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How to lower norepinephrine

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by ktred, Mar 26, 2013.

  1. ttt

    ttt

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    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.
  2. triffid113

    triffid113 Day of the Square Peg

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    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.
  3. triffid113

    triffid113 Day of the Square Peg

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    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).
    helen1 likes this.
  4. triffid113

    triffid113 Day of the Square Peg

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    Oh, fyi, the Thorne multis contain the picolinate forms of zinc and copper. If you don;t have allergies this is prolly enough.
  5. triffid113

    triffid113 Day of the Square Peg

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    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.
    helen1 likes this.
  6. ttt

    ttt

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    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!
  7. greenshots

    greenshots Senior Member

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    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.
  8. greenshots

    greenshots Senior Member

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    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.


  9. ttt

    ttt

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    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?
  10. triffid113

    triffid113 Day of the Square Peg

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    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.
    Valentijn likes this.
  11. ttt

    ttt

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    Thank you, triffid!
  12. Christopher

    Christopher Senior Member

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  13. ttt

    ttt

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

    Christopher Senior Member

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    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.
  15. ttt

    ttt

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    Does the OAT measure norepinephrine?

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