FADS1 and FADS2 SNPs?

[alicec]

It looks like FADS2 minor alleles are sped up

I'm sorry I'm just not finding this. Which particular snps correlate with an increase in desaturase activity?

 

[ppodhajski]

I'm sorry I'm just not finding this. Which particular snps correlate with an increase in desaturase activity?

I know, I'm still trying to work through the data. There is definitely more Anchrondic Acid with these SNPs so I made an assumption they were fast. I think that MY FADS2 is fast and my FADS1 is slow which would mean I would have more inflammation and heart disease. Which I do have in my family. I also know that when I go in a high-fat omega 6 diet I get lower back pain that is relieved when I take vitamin B6. This makes sense since B6 is the cofactor for FADS1 and FADS2.

I have a black out at my house right now so I can't really look anything up but I'll see what I can find. The literature on this is very confusing.

 

[alicec]

When I looked at the FADS snps previously I must say I ran out of energy and interest and did not follow them down every last rabbit hole. Still I only recall finding loss of function. Since I had quite a few heterozygous snps with known effects I figured this could mean a slightly decreased capacity to make longer chain PUFAs.

Coupled with my general understanding that desaturase activity is something that falls off with age, I just decided to be careful to obtain these end products from diet (eggs, meat, oily fish) plus some modest supplementation of borage and fish oils.

I've had several thoughts after reading your posts since this is the first time I have encountered concerns about increased desaturase activity.

I'd certainly be interested to know if there are some snps which increase desaturase activity and if these have any correlation with CHD.

I was worried when you said you maybe needed a vegetarian diet. Unless you really know you have a serious problem with desaturase overactivity, this could be counterproductive. I can't put my hand on a reference at the moment but I believe there is a very serious fall off in desaturase activity with aging. The young and healthy can make all the different types of PUFAs they need from alpha linoleic and linolenic starting points but not indefinitely.

While I agree that a high omega 6 diet is not a good idea, the popular notion that omega 6 = inflammatory = bad and omega 3 = anti-inflammatory = good is simplistic and just plain wrong. Both types are absolutely essential and need to be in balance. In other words I don't think we should be fearful of things like arachidonic acid which after all constitutes something like 14% of brain lipids - we absolutely need it.

I guess I started to think that while its very understandable that you are concerned about inflammation and heart disease since they are in your family, maybe the desaturases are not the main problem.

 

[brenda]

I am aspie but dont have any ++ in the risk factors, just a few +-.

 

[ppodhajski]

When I looked at the FADS snps previously I must say I ran out of energy and interest and did not follow them down every last rabbit hole. Still I only recall finding loss of function. Since I had quite a few heterozygous snps with known effects I figured this could mean a slightly decreased capacity to make longer chain PUFAs.

Coupled with my general understanding that desaturase activity is something that falls off with age, I just decided to be careful to obtain these end products from diet (eggs, meat, oily fish) plus some modest supplementation of borage and fish oils.

I've had several thoughts after reading your posts since this is the first time I have encountered concerns about increased desaturase activity.

I'd certainly be interested to know if there are some snps which increase desaturase activity and if these have any correlation with CHD.

I was worried when you said you maybe needed a vegetarian diet. Unless you really know you have a serious problem with desaturase overactivity, this could be counterproductive. I can't put my hand on a reference at the moment but I believe there is a very serious fall off in desaturase activity with aging. The young and healthy can make all the different types of PUFAs they need from alpha linoleic and linolenic starting points but not indefinitely.

While I agree that a high omega 6 diet is not a good idea, the popular notion that omega 6 = inflammatory = bad and omega 3 = anti-inflammatory = good is simplistic and just plain wrong. Both types are absolutely essential and need to be in balance. In other words I don't think we should be fearful of things like arachidonic acid which after all constitutes something like 14% of brain lipids - we absolutely need it.

I guess I started to think that while its very understandable that you are concerned about inflammation and heart disease since they are in your family, maybe the desaturases are not the main problem.

First to clear up some things about my diet. I am not a vegetarian but I lean strongly that way. I will eat sardines a few times a week and I eat liver on and off. I am not NO fat I am low fat.

