Immune amensia, statins and diabetes, fat and mitochondria

AIDA...kinda

Well, fate threw a wrench into my schedule last week. I got acutely (developing disease fast) sick in ways I seldom do. For the most part, even when I am sick it doesn’t stop me from working, but this time it did.

Don’t ask me what I had, I only go see a doctor if I am literally dying. My best deduction would be some sort of infection in my whole digestive system. I am now recovered enough to start working again, and God has a fantastic sense of humor, and the next piece will take a slightly different turn =).

So here is somewhat another AIDA, a science news round-up, with an addition first.

For quite a long while I have been perplexed about why, and precisely how SARS-CoV-2 and consequentially the vaccines could induce a global, unique change in disease frequency. Atypical breakouts are followed by atypical breakouts, followed by bigger messes. I knew it would happen, but I didn’t know how. No singular mechanism could quite explain many of these changes at the time, except one. Measles and its known “immune amnesia” effect.

Measles causes levels of immune amnesia by infecting pre-existing memory cells and basically killing them. It does so by using the receptor known as SLAM. Often referred to as CD150. This is how SARS-CoV-2 could potentially have caused immune amnesia in the first few waves, to a minor degree.

So as I usually did back at those times, I asked the friend I often refer to if this was one of my insane ideas. Then, almost every proposition I had was just merely that, propositions, so asking about Measles and any SARS-CoV-2 we found this.

But presenting with something doesn’t mean it shares the same effects and especially mechanisms, so going further…

In this analysis, the RBD had an affinity for many receptors and one of them was CD150, expressed in B and T Cells. As far as we know, SARS-CoV-2 Spike or other proteins do not share any molecular similarity with measles, but what we do know is that most immune cells infected by SARS-CoV-2 die. If this effect is remotely true, it would probably be mostly present in Wuhan, Alpha, and perhaps Delta waves.

But we just don’t know, I just decided to share this one. This is what sent me into the search for the immune amnesia question. 2 years later, things are a lot more complicated. The virus can mess with literally every immune cell or any cell you have. It affects how some of your receptors behave. It can "wipe out" your immunity against fungi. Immune suppression, tolerance, and many of these effects are shared by the vaccines or sometimes worsened.

SARS-CoV-2, fungal infections and "Immune Amnesia"

Now to the AIDA section.

In a very recent paper, authors found that a high dosage of atorvastatin dysregulates autophagy and induces the onset of diabetes. Statin-induced New-Onset Diabetes (NOD) has been increasing for years but there was no clear underlying mechanism. Here the authors found that high, but not low dosage, decreased the number of Beta-Cells, the cells in the pancreas that produce insulin, and increased cell death leading to impaired insulin storage, cells not being as viable, and reduced the number of them.

This is rather paradoxical, as I explained once before, one of the most common signs of pre-diabetes in many people is higher cholesterol, your body going through a complex metabolic process and shifting all the excess sugar into fats (lipids). Instead of treating the cause, many doctors will treat the symptoms and worsen the cause.

I don’t think there is something more damaging to human metabolism than the loss of Beta Cells, since insulin is a systemic hormone, with deep effects on the body, and as such we have yet another instance of short-term (and short-sightedness) gains for long-term pains.

And taking the cue while we are talking about fats.

Another very recent paper, even making the round in news articles, where the authors uncovered how obesity affects our mitochondria (the powerhouse of the cell =P).

After consuming a high-fat diet, mitochondria in parts of the mice's adipose tissue underwent fragmentation, splitting into many smaller, ineffective mitochondria that burned less fat.

In addition to discovering this metabolic effect, they also discovered that it is driven by the activity of a single molecule, called RaIA. RaIA has many functions, including helping break down mitochondria when they malfunction. The new research suggests that when this molecule is overactive, it interferes with the normal functioning of mitochondria, triggering the metabolic issues associated with obesity.

Persistent and long-term activation of the RaIA protein significantly affects how your body spends energy by shifting how your mitochondria function, in turn leading to more fat accumulation leading to more activation of the protein, ladies and gentlemen, this is another of of “those” feedback loops. Mitochondria is one, if not the most important aspect of long-term health and longevity itself, so the more efficient they are, the better your health over the long-term is.

Would be a shame if a common denominator affects both liver and brain mitochondria from a very early age, right ?

Does acute exposure to thimerosal, an organic mercury compound, affect the mitochondrial function of an infant model?

