Alpha Androstenol link to early puberty in girls and sex drive in both sexes

Pheromone Science Pheromone Theory & Molecules
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Alpha Androstenol in my research seems to be the cause of some change in menstrual cycle and a large contributor to early puberty in girls. There have been many links between father absence and earlier puberty in girls. I was able to find an article that pointed me to the idea that its the presence of a non biological male in the household and not the absence of a father…

Without Dad little girls grow up too fast

Looking into that further as to what might cause that, alpha androstenol has been found in studies to decrease luteinizing hormone (LH) pulse frequency during the follicular phase of the human menstrual cycle causing a change. Lutenizing Hormone is a pituitary hormone that triggers ovulation in a woman. There is no question on the many studies by different authors on this part.

https://academic.oup.com/biolreprod/article/68/6/2107/2683595

https://academic.oup.com/chemse/article/25/4/465/342748

Married vs unmarried women had a difference
https://www.ncbi.nlm.nih.gov/pubmed/20977093

A few other of the reported adjustments in cycles included: two days closer together over a four to six-month interval (McClintock, 1971) and a 1.4 day shortening (Stern & McClintock, 1998).

Luteinizing Hormone also is highly correlated with sex drive in women, it surges just prior to ovulation time when sex drive is highest. It also causes secretion of testosterone in men from the testicular Leydig cells. So Alpha Androstenol will also have effects in both women and men there from the increase in LH.

https://www.ncbi.nlm.nih.gov/pubmed/20646176

I dont see strong evidence yet however that this also means women sync up their cycles simply from the pulse change, only that there is definate effect on luteinizing hormone causing a change from the exposure to alpha androstenol, as well as has been shown to start puberty earlier from the effect on LH in mice, and based on that article probably in those who are non related. The amount of change should also vary further based on exposure timeframe.

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Added some new research links so far.

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Another one I found:

Androstenol
Smelling Androstenol caused activation of a portion of the hypothalamus, which according to animal data mediates the pheromone triggered mating behavior. And its another that apparently hits the brain like A1, as well as Hedione which is man made as well.

I have other studies that show Androstenol makes you appear more attractive then you are.

I updated some of the links in the first post to the full study.

A-nol just needs a balance in a mix with some form of status/androsterone, especially if your T is lower. Scent of Eros as one example used 4 A-nol to 1 Androsterone.

Otherwise its possible you get so friendly and then further can appear more weak and lower status if too much is on without the balance or starting from a high testosterone level.

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This may be an explanation as to why A1/Anol is such an effective fallout/crushy base combination - And why Anol isn’t nearly so useful on other fallout applications?

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A cautionary note on pre-2000 studies. You may wonder why scientists after 20 years aren’t publishing many new sweat studies.

The funding dried up. 1990s research triggered a phero craze. Scientists attempted to repeat the findings. They failed. Nowadays techniques such as SPME are the gold standard. They’ve done headspace analysis (the air above the skin–body odor if you will) of practically every known human odorant.

A prevention for mosquitos (malaria) is worth billions. Pheros, not hardly. Numerous headspace studies have failed to indentify more than trace amounts of anol in odor. It’s in sweat but it doesn’t vaporize.

What continues to amaze me is that none of this headspace research makes it to the phero community. And for me it kind of crushed all the conventional wisdom and folk tales I’ve heard. Yes, there are numerous odorants in headspace. Most are similar in structure to copulins. And the same compounds in copulins (some) are found in male odor.

Yes, anol produces effects. However, its presence in body odor has been rejected. If there are any laboratory chemists here familiar with SPME vs solvent extraction of sweat from cotton pads, we’ll talk.

I know this is a tough pill to swallow. It’s the truth. Most of the assumptions from 20 years ago turned out to be wrong. The sweat studies generated false positives. They wrongly assumed the compounds in sweat would vaporize like they do in phero sprays. But sweat isn’t alcohol. It appears that only low mol. wt. compounds (generally less than 200) actually vaporize into the air.

And that’s why it’s near impossible to get scientists to take “phero sigs” seriously. No journal will accept it for publication.

