The Cause Of Baldness

[Travis]

Interesting to see these theories being worked out. I'm following the best I can, though I'm not a scientist. I mention this in case my question(s) show my glaring ignorance.

I've been using my hair topicals on my beard as well, in an attempt to stimulate growth in thinner areas. I was doing this, as I wasn't using anything anti-androgen/DHT in my solution. If I'm understanding the approach of this thread, it is an anti-androgen/DHT for scalp growth. Would it be safe to say, these ingredients should not be used on the beard area? Thanks for any input.

This may seem strange, but DHT actually stimulates hair growth of the beard—this is how it got there in the first place. Women with too many androgens also get facial hair.

A nice run-down on this is the articles of Valerie Randall:

• Randall, Valerie Anne. "Hormonal regulation of hair follicles exhibits a biological paradox." Seminars in cell & developmental biology. Vol. 18. No. 2. Academic Press, 2007.

I thought this had a free full-text link, but it doesn't. You might have to run it through sci-hub.cc first.

 

[Mossy]

This may seem strange, but DHT actually stimulates hair growth of the beard—this is how it got there in the first place. Women with too many androgens also get facial hair.

A nice run-down on this is the articles of Valerie Randall:

• Randall, Valerie Anne. "Hormonal regulation of hair follicles exhibits a biological paradox." Seminars in cell & developmental biology. Vol. 18. No. 2. Academic Press, 2007.

I thought this had a free full-text link, but it doesn't. You might have to run it through sci-hub.cc first.

Thank you, Travis, I'll take a look at that link.

Sorry for the poor wording of my original question, but that was my understanding, that pro-DHT substances would be good for the beard. What lead me to ask my question is that I had thought your cocktail list was anti-DHT /anti-beard, based on some of the discussions. After rereading, I see you speaking specifically about anti-cortisol and anti-mineralcorticoid actions you're attempting to achieve, and that you note this approach as being distinct from the anti-androgen approach, "...both theories of hair loss: the Androgen Theory, and the Cortisol–Mineralcorticoid Theory". Would it be wrong to attempt to categorize this Cortisol-Mineralxorticoid theory (which is the one I assume you're pursuing) as pro or anti DHT?

 

[Travis]

The cortisol–mineralcorticoid (receptor) theory is good name, and I would consider it DHT independent. The only reason to really bring DHT into this is that it's the prevailing theory. Androgens were seen back in the 30s as the only way to explain why men exclusively had hair loss, and we've been stuck with it ever since.

Enoxolone probably wouldn't interfere—unless massive amounts are used—at the androgen receptor because it has such a strong affinity for 11βHSD₁.

Spironolactone is a weak androgen receptor antagonist. It was designed as a mineralcorticoid receptor antagonist, but it's effects on hair growth are usually attributed—publicly, at least—to it's weak anti-androgenic activity.

These are unitless relative binding affinities in which the higher is better, since it's expressed as the IC₅₀/IC₅₀ ratio between the test compound and the natural ligand. This is informative, as it shows spironolactone having a much higher affinity for the mineralcorticoid receptor than for the androgen receptor.

I think a fair interpretation of this double-displacement, double-receptor data is that spironolactone's ability to displace aldosterone from the mineralcorticoid receptor is 12× greater than it's ability to displace methyltrienolone from the androgen receptor.

I wouldn't take it internally because it can effect blood pressure and cause hormonal effects.

• De Gasparo, M., et al. "Three new epoxy-spirolactone derivatives: characterization in vivo and in vitro." Journal of Pharmacology and Experimental Therapeutics 240.2 (1987): 650-656.

Spironolactone is a drug which is used world-wide to block aldosterone-dependent sodium transport in the distal tubule of the kidney in order to reduce edema and to treat essential hypertension and primary hyperaldosteronism (Mantero et at., 1973; Nicholls et at., 1979). Spironolactone is also used commonly in the treatment of other hyperaldosterone-related diseases such as liver cirrhosis and congestive heart failure (Saunders and Alberti, 1978). The drug acts at the mineralocorticoid receptor level by competitively inhibiting aldosterone binding. ―De Gasparo

 

[jago]

I appreciate all your replies here.

I'd like to be able to tag this reply as 'microbiome' because, due to timing this is my best theory for a particular case in my family. Her rapid hair loss started exactly 2 months after school term started and with a change to slightly 5'C drop in weather temp... but also starting to drink a new brand of Kefir. Gut / hair link is established in science so it seems a good start to disprove.

