The Role of MTHFR & Methylation in ADHD & Autism with Dana Kay

Рет қаралды 5,551

Күн бұрын

Пікірлер: 28

@sshaw70 3 күн бұрын

This was an amazingly clear video on these gene mutations! I don’t have adhd so that may be why I was able to stick with it? 😁

@judylandry302 9 ай бұрын

I am AuDHD. I have been researching the cause of why I have so many cormobidities and related symptoms. It all comes back to the MTHFR gene mutation. I have been trying to share the information you are talking about in this video with my community, but because I don't have the credentials, I am censored. Would you be interested in writing an article on Medium on this subj?

@ADHDThriveInstitute 9 ай бұрын

Hi Judy, thanks for tuning in. Please get in contact with me here to chat further: adhdthriveinstitute.com/contact-us/

@huntergulledge596 29 күн бұрын

I love the way you describe it: “AuDHD”. I hope you don’t mind if I reuse it😅

@myAmericanGirlLife 5 ай бұрын

Oh my gosh 😮 I am functioning at 25%. I just got my test results yesterday. I also have gene mutations in cbs, comt, mao-a, mthfd1, mtr and mtrr, and smht. I am a little over my head trying to figure everything out, but I very much appreciate this video. Thank you! Ps: if anybody has tips or exleriences dealing with several mutations, feel free to comment ❤

@asherasator 2 ай бұрын

It's not a gene mutation, but the reality that some ancestors were not consuming high levels of methionine foods that result in homocysteine byproducts. This has been understood in science for quite some time. [Pre 2003 MTHFR symptoms were understood by Homocystinuria]: (1) Geigy Scientific Tables, 7th edition, page 449; Inborn Metabolic Errors and their treatment, 'Homocystinuria' the treatment is 'Diet low in methionine, but higher in cysteine and pyridoxine [vitamin B6].' Which B6 is naturally found in fruits, veggies and grains. (2) Enzymatic Reaction Mechanisms, pages 846-850; 'Cobalt coenzymes with FADH enzymes attacking SAM [S-adenoslymethionine] creating methyl-CoB12, which then turned homocysteine back into methionine.' Normally SAM would create methyl-CoB12 by the enzyme NADPH, with a "defect" and lower ability to metabolize the Cobalt enzymes with FADH can also do the job. But the next pages 851-863 show that methyl-CoB12 '... appears to function secondary methylation category... methylates mercury, palladium, lead, platinum, gold, tin, arsenic, selenium, and chromium' in the environment creating toxic chemicals. High doses of methyl-CoB12 is well known to increase oxidative stress and has many other toxic reactions. So lowering methionine with focus on natural foods with cysteine along with B2 and B6 seems to be a better route and dealing with homosistinuria [MTHFR] for over 50+ years. Methionine is carcinogenic and involved in angiogenesis that creates blood vessels to tumors. The common ideas of methionine being "essential" is overrated because even with no MTHFR "defects" the toxic effects of methionine to homocysteine recycling can affect anyone.

@shred_pow_pow Ай бұрын

Get the book Dirty Genes by Dr. Ben Lynch. It will walk you through the proper steps to take.

@asherasator Ай бұрын

@@shred_pow_pow Most online trends look at methyl-CoB12 supplementation dealing with homocysteine and MTHFR "defect". I'm experienced in nuclear chemistry, biochemistry and enzymatic catalyzation. Pre-2003 MTHFR discovery symptoms were noticed by homocysteine in urine. I looked in two books of very detailed facts: (1) Geigy Scientific Tables, 7th edition [1970], page 449; Inborn Metabolic Errors and their treatment. 'Homocystinuria' the treatment is "Diet low in methionine, but higher in cysteine and pyridoxine [vitamin B6]. Which B6 is naturally found in fruits, veggies and grains. (2) Enzymatic Reaction Mechanisms [1979] by Christopher Walsh [MIT], pages 846-850; Cobalt coenzymes with FADH enzymes attacking SAM [S-adenoslymethionine] creating methyl-CoB12, which then turned homocysteine back into methionine. Normally SAM would create the methyl-CoB12 by the enzyme NADPH, with a "defect" and lower ability to metabolize the Cobalt enzymes with FADH can also do the job. But the the next pages 851-863 show that methyl-CoB12 '... appears to function secondary methylation category... methylates mercury, palladium, lead, platinum, gold, tin, arsenic, selenium, and chromium' in the environment creating toxic chemicals. High doses of methyl-CoB12 is well known to increase oxidative stress and has many other reactions. So lowering methionine with focus on natural foods with cysteine along with B2 and B6 seems to be a better route. Methionine is carcinogenic and involved in angiogenesis and creates blood vessels to tumors. The common ideas of methionine being "essential" is overrated because even with no MTHFR "defects" the toxic effects of methionine to homocysteine recycling can affect anyone.

