Guest guest Posted September 5, 2007 Report Share Posted September 5, 2007 >> So some *dogs* may also have a genetic makeup that >predisposes them to >> requiring extra support for their methylation cylce? Could human >breeding of >> dogs have interfered with this, in your opinion, since breeding >interferes >> with natural selection? > > >Heh. Potentially. Though I'm not sure of the use of autistic >dogs to humans. Unless they come in pretty colours or are >particularly good at lining up their balls in a row. Guess you've never met a Golden. <g> Actually, I wasn't thinking in terms of autism since many humans who apparently have issues with methylation, don't have autism. It could manifest in some other way in other species, I'd imagine. Suze Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 > > Gail, > > I eat folate rich foods such as liver, legumes and whole grains. (I get .... The remaining text is trimmed. Thanks Lana for the information. I look forward to seeing your document. It is really helpful to see a food list since I try to get appropriate nutrition through food instead of isolated and sometimes synthetic vitamin and mineral sources. I could have used this information years ago but the sources of information up until now have not been available in a cohesive form (and if it weren't for people like you that information would not ever be available in a cohesive form!). The information provided by many different doctors, nutrition types and other experts is useful but by the time you comb through it and decode it you practically have the equivalent of multiple degrees in chemistry, biology, nutrition, detoxification... etc. You understand how it all works but not the simple steps that could be taken to get started. Hope I haven't scared you off with this rant! Thanks again for the information. Gail Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 > > DMG doesn't methylate as well, > and therefore doesn't 'amine' as well, so 'overmethylators' are able > to use it with less risk of 'amining' than folate and TMG. It isn't just about how much methylation is occuring, it is about what is being methylated. Also, a subsection of people with BHMT mutations have problems with > TMG and/or DMG. > DMG doesn't go through BHMT. -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 Suze, This is from the old post Emma referred to: http://query.nytimes.com/gst/fullpage.html?res=9A0DE4DD103CF934A35753C1A9659C8B6\ 3 & sec=health & pagewanted=all " The unusual strain of mouse carries a kind of trigger near the gene that determines not only the color of its coat but also its predisposition to obesity, diabetes and cancer. When pregnant mice were fed extra vitamins and supplements, the supplements interacted with the trigger in the fetal mice and shut down the gene. As a result, obese yellow mothers gave birth to standard brown baby mice that grew up lean and healthy. " Since coat color can be tied to methylation and overall health, I would say: yes, human breeding of dogs could have interefered with the canine methylation cycle. -Lana On 9/5/07, Suze Fisher <suzefisher@... > wrote: > > > >> So some *dogs* may also have a genetic makeup that > >predisposes them to > >> requiring extra support for their methylation cylce? Could human > >breeding of > >> dogs have interfered with this, in your opinion, since breeding > >interferes > >> with natural selection? > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 People with food chemical sensitivities, fibromyalgia and autism are > predisposed to these syndromes due to a 'cocktail' of very common > genetic polymorphisms in their methylation cycle. What genetic mutations are we talking about specifically? How much does it cost to get tested for all of them? What percentage of failsafers have spent the money to get tested? What percentage came back positive for which mutations? Are you finding some mutations more common than others? -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 >Since coat color can be tied to methylation and overall >health, I would say: >yes, human breeding of dogs could have interefered with the >canine methylation cycle. > Thanks Lana. How does coat color tie into methylation? And does that mean human hair color is also tied into methylation? Suze Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 > > I just listed a number of them in the previous post. Thank you, didn't get that before I sent this one. The price is currently $625 - it has come down a lot in the last few > months as Yasko has pruned quite a few of the more unusual > polymorphisms. When last I looked back in the early spring I'm pretty > sure it was well over $1000. That's not *that* bad as medical tests go (provided you're not used to insurance paying everything for you). Since I do not own a genetic laboratory or have $10,000's with which > to do genetic research, I cannot answer those questions. I did not mean to suggest that you should be funding this: there are several groups which collect test results that their members have purchased to determine trends. I simply figured with how adamantly you insist food intolerance is genetic, you would have done something similar. The methylation theory however (which has been around for at least > thirty years in one form or another, this is just another reinvention > of the wheel with a bit more care to detail) is very well grounded in > medical fact. Theories are not facts, they may be based on facts but they are not thorough enough to be facts themselves. The way you present your opinion that food intolerance is genetic, would make one think you had more than theories to stand on (such