Photobiomodulation Low Level Laser Therapy Lectures at A4M

19th Annual World Congress on Anti-Aging and Aesthetic Medicine / American Academy of Anti-Aging

Orlando FL April 7-9 2011


Friday April 8, Morning Session 7am Crystal Ballroom H

7:00AM  - Photobiomodulation in Anti-Aging: Harnessing the Power of Low Level Laser Therapy (LLLT) for Healing and Regeneration - Michael Hamblin, PhD [Harvard/MIT/Wellman Center for Photomedicine]

7:25AM -  The Use of Low Level Laser Therapy in the Medical Management of Androgenetic Alopecia (Hereditary Hair Loss) - Alan J Bauman, MD [Bauman Medical Group]


Shedding on Minoxidil, Propecia/Finasteride or Laser Therapy

Are you seeing excessive shedding after just beginning hair loss treatment with minoxidil (formula 82m or rogaine), laser therapy (lasercap or other)?   You might be having the "Dread Shed!"  But don't worry, keep up with the treatment... here's why:

Keep in mind that any regimen (medication or laser therapy) that stimulates follicles to switch into a growth phase can cause shedding. Because all hair follicles cycle-on and cycle-off over the course of your life, shedding is a VERY poor barometer for the measurement of hair loss or hair growth. Regardless of treatment, the more hair follicles you have, the more shedding you will have. "Resting" follicles may still contain a hair-shaft. When you apply minoxidil, for example, and the follicle "switches on" and the newly growing hair pushes out the old, resting hairshaft. The result: a shed. It is my feeling that any hair that is shed from starting a particular therapy wasn't in an anagen/growth phase anyway.

Remember that minoxidil/rogaine is a proven 'anagen-stimulator' which shifts resting follicles into growing follicles. Female pattern hair loss (androgenetic alopecia) is characterized by miniaturizing follicles and a shortening of the natural growth-phases of the follicles.

Shedding when starting minoxidil, laser, or propecia (if it is noticeable) typically occurs within the first two to eight weeks of therapy. Keep in mind that it normally takes 10-20 weeks for microscopic hair density to peak with minoxidil AND six to twelve months to see visible results of the growth with minoxidil.

Normal Hair Growth
There are three stages in a hair's growth cycle. The hair follicles in the scalp are at different stages at any one time.

Stage 1 - Anagen Stage (growing phase) 1. Anagen Stage (Growing Phase)
The new hair grows from the base of the follicle. This growth phase usually lasts for 2 to 4 years and results in a full-grown hair.
Stage 2 - Catagen Stage (regression phase) 2. Catagen Stage (Regression Phase)
During this stage, the hair stops growing and the hair root shrinks. The base of the follicle breaks down and the hair moves upward, away from the root.
Stage 3 - Telogen Stage (resting phase) 3. Telogen Stage (Resting Phase)
The matured hair is now only loosely anchored to the hair root. It usually falls off after a few months or is pushed out by the next hair which grows from below.

Saw Palmetto, DHT, Hair Loss and the Prostate

Comparison of finasteride (Proscar), a 5 alpha reductase inhibitor, and various commercial plant extracts in in vitro and in vivo 5 alpha reductase inhibition.

Department of Biochemistry, Merck Research Laboratories, Rahway, New Jersey 07065.

Human prostate was used as a source of 5 alpha reductase. Compounds were incubated with an enzyme preparation and [3H]testosterone. [3H]-dihydrotestosterone production was measured to calculate 5 alpha reductase activity. IC50 values (ng/ml) were finasteride = 1; Permixon = 5,600; Talso = 7,000; Strogen Forte = 31,000; Prostagutt = 40,000; and Tadenan = 63,000. Bazoton and Harzol had no activity at concentrations up to 500,000 ng/ml. In castrate rats stimulated with testosterone (T) or dihydrotestosterone (DHT), finasteride, but not Permixon or Bazoton, inhibited T stimulated prostate growth, while none of the three compounds inhibited DHT stimulated growth. These results demonstrate that finasteride inhibits 5 alpha reductase, while Permixon and Bazoton have neither anti-androgen nor 5 alpha reductase inhibitory activity. In addition, in a 7 day human clinical trial, finasteride, but not Permixon or placebo, decreased serum DHT in men, further confirming the lack of 5 alpha reductase inhibition by Permixon. Finasteride and the plant extracts listed above do not inhibit the binding of DHT to the rat prostatic androgen receptor (concentrations to 100 micrograms/ml). Based on these results, it is unlikely that these plant extracts would shrink the prostate by inhibiting androgen action or 5 alpha reductase.

PMID: 8381228 [PubMed - indexed for MEDLINE]

1: Eur Urol. 1994;26(3):247-52. Links

Comparison of finasteride (Proscar) and Serenoa repens (Permixon) in the inhibition of 5-alpha reductase in healthy male volunteers.

Eclimed Pharmacologie Clinique, Hopital Universitaire Cochin, Paris, France.

