Why the interest in fevers? Fevers have been around forever, Autism has not.

To help you understand the importance of fevers, please look up what the mitochondria do in cells. If they are disordered, then fevers can cause problems. Which is explained in the article:

The crux of the matter is fever. Mitochodrial dysfunction appears to be largely triggered by fever. Without the fever there’s no dysfunction. Without the dysfunction theres no autism.

If you do not understand what mitochondria do, I fear we cannot have much faith in the quality of research you have done on vaccines.

How do you know autism has not been around for forever? And what possessed you to post on a year old thread?

All I am saying is people like to nitpick the ‘details’ before they take a step back and evaluate the big picture. Stop looking at JUST thimerosal, or JUST MMR, or JUST fevers, etc. For instance, it is known that what we eat impacts mitochrondrial function, which has a direct impact on how our individual system is able to tolerate and eliminate toxins (which have their own oxidative impact on mitochondria).

After extensive research on vaccines, I think vaccines play a large role in the neurological disorders we see in our children today, but I also think it is in conjunction with other environmental and nutritional factors. While fevers may be a small part of it, I seriously question the narrow focus on fevers as a cause of type of mitochondrial disorder that in turn leads to ASD while ignoring the more relevant issues right in front of you.

Simply because temperature can be measured, and there is elevated temperature, does not mean that the elevated temperature caused what ever adverse effect is observed. In Reyes Syndrome, one of the symptoms besides fever is fatty liver. How does elevated temperature cause fatty liver?

She was compensated for an encephalopathy – a vaccine act table injury – which the court, on a very low standard of evidence, intentionally set to favor claimants – accepted to have occurred within the time-frame set out in the table.

Most conspicuously, her claim made no reliance on the work of Dr Andrew Wakefield, Big Pharma’s friend, whose involvement in litigation has devastated the interests of thousands of families in the US and UK.

My research relates to basal levels of NO. These cannot be measured in vivo because there are no techniques to do so. The levels that are important are in the nM/L range, less than a ppb. All immune system responses are characterized by both pro-inflammatory and anti-inflammatory responses. When these two responses are balanced, nothing much bad happens. When they are not balanced, then the patient can die.

Nitric oxide is mostly an anti-inflammatory agent. Its production during immune system stimulation is balanced by the production of superoxide which is mostly pro-inflammatory. When these two things get out of whack, then the patient dies. In sepsis, too much NO can cause generalized vasodilatation and low blood pressure. That takes a very high NO level, around 10 nM/L (which for NO is very high). Usually NO that is so high that it causes systemic hypotension can be dealt with temporarily (in an ICU). If the high NO goes on for too long, then the patient becomes depleted in glucose and there is insufficient glucose to produce ATP via glycolysis, so the mitochondria have to turn on to generate ATP via oxidation. It is mitochondria turning on in a high NO environment that causes mitochondria failure. I think this is what causes the multiple organ failure of sepsis (my hypothesis).

Each tissue compartment and each cell, and each mitochondrion regulates the NO/superoxide balance itself. If a few get out of whack, a few mitochondria may be damaged. A few mitochondria are expendable. It probably takes a loss of 50-90% of mitochondria to cause cell death (depending on a lot of other things), but that is really hard to measure.

What determines the NO level during immune system stimulation is how much iNOS is expressed. That is regulated by NFkB, which is inhibited by NO. So the lower the basal NO level, the higher the NO level will be following immune system stimulation. Much of this NO is generated in immune cells, and these cells move around, and are also controlled by multiple cytokines and also by temperature.

A high fever is not necessary for a good immune response. I suspect that a vaccine with an adjuvant like aluminum hydroxide would be safer than a vaccine that produces the same antibody titer without an adjuvant. Much of the antigen in an aluminum hydroxide adjuvanted vaccine is sequestered on the aluminum hydroxide and so it takes a longer time for the immune system to process it. That longer time translates into a lower peak level of cytokines and (probably) a reduced peak fever.

I think that a lot of the malaise effects during fever are a consequence of the interaction between the pro and anti-inflammatory responses. Blocking those responses might (my hypothesis) adversely affect the body’s ability to regulate them and so keep them in balance.

The immune system is far too complex to be able to predict what is going to happen in great detail, particularly at the extreme ends of the distribution. Vaccines are demonstrably safe for virtually all children; there is no way to predict who they might not be safe for at which time under what conditions. It is inconceivable to me that a vaccine could possibly be worse than the disease. An actual infection with an actual disease agent would almost certainly be far worse than the vaccine which has been demonstrated to be safer in 99.99% of cases, which is about at the limit of what clinical trials can measure.

Virtually all cases of ASDs are not characterized by neuropathy and are not characterized by mitochondrial dysfunction. An acute vaccination can’t have long term effects on mitochondria unless the regulation of mitochondria biosynthesis is affected long term. There is nothing special about vaccines that would cause long term disruption of mitochondria regulation. An actual infection would be expected to be much worse. If Hannah Poling had gotten one of the diseases she had been vaccinated for, it might have killed her. A single dose of some antibiotics might affect long term regulation of mitochondria (months even). If Hannah Poling was given antibiotics that affected mitochondrial protein synthesis, that might explain her sensitivity to mitochondrial damage. I am speculating, but it might be the combination of an antibiotic and her mitochondrial polymorphism that gave her that increases sensitivity. If so, then the Polings are being reckless by not releasing information on her antibiotic history.

It isn’t the fever per se that damages neurons. Temperatures have to get very high to do that, it is something associated with the immune response that is associated with the fever that does it. That something is unknown.

Of course duration and severity of a febrile episode can have a profound effect on mitochondrial function or damage but the cause of the fever is irrelevant, be it via vaccination or natural infection.

However, the creation of cytokines, which can affect the severity and duration of fever isn’t necessarily equivalent between natural infection and vaccination, especially if, as did Hannah Poling, you get many vaccines simultaneously. Why? Because the toll like receptors which initiate the innate immune response respond synergistically when several are triggered simultaneously.

Toll-like receptor ligands synergize through distinct dendritic cell pathways to induce T cell responses: Implications for vaccines

Although TLR ligands individually may be ignored at certain low doses, the host may have evolved to recognize some together as a combinatorial assault and mount immune responses against these combinations in a synergistic manner. This strategy would allow the immune system to rapidly respond to infection. Studies have addressed the questions on what combinations of TLR ligands can synergistically increase the magnitude of cytokine production by DCs (15–22). However, in addition to discovering new synergistic combinations, questions still remain about whether there is a logic to the TLR synergistic patterns that can be identified, what the underlying mechanism is for TLR synergy within target cells, and from a translational point of view, what can be learned for vaccine design.

We first found that the MyD88-dependent and MyD88-independent DC functions are divergent in response to nonrandom, synergistic TLR ligands. MALP-2- and CpG-ODN-associated MyD88-dependent DC function in producing IL-12, TNF?, and IL-6 was remarkably augmented when poly(I·C) was included.

If your body believes it is under attack by several agents simultaneously, it responds synergistically; in this observation, by creating aditional pyrogenic cytokines. If our measurement of interest is robustness of the innate immune response, which can in turn affect febrile response, triggering several TLRs at once is qualitatively different than one at a time.

The argument has long been that getting one vaccine, two vaccine, or eight vaccines at once didn’t make a difference; but clinically we are beginning to understand that this isn’t true.

– pD