Stress Triggers But Magnesium Prevents Neurological Diseases

haidut

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This should not really be a surprise for followers of Peat and Selye, but it is always nice to see modern medicine make the connection between something considered benign, like stress and the associated NMDA "receptor", and serious diseases.
Interestingly, if stress works primarily through NMDA (and activation of the MMP-9 as shown by the study) then in theory a powerful NMDA "antagonist" should be able to mitigate some of the damage caused by stress, and maybe even prevent it altogether. Magnesium is currently the most powerful and non-specific known such NMDA antagonist.


http://www.eurekalert.org/pub_releases/ ... 091614.php

"...The investigations conducted by the researchers led them to an enzyme involved in the process of protein degradation: MMP-9. It was already known that chronic stress causes a massive release of glutamate, a molecule that acts on NMDA receptors, which are essential for synaptic plasticity and thus for memory. What these researchers found now is that these receptors activated the MMP-9 enzymes which, like scissors, literally cut the nectin-3 cell adhesion proteins...Interestingly, MMP-9 expression is also involved in other pathologies, such as neurodegenerative diseases, including ALS or epilepsy. "This result opens new research avenues on the still unknown consequences of chronic stress," concluded Carmen Sandi, the BMI’s director.
 

Ella

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Re: Stress may trigger, and magnesium prevent, brain disease

Hey haidut, thanks for the alert on MMP-9. MMP-9 - belongs to a group of gelatinase proteins known as matrix metalloproteinases (MMPs). MMPs are a family of zinc and calcium-dependent enzymes capable of degrading components of the extracellular matrix. As part of my research into a corneal degrading condition, this molecule was the focus of my research. This proteinase degrades collagen when inflammation is present. MMP-9 is also involved when tissue is being invaded by pathogens and for a long time, I was convince that the increased expression in MMP-9 was due to certain pathogenic micro-organisms and I spent a long time trying to figure out whether they were host or microorganism derived MMP-9s. I didn't get to finish my research, so I will never know. But what is really interesting to me now, since reading an listening to Peat is the following paper.

http://www.iovs.org/content/46/7/2388.long

Now the holy grail for me would be increasing tissue remodelling and wound healing without residual scarring in the cornea. What is interesting from a Peat perspective is that the authors of the above study used Thymosin beta-4 peptide derived from bovine thymus. Since the begining of my research (a long time ago), I wondered about the role stress played in this particular corneal disease. I am trained in the orthodox sciences and had never heard of Selye's work. I remember a time when people debated whether stress really existed and those individuals that complained of being stressed were regarded as malingers. Stress along with nutrition was never going to be accepted as credible areas of research by the gate-keepers of knowledge. The question I now ask is, could these MMPs be modulated by giving the body more sugar in preventing the dissolution of the thymus gland?
 
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haidut

haidut

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Re: Stress may trigger, and magnesium prevent, brain disease

Ella said:
Hey haidut, thanks for the alert on MMP-9. MMP-9 - belongs to a group of gelatinase proteins known as matrix metalloproteinases (MMPs). MMPs are a family of zinc and calcium-dependent enzymes capable of degrading components of the extracellular matrix. As part of my research into a corneal degrading condition, this molecule was the focus of my research. This proteinase degrades collagen when inflammation is present. MMP-9 is also involved when tissue is being invaded by pathogens and for a long time, I was convince that the increased expression in MMP-9 was due to certain pathogenic micro-organisms and I spent a long time trying to figure out whether they were host or microorganism derived MMP-9s. I didn't get to finish my research, so I will never know. But what is really interesting to me now, since reading an listening to Peat is the following paper.

http://www.iovs.org/content/46/7/2388.long

Now the holy grail for me would be increasing tissue remodelling and wound healing without residual scarring in the cornea. What is interesting from a Peat perspective is that the authors of the above study used Thymosin beta-4 peptide derived from bovine thymus. Since the begining of my research (a long time ago), I wondered about the role stress played in this particular corneal disease. I am trained in the orthodox sciences and had never heard of Selye's work. I remember a time when people debated whether stress really existed and those individuals that complained of being stressed were regarded as malingers. Stress along with nutrition was never going to be accepted as credible areas of research by the gate-keepers of knowledge. The question I now ask is, could these MMPs be modulated by giving the body more sugar in preventing the dissolution of the thymus gland?

