Tag: Fabry disease

LSD and Covid (Part 2)

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LSD and Covid (Part 2)

LSD stands for Lysosomal Storage Disorders and the first part can be found here.  The disorder is otherwise known as Fabry disease and although the lysosome is a separate organelle it’s signalling pathways connect to the mitochondria. 

The Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View

The main causes of NLRP3 inflammasome activation in ischemic conditions are ascribable to mitochondria dysfunction, as abnormal Ca2+ influx, ROS production, mitochondrial membrane permeabilization with the consequent release of DAMPs and mtDNA, all conditions that are tightly linked one to the other (Figure 3). Within minutes, OGD affects mitochondria functions leading to a strong reduction of OXPHOS and therefore of ATP synthesis. Neurons in the infarct core fail to compensate the ATP cell request leading to a bust of the Na+/K+ ATPase pump [185,192]. This results in neuronal membrane depolarization accompanied by an extreme release of glutamate in the extracellular space finally leading to neurons loss [193]. Glutamate is an important excitatory neurotransmitter, which binds several types of receptors such as N-methyl-D-aspartate (NMDA) receptor, a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor and kainate receptor [194]. Although these receptors originally were thought to be exclusive to neurons, several studies revealed their functional expression also on glial cells [195,196]. The excessive amount of glutamate after stroke leads to a hyperactivation of these receptors promoting a strong influx of Ca2+ into the cells [197,198,199]. Mitochondria are the crucial players in regulating cytosolic Ca2+ levels [200], thus the massive accumulation of cytosolic Ca2+ results into the activation of the mitochondria calcium uniporter (MCU) leading to mitochondrial depolarization, which in turn drives NLRP3 inflammasome activation and the consequently IL-1β release [201]. Consistently, it has been found that in response to the activation of NMDA receptors, MCU overexpression increases mitochondrial Ca2+ levels and provokes mitochondrial membrane depolarization. Inversely, genetic knockdown of MCU reduces the NMDA-induced increase in mitochondrial Ca2+ followed by lower levels of mitochondrial depolarization [202]. In line with these findings, in focal cerebral ischemia rat models, the early stages of cerebral ischemia are characterized by an upregulation of the mitochondrial calcium uptake 1 (MICU1) a crucial regulator of MCU [203]. Interestingly this occurs in the acute phase of IS right when the inflammatory response takes place [204,205,206]. To corroborate the role of Ca2+ in mitochondria dysfunction-induced inflammation, it has been shown that NLRP3 inflammasome activation is reduced following the inhibition of extracellular Ca2+ entry or the depletion of Ca2+ stores in the ER [207]. Albeit K+ efflux, a common NLRP3 inducer [208], has been proposed to be upstream of the Ca2+-induced NLRP3 inflammasome activation, thus indicating that high levels of extracellular K+ abolish NLRP3 activation [209], the crucial contribution of mitochondrial Ca2+ overload in sustaining inflammasome activation following IS and IR is not excluded.

I found this infomercial  promoting a supplement for nerve regeneration and thought it was very good so I cut it into segments and placed the links in the tweets. I was already using N-acetylcysteine (NAC) and had ordered Niacin and α-lipoic acid (A-ALA) and R-lipoic acid (R-ALA) which I have just started taking.  The one thing that seems to work across all the mitochondrial diseases is  Co-enzyme 10 (CoQ10) which I just bought today.

 

This Review (see page 15) more or less confirms what the infomercial said. These are the supplements mentioned (some are still being trialed).

Co-enzyme 10 (CoQ10)
CoQ10 analogue, idebenone
α-tocopherol
N-acetylcysteine (NAC)
α-lipoic acid (A-ALA)
R-lipoic acid (R-ALA)
Genistein, a natural isoflavone
Trehalose
synthetic quinone, EPI-743
Thiamine (vitamin B1)
Elamipretide is an aromatic cationic tetrapeptide

Some of the synthetics (EP-743) mentioned above:

https://www.thelilyfoundation.org.uk/get-informed/questions-answers/52/

https://www.scielo.br/j/jiems/a/dYFjkzQr577HyF87nJwBTMM/?lang=en

Many of these compounds can be found in natural food. Trehalose is found in Mushrooms, yeast, honey, and shellfish all contain trehalose but their combined dietary contribution is low in comparison to added sugars in processed foods. They have started adding it to food which causes other problems. The other compounds increased the reporter activity of GAL4-PGC-1β: Genistein, daidzein, and resveratrols stimulate PGC-1β-mediated gene expression. They can be found in high soy products dark chocolate and red wine. Let food be your medicine.

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Conclusion

The way forward is eating healthy and walking more and experimenting with the different supplements that boost mitochondrial health.  Intermittent fasting is also good. Meditation and positive thinking. Everything is in the hands of the Almighty and remember this…. your ancestors whose defects you inherited walked  this earth for generations.  They lived, built homes, had children and died.  We  are more than a collection of genes and our destiny through grace is eternal life.

