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I have some important new infomation that i need to relay to you all regarding this theory.

Firstly, it seems that h1 receptors (the ones that dilate blood vessels) are perhaps not involved. Rather that h2 receptors are the important receptors in acne-genesis.

Before i present my research, i have a couple of thoughts i have been considering over the last few days. I don't believe that acne is just due to histadelic affects on metabolism, but rather an important part of the effect of chronically high histamine levels. This explains why many who eat very health diets still get acne. The role of H2 receptors fully needs to be eludicated, and the effects of cimetidine on acne isnt simply due to a possible anti-androgen effect:as the following study suggests:

[I]H2-antagonists and possibilities for their therapeutic use in dermatology]

[Article in German]

Diller G, Orfanos CE.

H2-antagonists differ from the commonly applied antihistamines (H1-antagonists) by blocking a different spectrum of histamine-mediated pharmacologic reactions. Their effects on the skin as the target organ may be stronger, weaker, or even reverse. The main representative of this group of drugs is cimetidine. Other compounds are still in experimental stages. Some controversial effects were reported in urticaria, pruritus, atopic dermatitis, mastocytosis of the skin, [B]and also in acne [/B] and psoriasis. With polyetiologic symptoms, as are manifested in cases of urticaria and pruritus, the efficacy of the drug may depend on the underlying disease. In acne and psoriasis, the clinical type and stage of the disease may also play a major role in the outcome of such studies. [B]Experimental and clinical findings suggest that cimetidine has some immunomodulating effect in terms of influencing the delayed type skin hypersensitivity[/B]. The intake of cimetidine should be registered in patch testing. Application of H2-antagonists may be beneficial in diseases with reduced immune resistance (generalized mycotic infections). Serious group-specific side-effects of H2-antagonists are not yet known. Several side-effects have been reported following oral intake of cimetidine; however, their frequency seems rather low.[/I]

This study suggests that h2 receptor blockade reduce the delayed type hypersenstivity of the the skin to antigens (toxins, foods etc). So acne sufferers in addition to them producing more toxins (possibly through an effect of histamine-via h2 recpetors- on cellular metabolic rate), also catabolising carbohydrates more rapidly (leading to hyperglyceamia and insulin resistance) ALSO have increased inflammatory sensitivity to antigens, which manifests as acne.

NOW i have some interesting supportive research....This could be very important.

1. Histamine potently suppresses human IL-12 and stimulates IL-10 production via H2 receptors.
J Immunol 1998 Sep 1;161(5):2586-93 (ISSN: 0022-1767)
Elenkov IJ; Webster E; Papanicolaou DA; Fleisher TA; Chrousos GP; Wilder RL
Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA. [email protected]
IL-12 and IL-10, respectively, stimulate Th1 and Th2 immune responses. The development of some allergic reactions, infections, and tumors are associated with [B]excessive histamine production and a shift toward Th2 responses[/B]. [B]Here we address the possibility that this association is causally linked, at least in part, to modulation of IL-12 and IL-10 production by histamine[/B]. We report that histamine dose-dependently inhibited the secretion of human IL-12 (p70) and increased the production of IL-10 in LPS-stimulated whole blood cultures. [B]These effects of histamine were antagonized by cimetidine, an H2 receptor antagonist, but not by selective H1 and H3 receptor blockers, and were mimicked by an H2 receptor agonist[/B].

The effects of histamine on IL-12 and IL-10 secretion were independent of endogenous secretion of IL-10 or exogenous addition of IL-12, while Ro 20-1724, a phosphodiesterase inhibitor, potentiated the effects of histamine on IL-12 and IL-10 production, implicating cAMP in its actions. Similar modulatory effects of histamine on IL-12 and IL-10 production, which were reversed by the H2 antagonist cimetidine, were observed in PBMC and isolated monocytes stimulated by Staphylococcus aureus Cowan strain 1 and LPS, respectively. [B]Thus, histamine, via stimulation of H2 receptors on peripheral monocytes and subsequent elevation of cAMP, suppresses IL-12 and stimulates IL-10 secretion, changes that may result in a shift of Th1/Th2 balance toward Th2-dominance. This may represent a novel mechanism by which excessive secretion of histamine potentiates Th2-mediated allergic reactions[/B] and contributes to the development of certain infections and tumors normally eliminated by Th1-dependent immune mechanisms. [/I]

To summerize..chronically raised histamine levels (histadelia), cause increased release of IL-10 by white blood cells (called monocytes) which is a chemical messenger in the immune system. This IL-10 then activates T-Helper cells (Th2 cells) and suppresses Th1 cells.