Unfortunately so much data floating around the boards is now obsolete. That’s why Pherin let their patents expire and you notice they haven’t done much lately. Forensic chemists are working hard to identify the exact human scent fingerprint. What’s known now in textbooks is that steroidal compounds like anol and erone are generally irrelevant.

Any graduate students that undertake studies of anol in terms of natural phero sigs, it’s rare for faculty to accept these dissertations because so much of that 80s and 90s research is not supported. They were using A1 amounts 1000 times higher than normal. When you use say 10 micrograms, the findings don’t repeat. 1 study will look good, the other flops.

Almost all the graduate work done since 2005 is in volatile fatty acids in human odor. The scientific community has essentially abanonded erone, enone and anol.

But don’t take my word for it. Deep dive into Google Scholar.
The precursors for androstenes aren’t Test. It’s pregnenolone and progesterone. “Both are C21 steroids that lose their
C17 side chains to form the Δ16 double bond (81).”

https://www.researchgate.net/profile/Charles_Wysocki/publication/237780679_A_Sense_of_Smell_Institute_White_Paper_Human_Pheromones_What's_Purported_What's_Supported/links/0deec51f7a9a054f00000000/A-Sense-of-Smell-Institute-White-Paper-Human-Pheromones-Whats-Purported-Whats-Supported.pdf

As some of you know, Dr. Preti’s lab did most of these sweat studies in the 90s. He also did the current work in headspace with the negative finding for androstenes in body odor. He’s mostly abandoned that research into sweat androstenes as commercially unproductive. Journals just aren’t interested.

And that’s the truth.

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In current body odor studies they collect sweat on a pad. Then they collect the vapors in the vial above the sweat in the air.

These are the odors that would be present directly near the skin. Like if you smelled someone’s armpit from 1 cm away.

They’ve done probably 10+ SPME studies of the entire body. There about 25 human biomarkers that come up most often. I am going from memory here. NONE are androstenes. The computers they were using 20-30 years ago a less powerful than your cell phone.

As we have better technology (more sensitive, SPME) we find many of the old phero studies aren’t valid. Not to say that mones are a hoax. But as far as an erone or enone “sig,” that’s junk science by today’s standards.

But to be fair, if anyone has a current decade study showing androstenes in headspace (the air above the skin), I will take a look.

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This is what a gas chromatagram of male sweat looks like. Note the absence of steroidal compounds like anol. This is the natural phero sig. These copulin-like compounds are small and vaporize pretty well. Some are powerfully bad smelling.

http://onlinelibrary.wiley.com/doi/10.1002/ar.a.20125/full

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That’s exactly why phero-products do work in a way, the unnatural diffusion of the used substances are very different to regular chemosignals.

Mones, why don’t you join on other phero-forums. If you’re still interested in the fallout-theme, contact me via pm. I’ve pretty much singled out the molecules that old A413 consisted of … in actual name, not code.

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Yes. To make this less arcane for the general audience.

Sweat studies pre-2000 to 2005 found chemicals we call ‘pheros’ like androstenol in sweat.

Sweat is mostly water. But pheros like androstenone are poorly soluble in water. Phero sprays could use cheap distilled water instead of organic solvents (alcohol), but it won’t work.

Early sweat studies extracted molecules from sweat collected on cotton pads using organic solvents. And then they inject the extract into a GC-MS machine that spits out a readout showing molecules like DHEAS (mones) with a weight around 270.

Scientists assumed that if the compounds were on the pads, they would be in the headspace (body odor of the air near the skin). They were wrong.

The first websites selling mones kicked in around 2000-2005.

After 2005 SPME came in wide use. They would put the pad in a glass vial. Then a tiny fiber collects the molecules in the air above the pad.

SPME showed that androstenol and other commercial pheros didn’t turn up in the air in the vial. That means that compounds line anol (with a weight above 200) for whatever reason do not vaporize into the air. They don’t leave your skin, except in trace amounts.

This presents a paradox: anol for sure affects people (chatty), it’s in sweat, but modern lab techiniques like SPME indicate studies newer than 15 years do not show a natural phero odor signature (headspace is the scientific term) for anol, erone or enone.