Thanks Ella, excellent points! As far as wound healing without residual scarring, Peat has written about and I have confirmed that there were human trials in the 1950s, mostly in the former Soviet Union, using CO2 as therapy. Breathing 5% CO2 air for 2-3 days resulted in most patients recovering from major thoracic surgery without scars. The study was in Russian and very old, so I doubt it exists online. I saw it in a Russian magazine back in 2008, so it could be all a hoax but it matches well with Peat's writings. Peat also wrote that corneal damage will heal better if riboflavin intake is increased as well as retinol.
Nice to hear from a researcher who is discovering a new perspective on physiology!
I hope you enjoy the forum.
 

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TubZy

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Does anyone know anything about the safety of thymosin, specifically thymosin beta-4? It's effects resemble that of growth hormone.

TB-500 or Thymosin Beta 4 | JuicedMuscle.com

I used it for a brief time at a low dose, but would not suggest using it for long periods of time unless you are using it to repair an injury. It actually promotes angiogenesis more than growth hormone so you got the cancer factor to take into consideration.
 

DaveFoster

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I used it for a brief time at a low dose, but would not suggest using it for long periods of time unless you are using it to repair an injury. It actually promotes angiogenesis more than growth hormone so you got the cancer factor to take into consideration.
Thanks for the input TubZy; I was just reading a study where they used thymosin in chemo patients to restore the thymus and raise T-cell counts back to normal.

This is an excerpt from Asprin: More Than Just a Painkiller

On its own, thymosin reconstructs cellular immunity and raises T-cell rosette counts;[4] thymosin reconstitutes but does not raise T-cell counts above normal, which underscores its efficacy in the face of thymic deficiency.[5]


[4]
Wara DW, Goldstein AL, Doyle NE, Ammann AJ. Thymosin Activity in Patients with Cellular Immunodeficiency. New England Journal of Medicine. 1975 Jan 9;292(2):70–4.
[5]
Ibid.

Thymosin beta-4 seems to help cardiac patients as well. Source: Thymosin beta4: structure, function, and biological properties supporting current and future clinical applications. - PubMed - NCBI
 

Luann

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Would calcium have the same effect as Mg (isn't that the word around here about alkaline minerals substituting for each other)?
 

LeeLemonoil

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Re: Stress may trigger, and magnesium prevent, brain disease

Hey haidut, thanks for the alert on MMP-9. MMP-9 - belongs to a group of gelatinase proteins known as matrix metalloproteinases (MMPs). MMPs are a family of zinc and calcium-dependent enzymes capable of degrading components of the extracellular matrix. As part of my research into a corneal degrading condition, this molecule was the focus of my research. This proteinase degrades collagen when inflammation is present. MMP-9 is also involved when tissue is being invaded by pathogens and for a long time, I was convince that the increased expression in MMP-9 was due to certain pathogenic micro-organisms and I spent a long time trying to figure out whether they were host or microorganism derived MMP-9s. I didn't get to finish my research, so I will never know. But what is really interesting to me now, since reading an listening to Peat is the following paper.

http://www.iovs.org/content/46/7/2388.long

Now the holy grail for me would be increasing tissue remodelling and wound healing without residual scarring in the cornea. What is interesting from a Peat perspective is that the authors of the above study used Thymosin beta-4 peptide derived from bovine thymus. Since the begining of my research (a long time ago), I wondered about the role stress played in this particular corneal disease. I am trained in the orthodox sciences and had never heard of Selye's work. I remember a time when people debated whether stress really existed and those individuals that complained of being stressed were regarded as malingers. Stress along with nutrition was never going to be accepted as credible areas of research by the gate-keepers of knowledge. The question I now ask is, could these MMPs be modulated by giving the body more sugar in preventing the dissolution of the thymus gland?


Ella, are you still active around here?
I assume you refer to Keratoconus and the parasite-thesis made popular by Lombardi?

I've researched the topic quite a bit as well, due to former Girlfriend suffering heavly from it.
Not so much the pathogen-angle but the MMP-9 mediated tissue degradation.
NF-κB plays a major part I concluded, chronically overexpressed by activation of receptors that tissue fragments bind to - which itself is caused by a unbalanced ratio of MMPs in the Cornea, MMP-9 above all.
Interestingly, Magnesium is suspected to improve or stop Magnesium by some dudes over at longecity and a German University has recently recommended all Keratoconus patients to check for low thyroid, but I hav not found out yet why they see a connection there. Now this NMDA - MMP9 connection might shed some more light on the pathogenesis.