RESULTS

Hg accumulation in the brain and liver was higher in exposed animals when compared to the control. Liver-isolated mitochondria showed that TM improved respiratory control by 23%; however, states 3 and 4 of the ETC presented a decrease of 16 and 37%, respectively. Furthermore, brain-isolated mitochondria presented an improvement of 61% in respiratory control. Brain enzyme activities were significantly impacted in TM-exposed rats compared to unexposed rats as follows: decreases in SOD (32%) and AChE (42%) and increases in GPx (79%) and CAT (100%). GPx enzyme activity in the liver was significantly increased (37%). Among secondary oxidative stress markers, the brain’s total reduced thiol (SH) concentration was significantly increased (41%).

CONCLUSION

Acute TM treatment exposure in a Wistar rat model mimicking TM exposure in an infant following childhood vaccination significantly damaged brain bioenergetic pathways. This study supports the ability of TM exposure to preferentially damage the nervous system.

Thimerosal is a mercury-related compound widely used in vaccines as a preservative (it impedes bacterial growth for the most part). It has been a massive point of contention and discussion for quite a long time if it induces harm or not. Using a mouse model to mimic infant vaccination, the authors found exactly what one would guess.

A significant decrease in brain mitochondrial function and also a significant decrease in the potential of your brain to “clean itself” (alterations in the thiol-redox system). Mitochondrial dysfunction in any organ will lead to certain diseases, even chronic ones, but in the brain, it will lead to cognitive dysfunction. According to the CDC TM is not used in most vaccines since 2001 except the one most pushed to every single person on the planet after Covid. The flu.

Or, so just the most common, most used, overall useless, actually autoimmunity-inducing and harmful one ? Great.

Among the types of “drugs” with the most promise and high interest from many companies around the world, resides senolytics. Compounds that deal with senescent (zombie) cells, cells that contribute to most old-age related diseases, and can progress diseases at late adulthood. There are natural senolytics such as Quercetin and its stronger cousin Fisetin, and there are proprietary compounds.

Treatment of advanced atherosclerotic mice with ABT-263 reduced indices of plaque stability and increased mortality

Each type of drug has specific effects on different types of cells, and senolytics would be no different. Here the authors wanted to clarify and uncover the very specific effects and mechanisms by which ABT-263 commercially known as Navitoclax has on smooth muscle cells, the cells involved in blood flow.

Results indicate that ABT-263 may be inducing apoptosis of nonsenescent SMC and that, with long-term use, it may increase the risk for the development of unstable advanced atherosclerotic lesions and the incidence of myocardial infarction (MI) or stroke. This may be particularly severe, since our data also show that ABT-263 prevented adaptive increases in investment of EC-derived cells into the fibrous cap via beneficial EndoMT to myofibroblast transitions that we have shown normally occur when SMC investment into fibrous cap of lesions is impaired.

In simple terms, the long-term use of Navitoclax raised the mortality rate by over 50% by changing the smooth muscle cells, and how other cells contribute to lesions. It also reduced α-SMA+ fibrous cap thickness by 60%, this one needs a little more explanation.

The α-SMA+ fibrous cap is a protective layer that covers atherosclerotic plaques, which are the plaques in and on artery walls. Thickness is highly important because the thicker a cap is the more stable and less likely to rupture it will be, thus leading to a lower chance of heart attack or stroke. A reduction such as the one observed here means there are serious risk of heart attacks or strokes.

The authors bring to attention how their model differs from other models because this drug has been pushed among the scientific and pharma community and “hyped up” for a few years. Their mice model is more accurate because it more accurately portrays an older person, with older lesions and, therefore more build-up.

It is not the first time this drug was found to induce long-term damage when older age models were used, back in 2020, another group of researchers found that the same drug causes bone loss and effectively impaired cells related to bone function. I bring this to your attention because there are many of these novel drugs to deal with different forms of plaques, and I have yet to witness a miracle cure where one of these novel drugs or monoclonals doesn’t either facilitate fungal or bacterial infections after treatment or increase higher mortality by “unforeseen consequences”.

This also falls in line with a trial history I shared once here, where a company was testing a drug to remove misfolded proteins from the brain of Alzheimer’s patients, and the drug was indeed successful in the removal. Yet mortality of the patients was incredibly high, and this one was done in old humans, not mice. A similar trend will be found will all these “novel, miraculous misfolded protein removal” treatments in my opinion.

The next article will take longer than usual, not because of the disruptive sickness, but because of the sheer complexity. In comparison, the last few ones were fairly simple, and the scope of everything involved with it is also large. I may publish something very short on Wednesday related to SARS-CoV-2, otherwise, it will take a few more days than usual.

I appreciate the support and the patience !