@emilyhandschuh2209 13 күн бұрын

I'm pretty sure you said that folic acid can build up in the body. If its from a supplement, then yes. The body does not make folic acid (it's synthetic, and found in fortified foods), the body uses folate (also not made in the body), which can be obtained through dark leafy greens, beans, and meat.

@otherhumans6171 2 ай бұрын

Where can I get my son tested for these faulty genes? I’m in the uk. I want to treat him with vitamins and detoxing but no idea where to start . He has suspected autism and it’s so hard for us.

@ADHDThriveInstitute 2 ай бұрын

Hey there, you’re welcome to contact me here so we can chat further: adhdthriveinstitute.com/contact-us/

@asherasator 2 ай бұрын

It's not a gene mutation, but the reality that some ancestors were not consuming a lot of methionine foods that result in high homocysteine byproducts. This has been understood in science for quite some time. [Pre 2003 MTHFR symptoms were understood by Homocystinuria]: (1) Geigy Scientific Tables, 7th edition, page 449; Inborn Metabolic Errors and their treatment, 'Homocystinuria' the treatment is 'Diet low in methionine, but higher in cysteine and pyridoxine [vitamin B6].' Which B6 is naturally found in fruits, veggies and grains. (2) Enzymatic Reaction Mechanisms, pages 846-850; 'Cobalt coenzymes with FADH enzymes attacking SAM [S-adenoslymethionine] creating methyl-CoB12, which then turned homocysteine back into methionine.' Normally SAM would create methyl-CoB12 by the enzyme NADPH, with a "defect" and lower ability to metabolize the Cobalt enzymes with FADH can also do the job. But the next pages 851-863 show that methyl-CoB12 '... appears to function secondary methylation category... methylates mercury, palladium, lead, platinum, gold, tin, arsenic, selenium, and chromium' in the environment creating toxic chemicals. High doses of methyl-CoB12 is well known to increase oxidative stress and has many other toxic reactions. So lowering methionine with focus on natural foods with cysteine, B2 and B6 [from diet] seems to be a better route and dealing with homosistinuria [MTHFR] for over 50+ years. Methionine is carcinogenic and involved in angiogenesis that creates blood vessels to tumors. The common ideas of methionine being "essential" is overrated because even with no MTHFR "defects" the toxic effects of methionine to homocysteine recycling can affect anyone. From my point of view it is irrelevant if B fortified foods are a source, what is important is to lower methionine which is the starting point of the cycle.

@user-xv5gq7ne3e 11 күн бұрын

Susannah at interwellness 😊

@arjunagarwal3546 19 күн бұрын

Hello, i recently tested and i got both mthfr c677t and a1298c heterozygous mutated and i tested homocysteine which came to be 29. So i thought i must be deficient in b complex but surprisingly all my b vitamins levels were normal. I couldn't figure out why. Pls tell

@ADHDThriveInstitute 17 күн бұрын

I can not advise without working with you directly. Best to speak with your doctor who did the testing.

@TheSami774 Ай бұрын

thanks for your videos ..my son 7 years in the school has ADHD my be im living in germany how could you help me in terms of treatments and diagnose the kind of mutation .?

@ADHDThriveInstitute Ай бұрын

You're welcome! Sounds like you could use some support. Be sure to check out my free masterclass as a starting point: bit.ly/3GE3cLX and you’re welcome to contact me here so we can chat further: adhdthriveinstitute.com/contact-us/

@billybolton6555 3 ай бұрын

due to the possibility of myself being fragile x.. could actually having a decreased methylation reduce overal adverse effect's of fragile x and its retardation.. im soon to be tested for fragile x and as a child whilst ferrel and unweildly and hard to teach I was very smart.. durring a process where my primary school was trying to refuse me as a pupil they had me do a general IQ test where I scored a 148 from memory. which named me legible to stay in normal school. these values from my research are typically unheard of.. from someone with the high liklyhood of having fragile x. the dissorder itself has been found in my sibling etc. so could this be a case of cramming many different mutations which in act causes some of them to become actively more innert in their damaging affects than they should be..

@judylandry302 9 ай бұрын

Liposomal isn't the same as sublingual. Sublingual is under the tongue.

@oliviavaldez203 4 ай бұрын

How can I order these tests and which ones should I request?

@ADHDThriveInstitute 4 ай бұрын

You’re welcome to contact me here so we can discuss this further: adhdthriveinstitute.com/contact-us/

@KM-nl8xr 8 ай бұрын

my son has an homogeneus result fot MTHFR 677

@ADHDThriveInstitute 8 ай бұрын

Hi there, thanks for tuning in! If you need a good starting point to begin making changes for your son and family, be sure to check out my free masterclass: bit.ly/3GE3cLX or get in contact with me here to chat further: adhdthriveinstitute.com/contact-us/