Re: Anyone reading Survival of the Sickest?/methylation and genes

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

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

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

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?

>

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

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

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

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

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.

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.

>

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

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

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,

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/

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/

>

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

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

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: