Information on all 3 ingredients in pink magic
It contains 3 ingredients in an 800 mg capsule.
Previously someone identified that there is 500mg of Massularia Acuminate in it, giving us:
Massularia Acuminate - 500mg
Nelumbo Nucifera - ???mg
Rhamnus Nakaharai - ???mg
--Massularia Acuminate--
-It is a shrub/tree in Africa that can be found growing wild in forests in Gabon, Cameroon, and the Democratic Republic of Congo, as well as more sparsely in other West African countries.
(Source #1)
-"A shrub or small tree, 2-30 ft. high; corolla-tube greenish-white at base, shading into pink above, lobes pink or reddish-purple, often with white margins; in forest."
(Perhaps part of the 'Pink Magic' inspiration)
(Source #2)
-It is so prevalent in parts of Cameroon that it is referenced in one cultural study as being used to build fences with. So this cant possibly be the reason pink magic is so expensive, right?!?
-There has been several studies on Massularia Acuminata as it regards to oral hygeine, as they are used as chewing sticks in Africa.
-There has been one study on rats examining the androgenic potential of the plant. a pdf search of google turns up a full text (albeit proofed) version of the study for those that do not want to purchase it but want to read it (All of the raw data in the proof is identical to the final published study)
Here
In that study, varying doses ranging from 250 mg/kg to 1000 mg/kg were applied.
When scaled to humans those doses work out to:
Rat - Human
1000 mg/kg - 244 mg/kg (49% test increase) (at my weight: 18.3g)
500 mg/kg - 122 mg/kg (13% test increase) (at my weight: 9.1g)
250 mg/kg - 61 mg/kg (11% test increase) (at my weight: 4.6g)
It should probably be noted that these increases were in testicular testosterone, not plasma testosterone, and those two values do not exactly correlate (that could mean more effect or less effect)
Based on the earlier released information that one capsule contains 500mg of the plant, even on days where 4 servings are consumed, someone at my weight which is significantly lower than the bodybuilding average would fall under the minimum dose used in the rat study.
--Nelumbo Nucifera--
Nelumbo Nucifera is 'The Pink Lotus' (hey, pink again!)
The claimed PDE inhibitor in Nelumbo Nucifera is a chemical called 'neferine', which is found in the green seeds at very low concentrations (1-5%)
You can find the study on it Here.
It raised cAMP in a dose-dependant manner, while not affecting cGMP at all, indicating that it does not have an affect on NOS or GTP.
The study cited by the Pink magic write-up cites this study as claiming that: 'Chen et al. showed that neferin in N. nucifera inhibits PDE1, 2, 3, 4, 7, 8, and 10 [84]'
I am pretty sure this is NOT true, and I have an email sent out to the Ji-Hong Liu and Jun Chen asking about that.
In Chen's study, the discussion states the following:
PDE is a superfamily enzyme system, 11 types of which have been reported. Some of these isoenzyme families contain more than one gene (isogenes) and some genes are alternatively spliced [25_27]. In early 1990s, using anion exchange chromatography, Stief and co-workers [28] reported the separation of hydrolytic activities of PDE isoenzymes 3, 4 and 5 from cytosolic supernatants prepared from human cavernous smooth muscle, whereas others reported the presence of PDE 2, 3 and 5 [29]. Currently, the presence of mRNAs specific for 14 different human PDE isoenzymes and isoforms in human cavernous tissue has been shown by means of reverse transcription polymerase chain reaction (RT-PCR) and Northern blot analysis. The expression of the following genes were detected: PDE1A, PDE1B, PDE1C, PDE2A and PDE10A, which hydrolyze both cAMP and cGMP; the cAMP specific PDEs PDE3A, PDE4A-D, PDE7A and PDE8A, and the cGMP specific PDEs PDE5A and PDE9A [26, 27]. However, the mere expression of an enzyme does not yield any information regarding its functional relevance. PDE3 and 5 are the predominant isoenzymes in the degradation of cNMP in human corpus cavernosum musculature [26_32]. Because a PDE isoenzyme can be expressed in several organs or tissues, there might be side effects associated with the systemic administration of a PDE inhibitor. For example, PDE5 is not only expressed in corpus cavernosum smooth muscle, but also in the vascular and central nervous system and the gastrointestinal tract. Therefore, the main adverse events of sildenafil include headache, visual disturbances, flushing and dyspepsia [33]. Meanwhile, the distributions of PDE isozymes in the corpus cavernosum vary from species to species. In rabbit corpus cavernosum, the PDE is PDE5, 2 and 1. PDE3, which contributes significantly to the total PDE activity in human corpus cavernosum, is apparently lacking in rabbit corpus cavernosum [34]. Therefore, it is important to perform further research to determine whether Nef enhances cAMP accumulation by inhibiting PDE1, 2, 3, 4, 7, 8 and/or by inhibiting PDE10 in corpus cavernosum and other organs or tissues in different species.
The study specifically mentions that cGMP is NOT affected, meaning it CANT be inhibiting "PDE1A, PDE1B, PDE1C, PDE2A and PDE10A" or "PDE5A and PDE9A"
as inhibiting those would have raised cGMP. In this sectiont they are discussing which PDEs do what, not stating that neferine specifically inhibited any in particular.
Of particular note is the fact that since it didn't affect cGMP and thus not PDE5, and that kind of invalidates the numerous PDE5 inhibitor studies you quote in your claims, and reference i a LOT of your 'more MOA's section of the write-up
--Rhamnus Nakaharai--
Moving on to the third ingredient in Pink Magic, the PDE Inhibitor here is: '3-O-methylquercetin 5,7,3',4'-O-tetraacetate'. It was studied in this study:
Potent suppressive effects of 3-O-methylquercetin 5,7,3',4'-O-tetraacetate on ovalbumin-induced airway hyperresponsiveness.
Showing that it inhibits PDE3&4.
And this study:
-rolipram binding in guinea pig tissues]This Study
It should be noted that it is suggested that you do NOT take a PDE3 inhibitor for any extended period of time and its pharmacological uses are limited, due to the fact that PDE3A controls heart contractillity.
In fact, reaserch on PDE3 inhibitors for treating heart conditions has pretty much ceased because the stuff they tried led to increased mortality rates
PDE3A inhibition during development also reduces fertility. (obvious warning sign if your endocrine system is still developing)
PDE4 also has effects on heart contractillity, and inhibitors of PDE4 are also avoided for their cardiac side effects, with the exception of some acute dosing medicines for cardiac faulure and asthsma.
