Study of thymus glands and estrogen as PCOS cause-PCOS is an immune disorder

Abstract

The aim of the present study was to investigate whether dietary advanced glycation end-products (AGEs) can be detected in the ovarian tissue of normal female rats and whether they can affect their metabolic or hormonal profile. Sixty normal rats (20 animals in each group) were randomly assigned to regular diet, either high (H-AGE) or low (L-AGE) in AGE content for 6 months. H-AGE rats demonstrated higher levels of fasting glucose (P < 0.001), insulin (P < 0.069), and serum AGEs (P < 0.001) than control and L-AGE rats. Additionally, the H-AGE group showed increased AGE localization in the theca interna cells of the ovarian tissue compared to control/L-AGE rats (P = 0.003). Furthermore, increased receptor for AGE (RAGE) staining was also observed in granulosa cells compared to control/L-AGE samples (P = 0.038). In the H-AGE group, plasma testosterone was higher than in control rats (P < 0.001) and in the L-AGE group (P < 0.001). However, H-AGE rats did not exhibit higher body weight compared with normal (P = 0.118) and L-AGE-fed rats (P = 0.35). These results demonstrate for the first time that administration of high AGE diet in female rats for a prolonged period is associated with increased deposition of AGEs in the theca cells and of RAGE in the granulosa and theca interna cells of the ovarian tissue compared with the corresponding ovarian compartments of the control and L-AGE-fed animals. The metabolic alterations in conjuction with the increased deposition in ovarian tissues of dietary glycotoxins and elevated levels of testosterone in H-AGE-fed animals compared to the controls suggest an impact of environmental factors on ovarian tissue and these findings need further exploration.

http://www.springerlink.com/content/g872k677v1114520/

First of all, we clearly see that PCOS is an autoimmune disease.

Before we go on any further, I need to go on a tangent. THIS STUDY WAS DONE IN ATHENS GREECE.

Greece is under attack by Wall Street through the use of Interest rate swaps and Credit default swaps. (My background isn't in medicine, it's in finance).

As we can clearly see here, Greece's bonds are way undervalued. This is incredibly sophisticated research, one that the researchers were free to conduct because they seemed to lack a conflict of interest between Big Pharma and doctors of medicine.

It was the Greeks who came up with the Hippocratic Oath.

The Modern Version:

I swear to fulfill, to the best of my ability and judgment, this covenant:

I will respect the hard-won scientific gains of those physicians in whose steps I walk, and gladly share such knowledge as is mine with those who are to follow.

I will apply, for the benefit of the sick, all measures [that] are required, avoiding those twin traps of overtreatment and therapeutic nihilism.

I will remember that there is art to medicine as well as science, and that warmth, sympathy, and understanding may outweigh the surgeon's knife or the chemist's drug.

I will not be ashamed to say "I know not," nor will I fail to call in my colleagues when the skills of another are needed for a patient's recovery.

I will respect the privacy of my patients, for their problems are not disclosed to me that the world may know. Most especially must I tread with care in matters of life and death. If it is given to me to save a life, all thanks. But it may also be within my power to take a life; this awesome responsibility must be faced with great humbleness and awareness of my own frailty. Above all, I must not play at God.

I will remember that I do not treat a fever chart, a cancerous growth, but a sick human being, whose illness may affect the person's family and economic stability. My responsibility includes these related problems, if I am to care adequately for the sick.

I will prevent disease whenever I can, for prevention is preferable to cure.

I will remember that I remain a member of society, with special obligations to all my fellow human beings, those sound of mind and body as well as the infirm.

If I do not violate this oath, may I enjoy life and art, respected while I live and remembered with affection thereafter. May I always act so as to preserve the finest traditions of my calling and may I long experience the joy of healing those who seek my help.

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

Dioscorides was Greek.

Dioscorides wrote a five-volume book in his native Greek, Περὶ ὕλης ἰατρικής, known in English by its Latin title De Materia Medica ("Regarding Medical Materials") that is a "precursor to all modern pharmacopeias"."

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

Apparently the grounds to develop mathematical, medical and scientific achievements, cures, etc. were only possible under a democratic reign. Greece was the inspiration to the Romans who adopted their culture in a Republic, and we adopted many of Greeces' concepts to build the modern world in the U.S.