 

LSD and Covid (Part 1)

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LSD and Covid (Part 1)

This is my personal health detective story (not a story about dropping acid and psychedelic experiences while combating covid…lolz).  Although this investigation is primarily for my own benefit and that of my family it has wider implications.  LSD in this investigation stands for Lysosomal Storage Disorders.   A lysosome has three main functions: the breakdown/digestion of macromolecules (carbohydrates, lipids, proteins, and nucleic acids), cell membrane repairs, and responses against foreign substances such as bacteria, viruses and other antigens.  Now the Lysosome  and the Mitochondria (Power house of the cell)  talk to each other.  Sometimes, they tell each other jokes and swap rude stories but usually they signal different path ways that regulate many key processes such as autophagy, proliferation, and cell death.

You may have seen in a previous post (https://www.biblaridion.info/blog/herbals-and-more/) that I was having feet problems and I found out via a blood test that I had high Calcium levels and this reminded me of something that Walter Chestnut had written (but that tweet no longer exists because Walter has been suspended from Twitter but now he is on Gab). Now it turns out that calcium is critical in regulating Mitochondrial signalling.

Fabry is not Fab

So now we come back to Lysosomes and Mitochondria talking to each other and the fact that I know that I have 12% of Fabry disease.   How do I know that?   I know because I was tested years ago because my mother suffers chronic pain and fibromyositis/fibromyalgia and the endocrinologist asked if all her children could be tested because it is a rare genetic disease and they were studying it.  Apparently I have 12% (how can you have 12% of a disease?) one sister has over 40% (she is quite sick with covid at the moment) another about 30%  and another at 0%).  To be honest I forgot all about it until my feet swelled up and started hurting.  Even then it did not occur to me until I started digging (am I thick or what?) and finally the penny dropped. If you are still reading this stick with it to the end…..because this virus will find and amplify any genetic weakness you have (and so will the vaccine). Defective lysosomal storage in Fabry disease modifies mitochondrial structure, metabolism and turnover in renal epithelial cells.

People who have Fabry disease don’t have the enzymes that break down lipids or fats. These fats collect in blood vessels and tissue, raising the risk of heart attack, stroke and kidney failure. Fabry disease is caused by mutations in the GLA gene. This gene provides instructions for making an enzyme called alpha-galactosidase A.

Lysosomal disease

Walter Chestnut got kicked off Twitter for this article ASP: SPIKE PROTEIN AMYLOIDOSIS in which he states that the spike protein is inducing fatal, systemic Amyloidosis. In his table he classifies Lysozyme as an Hereditary fibril protein within the clinical setting of familial systemic amyloidosis.  Dr Kevin McCairn has been warning for two years about neurotropic disease and amyloidosis. In fact he just discussed this paper on a live stream; Accelerated biological aging in COVID-19 patients.  The disease profile is multi-faceted and we are seeing heart attacks and strokes as well as brain disease etc. There is literally something for everyone:

This review paper by Seneff et al. (2022) summarises the current literature on mRNA and its effects on the molecular biology within human cells. The findings are shocking.

👉🏻 mRNA vaccines promote sustained synthesis of the SARS-CoV-2 spike protein.

👉🏻 The spike protein is neurotoxic, and it impairs DNA repair mechanisms.

👉🏻 Suppression of type I interferon responses results in impaired innate immunity.

👉🏻 The mRNA vaccines potentially cause increased risk to infectious diseases and cancer.

👉🏻 Codon optimization results in G-rich mRNA that has unpredictable complex effects.

The authors conclude that “billions of lives are potentially at risk, given the large number of individuals injected with the […] mRNA vaccines […]. We call on the public health institutions to demonstrate, with evidence, why the issues discussed in this paper are not relevant to public health, or to acknowledge that they are and to act accordingly.”

Conclusion

Whether you caught covid or got the “vaccine” (transfection) you are bound to come down with something. Many of us may be unaware that we have a hereditary disease.  The virus will go for any systemic weak spot. And herein lies the problem, the very diversity of symptoms and diseases makes it virtually impossible to establish causality. There will be a spectrum of responses with some people immediately harmed and others facing longer term degeneration.  It is truly the work of an evil genius…but now we know.  And you cannot hide the excess deaths and the increases in all cause mortality. The truth will out.

As for me I believe that I have the type 2 “later-onset” subtype and that it was probably triggered by Covid but it looks like it was on the cards anyway.  It seems that nothing much can be done except treat the symptoms (kidney and heart failure) or the more exotic gene therapy or more accurately Enzyme replacement therapy (ERT) is the cornerstone for treatment of Fabry disease and synthetic enzyme, produced by recombinant DNA technology, is infused intravenously.  I think I will pass on that or any other interventions like transplants.  No thank you.

However, what I have learnt is that the mitochondria make a big difference in the way that the lysosome works. Outcomes can be substantially improved if you boost mitochondrial health.  In fact, mitochondrial health makes a difference in a number of diseases.  That is what we will be looking at in part 2.