purpose of the fever is to delete the body of iron AND also deplete tryptophan and tryptophan metabolites. I posted a study on that on the forum but can't find it right now. Also, tryptophan is required for the growth of many pathogenic bacteria. There are many studies to consider but here is one:
http://iai.asm.org/content/75/11/5105.full

Second, tryptophan is carcinogenic even in physiological doses. Chronic feeding of identical diets except that one contained an extra 0.2% tryptophan (human dose about 3g daily) increased cancer incidence in rats 5-fold. Also, as you probably know some of the tryptophan conversion pathways are neurotoxic and are implicated in diseases like ALS, MS, etc.
http://www.ncbi.nlm.nih.gov/pubmed/17956331
http://en.wikipedia.org/wiki/Kynurenine ... rotoxicity

In diseases of the GI like IBS, tryptophan depletion is one of the few known ways to arrest symptoms indefinitely (i.e. while maintaining tryptophan depleted state).
http://www.ei-resource.org/information/ ... l-syndrome

I agree with you that the conversion pathway matters but unless you want to mess with those there are only a few safe ways of steering tryptophan towards the niacin pathway using diet. Calcium intake is probably the primary method available to people not interested in taking drugs.
But, back to your chelation points - I agree with you on chelating mercury. If you know of a good iron chelation compound I would appreciate it if you share it with us.

Also , good points, but most of these studies are taken out of context and not valid. The cutting edge of cancer therapy these days are IDO inhibitors, IDO is the enzyme that breaks down tryptophan. Once again , it is not the tryptophan which is the bad guy but serotonin. IDO is iron based enzyme, same as the tryptophan to serotonin enzyme. IRON toxicity is what most of us have even with low ferritin levels.

I am on IDO inhibitors and my cancer is running away although 3 years ago , I could not even walk anymore. Tryptophan is essential anti cancer agent . ALl these studies are wrong. YOU need to block the conversion of tryptophan to serotonin that will give you tons of tryptophan and trust me you wont get cancer from it)) All these studies say to limit tryptophan , but it should say limit the conversion and increase tryptophan.

There are no good iron chelators honestly that I know of. Fulvic acid will chelate mercury amazingly and you need to drink that always, but not fulvic minerals, just fulvic acid. I dealt with about 1000 people this year since I am trying to help many , and these people tested extensively and most of them have one problem. Low bioavailable copper because of tons of estrogen mimics, high iron and this actually opens up IDO enzyme and opens up the enzyme which converts tryptophan to serotonin simulnatenously . this is the main problem with almost everyone. And these diets wont do anything, since even if you take care of couple of neurological symptoms with the diet or niacinamide , the main copper problem wont go away, and that will be getting worse. Mercury wont come out on its own .
And believe me DMSA and ALA works, but you need to use frequent chelation protocol with low dosages, like Andy Cutlers. it does work and it has very little side effects. At the same time, you can always balance your minerals with hair tests, so you dont crash while chelating, since estrogen mimics are what holding your adrenals up, and it should be held on copper , not on mercury or cadmium , so obviously when mercury comes out, adrenals will crash until copper goes there.

Anyway , this is what I am doing, and this is working. I tried every diet possible, and Ray Peat is a smart guy , but I think he misses what comes first and what comes second. The diet wont help , and actually can make it worse. I prefer to see my progression and not cover it up.
Chronic loss of copper is happening and I think Peat admits it too. But at the same time, people are toxic in it also because of leaky gut.

What I am doing , is trying to increase amino acids/ minerals ratio. Which is achieved by fasting and chelating at the same time. It works. WE are sick since we are full of minerals and not only toxic ones, people taking these multivitaimins all the time, and getting sicker and sicker and older. Since amino acids need to exceed minerals, that is why fasting works for health, it improves amino acids to minerals ratio. Peat admits it too, that we are protein deficient( actually we are systemic protein deficient) .he is very smart. I just dont agree with his way out of this.

Good luck , guys
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
gbolduev said:
haidut said:
gbolduev said:
Milklove said:
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.


Well , how would you explain this then http://www.ncbi.nlm.nih.gov/pubmed/23426511
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .

And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more

And it has nothing to do with tryptophan , you need tryptophan and you are all deficient in it. It is the conversion rate of tryptophan to serotonin which is the problem and actually lack of tryptophan for niacin. So not eating tryptophan is not a cure it is a death sentence. FIX the conversion issue, not the raw material which other systems including T killers depend on

You raise some good points, but I don't think aggressive chelation is what will fix the underlying problem. First, for mercury chelation I would not take fulvic acid, I'd take fumaric and succinic acid. Thiamine (B1) can also chelate mercury and lead. Second, the study you posted has been discussed before and 100mg dose of nicotinamide is certainly not "excessive" as the study suggests and might as well push the serotonin higher. Doses of nicotinamide that lower serotonin are in 4g-8g range and that's what I would call excessive.
Now - about tryptophan. You can survive perfectly fine on a tryptophan-free diet after the age of about 18 when skeletal growth is complete, and in fact it is used as a life extension protocol in rodents.
http://www.ncbi.nlm.nih.gov/pubmed/22255
http://www.nutritionj.com/content/10/1/107

The reports fro mainstream medicine of low tryptophan lowering mood seems to be due to increasing sensitivity to light deprivation, which IMO signifies the central role of light in metabolism:
http://www.ei-resource.org/information/ ... ng-of-mood

