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#1 sim

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Posted 28 April 2008 - 02:38 PM

Hi people.

this has been bothering me for a while. i have a degree in microbiology but i still don't understand why this happens. when bacteria such as p. acne grows in a blocked follicle it causes a spot.

the bodies immune system will quickly detect these microbes and begin to attacked using white cells on many types (mainly macrophages) this causes inflamtion dues to chemicles released by the white cells. as time goes by puss occurs signalling death of the bacteria then healing and repair phase.

once we have been exposed once shouldn't our immune system destroy any p .acnes in the follicle before a spot forms? this would be true for any microbe that invades our body. antibodies would still linger in the body, macrophages would be more effective against the bacteria and memory cells would be made. so why are we still prone to them?

Edited by SweetJade1980, 04 May 2008 - 09:10 PM.
Added topic description


#2 bug

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Posted 29 April 2008 - 11:46 AM

you're the microbio major, so you'd know better than me. but all i can think is that either 1. cuz the follicle is blocked in the 1st place, so all that dead crap buildz up or 2. (which maybe makes more sense) it's bacteria that invadez from the external environment (like touching your face or shaving). not like, creating Abs for something already in your blood. i'm probably way off...

#3 Shadeonyx

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Posted 02 May 2008 - 03:49 PM

Well I have seen a few of these and you are a microbiologist, maybe you could look into some of these claims and tell us if it's true? I mean honestly it would make sense to me because all my worst acne started a huge influxes of hormones. When I got through puberty I started getting acne then, it got worse with every pregnancy I went through. Now... I am way past the age I should have acne and it's only getting worse....
These people clame it's some sort of Demolex Mite that is microscopic, I am assuming someone in your field can perhaps answer their claims about these oils in the articles and also some are saying it's the Mineral Zinc that helps to balance our body out?

Please let me know, I have tried everything including Accutane to no avail and it makes me want to cry.

http://www.pressrele...search-1987.htm

#4 SweetJade1980

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Posted 04 May 2008 - 08:55 PM

Because P.acnes may contribute to an inflammatory response, but in 99% of the cases, it is not the cause of our initial inflammatory response.

Please review the following exercept from:

ACNE DIET, CLEANSING & LEAKY GUT SYNDROME RESOURCE GUIDE

http://www.acne.org/...p...t=0&start=0 (perhaps one day I'll finish this, LOL)


Part B: Chronic Silent Inflammation

Acne is an Inflammatory Skin Disease


Please do not let this title deter you from thinking that acne is not genetic, that acne is not hormonal, that acne is not a form of skin diabetes, etc. These are ALL true...it's just that currently the evidence points to what's activating the acne, causing the hormonal disorder, skin diabetes, insulin resistance, etc is due to Subclinical (no obvious outward signs) Long-term Inflammation.

Ever wondered why certain drugs are prescribed for acne?

Why Accutane or Antibiotics are probably the most prescribed methods of treatment for acne sufferers?

Ever wonder why if acne is caused by a bacteria, why you would be prescibed Accutane, or Spironolactone or Birth Control, when NONE of these kill bacteria?

Ever wondered if the problem has to do with androgens, WHY are the dermatologists still prescibing antibiotics....long-term?

Acne has been called an Inflammatory Skin Disease for decades. Based on available articles, science and the medical community have known about some of these immunological events preceeding two specific immune responses (Type III & Type IV) which initiate the inflammatory events found in the development of acne since the 1970s! As a response to this inflammation, antibiotics was chosen as one of the first methods to fight against this in acne eusa_doh.gif

Unfortunately, due to the past and present mindset of certain doctors and scientists, 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 developing some of the known side effects of antibiotics. eusa_naughty.gif

Now, after reading numerous scientific articles/abstracts what I've noticed is that antibiotics do indeed work to kill certain types of inflammation. Antibiotics are used:

To kill the inflammation that clogged the pores and then to kill the inflammation caused by overgrown TRAPPED bacteria!

This is why it's continually 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 antioxidants



Not to mention, this includes a host of other drugs or topicals used in the treatment of acne. Omega 3s are obviously anti-inflammatory. AHAs (Glycolic, Mandelic, etc) are anti-inflammatories. Salicylic Acid/BHA is an anti-inflammtory. Retinoids and Accutane are anti-inflammatories. Benzoyl Peroxide is an anti-inflammatory. Hydrocortisone and Glucocorticoids (to a point) are anti-inflammatory. Tylenol, Asprin, & Motrin which some members use (and SHOULDN'T) are anti-inflammatories. B5 Therapy...Anti-inflammatory..........