as genetic test results). Since you have no proof that failsafers tend to have these mutations: why is it you completely dismiss the possibility that for at least some people, these are truly nutritional issues? -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 Suze, I was speaking more as to possiblity than actuality. According to the article here: http://query.nytimes.com/gst/fullpage.html?res=9A0DE4DD103CF934A35753C1A9659C8B6\ 3 & sec=health & pagewanted=all <http://query.nytimes.com/gst/fullpage.html?res=9A0DE4DD103CF934A35753C1A9659C8B\ 63 & sec=health & pagewanted=all> " The unusual strain of mouse carries a kind of trigger near the gene that determines not only the color of its coat but also its predisposition to obesity, diabetes and cancer. " I know a lot of animals share similar coat color genetics, but I am not sure exactly how this would apply to humans or dogs - only that it is possible that these links between appearance and methylation do occur in some species. Seeing as the dog is descended from wolves which are usually grey or brown, most coat colors we see in dogs nowadays are recessive. When you start breeding to obtain recessive genes, you can open up a can of worms. Add that to the closed gene pool concept that kennel clubs support and problems are pretty much guarenteed to manifest. My dog isn't KC - she's from an open gene pool (which is restricted by appearance/health at age 1 - dogs with defects are not registered, unlike with KCs where all dogs are registered at birth regardless of their quality as per the breed standard - they do allow the breeder to choose to register pups as pets, but not everyone does). My dog was an outcross breeding according to her 6 generation pedigree. When I researched back to 11 generations in her pedigree, I found that between generations 7 and 11 she was very linebred on 4 popular sires. Sure, having the dogs that far back in her pedigree allowed for more diversity, but they still had an stronger influence on her genetics than a complete outcross would have. Some breeds have far less genetic diversity than others, and this is viewed as desireable by the kennel clubs since it produces consistency in appearance (but it also produces consistency in disease - such as hip dysplasia, cataracts, etc.) Not to mention some of the stupid breed standards (chihuahua males are smaller than females so they need to stand on a box to mate, some bulldogs don't deliver naturally anymore due to the skulls being bred to be too big, a lot of short nosed dogs have respiratory problems)... So honestly, I think the human breeding of dogs interferes quite a bit with their health - methylation-related or not. -Lana Thanks Lana. > > How does coat color tie into methylation? And does that mean human hair > color is also tied into methylation? > > Suze Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 --- Lana Gibbons <lana.m.gibbons@...> wrote: > Some breeds have far less genetic diversity than others, and this is > viewed as desirable by the kennel clubs since it produces > consistency in appearance (but it also produces consistency in > disease - such as hip dysplasia, cataracts, etc.) Lana and Suze, Could problems like hip displasia and cataracts have dietary influences as well? Is it possible to prevent them, or at least minimize them, with proper diet, or are some dogs genetically doomed? My suspicion is that poor diet makes these problems much worse and brings them out sooner. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 I know of several people who have conquered hip dysplasia and cataracts in their lines with the raw diet. On the other hand: back when I was on the non-raw specific breeding lists, there were some people that believed that by feeding a dog an excellent diet, you are only " masking " a " disease " . These people proclaimed they preferred to feed their dogs an inferior diet such as Ol' Roy or Pedigree because they want to see what " diseases " they have in their lines - while I disagree with the argument, I do see their point (being that most people that buy those puppies feed their dogs what is cheapest, and those people want their dogs to be free of things like hip dysplasia.) -Lana Lana and Suze, > > Could problems like hip displasia and cataracts have dietary > influences as well? Is it possible to prevent them, or at least > minimize them, with proper diet, or are some dogs genetically doomed? > My suspicion is that poor diet makes these problems much worse and > brings them out sooner. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 > > If you take the time to look in PubMed, you will find literally > hundreds of papers showing correlations between different methylation > cycle genes and neurotransmitter transporter/receptor genes and autism > spectrum and other related syndromes like ADHD, bipolar, OCD, > depression, histamine and tyramine intolerance, you name it. You will > also find hundreds of papers on the effects of salicylates and amines > and how they cause the very same symptoms, and even direct links > between the effects of food chemicals and genetic susceptibility. I've looked at plenty of these in the course of determining exactly what nutritional deficiencies may be at play. The fact these articles exist does not prove that failsafers have these genetic defects. What you asked me was whether failsafers had genetic proof of their > illness. Of course this doesn't exist, the science is not that far > advanced. In other words, there's no way to prove failsafers need to be on failsafe due to genetic defects. You can *imply* that they do by referencing the above PubMed articles, but you