So, based on what I have seen tryptophan does not seem to be essential in any way in adult organisms except for being the source of niacin. The role of tryptophan in infections/immunity you bring up is also disputed and there is some evidence that the purpose of the fever is to delete the body of iron AND also deplete tryptophan and tryptophan metabolites. I posted a study on that on the forum but can't find it right now. Also, tryptophan is required for the growth of many pathogenic bacteria. There are many studies to consider but here is one:
http://iai.asm.org/content/75/11/5105.full

Second, tryptophan is carcinogenic even in physiological doses. Chronic feeding of identical diets except that one contained an extra 0.2% tryptophan (human dose about 3g daily) increased cancer incidence in rats 5-fold. Also, as you probably know some of the tryptophan conversion pathways are neurotoxic and are implicated in diseases like ALS, MS, etc.
http://www.ncbi.nlm.nih.gov/pubmed/17956331
http://en.wikipedia.org/wiki/Kynurenine ... rotoxicity

In diseases of the GI like IBS, tryptophan depletion is one of the few known ways to arrest symptoms indefinitely (i.e. while maintaining tryptophan depleted state).
http://www.ei-resource.org/information/ ... l-syndrome

I agree with you that the conversion pathway matters but unless you want to mess with those there are only a few safe ways of steering tryptophan towards the niacin pathway using diet. Calcium intake is probably the primary method available to people not interested in taking drugs.
But, back to your chelation points - I agree with you on chelating mercury. If you know of a good iron chelation compound I would appreciate it if you share it with us.

Also , good points, but most of these studies are taken out of context and not valid. The cutting edge of cancer therapy these days are IDO inhibitors, IDO is the enzyme that breaks down tryptophan. Once again , it is not the tryptophan which is the bad guy but serotonin. IDO is iron based enzyme, same as the tryptophan to serotonin enzyme. IRON toxicity is what most of us have even with low ferritin levels.

I am on IDO inhibitors and my cancer is running away although 3 years ago , I could not even walk anymore. Tryptophan is essential anti cancer agent . ALl these studies are wrong. YOU need to block the conversion of tryptophan to serotonin that will give you tons of tryptophan and trust me you wont get cancer from it)) All these studies say to limit tryptophan , but it should say limit the conversion and increase tryptophan.

There are no good iron chelators honestly that I know of. Fulvic acid will chelate mercury amazingly and you need to drink that always, but not fulvic minerals, just fulvic acid. I dealt with about 1000 people this year since I am trying to help many , and these people tested extensively and most of them have one problem. Low bioavailable copper because of tons of estrogen mimics, high iron and this actually opens up IDO enzyme and opens up the enzyme which converts tryptophan to serotonin simulnatenously . this is the main problem with almost everyone. And these diets wont do anything, since even if you take care of couple of neurological symptoms with the diet or niacinamide , the main copper problem wont go away, and that will be getting worse. Mercury wont come out on its own .
And believe me DMSA and ALA works, but you need to use frequent chelation protocol with low dosages, like Andy Cutlers. it does work and it has very little side effects. At the same time, you can always balance your minerals with hair tests, so you dont crash while chelating, since estrogen mimics are what holding your adrenals up, and it should be held on copper , not on mercury or cadmium , so obviously when mercury comes out, adrenals will crash until copper goes there.

Anyway , this is what I am doing, and this is working. I tried every diet possible, and Ray Peat is a smart guy , but I think he misses what comes first and what comes second. The diet wont help , and actually can make it worse. I prefer to see my progression and not cover it up.
Chronic loss of copper is happening and I think Peat admits it too. But at the same time, people are toxic in it also because of leaky gut.

What I am doing , is trying to increase amino acids/ minerals ratio. Which is achieved by fasting and chelating at the same time. It works. WE are sick since we are full of minerals and not only toxic ones, people taking these multivitaimins all the time, and getting sicker and sicker and older. Since amino acids need to exceed minerals, that is why fasting works for health, it improves amino acids to minerals ratio. Peat admits it too, that we are protein deficient( actually we are systemic protein deficient) .he is very smart. I just dont agree with his way out of this.

Good luck , guys

Again, good points. Just out of curiosity, what is your take on this issue?
http://en.wikipedia.org/wiki/Eosinophil ... a_syndrome
Peat said that tryptophan caused this issue and it was not due to the impurities but the amino acid itself. I personally get double vision whenever I eat protein high in tryptophan, but do not get this when I eat tryptophan-depleted foods or take BCAA with the high tryptophan foods. I doubt it is purely psychological.

If iron toxicity is so bad how about using some aspirin to deplete iron stores? Have you seen this study?
http://ajcn.nutrition.org/content/74/2/219.full
The old study on fever I posted somewhere on the forum said that higher body temperatures depletes iron stores. Maybe that's another reason high metabolism is good - chronically higher temperature will lower iron stores.
 

gbolduev

Member
Joined
Jun 26, 2014
Messages
464
haidut said:
gbolduev said:
haidut said:
gbolduev said:
Milklove said:
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.


Well , how would you explain this then http://www.ncbi.nlm.nih.gov/pubmed/23426511
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .

And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more

And it has nothing to do with tryptophan , you need tryptophan and you are all deficient in it. It is the conversion rate of tryptophan to serotonin which is the problem and actually lack of tryptophan for niacin. So not eating tryptophan is not a cure it is a death sentence. FIX the conversion issue, not the raw material which other systems including T killers depend on

You raise some good points, but I don't think aggressive chelation is what will fix the underlying problem. First, for mercury chelation I would not take fulvic acid, I'd take fumaric and succinic acid. Thiamine (B1) can also chelate mercury and lead. Second, the study you posted has been discussed before and 100mg dose of nicotinamide is certainly not "excessive" as the study suggests and might as well push the serotonin higher. Doses of nicotinamide that lower serotonin are in 4g-8g range and that's what I would call excessive.
Now - about tryptophan. You can survive perfectly fine on a tryptophan-free diet after the age of about 18 when skeletal growth is complete, and in fact it is used as a life extension protocol in rodents.
http://www.ncbi.nlm.nih.gov/pubmed/22255
http://www.nutritionj.com/content/10/1/107

The reports fro mainstream medicine of low tryptophan lowering mood seems to be due to increasing sensitivity to light deprivation, which IMO signifies the central role of light in metabolism:
http://www.ei-resource.org/information/ ... ng-of-mood

So, based on what I have seen tryptophan does not seem to be essential in any way in adult organisms except for being the source of niacin. The role of tryptophan in infections/immunity you bring up is also disputed and there is some evidence that the purpose of the fever is to delete the body of iron AND also deplete tryptophan and tryptophan metabolites. I posted a study on that on the forum but can't find it right now. Also, tryptophan is required for the growth of many pathogenic bacteria. There are many studies to consider but here is one:
http://iai.asm.org/content/75/11/5105.full

Second, tryptophan is carcinogenic even in physiological doses. Chronic feeding of identical diets except that one contained an extra 0.2% tryptophan (human dose about 3g daily) increased cancer incidence in rats 5-fold. Also, as you probably know some of the tryptophan conversion pathways are neurotoxic and are implicated in diseases like ALS, MS, etc.
http://www.ncbi.nlm.nih.gov/pubmed/17956331
http://en.wikipedia.org/wiki/Kynurenine ... rotoxicity

In diseases of the GI like IBS, tryptophan depletion is one of the few known ways to arrest symptoms indefinitely (i.e. while maintaining tryptophan depleted state).
http://www.ei-resource.org/information/ ... l-syndrome

I agree with you that the conversion pathway matters but unless you want to mess with those there are only a few safe ways of steering tryptophan towards the niacin pathway using diet. Calcium intake is probably the primary method available to people not interested in taking drugs.
But, back to your chelation points - I agree with you on chelating mercury. If you know of a good iron chelation compound I would appreciate it if you share it with us.

Also , good points, but most of these studies are taken out of context and not valid. The cutting edge of cancer therapy these days are IDO inhibitors, IDO is the enzyme that breaks down tryptophan. Once again , it is not the tryptophan which is the bad guy but serotonin. IDO is iron based enzyme, same as the tryptophan to serotonin enzyme. IRON toxicity is what most of us have even with low ferritin levels.

I am on IDO inhibitors and my cancer is running away although 3 years ago , I could not even walk anymore. Tryptophan is essential anti cancer agent . ALl these studies are wrong. YOU need to block the conversion of tryptophan to serotonin that will give you tons of tryptophan and trust me you wont get cancer from it)) All these studies say to limit tryptophan , but it should say limit the conversion and increase tryptophan.

There are no good iron chelators honestly that I know of. Fulvic acid will chelate mercury amazingly and you need to drink that always, but not fulvic minerals, just fulvic acid. I dealt with about 1000 people this year since I am trying to help many , and these people tested extensively and most of them have one problem. Low bioavailable copper because of tons of estrogen mimics, high iron and this actually opens up IDO enzyme and opens up the enzyme which converts tryptophan to serotonin simulnatenously . this is the main problem with almost everyone. And these diets wont do anything, since even if you take care of couple of neurological symptoms with the diet or niacinamide , the main copper problem wont go away, and that will be getting worse. Mercury wont come out on its own .
And believe me DMSA and ALA works, but you need to use frequent chelation protocol with low dosages, like Andy Cutlers. it does work and it has very little side effects. At the same time, you can always balance your minerals with hair tests, so you dont crash while chelating, since estrogen mimics are what holding your adrenals up, and it should be held on copper , not on mercury or cadmium , so obviously when mercury comes out, adrenals will crash until copper goes there.

Anyway , this is what I am doing, and this is working. I tried every diet possible, and Ray Peat is a smart guy , but I think he misses what comes first and what comes second. The diet wont help , and actually can make it worse. I prefer to see my progression and not cover it up.
Chronic loss of copper is happening and I think Peat admits it too. But at the same time, people are toxic in it also because of leaky gut.

What I am doing , is trying to increase amino acids/ minerals ratio. Which is achieved by fasting and chelating at the same time. It works. WE are sick since we are full of minerals and not only toxic ones, people taking these multivitaimins all the time, and getting sicker and sicker and older. Since amino acids need to exceed minerals, that is why fasting works for health, it improves amino acids to minerals ratio. Peat admits it too, that we are protein deficient( actually we are systemic protein deficient) .he is very smart. I just dont agree with his way out of this.

