Girl Heals SEVERE Acne In 6-12 Months With Diet And Lifestyle Only

Travis

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Insinuating in any capacity that one should inhibit androgens or for the sake of decreasing sebum production is reckless.
Agreed. I was just pointing out the wealth of data, from all directions, that androgens increase the sebum production rate. The sebum production rate is also correlated with acne.
 

Orion

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Agreed. I was just pointing out the wealth of data, from all directions, that androgens increase the sebum production rate. The sebum production rate is also correlated with acne.

B5 is known to reduce sebum production(and clear up acne) in higher doses 1g and up. There are studies showing that it up-regulates progesterone production as well.

Effects of pantothenic acid supplementation on adrenal steroid secretion from male rats. - PubMed - NCBI

I believe B5 is similar to this study: Inhibition of Sebum Production with the Acetyl Coenzyme A Carboxylase Inhibitor Olumacostat Glasaretil. - PubMed - NCBI

B5 -> panthethine -> cystamine = inhibitor of acetyl coenzyme A (CoA) carboxylase (ACC)
 

DuggaDugga

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Agreed. I was just pointing out the wealth of data, from all directions, that androgens increase the sebum production rate. The sebum production rate is also correlated with acne.

Again, I think that's a massive oversimplification of the relationship between the sebaceous gland and androgens. The skin is very active in metabolism of hormones, both catabolic and anabolic. Stating that they're associated with high or low levels of a particular hormone without providing a reasonable causal pathway doesn't do much to advance the conversation unfortunately.

I'm working on a paper outlining an integrated, bioenergetic view of acne vulgaris, which I will share once it's farther along. In the mean time, I think it is reasonable to avoid the dissemination of crude associations that might be unintentionally misleading.

More to come.

The skin as an endocrine organ
Human skin produces hormones which are released in the circulation and are important for functions of the entire human organism.21 Major examples are sex steroids, whereas a large proportion of androgens and estrogens in men and women are synthesized locally in peripheral target tissues from the inactive adrenal precursors DHEA and androstenedione.10,11,16 DHEA and androstenedione are converted to testosterone or to 5α-DHT by different pathways through the involvement of the three isotypes of the intracellular enzyme 5α-reductase and of the isotypes of 17β-hydroxysteroid dehydrogenase,11,16 thus making the skin responsible for considerable amounts of the circulating 5α-DHT levels. The best estimate of the intracrine formation of estrogens in peripheral tissues in women is in the order of 75% before menopause and close to 100% after menopause, except for a small contribution from ovarian and/or adrenal testosterone and androstenedione.12 Thus, in postmenopausal women, almost all active sex steroids are made in target tissues by an intracrine mechanism.

Hormones and the pilosebaceous unit
Androgen-mediated dermatoses such as acne, androgenetic alopecia and seborrhea are among the most common skin disorders, with most patients exhibiting normal circulating androgen levels. The “cutaneous hyperandrogenism” is caused by in stiu overexpression of the androgenic enzymes and hyperresponsiveness of androgen receptors. Regulation of cutaneous steroidogenesis is analogous to that in gonads and adrenals.

Cutaneous androgen metabolism: basic research and clinical perspectives. - PubMed - NCBI
The skin, especially the pilosebaceous unit composed of sebaceous glands and hair follicles, can synthesize androgens de novo from cholesterol or by locally converting circulating weaker androgens to more potent ones. As in other classical steroidogenic organs, the same six major enzyme systems are involved in cutaneous androgen metabolism, namely steroid sulfatase, 3beta-hydroxy-steroid dehydrogenase, 17beta-hydroxysteroid dehydrogenase, steroid 5alpha-reductase, 3alpha-hydroxysteroid dehydrogenase, and aromatase.
Strong steroid sulfatase immunoreactivity was observed in the lesional skin but not in unaffected skin of acne patients. 3beta-hydroxysteroid dehydrogenase has been mainly immunolocalized to sebaceous glands, with the type 1 being the key cutaneous isoenzyme. The type 2 17beta-hydroxysteroid dehydrogenase isoenzyme predominates in sebaceous glands and exhibits greater reductive activity in glands from facial areas compared with acne nonprone areas. In hair follicles, 17beta-hydroxysteroid dehydrogenase was identified mainly in outer root sheath cells. The type 1 5alpha-reductase mainly occurs in the sebaceous glands, whereby the type II isoenzyme seems to be localized in the hair follicles.