Pray for Greece. Wall Street is attacking it with subprime derivatives to get their assets for cheap, I feel that I owe Greece a world of thanks for a genuine understanding of this horrible problem and hopefully a cure for it. Remember, money is just a bartering tool. Money can't cure people, doctors, God and you can.

This study was done in NY?

"An examination of the literature indicates a strong likelihood

of thymus involvement in estrogen and/or testosterone-

induced anovulation in other animal species. For

example, Kincl et al. [24,25] reported that anovulation in

E2- and T-injected female rats could be prevented by thymocyte

infusion. Notably, only thymocytes from adult

donors were effective. Thymocytes from 5-day-old animals

did not prevent anovulation. In primates the thymus

undergoes its final development prenatally [7]. Steroid

action would thus occur in utero. This could explain why

injections of testosterone propionate (TP) given to pregnant

rhesus monkeys on gestational day's 40–55, produces

anovulatory female offspring [26,27]. The female

offspring have enlarged ovaries with multiple small follicles;

an elevated LH/FSH ratio; and, high levels of serum

17αOH-progesterone and testosterone.

Additional evidence of steroid influence in utero is

detailed in reports of the consequences of using DES in

pregnant women [28-35]. Prescribed from the 1940s until

1971, DES was banned by the FDA due to the large

number of reproductive problems in daughters exposed in

utero. Problems included an increased rate of primary

infertility, oligomenhorrhea, amenorrhea, high levels of

androstenedione and testosterone, facial hirsutism, and

an elevated LH/FSH ratio. These symptoms are all associated

with the formation of cysts [36,37]. Notably, exposure

to DES on gestational weeks 9 through 12 produced

the highest rate of infertility [35]. This timeframe is coincident

with the final developmental stages of the thymus

[7].

The identity of the self-antigen(s) that CD8+

Autoreactive T

cells regard as nonself, is at present, a matter for conjecture.

MECs synthesize approximately 300 ectopic tissue

proteins [20]. At least two are involved in autoimmune

disease. A peptide epitope of insulin initiates CD8+

Autoreactive

T cell destruction of pancreatic β cells [38], and zona

pellucida glycoprotein 3 (ZP3) is implicated as the selfantigen

involved in ovarian dysgenesis [39]. Synthesized

in the ovary by the oocyte and granulosa cells [40], ZP3 is

a prime candidate for the self-antigen involved in the formation

of follicular cysts. Destruction of granulosa cells

by CD8+

Autoreactive T cells would seriously impair the follicle's

capacity to synthesize estrogen. Restoration of this

ability might explain why injections of FSH cause ovulation

in clomiphene-resistant PCOS women without intervention

by either exogenous LH or hCG [41].

In conclusion: we have proposed that follicular cysts

formed in a popular animal model of PCOS represent an

autoimmune disease initiated by steroid administration.

An increased incidence of autoimmune disease in DESexposed

women [42], lends further support for the

autoimmune nature of PCOS. As maternally derived

androgens and estrogens diffusing into the fetal area are

limited by the amnion [43], and are normally at nanogram

levels, it is unlikely that this source of steroid causes

PCOS. The reproductive problems observed with DES

came from milligram levels [44]. Potential sources of steroids

at this level are phytoestrogens, contained in food

supplements and ingested by some pregnant women. The

Centers for Disease Control and Prevention, for example,

report that 10% of representative samples of women in

the United States contain urinary levels in the milligram

range, of phytoestrogens found in flax seed [45]. Flax seed

and soy bean products cause reproductive problems in

female rats [46] and mice [47], and mice suffer thymocyte

loss and thymic atrophy when given genistein, the phytoestrogen

contained in soy beans [47]. Our future

research will determine whether or not phytoestrogens

cause anovulation and follicular cysts when administered

to female mice during the thymus' critical period. We will

also be investigating the impact of adrenal corticoids.

