How to lower norepinephrine

[ttt]

Triffid, I don't have any suggestions, but just more questions. I don't understand the potassium thing and why it's so important. What I can say is that I have really bad adrenal fatigue, and outrageous salt cravings, so I have about a tablespoon of sea salt per day. I realize that sodium needs to be balanced by potassium, but my understanding was that it's not a good idea to take potassium if you have adrenal fatigue. I've started taking 100mg of Krebs potassium a day, because Yasko recommended it, and I also take electrolyte drops in my water. But I don't understand how the methylation creates problems with potassium. Would love to understand this more, since I think I have a big electrolyte issue.

 

[triffid113]

Triffid, how much P5P do you take? The Yasko camp has said to avoid it, but I just don't think that's right. So I've started taking about 40-50mg, and I wonder if I'm taking too much or too little. Here, I'm hearing that a lot of people disagree with Yasko about CBS. I'm CBS+/-, but my ammonia is low and my sulfur is high.

I have been taking 50mg P5P for years (5) in addition to what I get in 2x/day of Thorne Basic B (some small amount there). My homocysteine is normal per lab tests with 2x/day Thorne Basic B, 2g TMG, 50mg P5P, 800 mcg mfolate. It is not normal with only 2x/day Thorne Basic B (it is elevated 50% on that protocol). I tried 300 mg P5P and it made no difference vs 50mg as far as methylation , so I have been taking 50mg for years. However I recently read that P5P also helps make neurotransmitters and I am low in dopamine and serotonin so I decided to try 100mg P5P for that reason and it DID raise my dopamine (you get euphoric on raised dopamine). There is a $64 blood test for homocysteine you can order from www.lef.org (or your doc) and there is a neurotransmitter test you can order but it is expensive ($300?) and I always had it ordered by docs so I don't remember the company. Anyway, you can tell about the dopamine...if you raise it it causes euphoria although people say this feeling fades as you become used to the extra dopamine (so maybe it's more accurate to say that you can feel a RISE in dopamine). Someone else who who felt they could not tolerate the methylation protocol as it caused terrible itching found they were fine if they took P5P. If I were you I would try just taking a good B complex 2x/day (as far as methylation) and test my homocysteine and see if it is right or if I have to do any further tinkering. That presupposes a good diet with sufficient choline and TMG. You can look here to see how much betaine is in your diet: http://nutritiondata.self.com/tools/nutrient-search
People who get tghe most betaine (TMG) by diet get 2g/day. I highly advise everyoe to take a good multi to get a wide assortment of nutritional substances needed for biochemistry and also to take antioxidants. You shoudl have your D3 levels tested as well.

 

[triffid113]

I have adrenal issues as well. But I have 3 genes that cause very very high blood pressure and blood pressure issues make it easy to surmise potassium levels. I measured my b.p. many times per day to determine how it was affected by what and I wrote down what I ate etc. I discovered that if I ate too much salt it would most affect the bottom number, which would stay raised for 3 days as it took that long to drain the salt out of me. If I did not eat enough fruits and veggies (7 or more!) then the top number would primarily rise and that would come down right away with potassium. Now low potassium and/or high salt affects both numbers of the b.p., but the potassium affects the top number much more whereas salt affects the bottom number much more. So if the top number of my bp is above 120 but the bottom number is not above 90, then I know I am low in potassium, for instance. SInce I can measure what is going on instantaneously, I can tell you that this number DOES JUMP AROUND instantaneously. Thus I am nervous about controlling it via an even monthly blood test. I am very aware that electrolytes changes instantaneously.

Freddd is the guy who found that active methylation causes electrolyte issues and he found this through blood tests with his doc and emergency visits. Other people here who were unaware of this have also found themselves making emergency doctor visits to have it diagnosed. Freddd theorized that starting up methylation opens up previously closed biochemical pathways which require more use of potassium. Methyls are used by the body to turn off/on chemical reactions. Our biochemistry is like a big blueprint and methyls are like coffee cups. When a coffee cup covers a certain portion of the map we cannot see what is behind it ad thus cannot build whatever is specified under the coffee cup. (This is an analogy for gene expression). Anyway the point is the methyls are the on/off switch. If you now are able to turn things on that you could not before you can surely see that these chemical reactions will need various vitamins, minerals, and cofactors to work.