There are over 25 compounds routinely tested in human odor. They aren’t anol or erone.

According to modern science that wasn’t available when Androtics started, androstenone and androsterone do not exist (except in trace amounts) in the human scent fingerprint. Advertising claims to the contrary are not scientifically supported at this time.

“Literature review: 25
compounds most frequently isolated from headspace samples of
human skin, based on compilation of 31 references (see
Table 1).” 2013. The evidence is overwhelming. From a review of 31 studies using SPME and solvent extraction, none of the top 25 compunds in human odor are anol, enone or erone, or DHEA, DHEAS, AS, preg, or any of the other pheros on most product labels.

This was published in the prestigious Journal of Chemical Ecology. If any hobbyist or vendor can demonstrate why the article is not sound, please present the evidence. It is because of accepted science like this that most universities don’t consider enone a pheromone in natural human communication. It only seems to work as an aritifical spray. And journals will not publish ‘pheromone studies’ contradictory to this work with out new data, which currently does not exist.

A couple years ago I completely changed my approach to everything, becuase I found out most of what I thought I knew…was wrong.

Most message board posts about phero sigs are, unfortunately, no longer scientifically valid.

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I am most interested in compounds with a mol. wt. less than 200, as these are probably candidates for the natural male scent fingerprint. See 2013 study above.

This is not to disparage people like Dodd, who assisted Androtics with its early work. To my knowledge Dodd didn’t use SPME back then. Sweat studies from Gower 30 years ago aren’t wrong, they just don’t measure actual chemicals in body odor.

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This is very interesting! thanks data

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Another method of Pheromone transport: (Lipocalin - wikipedia)
The lipocalin family has been connected with the transport of mammalian pheromones due to easily observable protein-pheromone interactions. Lipocalins have been detected as carrier proteins of important pheromones in the nasal mucus of rodents. Major urinary proteins, a lipocalin subfamily, are found in mouse and rat urine and may act as protein pheromones themselves.

https://onlinelibrary.wiley.com/doi/full/10.1002/ar.a.20125

They further demonstrate the similarity between human axillary secretions and nonhuman mammalian odor sources where lipocalins carry chemical signals used in pheromonal communication. In rodents (Novotny, 2003), pigs (Spinelli et al., 2002), and hamsters (Singer et al., 1989), volatile molecules appear to be bound to lipocalin proteins that transport them and are in part responsible for some of the activity. Hence, the chemistry of human axillary secretions appears to be analogous to other mammalian pheromone systems
an interesting and thought‐provoking analogy.

As far as naturally, Androstenone and androstenol were found to be present in the characteristic odor fraction, at levels 50 to 100 times below the concentration of 3M2H and other organic acids (Zeng et al., 1992).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987372/

Although these steroids are present at concentrations 50-100 times below those of some organic acids mentioned previously, their effect ultimately depends on the volatility and the perceptive threshold for these compounds as well as the duration of exposure.

E‐3M2H and androstenone have comparable low olfactory thresholds (Baydar et al.,1992; Gower and Ruparelia,1993; Wysocki et al.,1993; Zeng et al.,1996b)

Odor dispersal is modulated by several factors including clothing layers, axillary temperature, total hair surface, arm movements and the proximity of one’s nose.

Androstenol

Considering that this compound (Androstenol) also is highly volatile (vapor pressure at 37?C is 254 microtorr), it could be expected to act as a pheromone, provided that its signals can be transduced to the brain.