While the bulk of this paper has concentrated on the role

of gonadal steroids, the observation that adrenal steroids

diminish thymic/spleen weight and numbers of thymocytes/

splenocytes (Table 2), and can instigate cyst formation

[6], raises the possibility that severe stress during

pregnancy may be a factor in PCOS development."

http://www.rbej.com/content/pdf/1477-7827-7-47.pdf

High Levels of Oestrogen in Utero May Cause PCOS

Anne Seccombe

“We propose that in utero exposure to excessive levels of steroids such as estrogen has a long-term effect on the ability of the thymus to produce regulatory T cells. In female offspring this can lead to PCOS.”

Researchers from Binghamton University in New York published an article on 18 May 2009 in the Journal of Reproductive Biology and Endocrinology hypothesizing a new cause for PCOS.

Essentially they suggest, and their study supports, the theory that exposure of a foetus to high levels of steroids (such as eostrogen, testosterone or corticosteroids) whilst it is in utero may cause a cascade of auto-immune dysfunctions involving the thymus gland and it’s production of regulatory T-cells, eventually resulting in polycystic ovarian syndrome if the child is female. Sources of steroid exposure are likely to be from dietary phytoestrogens in the case of oestrogen or severe maternal stress whilst pregnant in the case of corticosteroids.

In the study, mice were injected with oestrogen at between 5 & 7 days old. This is known to cause anovulation and follicular cysts, a disease model that bears a similarity to PCOS in humans.

It is generally believed (but not proven) that this response is due to the hypothalamus responding to the excess oestrogen and a disruption in the GnRH delivery system.

This group of researchers, however, had a new idea which they sought to prove, namely that the anovulation and follicular cysts may be part of an immune response to the oestrogen and involving the thymus gland and it’s production of a specialised type of white blood cells called T cells and which help to fight infection or potential infection and also have a regulatory effect. High levels of oestrogen appear to prevent the thymus gland from producing fully developed regulatory T-cells. The absence of T-regulatory cells is known to cause a number of auto-immune diseases.

The researchers found that mice who had their thymus gland removed when they were 3 days old, prior to the injection of oestrogen, they did not develop follicular cysts and anovulation. When these mice later received an infusion from older mice who had been exposed to oestrogen, they found that the disease was transferable in a large percentage of the mice through the lymphocytes. Thus it would appear that the absence of regulatory T-cells is a prerequisite for the formation of follicular cysts.

The researchers concluded that exposure in utero to steroid hormones such as oestrogen or testosterone are unlikely to be derived from the mothers’ own hormones as these are usually only present in nanogram levels, whereas milligram levels are required to produce these effects. Therefore, the researchers hypothesize that it is more likely that these levels are achieved through the ingestion of phytoestrogens from the mothers’ diet, such as are found in soy and flaxseed products. Although it wasn’t covered in depth in the present study, the researchers highlighted that severe stress in pregnancy would raise levels of corticosteroids which are also known to negatively affect the spleen and thymus development of a foetus and the subsequent production of lymphocytes/thymocytes respectively.

http://pcosinfo.wordpress.com/news-research/elevated-oestrogen-in-utero/

Inflammation & Auto-Immune. It's those darn T-cells causing those cysts!!

Inflammatory issues and Auto-Immune disease is a major contributor to PCOS fun.

First of all, without these T-cells, none of these ovarian cysts would happen. (I can't make this up.)

"A study of female mice is suggesting that ovarian cysts may at least partially be the result of an immune system dysfunction. The gland involved is the thymus gland, which is responsible for the management of major aspects of your immune system. One of the functions of the thymus gland is to produce T-cells, which are white blood cells that help protect you from infection and also perform other important activities.

The researchers reported that ovarian cysts in the female mice did not develop unless there was an absence of regulatory T-cells."
http://www.ovarian-cysts-pcos.com/news81.html

I'm taking notes on how to fight the inflammation:

http://pcossurvivor.blogspot.com/2011/02/food-is-medicine-low-glycemic-index.html

A friend of mine with an auto-immune disorder confirmed that auto-immune disease and inflammation disorders can happen without insulin resistance. Sugar doesn't make it any better, but it's not caused by insulin resistance. Trust me, I have it and my glucose level is at 86. (they're overprescribing Metformin erroneously as the "cure all")

T-cells and Advanced Glycation Products can cause diabetes. Diabetes is the symptom, not the cause of PCOS.
http://diabetes.diabetesjournals.org/content/53/6/1452.full.pdf

In some people, iodine deficiency and hypothyroidism can cause immune disorders.

