Yes, I also
agree with this post.
It's funny because if one were to read the studies and the abstracts you would see how it mentions that
THANKS to the use of antibiotics, acne sufferers can:
* Activate (dormant) autoimmune diseases
* Increase liver toxicity
* Increase their DHT Testosterone Levels (some can also decrease testosterone)
* Develop resistance to antibiotics
* Develop OTHER bacterial infections (that WILL then cause acne or some other problem)
* Develop Candida
* Develop Intestinal Hyperpermeability (Leaky Gut Syndrome)
* Develop Ulcers
http://www.acne.org/messageboard/index.php?showtopic=100399 (for abstracts)
Furthermore from reading these scientific articles I've noticed that antibiotics work to kill certain types of inflammation,
Initiated to clog the pores and then to kill the inflammation caused by overgrown TRAPPED bacteria,which is why it's prescribed for acne, except these SAME sources of inflammation can be inhibited or prevented, in acne sufferers, by using:
* Anti-fungals (and they don't kill p.acnes)
* Anti-parasitics
* NAC
* ALA
* Green, White, Red Tea
* Boswellia
* among other HIGH powered antioxidantsThese supplements, which are usually antioxidants, can multitask by lowering our testosterone levels, our IGF-1 levels, and boosting our Glutathione Levels, or SOD levels, and our PGE1 Anti-inflammatory Prostaglandins, among other things.
So it's interesting because chronic inflammation can cause biochemical imbalances and those biochemical imbalances can cause (further) inflammation...Hmm
When I speak of inflammation, with regards to acne sufferers, I'm referring to biomolecules such as:
* Histamine
* Free Radicals
* ROS - Reactive Oxygen Species
* PGE2- Proinflammatory Prostaglandins
* Leukotriene B4
* Cytokines (Interleukines 1 - 12a/b sometimes, TNF-a/Tumor Necrosis Factor-a, etc)
* NO - Nitric Oxide
* Peroxide (from lysed PMN/Polymorphonuclear leukocytes (white blood cells/neutrophils))
* Lactic Acid
* PPAR beta/delta - Peroxisome Proliferator Activated Receptors beta/delta
* Substance P
etc...
For example:
QUOTE
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)
And excerpts from
"What is the pathogenesis for acne?"QUOTE
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.
QUOTE
Inflammatory signalling is involved in the initiation
of acne lesionsHyperproliferation 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 acneThere is current evidence that regulatory neuropeptides with
hormonal and non-hormonal activity may control the development
of clinical inflammation in acne. Numerous
substance Pimmunoreactive 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 acneTopically 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 acneSmoking 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.
ConclusionAcne 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
(Funny Splenda/Sucralose is a Chlorinated/Halogenated Polycyclic Aromatic Hydrocarbon (LabGirl, True or False) and based on reports on this board as well as on the web, just as with Dioxin, it is capable of increasing acne in those prone and initiating acne in those not prone.)Obviously P.acnes doesn't play a PRIMARY role in acne development, otherwise why the use of RetinA, Accutane, Spironolactone, other antiandrogens, anti-fungals, and Insulin Sensitizers (some are PPAR-gammas),etc???
Acne has been called an Inflammatory Skin Disease for decades. Furthermore, based on available articles,
science and the medical community have known about some of these immunological events preceeding Type III and Type IV Hypersenstivity reactions which initiate the inflammatory response found in the development of acne since the 1970s! Yet, for the most part, they never bothered to do anything beyond throwing overprescribed antibiotics our way as a quick way of dealing with our CHRONIC (silent & systemic) inflammation.
As a result, a percentage of us are worse off because of it either
mentally (people still think it's about bacteria or sebum) or at least
physically, thanks to the side effects of antibiotics.
Home
0