The list goes on, some do it directly and others indirectly by inhibiting or regulating our ability, in some way, to make inflammatory products! Most of these drugs, topicals, supplements, as well as specialized diets also have other abilities and due to this, or the fact that some have stronger anti-inflammatory properties, make certain "treatments" a better choice than other methods based on an individuals circumstances.

Now, the above list of supplements, which are usually antioxidants, and some of these drugs, and certain diets, 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.



Chronic inflammation can cause biochemical imbalances and those biochemical imbalances can cause (further) inflammation! eusa_think.gif




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...



Like for me to back up back up my statements? Read on!



QUOTE
Skinmed. 2003 Jul-Aug;2(4):222-8. Related Articles, Links


Assessment of etiologic agents in acne pathogenesis.

Burkhart CN, Gottwald L.

The Department of Microbiology, Medical College of Ohio at Toledo, Toledo, OH 43623, USA. cburkhart@mco.edu

Acne is a chronic inflammatory disease of the pilosebaceous units. Traditional etiologic factors include increased sebum production, ductal hyperkeratosis, abnormality of the microbial flora within the pilosebaceous unit, and mediators of inflammation. Recent developments do not refute these familial elements, but rather refine particular aspects. Interleukin-1a influences hypercornification of the infundibulum as well as the inflammatory response by inducing the production of vascular endothelial growth factor in dermal papilla cells and follicular keratinocytes of the pilosebaceous unit. New retinoids have been developed based on controlling cellular proliferation and differentiation in the pilosebaceous unit by their action on nuclear receptors of cells. Dermal inflammation is not due to presence of bacteria, but from biologically active mediators produced by Propionibacterium acnes. The environment within the pilosebaceous unit is probably more important than the absolute number of P. acnes organisms. Indeed, the major role of the sebaceous gland appears to be supplying P. acnes needed nutrients. Moreover, the microbiologic principle of biofilms appears to be applicable to P. acnes in acne.

Publication Types:
Review

PMID: 14673275

(Thankfully further studies refine THIS study as well)


QUOTE
Rev Med Chir Soc Med Nat Iasi. 2004 Apr-Jun;108(2):319-24. Related Articles, Links


[Immunohistochemical evidence of chronic inflammation in acne vulgaris]

[Article in Romanian]

Branisteanu D, Cianga C, Cianga P, Petrescu Z, Carasevici E.

Universitatea de Medicina si Farmacie Gr.T. Popa Iasi, Facultatea de Medicina, Clinica Dermatologica.

The etiology and pathogenesis of acne vulgaris are not yet completely understood. Therefore we have investigated 5 patients with different clinical forms of disease, including the rare form of acne fulminans. Taking into consideration the four factors that are currently incriminated in the development of acne, sebaceous hypersecretion, hyperkeratosis of the pilosebaceous infundibulum, bacterial colonisation and perifollicular inflammation, we have focused our study on a set of cells involved in the chronic inflammatory process. We have evidenced by immunohistochemistry methods, using appropriate monoclonal antibodies, the presence of T lymphocytes and macrophages, while the B cells could be evidenced only in the severe forms. We were also interested to investigate the occurrence of new capillary formation, as an accompanying phenomenon of the inflammatory process. The presence and histological distribution of these cells highly supports the hypothesis that the mechanisms underlying the development of acne vulgaris belong to the Delayed Type Hypersensitivity.

PMID: 15688807 http://www.ncbi.nlm....l=pubmed_docsum


(This was one I had been looking to post again for awhile and I thought they had removed this article! This is a Type IV Hypersensitivity Reaction and was a key part of my arguement for WHY, sometimes, there's such a huge variance among the anti-inflammatory/anti-acne diets.)


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...-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 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.blackwell.../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.)



Therefore, while inflammation is at play, it's obvious P.acnes doesn't play a PRIMARY role, otherwise why the use of RetinA, Accutane, Spironolactone, other antiandrogens, anti-fungals, and Insulin Sensitizers (some are PPAR-gammas), etc???

Yes, they all work to kill some aspect of the inflammatory process, which in turn, or in conjunction, allows them to also regulate blood sugar, regulate androgen production, regulate IGF-1 production, etc.

Now, if we can all begin to think of acne as an inflammatory skin disease first, and for now everything else about it second, we can move on to figuring out WHAT we need to do to trace the source of inflammation and HOW to stop it!



#5 john1234

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Posted 05 May 2008 - 09:01 AM

Hey Sweet Jade, what elicits DTH response in the first place? I think that's an important question to ask. What is the antigen that leads to the activation of Thelper cells? The Th cells will then activate the macrophages, which then lead to the secretion of cytokines that mediate the inflammation process...