Good luck , guys

Again, good points. Just out of curiosity, what is your take on this issue?
http://en.wikipedia.org/wiki/Eosinophil ... a_syndrome
Peat said that tryptophan caused this issue and it was not due to the impurities but the amino acid itself. I personally get double vision whenever I eat protein high in tryptophan, but do not get this when I eat tryptophan-depleted foods or take BCAA with the high tryptophan foods. I doubt it is purely psychological.

If iron toxicity is so bad how about using some aspirin to deplete iron stores? Have you seen this study?
http://ajcn.nutrition.org/content/74/2/219.full
The old study on fever I posted somewhere on the forum said that higher body temperatures depletes iron stores. Maybe that's another reason high metabolism is good - chronically higher temperature will lower iron stores.

I doubt aspirin chelates iron, I think it simply lowers COX-1 and COX-2 which in turn lowers inflammation causing copper to be more bioavailable and ferritin lower. I doubt if you have high iron in your organs it will chelate it, I think it can regulate iron stores by reducing inflammation , but that is quite different from chelating free iron from organs.

As far as tryptophan, personally I never get double vision from tryptophan rich food or supplements , I am less iron toxic now and I used to get so much blurry vision from iron rich foods before. I mean you can always follow up on what you doing with blood tests or hairtests and see if you are doing good and going in the right path.
I am not sure about that case of eosinophilia , I think peats point is speculative . I know that many people are trying to inhibits IDO , and this raises tryptophan to niacin availability and they have amazing results against cancer. This is well documented and you can find many cases online, although that eosiniphillia thing is as if taken from the horror book and no one really can read solid facts on it.

I think, yes, higher temperatures can deplete iron, may be that is why hypertermia works for cancer where they put you in the special camera and raise your temperatures to 41C.
Although I doubt if you have high metabolism that will deplete iron. HIgh metabolism usually goes along with high stomach acid and lower copper stores, so may be high iron to copper ratio. I think chronic copper loss from the system is what makes your body slow down as we get older. May be that is the reason we see slow oxidizers on hairtests, their body needs to slow down to retain copper . OF course mineral transport could be also impaired with the presence of estrogen mimics.
To me higher metabolism is good, since your detox is higher and it might regulate iron stores if you have pure high metabolism , but most people dont have pure high metabolism . If they have high metabolism it is caused by toxic metals, like cadmium which in turn raises your adrenals and thyroid. So to me this kind of metabolism is not healthy. Of course if you chelate everything out and then you are so clean that you have higher metabolism on your own , then I would say yes it is very good. Other than that, I think only kids have pure higher metabolism . Most adults if they do, that is because they are toxic in something causing it


Chelating iron is tough. Exercise while staying away from iron rich food , will chelate it over time

It is just too tough to follow these studies, you need to test yourself, ALL these studies are taken out of context. And I used to create theories based on studies before, but then my theories would be broken by trying it in real life and testing.

good luck , and I hope this helps
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
gbolduev said:
haidut said:
gbolduev said:
haidut said:
gbolduev said:
Milklove said:
gbolduev said:
haidut said:
janna0805 said:
Also, there is a much older article about the role of nicotinamide on uptake and release of serotonin, in which very high doses of nicotinamide are used in the brain cortex of diabetic rats:

http://www.ncbi.nlm.nih.gov/pubmed/8588246

Ukr Biokhim Zh. 1995 Jan-Feb;67(1):105-11.

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].
[Article in Russian]
Donchenko GV, Kuchmerovskaia TM, Parkhomets PK, Obrosova IG, Klimenko AP, Efimov AS.

Abstract
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.

Actually, I think with this study you got it backwards. It does not show increase of serotonin but a "decrease" of sorts. Remember, we want a HIGH uptake of serotonin so that it does not freely float around. In one of Ray's article he talks about how caffeine "promotes uptake of serotonin" and how that is a good thing. In addition, the drug tianeptine is a Selective Serotonin Reuptake Enhancer (SSRE) and is used to lower levels of serotonin by, well, increasing uptake. Here is the quote from the posted study:

"Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels"

So, niacinamide / nicotinamide administration of what amounts to a human dose of about 2,500mg a day resulted in normalizing serotonin uptake to the levels of control animals. So, niacinamide does indeed lower serotonin in this dose in a manner similar to tianeptine.


It looks like you did not read this study correctly, it says it increases serotonin uptake within first 3 minutes huge. Where did you read that it lowered it.

Haidut did read the study correct. HIGH serotonin uptake leads to LOW plasma serotonin levels, which is what we want. In the study niacinamide restored low serotonin uptake to normal - it increased serotonin uptake.


Well , how would you explain this then http://www.ncbi.nlm.nih.gov/pubmed/23426511
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .

And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more

And it has nothing to do with tryptophan , you need tryptophan and you are all deficient in it. It is the conversion rate of tryptophan to serotonin which is the problem and actually lack of tryptophan for niacin. So not eating tryptophan is not a cure it is a death sentence. FIX the conversion issue, not the raw material which other systems including T killers depend on

You raise some good points, but I don't think aggressive chelation is what will fix the underlying problem. First, for mercury chelation I would not take fulvic acid, I'd take fumaric and succinic acid. Thiamine (B1) can also chelate mercury and lead. Second, the study you posted has been discussed before and 100mg dose of nicotinamide is certainly not "excessive" as the study suggests and might as well push the serotonin higher. Doses of nicotinamide that lower serotonin are in 4g-8g range and that's what I would call excessive.
Now - about tryptophan. You can survive perfectly fine on a tryptophan-free diet after the age of about 18 when skeletal growth is complete, and in fact it is used as a life extension protocol in rodents.
http://www.ncbi.nlm.nih.gov/pubmed/22255
http://www.nutritionj.com/content/10/1/107

The reports fro mainstream medicine of low tryptophan lowering mood seems to be due to increasing sensitivity to light deprivation, which IMO signifies the central role of light in metabolism:
http://www.ei-resource.org/information/ ... ng-of-mood

So, based on what I have seen tryptophan does not seem to be essential in any way in adult organisms except for being the source of niacin. The role of tryptophan in infections/immunity you bring up is also disputed and there is some evidence that the purpose of the fever is to delete the body of iron AND also deplete tryptophan and tryptophan metabolites. I posted a study on that on the forum but can't find it right now. Also, tryptophan is required for the growth of many pathogenic bacteria. There are many studies to consider but here is one:
http://iai.asm.org/content/75/11/5105.full

Second, tryptophan is carcinogenic even in physiological doses. Chronic feeding of identical diets except that one contained an extra 0.2% tryptophan (human dose about 3g daily) increased cancer incidence in rats 5-fold. Also, as you probably know some of the tryptophan conversion pathways are neurotoxic and are implicated in diseases like ALS, MS, etc.
http://www.ncbi.nlm.nih.gov/pubmed/17956331
http://en.wikipedia.org/wiki/Kynurenine ... rotoxicity

In diseases of the GI like IBS, tryptophan depletion is one of the few known ways to arrest symptoms indefinitely (i.e. while maintaining tryptophan depleted state).
http://www.ei-resource.org/information/ ... l-syndrome

I agree with you that the conversion pathway matters but unless you want to mess with those there are only a few safe ways of steering tryptophan towards the niacin pathway using diet. Calcium intake is probably the primary method available to people not interested in taking drugs.
But, back to your chelation points - I agree with you on chelating mercury. If you know of a good iron chelation compound I would appreciate it if you share it with us.

Also , good points, but most of these studies are taken out of context and not valid. The cutting edge of cancer therapy these days are IDO inhibitors, IDO is the enzyme that breaks down tryptophan. Once again , it is not the tryptophan which is the bad guy but serotonin. IDO is iron based enzyme, same as the tryptophan to serotonin enzyme. IRON toxicity is what most of us have even with low ferritin levels.

I am on IDO inhibitors and my cancer is running away although 3 years ago , I could not even walk anymore. Tryptophan is essential anti cancer agent . ALl these studies are wrong. YOU need to block the conversion of tryptophan to serotonin that will give you tons of tryptophan and trust me you wont get cancer from it)) All these studies say to limit tryptophan , but it should say limit the conversion and increase tryptophan.

There are no good iron chelators honestly that I know of. Fulvic acid will chelate mercury amazingly and you need to drink that always, but not fulvic minerals, just fulvic acid. I dealt with about 1000 people this year since I am trying to help many , and these people tested extensively and most of them have one problem. Low bioavailable copper because of tons of estrogen mimics, high iron and this actually opens up IDO enzyme and opens up the enzyme which converts tryptophan to serotonin simulnatenously . this is the main problem with almost everyone. And these diets wont do anything, since even if you take care of couple of neurological symptoms with the diet or niacinamide , the main copper problem wont go away, and that will be getting worse. Mercury wont come out on its own .
And believe me DMSA and ALA works, but you need to use frequent chelation protocol with low dosages, like Andy Cutlers. it does work and it has very little side effects. At the same time, you can always balance your minerals with hair tests, so you dont crash while chelating, since estrogen mimics are what holding your adrenals up, and it should be held on copper , not on mercury or cadmium , so obviously when mercury comes out, adrenals will crash until copper goes there.

Anyway , this is what I am doing, and this is working. I tried every diet possible, and Ray Peat is a smart guy , but I think he misses what comes first and what comes second. The diet wont help , and actually can make it worse. I prefer to see my progression and not cover it up.
Chronic loss of copper is happening and I think Peat admits it too. But at the same time, people are toxic in it also because of leaky gut.

What I am doing , is trying to increase amino acids/ minerals ratio. Which is achieved by fasting and chelating at the same time. It works. WE are sick since we are full of minerals and not only toxic ones, people taking these multivitaimins all the time, and getting sicker and sicker and older. Since amino acids need to exceed minerals, that is why fasting works for health, it improves amino acids to minerals ratio. Peat admits it too, that we are protein deficient( actually we are systemic protein deficient) .he is very smart. I just dont agree with his way out of this.

Good luck , guys

Again, good points. Just out of curiosity, what is your take on this issue?
http://en.wikipedia.org/wiki/Eosinophil ... a_syndrome
Peat said that tryptophan caused this issue and it was not due to the impurities but the amino acid itself. I personally get double vision whenever I eat protein high in tryptophan, but do not get this when I eat tryptophan-depleted foods or take BCAA with the high tryptophan foods. I doubt it is purely psychological.