Iodine is essential for human T cell recognition of human thyroglobulin.
Here we describe for the first time that recognition by human T cells of human thyroglobulin depends upon its iodine content. We have examined the proliferation of lymphocytes from blood of autoimmune thyroiditis patients and normal individuals to thyroglobulin preparations containing different amounts of iodine. A minimal degree of iodination was required to elicit the proliferative response of both patients and normal individuals since thyroglobulin preparations containing no detectable iodine did not induce proliferation. A non-iodinated thyroglobulin preparation that was iodinated in vitro produced significant proliferation of both patient and normal lymphocytes. Addition of IL-2 to the culture medium enhanced proliferation but did not change the pattern of response.
http://www.ncbi.nlm.nih.gov/pubmed/9623499

In return, the auto-immune disease can actually cause the body to attack the thyroid as if it were an invader to the body. Causing a nasty, vicious cycle.

Not only does T-cells cause PCOS, but it's the T-cells that cause a rise in androgen hormones!

Increased dietary intake of AGEs in hypocaloric diet is associated with significant increases in androgen levels, contributing to abnormal hormonal profile in women with PCOS. Since in the ovarian compartments from polycystic ovarian tissue the AGE and their receptor RAGE have been determined immunochemically, the role of dietary AGEs in PCOS needs to be explored http://www.endocrine-abstracts.org/ea/0016/ea0016p171.htm

http://www.ncbi.nlm.nih.gov/pubmed/19450261?ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Now, watch this!

"Analysis revealed 60% higher blood levels of BPA among lean women with PCOS and 30% higher levels among obese women with PCOS compared with healthy women.

Although BPA is a weak estrogen, EXCESSIVE ANDROGENS, as it occurs in women with PCOS, interfere with BPA detoxification by the liver, contributing to accumulation of BPA blood levels, Diamanti-Kandarakis told Endocrine Today.

"On the other hand, BPA may aggravate HYPERANDROGENIMIA in these women by stimulating their predisposed ovaries to secrete more androgens and therefore worsen their hormonal status and possibly play a role in the pathophysiology of the syndrome," she said. – by Katie Kalvaitis'
http://www.endocrinetoday.com/view.aspx?rid=65717

Who else has PCOS without insulin sensitivity caused by PCOS?

"Japanese PCOS might have insulin-resistance but the factor of obesity had a stronger effect on insulin-resistance than did the existence of PCOS. The possibility of a different type of glucose-intolerance was suggested in the patients with ultrasonographical PCO in whom gonadotropin secretion was abnormal."

http://www.ncbi.nlm.nih.gov/pubmed/16972071

Basically the Japanese live amongst plastics and BPA's.

How do we know that our OBGYNs are not pimping us out to Metformin distributors?
"The possibility of a different type of glucose-intolerance was suggested in the patients with ultrasonographical PCO in whom gonadotropin secretion was abnormal".


On that note, I'm sending prayers, wishes and donations to Japan. The only problem with them, they invented high fructose corn syrup. However, they've helped us tremendously with research and invented Benfotiamine. Their contributions to medicine is priceless.

But anyways, about this androgen stuff! This is incredibly important. Inflammatory markets, T-Cells and cytokenes causes the ovaries to produce too much of a male testosterone called androgen. We all have androgens, we're only supposed to have a moderate amount of it.

Look at the PCOS women with male like characteristics, they ALWAYS have some sort of auto-immune disease. Too much androgen in a woman causes hirutism, smaller breasts, etc.

Now here's another interesting twist that plays into socio-political fun. Lesbians are twice as likely to be suffering from PCOS than straight women. Think about those androgens. I'm a straight woman who is looking at pretty solid scientific evidence supporting why they prefer women over guys. I'm not trying to "cure them". I'm sure their PCOS might have been a combo of pollution, iodine blockers, mutated proteins (fast food/precooked foods), processed sugars and BPAs. I refuse to get political about this. However it's pretty clear that if they said, "I didn't choose to be gay"- they're probably telling the truth. And regardless, they deserve and need their dignity in society and I'm happy to support their civil rights. It's 2011, why are we discriminating against people again? Anyways...

