For one you make some sense........although it is just a copied and pasted article.......any thoughts of you rown on this matter?..............

What functions does P. Acnes play on the skin that are positive? It is no secret that antibacterial washes and antibiotics will just produce resistant bacteria. But there are some things, such as benzoyl peroxide and sulfur that will not do this. Some bacteria is good. But when bacteria causes problems it needs to be killed.

Of course,

I have time and again spoken about the natural stress free life without cosmetics, makeup, BP etc.

I have also spoken about a little bit of sunlight.

Again I have said to avoid all artificial forms of living as much as possible.

What more can I say.



Do you hate me because I speak the truth and only the truth

P. Acnes does actually have a function on our skin. It exists in a symbiotic relationship with us actually. It feeds off our sebaceous lipids and cellular debris and in turn actually protects us against infections by harmful bacteria like strep or staph...........If skin cells are able to properly keratinize and desquamate then the pores wouldn't be clogged up in the first place and the P. Acnes bacteria wouldn't be a problem.......




I don't hate you kid.......Sometimes I wonder a bit about your sanity, but I don't hate you.......

I realize that you probably have acne just like the rest of us and are trying to make sense of it.....it's annoying having a condition that cannot be fully explained by doctors and scientists......we all have out theories.....but what causes acne for one, may not cause it for another........yso you can't really generalize things.....you may speak what is the truth for you, but it might not work for me or someone else......
I don't agree with everything you post, but I do agree with this one.....

I knew you did not hate me

HeHe

And most of what I speak is the absolute truth as far as I am concerned.

Also a little sunlight moderates the quantities of all bacteria to a optimum level.

You are a chemist and explain theory behind things.

I posses common sense and know the truth intutively, instinctly and naturally

If what you say has cleared you acne (assuming you didn't just grow out of it as young men can) then what you say are "truths" for you and you only........As far as you're concerned you speak the turth as it applies to you and your world........the "truth" is relative not absolute.........

Melbourne you do not know any truth naturally as most of your posts are copied and pasted. pssh

Acta Dermatovenerol Alp Panonica Adriat. 2005 Jun;14(2):39-42. Related Articles, Links


Superoxide dismutase and myeloperoxidase activities in polymorphonuclear leukocytes in acne vulgaris.

Kurutas EB, Arican O, Sasmaz S.

KSU Medical Faculty, Department of Biochemistry, TR-46000 Kahramanmaras, Turkey.

BACKGROUND AND DESIGN: Acne vulgaris frequently occurs in the second decade of life. The pathogenesis of the disease is multifactorial and in the present study, we aimed to investigate the role of reactive oxygen species in the inflammation of acne by determining the activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) in polymorphonuclear leukocytes (PMN).

MATERIALS AND METHODS: Forty-three patients with acne vulgaris and 24 healthy controls were enrolled. The severity of the acne was categorized from mild (subjects with only comedonic lesions) to severe (subjects with nodulocystic lesions). SOD and MPO activities in PMN were measured spectrophotometrically.

RESULTS: There was no significant difference in the activity of MPO between the patients and controls.However, SOD activity in PMN was significantly lower in the patients than in the controls (p<0.001). Nocorrelation was detected between the activities of enzymes and the severity of the disease.

CONCLUSION: Propionibacterium acnes may not play a primary role in the pathogenesis of acne as a bacterium. However, the low activity of SOD in PMN may be responsible for the increased levels of superoxide anion radicals in the epidermis. New anti-acne drugs should include substances with lymphocyte stimulating and anti-oxidative properties.
PMID: 16001098 [PubMed - indexed for MEDLINE]
http://www.mf.uni-lj.si/acta-apa/acta-apa-05-2/1.pdf (full text)

Zouboulis CC, Eady A, Philpott M, Goldsmith LA, Orfanos C, Cunliffe WC
Rosenfield R. What is the pathogenesis of acne?