If you like, pls cotact my so we can exchange further or open a thread about Keratoconus here
 

TubZy

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Thanks for the input TubZy; I was just reading a study where they used thymosin in chemo patients to restore the thymus and raise T-cell counts back to normal.

This is an excerpt from Asprin: More Than Just a Painkiller

On its own, thymosin reconstructs cellular immunity and raises T-cell rosette counts;[4] thymosin reconstitutes but does not raise T-cell counts above normal, which underscores its efficacy in the face of thymic deficiency.[5]


[4]
Wara DW, Goldstein AL, Doyle NE, Ammann AJ. Thymosin Activity in Patients with Cellular Immunodeficiency. New England Journal of Medicine. 1975 Jan 9;292(2):70–4.
[5]
Ibid.

Thymosin beta-4 seems to help cardiac patients as well. Source: Thymosin beta4: structure, function, and biological properties supporting current and future clinical applications. - PubMed - NCBI

Another thing I noticed was my hair started to darken more and had slight thickening. I was using it sub Q. supposely it works better locally though so for injuries and hair purposes. I didn't feel comfortable injecting into my scalp but a few guys on a private forum did and had pretty decent results. Immune system wise it is pretty interesting. I believe Thymosin alpha 1 is better for immune system purposes though.

Thymosin Alpha-1 is a component of Thymosin Fraction 5 responsible for restoring immune function in animals lacking thymus glands. It was the original peptide synthesized from the Thymosin Fraction 5. Unlike β thymosins, which are genetically and chemically unrelated, Thymosin α1 is produced as a 28-amino acid peptide fragment from a longer, 113-amino acid precursor,prothymosin alpha. Research has shown it to enhance cell-mediated immunity in experimental animals and research subjects..

Thymosin Alpha-1 is being researched for the treatment of Hepatitis B and C, and it is also approved for inclusion with vaccines to boost the immune response in the treatment of other diseases.

Exhibiting a variety of immunoregulating properties, thymosin-alpha-1 induces differentiation of murine T-cell precursors and human thymocytes and the terminal differentiation of functionally immature cord blood lymphocytes and induces production of IL-2, high affinity IL-2 receptors, and B-cell growth factors by peripheral blood mononuclear cells. T-helper and cytotoxic/suppressor T-cell populations are targets of thymosin activity. Thymosin-alpha-1 has been shown to increase the efficiency of antigen presentation by macrophages and to be an endogenous modulator of alpha-thrombin activity.
 

DaveFoster

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Another thing I noticed was my hair started to darken more and had slight thickening. I was using it sub Q. supposely it works better locally though so for injuries and hair purposes. I didn't feel comfortable injecting into my scalp but a few guys on a private forum did and had pretty decent results. Immune system wise it is pretty interesting. I believe Thymosin alpha 1 is better for immune system purposes though.

Thymosin Alpha-1 is a component of Thymosin Fraction 5 responsible for restoring immune function in animals lacking thymus glands. It was the original peptide synthesized from the Thymosin Fraction 5. Unlike β thymosins, which are genetically and chemically unrelated, Thymosin α1 is produced as a 28-amino acid peptide fragment from a longer, 113-amino acid precursor,prothymosin alpha. Research has shown it to enhance cell-mediated immunity in experimental animals and research subjects..

Thymosin Alpha-1 is being researched for the treatment of Hepatitis B and C, and it is also approved for inclusion with vaccines to boost the immune response in the treatment of other diseases.

Exhibiting a variety of immunoregulating properties, thymosin-alpha-1 induces differentiation of murine T-cell precursors and human thymocytes and the terminal differentiation of functionally immature cord blood lymphocytes and induces production of IL-2, high affinity IL-2 receptors, and B-cell growth factors by peripheral blood mononuclear cells. T-helper and cytotoxic/suppressor T-cell populations are targets of thymosin activity. Thymosin-alpha-1 has been shown to increase the efficiency of antigen presentation by macrophages and to be an endogenous modulator of alpha-thrombin activity.
Awesome info TubZy, much obliged. I wonder how thymosin beta-4 acts on the prostaglandin system (judging from its effects on hair growth). Time to do some reading.
 