Second, I do not think that desaturase activity is the ONLY cause of heart disease, just a factor. But it is also a factor in the autoimmune and mood issues my family has struggled with.

I know the importance of omega 6 and to eliminate it would be foolish. To me it is finding what out genetic balance of these things needs be. The good omega 3/bad omega 6 in general is correct. But we are all different genetically so some will need a bit more omega 6 and others a lot less.There are people who are typically less inflammatory and people who are more inflammatory based solely on genetics.

Also destaurase activity is dependent on B6 (P5P), so othere genes that might need more B6 might causes a deficiency in P5P and therefor slow FADS2 activity. A high fat diet will also reduce B6.

And on age and desaturase activity, it seems there is more AA (omega 6) being left around as we age because Delta 6 (FADS2) activity slows down. This would say to me that as we age we need to increase Omega 3 in the diet.
http://www.ncbi.nlm.nih.gov/pubmed/2051894

This is why my family has early heart disease, it is like they are aging more quickly.

So it is making sense now that it is in fact they are both slow, and since they are both slow I make a greater amount of prostoglandins, both good and bad, the amount of each depends on my diet. This increase in prostoglandins will create one reaction or another based on how genetically sensitive I am to those.

Note that prostoglandins seem to have some effect on neurotransmitters:
http://www.karger.com/Article/Abstract/301973
http://pubs.acs.org/doi/abs/10.1021/ja00725a064
http://www.sciencedirect.com/science/article/pii/S0969996105003128
http://www.sciencedirect.com/science/article/pii/S0002937809005535

I cannot begin to tell you the extreme diets I endured and the suffering I went threw to see how omega 3 and omega 6 balance effected me. There is no doubt, that for me Omega 6 makes brings my body down (depression, pain, inflammation, excess sleep) and omega 3 brings it up (manic, no pain, insomnia) makes it excited.

When I was depressed and in pain on a high omega 6 diet I took P5P (B6) and a lot of my issues resolved. And when I took it now on a low fat diet I had a bad rosecia outbreak. So this follows that my FADS are slow. I also got a rosecia flare up when I drank red wine recently while on the low fat diet.

 

[Valentijn]

Almost identical.

I wouldn't bother worrying about it. @ppodhajski just randomly decides SNPs are having an impact, without any concern for whether or not there is any research done into those SNPs. You both have the same variations for a lot of them because they are extremely common.

If you want to know if SNPs are relevant, someone has to read the research at some point. There's no short cuts.

 

[out2lunch]

I wouldn't bother worrying about it. @ppodhajski just randomly decides SNPs are having an impact, without any concern for whether or not there is any research done into those SNPs. You both have the same variations for a lot of them because they are extremely common.

If you want to know if SNPs are relevant, someone has to read the research at some point. There's no short cuts.

Thanks, Valentijn. I pretty much came to the same conclusion myself, especially since so many of us with ME/CFS/FMS have ASD running through our families. If these alleles are commonly seen in ASD, then they're going to be prevalent here. And since biology is never absolute destiny except for a few rare diseases, having these SNPs doesn't mean much, unless they're expressing themselves, which isn't necessarily an easy thing to determine.

 

[out2lunch]

Hysterectomy. That will throw all genetics out the window….

Especially when the hystero was done for endometriosis, which many researchers now believe is an autoimmune disease.

There is enough of evidence that high fat diet is one of the major causes of gallstones for people at risk.

You're making no sense here. I got the bad genes from my mom, who died stone free after eating a high fat diet for over four decades. Her cholesterol levels were low normal. Only my total and LDL are elevated because of lack of estrogen. The times I've tried to replace my estrogen, the LDL dropped and the total normalized. For my family, the diet has nothing to do with it.

You are mistaken about the bile sticking around and causing gallstones.

Nope, not always true. Sludgy bile that doesn't flow easily from the bladder will precipitate out and form stones. That's why GI docs recommend cholecystectomy for this condition. The risk of small stones forming in the bile duct and blocking it from bile sludge is too great.

I would guess it is more likely that you are getting gall stones because of your bad BCMO1 genes

Then explain the lack of stones in my mom who had the same genes! Geez, this is the stuff that makes me crazy!