Exp Dermatol 2005: 14: 143–152. # Blackwell Munksgaard, 2005

Abstract: For a long time, the mantra of acne pathogenesis debates has been that
acne vulgaris lesions develop when (supposedly largely androgen-mediated)
increased sebum production, ductal hypercornification, and propionibacteria come
together with local inflammatory process in the unlucky affected individual. And
yet, the exact sequence, precise interdependence, and choreography of pathogenic
events in acne, especially the ‘match that lights the fire’ have remained surprisingly
unclear, despite the venerable tradition of acne research over the past century.

However, exciting recent progress in this – conceptually long somewhat stagnant, yet
clinically, psychologically, and socioeconomically highly relevant – everyday battlefield
of skin pathology encourages one to critically revisit conventional concepts of acne
pathogenesis. Also, this provides a good opportunity for defining more sharply key
open questions and intriguing acne characteritics whose underlying biological basis has
far too long remained uninvestigated, and to emphasize promising new acne research
avenues off-the-beaten-track – in the hope of promoting the corresponding
development of innovative strategies for acne management.

Inflammatory signalling is involved in the initiation
of acne lesions

Hyperproliferation of the follicular epithelium leads to formation
of microcomedones, which are the first acne lesions and
can be found in normal-looking skin (23). The sebaceous
follicle undergoes a cycling process which may explain a natural
resolution of microcomedones and also comedones and,
on a longer term, the resolution of the disease itself (24)
(Fig. 1). The very early stage of acne lesion development,
namely the beginning of microcomedones, is associated with
vascular endothelial-cell activation and involvement of inflammatory
events (25) which corroborates the suggestion that acne
may represent a genuine inflammatory disorder without involvement
of bacteria in its initiation (26).

Similar results have been reported by Ingham et al. (27) who found bioactive interleukin
(IL)-1a-like material in the majority of open acne comedones
from untreated acne patients. There was no correlation
between levels of any cytokine, in particular IL-1a, and the
numbers of follicular microorganisms. It seems that healthy
sebaceous glands also express various cytokines. In our laboratories,
we stressed sebocytes in vitro by maintaining them in
serum-free medium and detected IL-1a expression at the
mRNA and protein levels (28). Antilla et al. (29) showed that
IL-1 is present in normal sebaceous glands and Boehm et al.
(30) detected mRNA for IL-1a, IL-1b, and tumor necrosis
factor-a in normal sebaceous glands by in situ hybridization.
Interestingly, IL-1a induced hyperproliferation of follicular
keratinocytes in isolated sebaceous follicle infundibula maintained
ex vivo (31).

Which factors interrupt cycling of the sebaceous
follicle?

Overstimulation of the initiation of the preclinical inflammatory
process or defect negative feedback regulation may be major
reasons for the interruption of the normal cycling of the sebaceous
follicle and be responsible for the initiation of the clinical
inflammatory process in acne (Fig. 1). As mentioned above, hereditary
factors and excess androgen activity, e.g. in puberty, may
cause overstimulation, thus triggering sterile inflammatory phenomena
(Fig. 2). Neuroendocrinologic regulation and environmental
factors, such as dietary lipids and smoking, have also
been suggested to represent trigger mechanisms.

Role of neuropeptides for regulation of clinical
inflammation in acne

There is current evidence that regulatory neuropeptides with
hormonal and non-hormonal activity may control the development
of clinical inflammation in acne. Numerous substance P
immunoreactive nerve fibers were detected in close apposition to
the sebaceous glands, and expression of the substance P-inactivating
enzyme neutral endopeptidase was observed within sebaceous
germinative cells of acne patients (32). In vitro experiments
using an organ culture system demonstrated that substance P induced
expression of neutral endopeptidase in sebaceous glands
in a dose-dependent manner. On the other hand, treatment of
sebocytes with IL-1b which resulted in marked increase of IL-8
release (33) was partially blocked by co-incubation of the cells
with a-melanocyte-stimulating hormone in a dose-dependent
manner (34). Corticotrophin-releasing hormone induces the
synthesis of sebaceous lipids in vitro (33), and adrenocorticotropic
hormone evokes adrenal dehydroepiandrosterone [DHEA androgen] to regulate skin
inflammation (35). These current findings indicate that central
(36) or topical stress (33,37) may, indeed, influence the feedback
regulation, thus inducing the development of clinical inflammation
in early acne lesions.