Testing needs to be more systematic:
- swap scalp and DNA barcode for x bacteria, yeast, fungus at your local DIY Bio hacking lab, or get it sent a way for analysis... but how to swab correctly?
- as above for stool and skin
- test thyroid,
- test hormones levels,
- test nutrient & diet

Anecdotally I can say that sunlight and moisture have been factors for me. Both of those effect bacteria. I don't think bacteria is the only aspect, with the body and bacteria in conversation with each other, making it a complex thing. However, try to keep things simple where possible.

-j


As an possibly useful aside I can say that after having tried 6-7 different strains from around the world of kefir, they are all very different. The first time I tried it I felt it hit my stomach and wow! What a feeling. I haven't experienced that again. Some other strains have helped me in different ways and others not so much. It's hard to find a common thread due to changing conditions. I think what needs to happen is to find out what each strain actually is and start to get to know individual species of bacteria.

 

[Mossy]

The cortisol–mineralcorticoid (receptor) theory is good name, and I would consider it DHT independent. The only reason to really bring DHT into this is that it's the prevailing theory. Androgens were seen back in the 30s as the only way to explain why men exclusively had hair loss, and we've been stuck with it ever since.

Enoxolone probably wouldn't interfere—unless massive amounts are used—at the androgen receptor because it has such a strong affinity for 11βHSD₁.

Spironolactone is a weak androgen receptor antagonist. It was designed as a mineralcorticoid receptor antagonist, but it's effects on hair growth are usually attributed—publicly, at least—to it's weak anti-androgenic activity.

View attachment 7125

These are unitless relative binding affinities in which the higher is better, since it's expressed as the IC₅₀/IC₅₀ ratio between the test compound and the natural ligand. This is informative, as it shows spironolactone having a much higher affinity for the mineralcorticoid receptor than for the androgen receptor.

I think a fair interpretation of this double-displacement, double-receptor data is that spironolactone's ability to displace aldosterone from the mineralcorticoid receptor is 12× greater than it's ability to displace methyltrienolone from the androgen receptor.

I wouldn't take it internally because it can effect blood pressure and cause hormonal effects.

• De Gasparo, M., et al. "Three new epoxy-spirolactone derivatives: characterization in vivo and in vitro." Journal of Pharmacology and Experimental Therapeutics 240.2 (1987): 650-656.

​

I appreciate the clarification and additional information -- especially the safety concerns about spironolactone.

Of the items on your cocktail list, I must confess, I'm apprehensive to use synthetics, and would prefer a natural alternative, if available. I realize natural is not always safer, and that nature can produce some pretty damaging substances, but for starters I'd like to use this approach. I may venture into synthetics as I gain confidence through my understanding of them.

So, from this perspective, my thought is to use licorice root extract (glychyrrizic acid) as an alternative to enoxolone. I am using this simply because I already have it, and it's a natural substance I feel pretty safe with. Beyond this, I don't have any reason to know that it's a viable alternative to enoxolone -- you're welcome to set me straight on this. I'll use coconut oil as well, which is of no safety concern. Instead of olive oil, I'll use emu oil to promote absorption of all the substances -- at least it's my understanding that it will. For Cholecalciferol, I'll use liquid Thorne D/K2. This covers all on this list but the remaining two synthetics (at least I think they are). Once again, if you, or anyone else, sees an issue with any of this, I welcome any input.

Thanks again for sharing your findings.

 

[Mossy]

DELETED (duplicate post)

 

[ivy]

I appreciate the clarification and additional information -- especially the safety concerns about spironolactone.

Of the items on your cocktail list, I must confess, I'm apprehensive to use synthetics, and would prefer a natural alternative, if available. I realize natural is not always safer, and that nature can produce some pretty damaging substances, but for starters I'd like to use this approach. I may venture into synthetics as I gain confidence through my understanding of them.

So, from this perspective, my thought is to use licorice root extract (glychyrrizic acid) as an alternative to enoxolone. I am using this simply because I already have it, and it's a natural substance I feel pretty safe with. Beyond this, I don't have any reason to know that it's a viable alternative to enoxolone -- you're welcome to set me straight on this. I'll use coconut oil as well, which is of no safety concern. Instead of olive oil, I'll use emu oil to promote absorption of all the substances -- at least it's my understanding that it will. For Cholecalciferol, I'll use liquid Thorne D/K2. This covers all on this list but the remaining two synthetics (at least I think they are). Once again, if you, or anyone else, sees an issue with any of this, I welcome any input.

