Re: VITAMIN K -- maybe better for you than you think...

[Guest guest]

Janet -- new studies say that vitamin K actually has ANTI-CLOTTING factors as

well as

antiinflammatory, heart protective, etc., etc.. Check out this link from the

LEF website:

http://www.lef.org/magazine/mag2000/feb00-report.html

" Strangely enough, vitamin K also plays a role in activating two factors that

reverse

clotting: proteins S and C. Studies show that people who have a deficiency of

protein S and

C get blood clots. "

Dan

> Janet,

>

> Here is some info from Dr. Amy - hopefully this will be helpful. I think you

> will greatly benefit form vitamin D, K, & Ora Pancreas with your VDR

> mutations.

>

> Marisha.

>

> Mom to

>

> Lake, 5 years old, Recovered

>

> Continuing to support his mutations.

>

> NULL GSTM1, GSTP1+-, SOD2+-

>

> ACE-Del, MAO A R297R++, NOS D298E+-

>

> AHCY L135T++R38W++

>

> CBS A360A+-C699T+-

>

> COMT H62H+-V158M+-

>

> MTHFR F435F++A1298C+-

>

> MTRR S175L+-K350A+-A66G+-

>

> SUOX L300L++S370S++

>

> VDR Taq++Bsm/Taq++Fok+-

>

> There are two pathways that will take you around the methylation cycle from

> homocysteine to methionine. The first is the " long way " around the cycle via

> the MTR and MTRR enzymes that require B12 and the forward reaction of the

> MTHFR (where the C677T impairs the activity) for function. The other is a

> " short cut " through the middle of the cycle that bypasses MTR, MTRR and

> MTHFR via the BHMT enzyme. If you think of this portion of the cycle as a

> clock, the BHMT enzyme can use phosphatidyl serine, phosphatidyl choline and

> TMG as substrates to go directly from homocysteine at 6:00 to methionine at

> 12:00 skipping 7:00 through 11:00. The use of phosphatidyl choline,

> phosphatidyl serine and TMG therefore help to bypass these mutations. This

> backdoor reaction (or short cut) generates more norepinephrine relative to

> dopamine. The BHMT enzyme is also triggered by stress. Imbalances in

> dopamine relative to norepinephrine have been implicated in ADD and ADHD

> behaviors.

>

> 1) Address CBS/ammonia imbalances using the ammonia support program. This is

> an important first step so that added methylation cycle support does not

> lead to increased levels of ammonia, hydrogen sulfide and other toxic sulfur

> byproducts. If there are no CBS up regulations you can skip this step.

>

> 2) Wait at least one month after (1) before looking to add the rest of

> methylation cycle support as indicated by the nutrigenomic profile. During

> this time period you can look at integrating the use of the comprehensive

> gut/bacterial support program while the CBS/ammonia issues get in better

> balance.

>

> 3) Support the rest of the methylation cycle imbalances using support for

> both pathways around the methylation cycle. You are looking to support the

> " long way " around the cycle via the MTR/MTRR as well as the " short cut "

> through the cycle via the BHMT enzyme.

>

> 4) Creatinine levels will increase as a function of proper methylation cycle

> function as well as by virtue of the decreased ammonia levels as CBS up

> regulations are addressed. Increased creatinine will cause detoxification

> reactions.

>

> 5) Increased beta alanine, anserine, carnosine may be seen as the " short

> cut " around the methylation cycle is supported as and ammonia levels drop.

>

> 6) Once the levels of beta alanine, anserine, carnosine drop you can

> consider the addition of DMG. This will emphasize the long route around the

> cycle rather than the short cut. Before adding DMG, first verify that the

> long route around the cycle is in balance by checking methionine and taurine

> levels on a urine AA test, and FIGLU and methylmalonic acid on an OAT/ MAT

> test.

>

> 7) Add in metals RNA program if needed.

