FACTORS THAT INCREASE Th2 CYTOKINES

The three most common factors that drive Th2 cytokine responses are:

1. Faulty digestion leading to absorption of partially digested and unusable proteins and other food particles (increases IgG and IgE antibody responses that are directed against these foreign food particles). This is the condition called leaky gut due to increased intestinal permeability. Instead of the intestines serving as a barrier to the outside world, it allows an excessive amount of particles to be presented to the body through a non-physiologic entryway. Just as if you entered a home with a security system through a window, the alarm is triggered and you are alerted to a foreign invader. The result is a recruitment of police and other protective mechanisms, in the case of the food this represents the immune system. Proper digestion, a balance of friendly supportive bacteria, and a healthy gastrointestinal lining create a strong barrier to improper entry. Likewise, use of digestive enzymes, eating slowly mixing lots of saliva with food, avoiding over-eating or processed foods that are difficult to digest, anti-microbial therapy, etc. are necessary components to establishing immune balance. To emphasize the importance of proper digestion is the fact that the largest immune organ in the body is the gastrointestinal tract!

2. White sugar and glucose and all processed foods containing these (Coke, canned soda, candy bars, cake, pie, sweet rolls etc.) - directly weakens the functioning of macrophages, natural killer cells and other white blood cells and weakens systemic resistance to all infections. This statement is not just politically correct but has been documented in several scientific studies. The effects last for up to six hours, which means if you consume this at every meal, you are basically immune -suppressed all of the time. It may also explain that in an otherwise nutritionally repleted individual, fasting extends lifespan...

3. Consuming trans-fatty acids found in almost all heated and processed vegetable oils (soy, canola, safflower, corn and sunflower) and food products made with them (i.e. French fries, potato chips, almost any crunchy snack) stimulate IL-6 and depress delayed type hypersensitivity (DTH) thus weakening CD8 Killer-T cell activity. The trans-fatty acids are twisted out of their normal "cis" shape and produce cell membranes that are porous and vulnerable to viral infections. In his book Fats that Heal and Fats that Kill, Udo Erasmus states: "Besides producing atherosclerosis in the arteries of animals, fried and deep fried (vegetable) oils can also impair cell respiration and other cell functions, inhibit immune functions, and lead to cancer."

Among the most problematic hydrogenated vegetable oils are in margarine and shortening due to their high content of trans-fatty acids. Soybean oil, safflower, corn, sunflower, canola and most other vegetable oils should also be avoided by persons with chronic illness who have a predominant TH2 cytokine profile (too much Il-6, Il-10, TNF and triglycerides). It is nearly impossible to find vegetable oils that are strictly cold processed. Except for expeller pressed oils, nearly all other vegetables are processed with solvents, hexane or gasoline, to remove the oils from the seeds. The oil and hexane/gasoline mixture is then heated to 302 degrees F. to remove the hexane or heptane (gasoline) (1). At this point, the oils are now toxic for human use as they are twisted out of their natural "cis" shape and become trans-fatty acids. Add heat, light and oxygen to oils and the lipid peroxides increase and they become rancid and develop a strong taste. The safest and freshest oils to buy are cold pressed (best choice) or expeller that are stored in a can or black bottle to keep out light. It is even better if Vitamin E or BHT is added as an antioxidant to prevent lipid peroxide formation.

It should be clear that consuming canned soda (i.e. Coca-cola) and French fries regularly will make you immune compromised. Any situation that allows you to become infected will be much more likely to progress into a chronic condition just on the basis of your dietary choices.

laut dem aussagen müsste der westen schon längst ausgestorben sein...na ja von wegen

pilos schrieb am Tue, 21 July 2015 15:43

laut dem aussagen müsste der westen schon längst ausgestorben sein...na ja von wegen

Doch doch, gehirntot ist man im Westen schon längst.

es ging um die lebenserwartung totz der ganzen gifte

Naja die Lebenserwartung Karte ist nicht so Objektiv. Die höchste Lebenserwartung in Europa (wo auch die Ältesten Menschen von ganz Europa wenn nicht sogar der Welt) leben sollte dunkelgrün sein.
Afrika ist klar wegen den Umweltgiften (Elektroschrott Metal Gewinnung) , Abfall, Verseuchtes Wasser und natürlich Krieg. Hunger kommt da ganz weit hinten..

Es geht in dem Artikel ja auch nicht um die Lebenserwartung sondern das uns die Ernährung vorallem die Herstellung der verschiedenen Pflänzenöle Gift für unser Imunn System ist.
Zucker den wir in Unmengen auch Aufnehmen wird in den Fettzellen eingelagert.
Diverse Krankheiten (Krebs, Arteriesklerose, Herzinfarkt, AutoImmunkrankheiten, Diabetis, etc etc) ist alles auf die Öle zurück zuführen.

Es könnte sein das die Öle / Fette welche über die Haut (Wenn Leber überlastet ist) versucht ausgeschieden zu werden sich in der Kopfhaut Sammelt (Talgdrüssen) und verhärtet / ansammelt.
Da das Immunsystem geschwächt ist können Pilze auf der Kopfhaut vermehren (Essen den Talg und auch Hormone)
Glazen Träger haben immer eine schimmernde Kopfhaut.

Recent studies suggest that androgen-driven alteration to the autocrine and paracrine factors produced by scalp dermal papilla (DP) cells may be a key to androgen-potentiated balding.
Here, we found that interleukin-6 (IL-6) level is higher in conditioned media of balding dermal papilla cells compared with non-balding dermal papilla cells by ELISA. IL-6 mRNA is up-regulated after dihydrotestosterone (DHT) treatment. Immunostaining showed that IL-6 receptor (IL-6R) is expressed in outer root sheath (ORS) keratinocytes. Recombinant human IL-6 (rhIL-6) caused apoptotic cell death in ORS keratinocytes in a dose-dependent manner. Also, immunoblot and immunostaining showed that STAT3, a IL-6 signaling pathway mediator, is activated by rhIL-6 in ORS keratinocytes. Histological analysis demonstrated that injection of rhIL-6 induced catagen phase in back skin of 5 weeks old mice. Also, implantation with agarose beads containing rhIL-6 delayed onset of anagen phase. Our data suggest that DHT-inducible IL-6 may be one of the factors involved in the pathogenesis of DHT-driven balding.

DHT trigger Interleukin 6 which is a pro-inflammatory cytokine. Estrogen inhibits IL6! This is really interesting!! There is also a relationship between PGD2 and IL6

Prostaglandin D2 induces interleukin-6 synthesis via Ca2+ mobilization in osteoblasts: regulation by protein kinase C.Tokuda H (http://www.ncbi.nlm.nih.gov/pubmed?term=Tokuda%20H%5BAuthor%5D&cauthor=true&cauthor_uid=10582659), Kozawa O (http://www.ncbi.nlm.nih.gov/pubmed?term=Kozawa%20O%5BAuthor%5D&cauthor=true&cauthor_uid=10582659), Harada A (http://www.ncbi.nlm.nih.gov/pubmed?term=Harada%20A%5BAuthor%5D&cauthor=true&cauthor_uid=10582659), Uematsu T (http://www.ncbi.nlm.nih.gov/pubmed?term=Uematsu%20T%5BAuthor%5D&cauthor=true&cauthor_uid=10582659).
SourceDepartment of Internal Medicine, Chubu National Hospital, National Institute for Longevity Sciences, Obu, Japan.

AbstractWe previously showed that prostaglandin (PG) D2 stimulates Ca2+ influx from extracellular space and activates phosphoinositidic (PI)-hydrolyzing phospholipase C and phosphatidylcholine (PC)-hydrolyzing phospholipase D independently from PGE2 or PGF2alpha in osteoblast-like MC3T3-E1 cells. In the present study, we investigated the effect of PGD2 on the synthesis of interleukin-6 (IL-6) and its regulatory mechanism in MC3T3-E1 cells. PGD2 significantly stimulated IL-6 synthesis dose-dependently in the range between 10 nM and 10 microM. The depletion of extracellular Ca2+ by EGTA reduced the PGD2-induced IL-6 synthesis. TMB-8, an inhibitor of intracellular Ca2+ mobilization, significantly inhibited the PGD2-induced IL-6 synthesis. On the other hand, calphostin C, a specific inhibitor of protein kinase C (PKC), enhanced the synthesis of IL-6 induced by PGD2. In addition, U-73122, an inhibitor of phospholipase C, and propranolol, a phosphatidic acid phosphohydrolase inhibitor, enhanced the PGD2-induced IL-6 synthesis. These results strongly suggest that PGD2 stimulates IL-6 synthesis through intracellular Ca2+ mobilization in osteoblasts, and that the PKC activation by PGD2 itself regulates the over-synthesis of IL-6.

es ging um die lebenserwartung totz der ganzen gifte

es fragt sich nur WIE man so alt wird. die letzten zehn jahre 3/4 meiner grosseltern war ein einziges siechtum. mit leben hatte das nicht mehr viel zu tun. darauf kann ich verzichten.

woher kommen denn die ganzen zivilisationskrankheiten? autoimmunerkrankungen breiten sich gradezu epidemisch aus.