#6 allo12345

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Posted 05 May 2008 - 01:01 PM

Sweetjade -

What kind of acne do you get if you eat bananas and pineapples, and let's say you ate those, how much time does it take after you eat them to eliminate the inflammation response?

Another thing, do you recommend we try some of the things you are doing in "Stage 3 (Correction)?

Thanks

#7 SweetJade1980

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Posted 05 May 2008 - 08:30 PM

QUOTE (john1234 @ May 5 2008, 08:01 AM) <{POST_SNAPBACK}>
Hey Sweet Jade, what elicits DTH response in the first place? I think that's an important question to ask. What is the antigen that leads to the activation of Thelper cells? The Th cells will then activate the macrophages, which then lead to the secretion of cytokines that mediate the inflammation process...



LOL, a very good question and it's the reason for any big "diet" debate in the nutrition forum, let alone in other area on this board if you mention diet.

Anything. (Ingredient topical or oral, chemical, preservative, microbe, supplement....)

It's that easy...and that's why it's so hard for people to "pinpoint" what IT is for them.

People with allergies (Type I Hypersensitivity) can be allergic to anything, but there's a most common allergen list. Regarding food there is

Wheat
Dairy
Eggs
Soy
Tree Nuts
Peanuts
Fish
Shellfish
..... there's more (let me find a list)


Basically the above are the MOST allergenic/antigenic and some people (with acne, etc) will find that at least one of their "trigger food items" will be on the list.

Food Allergies: When Food Becomes the Enemy
http://www.fda.gov/F...1/401_food.html

Another way to determine is through Hypersensitivity Testing (sometimes covered by insurance), in particular the most affordable would be through www.ALCAT.com (looks only at white blood cell activity), which covers DTH Reactions. Any food intolerance test that will look for IgG antibodies will cover Type III Reactions.

However, the Gold Standard and Cheapest method is to do an Elimination and Revocation Diet.

1. Bascially you would consume the least allergenic foods (chicken, rice, pears, etc) for a few weeks to allow for the inflammatory process to cease (not neccessarily the presence of current acne, but the development of NEW acne).

2. Then add in ONE food item (in as pure as state as possible) at time every 2 - 4 weeks. The length of time is determined by whether or not you breakout.

3. After two weeks you should know if you will or not. If you don't, you can add another food item in and so forth.

4. IF the food item breaks you out, then 2 weeks after that, you can add in another food item.

5. Of course. You always want to go back and retest any suspected food items to determine if it really did break you out.


That being said....I did not do that!

I opted to eliminate Gluten. Then Dairy. Then Sweetners. Then Nuts. Then certain fruits. Somewhat in that order based on how my skin reacted when I ate certain foods.

- I eliminated not just Gluten (wheat, barley, rye and derivate grains) from my diet by going "Gluten-Free", because there was also some dairy, sweeteners (incl HFCS), and trans fats in the Gluten containing products! I had THE biggest improvement from doing that alone.

--I soon discovered that I sometimes I was breaking out in NEW areas and with NEW types of acne! (will explain further later)

-- Basically it was through being very observant as to what I was eating and seeing when I would break out is what lead my to finding what foods break me, when, for how long, and the type of acne they give me.

#8 SweetJade1980

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Posted 05 May 2008 - 08:35 PM

Most Common Allergens


QUOTE
Cow's Milk:

Two out of a hundred infants under one year old suffer from cow's milk allergy, making it the most common food allergy of childhood. In general children lose this sensitivity as they grow up with nine out of ten losing it by the age of three; it is unusual for adults to suffer from this allergy.

Symptoms are frequently vomiting and diarrhoea in children, with 30-50% also having skin rashes of some type. A small number of children have an anaphylactic reaction to milk which tends to be lifelong.

The major allergens in milk are the caseins and the whey protein b -lactoglobulin. People are usually allergic to more than one kind of milk protein.

The proteins from cow's milk are very similar to those from goats and sheep, and can cause the same sorts of reaction in cow's milk-allergic subjects. Thus goat's or sheep's milk cannot be used as a cow's milk substitute in allergic individuals.

Eggs:

Allergy to eggs is usually observed in young children rather than adults, and like cow's milk allergy, fades with time. Occasionally children suffer from a severe form of allergy which is not outgrown.

The main allergens are the egg white proteins ovomucoid, ovalbumin, and ovotransferrin.

The eggs of other poultry, such as ducks, are very similar to those of hens and can cause reactions in egg-allergic individuals.

Fish and shellfish:

Allergies to shellfish are unusual in children, mostly being experienced by adults. Reactions to fish are found in children and adults. The incidence of seafood allergy is higher in those countries with a high consumption of fish and shellfish.