I have such bad allergies fyi that my adrenal gland goes out during allergy season and my bp goes low. At that time I have to eat salt or pass out. It is very weird that despite high bp normally (cant eat salt) suddenly I have low bp (and have to eat salt). I find I need higher zinc to help both my thyroid and adrenal gland during allergy season. My doc also put me on 1g tyrosine / day to help my thyroid and said there was a tie between thyroid and adrenal performance so I need to supplement for my thyroid to protect my adrenals. Well since I take a multi I am actually covered for all the low level supplements needed by the thyroid and only need to worry about things needed in higher dose like tyrosine and zinc. The adrenal gland supposedly benefits from B5 (pantothene) but I get that from my B complex. I find with my supplementation regime, that as soon as I stop going through zinc at a ferocious rate (as soon as allergy season is over in other words) that my adrenal gland recovers right away).

Oh, I take zinc picolinate. I found a study showing the picolinate form of zinc is extremely more absorbable than other forms and since I switched to zinc picolinate I can get buy with only 50mg zinc. Zinc helps me breathe during allergy/cold/rhinitis. The amount of zinc I have to take to be able to breathe is far greater if I do not use the picolinate form. Since I supplement zinc I also supplement copper picolinate (if I did not it would cause neuropathy).

 

[triffid113]

Oh, fyi, the Thorne multis contain the picolinate forms of zinc and copper. If you don;t have allergies this is prolly enough.

 

[triffid113]

I want to say one more thing -- it is accepted medical knowledge based on sufficient studies - that P5P/B6 completely erases CBS mutation effects in a huge percent of the population (I forget how many - 40-60% or something like that). Other studies are showing that those with CBS mutation not fixed by B6/P5P can be fixed with TMG. That said, it looks like CBS is not much of an issue in adults anyway regarding methylation (it only makes a 2% difference in adults between those with wild type vs mutations). idk about any other effects of CBS mutations (such as Yasko claims CBS mutations cause some glycogen storage issues and I do seem to have that problem, don't know if that's why). My glycogen storage issues are solved by DHEA and hormones do regulale gene expression including CBS.

 

[ttt]

Thanx, triffid! I have to stay away from the multis, cause they mostly have methyl B12, and I need to go less methyl donors, rather than more. What you're saying about TMG, though, is interesting. I've been shying away from that, because it can increase norepinephrine by contributing to the shortcut through the methionine cycle (at least that's my understanding), and I'm already so hopped up on norepinephrine that that's the last thing I need.

Interesting to hear you say that about the blood pressure. I'm not sure how I would apply that to myself. My BP tends to be low (96/66 or 104/64), for instance. It's rare that my bottom number goes above 70. I don't know how that translates in terms of potassium, but I sure do know that I need sodium!

 

[greenshots]

Triffid, how much P5P do you take? The Yasko camp has said to avoid it, but I just don't think that's right. So I've started taking about 40-50mg, and I wonder if I'm taking too much or too little. Here, I'm hearing that a lot of people disagree with Yasko about CBS. I'm CBS+/-, but my ammonia is low and my sulfur is high.

Whoa nelly! Thats alotta P5P!!! Especially if you are SNS like me. I think its important to remember that the CBS & MTHFR c677T isn't the only factor with homocysteine since having BHMT defects will also increase homocysteine levels, especially if you have several. I think its good to remember that nothing seems to work alone, its probably more of a combination of factors. There are probably more defects that increase these levels as well but we haven't found them yet. If you already have a CBS defect and you take too much P5P or B6, you'll speed it up. This might not be a big deal if your other snps are working ok and filtering out garbage normally. But then again, they're probably not.

 

[greenshots]

I think your probably talking about the CBS that most people study for strokes, heart disease, and dementia. Their CBS is downregulated so going way too slow and homocysteine builds up, causing alotta inflammatory changes. These people really need P5P but thats not the same as the upregulated CBS. Come to think of it, you could have both the upreg and the down reg as well as several bhmts and have high homocysteine. Its a huge snowball fest so looking at one area can be a problem.