If anyone wants to call this "junk science", tell Blue Cross that they rejected me as an applicant for having PCOS since PCOS is "junk science" amongst misogynists.

Further research and notes on Vitamins to relieve inflammation:

Autoimmune diseases.

THE BAD GUYS:

Cytokine
T-cells
174 G/C promoter polymorphism of IL-6
174 C alleles = interleukin-6
Adipose tissues make large amounts of IL-6. Increased blood sugar levels also lead to more manufacture of IL-6.
http://www.inflammationremedy.com/herbal-remedies/inflammationremedy/inflammatory-markers

-(ADIPOSE TISSUES=body fat. Adipose tissue also serves as an important endocrine organ[1] by producinghormones such as leptin, resistin, and the cytokine TNFα.)

--(TUMOR NECROSIS FACTOR(TNF, cachexin or cachectin and formerly known as tumor necrosis factor-alpha or cytokine TNFα) is a cytokine involved in systemic inflammation and is a member of a group of cytokines that stimulate the acute phase reaction. Stimulation of the hypothalamic-pituitary-adrenal axis by stimulating the release of corticotropin releasing hormone (CRH) On the liver: stimulating the acute phase response, leading to an increase in C-reactive protein and a number of other mediators. It also induces insulin resistance by promoting serine-phosphorylation of insulin receptor substrate-1 (IRS-1), which impairs insulin signaling). On macrophages: stimulates phagocytosis, and production of IL-1 oxidants and the inflammatory lipid prostaglandin E2 PGE2

(interleukin-6(Il-6)) + (C-reactive protein (CRP))=INFLAMMATION

http://www.inflammationremedy.com/herbal-remedies/inflammationremedy/natural-inflammation-remedies

INFLAMMATORY CYTOKENES INHIBIT IODINE UPTAKE (possibly leading to thyroid disorders)
OSM inhibited iodide uptake stimulated by TSH; while IL-6 also inhibited iodide uptake, it was only about one-tenth as potent. IL-6 had about the same potency as OSM when it was added with soluble IL-6 receptor. OSM had no effect on cAMP production but inhibited iodide uptake stimulated by 8-bromo-cAMP and forskolin.
http://www.ncbi.nlm.nih.gov/pubmed/9086575

Apparently running and exercise can reduce C-Reactive Proteins, part of the inflammatory chain. If you can lose the IL-6, then running might even help stop allergy attacks, amongst other things.

Strikingly Low Circulating CRP Concentrations in Ultramarathon Runners Independent of Markers of Adiposity
http://atvb.ahajournals.org/cgi/content/short/23/9/1640

Relaxing is one way to get the IL-6 down.

“yoga had lower amounts of the cytokine interleukin-6 (IL-6) in their blood”
http://www.sciencedaily.com/releases/2010/01/100111122643.htm

VITAMIN EFFECTS ON INFLAMMATION:

Vitamin A deficiency

Other signs of VAD include excessive deposition of periosteal bone secondary to reduced osteoclastic activity, anemia, keratinization of mucous membranes, and impairment of the humoral and cell-mediated immune system.

http://emedicine.medscape.com/article/126004-overview

Purpose

To evaluate the effect of thiamine (B1) administration on metabolic profile, cytokines and inflammatory markers in drug-naïve patients with type 2 diabetes mellitus (T2DM).
Methods
A randomized, double-blind, placebo-controlled, pilot-scale clinical trial was carried out in 24 patients with T2DM. Twelve subjects received thiamine orally (150 mg), once daily during a fasting state for 1 month. An additional 12 patients (control group) were given placebo for the same period of time. Before and after the intervention, fasting glucose, A1C, creatinine, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, very low-density lipoprotein, high-sensitive C-reactive protein, interleukin 6, tumor necrosis factor-alpha, leptin and adiponectin levels were estimated. Wilcoxon’s signed-rank and Mann–Whitney U test were used for statistical analyses.
Results
There were significant decreases in glucose (6.7 ± 1.0 mmol/l vs. 6.0 ± 1.0 mmol/l, p = 0.024) before and after the intervention, respectively, and leptin concentrations (32.9 ± 13.3 ng/ml vs. 26.9 ± 12.8 ng/ml,p = 0.027) before and after the intervention, respectively, with thiamine administration. There were no changes with the rest of the measurements.
Conclusions
Thiamine administration for 1 month decreased glucose and leptin concentrations in drug-naïve patients with T2DM.
http://www.springerlink.com/content/f28425v554815256/

