Spike protein, a cellular torture!

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Re-posted WALTER M CHESNUT's article from Substack: "A Cellular Peine Forte et Dure: The Spike Protein Induces Almost Imperceptible Chronic Inflammation with Devastating Consequences The key cytokine is almost certainly CCL2, and this was known in 2010!", by WALTER M CHESNUT APR 15, 2024

Quote:

Upregulation of the Chemokine (C-C Motif) Ligand 2 via a Severe Acute Respiratory Syndrome Coronavirus Spike-ACE2 Signaling Pathway
Upregulation of the Chemokine (C-C Motif) Ligand 2 via a Severe Acute Respiratory Syndrome Coronavirus Spike-ACE2 Signaling Pathway

Why is upregulation of CCL2 (MCP-1) important and why is it dangerous?

CCL2 is expressed in, among other cells, endothelial cells. It is at Ground Zero of what I have called Spike Protein Endothelial Disease (SPED). I believe this to be an initial condition (invasion) that leads to global organ dysfunction and destruction. Please search my Substack for background. CCL2 is involved in much SARS-CoV-2 sequelae.

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Chemokines in tissue fibrosis

Just as I have previously hypothesized that the Spike Protein is inducing almost imperceptible “micro-tumors,” I have also hypothesized about it causing constant organ damage. This is through inducing almost imperceptible constant inflammation, which, ultimately also explains the accelerated aging I predicted the virus and its Spike Protein would cause. There is now proof of this mechanism.

A study published Friday proves that this low-level, constant inflammation is, indeed, occurring.

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Cardiovascular symptoms of PASC are associated with trace-level cytokines that affect the function of human pluripotent stem cell derived cardiomyocytes

This slow burn. Eroding all organs little by little. It is Bond-level diabolical. Of course, certain authorities would have us believe that the Bat and the Pangolin have managed to "create" one of the most stealthy and cruel conditions one could conceive – imagine what Humans could do!

We must investigate further. I believe that the Spike, via its amyloidogenic properties, either self-replicates, or is retrotranscribed into host DNA, or both. This is also further evidence that avoiding the Spike Protein (in ALL of its forms) and keeping an anti-inflammatory diet is critical. At least until we have a full understanding of the long-term effects of the Spike Protein and how to deal with them.

Thank you, as always, for your support, readership and dialog.

Meat-free diet six times more likely to suffer brain shrinkage

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"Vitamin B12 status and rate of brain volume loss in community-dwelling elderly." by Vogiatzoglou A1, Refsum H, Johnston C, Smith SM, Bradley KM, de Jager C, Budge MM, Smith AD., published in Neurology. 2008 Sep 9;71(11):826-32. doi: 10.1212/01.wnl.0000325581.26991.f2.


(after @shashiiyengar Twitter post)

(Sorry for not being able to post any comments figures or quotes, the original paper is paywalled!)

How ketogenic diet protects against vascular aging

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It has been noticed that ketone bodies producing diets such as calorie-restricted diet and ketogenic diets exert some anti-aging effects (on test animals). This study, see the article linked below, pinpoints the mechanism of this effect to the specific ketone body molecule: β-Hydroxybutyrate.

Natural “Fasting” Molecule Exerts Anti-Aging Effects to Protect Vascular System
By NutritonReview.org - May 16, 2019


Quote:

In their study, the research team explores the link between calorie restriction (eating less or fasting) and delaying aging, which is unknown and has been poorly studied. The findings are published in the journal Molecular Cell.

The researchers identified an important, small molecule that is produced during fasting or calorie restriction conditions. The molecule, β-Hydroxybutyrate, is one type of a ketone body, or a water-soluble molecule that contains a ketone group and is produced by the liver from fatty acids during periods of low food intake, carbohydrate restrictive diets, starvation and prolonged intense exercise.

The researchers reported that β-Hydroxybutyrate delays vascular aging by providing a chemical link between calorie restriction and fasting and the anti-aging effect.

This compound can delay vascular aging of the endothelial cells, which line the interior surface of blood vessels and lymphatic vessels, preventing a type of cell aging called senescence, or cellular aging.

Senescent cells can no longer multiple and divide. The researchers found β-Hydroxybutyrate can promote cell division and prevent these cells from becoming old. Because this molecule is produced during calorie restriction or fasting, when people overeat or become obese this molecule is possibly suppressed, which would accelerate aging.

In addition, the researchers found when β-Hydroxybutyrate binds to a certain RNA-binding protein, this increases activity of a stem cell factor called Octamer-binding transcriptional factor (Oct4) in vascular smooth muscle and endothelial cells in mice.

Stem cell factor Oct4 increases a key factor against DNA damage-induced senescence, which can keep blood vessels young.

Reference:

1. "β-Hydroxybutyrate Prevents Vascular Senescence through hnRNP A1-Mediated Upregulation of Oct4",
Young-min Han et al., Molecular Cell, VOLUME 71, ISSUE 6, P1064-1078.E5, SEPTEMBER 20, 2018.

Example of a ketogenic (high fat low carb) dish.  Ketogenic diet has been described by some as BBB diet, meaning Butter, Bacon and Brie.  It is not limited to that!  

How Carbohydrates and Not Protein Promote Aging

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Interesting article:

How Carbohydrates and Not Protein Promote Aging

Longevity genes, glucose and insulin sensitivity

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Some of the most interesting longevity research concerns FOXO3A (homozygotic GG) and SIRT6 genes. In the case of FOXO3A, it seem to be associated also with the improved insulin sensitivity (thus allowing the body to maintain consistently LOW insulin level, reducing the risk of insulin resistance, metabolic factor and diabetes t2) throughout one's life. In the case of SIRT6 which plays a major role in DNA repair process, it appears to be upregulated with lower glucose consumption. Insulin and carbohydrates, carbohydrates and insulin...