If iron toxicity is so bad how about using some aspirin to deplete iron stores? Have you seen this study?
http://ajcn.nutrition.org/content/74/2/219.full
The old study on fever I posted somewhere on the forum said that higher body temperatures depletes iron stores. Maybe that's another reason high metabolism is good - chronically higher temperature will lower iron stores.

I doubt aspirin chelates iron, I think it simply lowers COX-1 and COX-2 which in turn lowers inflammation causing copper to be more bioavailable and ferritin lower. I doubt if you have high iron in your organs it will chelate it, I think it can regulate iron stores by reducing inflammation , but that is quite different from chelating free iron from organs.

As far as tryptophan, personally I never get double vision from tryptophan rich food or supplements , I am less iron toxic now and I used to get so much blurry vision from iron rich foods before. I mean you can always follow up on what you doing with blood tests or hairtests and see if you are doing good and going in the right path.
I am not sure about that case of eosinophilia , I think peats point is speculative . I know that many people are trying to inhibits IDO , and this raises tryptophan to niacin availability and they have amazing results against cancer. This is well documented and you can find many cases online, although that eosiniphillia thing is as if taken from the horror book and no one really can read solid facts on it.

I think, yes, higher temperatures can deplete iron, may be that is why hypertermia works for cancer where they put you in the special camera and raise your temperatures to 41C.
Although I doubt if you have high metabolism that will deplete iron. HIgh metabolism usually goes along with high stomach acid and lower copper stores, so may be high iron to copper ratio. I think chronic copper loss from the system is what makes your body slow down as we get older. May be that is the reason we see slow oxidizers on hairtests, their body needs to slow down to retain copper . OF course mineral transport could be also impaired with the presence of estrogen mimics.
To me higher metabolism is good, since your detox is higher and it might regulate iron stores if you have pure high metabolism , but most people dont have pure high metabolism . If they have high metabolism it is caused by toxic metals, like cadmium which in turn raises your adrenals and thyroid. So to me this kind of metabolism is not healthy. Of course if you chelate everything out and then you are so clean that you have higher metabolism on your own , then I would say yes it is very good. Other than that, I think only kids have pure higher metabolism . Most adults if they do, that is because they are toxic in something causing it


Chelating iron is tough. Exercise while staying away from iron rich food , will chelate it over time

It is just too tough to follow these studies, you need to test yourself, ALL these studies are taken out of context. And I used to create theories based on studies before, but then my theories would be broken by trying it in real life and testing.

good luck , and I hope this helps

OK, thanks. Couple of more things. In your post you said that IDO inhibitors inhibit the conversion of tryptophan to serotonin. However, based on what I read IDO is the enzyme that steers tryptophan into the kynurenine pathway.
http://en.wikipedia.org/wiki/Indoleamin ... ioxygenase

This is in line with my post where I said that tryptophan has a least 2 toxic pathways - serotonin and kynurenine. So, I absolutely agree with you that IDO inhibitors will be helpful in cancer b/c the kynurenine pathway is toxic and implicated in many diseases like cancer and pretty much every neurodegenerative disease as well. However, if you inhibit IDO then you will also be inhibiting niacin synthesis b/c niacin is the end-product of the kynurenine pathway. Also, in line with your post if one wants to do get even more benefits one should inhibit both IDO and TPH. TPH1 is what synthesizes serotonin in the brain. For best results, one should probably inhibit both TPH1 and TPH2 since serotonin can wreak havoc in the gut as well.
If you inhibit both TPH and IDO then tryptophan will probably get excreted or used to synthesize muscle tissue if there is enough BCAA to cause anabolic action.
So, I think we can agree that both patways of tryptophan metabolism (IDO and TPH) are pretty toxic and only the IDO pathway can result in a beneficial metabolite at the very end (niacin). We also agree that inhibitong both pathways IDO and TPH (e.g. p-choloro-phenylalanine inhibits both TPH1 and TPH2) would be optimal for cancer but then one has to supplement niacin.
However, with all that being said, there is still evidence that tryptophan is directly carcinogenic to cells even without being metabolized. Here are some things to consider:
http://www.ncbi.nlm.nih.gov/pubmed/3591519
http://www.ncbi.nlm.nih.gov/pubmed/9457738
http://cancerres.aacrjournals.org/conte ... 7.abstract

After reading the studies, I think the effect is very small and it is likely that if tryptophan is ingested as part of high protein meals then it probably is mostly harmless, assuming one inhibits both IDO and TPH.
BUT, for people who overexpress IDO or TPH (or both) due to heavy metal toxicity like you said, tryptophan can be rather dangerous. Agree?

The points on iron and copper you raise are very good. Ray has written on the positive effects of tocopherol (vitamin E) on the age pigment lipofuscin. It seems that tocopherol may also inhibit iron accumulation as well.
http://link.springer.com/article/10.1007%2FBF01277665
"...The results demonstrated that both DFO and vitamin E inhibit the iron accumulation and thus reverses the increase in oxidized glutathione (GSSG), oxidized to reduced glutathione ratios, .OH and lipid peroxidation levels."

