Guest guest Posted September 3, 2010 Report Share Posted September 3, 2010 I get scared when it comes to amino acids. I read that with AA, it is important to keep balance of all of them, not just give the one which is low. They kind a compete in the body and if one goes high, another goes low right away. To: mb12 valtrex Sent: Tue, August 31, 2010 11:08:52 PMSubject: Re: Yasko results I believe her recommendation is to go thru the list and try them, adding and keeping what works, removing that which doesn't have a positive effect. I think that's what she advises anyway... I certainly wouldn't want to do everything all at once LOL I'd be bankrupt in a month! LOLRight now we are just doing basics + diet. I don't think I've added any herbs at all... funny I don't mind amino acids and vitamins but when it comes to herbs, I get scared! ;-) --- Toni To: mb12 valtrex Sent: Tue, August 31, 2010 4:10:19 PMSubject: Re: Yasko results Toni, thanks for sharing your son's results! This is quite a long list of recomended supplements. Even though some of them are quite familiar, like probiotics and others, but some are not so known. Are you going to give your child all of them? What the expected effect of each of them, is there any explanation about them? Thank you very much again for sharing your experience, Regards, To: mb12 valtrex Sent: Thu, August 26, 2010 3:53:51 AMSubject: Yasko results I uploaded my son's report but I did remove his name.You can find it here http://health.groups.yahoo.com/group/mb12 valtrex/files/Yasko%20Test%20Results/ I originally uploaded it in another location, but moved it.So if you get two messages telling you where the file is, go to this one. :-)--- Toni Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 13, 2010 Report Share Posted November 13, 2010 I hope ,I could help you... COMT (catechol-O-methyltransferase): A primary function of this gene is to help to break down dopamine. Dopamine is a neurotransmitter that is recognized for its role in attention, as well as reward seeking behavior. Dopamine helps to cause pleasurable feelings that aid in reinforcing positive behaviors and motivating individuals to function in certain reward gaining activities. COMT is also involved in the breakdown of another neurotransmitter, norepinephrine. The balance between norepinephrine levels and dopamine levels has been implicated in ADD/ADHD; in addition, dopamine levels are important in conditions such as Parkinson’s disease. COMT is also involved in the proper processing of estrogen in the body. Sensitivity to pain has recently been found to be correlated with COMT activity, such that COMT + + individuals may be more sensitive to pain. VDR/Taq and VDR/Fok (vitamin D receptor): The panel looks at more than one portion of the vitamin D receptor, the Taq as well as the Fok sites. While the Fok change has been related to blood suMPA regulation, changes at Taq can affect dopamine levels. For this reason it is important to look at the composite of the COMT and VDR/Taq status and make supplement suggestions based on the combined results at these two sites. The focus on changes in the Fok portion of the VDR is in reMPAd to supplements that support the pancreas and aid in keeping blood suMPA in the normal healthy range. MAO A (monoamine oxidase A): MaoA is involved in the breakdown of serotonin in the body. Like dopamine, serotonin is another neurotransmitter in the body. It is involved with mood, and imbalances in serotonin levels have been associated with depression, aggression, anxiety and OCD behavior. Since Mao A is inherited with the X chromosome and is considered a dependent trait it may not show standard inheritance characteristics in males. Since the X chromosome in males can only come from the mother, this means that the fathers Mao A mutations (or lack there of) does not play a role in their son’s Mao A status. For females, since one X chromosome is inherited from each parent, the genetics tend to reflect the Mao A status of both parents. ACE (angiotensin converting enzyme): Changes can occur that affect the activity of the ACE gene that can lead to elevated blood pressure. In animal studies imbalances in this pathway were also correlated with increased anxiety and decreases in learning and memory. Increased ACE activity can also throw off the essential mineral balance in the your system due to decreased excretion of sodium in the urine and increased excretion of potassium in the urine. This reaction is also tied to the stress response such that situations of chronic stress can result in additional sodium retention and increased potassium excretion. This excess potassium is excreted