A total of 32 healthy male volunteers (age range 20-30 years) were enrolled in a 1-week open, randomized, placebo-controlled study comparing finasteride (Proscar), a 5 alpha-reductase inhibitor, with Permixon, the plant extract of Serenoa repens. The objective of the study was to evaluate the effect of single and multiple doses of the drugs on the inhibition of 5 alpha-reductase as assessed by serum dihydrotestosterone level determination. Following baseline measurements on day 1, the subjects were randomized to finasteride 5 mg once a day (n = 10), Permixon 80 mg x 2 twice a day (n = 11), or to placebo once a day (n = 11) for 7 days. Serum testosterone and dihydrotestosterone levels, were determined on day 1 (baseline and 12 h) and on days 2 (24 h), 3 (48 h), 4 (72 h), 6 (120 h), and 8 (168 h). After 12 h, a single dose of finasteride 5 mg reduced the serum dihydrotestosterone level by 65% (p < or = 0.01). The decreases ranged from -52 to -60% with multiple doses of finasteride 5 mg once a day (p < or = 0.01). As in the placebo group, there was no effect of Permixon on the serum dihydrotestosterone level. No significant difference was detected between finasteride and Permixon or between finasteride and placebo with respect to serum testosterone, except on days 3 and 6, respectively (p < or = 0.05). However, the corresponding serum testosterone levels remained within the normal ranges. These data confirm the efficacy of finasteride as inhibitor of 5 alpha-reductase.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 7805711 [PubMed - indexed for MEDLINE]

1: Prostate. 2006 Feb 1;66(2):115-23.Click here to read Links

Saw palmetto is an indirectly acting sympathomimetic in the rat-isolated prostate gland.

Prostate Research Co-Operative, Faculty of Pharmacy, Monash University, Parkville, Victoria, Australia.

BACKGROUND: To investigate whether saw palmetto that inhibits alpha1-adrenoceptor binding in vitro affects contractility of the rat prostate gland. METHODS: The effects of a commercially available saw palmetto extract were examined on the contractility of rat-isolated prostate glands. The extract was tested in the presence and absence of phentolamine, prazosin, yohimbine, propranolol, hexamethonium, cocaine, desipramine, nifedipine, guanethidine, atropine, and alpha,beta-methylene ATP to evaluate the mechanism of action. Isolated preparations of rat vas deferens and bladder were used for comparison. RESULTS: Unexpectedly, saw palmetto extract caused contractions of the rat prostate gland that could be attenuated by prazosin, phentolamine, nifedipine, guanethidine, cocaine, and desipramine but not by any of the other pharmacological tools. Similar contractile effects were observed in rat-isolated vas deferens preparations but not in rat-isolated bladder preparations. CONCLUSIONS: In the rat prostate gland, saw palmetto extract causes indirect alpha1-adrenoceptor-mediated contractions via the release of noradrenaline from sympathetic neurons. Copyright 2005 Wiley-Liss, Inc.

PMID: 16114061 [PubMed - indexed for MEDLINE]

: Prostate. 1999 Feb 15;38(3):208-15.Click here to read Links

Saw palmetto extracts potently and noncompetitively inhibit human alpha1-adrenoceptors in vitro.

Department of Urology, University of Essen, Germany.

BACKGROUND: We wanted to test whether phytotherapeutic agents used in the treatment of lower urinary tract symptoms have alpha1-adrenoceptor antagonistic properties in vitro. METHODS: Preparations of beta-sitosterol and extracts of stinging nettle, medicinal pumpkin, and saw palmetto were obtained from several pharmaceutical companies. They were tested for their ability to inhibit [3H]tamsulosin binding to human prostatic alpha1-adrenoceptors and [3H]prazosin binding to cloned human alpha1A- and alpha1B-adrenoceptors. Inhibition of phenylephrine-stimulated [3H]inositol phosphate formation by cloned receptors was also investigated. RESULTS: Up to the highest concentration which could be tested, preparations of beta-sitosterol, stinging nettle, and medicinal pumpkin were without consistent inhibitory effect in all assays. In contrast, all tested saw palmetto extracts inhibited radioligand binding to human alpha1-adrenoceptors and agonist-induced [3H]inositol phosphate formation. Saturation binding experiments in the presence of a single saw palmetto extract concentration indicated a noncompetitive antagonism. The relationship between active concentrations in vitro and recommended therapeutic doses for the saw palmetto extracts was slightly lower than that for several chemically defined alpha1-adrenoceptor antagonists. CONCLUSIONS: Saw palmetto extracts have alpha1-adrenoceptor-inhibitory properties. If bioavailability and other pharmacokinetic properties of these ingredients are similar to those of the chemically defined alpha1-adrenoceptor antagonists, alpha1-adrenoceptor antagonism might be involved in the therapeutic effects of these extracts in patients with lower urinary tract symptoms suggestive of benign prostatic obstruction.

PMID: 10068345 [PubMed - indexed for MEDLINE]