Severe reactions are more frequently found with these foods, including anaphylaxis.

Cooking does not destroy the allergens in fish and shellfish, and some individuals maybe allergic to the cooked, but not raw, fish.

The major allergens in fish are flesh proteins called parvalbumins which are very similar in all kinds of fish. This is why people allergic to cod tend to be allergic to fish such as hake, carp, pike, and whiting as well.

Shellfish allergens are usually found in the flesh and are part of the muscle protein system, whilst in foods such as shrimps, allergens have also been found in the shells.

Fruits:

In general allergic reactions to fruits and vegetables are mild, and are often limited to the mouth, and are called the oral-allergy syndrome (OAS).

Around four out of ten people having OAS are also allergic to tree and weed pollens. Thus people who are allergic to birch pollen are much more likely to be allergic to apples.

There allergens in fruits and vegetables are not as complicated as other foods. Many of them are very like the allergens in pollens, which is why people with pollen allergies are also allergic to certain fruits.

Many fruit allergens are destroyed by cooking, and thus cooked fruits are often safe for fruit allergic people to eat.

Allergies to latex gloves, especially amongst health professionals, are increasing. As many of the latex allergens are like those found in certain tropical fruits, such as bananas, these people can get an allergic reaction to handling or eating these foods .

Legumes:

This group of foods includes soya beans and peanuts. Peanuts are one of most allergenic foods and frequently cause very severe reactions, including anaphylaxis.

Allergy to peanuts is established in childhood and usually maintained throughout life.

Both these foods have multiple allergens which are present in the raw and cooked foods.

Peanut allergy can be so severe that only very tiny amounts of peanut can cause a reaction. Thus the traces of nuts found in processed oils, or the carry over of materials on utensils used for serving foods, can be enough in some individuals, to cause a reaction.

The main allergens in peanuts and soya are the proteins used by the seed as a food store for it to grow into a seedling. One of the allergens in soya bean is very similar to a major allergen from dust mites, a common environmental allergen. We aren't sure yet whether this means there is a link between dust allergy and soya allergy.

Tree nuts:

This group includes true tree nuts, such as Brazil nuts, hazelnuts, walnut and pecan.

Whilst not as intensively studied as peanuts, indications are that tree nuts can cause symptoms as severe which can occasionally be fatal.

Children who become sensitised to tree nuts tend to remain allergic throughout life.

Hazelnut and almond allergies are more like those people get to fruit, and are linked to pollen allergies.

Nut allergens can be both destroyed by, or resistant, to cooking and we think that roasting may actually create new allergens.

The allergens can be the seed storage proteins, or other molecules which are also found in pollen.



Cereals:

Suffered by children and adults alike, wheat allergy appears to be particularly associated with exercise-induced anaphylaxis.

The more of a cereal (wheat, rye, barley, oats, maize or rice) we eat the more likely we are to suffer an allergy. Thus rice allergy is found more frequently in populations eating ethnic diets.

Seed storage proteins (such as wheat gluten) and other proteins present in grain to protect it from attack by moulds and bacteria, have been found to be major allergens.

http://www.ifr.ac.uk...l/infosheet.htm


#9 SweetJade1980

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Posted 05 May 2008 - 09:31 PM

QUOTE (allo12345 @ May 5 2008, 12:01 PM) <{POST_SNAPBACK}>
Sweetjade -

What kind of acne do you get if you eat bananas and pineapples, and let's say you ate those, how much time does it take after you eat them to eliminate the inflammation response?

Another thing, do you recommend we try some of the things you are doing in "Stage 3 (Correction)?

Thanks



Hi Allo,

As best as I can determine the inflammatory response will last as long as what Triggered the inflammation is still being consistently introduced into the body.

The inflammatory reaction is dose dependent, meaning if you eat one piece of candy...you may not break out or maybe you will get a zit or two. It will depend on your sensitivity level...and what's in the candy. If you eat more and daily...you will pretty much have some type of acne every day.


For example....almonds (Genus Prunus actually) give me weird under the chin & neck acne. I can bath in almond oil....but if I consume it....even the tiny bit from Lip Balm and I will get at least 1 zit.


Another example...A few months ago, I purchased Pina Colada flavored Liquid Calcium. All naturally flavored which should mean....Pineapples and Coconut flavorings (doesn't specify). Well I tried to be in denial about it but...I started breaking out along the ear & jawline (pineapple does this to me). They weren't HUGE, but small pimples that were stubborn to disappear over the course of 6-8 weeks. Finally I decided to give up this particular flavored supplement and after a few weeks....my skin cleared up again. I've previously and since consumed other flavors of liquid calcium, but sadly this won't be one of them.