provided that the kidneys are functioning properly. In the event that kidney function is compromised, it can lead to the retention of potassium in the body. ACE is a deletion, it is not a SNP. As a consequence it does not associate in the same manner that the other single nucleotide polymorphisms (SNP) on this panel do, so the inheritance pattern of the ACE deletion may not distribute in the same manner as single base changes. MTR/MTRR (methionine synthase/ methionine synthase reductase): These two gene products work together to regenerate and utilize B12 for the critical “long way†around the methylation pathway, helping to convert homocysteine to methionine. High levels of homocysteine have been implicated as risk factors in a number of health conditions including heart disease as well as Alzheimer’s disease. As is the case for COMT and VDR Bsm/Taq, the MTR and MTRR composite status is also important. Mutations in MTR can increase the activity of this gene product so that it leads to a greater need for B12 as the enzyme is using up B12 at a faster rate. The MTRR helps to recycle B12 for use by the MTR. Mutations that affect its activity would also suggest a greater need for B12. BHMT (betaine homocysteine methyltransferase): The product of this gene is central to the “short cut†through the methylation cycle, again helping to convert homocysteine to methionine. The activity of this gene product can be affected by stress, by cortisol levels and may play a role in ADD/ADHD by affecting norepinephrine levels. CBS (cystathionine-beta-synthase): The CBS enzyme basically acts as a gate between homocysteine and the downstream portion of the pathway that generates ammonia in the body. The types of CBS mutations that are identified on this SNP panel cause this “CBS gate†to be left open, this “open gate†is not a neutral situation. The “open gate†can allow support that is added for the rest of the methylation pathway to be depleted, including any B12 that is used to address MTR and MTRR mutations. While there are some positive end products that are generated via the downstream portion of the pathway such as glutathione and taurine, there are also negative byproducts such as excess ammonia and sulfites. By virtue of increased CBS activity, these sulfur groups that were complexed as part of the methylation cycle can now be released into the system as sulfites which are toxic to the body and put an additional burden on the SUOX gene product. NOS (nitric oxide synthase): The NOS enzyme plays a role in ammonia detoxification as part of the urea cycle. Individuals who are NOS + + have reduced activity of this enzyme. NOS mutations can have additive effects with CBS up regulations due to the increased ammonia that is generated by the CBS up regulations. To: mb12 valtrex Sent: Sat, November 13, 2010 4:12:14 AMSubject: Yasko results Got my ds's genetics back today. I understand just enough to know that I don't understand! Lol! I know what he doesn't have a problem with but that's about it. I know that he doesn't have the MTHFR mutation at all, no SUOX mutation and those are the mutations that are fine that I understand enough to breath a sigh of relief but he is NOS +- and ACE is ++ which sort of explains a few things but not really since I don't understand. Ugh! And I'm still waiting for the admin on the yasko board to approve me... Anyone want to explain some of this to me???? It doesn't seem to me like to it's *too* bad but what do I know? Lol! If there's anyone available that knows this stuff, here's the list of mutations/deletions: COMT V158M +- COMT H62H +- VDR Taq +- VDR FOK ++ (I know enough to know that this explains his D deficiency...I think) ACE Del16 ++ MTR A2756G +- MTRR A66G +- MTRR R415T +- MTRR S257T +- BHMT 2 +- BHMT 4 +- BHMT 8 +- CBS A360A +- NOS D298E +- (I think this explains his high ammonia?) But really, that's all I understand. I'm still trying to figure out what the heck the CALL column is supposed to mean with all it's T's, G's, A's and C's and such. The book is helpful but only barely since it's not exactly detailed enough. It mentions things about being COMT +- and such but it doesn't say anything about the specific COMT's. I'm so confused. Help? Cheryl ~http://www.gryffins-tail.blogspot.com ~@midian42~ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 13, 2010 Report Share Posted November 13, 2010 Well, I actually have all that information. I guess I'm looking for something more specific. For instance, my son doesn't have all the COMT mutations, he only has 2 of 3. What does that mean and what do the individual mutations mean? That kind of thing. Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ I hope ,I could help you...COMT (catechol-O-methyltransferase): A primary function of this gene is to help to break down dopamine. Dopamine is a neurotransmitter that is recognized for its role in attention, as well as reward seeking behavior. Dopamine helps to cause pleasurable feelings that aid in reinforcing positive behaviors and motivating individuals to function in certain reward gaining activities. COMT is also involved in the breakdown of another neurotransmitter, norepinephrine. The balance between norepinephrine levels and dopamine levels has been implicated in ADD/ADHD; in addition, dopamine levels are important in conditions such as Parkinson’s disease. COMT is also involved in the proper processing of estrogen in the body. Sensitivity to pain has recently been found to be correlated with COMT activity, such that COMT + + individuals may be more sensitive to pain. VDR/Taq and VDR/Fok (vitamin D receptor): The panel looks at more than one portion of the vitamin D receptor, the Taq as well as the Fok sites. While the Fok change has been related to blood suMPA regulation, changes at Taq can affect dopamine levels. For this reason it is important to look at the composite of the COMT and VDR/Taq status and make supplement suggestions based on the combined results at these two sites. The focus on changes in the Fok portion of the VDR is in reMPAd to supplements that support the pancreas and aid in keeping blood suMPA in the normal healthy range. MAO A (monoamine oxidase A): MaoA is involved in the breakdown of serotonin in the body. Like dopamine, serotonin is another neurotransmitter in the body. It is involved with mood, and imbalances in serotonin levels have been associated with depression, aggression, anxiety and OCD behavior. Since Mao A is inherited with the X chromosome and is considered a dependent trait it may not show standard inheritance characteristics in males. Since the X chromosome in males can only come from the mother, this means that the fathers Mao A mutations (or lack there of) does not play a role in their son’s Mao A status. For females, since one X chromosome is inherited from each parent, the genetics tend to reflect the Mao A status of both parents. ACE (angiotensin converting enzyme): Changes can occur that affect the activity of the ACE gene that can lead to elevated blood pressure. In animal studies imbalances in this pathway were also correlated with increased anxiety and decreases in learning and memory. Increased ACE activity can also throw off the essential mineral balance in the your system due to decreased excretion of sodium in the urine and increased excretion of potassium in the urine. This reaction is also tied to the stress response such that situations of chronic stress can result in additional sodium retention and increased potassium excretion. This excess potassium is excreted provided that the kidneys are functioning properly. In the event that kidney function is compromised, it can lead to the retention of potassium in the body. ACE is adeletion, it is not a SNP. As a consequence it does not associate in the same manner that the other single nucleotide polymorphisms (SNP) on this panel do, so the inheritance pattern of the ACE deletion may not distribute in the same manner as single base changes. MTR/MTRR (methionine synthase/ methionine synthase reductase):These two gene products work together to regenerate and utilize B12 for the critical “long way” around the methylation pathway, helping to convert homocysteine to methionine. High levels of homocysteine have been implicated as risk factors in a number of health conditions including heart disease as well as Alzheimer’s disease. As is the case for COMT and VDR Bsm/Taq, the MTR and MTRR composite status is also important. Mutations in MTR can increase the activity of this gene product so that it leads to a greater need for B12 as the enzyme is using up B12 at a faster rate. The MTRR helps to recycle B12 for use by the MTR. Mutations that affect its activity would also suggest a greater need for B12.BHMT (betaine homocysteine methyltransferase):The product of this gene is central to the “short cut” through the methylation cycle, again helping to convert homocysteine to methionine. The activity of this gene product can be affected by stress, by cortisol levels and may play a role in ADD/ADHD by affecting norepinephrine levels.CBS (cystathionine-beta-synthase):The CBS enzyme basically acts as a gate between homocysteine and the downstream portion of the pathway that generates ammonia in the body. The types of CBS mutations that are identified on this SNP panel cause this “CBS gate” to