I want to say one more thing -- it is accepted medical knowledge based on sufficient studies - that P5P/B6 completely erases CBS mutation effects in a huge percent of the population (I forget how many - 40-60% or something like that). Other studies are showing that those with CBS mutation not fixed by B6/P5P can be fixed with TMG. That said, it looks like CBS is not much of an issue in adults anyway regarding methylation (it only makes a 2% difference in adults between those with wild type vs mutations). idk about any other effects of CBS mutations (such as Yasko claims CBS mutations cause some glycogen storage issues and I do seem to have that problem, don't know if that's why). My glycogen storage issues are solved by DHEA and hormones do regulale gene expression including CBS.

 

[ttt]

Whoa nelly! Thats alotta P5P!!!

Eeek! How much P5P do you take? Angela, I think part of my concern is that P5P is such an important co-factor for so many things, including, I think, conversion of glutamate to GABA. Also, even though I've got the CBS mutation, my ammonia is low (not sure if that's relevant, though).

I'm looking through my lab work for homocysteine levels, but I don't see anything. Is that measured on the standard Yasko tests? If not, is that a blood test or is it best measured some other way?

 

[triffid113]

Here is a cogent rebuttal of Yasko regarding CBS: http://onibasu.com/archives/am/218588.html
CBS Upregulation, Myth or Reality?
By Mark London

Upregulation of the CBS enzyme via two genetic polymorphisms has been
theorized to be possibly detrimental for some conditions, based on the
work by Dr. Amy Yasko in autism. These two polymorphisms were studied
in 2000, and in that study, the Post Methionine Load (PML) test was
used to determine the effects of different CBS polymorphism genotypes.
That loading test can detect subtle defects in the transsulfuration
pathway, which is the metabolic process that is affected by the CBS
enzyme. The polymorphism with the greatest effect, as shown by the
PML test, was found to be 699CàT (Y233Y). People with the TT (+/+)
genotype of that polymorphism, and to a lesser degree CT (-/+),
produce lower levels of homocysteine levels in response to the PML
test, when compared with the CC (-/-) genotype. Lower homocysteine
levels from that test infers greater CBS activity. By the way, none
of these genotypes are rare. About 40% of the population has CC, 40%
has CT, and 20% have TT. Thus, all the genotypes of this polymorphism
are quite common. The study also looked at the CBS polymorphism
1080CàT (A360A), but that was found to have less a significant effect.
The TT genotype of that polymorphism only showed a significant
decrease in homocysteine in the PML test, if 2 other polymorphisms
were also excluded. Thus, 699TT seems to have the most significant
affect on CBS activity.

On the other hand, a similar study in 2003 on these polymoprhisms did
not show a significant difference in homocysteine levels due to the
different genotypes, in response to the PML test. One difference with
this new study is that it was done on a different ethnic group, which
is sometimes a factor in genetic studies. Also, while the mean age
was the same in both studies, this new study had a much smaller range
of ages, and did not include anyone younger than about 40 years old.
This might be a factor, since CBS activity is known to decrease as a
person gets older.

Even more interestingly, is that a study on pregnant women in 2003
surprisingly showed an increase in basal homocysteine levels from the
TT genotype, the same genotype that had the lowest homocysteine level
in the 2000 study. This study did not give any possible reason for
this result.

In any event, even in studies which showed increased CBS activity
effects from the TT genotype, such as the one from 2000, and a more
recent one from 2007, only small changes in homocysteine levels were
observed. For example, in the latest study, which used a very large
population of 10000, the basal homocysteine levels only differed by
2.7%, between the TT genotype, which has the highest CBS activity,
compared to the CC genotype, which has the lowest CBS activity.

This minor decrease in homocysteine levels is in contrast to that
which is seen in Down's syndrome, where CBS upregulation is definitely
known to occur. In one study on Down's syndrome children, basal
homocysteine levels were reduced by 25%, and plasma levels of
cystathionine, which is produced by the transsulfuration pathway, was
increased by 3.8 fold.