Genes are not absolute destiny! Bad genes are only bad when they express themselves. And what triggers them off? Who knows? Perhaps in my family, it's the lack of estrogen and elevated LDL that does it. My mom didn't have estrogen problems, had normal cholesterol levels, and no stones. Even on a high fat diet.

If you do not get enough Vitamin A you will limit the amount of bile acids you make. Bile acids are what breakdown and inhibit gallstones from forming.

So when I don't eat fat and have imaging done of my gallbladder, and it's swollen up to the size of a small peach, you're telling me that it's not filled up with bile but with something else? And that's why I have stones? If I told that to my GI doc, he'd laugh in my face.

I know all this because I have a woman friend who had a history with gallstones and she has the same SNPs. She takes Vitamin A now and she has no more gallbladder pain.

So the vitamin supplements I've taken my entire life which includes vitamin A -- not beta carotene -- isn't keeping me from being deficient, even though my serum metabolic profile tests demonstrate otherwise? You just know that because I have stones that my body isn't getting enough vitamin A, even though I eat a high fat diet and supplement?

You probably feel better eating the high fat because you are more likely get get Vitamin A. On a vegetarian diet you are only getting beta carotine which is hard for you to convert to Vitamin A.

Before popping off and assuming that I don't do any testing and don't take any supplements, even when I was eating a vegetarian diet, why not ask me if I've done testing and whether or not I supplement my crappy methylation genes and dietary deficiencies?

Seriously, you need to understand that there are MANY factors that contribute to diseases like gallstone formation, and not just high fat diets and lack of vitamin A.

If you can show me evidence of this I will be glad to see it. I used to have IBS-D. BAD. I got every test in the book; fungus, bacteria, SIBO breath test, H Pylori. I tried antibiotics, manuka homey, low card, high carb, probiotics, prebiotics. Sometimes it would get a little better but never better.

I developed severe IBS-D from SIBO about three years ago. The SIBO was prevotella out of control in the distal part of my small intestine. Two weeks of Xifaxan wiped it out and the diarrhea went away. Just like that.

SIBO is a simple test that any doctor can and will do and it is not caused by a fungus, it is caused by an overgrowth of bacteria.

I didn't state that it was. I stated that fibro patients are prone to IBS and SIBO, which also makes them prone to gut fungal infections as well, because of the overall dysbiosis caused by the SIBO. Even when "good bacteria" like prevotella becomes overpopulated, other bad players like fungus, especially candida, can also get out of control. And some of us, especially those with allergies on the autism spectrum, tend to have difficulties with keeping fungus under control, even on low sugar/low carb diets. I still wrestle with gut fungus on my low carb diet, which tends to worsen when the SIBO returns.

There is zero evidence that IBS is caused by anything pathogenic. But plenty of evidence is is related to neurotransmitter function.

That is simply no longer believed by knowledgable GI docs. There is a HUGE correlation between IBS and SIBO now, enough so that many docs are prescribing one 200mg Xifaxan tablet to be taken at bedtime every night to keep the SIBO at bay. Those IBS patients who've adopted this routine are reporting significant reduction if not complete elimination of their IBS symptoms with this regimen. You need to keep up with your reading.

You know how I got rid of my IBS-D? Flavin Mononucliotide. (a form of B2). Gone in one day.
IBS-C, the opposite I imagine, not enough serotonin, I have issues with too much. (MAOA, MAOB, and SERT)
http://www.ncbi.nlm.nih.gov/pubmed/19361459

Since you have the mood and addiction issues in the family I would say this is probably a more likely notion.

And once again, you make assumptions that I even have a serotonin problem that's not being addressed and monitored and treated!

Besides, you're forgetting about the hysterectomy. Scar tissue. It keeps the bowel function tamped down. It alters placement anatomy, adding loops to the distal small intestine because there's no uterus to prop it up.

And FWIW, I don't believe you ever had IBS-D. IBS never resolves in one day with ANY treatment. Whatever it is you had, it wasn't IBS.

 

[ppodhajski]

You're making no sense here. I got the bad genes from my mom, who died stone free after eating a high fat diet for over four decades. Her cholesterol levels were low normal. Only my total and LDL are elevated because of lack of estrogen. The times I've tried to replace my estrogen, the LDL dropped and the total normalized. For my family, the diet has nothing to do with it.

