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Some information regarding LEDs and their therapeutic uses

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  • Some information regarding LEDs and their therapeutic uses

    I'm going to copy and paste two documents I've gotten from Adrian Warburton regarding LEDs. If you're interested, PM me and I can help you build your own array. I'm having alot of success with mine of late, and I'm planning to double the number of LEDs I'm using once I have to cash to spare.

    Both documents were emailed to me as attachments by Adrian Warburton.

    Document 1:


    A large number of studies both in﷓vitro and in﷓vivo have been undertaken using laser light of a wide range of wavelengths and doses. Protocols have also varied widely and it is extremely difficult to dissect out the real from the ridiculous. This has been recognised by the FDA who have consistently refused to sanction this therapeutic tool. However, recent studies have been much more closely controlled and approval is likely. This has, to some extent, been due to intense interest in photodynamic therapy, which has produced a flood of publications and much development of laser technology.


    One of the most interesting and potentially useful effects of light is that wavelengths around 660nm induce cell proliferation. It is probably the basis of light﷓induced accelerated wound healing, a very promising field for future development. We can determine the following facts from our own studies, those of our colleagues Mary Dyson and Jim Allen and the literature:

    A. Light exposure increases rate of cell division significantly, but the time of exposure
    is critical. A five-minute exposure can cause significantly increased proliferation
    detectable up to 7 days subsequently whereas longer exposures do not have this effect.

    B. The proliferative effect induced by 660mn light is not reproducible using longer
    Wavelengths of 820nm and 950nm.

    C. The light effect acts directly on cell function to produce proliferation and is not produced
    by a laser photolytic effect on the cell culture medium.

    D. The proliferative effect of 660nm light exposure may be linked to the length of cell cycle.
    We and others have shown that endothelial cells and keratinocytes which grow more
    slowly than fibroblasts, require a longer exposure to laser fight, i.e., 20 minutes, to
    produce a significant increase in growth rate.

    The mechanism for proliferation is not known and for the purposes of clinical effectiveness this is an important area. There are, however, interesting possibilities:

    Warnke and Weber (1) suggest that Laser stimulation is the result of respiratory chain complex 1
    as primary light absorbers. A wide variety of pro and eukaryotic cells have similar
    long and short term photoresponses to irradiation with visible light of the same spectral band suggesting a common photoreceptor to all these cells(2). Such photoreceptors, of which three are definitively known (3), are well described in a variety of organisms and are thought to mediate DNA repair in plant growth via photo﷓induced electron transfer reactions. In the blue﷓red region the absorbing compounds are the semiquinone forms of flavoproteins as well as terminal cytochrome oxidases (2). Last year, two human photoreceptor genes (CRY1 and 2) were identified and their products are flavoproteins containing FAD and a pterin co﷓factor (3,4). Light irradiation would, therefore, act as a trigger altering the redox status of the cell. We know that the accelerated growth is accompanied by increased respiratory activity and DNA synthesis. There are also related changes in Ca2+ and cAMP levels within cells (2).

    Such reactions do, however, appear to need continued irradiation for their effect to persist, whereas brief, one﷓off low dose light irradiation appears to have extended effect. HeLa cells stimulated for 5 mins ( 102 ﷓ 103 J/m2) exhibit exponential growth for at least 6﷓7 days. Longer exposure times tended to be cytotoxic and there is a lag phase (about 30 mins) between irradiation and biological effect (2). Other cellular effects appear extremely varied as indicated in the table below.

    Biosystem (references) Changes Induced Model System Light Source
    DNA Synthesis (2,5) increase Skin HeNe 633nm
    DNA Repair (6) increase HL60 irradiated GaAs 660nm
    Cell Prolferation (7-15) increase, decrease Micro, fibro, lympho, mono, keratino Ruby, 697nm HeNe, GaAs,
    Cell motility (16) increase Sperm Kr. 647nm
    Cell granule release (17) increase Mast cells HeNe
    Cytokine release (18) increase Fibroblasts Argon 500nm
    Membrane potential (19-21) increase Mitochondria, fibro, lympho HeNe
    Neurotransmitter release (22) increase Acetylchlorine Ruby
    Nerve conduction (23,24) increase Skin, Median nerve
    Phagocytosis (25) increase Polymorphs Ruby
    ATP synthesis (19,26) increase Mitochondria HeNe
    Prostaglandin synthesis (27) increase Skin HeNe
    Collagen synthesis (28-30) (independent of prolif.) increase, decrease Skin, fibro, synovium HeNe, GaAs, Nd: 1060nm