Thanks again for sharing your findings.

Actually, enoxolone is glychyrrizic acid.
There might be something else worth pondering as part of a natural stack, Oleuropein. @Travis, would this fit the cortisol–mineralcorticoid (receptor) theory?

Topical Application of Oleuropein Induces Anagen Hair Growth in Telogen Mouse Skin

 

[Travis]

Oleuropein is different; it appears to word by lowering leukotriene B₄ leves, an eicosanoid, by inhibiting it's generative enzyme 5-lipoxygenase.

• de la Puerta, Rocio, Valentina Ruiz Gutierrez, and J. Robin S. Hoult. "Inhibition of leukocyte 5-lipoxygenase by phenolics from virgin olive oil." Biochemical pharmacology 57.4 (1999): 445-449.

The effect of olive oil has been tested indirectly, as control, in an experiment on cylcosporine A.

• Watanabe, Shinichi, et al. "Hair growth on nude mice due to cyclosporin A." The Journal of dermatology 18.12 (1991): 714-719.
• Excerpt:
  • "The distribution of the new hair depended on the natural pattern of hair growth in the mice. There was no hair growth in the control mice which were given only olive oil topically (Fig. 1C). The hair growth in the CsA-treated mice stopped after cessation of the treatment, and returned to the level of the control mice on day 14 after the end of the treatment." ―Watanabe

This pathway overlaps with the vitamin D pathway, and eicosanoid production can also be inhibited by avoiding linoleic acid—the only precursor.

But the concentrations in olive oil can vary widely, 1.5 to 11,226 milligrams per kilogram.*

click to embiggen

Taking the density of oil to be one, for simplicity, this yields a concentration of 1.5 – 11,226 mM. Rocio de la Puerta measured the enzyme-inhibiting effect, as EC₅₀, of oleuropein at 80 μM; the concentration used for hair growth in rats by Dr. Tao was 3.7 mM. Most olive oils, it would seem, have concentrations of oleuropein fulfilling both of these conditions, but the same cannot be said about all olive oil. Olive oil is notorious for being adulterated with cheaper oils, so it's hard to tell much of this is from regional and climactic variability or from mixing.

• Errico, Sally. "Olive Oils Dark Side." The New Yorker, Feb. 2002
• Mueller, Tom. "Slippery Business." The New Yorker, Aug. 2007

I would imagine you'd be able to discriminate a high-phenolic olive oil from a low one by taste.

*Perri, Enzo, Andrea Raffaelli, and Giovanni Sindona. "Quantitation of oleuropein in virgin olive oil by ionspray mass spectrometry− selected reaction monitoring." Journal of agricultural and food chemistry 47.10 (1999): 4156-4160.

 

[Travis]

Actually, enoxolone is glychyrrizic acid.

Enoxolone is the aglycone of glycyrrhizic acid.

Beyond this, I don't have any reason to know that it's a viable alternative to enoxolone -- you're welcome to set me straight on this.

The only study on hair growth with this was actually done with ethanolic licorice extract, but you would expect enoxolone to be slightly more effective. Enoxolone is also more oil-soluble.

It wouldn't be unreasonable to assume that the glycosidic bond gets cleaved by an enzyme in the skin; both compounds should work to inhibit 11βHSD₁.

 

[ivy]

Enoxolone, also called glycyrrhetinic acid, is the aglycone of glycyrrhizic acid.

Thanks for the clarification. But that doesn't imply it's less safe, does it?

I think you missed a previous question from Mossy:

P.S. I just noticed your distinction of Glycyrrhetin from Glycyrrhizic acid; is Glycyrrhetin preferred, or just an alternative to Glycyrrhizic acid?

 

[Travis]

Thanks for the clarification. But that doesn't imply it's less safe, does it?

It's probably slightly more so, but they are both safe externally. Enoxolone is cleaved from glycyrrhizic acid during digestion, and this is what inhibits the mineralcorticoid receptor in the kidneys.

The glucose would simply be metabolized.

