For starters....

[boxa06]

Yes. Any time you're using testosterone outside of TRT guidelines you're introducing high levels of testosterone, more of an androgenic hormone, more of a hormone to interact with the 5AR.

Activity from 5-alpha is the conversion from Test into DHT. So by taking anavar which is a DHT derived AAS would cause acne if you are prone DHT derived acne. Back to my original debate of why one should take only one substance at a time is valid for this reason also.

[Metalject]

Maybe I'm retarded...it happens sometimes, lol! I'm not sure I'm following your question.

[Metalject]

Activity from 5-alpha is the conversion from Test into DHT. So by taking anavar which is a DHT derived AAS would cause acne if you are prone DHT derived acne. Back to my original debate of why one should take only one substance at a time is valid for this reason also.

You're right, it is a DHT derivative, but it lacks the interaction with the 5AR, which is necessary to enhance the androgenic action in the target tissue of the skin, scalp, prostate, etc. Again, I'm not saying acne is impossible with Anavar , just that high testosterone doses would be more apt to produce it in a predisposed individual than Anavar.

[boxa06]

Ok I've done a crap load of reading and have come to the conclusion that unstable hormone levels and high hormone levels may cause acne in individuals. Everyone is different so there is no predicting who will get it or who won't. I still think the OP should take only 1 substance for his first cycle and if you don't agree I am done debating LOL everyone will have there own opinion and there are no rights or wrongs. I have learnt a fair bit from this debate

[Sworder]

Here is some information on acne. How it applies to AAS use et cetera


Localization of sex steroid receptors in human skin
http://digitum.um.es/jspui/bitstream...20skin.pdf.txt

We have recently
observed that 20?-hydroxysteroid dehydrogenase the
enzyme which catalyzes the conversion of progesterone
into its inactive form 20?-hydroxyprogestgerone was
highly expressed in sebaceous glands in the mouse skin
(Pelletier et al., unpublished data). The enzyme could
regulate the availability of circulating progesterone for
PR and thus control the influence of progesterone on
sebaceous gland cell activity.
Concluding remarks

An update on the role of the sebaceous gland in the pathogenesis of acne
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051853/
Enhanced sebaceous gland activity is attributed to the potent androgen 5α-DHT5 as sebaceous gland cells possess all necessary enzymes for conversion of testosterone to 5α-DHT.33 The isozyme 5α-reductase type I, which catalyses the conversion from testosterone to 5α-DHT in peripheral tissues by a NADPH-dependent reaction is expressed predominantly in skin.
Human SZ95 sebocytes treated with hormone levels that can be found in 60 year-old women produce less lipids than sebocytes treated with a hormone mixture representing that found in serum of 20 year-old women

Acne and sebaceous gland function.
http://www.ncbi.nlm.nih.gov/pubmed/15556719/
The sebaceous gland is an important formation site of active androgens. Androgens are well known for their effects on sebum excretion, whereas terminal sebocyte differentiation is assisted by peroxisome proliferator-activated receptor ligands. Estrogens, glucocorticoids, and prolactin also influence sebaceous gland function.
Current data indicate that acne vulgaris may be a primary inflammatory disease. Future drugs developed to treat acne not only should reduce sebum production and Propionibacterium acnes populations, but also should be targeted to reduce proinflammatory lipids in sebum, down-regulate proinflammatory signals in the pilosebaceous unit, and inhibit leukotriene B(4)-induced accumulation of inflammatory cells. They should also influence peroxisome proliferator-activated receptor regulation. Isotretinoin is still the most active available drug for the treatment of severe acne.


Skin Lipids. Sebaceous gland lipids: friend or foe?
http://www.jlr.org/content/49/2/271.full
Clinical and experimental evidence indicates that androgens affect sebaceous gland function. The majority of circulating androgens are produced by the gonads and the adrenal gland, but they can also be produced locally within the sebaceous gland from dehydroepiandrosterone sulfate, an adrenal precursor hormone. Androgen receptors are expressed in the basal layer of the sebaceous gland and in the outer root sheath keratinocytes of the hair follicle (35, 36). When free testosterone enters the cell, it is quickly reduced to 5α-dihydrosterone (DHT) by the 5α-reductase enzyme. The activity of 5α-reductase is increased in the sebaceous gland in proportion to the size of the gland (37). DHT is ∼5–10 times more potent than testosterone in its interaction with the androgen receptor. Upon binding to its receptor protein, DHT is translocated to the nucleus and initiates the transcription of androgen-responsive genes. It has been shown in a hamster ear model that DHT increases sebaceous gland size by increasing sebocyte proliferation and the rate of total lipid synthesis. DHT increases the mRNA of proteins involved in fatty acid, triglyceride, squalene, and cholesterol synthesis. This effect is mediated by the SREBPs. By inhibiting SREBP's effect with 25-hydroxycholesterol, there was a 50% decrease in the lipid synthesis increase by DHT alone (38). Androgens exert their effect on sebaceous glands by increasing the proliferation of sebocytes and increasing lipid production through SREBPs.
An increase was found in the activity of the androgen-metabolizing enzymes found on the face, chest, and back compared with the sebaceous glands in non-acne-prone areas when normalized for gland size (43). Determining what causes this increase in androgens that increases sebum production is important to understanding sebaceous gland pathophysiology.
There are currently several hypotheses that suggest a mechanism for the suppression of sebum production by estrogens. These include the notions that estrogens directly antagonize androgen activity, estrogens inhibit the production of androgens by gonandal tissue through a negative feedback loop, and estrogens regulate genes involved in lipid production. Rats given testosterone and estrogen simultaneously have a high rate of mitosis but a reduction in gland size and sebum secretion (48, 49). Based on these results, it is thought that estrogens work principally to decrease intracellular lipid production.
These include the notions that estrogens directly antagonize androgen activity, estrogens inhibit the production of androgens by gonandal tissue through a negative feedback loop, and estrogens regulate genes involved in lipid production. Rats given testosterone and estrogen simultaneously have a high rate of mitosis but a reduction in gland size and sebum secretion


Role of FGFR2-signaling in the pathogenesis of acne
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835907/
Exogeneous androgen excess or hyperandrogenism are associated with increased sebum production and severe acne.
Acne-prone skin exhibits a higher androgen receptor (AR) density and higher 5α-reductase type-I activity than uninvolved skin.
Androgen-mediated upregulation of FGFR2b-signaling in acne-prone skin appears to be involved in the pathogenesis of acne vulgaris.
Insulin -like growth factor-1 (IGF-1), the mediator of growth hormone during puberty, intracts with androgen-dependent FGFR2b-signaling and links androgen- and FGF-mediated signal transduction important in sebaceous gland homeostasis.

[kid tastic1]

Thanks guys haha was getting a bit confused. I will be reviewing everyone's comments as well as adding my stats and doing more research. I Am not going to jump ahead until i know 100% what i am taking/ doing thanks again guys.

[Sworder]

Thanks guys haha was getting a bit confused. I will be reviewing everyone's comments as well as adding my stats and doing more research. I Am not going to jump ahead until i know 100% what i am taking/ doing thanks again guys.

Sorry that we clusterf*cked this for you. Lets start fresh by providing your stats, experience, diet and pretty much everything that may be relevant so we can tailor a program for you!!

[Synergy1]

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