NEW HAIR GROWTH SHAMPOO LOOKS LEGIT
Revita, a new shampoo for hair loss, will be hitting the shelves at local drugstores soon. In the midst of generic Rogaine and other laughable “hair loss” drug store based products, this one actually looks legit.
It is essentially Nizoral with a potent kick. It has the same active ingredient as prescription strength Nizoral (2% Ketoconazole), but requires no prescription.
It also contains a WHOLE lot more, including topical caffeine and apple polyphenols, of which there is some evidence of efficacy. It will cost about the same as 2 % Nizoral, approximately $30.00, which will last 2 months according to the manufacturer, DS labs.
We will not hesitate to slam treatments that are generally ineffective and over-hyped, such as Fabao 101,Avacor, Nuhair, Hair Genesis, Nisim and even the sacred cow, Rogaine.
However when a seemingly legit product appears, we feel obligated to get the word out.
Here is a brief rundown on the active ingredients:
DS Labs Revita active ingredients:
Amino Acids: Ornitine, Taurine, Cysteine
It comes in 200 ml size which is approximately a two month supply. It is recommended to be used 5 times a week for best results.
Revita will replace 2% Nizoral Shampoo in our primary treatment protocol as soon as it becomes commercially available.
It is designed to be used 5 times a week, which would allow Dr Proctor’s Hair Regrowth Shampoo on the off days,(Dr. Proctor’s Hair Regrowth Shampoo, which has a high concentration of Pyridine-N-Oxides, has a hair growth stimulation effect even at a twice a week usage rate).
Dr. Proctor’s Hair Regrowth Shampoo
Dr. Proctor’s Hair Regowth Shampoo contains the minoxidil-like (without the side effects) hair growth stimulator NANO (nicotinic acid N-Oxide). In addition, NANO shampoo contains an SODase-type hair growth stimulating agent. Dr. Proctor’s Hair Regrowth Shampoo is a good adjuvant treatment for either prescription Nizoral or Revita shampoo.
Here’s a study on topical caffeine, one of Revita’s primary ingredients, and hair growth.
Int J Dermatol. 2007 Jan; 46(1):27-35.
Effect of caffeine and testosterone on the proliferation of human hair follicles in vitro
Department of Dermatology and Allergology, Friedrich-Schiller-University, Jena, Germany. firstname.lastname@example.org
BACKGROUND: Androgenetic alopecia (AGA) is a common problem in men of all ages, affecting approximately 50% at 50 years of age. The underlying cause is an androgen-dependent miniaturization of genetically predetermined hair follicles. Here, the hair organ culture model was used to investigate the effects of testosterone and caffeine; the latter being a promising candidate for hair growth stimulation. METHODS: Hair follicles from 14 biopsies, taken from the vertex areas from male AGA patients, were cultivated for 120-192 h in vitro with normal William's E medium (control) or William's E medium containing different concentrations of testosterone and/or caffeine. Hair shaft elongation was measured daily and at the end of cultivation, cryosections of follicles were stained with Ki-67 to evaluate the degree and localization of keratinocyte proliferation. RESULTS: Significant growth suppression was found in hair follicles treated with 5 microg/ml testosterone. This was counteracted by caffeine in concentrations of 0.001% and 0.005%. Moreover, caffeine alone led to a significant stimulation of hair follicle growth. These results were confirmed immunohistochemically by Ki-67 staining. CONCLUSIONS: Androgen-dependent growth inhibition of ex vivo hair follicles from patients suffering from AGA was present in the human hair organ culture model, a constellation which may serve for future studies to screen new substances against androgen-dependent hair loss. Caffeine was identified as a stimulator of human hair growth in vitro; a fact which may have important clinical impact in the management of AGA.
Here is a paper by Dr. Proctor, describing the mechanisms of the active ingredients in his Regrowth shampoo.
Endothelium-Derived Relaxing Factor and Minoxidil: Active Mechanisms in Hair Growth
In: Archives in Dermatology, vol. 125, August, 1989
To the Editor. -Recent discoveries imply a role for the nitroxide free radical (NO) in the control of vascular tone, platelet function, and in the central nervous system.(1-2) The NO is apparently endothelium-derived relaxing factor, or EDRF,(1~2) an endogenous compound probably accounting for the action of nitrovasodilators such as nitroglycerin. Because many other vasodilators act by increasing the endothelial production and release of EDRF, the elucidation of this system has caused a revolution in vascular physiology.