can never prove such. However if you ask failsafers whether they have close family > members with similar symptoms as them, most of them will respond that > they do. Price wrote about many families that had healthy parents but unhealthy children in NAPD. It was malnutrition that caused these similarites, not genetics. > As I have repeatedly stated on this group, the FailsafeNT group, and > my own blog, I am quite sure that some people are able to totally > screw their bodies up to the extreme extent that they become food > chemical intolerant due to nutritional deficiency. I don't know why > you keep claiming I say otherwise. I am not the only person that has gotten this impression from you. Every time anyone ever mentions nutrition in terms of food sensitivity, you jump in insisting it is genetic. You've even actively discourage people from supplementing with vitamins that may help them - vitamins that the failsafe diet does not provide adequate amounts of because of how it restricts nutrient dense foods such as liver. Maybe if you prefaced the adamant claims that these things are genetic with a disclaimer like the above and stopped naysaying those who compensate for failsafe's inferiority with supplements, people wouldn't get that impression. And I do not believe it is the fault of the people who have these nutritional deficiencies - it is the fault of our food supply - that's the whole point of NAPD! However, nutritional deficiencies > are pretty quickly corrected with normal high street vitamins. Not necessarily - for example, someone with a bad liver* will have a decreased level of FAD and FMN, the active forms of B2. This will prevent them from properly absorbing B3, B6 and folate from diet, causing disruption in the methylation cycle. One can not correct the conversion error until the liver is working optimally so " normal high street vitamins " won't work - they will need the coenzyme forms of these vitamins. These can typically be found in nutrient dense liver, which is disallowed on failsafe. *One can have a bad liver for many reasons, including having a mother that had inadequate stores of Vitamin A at the start of the thrid trimester, when that Vitamin A is typically transferred to the fetus. Other possibilities include a mother with a thyroid disorder (or having a thyroid disorder yourself), and toxic compounds such as heavy metals and Rx drugs (like warfarin). However, I DON'T believe that they are the majority of cases, because > I have yet to come across anyone who has come to failsafe after eating > SO BADLY that this would ever happen. Even junk food is regularly > fortified with folic acid! Price regularly found people who ate SO BADLY within the 1st generation of consuming western foods that they would get diseased and possibly die unless returned to a native dietary. Price proved the western food supply inferior - why you would support that it can maintain health is beyond me. Folic acid is a synthetic vitamin that was never consumed regularly in the US until the 1980s - and in the UK, they are only just now passing mandatory fortification laws. Anyone consuming enough food folate such as liver would never have an issue with a MTHFR defect, because they would not have to form their own 5-MTHF. Junk food is not fortified with B2, which is necessary for the absorbtion of folate - and it is missing many, many other absolutely vital nutrients so I don't see how you can claim that fortification is supposed to properly compensate for a bad food supply! People who are diagnosed as food chemical > intolerant are normal people who eat a regular Western diet, it's just > they are less tolerant of that diet than most Westerners. In fact what > you tend to find is that they eat better than most Westerners, because > they know that some foods, particularly junk foods, cause them problems. I am not supporting, and will never support the SAD. The SAD is what is causing all these problems - why else would Price have written NAPD? If you do not have a MTHFR or DMG polymorphism Lana, you should be > able to use artificial folic acid without any problems whatsoever, > just like most of the population can. Actually, most of the population can absorb 200-400 mcg folic acid a day with the rest staying in their blood until their body gets to it. If folate comes from food, there is no limit on the amount that can be used daily. On top of that, synthetic folic acid can damage the kidneys. So where they may be able to use folic acid to stay out of deficiency, I don't believe anyone can use folic acid and achieve optimal health. That's why you need liver and whole grains (not fortified white flour). And how come most of the > population eat junk food and additives, yet do not have aspergers, > asthma, fibromyalgia or ADHD, do not require huge amounts of B12 and > food folate, but also have amalgam fillings and have used > mercury-containing vaccines?Do you have a non-genetic explanation for > all of this that holds as much water as genetics? Our livers are substandard compared to theirs. The liver is an amazing thing - it is a form of nutritional storage that is handed down from generation to generation. It has an exceptional capacity and it can sometimes support generations of descendants before being run down enough to cause disease. The chinese call it " liver qi stagnation " and reccomend consuption of liver and mollusks to fix it. Just because these people get by now doesn't mean a few generations down the line their children won't have issues - it all depends on if they get enough of the nutrients needed for conception. The fact is, the pre-conception diet needs to come back