On the other hand, a later study on Down's syndrome adults did not
show decreased homocysteine levels. This surprising result was
theorized to be due to the fact that adults have a much lower
requirement for folic acid. When folic acid was given to the Down's
syndrome children, their homocysteine levels rose significantly.

Thus, age may become a factor when considering the effects from CBS
upregulation. Dr. Yasko claims that these CBS polymorphisms can have
significant effects for autistic children. Even if that claim is
true, it is possible that it only has relevancy for children. Also,
the claim may have no relevancy for other conditions, due to the fact
that autism has many other metabolic disturbances that are not found
in other conditions.

It's also been claimed that increased urinary taurine and ammonia can
help diagnose CBS upregulation. While it's true that CBS upregulation
can cause increased taurine and ammonia production, there's no
evidence that this increased production can be detected by measuring
their urinary levels.

Urinary taurine is an unreliable test for CBS upregulation, due to
fact that urinary taurine is dependent on many factors, including age,
genetics, gender, renal function, clinical conditions, and especially
dietary intake. Thus, even though a study on Down's syndrome found a
significant increase in plasma taurine, another study on Down's
syndrome found that urinary taurine levels were normal. Urinary
inorganic sulfur was also not significantly different, which doesn't
confirm Dr. Yasko's prediction of excess sulfur byproducts from CBS
upregulation .On the other hand, urinary thiosulfate was
significantly increased. Thiosulfate is a metabolite of hydrogen
sulfide, and CBS is one of only three enzymes known to be able to
produce hydrogen sulfide. Thus, significant CBS upregulation was
likely occurring, even though urinary taurine and sulfur levels were
normal.

Urinary ammonia is an even less reliable method for testing for CBS
upregulation. This is because most of the ammonia (NH4+) in urine is
produced by the kidneys for ph regulation. The ammonia that is
produced elsewhere in the body, is usually detoxified by being
converted to urea, which is then excreted. This process mainly occurs
in the liver, and the liver is quite capable of handling the large
amount of ammonia that is produced in the body, which occurs due to
the metabolization of amino acids. The liver has to be able to do
this, because the nervous system can only tolerate very low levels of
ammonia. Excess ammonia, i.e., hyperammonia, only usually occurs
either when liver functioning has been greatly reduced, or where a
genetic defect in the urea cycle exists. Only by testing serum
ammonia, can such a condition be diagnosed.

In conclusion, the medical literature states that these CBS
polymorphisms have only very mild effects on CBS activity. And even
if there is significant CBS upregulation, there is no evidence that it
can significantly cause any negative effects, such as overproduction
of ammonia. Furthermore, the medical literature doesn't support the
claim that elevated levels of urinary ammonia or taurine is indicative
of CBS upregulation.

Dr. Yasko claims that CBS upregulation can lead to "a lack of
glutathione." However, while glutathione is reduced in Down's
syndrome, medical researchers do not believe that this is due to the
CBS upregulation. Instead, they believe it is due to the
overexpression of the superoxide dismutase (SOD) gene, which also
occurs in Down's syndrome: "The reduced plasma glutathione observed in
the children with DS most likely reflects an adaptive antioxidant
response to chronic oxidative stress, resulting from SOD
overexpression." This conclusion is possibly confirmed by a lab study
on CBS overexpression in mice, where even though homocysteine levels
were significantly reduced by the CBS upregulation, gluathione levels
were unchanged.

Thus, while some of the aspects of Dr. Yasko's treatment plan may have
usefulness, there is no support that CBS upregulation can have any
negative effects.

 

[ttt]

Thank you, triffid!

 

[Christopher]

http://www.greatplainslaboratory.com/home/eng/hphpa.asp

perhaps this would be related for some.

 

[ttt]

Thanx, Christopher. If I'm understanding the article correctly, they're saying that clostridia can increase HPHPA, which is similar to norepinephrine?

 

[Christopher]

I think basically. The toxins those bacteria create interfere with normal dopamine/norepinephrine function. It's something I've been researching for a while now - I plan to get the OAT soon which measures this.

 

[ttt]

Does the OAT measure norepinephrine?