be left open, this “open gate” is not a neutral situation. The “open gate” can allow support that is added for the rest of the methylation pathway to be depleted, including any B12 that is used to address MTR and MTRR mutations. While there are some positive end products that are generated via the downstream portion of the pathway such as glutathione and taurine, there are also negative byproducts such as excess ammonia and sulfites. By virtue of increased CBS activity, these sulfur groups that were complexed as part of the methylation cycle can now be released into the system as sulfites which are toxic to the body and put an additional burden on the SUOX gene product.NOS (nitric oxide synthase): The NOS enzyme plays a role in ammonia detoxification as part of the urea cycle. Individuals who are NOS + + have reduced activity of this enzyme. NOS mutations can have additive effects with CBS up regulations due to the increased ammonia that is generated by the CBS up regulations. To: mb12 valtrex Sent: Sat, November 13, 2010 4:12:14 AMSubject: Yasko results Got my ds's genetics back today. I understand just enough to know that I don't understand! Lol! I know what he doesn't have a problem with but that's about it. I know that he doesn't have the MTHFR mutation at all, no SUOX mutation and those are the mutations that are fine that I understand enough to breath a sigh of relief but he is NOS +- and ACE is ++ which sort of explains a few things but not really since I don't understand. Ugh! And I'm still waiting for the admin on the yasko board to approve me... Anyone want to explain some of this to me???? It doesn't seem to me like to it's *too* bad but what do I know? Lol! If there's anyone available that knows this stuff, here's the list of mutations/deletions: COMT V158M +- COMT H62H +- VDR Taq +- VDR FOK ++ (I know enough to know that this explains his D deficiency...I think) ACE Del16 ++ MTR A2756G +- MTRR A66G +- MTRR R415T +- MTRR S257T +- BHMT 2 +- BHMT 4 +- BHMT 8 +- CBS A360A +- NOS D298E +- (I think this explains his high ammonia?) But really, that's all I understand. I'm still trying to figure out what the heck the CALL column is supposed to mean with all it's T's, G's, A's and C's and such. The book is helpful but only barely since it's not exactly detailed enough. It mentions things about being COMT +- and such but it doesn't say anything about the specific COMT's. I'm so confused. Help? Cheryl ~http://www.gryffins-tail.blogspot.com ~@midian42~ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 14, 2010 Report Share Posted November 14, 2010 You don't need all the COMT mutations to be affected. I think the COMT mutations mean to be careful with sulfur-containing things. I am not really sure anymore LOL because we had so many big mutations that everything was contradicting. Try to go back into the web board. I never got a confirmation once I was allowed in. If you still can't get in, email me back and I'll give you my password... you can at least look around and see... I think the COMT people have their children on reduced meat diets, again I really can't remember off the top of my head. Our big mutation is the MAO-A one. I believe it is the root of most of the problems in my kiddos, well my son anyway. I am glad you don't have that one! Well, I actually have all that information. I guess I'm looking for something more specific. For instance, my son doesn't have all the COMT mutations, he only has 2 of 3. What does that mean and what do the individual mutations mean? That kind of thing. Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ I hope ,I could help you...COMT (catechol-O-methyltransferase): A primary function of this gene is to help to break down dopamine. Dopamine is a neurotransmitter that is recognized for its role in attention, as well as reward seeking behavior. Dopamine helps to cause pleasurable feelings that aid in reinforcing positive behaviors and motivating individuals to function in certain reward gaining activities. COMT is also involved in the breakdown of another neurotransmitter, norepinephrine. The balance between norepinephrine levels and dopamine levels has been implicated in ADD/ADHD; in addition, dopamine levels are important in conditions such as Parkinson’s disease. COMT is also involved in the proper processing of estrogen in the body. Sensitivity to pain has recently been found to be correlated with COMT activity, such that COMT + + individuals may be more sensitive to pain. VDR/Taq and VDR/Fok (vitamin D receptor): The panel looks at more than one portion of the vitamin D receptor, the Taq as well as the Fok sites. While the Fok change has been