Sebocytes are the key regulators of androgen homeostasis in human skin. - PubMed - NCBI
The major metabolic steps of testosterone in SZ95 sebocytes, primary sebocyte cultures, and HaCaT keratinocytes were its conversion to androstenedione by 17beta-hydroxysteroid dehydrogenase and further to 5alpha-androstanedione by 5alpha-reductase. The type 1 5alpha-reductase selective inhibitor 4,7beta-dimethyl-4-aza-5alpha-cholestan-3-one, but not the type 2 selective inhibitor dihydrofinasteride, inhibited 5alpha-reductase at low concentrations in SZ95 sebocytes and HaCaT keratinocytes. 5alpha-androstanedione was degraded to androsterone by 3alpha-hydroxysteroid dehydrogenase, which exhibited a stronger activity in HaCaT keratinocytes than in SZ95 sebocytes and in primary sebocyte cultures. Lower levels of 5alpha-dihydrotestosterone and 5alpha-androstanediol were also detected in all cells tested. Our investigations show that specific enzyme expression and activity in cultured sebocytes and keratinocytes seem to allocate different duties to these cells in vitro. Sebocytes are able to synthesize testosterone from adrenal precursors and to inactivate it in order to maintain androgen homeostasis, whereas keratinocytes are responsible for androgen degradation.[/QUOTE]
 

Travis

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Stating that they're associated with high or low levels of a particular hormone without providing a reasonable causal pathway doesn't do much to advance the conversation unfortunately.
I have provided reasonable causal evidence for increased sebum production stimulated by androgens.

Would you really like the specific pathway? We can always read studies such as these with DNA microarray analysis to show exactly what proteins are transcribed.

Barrault, Christine, et al. "Androgens induce sebaceous differentiation in sebocyte cells expressing a stable functional androgen receptor." The Journal of steroid biochemistry and molecular biology 152 (2015): 34-44.
 
OP
B

beta pandemic

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"Avocado, coconut oil = fatty blood = fatty skin" oh, those mechanical bodies

Does low fat high carb vegan diet work? Yes
How? I think By elevating cortisol through the roof, she is basically lives like on corticosteroid shots.
Does it work? Yes. Does it down regulate inflamation? Yes. Would it help with arthritis? Yes. Thats mainstream basically therapy.
In her case its endogenous, because of extremely low protein diet deficient in some minerals and vitamins.
Is it good for you in a long time?
Is elevated cortisol good for you for prolonged periods of time?

I know this, because ive been there. Ive been low fat high carb raw vegan for 3 years.
Did my psoriasis disappear? Yes! Was gone completly, i became a beliver.
But
As the cortisol supply started to drop in couple years it all returned twice as bad.
Good thing it was the final call to drop veganism.

I wish we could see this girls testimontials two years from now, then tree and so on (if she will be able to sustain this lifestyle).

Corticosteroids (endogenous or exogenous) bring instant relief, but there is a price tag on that one.

And low fat vegan avoids PUFA and depletes them as well. That probably is one positive in this situation
.

good points

yeah i dont agree with everything she says. i dont agree 100% with any authority/expert either. but with enough self experimentation and learning one becomes better at sifting through nuggets of gold

i think we should be appreciative of people who are willing to share before/afters (of any chrnoic condition), especially through 'natural' ways.

the length of time it took her to imrpove leads me to believe it could be a permanent fix for her, but will it be at a cost, like you say? nobody can know really, so i guess we'll see in a couple years :)
 

DuggaDugga

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I have provided reasonable causal evidence for increased sebum production stimulated by androgens.

Would you really like the specific pathway? We can always read studies such as these with DNA microarray analysis to show exactly what proteins are transcribed.

Barrault, Christine, et al. "Androgens induce sebaceous differentiation in sebocyte cells expressing a stable functional androgen receptor." The Journal of steroid biochemistry and molecular biology 152 (2015): 34-44.

Great reference- thank you. Doesn't really have anything to do with acne specifically, but it'll be great in the background section.
 