As for bananas...the only thing I can recall (I do have a list somewhere - check the Taurine thread) is that I broke out underneath my arms! You can feel them (nodular), but they don't really surface...and they hurt.

HTH =)

#10 Madworld

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Posted 07 May 2008 - 07:32 AM

instead of making life hard for yourself by not eating anything, why not EAT everything and build up a tolerance to the allergens?

#11 SweetJade1980

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Posted 07 May 2008 - 05:47 PM

QUOTE (Madworld @ May 7 2008, 07:32 AM) <{POST_SNAPBACK}>
instead of making life hard for yourself by not eating anything, why not EAT everything and build up a tolerance to the allergens?



Hmm...and how exactly is my life or anyone else's, that follows a diet that usually get's them 95% - 100% clear hard?

#12 SweetJade1980

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Posted 07 May 2008 - 05:52 PM

QUOTE (Madworld @ May 7 2008, 07:32 AM) <{POST_SNAPBACK}>
instead of making life hard for yourself by not eating anything, why not EAT everything and build up a tolerance to the allergens?



2nd of all....I'm not allergic to certain foods items. I have an intolerance which can be caused by a variety of things but the official definition is that "people over a period of time develop intolerances to foods they consume the most." Hence, why some acne sufferers. and even other dieters, have discovered that some of their favorite foods will be on the "trigger" list. Oh well, there's ways to get your favorites back using different grains, milk, sweeteners, etc. Of course, now we have the opportunity to expand our dietary palate by eating new foods!

#13 john1234

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Posted 07 May 2008 - 08:18 PM

Are intolerances still characterized by a degranulation of mast cells, leading to the release of histamine? If that were teh case, maybe anti-histamines will have an affect on acne. We can also search for natural anti-histamines.....One person has reported that SODIUM improves his acne. In fact, sodium is nature's anti-histamine.
Sometimes the bumps that appear after I eat a certain food certainly LOOK and FEEL like allergies--itchy and weepy. They definitely aren't the garden variety acne.
I've seen lots of pictures of people with acne on this board--some of that stuf definitely does not look like what we define as "acne." But we still lump them in the category, because its red and detrimental to one's appearances.....

#14 SweetJade1980

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Posted 07 May 2008 - 10:28 PM

QUOTE (john1234 @ May 7 2008, 08:18 PM) <{POST_SNAPBACK}>
Are intolerances still characterized by a degranulation of mast cells, leading to the release of histamine? If that were teh case, maybe anti-histamines will have an affect on acne. We can also search for natural anti-histamines.....One person has reported that SODIUM improves his acne. In fact, sodium is nature's anti-histamine.
Sometimes the bumps that appear after I eat a certain food certainly LOOK and FEEL like allergies--itchy and weepy. They definitely aren't the garden variety acne.
I've seen lots of pictures of people with acne on this board--some of that stuf definitely does not look like what we define as "acne." But we still lump them in the category, because its red and detrimental to one's appearances.....



Yes, some people had success using Ranitidine, especially those that self-dx'd as being Histadelics.... but of course how long do you want them to continue with taking an anti-histamine that can expose them to getting other illnesses? There was also talk of a specific oil....perilla oil (?)....(try searching the board and healthboards)

Furthermore, that drug works for Histamine (Hz-blocking) and apparently reducing stomach acid (hmm), if that were the only problem, it would be perfect, yet Histamine is only one of a long list of inflammatory products, with regards to acne sufferers:

* 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...


Unfortunately, no matter what we do, if you are taking a drug that works in some way to combat inflammation, you are still consistently exposing yourself to something that is causing your inflammation...unless you are able to get to and treat the root cause (top suspect - increased intestinal hyperpermeability due to lifestyle?).

It's like it is with any other drug/supplement. If your lifestyle is antagonistic to what the drug/supplement is doing....how effective will it ultimately be for you?

Some people, all they need is a pill.

Others it's combination of pill and diet.

Other's it's diet alone.

Though mind you, it could also be an intolerance to something that is found in your skin care products, a supplement or your diet like a preservative, an artificial sweetener, a chemical (i.e. pesticide residue), or even a microbe (the body initially attacked the microbe the food was attached to) or microbial by-product (aflatoxin).