related to blood suMPA regulation, changes at Taq can affect dopamine levels. For this reason it is important to look at the composite of the COMT and VDR/Taq status and make supplement suggestions based on the combined results at these two sites. The focus on changes in the Fok portion of the VDR is in reMPAd to supplements that support the pancreas and aid in keeping blood suMPA in the normal healthy range. MAO A (monoamine oxidase A): MaoA is involved in the breakdown of serotonin in the body. Like dopamine, serotonin is another neurotransmitter in the body. It is involved with mood, and imbalances in serotonin levels have been associated with depression, aggression, anxiety and OCD behavior. Since Mao A is inherited with the X chromosome and is considered a dependent trait it may not show standard inheritance characteristics in males. Since the X chromosome in males can only come from the mother, this means that the fathers Mao A mutations (or lack there of) does not play a role in their son’s Mao A status. For females, since one X chromosome is inherited from each parent, the genetics tend to reflect the Mao A status of both parents. ACE (angiotensin converting enzyme): Changes can occur that affect the activity of the ACE gene that can lead to elevated blood pressure. In animal studies imbalances in this pathway were also correlated with increased anxiety and decreases in learning and memory. Increased ACE activity can also throw off the essential mineral balance in the your system due to decreased excretion of sodium in the urine and increased excretion of potassium in the urine. This reaction is also tied to the stress response such that situations of chronic stress can result in additional sodium retention and increased potassium excretion. This excess potassium is excreted provided that the kidneys are functioning properly. In the event that kidney function is compromised, it can lead to the retention of potassium in the body. ACE is a deletion, it is not a SNP. As a consequence it does not associate in the same manner that the other single nucleotide polymorphisms (SNP) on this panel do, so the inheritance pattern of the ACE deletion may not distribute in the same manner as single base changes. MTR/MTRR (methionine synthase/ methionine synthase reductase): These two gene products work together to regenerate and utilize B12 for the critical “long way” around the methylation pathway, helping to convert homocysteine to methionine. High levels of homocysteine have been implicated as risk factors in a number of health conditions including heart disease as well as Alzheimer’s disease. As is the case for COMT and VDR Bsm/Taq, the MTR and MTRR composite status is also important. Mutations in MTR can increase the activity of this gene product so that it leads to a greater need for B12 as the enzyme is using up B12 at a faster rate. The MTRR helps to recycle B12 for use by the MTR. Mutations that affect its activity would also suggest a greater need for B12. BHMT (betaine homocysteine methyltransferase): The product of this gene is central to the “short cut” through the methylation cycle, again helping to convert homocysteine to methionine. The activity of this gene product can be affected by stress, by cortisol levels and may play a role in ADD/ADHD by affecting norepinephrine levels. CBS (cystathionine-beta-synthase): The CBS enzyme basically acts as a gate between homocysteine and the downstream portion of the pathway that generates ammonia in the body. The types of CBS mutations that are identified on this SNP panel cause this “CBS gate” to be left open, this “open gate” is not a neutral situation. The “open gate” can allow support that is added for the rest of the methylation pathway to be depleted, including any B12 that is used to address MTR and MTRR mutations. While there are some positive end products that are generated via the downstream portion of the pathway such as glutathione and taurine, there are also negative byproducts such as excess ammonia and sulfites. By virtue of increased CBS activity, these sulfur groups that were complexed as part of the methylation cycle can now be released into the system as sulfites which are toxic to the body and put an additional burden on the SUOX gene product. NOS (nitric oxide synthase): The NOS enzyme plays a role in ammonia detoxification as part of the urea cycle. Individuals who are NOS + + have reduced activity of this enzyme. NOS mutations can have additive effects with CBS up regulations due to the increased ammonia that is generated by the CBS up regulations. To: mb12 valtrex Sent: Sat, November 13, 2010 4:12:14 AMSubject: Yasko results