The Pheromone Androstenol (5

Androstenol has certain physiochemical properties that make it better suited to serve as a pheromone than other neurosteroids. The calculated vapor pressure of androstenol at 37?C is 254 μtorr, which is markedly greater than other neurosteroids (values for allopregnanolone, allotetrahydrodeoxycorticosterone, androstanediol, and androsterone are 26, 4, 55, and 60 μtorr, respectively). Thus, androstenol is more volatile than other neurosteroids and is better able to serve as an airborne vapor-phase chemical messenger. By the universal gas law, the concentration of androstenol in air at 37?C is estimated to be 13 nM. Interestingly, this value is comparable to the basal serum concentrations of allopregnanolone (3?10 nM) (Paul and Purdy, 1992), indicating that whether neurosteroids are delivered as blood-borne hormones or as pheromones carried in a vapor, the concentrations in the delivery medium are remarkably similar. The estimated vapor-phase concentration of androstenol is below the concentration active on GABAAreceptors (threshold concentration, ∼100 nM). However, it is likely that the steroid would reach the required concentration in mucus within seconds or less (T. H. Morton, personal communication). A second characteristic of androstenol that makes it well suited as a pheromone is its hydrophobicity. Androstenol has a calculated logP(octanol-water partition coefficient) value of 5.9. Thus, it has significantly greater hydrophobicity than other neurosteroids (comparable values, 3.8?4.9), which would promote accumulation in mucus and transcellular delivery following exposure to a vapor.

Molecular Weight: Androstenol 274.44 g/mol, Androstenone 272.43, Androstadienone 270.408, Androsterone 290.4403. All and many more in this range we have found effects on others.

https://academic.oup.com/chemse/article/28/5/423/349663

Many other Volatile Organic Compounds in human odor. There are more then 500 on skin as well. Guess we all will have a lot of testing to do :wink:
https://www.semanticscholar.org/paper/Comparison-of-the-Volatile-Organic-Compounds-in-Curran-Rabin/70b2795f8085e2c37d37033880c681ce1d97a9e8
https://www.researchgate.net/publication/259721564_A_review_of_the_volatiles_from_the_healthy_human_body

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Humans also have lipocalin protein transporters:
http://www.pnas.org/content/pnas/93/13/6626.full.pdf

A human lipocalin protein transporter, apolipoprotein D, was recently found expressed in apocrine sweat glands, and was shown to bind the axillary odorant, E-3-methyl-2-hexenoic acid (E-3M2H). These results further suggest a remarkable similarity between human axillary secretions and nonhuman mammalian odor sources, where lipocalins have been shown to carry the odor signals used in pheromonal communication.

In pigs pheromones such as androstenol and androstenone are first bound to a lipocalin transporter:
https://pdfs.semanticscholar.org/6ce3/9d8255be785e67c406435ab45ca06a08e429.pdf

Low molecular mass proteins are implicated in chemical communication throughout mammalian species, and are involved in both perception and delivery of pheromonal
compounds. The submaxillary glands of the male pig secrete large quantities of saliva when aroused by female pigs. The presence of pheromones within the saliva cause oestrous sows to take up the mating stance. These pheromones are the 16-androstene steroids, 5a-androsten-3a-ol (Androstenol) and 5a-androsten-3-one (Androstenone). Biochemical studies have shown that the submaxillary glands of pigs, particularly Go?ttingen boars, contain a low molecular mass protein, pheromaxein, which is capable of binding these 16-androstene steroids. When the binding affinities of various steroids to pheromaxein were assessed relative to 5a-androsten-3-one (100%) at 50% binding of 5a-[3 H]androsten-3-one, all 16-androstenes tested had strong affinities for pheromaxein, with 4,16-androstadienone the highest at 176%. Other steroids, which had poor binding affinities, were saturated at the C16 position and reduced at C5. In general, 5a-androstanes bound better than 5b-androstanes.

https://pheromonetalk.com/t/human-lipocalin-protein-patents/4353

Booth and White reported a partially characterized porcine extracellular protein, pheromaxein, that binds androstenol and related steroids in boar submaxillary gland saliva (Booth and White, J. Endrocr. 118:47 (1988)). A salivary gland lipocalin, which binds 16-androstrenes, was later isolated from boar submaxillary gland (Marchese et al., Eur. J. Biochem. 252:563 (1998)). A cDNA encoding this protein, termed sex-specific salivary lipocalin (SAL), was recently reported, and shown to encode a polypeptide with high homology to the murine MUPs (Loebel et al., Biochem. J. 350:369 (2000)). It is not known whether boar SAL or pheromaxein has phermone activity itself, or only contributes to the phermone activity of cognate androstene ligands. Human homologs of boar pheromaxein or SAL have not been characterized.