Vitamin B(6) supplementation improves pro-inflammatory responses in patients with rheumatoid arthritis.
Huang SC, Wei JC, Wu DJ, Huang YC.
School of Nutrition, Chung Shan Medical University, Taichung, Taiwan.
Abstract
BACKGROUND/OBJECTIVES: The purpose of this study was to investigate whether vitamin B(6) supplementation had a beneficial effect on inflammatory and immune responses in patients with rheumatoid arthritis (RA).
SUBJECTS/METHODS: This was a single-blind co-intervention study performed at the Division of Allergy, Immunology and Rheumatology of Chung Shan Medical University Hospital, Taiwan. Patients were diagnosed with RA according to the 1991 American College of Rheumatology criteria for RA. Patients were randomly allocated into two groups: control (5 mg/day folic acid only; n=15) or vitamin B(6) (5 mg/day folic acid plus 100 mg/day vitamin B(6); n=20) for 12 weeks. Plasma pyridoxal 5'-phosphate (PLP), serum folate, inflammatory parameters (that is, high-sensitivity C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)) and immune parameters (that is, white blood cell, total lymphocyte, T-cell (CD3), B-cell (CD19), T-helper cell (CD4), T-suppressor (CD8)) were measured on day 1 (week 0) and after 12 weeks (week 12) of the intervention.
RESULTS: In the group receiving vitamin B(6), plasma IL-6 and TNF-alpha levels significantly decreased at week 12. There were no significant changes with respect to immune responses in both groups except for the percentage of total lymphocytes in the vitamin B(6) group when compared with week 0 and week 12. Plasma IL-6 level remained significantly inversely related to plasma PLP after adjusting for confounders (beta=-0.01, P=0.01).
CONCLUSIONS: A large dose of vitamin B(6) supplementation (100 mg/day) suppressed pro-inflammatory cytokines (that is, IL-6 and TNF-alpha) in patients with RA.
http://www.ncbi.nlm.nih.gov/pubmed/20571496

Cobalamin (vitamin B12) positively regulates interleukin-6 levels in rat cerebrospinal fluid
G. Scalabrino ae , M.M. Corsiae, D. Vebera, F.R. Buccellatoae, G. Pravettonib, A. Manfridic, P. Magnide
Received 30 November 2001; received in revised form 23 January 2002; accepted 13 March 2002.
Abstract
We have previously demonstrated that the repeated intracerebroventricular (i.c.v.) microinjection of interleukin-6 (IL-6) prevented the myelinolytic lesions of cobalamin-deficient (Cbl-D) central neuropathy [or subacute combined degeneration (SCD)] in totally gastrectomized (TGX) rats. We therefore hypothesized that cobalamin (Cbl) may actually regulate IL-6 levels in rat cerebrospinal fluid (CSF). We measured IL-6 levels in the CSF of rats made Cbl-D by means of total gastrectomy (TG) or chronic feeding with a Cbl-D diet and killed at different times from the beginning of the experiment, and found that IL-6 levels significantly and progressively decreased over time. Chronic 2-month Cbl administration started 1 week after surgery prevented the decrease in IL-6 levels and, when it was started 2 months after surgery, it significantly increased IL-6 levels, but not to presurgical values. We also investigated whether IL-6 decrease might be ultimately due to the Cbl-deficiency-linked decrease in epidermal growth factor (EGF) synthesis. Repeated i.c.v. administrations of EGF to TGX rats did not modify CSF IL-6 levels. These results, together with those of a previous study showing the preventive effect of IL-6 treatment on SCD lesions, demonstrate that: (i) Cbl selectively regulates CSF IL-6 levels; and (ii) decreased IL-6 availability plays a role in the pathogenesis of the experimental SCD, in which no evidence of inflammatory and/or immunological reaction has been observed.
http://www.jni-journal.com/article/S0165-5728(02)00095-4/abstract

VITAMIN D
“Many people suffer and die from influenza, or the "flu." They don't die of the viral infection per se, as much as they die from the body's over-reaction. The influenza virus causes an uncontrolled over-production of inflammatory cytokines. Interestingly, vitamin D turns down this process by "down regulating" the expression of pro-inflammatory cytokines, such as tumor necrosis factor-alpha.