Got my ds's genetics back today. I understand just enough to know that I don't understand! Lol! I know what he doesn't have a problem with but that's about it. I know that he doesn't have the MTHFR mutation at all, no SUOX mutation and those are the mutations that are fine that I understand enough to breath a sigh of relief but he is NOS +- and ACE is ++ which sort of explains a few things but not really since I don't understand. Ugh! And I'm still waiting for the admin on the yasko board to approve me... Anyone want to explain some of this to me???? It doesn't seem to me like to it's *too* bad but what do I know? Lol! If there's anyone available that knows this stuff, here's the list of mutations/deletions: COMT V158M +- COMT H62H +- VDR Taq +- VDR FOK ++ (I know enough to know that this explains his D deficiency...I think) ACE Del16 ++ MTR A2756G +- MTRR A66G +- MTRR R415T +- MTRR S257T +- BHMT 2 +- BHMT 4 +- BHMT 8 +- CBS A360A +- NOS D298E +- (I think this explains his high ammonia?) But really, that's all I understand. I'm still trying to figure out what the heck the CALL column is supposed to mean with all it's T's, G's, A's and C's and such. The book is helpful but only barely since it's not exactly detailed enough. It mentions things about being COMT +- and such but it doesn't say anything about the specific COMT's. I'm so confused. Help? Cheryl ~http://www.gryffins-tail.blogspot.com ~@midian42~ -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 16, 2010 Report Share Posted November 16, 2010 No I think I need to send someone a message that I'm still waiting... Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ On Nov 16, 2010, at 6:10 AM, Toni Marie Lombardo wrote: Cheryl,Did you get access to the board? Got my ds's genetics back today. I understand just enough to know that I don't understand! Lol! I know what he doesn't have a problem with but that's about it. I know that he doesn't have the MTHFR mutation at all, no SUOX mutation and those are the mutations that are fine that I understand enough to breath a sigh of relief but he is NOS +- and ACE is ++ which sort of explains a few things but not really since I don't understand. Ugh! And I'm still waiting for the admin on the yasko board to approve me... Anyone want to explain some of this to me???? It doesn't seem to me like to it's *too* bad but what do I know? Lol! If there's anyone available that knows this stuff, here's the list of mutations/deletions: COMT V158M +-COMT H62H +- VDR Taq +-VDR FOK ++ (I know enough to know that this explains his D deficiency...I think) ACE Del16 ++MTR A2756G +- MTRR A66G +-MTRR R415T +- MTRR S257T +-BHMT 2 +- BHMT 4 +-BHMT 8 +- CBS A360A +-NOS D298E +- (I think this explains his high ammonia?) But really, that's all I understand. I'm still trying to figure out what the heck the CALL column is supposed to mean with all it's T's, G's, A's and C's and such. The book is helpful but only barely since it's not exactly detailed enough. It mentions things about being COMT +- and such but it doesn't say anything about the specific COMT's. I'm so confused. Help? Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 16, 2010 Report Share Posted November 16, 2010 I sent you my password info and I also sent a PM to a mod to advice my friend is waiting... and used this email cheryl.lowrance@... to let her know who you are. Hope that's right. ;-) No I think I need to send someone a message that I'm still waiting... Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ On Nov 16, 2010, at 6:10 AM, Toni Marie Lombardo wrote: Cheryl,Did you get access to the board? Got my ds's genetics back today. I understand just enough to know that I don't understand! Lol! I know what he doesn't have a problem with but that's about it. I know that he doesn't have the MTHFR mutation at all, no SUOX mutation and those are the mutations that are fine that I understand enough to breath a sigh of relief but he is NOS +- and ACE is ++ which sort of explains a few things but not really since I don't understand. Ugh! And I'm still waiting for the admin on the yasko board to approve me... Anyone want to explain some of this to me???? It doesn't seem to me like to it's *too* bad but what do I know? Lol! If there's anyone available that knows this stuff, here's the list of mutations/deletions: COMT V158M +-COMT H62H +- VDR Taq +-VDR FOK ++ (I know enough to know that this explains his D deficiency...I think) ACE Del16 ++MTR A2756G +- MTRR A66G +-MTRR R415T +- MTRR S257T +-BHMT 2 +- BHMT 4 +-BHMT 8 +- CBS A360A +-NOS D298E +- (I think this explains his high ammonia?) But really, that's all I understand. I'm still trying to figure out what the heck the CALL column is supposed to mean with all it's T's, G's, A's and C's and such. The book is helpful but only barely since it's not exactly detailed enough. It mentions things about being COMT +- and such but it doesn't say anything about the specific COMT's. I'm so confused. Help? Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 17, 2010 Report Share Posted November 17, 2010 Thank you. Still waiting. Thanks for sending your login info to me! Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ On Nov 16, 2010, at 9:44 AM, Toni Marie Lombardo wrote: I sent you my password info and I also sent a PM to a mod to advice my friend is waiting... and used this email cheryl.lowrance@... to let her know who you are. Hope that's right. ;-) No I think I need to send someone a message that I'm still waiting... Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ On Nov 16, 2010, at 6:10 AM, Toni Marie Lombardo wrote: Cheryl,Did you get access to the board? Got my ds's genetics back today. I understand just enough to know that I don't understand! Lol! I know what he doesn't have a problem with but that's about it. I know that he doesn't have the MTHFR mutation at all, no SUOX mutation and those are the mutations that are fine that I understand enough to breath a sigh of relief but he is NOS +- and ACE is ++ which sort of explains a few things but not really since I don't understand. Ugh! And I'm still waiting for the admin on the yasko board to approve me... Anyone want to explain some of this to me???? It doesn't seem to me like to it's *too* bad but what do I know? Lol! If there's anyone available that knows this stuff, here's the list of mutations/deletions: COMT V158M +-COMT H62H +- VDR Taq +-VDR FOK ++ (I know enough to know that this explains his D deficiency...I think) ACE Del16 ++MTR A2756G +- MTRR A66G +-MTRR R415T +- MTRR S257T +-BHMT 2 +- BHMT 4 +-BHMT 8 +- CBS A360A +-NOS D298E +- (I think this explains his high ammonia?) But really, that's all I understand. I'm still trying to figure out what the heck the CALL column is supposed to mean with all it's T's, G's, A's and C's and such. The book is helpful but only barely since it's not exactly detailed enough. It mentions things about being COMT +- and such but it doesn't say anything about the specific COMT's. I'm so confused. Help? Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 17, 2010 Report Share Posted November 17, 2010 Thank you. Still waiting. Thanks for sending your login info to me! Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ On Nov 16, 2010, at 9:44 AM, Toni Marie Lombardo wrote: I sent you my password info and I also sent a PM to a mod to advice my friend is waiting... and used this email cheryl.lowrance@... to let her know who you are. Hope that's right. ;-) No I think I need to send someone a message that I'm still waiting... Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ On Nov 16, 2010, at 6:10 AM, Toni Marie Lombardo wrote: Cheryl,Did you get access to the board? Got my ds's genetics back today. I understand just enough to know that I don't understand! Lol! I know what he doesn't have a problem with but that's about it. I know that he doesn't have the MTHFR mutation at all, no SUOX mutation and those are the mutations that are fine that I understand enough to breath a sigh of relief but he is NOS +- and ACE is ++ which sort of explains a few things but not really since I don't understand. Ugh! And I'm still waiting for the admin on the yasko board to approve me... Anyone want to explain some of this to me???? It doesn't seem to me like to it's *too* bad but what do I know? Lol! If there's anyone available that knows this stuff, here's the list of mutations/deletions: COMT V158M +-COMT H62H +- VDR Taq +-VDR FOK ++ (I know enough to know that this explains his D deficiency...I think) ACE Del16 ++MTR A2756G +- MTRR A66G +-MTRR R415T +- MTRR S257T +-BHMT 2 +- BHMT 4 +-BHMT 8 +- CBS A360A +-NOS D298E +- (I think this explains his high ammonia?) But really, that's all I understand. I'm still trying to figure out what the heck the CALL column is supposed to mean with all it's T's, G's, A's and C's and such. The book is helpful but only barely since it's not exactly detailed enough. It mentions things about being COMT +- and such but it doesn't say anything about the specific COMT's. I'm so confused. Help? Cheryl~http://www.gryffins-tail.blogspot.com~@midian42~ -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. -- Toni------Mind like a steel trap...Rusty and illegal in 37 states. Quote Link to comment Share on other sites More sharing options...
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