and it needs to be maintained for several generations before we're going to see significant improvement in human health. A good start is stopping the bombardament of our food animals with liver-toxifying compounds and inappropriate foods such as grains which cause them to develop fatty livers, so that we actually have a source of healthy liver to help fix our own deficient livers with. -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 I'm not desperate to start a fight and I'm not saying that it can't be genetic, I'm just saying it is absolutely rediculous to assume it is when there are so many other factors at play. And even if it is genetic, persuing optimal nutrition can and does help. And by optimal, I'm not talking about the rediculously low RDA values that were set forth to prevent scurvy, pellega and the other avitaminosis. Some of the RDAs need to be doubled (at least!) for optimal health. That's because genetics are the main cause, Which you have stated you have no proof of, other than the implications that PubMed articles suggest occur in some people. Just because someone has a symptom doesn't mean they have a genetic defect - they could simply be missing the cofactor needed for the enzyme. You assume that genetics must play a part *most* of the time, whereas I have a much higher view of our gene pool and resultantly believe nutrition plays a part at least half the time (and that is being very, very generous). unless you believe an NT > diet is nutritionally deficient? I certainly don't. I think an NT diet without liver, shellfish, etc is deficient (and I don't really see how you could call it an NT diet quite frankly). I also think anyone who tries to westernize the NT diet is at risk for being deficient. This is why > you need to know your genetic profile. Otherwise you can make > dangerous mistakes. So wait, I'm supposed to know my genetic profile, but you don't reccomend people get genetic testing because it is too expensive? This is the point I'm making - until testing has been done, there is no way to know for sure which is culprit. I'll be happy to compromise with you on the idea that those considering supplementing should also seriously consider testing in order to avoid serious side effects. Liver isn't the only source > of folate in the universe, just a particularly aminey one. No, but it is one of the best sources of B12 available outside of mollusks which are also particularly " aminey " . Beef liver has almost 10x the B12 as tuna does per 200 calories. That's your explanation? You realise methylation takes place in the > brain and the rest of the body, not just in the liver? > As I said in my previous post: Methylation is dependant on several nutrients that are dependant on having adequate amounts of the coenzyme forms of riboflavin, which someone with a compromised liver does not produce in adequate amounts. Without FAD and FMN, it doesn't matter where else in the body can execute methylation because it won't be absorbing B3, B6 or Folate correctly. As you said, it really isn't worth arguing since we obviously have different views. I won't waste anymore time. -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 I've been following this discussion with great interest, although I know nothing about methylation and genes. However, my husband, who has ADHD, has a close family member with Ehlers-Danlos syndrome. She has a very rare form of this, but DNA tests confirm she has it. Also, his father and brother carry the gene. There are other symptoms in the family, such as bowed legs, sunken chest, scoliosis, etc. Mother-in-law had goiter as a child, and suspect thyroid problems now. Never been tested because they believe they are all very healthy. My question is whether anyone knows anything about this syndrome and specifically if it might be connected to methylation. I found a great website by a woman who has been able to control her Ehlers-Danlos symptoms using a nutritional approach, somewhat based on WAPF. Just wondering if there's anything I can do to protect my two children, who up until now haven't been tested, but appear to be very healthy. Thanks, Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 --- In , " Emma Davies " vitaminkgirl@... wrote: >If you take the time to look in PubMed, you will find literally >hundreds of papers showing correlations between different methylation >cycle genes and neurotransmitter transporter/receptor genes and autism >spectrum and other related syndromes like ADHD, bipolar, OCD, >depression, histamine and tyramine intolerance, you name it. You will >also find hundreds of papers on the effects of salicylates and amines >and how they cause the very same symptoms, and even direct links >between the effects of food chemicals and genetic susceptibility. Is autism in Pub Med related to deficient acetylcholine , ADHD dopamine, OCD, depression, salicylate, amine intolerance to serotonin, bipolar to GABA? Everyone is genetically predisposed to one dominant neurotransmitter with more or less of the other three needed to maintain the dominant according to Braverman M.D.'s book The Edge Effect. You've disagreed with Braverman's protocols in this article before. http://www.douglaslabs.com/pdf/nutrinews/The%20Edge%20Effect%20NN%20(Spring-05).