Do you have your mother's actual gene profile or are you assuming you have your mothers genes? She might not have had your genes after all, yes? I mean that is a possibility. I showed you the research on how a high fat diet leads to gallstones and how bile acid degrads them, but you say I am wrong but show me not proof.

At this point I am not replying because there seems to be an inordinate amount of proof I need to show, and even when I do some say it is "not proof". And yet the rest of this post is filled with anecdotal examples that might be the result of coincidence.

And this bit:

And FWIW, I don't believe you ever had IBS-D. IBS never resolves in one day with ANY treatment. Whatever it is you had, it wasn't IBS.

Well, I just do not know what to say about it. I wish I would have taken video of myself on the crapper or had the doctor reports that showed you the diagnosis. All I can say now is that I am no longer in the bathroom every time after I eat. And you remarked that I resolved it with out "any treatment". No, I never said that. I said I resolved it by watching my dietary amines and taking high does FMN. But that is a rather sad thing to hear from another person with CFS, after all we go through with people not believing us.

But I will not be responding to your posts either after that last comment. It is not helpful. People can either not believe me or look at the connection in the research I am making. I have no proof why it worked, I just know it worked. What I am trying to figure out is why.[/QUOTE][/QUOTE]

 

[Valentijn]

Do you have your mother's actual gene profile or are you assuming you have your mothers genes? She might not have had your genes after all, yes?

@out2lunch 's mother had gallstone problems. And he has a rare pathogenic missense mutation known to cause gallstone problems. That rare pathogenic missense mutation came from one of his parents. It's safe to assume it came from the parent with gallstone problems

It's pretty likely that the gallstone problems are related to the mutation known to cause that exact problem, versus whatever theory you're currently trying to sell.

 

[ppodhajski]

@out2lunch 's mother had gallstone problems. And he has a rare pathogenic missense mutation known to cause gallstone problems. That rare pathogenic missense mutation came from one of his parents. It's safe to assume it came from the parent with gallstone problems

It's pretty likely that the gallstone problems are related to the mutation known to cause that exact problem, versus whatever theory you're currently trying to sell.

Would you mind sharing what that mutation was?

 

[Valentijn]

Would you mind sharing what that mutation was?

It's the one he listed as being a gallstone mutation in his post.

 

[ppodhajski]

It's the one he listed as being a gallstone mutation in his post.

There is not one listed. If you can tell me what the gene is or link directly to the post I would appreciate it.

 

[out2lunch]

@out2lunch 's mother had gallstone problems. And he has a rare pathogenic missense mutation known to cause gallstone problems. That rare pathogenic missense mutation came from one of his parents. It's safe to assume it came from the parent with gallstone problems

It's pretty likely that the gallstone problems are related to the mutation known to cause that exact problem, versus whatever theory you're currently trying to sell.

Not to split hairs here, but I'm actually not male. Hysterectomy 30 years ago. Well, I guess that's pretty close then.

And my mom's family had gallbladder disease out the wazoo. But she did not. All of her sisters did, having cholecystectomies post-menopause. Was it the difference in dietary fat? Nope. They all ate a high fat diet. They ate SAD, and my mom ate ketogenic. Maybe it was other dietary differences, like carbs. But it certainly wasn't fat.

If the SNPs were the bullets in the gallstone chamber, then something other than dietary fat pulled the trigger. Given my mom's family's history, I'm betting it's cholesterol levels.

Before the surgery, I had plenty of estrogen and very low cholesterol levels, like my mom. But once I lost my ovaries and estrogen, my LDL shot straight up. My aunts had high cholesterol but my mom did not. I didn't have gallstones before the surgery, and I ate a low fat high carb vegetarian diet for several years afterwards, when the stones started to form.

Then there's the estrogen replacement factor. The times I've attempted HRT, my LDL drops down to low pre-hysterectomy levels. But I can't do HRT for any length of time without severe side effects, so the LDL stays elevated in my body's effort to make the estrogen that's missing. And that's what my aunts and I had in common: low estrogen. They didn't do HRT after menopause but my mom did. Their cholesterol levels rose like mine but her levels stayed low. They got stones, she didn't. But all of them ate high fat diets.