 

[HealthAdvocate1]

Look at Gestalts stuff on nervous system. People who are sympathetic dominant tend to have a fight or flight response naturally and then supplements, methylation defects, and toxins will sorta tweak you more in that direction. He had a good methylation posting of his defects and treatments and the nervous system part was just one piece of the puzzle. Since I happen to be a SNS person, as opposed to a mixed or parasympathetic, I know that higher doses of Magnesium and some potassium are needed to roll me back. In fact, now that I think about it, ever since I started all of the supplements for SNS dominance I'm much more chilled out then I used to be and I'm not nearly as compulsive. My emails and posts are usually shorter and more concise then the endless stuff I used to write and things like staying up half the night researching and making diagrams and tables is all gone. Funny now that I think about it. I also don't have anxiety, insomnia, or endless brain chatter. Come to think of it, its pretty nice.

I am new to this discussion board. I have been suffering from extreme insomnia (sleeping between 1-4 hours nightly, with 4 hours being a very good night - and not without the help of both natural and prescription sleep aids.) There have been many nights where I have not slept at all.

A test from NeuroScience of my neurotransmitters showed extremely high norepinephrine (NE). I can actually gauge the level of NE - at least whether it is really high - by the volume of the ringing in my ear! This has been going on since about April. The lack of sleep is killing me. I have aged 10 years in that time. I can't find a doctor of any kind who can help me.

I have two questions, at least for now : The first is for "greenshots" - What is the protocol for a sympathetic dominant person? Where can I find more information about this and the supplemental protocol for SNS dominance? You probably are already aware of this but I thought I'd mention it: I used to do a test in the physician's office where I worked called ANSAR (ANX 3.0), a diagnostic evaluation of both branches of the autonomic nervous system (ANS) based on Heart Rate Variability (HRV). The test was developed by MIT and others.

According to them, the best single supplement to help balance the ANS is Alpha Lipoic Acid. I'm actually an RN but I'm not familiar with many of the abbreviations used in these discussions. I know a few, such as DHEA (the hormone), CFS (Chronic fatigue), MTHFR (methylation), but reading some of the posts is like reading a foreign language! It would be awesome if someone could post a list of all the meanings of all the various abbreviations such as CBS, ACE, VDR taq, BHMT, COMT, etc., - or provide a link to a resource with such a list. Thanks so much!

CBS, COMP,

 

[Sushi]

@HealthAdvocate1

Greenshots has not been here since July so you might have better luck using a google site search (click on search to find this option).

Welcome to the forum!
Sushi

 

[HealthAdvocate1]

@HealthAdvocate1

Greenshots has not been here since July so you might have better luck using a google site search (click on search to find this option).

Welcome to the forum!
Sushi

Got it - thanks

 

[Phred]

I'm actually an RN but I'm not familiar with many of the abbreviations used in these discussions. I know a few, such as DHEA (the hormone), CFS (Chronic fatigue), MTHFR (methylation), but reading some of the posts is like reading a foreign language! It would be awesome if someone could post a list of all the meanings of all the various abbreviations such as CBS, ACE, VDR taq, BHMT, COMT, etc., - or provide a link to a resource with such a list. Thanks so much!

CBS - Cystathionine-β-synthase
ACE - Angiotensin-converting enzyme
VDR taq - Vitamin D receptor
BHMT - Betaine-homocysteine methyltransferase
COMT - catechol-O-methyltransferase

are all genetic snp's (single nucleotide polymorphisms) that affect the methylation cycle.

MTHFR is not methylation per se. It's Methylenetetrahydrofolate reductase (another snp) and works in the folate cycle.

 

[HealthAdvocate1]

CBS - Cystathionine-β-synthase
ACE - Angiotensin-converting enzyme
VDR taq - Vitamin D receptor
BHMT - Betaine-homocysteine methyltransferase
COMT - catechol-O-methyltransferase

are all genetic snp's (single nucleotide polymorphisms) that affect the methylation cycle.

MTHFR is not methylation per se. It's Methylenetetrahydrofolate reductase (another snp) and works in the folate cycle.

@Phred Thank you for the information. I am so new to all of this... I have a huge learning curve.