The whole immune system function depends on the relative balance in activity of Th1 and Th2 cells. If there is an overactivity in Th2 then the person is more prone to certain conditions, and allergies etc.
The following artical explains the relevance of this much better...:

[I]The important message is that there are 2 types of Helper T-cells in the immune system called Th1 and Th2. The Th1 cells deal with acute infection - like colds and flu's, infected cuts etc. The Th2 cells are responsible for antibody production so that the body can overcome a repeat infection much faster. In simple terms - Th1 are the soldiers fighting in hand to hand combat and the Th2 cells are those on guard duty to sound the alarm and repel invaders.

Problems occur when the Th2 cells become dominant unbalancing the Th1 cells. When this occurs we tend to develop chronic allergies, depressive psychological disturbances, auto-immune diseases, leaky gut and constant infections that are difficult to resolve.

The pattern can be set in childhood as vaccination stimulates Th2 production (can be further stimulated by fluvac etc) and lowers Th1 cells. So a pattern is set up with frequent colds, flu's and ear infections etc that are hard to throw off. We may then end up on antibiotics which kill off the good gut flora, leading to overgrowth of candida and causing damage to the gut lining. This results in decreased nutrient absorption, indigestion, gut ulceration, leaky gut, food intolerances allergic reactions, chronic illness like asthma etc, build-up of toxic metals, chronic ill health and auto immune disease such as Chronic Fatigue, diabetes, Lupus, rheumatoid arthritis, cancer and autism in susceptible individuals as the Th2 climbs higher. So at any point in our lives we can be thrown into this vicious cycle of ill-health that is self perpetuating.

T Helper 2 Cells are raised by infection, vaccines, stress, faulty digestion, leaky gut, candida, eating processed sugars & flours, trans-fats like margarine, omega 6 fatty acids like canola oil - all of which can lead to adrenal exhaustion, a further complication. [/I]

NOTICE that this above list is also the list of acne triggers....
So all the bits of the puzzel are slowly making sence..All the things that are widely supposed to cause acne are in the above list..stress, faulty digestion, leaky gut, candida, processed foods, sugars, trans-fats' AND what isnt mentioned in the list but also causes activation of Th2 cells: High levels of Histamine...!!!!!! I WANT YOU TO REALISE THE SIGNIFICANCE OF THIS...FOR THE FIRST TIME EVER ALL THE THINGS THAT WE HAVE ALL LINKED TO OUR ACNE ERUPTIONS, IN A CAUSE-EFFECT MANOR..ARE IN THE ABOVE LIST...NOW WE CAN SEE HOW THE CAUSAL FACTORS ARE [B]CONNECTED WITH EACH OTHER!![/B] They ALL increase the Th2:Th1 imbalance..

So to summarize chronic acne, is due to an imbalance in Th2:Th1 activity which promotes a delayed type hypersensitivity of the skin (to toxins, foods, and bacterial products) which is due to many things (see above list), including high histamine, thus all of these things must be addressed to normalise the balance.

Lastly, this thoery would be further proven if it was found that there is an association between vaccination (which is one of the factors that increase the th2:th1 ration) and acne, in suseptible individuals, i.e. ones that worsen the imbalance through other means as well such as histadelics...I found this:

[I][I]The national smallpox vaccine program proved last year to be a bumpy road; it was also especially spotty for about 10 percent of Vanderbilt’s vaccinated volunteers who broke out in a curious acne-like rash.

“Several of the volunteers said their acne worsened, and we weren’t sure it was the vaccine,” said Dr. Tom Talbot, an Infectious Diseases fellow and co-investigator in Vanderbilt’s smallpox vaccine clinical trials. (The national trials also were coordinated here.)
“Then in late October (2002, during the clinical trial), we saw two volunteers with generalized rashes on their backs and legs and we became more attuned to a possible association with the vaccine,” Talbot said. “The second light bulb to go off was in a news story in which one volunteer noted new ‘acne’ on his back after vaccination. He said he ‘felt like a teen-ager again"[/I]

All that this proves is that vaccination, which worsens the Th2:Th1 imbalnce is associated with an acne like rash in some individuals...still this is an interesting development.

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