 

[johnwester130]

It's probably slightly more so, but they are both safe externally. Enoxolone is cleaved from glycyrrhizic acid during digestion, and this is what inhibits the mineralcorticoid receptor in the kidneys.

View attachment 7129

The glucose would simply be metabolized.

what explains the people who regrow hair with finasteride (40% success rate) ?

 

[Travis]

what explains the people who regrow hair with finasteride (40% success rate) ?

What do you mean by 40%? Sounds like the results from a coerced "satisfaction" survey.

Cyclosporine A causes real, unequivocal hair growth in 94.6% of patients.

• Wysocki, G. P., and T. D. Daley. "Hypertrichosis in patients receiving cyclosporine therapy." Clinical and experimental dermatology 12.3 (1987): 191-196.
  • "Hypertrichosis is a cosmetically undesirable side-effect of cyclosporine therapy. A study of 56 insulin-depetident diabetics on long-term cyclosporine therapy indicated that unequivocal hypertrichosis occurred in 94.6% of the patients." ―Wysocki

Cyclosporine A is not thought to work on the androgen receptor. If androgens go against their natural hair stimulatory role on the scalp only, I could only guess that it's by inhibiting sebum—the classic and undeniable effect of androgens on the skin.

――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――

The cortisol theory in the early days was confounded by a lack of understanding. The removal of the adrenal cortex causes undeniable hair growth in animals, while the removal of the adrenal medulla causes hair loss. The removal of of the entire gland can produce paradoxical results, depending on the animal and season.

• Stein, L., and E. Wertheimer. "Hair-loss as deficiency test of medullectomy in rats." Journal of Endocrinology 2.2 (1940): 418-427.
  • "Active hair-loss inhibiting preparations were obtained by extraction of fresh cattle adrenals with 0-2N HCl or with alcohol. The active principle was highly sensitive to oxygen and to alkali. [...] When cortex and medulla were separated as completely as possible, by far the predominant quantity of active principle was found in the medulla. The low activity noted for the cortex can probably be completely accounted for as due to the incomplete separation of cortex from medulla." ―Stein
  • "Medullectomy was carried out in part according to the method of Evans [1935/36], but generally according to a modification of this method, wherein one adrenal gland was completely removed, and the second adrenal was treated as indicated by Evans. [...] The operated animals showed largely the same course of hair-loss as did the adrenalectomized rats." ―Stein
  • "The hair-loss of medullectomized rats rose steeply to a maximum within 3-7 days of the operation, remained at the maximum for about a week, then fell sharply, though frequently still exceeded the normal maximum (20 mg.)" ―Stein
  • "Out of 17 medullectomized rats maintained under observation during prolonged time intervals, 13 developed distinct bald spots
  • "The effect of adrenalin on hair-loss: It has been pointed out that acid extract of adrenal medulla inhibits the hair-loss reaction of adrenalectomized rats." ―Stein
  • "In a subsequent series of experiments the effect of pure adrenalin rather than medulla extract was examined. Adrenalin was found to be markedly active. I-Adrenalin of Poulenc Frères was used." ―Stein
  • "Butcher & Richards [1939], working with rats, have shown that adrenalectomy strongly stimulates the growth of the second hair coat, previously inactive hair buds being found to show signs of development 40 hours after the operation. According to these authors, the effect is dependent on the removal of the adrenal cortex. It appears justified, therefore, in view of this and of our own findings, to conclude that hair-moult in rats is regulated by the adrenal glands." ―Stein
    • Butcher, Earl O., and R. A. Richards. "The relation of the adrenals to the retarded hair growth in underfed albino rats." Endocrinology25.5 (1939): 787-792.

It would seem pretty clear that adrenaline (epinephrine) from the adrenal medulla stimulates hair growth, while a product of the adrenal cortex—either aldosterone, cortisone, cortisol, dehydroepiandrosterone (or some combination thereof)—powerfully inhibits it.

The below article makes absolutely no mention of testosterone being produced by the adrenals (although Wikipedia claims "small amounts," less than 5% of total.)

• Rainey, William E., et al. "Dissecting human adrenal androgen production." Trends in Endocrinology & Metabolism 13.6 (2002): 234-239.

While it's true that castration prevents hair loss at an early age, castration after a certain age produces no such effect. If it was simply testosterone doing this, then any castration before the age of 30 would be be expected to have the same effect.