\ pdf From Braverman's work I can see that failsafe would more likely work best for the serotonin deficient serotonin dominant portion of the population and would less likely work as well alone in varying degrees for the remainder of the population dominant to dopamine, acetylcholine or GABA instead. Braverman suggests a failsafe principle diet for the deficient serotonin type. Wanita ________________________________________________________________________________\ ____ Park yourself in front of a world of choices in alternative vehicles. Visit the Auto Green Center. http://autos./green_center/ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 Wanita, Thanks for posting this, I find it very interesting! I don't really agree with the use of Rx meds... but regarding the serotonin-failsafe connection: one of the deficiencies I had to fix was before getting better was a B3/Tryptophan deficiency and that directly relates to low serotonin levels. Thing is, I can't really figure out which subset I am. I do know I'm an INTJ meyers-briggs and that would put me as a Dopamine type, but this says people arn't always what their meyers-briggs implies. It references a self-test if you're unsure - but doesn't give a link. Is there a self-test that you would reccomend? -Lana Is autism in Pub Med related to deficient acetylcholine , ADHD dopamine, > OCD, depression, salicylate, amine intolerance to serotonin, bipolar to > GABA? Everyone is genetically predisposed to one dominant neurotransmitter > with more or less of the other three needed to maintain the dominant > according to Braverman M.D.'s book The Edge Effect. > > You've disagreed with Braverman's protocols in this article before. > > http://www.douglaslabs.com/pdf/nutrinews/The%20Edge%20Effect%20NN%20(Spring-05).\ pdf > > From Braverman's work I can see that failsafe would more likely work best > for the serotonin deficient serotonin dominant portion of the population and > would less likely work as well alone in varying degrees for the remainder of > the population dominant to dopamine, acetylcholine or GABA instead. > Braverman suggests a failsafe principle diet for the deficient serotonin > type. > > Wanita > > > > > > > ________________________________________________________________________________\ ____ > Park yourself in front of a world of choices in alternative vehicles. > Visit the Auto Green Center. > http://autos./green_center/ > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 8, 2007 Report Share Posted September 8, 2007 Emma, I'm not actually replying to you here since we've decided our views are too different - there are just some things that were in this post that I think need some fleshing out for others following this thread. Everyone else: > You seem to think that it is bad to recycle homocysteine with anything > other than folate or you will somehow 'lose' your folate, which is not > true. I didn't say you lose your folate, it is just there are far more forms of folate than 5-MTHF that the body does need to use for things like DNA replication and if all the folate gets stuck as 5-MTHF, you can end up with too little of the other forms. This is the " folate trap " hypothesis - it isn't always an issue, as you don't always need the other forms of folate, but it can be. For a start, folate donates methyl to B12 to make MeB12, and > methionine synthase uses MeB12 (not folate) to recycle homocysteine. MS is what takes the methyl from 5-MTHF and passes it to homocysteine using B12 as a cofactor. So technically, it is the 5-MTHF that is methylating homocysteine. ( http://www.online-medical-dictionary.org/Methionine+Synthetase.asp?q=Methionine+\ Synthetase) These are not two seperate reactions as they are powered by the same enzyme. > if you have a BHMT downregulation, neither TMG or DMG are going to > help with anything much. > If you have a BHMT downregulation, you are incapable of making DMG from TMG, thus supplemeting it *could* help. However, there are alternate pathways for recycling used folate (THF): One uses B3 and Glycine (a conditionally essential amino acid) with a cofactor of B6, the other uses Serine (another conditionally essential amino acid) with a cofactor of B6. As conditionally essential amino acids, neither of these have reccomended dietary intakes so there is no guarentee the person would be getting enough of them to properly recycle used folate in the event of a BHMT downregulation. -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 > > Methylation supplements had me on the verge of epileptic seizures last > year. Emma, I'm a bit concerned you found seizures to be a side effect of methylation supplements. I've been pondering this and I've come up with two ideas as to why this could have occured. I'm not looking to debate or anything, just wanted to put out some " food for thought " - especially for others who may have had a similar experience as you. 1) Synthetic folic acid is chemically known as PterylMonoGlutamate. It needs to pass through DHFR twice to get to be THF (aka used folate). PterylMonoGlutamate is more affinitive for the DHFR enzyme than it's metabolite PetrylPolyGlutatmate, and as a result megadoses of folic acid can increase your blood PterylPolyGlutamate levels temporarily. I have met a few people who have felt folic acid has given them glutamate toxicity symptoms. MSG has a possible side effect of seizures, so if you were taking synthetic folic acid this may be a possible cause. 