This helps destroy harmful, dangerous cytokines that can get us very sick…
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Prostaglandins are potentially dangerous lipid hormones.
Besides being truly unique among hormones in structure (on account of being lipids), they are unique in yet another way:
The specific types and quantity of prostaglandins within the body are largely influenced by diet.
This means that choosing the right foods can logically be expected to prevent prostaglandin formation and cancer.
(Cancer is a well-known consequence of increased prostaglandin E₂ levels.)
But what is generally not known is that prostaglandin E₂ (PGE₂) powerfully affects the immune system.
This is often not even considered, even though this too has been sufficiently proven.
The immune response caused by PGE₂ is usually neglected because we all can fight bacteria just fine…
BUT poor immunity can and does allow fungi, mycoplasma, and spirochetes to proliferate unchecked.
These infections can sap energy and lead to further problems… and very often go unrecognized.
Notably, Candida albicans (a fungal or yeast infection) is capable of producing its very own PGE₂.
This lipid hormone is then released, which shifts the host’s immune response towards the inactive state.
And this is the primary cloaking mechanism of Candida albicans.
These immune effects give us yet another reason to avoid linoleic and gamma-linolenic acids.
Both of those are omega-6 fatty acids.
People who were not previously concerned lowering their omega-6 intake might want to think about it now, after reading about immunity.
These immune effects are real, they are undeniable – and they are surprisingly powerful, coming from a lipid hormone:These effects started being reported in 1995 after a group of Dutch researchers published this experiment.
They used human blood, added PGE₂, and then measured the cytokines released.
Cytokines are protein signalers… The cells of the immune system use them to communicate with each other and with other cell types.
The researchers observed a profound shift in two main cytokines:
Interleukin-10 (IL-10) and interleukin-12 (IL-12) are two of the most important cytokines.
They operate on a higher level and dictate the expression of many other important cytokines.
These two cytokines control the differentiation of helper T-cells…
Helper T-cells are immune cells that our bodies need for almost all adaptive immune responses.
These helper T-cells can become either one of two types:
- Type one (TH1)
- Type two (TH2) helper T-cells
As you can see on the graph above, the cytokines IL-10 and IL-12 influence the direction in which these T-cells differentiate:
- IL-10 leads to more TH2 cells, which generally have an immune-suppressive nature.
- IL-12 always produces more TH1 cells, the powerful microbe-killing cells that produce the attacking cytokines interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β).
“Thus, the balance between the secretion of IL-12 and PGE₂ by the antigen-presenting monocyte will be crucial in determining whether a TH1 or TH2 response will dominate.”
There is simply no other way to kill fungi, mycoplasma, and spirochetes.
These cytokines also go on to other cells to induce an enzyme called inducible nitric oxide synthase (iNOS).
And the nitric oxide (NO) produced from that combines with superoxide to form the most potent microbe-destroying molecule in the body: peroxynitrite.
TH1 cytokines have a bad reputation for being involved in inflammation.
This is true… They are undeniably involved in inflammation…
But these cytokines are simply trying to do their job – to destroy bad microbes.
The inflammation associated with these cytokines wouldn’t exist to begin with if not for the invading microbes that initiate the response.
The fact that NO-producing cytokines such as IFN-γ are necessary to destroy certain pathogens has been proven beyond any doubt…
And so has inhibition by IL-10:
This study proved three things:
- NO is necessary to destroy Candida albicans
- INF-γ could cause this destruction
- IL-10 inhibits this from occurring
In this study, they used human blood cells and rats.
They even used an arginine analogue to inhibit the enzyme iNOS, preventing NO formation that way.
The effect then can be known with complete certainty:
Although nitric oxide is actually necessary when the immune system is going after pathogens, too much is certainly not good.
This is where the immunosuppressive cytokines IL-4 and IL-10 must come in, to balance the destruction.
A perfect TH1 to TH2 cytokine balance is capable of making large amounts of NO on demand…
And it can also limit excessive NO production to keep it from destroying the body as well.
“Production of nitric oxide is considered to be a crucial event in macrophage killing of Leishmania major, Schistosoma mansoni, and the fungal pathogen Cryptococcus neoformans.”
Prostaglandin E₂ (PGE₂) causes noise and distortion in this system by creating an improper TH1 ⟶ TH2 shift.
This prostaglandin occurs when we eat unnatural fatty acids.
But (as mentioned above) it is also produced as a cloaking mechanism by pathogenic yeast, fungi, and parasites.
These types of pathogens can synthesize linoleic acid… And from this, they produce the 2-series prostaglandins…
Not even bacteria can do this.
These trends are consistent… And they occur with the other nitric oxide-producing cytokines as well.
PGE₂ has been shown to lower IFN-γ, TNF-α, and IL-1β.
And it does so simply by lowering IL-10 (again, the primary immune-suppressing cytokine that controls so many others).
PGE₂ has also been shown to lower chitotriosidase, an enzyme created by the body specifically to kill yeast-fungi by breaking down the chitin on the walls of their cells.
With PGE₂, and hence IL-10, an effective immune response is impossible.
This is probably best shown by giving Candida-infected mice antibodies against IL-10.
These will bind to and then neutralize IL-10, preventing it from having any effe
Four hours before the Candida albicans injections, they injected one group of mice with anti-interleukin-10 antibodies.
They repeated the same antibody dose four hours after the C. albicans injection.
They also had a group of control mice that got the Candida albicans injection but not the neutralizing antibodies…
By the end of the experiment, all the control mice were dead.
But, amazingly, simply neutralizing immune-suppressive IL-10 facilitated survival in the other group of mice:
These researchers confirmed that, by neutralizing IL-10, the concentrations of INF-γ had increased.
This was perfectly correlated with both NO and Candida-killing potential, as had been found in the previous experiment.
Some steroids can cause the same shift in immune balance.
Behind prescription antibiotics, glucocorticoids are the second major risk factor for invasive fungal infections.
Since two very common medication classes lead directly to certain invasive infections, it’s easy to see why the AMA would tend to downplay and marginalize the issue to an extent.
These side effects are very common, ranging from toxoplasmosis in the bloodstream to aspergillosis in the lungs.
A person with a history of antibiotic and/or glucocorticoid use is especially at risk for fungal, yeast, and parasite infections.
“Table I shows that anti-IL-10 monoclonal antibody (mAb) therapy resulted in a 100% cure rate of the treated animals, and this was associated with enhanced clearance of the yeast from kidneys at 1 and 2 weeks after challenge.”
So, besides avoiding excessive glucose, glutamine, and N-acetylglucosamine, avoiding omega-6 is also necessary to avoid and/or eliminate invasive yeast and fungi.
So, perhaps not surprisingly, cyclooxygenase inhibitors such as aspirin are really very powerful antifungal agents…
They inhibit yeast and human cyclooxygenase to the same degree.
Gamma-tocopherol can prevent reactive nitrogen species from harming the body by trapping and removing them…
And it can do this while having little effect on the reactive nitrogen intended for pathogens.
Microbe-directed nitric oxide and superoxide can be found inside macrophages, on killer T-cells, and on neutrophils.
Gamma-tocopherol can safely intercept any stray reactive nitrogen species, lowering PGE₂ in the process.
These unnatural 1- and 2-series prostaglandins have been interfering with the human metabolism for millennia…
…starting around the time humans migrated from the tropics and began to consume the unnatural (to us) cold-climate seed oils.
The 3-series prostaglandins derived from eicosapentaenoic acid are the natural ones for tropical humans…
This class has about one-fourth the potency as the 2-series prostaglandins.
Three-series prostaglandins have never been implicated in disease, and have even been found “protective” in studies.
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