It has been conclusively shown—in more than one experiment—that during adolescence testosterone changes the hormonal profile of the adrenals. You could see this as an evolutionary advantage to provide males with more adrenal hormones. At Wimbleton and the French Open, men play 5 sets per match; women play three.

I think the only thing DHT has going for it is academic inertia, and nearly full endorsement from the media and pharmaceutical companies. Judging by how the AMA has treated some highly-effective historical cancer therapies—and some undeniable evidence pertaining to cardiovascular disease—you might be tempted to think that cures are not considered profitable by them, especially when pharmaceutical patents are still in force.

 

[Mossy]

Actually, enoxolone is glychyrrizic acid.
There might be something else worth pondering as part of a natural stack, Oleuropein.

I did read about oleuropein some time back, but discarded it based on comments by swissTemples. I'm guessing most who've been searching out hair-loss remedies know who he is; but, if not, he made popular the "ghetto protocol", which seemed to give him great results. The ghetto protocol was his improvised approach of the professionally formulated prostaglandin protocol, which seems to rooted in the androgen theory.

I can't say my reasoning was well-founded for dismissing oleuropein, I was just going with what someone who clearly knew more about it was advising. As Travis shows, there are potential potency issues if you attempt to get it from olive oil. When I was researching it, I did find some suppliers of the extract, with up to 40% oleuropein, should it interest you.

 

[Mossy]

Enoxolone is the aglycone of glycyrrhizic acid.
The only study on hair growth with this was actually done with ethanolic licorice extract, but you would expect enoxolone to be slightly more effective. Enoxolone is also more oil-soluble.

It wouldn't be unreasonable to assume that the glycosidic bond gets cleaved by an enzyme in the skin; both compounds should work to inhibit 11βHSD₁.

Great -- thank you.

 

[Travis]

Thanks for the heads-up on 40% oleuropein, a molecule that inhibits the production of an eicosanoid. There are so many types of eicanoids, from the prostaglandins to the leukitrienes, that probably only students—studying before a test—can list them all from memory. They all seem to have slightly different effects, and oleuropein inhibits the production of leukitriene B₄.

Aspirin and indomethacin inhibit cyclooxygenase, which prevents the formation of prostaglandins—another subset of eicosanoids. This is the first leukitriene-inhibitor that I've come across, and I should examine its role in biology someday.

But nearly all eicosanoids can be avoided by restricting its only precursor: linoleic acid, the singly worst polyunsaturated fatty acid.

 

[Mossy]

...linoleic acid, the singly worst polyunsaturated fatty acid.

Wow -- that statement is sobering. I have a lot of work to do, then, to reverse what is probably some extensive build-up/damage. Prior to Peating, I was on the Budwig protocol, consuming large amounts of flax seed and flax oil daily. Let me put it this way, at one point, I purchased a 25lb bag of flax seed, which I completely consumed over the course of being on that protocol -- not to mention that bottles and bottles of flax seed oil.

 

[Travis]

I just found out that DHT is a more powerful androgen than testosterone. This should be no surprise, really, as the hydrogenated (reduced) forms are always more active; cortisol is more active than cortisone, and estradiol is more active than estrone.

I've seen the in vitro binding data, I've seen a few bioassays, and not even Wikipedia can deny this:

Relative to testosterone, DHT is considerably more potent as an agonist of the androgen receptor (AR). ―Wiki

Testosterone can be seen like estrone, and DHT would be analogous to estradiol. This is certainly the way things appear in the literature, and many people freely state that DHT is more potent.

This is not the message people hear from Merck, from the television. They are almost led to imagine DHT as a testosterone byproduct of sorts, or an evolutionary accident which causes hair loss.

Dihydrotestosterone is most potent androgen, and is involved in neurite growth. It upregualtes the neuritin protein through the androgen receptor, and can even induce transcription and translation of myelin protein zero (P₀) by activating the progesterone receptor.

The female phenotype is the default phenotype, and males diverge from this through the action of testosterone DHT. Motor neurons are grown in certain areas and there is even an androgen (DHT) receptor in muscle. Taking Finasteride not only lowers DHT, but it raises estradiol as testosterone backs-up and is forced down the aromatase pathway. This explains Finasteride-gynecomastia.

Finasteride impotence is best explained by the regression of the neurons emanating from the spinal nucleus of bulbocavernosus. It was previously thought that such things only happened at an early age, but this idea was proven false in 1986.