2) Pyridoxine (B6). The pyridoxine form of B6 is found in plants, where the Pyridoxal form is found in animals. The pyridoxine form requires B2 to be converted into Pyridoxal. If megadoses of this vitamin are taken without adequate B2, it can accumulate near nerve tissue and cause intereferance. Peripheral neuropathy is a recognized side effect of pyridoxine megadosing and pyridoxine is known to be associated with nerve damage as a result. I met one woman who claimed her daughter developed seizures after megadoses of B6 - this was a young child who was being given 250 mg/day (12,500% RDV). Nerve damage has been seen in adults with as little as 100 mg/day. I honestly don't believe pyridoxine should be used in amounts greater than 250 mcg per day because of these side effects. A lot of people go to the store and don't realize they're picking out 250 mg instead of 250 mcg (myself included when I started out on this journey). P5P, the activated form of B6 is a far better choice for correcting severe B6 deficiency as it doesn't need B2 and doesn't have these nerve-related side effects. -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 Lana, Don't agree with Rx either. They're the neurotransmitter specific ones he suggests. His case histories are on weaning off or getting more specific temporarily. There is an free online test , same as book's at http://www.antiagingnow.com/secure/test_forms/edge_effect_intro.html. I scored highest to my INFJ acetylcholine but am not overly dominant. Have possible lifelong serotonin or dopamine deficiency with GABA moderately deficient to other three minor deficiencies now. One MBTI test I took with % gave my F as 51% to T at 48% so I'm a borderline INTJ and should look at dopamine. Wanita " Lana Gibbons " lana.m.gibbons@... wrote: Wanita, Thanks for posting this, I find it very interesting! I don't really agree with the use of Rx meds... but regarding the serotonin-failsafe connection: one of the deficiencies I had to fix was before getting better was a B3/Tryptophan deficiency and that directly relates to low serotonin levels. Thing is, I can't really figure out which subset I am. I do know I'm an INTJ meyers-briggs and that would put me as a Dopamine type, but this says people arn't always what their meyers-briggs implies. It references a self-test if you're unsure - but doesn't give a link. Is there a self-test that you would reccomend? -Lana Is autism in Pub Med related to deficient acetylcholine , ADHD dopamine, > OCD, depression, salicylate, amine intolerance to serotonin, bipolar to > GABA? Everyone is genetically predisposed to one dominant neurotransmitter > with more or less of the other three needed to maintain the dominant > according to Braverman M.D.'s book The Edge Effect. > > You've disagreed with Braverman's protocols in this article before. > > http://www.douglaslabs.com/pdf/nutrinews/The%20Edge%20Effect%20NN%20(Spring-05).\ pdf > > From Braverman's work I can see that failsafe would more likely work best > for the serotonin deficient serotonin dominant portion of the population and > would less likely work as well alone in varying degrees for the remainder of > the population dominant to dopamine, acetylcholine or GABA instead. > Braverman suggests a failsafe principle diet for the deficient serotonin > type. > > Wanita > ________________________________________________________________________________\ ____ Choose the right car based on your needs. Check out Autos new Car Finder tool. http://autos./carfinder/ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 > > > This is the " folate trap " hypothesis - it > > isn't always an issue, as you don't always need the other forms of > folate, > > but it can be. > > It is never an issue unless you have clinical B12 deficiency. Or a MS defect or a clinical folate deficiency, but yeah, the B12 deficiency is likely to be the most common culprit. > If you have a BHMT downregulation, you are incapable of making DMG > from TMG, > > thus supplemeting it *could* help. However, there are alternate > pathways > > for recycling used folate (THF) > > > Yes, at least six of them, and one of those is achieved by non-enzymic > equilibrium. I dunno much about the one that is achieved by non-enzymatic equillibrium other than my chart says it is HCHO -> H2O. I didn't know what HCHO was so I googled it and it is formaldehyde? That's not something I want my body thinking it needs... Could you elaborate a bit on this reaction? Do we really have enough formaldehyde to power this in the event the other pathways fail? Would there be any adverse effects to relying on formaldehyde for folate recycling? I mean, I'd think it'd be nice to convert it all to water, but I'm concerned the body will carry/produce higher levels of it to ensure folate can be recycled and I'm wondering if that can cause issues? -Lana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 I'm not saying you have to do anything Emma, nor am I saying anyone else has to do anything. I'm providing data for those who may be interested in persuing this - I was just thinking that those two forms of vitamins can cause issues and even if you wern't taking them, letting everyone else be aware of their flaws to prevent possible issues is important because seizures arn't good for anyone, no matter what causes them! Now, I'm not saying this is what is occuring with you, but tyrosine and tryptophan deficiency can just as easily cause insufficient production of neurotransmitters as MTHFR issues (The pdf Wanita posted touches on this, although it could definately be a bit more thourough). Most ingested amines should be neutralized in the gut, the fact that they get to some people's brains either indicates genetic issues with MAO-A, neurotransmitter deficiencies or a bad gut. We *are* all different - it would just be nice to talk about what *can* be different so those that are simply missing vital nutrients can get enough data to heal themselves. I apologize you feel hurt that I am trying to help the people who share more similarities with me than with you. I don't think it is embarrasing at all to share what I have learned just because it may not apply to some people. You are more than welcome not to read or reply to my emails. -Lana On 9/9/07, Emma Davies <vitaminkgirl@...