Dante

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Again, I think that's a massive oversimplification of the relationship between the sebaceous gland and androgens. The skin is very active in metabolism of hormones, both catabolic and anabolic. Stating that they're associated with high or low levels of a particular hormone without providing a reasonable causal pathway doesn't do much to advance the conversation unfortunately.

I'm working on a paper outlining an integrated, bioenergetic view of acne vulgaris, which I will share once it's farther along. In the mean time, I think it is reasonable to avoid the dissemination of crude associations that might be unintentionally misleading.

More to come.

The skin as an endocrine organ


Hormones and the pilosebaceous unit


Cutaneous androgen metabolism: basic research and clinical perspectives. - PubMed - NCBI


Sebocytes are the key regulators of androgen homeostasis in human skin. - PubMed - NCBI
@DuggaDugga ,great references. This is very similar to the case of MPB where there is a localized increase in the expression of 5-AR type II ,3ß-HSD and possibly other enzymes. So, it's the localized hyperactivity(intracrine activity) not the gonadal hyperactivity that is evident in both MPB and hormonal acne (some rare cases of adrenal hyperactivity due to tumors but rule that one out).
Regional scalp differences of the androgenic metabolic pattern in subjects affected by male pattern baldness. - PubMed - NCBI
Guanylate cyclase activity in male pattern baldness. Stimulating effect of 3-beta-androstanediol. - PubMed - NCBI
A possible specific receptor for 3-beta-androstanediol in the human sebaceous gland. - PubMed - NCBI
Hair Steroid Profiling Reveals Differences In Male Pattern Baldness Between Korean & Caucas. Men
I have just started reading a on old book by a Japanese author whose hypothesis was that MPB can't happen if there is no sebaceous gland hypertrophy. A paragraph from the foreword of the book :-
"The prevailing belief is that the male hormone acts directly on the hair root to cause male pattern baldness. However, Dr. Inaba has found that the male hormone is affected by an enzyme in the sebaceous gland which exercises a secondary effect on the hair root. An important factor in baldness is the size of the sebaceous gland; the relative size of the gland is influenced by diet and animal fats. Thus, baldness is not primarily a hereditary condition but rather a result of the combination of the hereditary strength of the hormone and individual dietary habits. This new theory helped Dr. Inaba to develop a treatment for baldness based on the prevention of the enlargement of the sebaceous gland"
 

Travis

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Great reference- thank you. Doesn't really have anything to do with acne specifically, but it'll be great in the background section.
The background section? But this is such an informative study. This should be placed firmly in the foreground.

This was a very comprehensive study by Barrault & Garnier. They used sebocyte cells with an androgen receptor and measured mRNA and protein expression in response to the androgen DHT..
We showed for the first time that in a simple defined low calcium keratinocyte medium, without any additive or complement, active androgens can engage immature sebocytes in a clear differentiation process. –Barrault
The they used both PCR and microarray to measure certain mRNA fragments, and found some genes involved in lipid biosynthesis were upregulated. Probably the most important was RASD1.
Recently, RASD1 was shown to be involved in glucocorticoidinduced adipogenesis in preadipocytes. When analyzed by
RT-qPCR, the DHT-induced overexpression of RASD1 is above 3 log (Fig. 1D and Fig. S2), indicating that this biomarker should
constitute a robust pharmacological read-out for testing androgen function modulators. –Barrault

sebum.png


But probably the most interesting part of the entire experiment, to me, was that they extracted the lipids from sebocytes with and without DHT treatment. They used thin layer chromatography to separate the lipid. These cells were cultured with ¹⁴carbon-labeled acetate, so what you are actually seeing is an autoradiograph. The radiation emitted by the radioactive carbon in the lipids had exposed the photographic plate.

lipo.png


You can plainly see an increase in lipid production. Notice the change in wax esters (WE). Remember how these were found significantly increased in the sebum from acne-prone individuals?
Here we show that DHT alone induces lipogenesis and lipid storage in SEBO662 AR+ cells, with a clear increase in lipid
labeling after 72 h of treatment and later. –Barrault
Now, there are many proteins and enzymes that are upregulated by the androgen receptor so it's hard to point to just one and say, "this is what's making the wax esters!"