#15 john1234

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Posted 07 May 2008 - 11:02 PM

Since inflammatory mediators cause the symptoms, an anti-inflammatory diet is the best mode of action, is it not?. Intolerances manifest themselves because the body's defense system is unable to clear the antigen effectively enough. If we strengthen our bodies so that we can deal with substances that might be a bit more intolerable--that would be ideal. I truly doubt that most of us are genetically inclined to be so sensitive to every food, every product. Perhaps thats the optimisitc in me speaking. A healthy body should not react so negatively to stimuli. Removing the stimulus is of course a solution, but is it the best solution? I'm not so sure...because our oversensitivity to foreign substances is a sign of a faulty immune system, in a manner of speaking.


That being said, I've been clear for quite awhile now. I'm not embarassed to say, but masturbation was actually the biggest cause in clearing my acne, I believe. I did not know until after I became clear. I thought it was diet, exercise....but masturbation played a bigger role than I thought. Switcihng from daily to once or twice a week has done crazy things for my skin tone... In chinese medicine, there is the concept of semen loss through masturbation, which is detrimental. Normal sex is not considered detrimental because the couple complement and restore each other. Althoguh abstract, I think it makes sense in some spiritual way. There is a instance where a indian wrestler guru (who are required to swear into abstinence) attended a wedding. He gave a look at the groom, and shook his head in disapproval. "The groom obviously does not practice abstinence--his skin tone is poor and his eyes are dim."

Anyhow, i do not know why i'm sharing this, but I'm just saying that limiting masturbation might help lots of people. (My skin tone is crazy right now, even though I was forced to eat all my trigger foods this week, hanging out with some friends ) Unforunately, this is a concept that lots of poeople will not embrace.

Okay, life story over. Back to topic...

I'm currently planning to apply for a research position investigating the formation of acne. If I find one, I'll be sure to add more to this topic as I learn more about the immune response. smile.gif








QUOTE (SweetJade1980 @ May 7 2008, 11:28 PM) <{POST_SNAPBACK}>
QUOTE (john1234 @ May 7 2008, 08:18 PM) <{POST_SNAPBACK}>
Are intolerances still characterized by a degranulation of mast cells, leading to the release of histamine? If that were teh case, maybe anti-histamines will have an affect on acne. We can also search for natural anti-histamines.....One person has reported that SODIUM improves his acne. In fact, sodium is nature's anti-histamine.
Sometimes the bumps that appear after I eat a certain food certainly LOOK and FEEL like allergies--itchy and weepy. They definitely aren't the garden variety acne.
I've seen lots of pictures of people with acne on this board--some of that stuf definitely does not look like what we define as "acne." But we still lump them in the category, because its red and detrimental to one's appearances.....



Yes, some people had success using Ranitidine, especially those that self-dx'd as being Histadelics.... but of course how long do you want them to continue with taking an anti-histamine that can expose them to getting other illnesses? There was also talk of a specific oil....perilla oil (?)....(try searching the board and healthboards)

Furthermore, that drug works for Histamine (Hz-blocking) and apparently reducing stomach acid (hmm), if that were the only problem, it would be perfect, yet Histamine is only one of a long list of inflammatory products, with regards to acne sufferers:

* 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...


Unfortunately, no matter what we do, if you are taking a drug that works in some way to combat inflammation, you are still consistently exposing yourself to something that is causing your inflammation...unless you are able to get to and treat the root cause (top suspect - increased intestinal hyperpermeability due to lifestyle?).

It's like it is with any other drug/supplement. If your lifestyle is antagonistic to what the drug/supplement is doing....how effective will it ultimately be for you?

Some people, all they need is a pill.

Others it's combination of pill and diet.

Other's it's diet alone.

Though mind you, it could also be an intolerance to something that is found in your skin care products, a supplement or your diet like a preservative, an artificial sweetener, a chemical (i.e. pesticide residue), or even a microbe (the body initially attacked the microbe the food was attached to) or microbial by-product (aflatoxin).


#16 SweetJade1980

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Posted 09 May 2008 - 10:45 PM

QUOTE (john1234 @ May 7 2008, 10:02 PM) <{POST_SNAPBACK}>
Since inflammatory mediators cause the symptoms, an anti-inflammatory diet is the best mode of action, is it not?. Intolerances manifest themselves because the body's defense system is unable to clear the antigen effectively enough. If we strengthen our bodies so that we can deal with substances that might be a bit more intolerable--that would be ideal. I truly doubt that most of us are genetically inclined to be so sensitive to every food, every product. Perhaps thats the optimisitc in me speaking. A healthy body should not react so negatively to stimuli. Removing the stimulus is of course a solution, but is it the best solution? I'm not so sure...because our oversensitivity to foreign substances is a sign of a faulty immune system, in a manner of speaking.



LOL, John, I agree with you 100%!

Well, regarding our immune systems gone wild part that is. wink.gif

No, a healthy body should not be so sensitive to various stimuli. Keep in mind that this stimuli varies per individual (as you can tell by the variety of diets on the other forum).