• Kurz, Elizabeth M., Dale R. Sengelaub, and Arthur P. Arnold. "Androgens regulate the dendritic length of mammalian motoneurons in adulthood." Science 232 (1986): 395-399.

what explains the people who regrow hair with finasteride (40% success rate) ?

I came across this passage in an article:

‘It turns out that 5α reductase not only converts testosterone to dihydrotestosterone, but it also irreversibly reduces glucocorticoids and progestins: deoxycorticosterone to 5α-dihydrodeoxycorticosterone and progesterone to 5a-dihydroprogesterone.' ―Irwig

Perhaps 5α-dihydrodeoxycorticosterone is a ligand for the mineralcorticoid receptor?

I found just now a better one:

• Traish, Abdulmaged M., et al. "Adverse effects of 5α-reductase inhibitors: What do we know, don’t know, and need to know?." Reviews in Endocrine and Metabolic Disorders 16.3 (2015): 177-198.

The substrates for 5α- Rs include T, progesterone (PROG), deoxycorticosterone (DOC), corticosterone, cortisol and aldosterone. The products of these reactions result in formation of 5α-dihydro-derivatives such as 5α-DHT, 5α-dihydroprogesterone (5α-DHP) and 5α- dihydrodeoxycorticosterone (5α-DHDOC), 5α- dihydrocorticosterone, 5α-dihydrocortisol and 5α- dihydroxyaldosterone. The latter two metabolites are thought to act as potential active mineralocorticoids [17]. ―Traish

[17] Marver D, Edelman IS. Dihydrocortisol: a potential mineralocorticoid. J Steroid Biochem. 1978;9:1.

Perhaps it works by inhibiting 5α-dihydrocortisol?

 

[Travis]

I guess the question is: is 5α-dihydrocortisol a more potent mineralcorticoid that cortisol? and is 5α- dihydroxyaldosterone a more potent mineralcorticoid than aldosterone? Keep in mind that reduced forms are generally more active; the body detoxifies steroids by sulfation, acetylation, and shedding from hair and skin—not by chemical reduction.

• Marver, Diana, and Isidore S. Edelman. "Dihydrocortisol: a potential mineralocorticoid." Journal of steroid biochemistry 9.1 (1978): 1-7.

*Some people think that methylation of hydroxyl groups is also a detoxification pathway, but this is strange since this actually makes the molecule harder to eliminate. O-methylated analogues of estrogen and dopamine are produced in the body by COMT, but these molecules are always more toxic and lipophillic. If anything, this is more of a toxicification pathway; although in truth it's probably neither. Methylated derivatives have functions in their own right—melatonin is O-methylated serotonin.

 

[Travis]

The answer is no. The 5α-reductase product 5α-dihydrocortisol is less of a mineralcorticoid than cortisol. Here are some binding affinities and assays which show both this and the relative strength of cortisol:aldosterone on the mineralcorticoid receptor. From the article:

mineralocorticoid receptor:

aldosterone (1.00) > cortisol (0.20) > 5α-DHF (0.083) > 5β-DHF (0.042)​

glucocorticoid receptor:

dexamethasone (1.00) > cortisol (0.10) > 5α-DHF (0.002) > 5β-DHF (0.001).
​

bioassay: mineralcorticoid activity on toad bladder:

aldosterone (1.00) > cortisol (0.80) > 5α-DHF (0.65) > 5β-DHF (none).​

That that entire quote in the Traish article is just mindless, since it makes no sense to even mention 5α-dihydrocortisol as a "potential mineralcorticoid" when:

• It has been shown to be a mineralcorticoid, with an activity 65% that of aldosterone, and.. . . .
• It's even less of a mineralcorticoid than cortisol itself. Traish et al give the impression that mineralcorticoid activity was increased—or actually created—by this process, while the truth is that it actually decreases. The line by Traish "The latter two metabolites are thought to act as potential active mineralcorticoids" would be better expressed as "The latter two metabolites still have mineralocorticoid activity, but less so than the substrate cortisol—representing an attenuation of total mineralcorticoid activity (assuming no potentiating modifications downstream.)" It's almost as if Traish, or one of the others had simply glanced at the title and chose to cite it—padding the footnote section and giving the impression that they'd read more than they had; a cheap move by Traish et al.