And unfortunately, he didn't actually measure for the genes involved in the wax ester biosynthetic pathway. But since pore-clogging wax esters increased in response to DHT, we can probably assume that these were upregulated along with the other lipogenic genes.
Interestingly, in these conditions, the amount of squalene was increased by almost two-fold in the presence of DHT (Fig. 4A), leading to an increased level of squalene/cholesterol. –Barrault
We do need androgens, but there is strong evidence that excessive amounts increase wax esters in the pores. This might be expected to clog them; use your imagination.

People with low amounts of plasma steroid hormone binding globulin would be expected to be more sensitive to endogenous steroid hormones.
Conflicts of interest: The authors are employees of BIOalternatives SAS; –Barrault & Garnier


Barrault, Christine, et al. "Androgens induce sebaceous differentiation in sebocyte cells expressing a stable functional androgen receptor." The Journal of steroid biochemistry and molecular biology 152 (2015): 34-44.
 
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Dante

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People with low amounts of plasma steroid hormone binding globulin would be expected to be more sensitive to endogenous steroid hormones.
.
True, low serum SHBG is one of findings in case of MPB also but the question is even in case of similar gonadal and adrenal androgen concentration and similar sex hormone binding globulin , why does the skin upregulate the expression of certain "strong" androgenic enzymes ? Why is this happening locally in both the cases ?
Also, it's interesting that DHT treatment on sebocytes increased lipogenesis whereas taking exogenous DHT has the opposite effect !
 

DuggaDugga

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The background section? But this is such an informative study. This should be placed firmly in the foreground.

This was a very comprehensive study by Barrault & Garnier. They used sebocyte cells with an androgen receptor and measured mRNA and protein expression in response to the androgen DHT..

The they used both PCR and microarray to measure certain mRNA fragments, and found some genes involved in lipid biosynthesis were upregulated. Probably the most important was RASD1.


View attachment 6226

But probably the most interesting part of the entire experiment, to me, was that they extracted the lipids from sebocytes with and without DHT treatment. They used thin layer chromatography to separate the lipid. These cells were cultured with ¹⁴carbon-labeled acetate, so what you are actually seeing is an autoradiograph. The radiation emitted by the radioactive carbon in the lipids had exposed the photographic plate.

View attachment 6227

You can plainly see an increase in lipid production. Notice the change in wax esters (WE). Remember how these were found significantly increased in the sebum from acne-prone individuals?

Now, there are many proteins and enzymes that are upregulated by the androgen receptor so it's hard to point to just one and say, "this is what's making the wax esters!"

And unfortunately, he didn't actually measure for the genes involved in the wax ester biosynthetic pathway. But since pore-clogging wax esters increased in response to DHT, we can probably assume that these were upregulated along with the other lipogenic genes.

We do need androgens, but there is strong evidence that excessive amounts increase wax esters in the pores. This might be expected to clog them; use your imagination.

People with low amounts of plasma steroid hormone binding globulin would be expected to be more sensitive to endogenous steroid hormones.



Barrault, Christine, et al. "Androgens induce sebaceous differentiation in sebocyte cells expressing a stable functional androgen receptor." The Journal of steroid biochemistry and molecular biology 152 (2015): 34-44.


The couple studies I've ready found that squalene was disproportionately high in the sebum of an individual with acne, whereas the other lipid components were relatively the same.
Squalene is a long and unsaturated organic compound that is a precursor to the steroid hormones.
420px-Squalene.svg.png


Sebum analysis of individuals with and without acne
It is apparent that only the total amount of lipid (micrograms, p = 0.002) and the amount of squalene (micrograms, p = 0.038) are increased in the sebum of acne subjects with a statistical significant difference. The subjects with acne had more sebum (59%) than the control subjects. The lipid that differed the most between the two groups was Squalene, which was upregulated in acne sebum by a 2.2-fold. The only class of lipids that was reduced in the sebum of acne subjects was the free fatty acids, which were suppressed more than 20%. However, this result did not demonstrate statistical significance. Note that in addition to the sum of the total lipid classes (FFA, TG, WE, ChoE, Squalene), the total amount of Sapienic acid was also included in Figure 3 (since it is the major fatty acid in human sebum). Squalene was subtracted from the total amount of the WE/ChoE fraction and was also graphed separately.

It's highly susceptible to oxidation.