Some stimuli are going to impact the majority of us negatively no matter what because they are known irritants (in skin care products) or are chemicals that are linked to causing acne such as Dioxin (& Splenda...is very similar).

Other stimuli seem to pop us as triggers because they are the most allergenic/antigenic among the consumables. Although, I recall a member that cleared their skin from just eliminating Pork and another woman healed her PCOS by removing Poultry products. So, there are people that avoid different foods other than what is the most allergenic.

Keeping the above in mind, the only logical reason, outside of genetics, would be that we are living a lifestyle conducive for developing an altered and overreactive immune response, to typically harmless foods.


Our environment, internally and externally, has become filled with a variety of the following:

chronic stress
antibotic abuse
non-steriodal anti-inflammatory drugs/NSAIDs abuse
alcohol abuse
smoking
poor diet
lack of sleep
sedentary lifestyle
pollutants
artificial additives
microbes & by-products (parasites, fungi, etc)
etc

The above factors have helped to alter our bodies internal environment in a way that has theoretically negatively affected our digestive system. Hence, the prime suspect in what needs to be healed is our intestinal mucosal lining. There are tests to see if we have Intestinal Hyperpermeability (leaky gut syndrome)...though some people fail these tests. Just as I failed to show a form of Gluten Intolerance neccessary to be deemed a Celiac. Though, I am not a celiac...my diet still works....luckily there are other tests to determine hypersensitivities to foods.

Although, your thought are that we should just....heal our Leaky Guts then, right? That's what Glutamine (certain types are better than others), Aloe Vera, Probiotics are for. However, this is where the controversy comes in....the protocol also requires Liver Flushes.

Now, how popular is liver flush on Nutrition & Holistic Forum? Can you see it going over well in this forum? Placebo or Nocebo effect, there IS something behind it. We've had members improve the skin clarity by doing multiple flushes and then follow up with maintence flushes over the year. We've had members that not only cleared their skin, reduced their multiple food & chemical sensitivites, and even their hirstutism (Denise). So, it can work. It is hard work and expensive (the detox formulas and everything else used). Though....it's nothing compared to the cost of being on medication and the side effects that those drugs would cost, right?

So the biggest problem here is...because it is so controvesial, unknown, etc...it's sometimes easier to avoid a few food items. That being said, I do have it listed as being Stage 3 on my signature, because if you do all the cleansing, detoxes, flushes, re-populate the good bacteria, heal your intestinal linining and reduce your exposure to the factors that probabaly got you there to begin with....You would truly be cured! Of course, you will have to continue to do maintenance work...because you will always be exposed to some of those factors.

#17 john1234

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Posted 09 May 2008 - 10:47 PM

Lol!!!

For a second I thought you agreed with me about the masturbation part. : )

Phooey. eusa_dance.gif


#18 SweetJade1980

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Posted 09 May 2008 - 11:59 PM

Psst...I updated the prior post.

OK, now second line of thought....what's up with grains, especially Wheat?

If you've read what I've posted in topics relating to Insulin Resistance, Diabetes, and Cholesterol you know that I've been posting a lot studies showing the negative impact wheat has on our health.

It's not just Insulin Resistance, Diabetes, Cardiovascular Disease, but also....ADHD, Autism, Arthritis, Thyoriditis, Adrenal Disorders and....even Cancers.

Some of which, are of course linked to the development of acne:

Insulin Resistance
Thyroid Disorders
Adrenal Disorders

Most of the previously mentioned disorders are linked to being either an Auto-Immune disease or a Silent Chronic Inflammatory Disease...

So, why would wheat have such an impact on our immune system? Well there's a few lines of thought here:

* Highly Antigenic

*Problematic Lectin - WGA (wheat germ agglutinin)

* Mycotoxin Level - some believe that there's permenant mycotoxins in grains, peanuts and select other foods contributing to....systemic yeast/candida infections and other disease (sinus, diabetes, cholesterol, etc).

* Evolution - have all ethnicities evolved enough to consume this grain (or certain others)?


The one that hasn't been mentioned the most is....Problematic Lectins. On another thread I mentioned that this was how I came to selecting the diet that did at the time. Problematic lectins include all grains, legumes and nightshades for this particular diet that acneic members were following. The theory IS, that these lectins cause the blood to agglutinate, cluster together, thus setting the stage for problems within the body.

While doctors don't support the idea that certain lectins will be problematic for certain blood types...see Eat Right 4 Your Type, there is scientific evidence to support that lectins do cause agglutination within the blood stream and there this can be linked to certain diseases (as mentioned above)!

