SAM-e and MTHFR Heightmaxxers GTFIH

[bruh3610]

What is the view on this? Apparently there is only one source that claims SAM-e and stuff can cause mercury poisoning(Seth Walsh) and @Strike_Poseidon claims there isn’t enough studies to back this up.

So does SAM-e redistribute mercury to the brain? Let’s have a discussion instead of roasting each other

@Strike_Poseidon @Dyorotic2 @rax1337 @Bruh567

 

[Deleted member 4946]

What is the view on this? Apparently there is only one source that claims SAM-e and stuff can cause mercury poisoning(Seth Walsh) and @Strike_Poseidon claims there isn’t enough studies to back this up.

So does SAM-e redistribute mercury to the brain? Let’s have a discussion instead of roasting each other

@Strike_Poseidon @Dyorotic2 @rax1337 @Bruh567

no no no and NO end of discussion (various genes control the methylation cycle and mercury detox, not just MTHFR LMFAO)

 

[bruh3610]

no no no and NO end of discussion (various genes control the methylation cycle and mercury detox, not just MTHFR LMFAO)

Yea there are others but MTHFR is a critical one

 

[rax1337]

Genetic Variation Associated with Hypersensitivity to Mercury

Very little is known about mechanisms of idiosyncratic sensitivity to the damaging effects of mercury (Hg); however, there is likely a genetic component. The aim of the present study was to search for genetic variation in genes thought to be involved ...

www.ncbi.nlm.nih.gov

We have identified two genetic polymorphisms associated with increased sensitivity to Hg. Genetic variation in MTHFR and PON1 significantly differentiated a group formerly diagnosed with PD (a condition of Hg hypersensitivity) with age- and gender-matched healthy controls.

I mean, im still taking the SAM-e but thats because i probably wasnt exposed to much mercury or lead growing up in a first world country. But suggesting that SAM-e doesnt redistribute mercury is untrue

As a soft acid, mercury binds strongly to reduced sulfur (a soft base). Many of the transformation reactions therefore, involve the association of Hg to reduced sulfur compounds

https://opencommons.uconn.edu/cgi/viewcontent.cgi?article=7554&context=dissertations

SAM-e:

 

[GigaMogger]

After your teens heightmaxxing is only possible by wear boots

During by increasing growth hormone, testosterone and protein intake

 

[PubertyMaxxer]

Peak autism

 

[bruh3610]

Peak autism

U Wasted $8K on gh u salty boi?

 

[Deleted member 4946]

Genetic Variation Associated with Hypersensitivity to Mercury

Very little is known about mechanisms of idiosyncratic sensitivity to the damaging effects of mercury (Hg); however, there is likely a genetic component. The aim of the present study was to search for genetic variation in genes thought to be involved ...

www.ncbi.nlm.nih.gov

I mean, im still taking the SAM-e but thats because i probably wasnt exposed to much mercury or lead growing up in a first world country. But suggesting that SAM-e doesnt redistribute mercury is untrue

https://opencommons.uconn.edu/cgi/viewcontent.cgi?article=7554&context=dissertations

SAM-e:
View attachment 469231

sam-e and all this methylation stuff is a slow ass process, plus you aren't even taking the full stack so why do you bother with half hearted results? We need to research more into BMP's like BMP-2 and BMP-7 the makers of the BMP formula: https://evolutionarymuse.com/products/bmp are looking at my research now for a more potent formula for increasing height, their BMP formula brings about osteogenesis mainly instead of chondrogenesis, I need either your help or someone else's help to figure out the pathway and transcriptional factors for BMP-7 to bring chondrogenesis, evomuse (https://evolutionarymuse.com/products/bmp) will make an effective height formula, In terms of BMP-2 I have figured out how this can revert inactive growth plate back into MSC, we need compounds which upregulate BMP's but don't use any smad-dependent pathway and transcriptional factors like cbfa1/runx2 (this is for osteosgenesis), we need chondrogenesis and for that you can target a smad-independent possible mechanism for this is activating the MAPK pathway by downregulation FGFR3 and regulating FGFR2 from BMPR-IA, this is most effective way with BMP-2. But for BMP-7 (since BMP is far better for chondrogenesis) it may be a different pathway or protein component, again we are trying to bring about chondrogenesis, not osteogenesis, that BMP formula is only good for people with active plates who are also taking sam-e and shit for methylation, if u took that formula alone if u had closed/inactive plates you would not grow with it as it induces osteogenesis not chondrogenesis

P.S for inhibiting noggin we have meclizine and it also helps with one part of activating MAPK, FGFR3 downregulation