It's not fat in the diet. It's the SNPs and the high cholesterol. And since gallstones are made from cholesterol, that makes perfect sense. The SNPs most likely predispose the excess cholesterol to settle out of the bile into stones. How any other trigger like a high fat diet could be logically postulated from this data is beyond me.

 

[ppodhajski]

Not to split hairs here, but I'm actually not male. Hysterectomy 30 years ago. Well, I guess that's pretty close then.

And my mom's family had gallbladder disease out the wazoo. But she did not. All of her sisters did, having cholecystectomies post-menopause. Was it the difference in dietary fat? Nope. They all ate a high fat diet. They ate SAD, and my mom ate ketogenic. Maybe it was other dietary differences, like carbs. But it certainly wasn't fat.

If the SNPs were the bullets in the gallstone chamber, then something other than dietary fat pulled the trigger. Given my mom's family's history, I'm betting it's cholesterol levels.

Before the surgery, I had plenty of estrogen and very low cholesterol levels, like my mom. But once I lost my ovaries and estrogen, my LDL shot straight up. My aunts had high cholesterol but my mom did not. I didn't have gallstones before the surgery, and I ate a low fat high carb vegetarian diet for several years afterwards, when the stones started to form.

Then there's the estrogen replacement factor. The times I've attempted HRT, my LDL drops down to low pre-hysterectomy levels. But I can't do HRT for any length of time without severe side effects, so the LDL stays elevated in my body's effort to make the estrogen that's missing. And that's what my aunts and I had in common: low estrogen. They didn't do HRT after menopause but my mom did. Their cholesterol levels rose like mine but her levels stayed low. They got stones, she didn't. But all of them ate high fat diets.

It's not fat in the diet. It's the SNPs and the high cholesterol. And since gallstones are made from cholesterol, that makes perfect sense. The SNPs most likely predispose the excess cholesterol to settle out of the bile into stones. How any other trigger like a high fat diet could be logically postulated from this data is beyond me.

Please split hairs, I knew you were female, Val did not. I think it might point to something in her logical errors.

But you are ASSUMING that your Mom and her sisters all had the same genetics.It is the very fact that they all had the same diet, yet your Mother did NOT have gallbladder issues that shows that she could have had DIFFERENT genes. There is the possibility that your mother had genetiocs that protected her from the high fat diet. You see, it is the SNPs AND the fat. But you cannot say that you all had the same genetics for certain.

By the way, cholesterol is a sterol (lipid), a fat in the blood, derived from animal fat.
http://www.wisegeek.com/what-is-a-sterol.htm

So to say is was not the fat in the diet kind of does not make sense since fat is out source of all sterols.

And if gallstones are broken down by bile acid you are missing that part of the possibility. It could be that your mothers BCMO1 genes were fine. Right?

 

[Undisclosed]

Moderator hat on -- The initial reason I looked at this thread is because it has been reported a few times. As a moderator, I will ask that you be nicer to each other -- in other words, please avoid interjecting negative personal comments when responding to other members.

Moderator hat off

@ppodhajski I know very little about SNP's and genetics -- the one thing that I do know is that having bad genetics does not necessarily translate into illness and bad health. We do know quite a bit about single gene mutations causing specific diseases. All the SNP's have not been mapped, have they? Companies like 23andME only represent a very small part of the genome that's why they are able to provide information that doesn't cost thousands of dollars so a lot of information is being missed and basically what they are offering are correlations. It's a fascinating field but there is very little conclusive information you can get about your actual health status related to your snp's at this point except prediction. So really, any assertations you are making can't really be set in stone at this point of time.

If you believe something about your own SNP's causing your health issues then it would be your unique genetic make-up and epigenetics that are involved rather than being applicable to the rest of the people with similar SNP's who have some similar disease. You are practicing your own personalized medicine in a way, but how is it transferable to others that have a vastly different genetic make-up than you do as well as their own unique epigenetic history. I think it's really tempting to find out you have certain SNP's and then say those SNP's must be causing your health issues because there is some correlation but really there is much more to it at that. I also think it's important not to insist something when it's really better to use words like 'could be related' 'might be related' rather than insisting something 'is related'. It's much easier to have a discussion when you are open to the idea that something might have more than one explanation. I wonder if that is the problem on this thread?