> wrote: > > > Sorry Lana, I wasn't even taking those supplements. I don't take > artificial supplements. I know why I came close to seizing and I > already have a full explanation in my blog archives. > > You seem not to understand what I keep saying and questioning my > motivations in quite a hurtful way, so I will try to explain it again. > > Do you understand now that we are not all the same, and why I keep > urging people to be cautious with this stuff? > > Just because something seems to work for you doesn't mean it is going > to work for the rest of the world. Loudly proclaiming that it does is > just embarrassing. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 --- Emma Davies <vitaminkgirl@...> wrote: > Salicylates depress my neurotransmitters by interfering with > methylation and give me brain fog and exhaustion and tip the see-saw > in one direction. Amines give me too many neurotransmitters and send > me bipolar and overemotional and tip the see-saw in the other > direction. Emma, thanks for clarifying the difference in effects between salicylates and amines - I hadn't managed to pick that up yet. I assume that these effects are common to all of us, in lesser or greater degrees depending on genes and health status. > You should have seen what happened to me when I tried a liver diet a > couple of years back. Oh that was a laugh. A combination of dietary > amines and high doses of B vitamins is a great way to screw up an > amine-responder big time. I'm curious if you know which amines are most common in liver and if freshness is a big factor. I'm guessing that just about all of the many amino acids present in the meat can be converted into corresponding amines, but that bacterial action may favor certain amines and some amines may be more problematic than others. Also, when preparing meat, does washing the meat reduce the amine content. I'm guessing that most of the amine forming bacteria are on the surface of the meat and that is most likely where a majority (though not all) of the amines reside in aged meats. Of course, I'm also assuming that washing will remove significant amounts of the amines that are on the surface. I am not sure of either of these ideas. However, I have noticed that off-smelling meat does at least smell much better after washing. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 Nice test! Definately easy enough to complete. Turns out right now I don't have an " overly dominant " type - No wonder I couldn't decide. I scored highest to choline (INFJ) with dopamine (INTJ) following very closely behind (then serotonin and GABA). That makes sense as I do tend to totter between F and T, but T used to be more dominant than F. I come up with a moderate choline deficiency - this makes perfect sense considering the mercury and arsenic poisining that are interefering with my acetylcholine production. My GABA was also listed as moderate, this also makes sense as I've been suspecting an issue with my GABA production. My dopamine and serotonin came up as mild, probably since I've balanced the amino acid precursors over the last few months. I'm impressed! This fits in very well with what I've been doing. One of the things about dopamine is that it is produced from tyrosine in the body. The reccomended daily intake of tyrosine is combined with it's precursor phenyalanine - and I don't think this is necessarily wise as not everyone converts phenyalanine into tyrosine efficiently. (I have many, many complaints about the general reccomendations for amino acid intake...) The thing about serotonin that threw me for a long while is that it isn't easy to get tryptophan from foods, at least not in the amounts I needed. The body can convert B3 to tryptophan, and I find I need B3 more than tryptophan in terms of balancing my serotonin. I like how Braverman suggests both niacinamide and 5-HTP for this - the body interconverts the standard forms, niacin and tryptophan, at a great cost and someone deficient in both will definately get better results using both niacinamide and 5-HTP because these forms do not interconvert and thus do not cause the nutritional losses associated with consuming standard niacin and tryptophan for B3/tryptophan deficiency. I used niacinamide and 5-HTP for a while, until my serotonin normalized, and then I switched to probiotics - some strains produce B3 and as long as I don't kill them off by accident I do very well with just the probiotics. (I find quite a bit of food intolerance has to do with a bad gut.) Price found well nourished natives had very even psyches - I honestly think we can all get to that point with the proper diet (customized for our personal shortcomings). IMHO, Braverman's work is definately a step in the right direction. -Lana On 9/9/07, Wanita <wanitawa@...> wrote: > > Lana, > > There is an free online test , same as book's at > http://www.antiagingnow.com/secure/test_forms/edge_effect_intro.html. > I scored highest to my INFJ acetylcholine but am not overly dominant. Have > possible lifelong serotonin or dopamine deficiency with GABA moderately > deficient to other three minor deficiencies now. One MBTI test I took with % > gave my F as 51% to T at 48% so I'm a borderline INTJ and should look at > dopamine. > > Wanita Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 Actually, most of the population can absorb 200-400 mcg folic acid a day with the rest staying in their blood until their body gets to it. If folate comes from food, there is no limit on the amount that can be used daily. On top of that, synthetic folic acid can damage the kidneys. Lana, Can you direct me to primary research on folic acid damaging the kidneys? Was it mega doses? Also, there is commericially available folic acid made by bacterial synthesis, FWIW. Suze Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 --- Lana Gibbons <lana.m.gibbons@...