Some herbs that inhibit iron accumulation are basil, cinnamon, rosemary, and clove. However, clove is extremely estrogenic so probably not a good choice for an iron chelator.
http://onlinelibrary.wiley.com/doi/10.1 ... 0156.x/pdf
"...Hinneburg and others (2006) reported that hydrodistilled extracts from basil and laurel had the highest antioxidant activities of several herbs (basil, laurel, parsley, juniper, aniseed, fennel, cumin, cardamom, and ginger) but not the greatest iron chelation ability. In a linoleic acid peroxidation assay, basil extract was as effective as Trolox. Basil also exhibited significant iron-reducing capacity."
"...Cinnamon leaf oil has a significant inhibitory effect on hydroxyl radicals and acts as an iron chelator efficiently inhibiting formation of conjugated dienes and generation of secondary products from lipid peroxidation at a concentration equivalent to BHT."
"...Clove essential oil is inhibitory toward hydroxyl radicals and can chelate iron. Comparing 16 spices, Khatun and others (2006) found that clove had the highest radical-scavenging activity followed by allspice and cinnamon."
"...In lipid-based systems, carnosic acid and carnosol effectively chelate iron and scavenge peroxyl radical (Arouma and others 1992)."

Finally, as far as metabolism goes - I think Peat is in favor of achieving the "child-type" metabolism and not the adrenalin-driven metabolism of most adults. Since thyroid stimulates glucose oxidation and adrenalin stimulates fat oxidation I would say that they are mostly antagonistic to each other. Do you have an example or study with people who have both high adrenalin and AND thyroid activity b/c some heavy metal like cadmium is causing BOTH adrenals and thyroid to be overactive?
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
I just wanted to add that virtually all IDO inhibitors are also iron chelators of both heme and non-heme iron. So, the benefit in cancer @gbolduev reports is likely due to a large degree to iron depletion. Iron chelators are currently in clinical trials for pretty much all types of disease - cancer, autoimmune, neurological, GI tract, diabetes, and aging itself.
Here is one of the safe pharmaceutical-grade iron chelators that can be obtained without prescription.
http://www.scbt.com/datasheet-204192-Py ... azone.html

Some other safe inhibitors of iron absorption below.

Sugar:
http://www.sciencedirect.com/science/ar ... 0263912642

Coffee:
http://www.ncbi.nlm.nih.gov/pubmed/9501514

Milk Thistle (chelating iron is probably the main MOA behind its protective effects on liver):
http://www.ncbi.nlm.nih.gov/pubmed/11410232

Milk protein (and especially casein):
http://www.ncbi.nlm.nih.gov/pubmed/11382547
http://www.ncbi.nlm.nih.gov/pubmed/16189201

Vitamin K and possibly other quinones line Cascara and Aloe:
http://www.ncbi.nlm.nih.gov/pubmed/18274994

Calcium apparently also inhibits absorption of heme iron as long as each individual dosage of calcium exceeds 300mg, which is about the amount found in a glass of milk. The combination of calcium and milk proteins probably makes things like cheese/milk/yogurt a very powerful tool to control iron levels.
 

gbolduev

Member
Joined
Jun 26, 2014
Messages
464
haidut said:
I just wanted to add that virtually all IDO inhibitors are also iron chelators of both heme and non-heme iron. So, the benefit in cancer @gbolduev reports is likely due to a large degree to iron depletion. Iron chelators are currently in clinical trials for pretty much all types of disease - cancer, autoimmune, neurological, GI tract, diabetes, and aging itself.
Here is one of the safe pharmaceutical-grade iron chelators that can be obtained without prescription.
http://www.scbt.com/datasheet-204192-Py ... azone.html

Some other safe inhibitors of iron absorption below.

Sugar:
http://www.sciencedirect.com/science/ar ... 0263912642

Coffee:
http://www.ncbi.nlm.nih.gov/pubmed/9501514

Milk Thistle (chelating iron is probably the main MOA behind its protective effects on liver):
http://www.ncbi.nlm.nih.gov/pubmed/11410232

Milk protein (and especially casein):
http://www.ncbi.nlm.nih.gov/pubmed/11382547
http://www.ncbi.nlm.nih.gov/pubmed/16189201

Vitamin K and possibly other quinones line Cascara and Aloe:
http://www.ncbi.nlm.nih.gov/pubmed/18274994

Calcium apparently also inhibits absorption of heme iron as long as each individual dosage of calcium exceeds 300mg, which is about the amount found in a glass of milk. The combination of calcium and milk proteins probably makes things like cheese/milk/yogurt a very powerful tool to control iron levels.


Yes, I inhibit both IDO and TPH . IDO is iron based so is MAO-B , so is enzyme that converts tryptophan to serotonin. chelation of iron is one thing I am concentrated on. Also improving copper metabolism ruined by mercury cadmium and SIBO


I take nicotinamide and rosmarinic acid to inhibit IDO and increase tryptophan. Nicotanimide raises tryptophan in blood. Nicotinamide also increases uptake of serotonin as you mentioned.


Read this, it is not as straight forward as you think
http://www.csom.ca/wp-content/uploads/2 ... a-26.2.pdf

It says that niacinamide increases tryptophan level in blood. Well it would be obvious since its feed back cycle on
Kynurenine pathway. Now the question is , how is that lowering your serotonin?
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
gbolduev said:
haidut said:
I just wanted to add that virtually all IDO inhibitors are also iron chelators of both heme and non-heme iron. So, the benefit in cancer @gbolduev reports is likely due to a large degree to iron depletion. Iron chelators are currently in clinical trials for pretty much all types of disease - cancer, autoimmune, neurological, GI tract, diabetes, and aging itself.
Here is one of the safe pharmaceutical-grade iron chelators that can be obtained without prescription.
http://www.scbt.com/datasheet-204192-Py ... azone.html

Some other safe inhibitors of iron absorption below.