 

[ppodhajski]

I do not know how many times I can repeat that I know single SNPs will not always be pathogenic. I do not care about pathogenic SNPs, they are not my interest.

I see the basic misunderstanding some have with what I am saying but I cannot help you understand it. But I will try.

yes, we all have different genetics, but our metabolic pathways are always the same since we are all human. Those pathways just function at different rates because of our nonpathogenic SNPs. For example, we all breakdown tryptophan the same way and we all metabolize it into the same thing but the rates that we do that will vary from person to person. What makes us susceptible to different diseases and sensitive to different foods are the different SNPs on these pathways that determine the metabolic rate of that pathway. It is the same with skin color which might be a better example. We all have the same genes for producing melanin but some of us have darker skin and some of the lighter skin. This difference is due to the different metabolic rate of the pathway due to different SNPs on that pathway. There are not different dark skin genes and light-skinned genes, there is only the melanin pathway that produces melanin and how much melanin is produced depends on the metabolic rate of that pathway. Sun will speed up that pathway causing more melanin to be produced. But based on our different SNPs some Might tan and others might just get burnt.

So for example, they know in Parkinson's that people with the disorder seem to metabolize dopamine more quickly. They give these people drugs to either slowdown dopamine metabolism (MAOIs) or to speed up Dopamine production (loops and B6) The dopamine pathway is a long pathway and there are many SNpS that can change the amount of any product. By looking at anyone specific genes in the pathway we can get an idea of the possibility of why they have low dopamine. What I, and others in the field of nutritional genomics, are investigating is the possibility to do this simply with vitamin cofactors.

In other words I'm not looking at pathogenic diseases, I am looking at nutrition genomics.

http://nutrigenomics.ucdavis.edu/?page=information
http://www.eufic.org/article/en/expid/review-nutrition-genome/

This fact is why people get sick when they have vitamin deficiencies. With a vitamin deficiency the enzymes might not have the cofactor they need to function fast enough. This is why people here take vitamins and see changes. If the SNPs didn't matter and we would see no change when taking any vitamins.

And all this is why you keep seeing me ask me for different people's genetics. It is exactly because I know that are different genetics matter in some critical pathways.

But the most important factor in all of this is that by following this idea I Fixed some issues that we all seem to share. Yet, the response I got from you an Valentjin is that I was misdiagnosed? Really?

I'm not saying any of this stuff to win awards or get money or anything else. I know the suffering you were all going through because I've lived through it myself. I spent six years studying nutrition in the last year and a half studying nutrition genomics. This is all I do since I'm on disability and I do it obsessively.

Yes I know this is new, yes I know this is theory, yes I know there is not much evidence for what I am doing, but there's a lot of evidence for the parts of what I'm doing. All I did is put together those different parts and I seem to of had very good results. I am cured. 100%.

I know I'm not the most diplomatic person at times. I just ask of you to recognize that it's my aspergers and not to take it personally and instead look at the science that I'm talking about.

 

[Undisclosed]

But the most important factor in all of this is that by following this idea I Fixed some issues that we all seem to share. Yet, the response I got from you an Valentjin is that I was misdiagnosed? Really?

What I actually said was that it 'sounds like a misdiagnosis' not that it is a misdiagnosis. I have never heard of a case of IBS being cured in one day.

I'm not saying any of this stuff to win awards or get money or anything else. I know the suffering you were all going through because I've lived through it myself. I spent six years studying nutrition in the last year and a half studying nutrition genomics. This is all I do since I'm on disability and I do it obsessively.

Yes I know this is new, yes I know this is theory, yes I know there is not much evidence for what I am doing, but there's a lot of evidence for the parts of what I'm doing. All I did is put together those different parts and I seem to of had very good results. I am cured. 100%.

If you are on disability then why are you claiming 'I am cured. 100%'? It's really confusing. I took that to mean you are totally cured of all your physical issues. Maybe the disability is for your Asperger's but it would be helpful to add that to lessen the confusion. It appears for those who know nothing about you that you are claiming to be cured of ME because this is a website for ME/CFS. Please make it very clear to readers what you have cured yourself of. That would be very helpful.