A possible role for squalene in the pathogenesis of acne. I. In vitro study of squalene oxidation. - PubMed - NCBI
The results clearly show that squalene is a highly effective oxygen-scavenging agent. Its oxidation may first induce comedogenesis and, as a secondary event, cause a large reduction in oxygen tension in the human pilo-sebaceous duct.
A possible role for squalene in the pathogenesis of acne. II. In vivo study of squalene oxides in skin surface and intra-comedonal lipids of acne p... - PubMed - NCBI
The results showed that these lipids were enriched in polar lipids, as compared with the skin surface lipids obtained from controls without acne. In both open and closed comedones, these polar lipids appeared to be derived mainly from the oxidation of squalene, which is in agreement with our previous in vitro results. We suggest that squalene oxidation is the link between comedogenesis and bacterial colonization, and based on this, we propose a hypothesis of the pathogenesis of acne.
Oxidization of squalene, a human skin lipid: a new and reliable marker of environmental pollution studies. - PubMed - NCBI
Squalene by-products, mostly under peroxidized forms, lead to comedogenesis, contribute to the development of inflammatory acne and possibly modify the skin relief (wrinkling). Experimental conditions of oxidation and/or photo-oxidation mechanisms are exposed, suggesting that they could possibly be bio-markers of atmospheric pollution upon skin. Ozone, long UVA rays, cigarette smoke… are shown powerful oxidizing agents of squalene. Some in vitro, ex vivo and in vivo testings are proposed as examples, aiming at studying ingredients or products capable of boosting or counteracting such chemical changes that, globally, bring adverse effects to various cutaneous compartments.

So I am currently of the evolving opinion that oxidative stress is one of the primary causes of mitochondrial disruption and peroxidation of lipid compounds of the sebum, leading to low grade inflammation, and possibly esterification of other lipids in a chain-reaction as they make migration to the skin surface where they are exposed to ultraviolet light.

I absolutely agree androgens increase sebum production. In fact, I think it's a wonderfully healthy and desirable thing to produce sebum. Look at the glossy skin of a teenager versus an elderly man. One of the "side effects" is that the sebum apparently has the ability to become pathological (whether it's cause or effect, I'm not positive yet), but I think understanding why is the key.
 

DuggaDugga

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@DuggaDugga ,great references. This is very similar to the case of MPB where there is a localized increase in the expression of 5-AR type II ,3ß-HSD and possibly other enzymes. So, it's the localized hyperactivity(intracrine activity) not the gonadal hyperactivity that is evident in both MPB and hormonal acne (some rare cases of adrenal hyperactivity due to tumors but rule that one out).
Regional scalp differences of the androgenic metabolic pattern in subjects affected by male pattern baldness. - PubMed - NCBI
Guanylate cyclase activity in male pattern baldness. Stimulating effect of 3-beta-androstanediol. - PubMed - NCBI
A possible specific receptor for 3-beta-androstanediol in the human sebaceous gland. - PubMed - NCBI
Hair Steroid Profiling Reveals Differences In Male Pattern Baldness Between Korean & Caucas. Men
I have just started reading a on old book by a Japanese author whose hypothesis was that MPB can't happen if there is no sebaceous gland hypertrophy. A paragraph from the foreword of the book :-
"The prevailing belief is that the male hormone acts directly on the hair root to cause male pattern baldness. However, Dr. Inaba has found that the male hormone is affected by an enzyme in the sebaceous gland which exercises a secondary effect on the hair root. An important factor in baldness is the size of the sebaceous gland; the relative size of the gland is influenced by diet and animal fats. Thus, baldness is not primarily a hereditary condition but rather a result of the combination of the hereditary strength of the hormone and individual dietary habits. This new theory helped Dr. Inaba to develop a treatment for baldness based on the prevention of the enlargement of the sebaceous gland"

I totally agree. There are tons of parallels between acne and hair loss. For starters they're poorly understood, emotionally-disturbing given their cosmetic nature, have been crudely categorized as genetic in cause, constantly used to point blame at unequivocally healthy hormones, and are preyed on by pharmaceutical companies to push dangerous drugs.

I'm largely inspired by Danny Roddy's work on MPB to do similar research on acne. Look forward to continuing this discussion.
 