> wrote: > We *are* all different - it would just be nice to talk about what > *can* be different so those that are simply missing vital nutrients > can get enough data to heal themselves. Lana and Emma, I greatly appreciate the dialog you two are having, even though I don't fully understand half of it. I have read that science is all about dialog and listening to other points of view to come to a better understanding, even though there may not always be agreement. So, I hope the two of you will continue to enlighten us. > Now, I'm not saying this is what is occurring with you, but tyrosine > and tryptophan deficiency can just as easily cause insufficient > production of neurotransmitters as MTHFR issues (The pdf Wanita > posted touches on this, although it could definitely be a bit more > thorough). Most ingested amines should be neutralized in the gut, > the fact that they get to some people's brains either indicates > genetic issues with MAO-A, neurotransmitter deficiencies or a bad > gut. Now MTHFR looks like the abbreviation for a curse to me But what do I know? And I thought MAO-A was that despicable ruler of communist China a while back who was responsible for the deaths of millions? But seriously, I have noticed that tryptophan is in most foods, but in relatively small quantities compared to glutamic acid. Here are some foods high in tryptophan in g per 100 g: 0.37 Beef, variety meats and by-products, liver, cooked, braised 0.33 Seeds, sesame seed kernels, dried (decorticated) 0.33 Chicken, broilers/fryers, light meat, meat+skin, cooked, roasted 0.32 Pork, cured, bacon, cooked, pan-fried 0.32 Cheese, cheddar 0.32 Wheat germ, crude 0.32 Turkey, fryer-roasters, light meat, meat+skin, cooked, roasted 0.30 Turkey, fryer-roasters, dark meat, meat+skin, cooked, roasted 0.30 Cheese, mozzarella, whole milk, low moisture 0.30 Pork, fresh, loin, ribs, separable lean/fat, cooked, roasted 0.30 Seeds, sunflower seed kernels, dry roasted, without salt 0.29 Cocoa, dry powder, unsweetened 0.29 Crustaceans, shrimp, mixed species, cooked, moist heat 0.29 Chicken, broilers/fryers, dark meat, meat+skin, cooked, roasted 0.29 Lamb, ground, cooked, broiled 0.29 Fish, tuna, light, canned in water, drained solids 0.29 Mollusks, clam, mixed species, canned, drained solids 0.28 Fish, sardine, Atlantic, canned in oil, drained solids with bone 0.27 Fish, tuna, white, canned in water, drained solids 0.26 Fish, salmon, coho, wild, cooked, dry heat 0.25 Peanuts, all types, raw 0.25 Chicken, liver, all classes, cooked, simmered 0.25 Fish, salmon, Atlantic, farmed, cooked, dry heat It's interesting that beef liver is at the top of the list. For comparison, here are some foods high in glutamic acid in g/100 g: 6.09 Cheese, cheddar 5.64 Pork, cured, bacon, cooked, pan-fried 5.39 Peanuts, all types, raw 5.37 Nuts, almonds, dry roasted, without salt added 5.34 Nuts, almonds, blanched , unroasted 5.06 Cheese, mozzarella, whole milk, low moisture 5.02 Peanut butter, chunk style, without salt 4.74 Seeds, sunflower seed kernels, dry roasted, without salt 4.60 Seeds, sesame seed kernels, dried (decorticated) 4.57 Turkey, fryer-roasters, light meat, meat+skin, cooked, roasted 4.56 Beef, chuck, arm pot roast, 1/8 " fat, cooked, braised 4.40 Turkey, fryer-roasters, dark meat, meat+skin, cooked, roasted 4.25 Chicken, broilers/fryers, light meat, meat+skin, cooked, roasted 4.05 Beef, top sirloin, 1/8 " fat, cooked, broiled 4.00 Wheat germ, crude Hmmm ... maybe that explains why I like cheddar cheese, bacon, and peanuts Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 9, 2007 Report Share Posted September 9, 2007 --- Suze Fiser <suzefisher@...> wrote: > Also, there is commericially available folic acid made by > bacterial synthesis, FWIW. Suze, here's a list of foods high in folate (g/100g): 691 Turkey, liver, all classes, cooked, simmered 578 Chicken, liver, all classes, cooked, simmered 307 Spices, rosemary, dried 281 Wheat germ, crude 274 Spices, oregano, dried 253 Beef, variety meats and by-products, liver, cooked, braised 240 Peanuts, all types, raw 237 Seeds, sunflower seed kernels, dry roasted 194 Spinach, raw 181 Lentils, mature seeds, cooked, boiled 172 Beans, pinto, mature seeds, cooked, boiled 146 Egg, yolk, raw, fresh 140 Beans, navy, mature seeds, cooked, boiled, with salt 135 Asparagus, frozen, cooked, boiled, drained, without salt 121 Spinach, frozen, chopped or leaf, cooked, boiled, drained 115 Seeds, sesame seed kernels, dried (decorticated) 108 Broccoli, cooked, boiled, drained 106 Beans, navy, mature seeds, sprouted, cooked, boiled, drained 106 Spices, pepper, red or cayenne 98 Nuts, walnuts, english unroasted 92 Peanut butter, chunk style, without salt 81 Avocados, raw, all commercial varieties 81 Beans, white, mature seeds, cooked, boiled 80 Beets, cooked, boiled, drained 71 Broccoli, flower clusters, raw 69 Nuts, cashew nuts, dry roasted 66 Cabbage, chinese (pak-choi), raw 65 Beans, white, mature seeds, canned 65 Bread, wheat 62 Beans, navy, mature seeds, canned 60 Beans, pinto, mature seeds, canned 60 Brussels sprouts, cooked, boiled, drained 59 Peas, green, frozen, cooked, boiled, drained 57 Cauliflower, raw 56 Broccoli, frozen, chopped, cooked, boiled, drained 50 Bread, whole-wheat, commercially prepared Quote Link to comment Share on other sites More sharing options...
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