I know I'm not the most diplomatic person at times. I just ask of you to recognize that it's my aspergers and not to take it personally and instead look at the science that I'm talking about.

I do recognize some of your issues are likely caused by your Asperger's but you must understand that you need to stop speaking with seemingly absolute authority on issues that can have multiple answers.

I was trying kindly to point something out to you, I will say it again:

I also think it's important not to insist something when it's really better to use words like 'could be related' 'might be related' rather than insisting something 'is related'. It's much easier to have a discussion when you are open to the idea that something might have more than one explanation. I wonder if that is the problem on this thread?

There are appear to be some holes in your knowledge, that or you are not explaining things very well. Either way, you do come across as you think you are right about everything and maybe because of your Asperger's you can't accept that you could be erroneous. It's really hard to communicate on the internet but if people are reacting negatively to what you are saying, pay attention to it and try to figure out what it is that is causing all the issues and go from there. Leave yourself open to the opinions of others rather than insisting that you are correct. It adds to a good debate and it allows for learning from each other.

 

[ppodhajski]

What I actually said was that it 'sounds like a misdiagnosis' not that it is a misdiagnosis. I have never heard of a case of IBS being cured in one day.

Now you have heard of one case of IBS being cure in a day.

If you are on disability then why are you claiming 'I am cured. 100%'? It's really confusing. I took that to mean you are totally cured of all your physical issues. Maybe the disability is for your Asperger's but it would be helpful to add that to lessen the confusion. It appears for those who know nothing about you that you are claiming to be cured of ME because this is a website for ME/CFS. Please make it very clear to readers what you have cured yourself of. That would be very helpful.

Two things, after 15 years on disability is is hard to find work, especially in this economy. Second, I wanted to be sure I was stable. And to be cured does not mean the legacy of my illness was erased.

To be clear, what I cured/no longer suffer from:
ME/CFS
IBS-D
Anxiety
OCD
Sebhoeric Dermatisis
Costocondritis
Parethesia
Heart Palpitations
High Blood Pressure

There are appear to be some holes in your knowledge, that or you are not explaining things very well. Either way, you do come across as you think you are right about everything and maybe because of your Asperger's you can't accept that you could be erroneous. It's really hard to communicate on the internet but if people are reacting negatively to what you are saying, pay attention to it and try to figure out what it is that is causing all the issues and go from there. Leave yourself open to the opinions of others rather than insisting that you are correct. It adds to a good debate and it allows for learning from each other.

You say you know nothing about genetics yet you say there are holes in my knowledge? It is one thing for me to explain it well it is another to have the capacity to understand it. I do not understand quantum physics but I would not blame it on the person trying to tell me about it.

I see in my head are too complex for a forum. If you look carefully at my other posts you will see I certainly do not think I am right about everything. In fact you just have to look at this thread. "I know, I'm still trying to work through the data. There is definitely more Anchrondic Acid with these SNPs so I made an assumption they were fast." That is me correcting my wrongness. One thing I do not care about is being wrong, that is not an aspergers trait. What I care about is people just saying I am wrong and just saying "@ppodhajski just randomly decides SNPs are having an impact, without any concern for whether or not there is any research done into those SNPs." That is an insult and I reported it and nothing happened. I am not doing this randomly. You keep criticizing me but there is another party in all this which I have not heard you comment on. For me to respect her, she needs to respect me and my work and stop instigating and spreading "reasonable doubt".

You know, everytime Valentenjn says I am wrong she is ALSO insisting she is right. It is how SHE "comes across as [she] think [she] right about everything" which I am responding to. SHE is the "know it all". She is not always right that I am wrong about everything. I hope you can see your bias on this issue..

I am certain the FADS SNPs I have effect me. How and what that means is what I am trying to figure out.][/QUOTE]

 

[Gondwanaland]

Now you have heard of one case of IBS being cure in a day.

My husband started having severe D - no probiotics (boulardii, bifium, LAB, or charcoal would help with it until I thought it was the zinc supplementation. The D stopped in the same day I gave him copper.

I found a post I wrote a while ago about my flax intolerance:
http://forums.phoenixrising.me/inde...icum-a-game-changer.37324/page-18#post-599307
@ppodhajski what do you think about my hypothesis?