Lots of unanswered questions: is the link accidental or not? Which is the primary and which is the secondary factor in the longevity?
Is (a) FOXO3A the primary cause of longevity while in addition improving also the insulin sensitivity? - Or, (b) is the improved insulin sensitivity and low glucose caused by the gene (or by whatever other factors...) - the primary longevity factor?

So far, the second answer (b) seems to be already demonstrated for the SIRT6 while there seems to be a growing suspicion that it is may be so for the FOXO3A as well!

This situation reminds me that the life forms may deals with any adverse environmental threat in the two-fold fashion: - either evolving a special resistance against a threat or simply avoiding the threat (in this case by not consuming the excessive carbohydrates...)

So, you either may already have the protective genes and in this case you can safely consume whatever high carbohydrate food is being marketed your way, or you minimize or avoid that stuff altogether. Everybody has a choice - and that's excellent news!


More links:

Bradley Willcox et al., "FOXO3A genotype is strongly associated with human longevity", PNAS, September 16, 2008, vol. 105 no. 37

Quote:

Human longevity is a complex phenotype with a significant familial component, yet little is known about its genetic antecedents. Increasing evidence from animal models suggests that the insulin/IGF-1 signaling (IIS) pathway is an important, evolutionarily conserved biological pathway that influences aging and longevity.
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Long-lived men also exhibited several biological markers indicative of greater insulin sensitivity and this was associated with homozygosity for the FOXO3A GG genotype.

I also posted on this subject in post. See the following quote from this article about the SIRT6 gene:

Quote:

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One explanation for this failure may relate to SIRT6’s critical role in DNA repair. Several studies have indicated that SIRT6 helps catalyze repair of the damage at numerous types of DNA lesions, including single- and double-strand breaks. A characteristic feature of aging cells is an increase in the amount of DNA damage.
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While overexpression of SIRT6 may not be tractable in a therapeutic context, SIRT6 activity can be increased by caloric restriction, reducing glucose consumption, or increasing NAD+ bioavailability (**) - interventions that have already shown promise in increasing longevity in animal models. (Such interventions are also showing promise in slowing the progress of some age-related neurodegenerative disorders.

Just a spoonful of sugar (with CO2) helps the medicine go down

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http://en.wikipedia.org/wiki/Sugar

http://ajph.aphapublications.org/doi/abs/10.2105/AJPH.2014.302151

Quotes:

Objectives. We tested whether leukocyte telomere length maintenance, which underlies healthy cellular aging, provides a link between sugar-sweetened beverage (SSB) consumption and the risk of cardiometabolic disease.
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Results. After adjustment for sociodemographic and health-related characteristics, sugar-sweetened soda consumption was associated with shorter telomeres (b = –0.010; 95% confidence interval [CI] = −0.020, −0.001; P = .04). Consumption of 100% fruit juice was marginally associated with longer telomeres (b = 0.016; 95% CI = −0.000, 0.033; P = .05). No significant associations were observed between consumption of diet sodas or noncarbonated SSBs and telomere length.
Conclusions. Regular consumption of sugar-sweetened sodas might influence metabolic disease development through accelerated cell aging. (Am J Public Health. Published online ahead of print October 16, 2014: e1–e7. doi:10.2105/AJPH.2014.302151)

Notice the lack of correlation for non-carbonated sugar-sweetened beverages!

More on the carbohydraty poison, today's news.  Skim milk anyone?

Quote:

In women the adjusted mortality hazard ratio for three or more glasses of milk a day compared with less than one glass a day was 1.93 (95% confidence interval 1.80 to 2.06). For every glass of milk, the adjusted hazard ratio of all cause mortality was 1.15 (1.13 to 1.17) in women and 1.03 (1.01 to 1.04) in men. For every glass of milk in women no reduction was observed in fracture risk with higher milk consumption for any fracture (1.02, 1.00 to 1.04) or for hip fracture (1.09, 1.05 to 1.13). The corresponding adjusted hazard ratios in men were 1.01 (0.99 to 1.03) and 1.03 (0.99 to 1.07). In subsamples of two additional cohorts, one in males and one in females, a positive association was seen between milk intake and both urine 8-iso-PGF2α (a biomarker of oxidative stress) and serum interleukin 6 (a main inflammatory biomarker).

Interestingly, detrimental effects seem to be related to the milk lactose contents rather than fat or proteins, because consumption of milk products that are high in fat and lower in lactose, such as fermented milk, cheese or cream, seem to correlate with more favorable biomarkers profile.

Comparing milk with other dairy products
Particularly noteworthy is that intake of fermented milk products such as yogurt and soured milk and cheese were associated with lower rates of fracture and mortality. Furthermore, we observed a positive association only between milk intake and markers of oxidative stress (urine 8-iso-PGF2α) and inflammation (serum interleukin 6). Previously, we found a negative relation between bone mineral density and 8-iso-PGF2α.42 63 Interleukin 6 seems to be causally related to cardiovascular disease64 and may influence bone loss and osteoporosis.65 Importantly, those who consume high amounts of non-fermented milk have a more non-favourable cardiovascular risk factor profile, with higher blood pressure, lower high density lipoprotein cholesterol levels, and higher insulin resistance.18 In contrast, intake of cheese and fermented milk products is related to higher high density lipoprotein cholesterol levels, less insulin resistance, and a lower risk of myocardial infarction.18 22 23 24 In addition, a recent small randomised cross over study indicated that the intake of a fermented dairy diet seemed to provide a more favourable biomarker profile than that of a non-fermented dairy diet.66