Dietary lipids and inflammatory process in acne

Topically applied linoleic acid was shown to induce an almost
25% reduction in the overall size of microcomedones over a
1-month treatment period (38). On the other hand, arachidonic
acid, an essential, long-chain, pro-inflammatory o-6 fatty acid,
stimulates IL-8 and IL-6 synthesis in cultured human sebocytes
(39) and enhances synthesis of sebaceous lipids (21). Leukotriene
B4 inhibition in vivo reduces concomitantly pro-inflammatory
sebaceous fatty acids and inflammatory acne lesions (22). Inuit
Eskimos, the inhabitants of the Okinawa island and Chinese have
been observed to develop acne with the changing of their nutrition
habits (20,40,41). Westernized nutrition includes low
amounts of o-3-fatty acids and antioxidant vitamins and higher
amounts of the pro-inflammatory o-6 and trans-fatty acids. The
ratio o-6/o-3 fatty acids in westernized nutrition is 20 : 1, in
contrast to a 1 : 1 ratio in traditional nutrition (42).
Overall, the role of nutrition in acne still remains controversial. A
current study reported that the Kitavan islanders of Papua New
Guinea and the Ache hunter-gatherers of Paraguay do not present
acne (43), however, other authors suggested that these population
studies may have detected a genetic background rather than a nutritional
effect (44).

Smoking and acne

Smoking was currently reported to be a clinically important
contributor to acne prevalence and severity (45). Recent investigations
revealed that cigarette smoke contains high amounts of
arachidonic acid and polycyclic aromatic hydrocarbons which
induce a phospholipase A2-dependent inflammatory pathway
(46); this effect may further stimulate arachidonic acid synthesis
(37). On the other hand, smokers have a higher saturated fat
intake with their food and much lower polyunsaturated fat
intake, principally due to a lower linoleic acid intake compared
with nonsmokers (47).

Are Propionibacterium acnes (P. acnes) and tolllike
receptors involved in the initiation of acne
lesions?

Toll-like receptors 2 and 4 as well as CD14 are expressed in
human monocytes. Chemokine/cytokine synthesis in these cells
is induced through activation of Toll-like receptor 2 by P. acnes
(48). These findings in combination with the expression of active
Toll-like receptors 2 and 4 and of CD14 in human keratinocytes
(49) have implicated P. acnes and Toll-like receptors in acne
inflammation. However, P. acnes was unable to induce IL-1a
expression in human keratinocytes in vitro (50), therefore,
P. acnes seems to induce later events not being involved in
the initiation of acne lesions. The successful therapeutic
action of antibiotics in acne has been attributed to an antibacterial
activity but it may also be seen as a para-antibiotic,
anti-inflammatory effect.

Conclusion

Acne vulgaris is likely to be a genuine inflammatory disease with
androgens, PPAR ligands, regulatory neuropeptides, and environmental
factors being agents able to interrupt the natural
cycling of the sebaceous follicles and lead microcomedones to
form comedones and inflammatory lesions (Figs. 1 and 2). Proinflammatory
lipids and chemokines/cytokines seem to act as
mediators for the initiation of acne lesions. P. acnes is not initially
involved but may mediate later inflammatory events leading to
worsening of the lesions. This concept of acne pathogenesis may be controversially discussed,
however, it initiates a fruitful discussion for better understanding
this most common disease.

http://www.blackwellpublishing.com/dermato.../cont_feb05.pdf Full Text