Sugar:
http://www.sciencedirect.com/science/ar ... 0263912642

Coffee:
http://www.ncbi.nlm.nih.gov/pubmed/9501514

Milk Thistle (chelating iron is probably the main MOA behind its protective effects on liver):
http://www.ncbi.nlm.nih.gov/pubmed/11410232

Milk protein (and especially casein):
http://www.ncbi.nlm.nih.gov/pubmed/11382547
http://www.ncbi.nlm.nih.gov/pubmed/16189201

Vitamin K and possibly other quinones line Cascara and Aloe:
http://www.ncbi.nlm.nih.gov/pubmed/18274994

Calcium apparently also inhibits absorption of heme iron as long as each individual dosage of calcium exceeds 300mg, which is about the amount found in a glass of milk. The combination of calcium and milk proteins probably makes things like cheese/milk/yogurt a very powerful tool to control iron levels.


Yes, I inhibit both IDO and TPH . IDO is iron based so is MAO-B , so is enzyme that converts tryptophan to serotonin. chelation of iron is one thing I am concentrated on. Also improving copper metabolism ruined by mercury cadmium and SIBO


I take nicotinamide and rosmarinic acid to inhibit IDO and increase tryptophan. Nicotanimide raises tryptophan in blood. Nicotinamide also increases uptake of serotonin as you mentioned.


Read this, it is not as straight forward as you think
http://www.csom.ca/wp-content/uploads/2 ... a-26.2.pdf

It says that niacinamide increases tryptophan level in blood. Well it would be obvious since its feed back cycle on
Kynurenine pathway. Now the question is , how is that lowering your serotonin?

The study I posted at the beginning of the thread said that niacinamide acts like anti-metabolite of serotonin. The authors were not sure if it actually lowers plasma serotonin levels but niacinamide antagonized fully the effects of serotonin on the organs they tested. So, they called it an anti-metabolite and antagonist. I am not sure the human dose 4g-8g reported in the study is something I would take long term. There are probably better ways to lower serotonin synthesis as you point out.
 

pboy

Member
Joined
Jan 22, 2013
Messages
1,681
my goodness what a topic...im surprised I didn't find it earlier...I could only read the first page before wanting to post. That post above by haidut has to be the biggest quote in quote post I may have ever seen...lol. Very nice info

I just have 2 questions....

#1 it seems the various forms of niacin..nocotini acid, nicotinamide, and various active enzymatic forms are all present in food...but all just listed as 'NE', or niacin
equivalents....so theres no reliable way to tell which form is in the food based on most data. Do you know whether b3 in food is generally nicotinamide, or if foods high in b3 might be better avoided? As it stands my intake is pretty low from food but satisfies. Do you think it would be a better idea to split the various niacin equivalents into different classes of vits, so that people could make a more intelligent choice? Because as it stands, recommendations to people are made that all NE's go towards meeting your daily need and they pretty much are all the same...but from what haidut is eloquently stating, they are not the same...and in
fact it might be very important to make a distuingishment

#2 could nicotine itself just be another 'NE', niacin equivalent? And if so, is it detrimental or beneficial?

I smoke tobacco, it is a double edged sword or sorts in some ways, but man I think ive been able to flow through my life quite a bit better the past few years...in
many many ways, via using pipe tobacco. If nothing else the fact it can reliably induce sleep or a bowel movement (when one is due) whenever you use a high enough amount is like...beyond huge for every day ease of life
 
Joined
Nov 26, 2013
Messages
7,370
What is wrong with blood letting for iron excess?
 

jyb

Member
Joined
Nov 9, 2012
Messages
2,783
Location
UK
Such_Saturation said:
What is wrong with blood letting for iron excess?

The only downside I can think of is not knowing when a good level is reached, so you might need to test after a while of doing it every few months.
 

pboy

Member
Joined
Jan 22, 2013
Messages
1,681
I find it interesting that cacao beans were reserved mostly for the priest and political class in Aztec America...and the mayans generally relegated cacao use to men only. The reason I find it interesting is because they were apparently consuming copious amounts, and cacao is high in iron. Cacao was associated with many rituals around blood and a lot involved men blood letting. I wonder if this is an artifact of them realizing that cacao builds blood, but in excess is bad...so those consuming
a lot of cacao should blood let frequently or relatively frequently. The Aztec word for cacao was something like 'heart, blood'...and was known to build the blood...to me indicating copper and iron, iron mostly. The whole symoblogy is pretty cool and interesting...the essence of having so much blood you must give, that cacao was for the priest and more influential classes...its sort of a representation, the blood letting, of the duties of sacrifice or giving your blood, vital essence, to the people...cacao helped do this

Maybe none of this is related but I found it interesting. The fat European aristocrats in older times who ate all that organ meat and all had gout probably could have benefitted from blood letting...lol, maybe they wouldn't have been so domineering and aggressive if they had

I don't personally donate blood but I get cuts or scrapes now and then, and mosquitos like to take it from me
 

Similar threads

Back
Top Bottom