So in my case...Dad has Type B Blood, I have Type O Blood and diabetes type 2 runs on his side of the family. According to Eat Right 4 Your Type, Type B and Type O should avoid Gluten and select lectins because they are linked to us developing Insulin Resistance and then Type 2 Diabetes....

http://www.drlam.com...iet/blood_o.cfm

http://www.dadamo.com/

What's really interesting, again, while doctor's don't support the idea of Blood Type being used in this manner....Type O is THE most common blood type around. I wonder how many people with Diabetes or chronic Insulin Resistance have Type B or Type O blood (vs. the other types)?

http://www.acu-cell.com/btd.html (mulls over the possibility)

However, I mainly mention this because there's quite a few things going on with Wheat that makes it rather interesting when it comes to looking at it's role in disease development.

For those, unaware:

QUOTE
Agglutination is the clumping of particles. The word agglutination comes from the Latin agglutinare, "to glue to."

This occurs in biology in three main examples:

1. The clumping of cells such as bacteria or red blood cells in the presence of an antibody. The antibody or other molecule binds multiple particles and joins them, creating a large complex.

2. The coalescing of small particles that are suspended in solution; these larger masses are then (usually) precipitated.

3. An allergic reaction type occurrence where cells become more compacted together to prevent foreign materials entering them. This is usually the result of an antigen in the vicinity of the cells. http://en.wikipedia....ation_(biology)


Please note, this agglutination process also happens in Delayed Type Hypersensitivity Reactions (to whatever the foreign substance may be).

Night (yawn)

P.S. A patent for an anti-fungal drug and diet for diabetes... http://www.freepaten...05/0049208.html

P.P.S. Antifungals also work to treat acne because they affect a prime pathway in the inflammation process, w/o killing bacteria (obviously)....see

QUOTE
Dermatology. 1998;196(1):82-5. Links
The possible role of reactive oxygen species generated by neutrophils in mediating acne inflammation.Akamatsu H, Horio T.
Department of Dermatology, Kansai Medical University, Osaka, Japan.

The purpose of this study was to investigate the possible role of reactive oxygen species (ROS) generated by neutrophils in mediating acne inflammation. Antibiotics used for the treatment of acne significantly inhibited ROS generated by neutrophils, when compared to other antibiotics. Metronidazole, which is effective in the treatment of acne, markedly inhibited ROS generated by neutrophils. The drug is known to have no significant effect on the growth of Propionibacterium acnes. The proportion of linoleic acid is markedly decreased in acne comedones. Linoleic acid significantly suppressed ROS generated by neutrophils. The ability of neutrophils to produce ROS was significantly increased in patients with acne inflammation. These results seem to reveal the involvement of ROS generated by neutrophils in the disruption of the integrity of the follicular epithelium, which is responsible for inflammatory processes of acne. http://www.ncbi.nlm.nih.gov/pubmed/9557235?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


#19 ComplexIssues

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Posted 13 May 2008 - 08:48 PM

Uhm,

Can anybody simplify this into one coherent theory? And there has to be some way to document and unite all the various theories, this would help immensely.

#20 sie

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Posted 16 May 2008 - 01:23 AM

This all seems to make sense but I'd like to add one thing. I have hormonal break outs (but not during pregnancy--only menstrual) BUT I don't have PCOS or oily skin. I once read that it is monthly water retention that makes your skin look temporarily plump and beautiful and pores minimized...but that shortly after that time, that same water retention has caused pores to be blocked and then the bacteria accumulates and... you know the rest.

So, maybe "hormonal" monthly breakouts are simply a result of water retention and the very rapid spot development that occurs due to p.acnes inflammation creation. In this case, the person has no inflammation of their own. They had pores "swelled shut" due to water retention and then p.acnes causes inflammation, but nothing that the person is doing (re: diet, etc) causes initial inflammation.

In this case, the person needs to head off the water retention. I'm thinking of trying a mild diuretic (Midol or caffeine or something) next month, but I don't know when to take it, as the water retention happens earlier than the spots...maybe a week before my period??? Anybody care to comment on my theory (and recommend wrt diuretic timing)?

sidenote: At the same time, I am trying to avoid extracting/picking etc to retrain my immune system to handle break outs itself (antibody development). I believe that extracting prevents your body from learning to attack p.acnes colonies--or causes the body to attack every p.acnes (not allowing any cohabitation, causing more spots than necessary)..not sure which. I've also been nourishing my immune system w/white tea, rooibos and other herbal infusions, while eating well, etc. The last thing is SLEEP...something I don't get enough of and will be trying to address this as it seems to be a miracle cure for me, when i can get it.