TubZy

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Awesome info TubZy, much obliged. I wonder how thymosin beta-4 acts on the prostaglandin system (judging from its effects on hair growth). Time to do some reading.

I don't believe it has any interaction with prostaglandins (at least in terms with hair growth) but it seems to provide stem cell migration causing hair growth. Check out this detailed PDF. I have other studies if you are interested.

Thymosin B4 increases hair growth by activation of hair follicle stem cells.pdf
 

DaveFoster

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Ella

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Ella, are you still active around here?
I assume you refer to Keratoconus and the parasite-thesis made popular by Lombardi?

I've researched the topic quite a bit as well, due to former Girlfriend suffering heavly from it.
Not so much the pathogen-angle but the MMP-9 mediated tissue degradation.
NF-κB plays a major part I concluded, chronically overexpressed by activation of receptors that tissue fragments bind to - which itself is caused by a unbalanced ratio of MMPs in the Cornea, MMP-9 above all.
Interestingly, Magnesium is suspected to improve or stop Magnesium by some dudes over at longecity and a German University has recently recommended all Keratoconus patients to check for low thyroid, but I hav not found out yet why they see a connection there. Now this NMDA - MMP9 connection might shed some more light on the pathogenesis.

If you like, pls cotact my so we can exchange further or open a thread about Keratoconus here

Yes my luv, I am still around but have little time to be active. I had the privilege to work with Lombardi. I have seen the pathogen cultured from the cornea. My background is in biotechnology so I am trained in molecular microbiology. If you understood the pathogen involved then you would understand why it was important to determine whether MMP-9 was host derived or pathogen derived? How would you know if the inflammatory process is being driven by the pathogen or too much estrogen, nitric oxide etc etc. I think the German University people are perhaps nearly a century behind on the thyroid influence in this disease. It truly pains me and breaks my heart. I am sorry for your girlfriend because this is a horrid condition. There has been little to no credible research in this modern day with all our sophistication and technology. I am truly angry at the profession who for decades promoted this condition as genetic and continued to push the idea that KC was a non-inflammatory condition just to be sure researchers would be led down so many blind alleys. I keep reminding myself that they had to have known otherwise they must have been complete imbeciles, which is why we should not put too much faith in the research journals. I was pressured to look for the gene for this condition. I refused because I thought it would be a waste of my research career. Yeah, well I am still waiting for the gene - where is it?

You state not so much the pathogen-angle but the MMP-9 mediated tissue degradation. You know that is a lot of tissue destruction going on. A cornea is mighty tough collagen. Riddle me this, how can the disease manifest itself again in the donor cornea if not an infectious agent. There is more to this story. I had a complete breakdown due to the stress of this research during my Phd thesis. I could not find one supervisor that had any comprehension or expertise required to support my work. There is too much money in keeping these sufferers chained to their contact lenses.

Lombardi is truly passionate in understanding the root cause of this disease. Yes, everyone of his patients had thyroid issues. One day when I feel brave enough, I will reveal the whole sad sorry saga of this disease condition. Make no mistake about Lombardi, he is pure genius and extremely dedicated. Can't say the same about others in this field. It's the blind leading the blind. I feel nothing but disgust with some the optometrists who position themselves as saviours of these unfortunate sufferers. They don't like using the word sufferers because it implies that these poor unfortunate people are victims. Yes indeed, they are victims of the gatekeepers of the truth.

If your are no longer with this girlfriend, why are you still interested in KC?
 
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paymanz

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Would calcium have the same effect as Mg (isn't that the word around here about alkaline minerals substituting for each other)?
No,i know ray says all this ions can substitute each other,but that is for alkalizing effect probably.

I don't think Ca can replace Mg in ATP metabolism.they are quite opposite effects,Mg relax things and Ca excites.
 
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Jsaute21

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What are thoughts on adrenal fatigue? I know Peat is skeptical of its impact but I know many disagree. When looking at a full panel, what are best ways to track adrenals?
 
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My doctor recommended thymosin alpha I think and I have to decide soon whether to try it ? Sorta nervous and sounds not that peaty but interesting
 

Davsey85

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Hello Haduit

Curious what kind of magnesium

You reccomend and dose?

Appreciate it
 

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