Actually, the pro-inflammatory cytokine process is the same inflammatory process that occurs in chronic disease, such as inflammation of arteries in atherosclerosis, inflammation in arthritis, damage to neurons, and inflammation and damage caused by cancer cells and by the aging process itself.
Think about the possibilities of reducing inflammation, by down regulating cytokines (tumor necrosis factor alpha, etc.) and thus reducing the incidence and progression of many chronic degenerative diseases, including heart disease, cancer, Alzheimer's disease, arthritis, diabetes, respiratory infections, liver and kidney disease, and the aging process itself!”
http://ezinearticles.com/?High-Dose-Vitamin-D-and-the-Decreased-Incidence-of-Chronic-Disease&id=3835324

Vit E lowers CRP. If vitamin E supplementation dampens interleukin-6 production in circulating blood as it does in the test tube
http://www.sciencenews.org/view/generic/id/1502/title/Food_for_Thought__Vitamin_E_targets_dangerous_inflammation

http://www.inflammationremedy.com/herbal-remedies/inflammationremedy/vitamin-e-and-inflammation

Antioxidants are the remedy to this problem. They neutralize free radicals. In the last decade scientists have proven that some antioxidants have anti-inflammatory properties. In addition to scavenging free radicals, there are antioxidants that actually block inflammation. The antioxidant effect (the blocking of certain oxidizing proteins) lowers the activation of inflammatory signals.
Adding coenzyme Q10 further reduces CRP by about 20% more, for a 70% reduction overall.
The body manufactures its own antioxidants. Some of them are in the form of enzymes, such as glutathione peroxidase, superoxide dismutase, and catalase – all of which require selenium and zinc to do their job. Lipoic acid, N-acetylcysteine, and glutathione are enzymes which rely on sulfur. Supplemental lipoic acid, in conjunction with L-Carnitine, works in the mitochondria to reduce the harmful effects of free radicals and diminish the actions of inflammatory signals.
http://www.inflammationremedy.com/herbal-remedies/inflammationremedy/antioxidants-for-inflammation

Fatty Acids Isolated from Toxoplasma gondii Reduce Glycosylphosphatidylinositol-Induced Tumor Necrosis Factor Alpha Production through Inhibition of the NF- B Signaling Pathway
http://iai.asm.org/cgi/content/abstract/75/6/2886

To get into this bit, here are some neat nutrition tricks.

"Vit E fights Free Radicals –super oxide radical hydroxlyl radical chan breaking agent in prop phase of lipid peroxidation

COQ10-blocks initiation and propagation of lipid peroxidation

Vit C and COQ10- can recycle Vit E

Vit C and BetaCarotine-blocks free radicals within watery cells (cytosol) and inspace out of the cell

Glutathione (selenium)- recycles Vit C"

http://www.amazon.com/Excitotoxins-Taste-Russell-L-Blaylock/dp/0929173252

Excitotoxins: The Taste That Kills [Paperback]vRussell L. Blaylo

OTHER LINKS TO INFLAMMATION: (acephetamine leads to Magnesium deficiency)
http://leifgrunseth.com/2010/03/this-common-food-ingredient-is-as-addictive-as-cocaine/

Magnesium deficiency causes and underpins chronic inflammatory build ups.

Inflammation is the missing link to explain the role of magnesium in many pathological conditions. Dr. Mazur says, “Magnesium deficiency contributes to an exaggerated response to immune stress and oxidative stress is the consequence of the inflammatory response.” Magnesium deficiencies feed the fires of inflammation and pain and it is magnesium that modulates cellular events involved in inflammation. Increases in extracellular magnesium concentration cause a decrease in the inflammatory response while reduction in the extracellular magnesium results in cell activation.

http://imva.info/index.php/mercury-medicine/multiple-sclerosis/#_edn8

By the way, this is THE BEST Friends episode ever! This is where Ross goes to see his pediatrician, the same pediatrician he had when he was growing up. We're all babies when we're sick, I know I am.