Such discoveries may also explain the vasodilatory action of another nitro compound, whose name, "miNOxidil," betrays its chemical affinity to EDRF (Figure). That is, minoxidil or (more likely) an active metabolite may be an EDRF agonist. Further, EDRF and minoxidil both activate guanylate cyclase,(1-3) an action thought to account for their common vasodilatory properties and one that is shared by many electronically activated compounds. Perhaps a separate action of EDRF on hair growth also explains minoxidil-induced hypertrichosis.
Legend: Nitroxides form long-lived radicals. Spin traps such as DMPO (5,5 dimethyl-i -pyrroline-N-oxide) form stable adducts with short-lived radicals such as superoxide. Spin labels such as TEMPO (2.2,6.6-tetramethyl-1-piperidinyloxyl, free radical ) are stable radicals under biological conditions-the dot stands for the unpaired electron. Minoxidil itself resembles the spin traps, but the active form may be a radical analogous to endothelium-derived growth factor (EDRF) or TEMPO. Conversely, note that minoxidil is also a polyamine; cations (such as polyarginine) can show EDRF-like activity with activation of guanylate cyclase.
In addition, EDRF is a stable free radical. Significantly, other radical-formers such as psoralen plus UV-A, porphy-rins, and anthralin induce hypertrichosis, which also occurs in hairy nevi (eg, melanin as a stable radical species(4)). Thus, free radicals and the like may modulate hair growth as they apparently do inflammation, skin pigmentation, and neurotransmission.(4 )
Conversely, stable radicals are often potent antioxidants. Indeed, NO is an important industrial antioxidant, while NO's reactivity with superoxide radical explains the potentiation by superoxide dismutase of EDRF action.(2). Perhaps hair growth reflects protective systems rather than the active processes themselves. Such opposed interpretations are common in free-radical biology. In this regard, we have observed stimulation of hair growth by certain oxygen radical scavengers (P.H.P., unpublished data, 1988).
Moreover, minoxidil closely resembles nitroxide spin labels and spin traps(4) (Figure). By scavenging superoxide, the nitroxide spin trap DMPO (5,5 dimethyl-1-pyrroline-N-oxide) ameliorates postischemic injury to heart muscle (5). It is likely that EDRF plays a similar function in ischemia and inflammation, for which there may be some (controversial) role in pattern loss. In fact, this may account for some of the protective action of nitrovasodilators in myocardial infarction. For example, many current models for postischemic myocardial and stroke-induced tissue damage involve a combination of calcium ions and free radicals. Since calcium channel blockers also induce hair growth, perhaps balding is ultimately related to similar processes.
Peter H. Proctor, PhD, MD
Some things that have changed since this paper was published:
1): Presently, the action of both nitric oxide and Minoxidil on vascular smooth muscles is thought to be due to opening of membrane potassium channels ( "K-Channel agonism") rather than their action on cyclic GMP. Superoxide blocks this. According to UpJohn researchers, K-channel angonism also accounts for the action of minoxidil on hair follicles.
2) As well as breaking down NO, the "bad" effect of superoxide on nitric oxide is now thought to include the toxic reaction product peroxynirite. TEMPO, DMPO, and similar agents may work in heart attack, stroke, etc. by competitively inhibiting the reaction of superoxide and nitric oxide to form peroxynitrite.
1. Vanhouette PM. The endothelium: modulator of vascular smooth-muscle tone. N Engi J Med. 1988;319:512-513.
2. Moncada S, Radomski MW, Palmer RJM. Endothelium-derived relaxing factor: identification as nitric oxide and role in the control of vascular tone and platelet function. Biochen PharmacoL 1988;37:2495-2501.
3 Eoehme E, Graf H, Schultz C. Effect of sodium nitroprusside and other smooth muscle relaxants on cyclic GMP formation in smooth muscle. Adv Cyclic Nacleotide Protein Phosphorylation Res. 1978;9:131-143.>
4. Proctor PR. Free radicals and human disease. In: CRC Handbook of Free Radicals andAntioxidants in Biomedicine. Boca Raton, Fla: CRC Press; 1989~:209-222.
5. Kramer JR, Arroyo CM, Dickens BF, Weglicki WE. Spin-trapping evIdence that graded myocardial ischemia alters post ischemic superoxide production. Free Radic Biol Med. 1987;3:153-158.
Some in the beginning stages of hair loss are fortunate enough to be able to control Hair Loss and regrow hair with just shampoos alone. The most potent shampoo combo that has worked for many is 2% Nizoral and Dr. Proctor’s Hair Regrowth Shampoo, alternated on a day on day off basis. Head and Shoulders Shampoo *may* be useful as well. Revita Shampo will likely give us an even better option.
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