>

> VDR Fok:

>

> This VDR polymorphism is not related to dopamine levels. It is important in

> terms of blood sugar regulation - pancreatic support are useful for

> individuals who have a VDR Fok+ status.

>

> VDR Bsm/Taq:

>

> While this particular VDR polymorphism does not affect COMT activity

> directly it does affect overall dopamine levels. Since COMT breaks down

> dopamine, looking at the level of dopamine breakdown in conjunction with

> other genes that also affect dopamine levels will give you an overall sense

> of the dopamine levels in the system based on nutrigenomics.

>

> VDR Bsm/Taq - - is the norm and represents the higher level of dopamine. VDR

> Bsm/Taq 4- + represents changes in both copies of the genes such that the

> dopamine levels are reduced.

>

> COMT and VDR Bsm/Taq:

>

> Individuals who are COMTV158M + +

>

> COMT H62H + +

>

> COMTL136L--

>

> VDR Bsm/Taq - -

>

> wound tend to have the highest overall dopamine levels but also be the most

> susceptible to mood swings due to dopamine highs and low. This is because

> high dopamine levels can feedback and inhibit dopamine synthesis. Those who

> break down dopamine more slowly will tend to accumulate higher levels of

> dopamine. This is compounded by the presence of VCD Bsm/Taq - - status. The

> high level dopamine inhibits new synthesis such that the dopamine levels can

> fall until it reaches a point where the inhibition is relieved and new

> synthesis occurs.

>

> CBS:

>

> Both the CBS C699T as well as the CBS A360A lead to increased activity of

> the CBS enzyme. The C699T is the stronger of the two up regulations. Overall

> there are four possible CBS up regulations that have been characterized at

> this time.

>

> MTRR:

>

> The methionine synthase reductase helps to recycle B12 for use by the MTR.

> The A66G mutation appears to impair the acitivty of the enzyme.

>

> MaoA:

>

> This is the enzyme that breaks down serotonin. Individuals who are maoA +

> break down serotonin more slowly, but may also be subject to mood swings due

> to serotonin cycling from high to low levels. I have observed that

> aggressive behaviors may in part be associated with maoA + + status.

>

> ACE:

>

> The designation of ACE + + is the same as saying that an individual is

> positive for having deletions in both copies of the ACE gene. This can cause

> increases in aldosterone levels. Aldosterone is also increased by stress.

> The ACE deletions in combination with the maoA+ status may also play a role

> in low frustration thresholds and increased anxiety.

>

> SUOX:

>

> The SUOX enzyme helps to detoxify sulfites that are generated due to

> activity of the CBS gene. When we have increased CBS activity (CBS C699T+ or

> C1080T+) then it can put an additional strain on the SUOX enzyme. Changes in

> the SUOX S370S SNP appear to affect the function of this enzyme. Remember

> that the + or - status is in relative term that reflects a comparison to a

> database " norm " . In the case of SUOX, I find that a - denotes situations

> where we are having a potential issue with this SNP. In virtually all cases

> we are finding a + + status for the two SUOX markers. In rare cases I have

> seen a single - for one of the two SUOX SNPs and this single - for SUOX

> S370S appears to indicate a problem with SUOX function.

>

> Individuals who are

>

> CBS C699T+ (or CBS C1080T+) SUOX S370S -

>

> will have greater difficulties with the use of sulfur donors. The presence

> of CBS up regulations can serve to allow added methylation cycle support to

> flow at a high level into the transsulfuration pathway causing increased

> levels of sulfur byproducts and ammonia. The sulfites need to be detoxified

> by the SUOX enzyme with the help of molybdenum. The SUOX - status indicates

> that the ability to detoxify all of these sulfur (groups that are generated

> by the CBS+ +) may be compromised. For those individuals with a CBS+ status

> and the SUOX -status it will be really important to limit the ammonia and

> sulfur in their system. You will also need to keep a very close eye on

> molybdenum and magnesium levels as both of these essential minerals are

> involved in either ammonia or sulfur detoxification. sulfur detoxification.

>

>