Travis

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One of the "side effects" is that the sebum apparently has the ability to become pathological (whether it's cause or effect, I'm not positive yet), but I think understanding why is the key.
It seems to become pathological when the relative wax ester concentration doubles.
 
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Travis

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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. Antiandrogens reduce the synthesis of sebaceous lipids and improve acne, whereas androgen-insensitive subjects who lack functional AR do not produce sebum and do not develop acne. –Bodo Melnik

Melnik, Bodo. "Role of FGFR2-signaling in the pathogenesis of acne." Dermato-endocrinology 1.3 (2009): 141-156.
 

DuggaDugga

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Melnik, Bodo. "Role of FGFR2-signaling in the pathogenesis of acne." Dermato-endocrinology 1.3 (2009): 141-156.
Thanks for that, Travis.
Reminds me of the pseudo-hermaphrodite studies that made the inference that androgens and later androgen-receptors were the cause of hair loss (or lack thereof).

However I think there are many (perhaps the majority) of individuals with robust androgen sensitivity that do not suffer from acne. If the quality and quantity of the sebum plays a role in the pathogensis of acne, it would stand to reason that inhibiting sebum production (through mechanisms of antiandrogens) would therefore "treat" acne-- but at a considerable cost to the individual. A similar effect could be achieved by inhibiting the effects of natural retinoids but, again, I think you and I agree that that is not a reasonable solution for most individuals. But that's a decision each informed person should be allowed to make for them self.
 

tomisonbottom

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I don't think any do. Here is a chart of androgens extracted from beef. They are on the order of micrograms per kilogram (μg/kg).
View attachment 6139 Click to embiggen

The concentrations found in milk are a few micrograms per liter (μg/L). Concentrated milk, as in cheese, would be even higher.

Impact of extraction solvents on steroid contents determined in beef
Food Chemistry 76 (2002) 83–88
Analytical, Nutritional and Clinical Methods Section

I had horrible acne on a dairy-free diet, but my skin cleared up when I adding milk back in along with fruit, sugar, caffiene, etc
 

bohogirl

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While her acne was A LOT, I wouldn't consider that severe.

Her skin has no disfiguring scarring.

I get huge cystic acne which leaves deep holes in my skin.

I don't think that this is a cure. A cure is eating whatever you want and not breaking out.

I do agree with exercise though. I had the best skin of my life (keyword of my life because it still sucked compared to everyone else's) while exercising daily, intermittent fasting, grass fed beef, no dairy except low fat kefir, no grains, lots of fruits, lots of walnuts/pecans, eggs.

It's very hard for me to sleep at an early time and I've been struggling with sleep for about 5-6 years. Taping my mouth helps me sleep much better but still isn't perfect.

And sure if I don't eat anything my skin won't break out. But that's a crappy life to live. After awhile it's so restricting.

What I find helps my skin the most: sardines, tuna, salmon, oysters.

The thing is acne doesn't have one solution. Everyone has different types of acne.

But simply restricting yourself is not curing acne.
 

Travis

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I had horrible acne on a dairy-free diet, but my skin cleared up when I adding milk back in along with fruit, sugar, caffiene, etc
Were you eating eggs? (There is a significant amount of androgens also in eggs.)
 

Travis

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yes, but I eat eggs now too along with milk
So, you're saying that you had noticed a reduction in acne concomitant with an increased androgen intake?

This is certainly unusual (n=1), and most scientific articles that I had read imply that you could expect the exact opposite to occur.
 

tomisonbottom

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So, you're saying that you had noticed a reduction in acne concomitant with an increased androgen intake?

This is certainly unusual (n=1), and most scientific articles that I had read imply that you could expect the exact opposite to occur.

Yeah, lots of scientific articles are the opposite of my experience.

Fish oil lowers inflammation short term in studies but raises inflammation immediately in me.

But I didn't just add in milk, I changed to a ray peat style diet, so much less pufa too.

There are hundreds of things that can cause acne, so trying to narrow it down to just milk without context isn't that helpful.

Genetics, altitude, heavy metals, trauma, prescriptions, breathing patterns, endocrine disrupters, household and work toxins, emotional stress, and primarily the rest of the diet will all affects the levels of stress, and therefore acne.
 
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