    Activation of flavoproteins in the presence of oxygen Involves the production of O2 and H2O2 (31) and this could be accelerated following light activation, a possible contributory factor to cytotoxicity following long irradiation. ROS such as H2O2 are also activators of transcription factors including NfkB and AP﷓1 (32) leading to upregulation of cytokine expression. Such upregulation has been described, fibroblasts irradiated with 630﷓660nm red light from an argon laser for 4﷓8mins release TGF and PDGF into the culture medium (18). This is likely to apply to other cell types as well and could explain the mitogenic effect of culture medium from laser irradiated cells. Transcription factor activation may also be induced by laser irradiation directly, UV radiation being known to lead to modifications of c﷓jun and enhanced transcription of AP﷓ 1 ,genes leading to cell proliferation (33). We and others have also noticed pronounced protective effects of red light irradiation. HeLa cells irradiated with a HeNe (102 J/m2 ) and left for 30mins were then protected against Gamma radiation (5.0Gy/180min) (2). Rats total body irradiated with red light were protected against ocular toxicity induced both by hyperoxia and by the iron chelator desferrioxamine (34). This effect is possibly linked to the upregulation of stress protein genes by red light which may cause small rises in intracellular temperature (35). Light﷓induced photoreceptor damage in rats is significantly reduced following stress protein upregulation (36). Short wavelength UVA irradiation also induces stress protein responses. Activation of expression of one of these, haem, oxygenase (H0), is a known defence system in marnmahan cells (37), pre﷓ of skin fibroblasts with UVA protecting from subsequent UVA damage (38).

    Protection against tissue damage induced by UV is obviously a blockbuster involving both skin and eye protection. Previous work in this area indicates that red light exposure could protect against senile macular degeneration which results in rapid deterioration of vision in the over 60's living in sunny areas. 60% of the southern USA's elderly population suffer from this condition. Prof. Tyrrell's studies (38) suggest a similar use in skin protection.

    Other Areas of potential interest include photodynamic therapy (PDT) (39) in which protoporphyrins and similar derivatives are given to cancer patients (mainly). For reasons not clearly understood, protoporphyrins are taken up (or retained) rather more readily by tumours than normal tissue and produce cytotoxic singlet oxygen when laser irradiated. The advantages of this procedure are essentially restriction of toxicity to irradiated tissue, the disadvantages lack of laser penetration into deeper inaccessible tumours. Greater and more specific retention of such therapeutic agents is necessary and this may possibly be achieved by linked phototherapeutic agents and bioreductive drugs.

    Another recent development has been Colin Self's production of light activatable antibodies (presumably other moieties could be used as well) (40 and patent appl.WO﷓09634892). The technology involves creating a bispecific antibody capable of binding to a tumour through its first antibody component reactive with a tumour marker and also to an anti﷓tumour agent. The anti-tumour agent moiety is blocked by a visible/UV light photocleavable nitrophenyethan﷓l﷓ol activated at the tumour site. his type of technology would appear to have great potential.


    1 Warnke U, Weber WM. ATP﷓synthesis of non﷓vegetable cells through laser light
    stimulation Lasers Surg. Med 1987;7:

    2. Karu TI. Photobiological fundamentals of low﷓power laser therapy. lEEE Journal of Quantum Electronics 1987; QE﷓23: 1703.

    3. TodoT, Ryo H,Yamarnoto K, Toh H. Science 1996; 272: 109﷓112.

    4. Hsu DS, Xiaodong Yao, Shaying Zhao. Putative human blue light photoreceptors
    hCRY1 and h CRY2 are flavoproteins. Biochemistry 1996; 35: 13871﷓13877.

    5. Glassberg E, Lask GP, Uitto J. Biological effects of low energy laser irradiation.
    American Society for Laser Medicine and Surgery Abstracts. Lasers Surg Med 1988; 8:

    6. Logan ID, Bristow HE, Barrett YA. The induction of DNA repair in X﷓ray irradiated
    Friend erythroleukeamia and human myeloid HL60 cells by low intensity laser irradiation.
    Laser Therapy 1994; 6: 189﷓194.

    7. Hardy LB, Hardy FS, Fine S, Sokal J. Effect of ruby laser radiation on mouse fibroblast
    culture (abstract). Fed Proc 1967; 26: 668.

    8. Abergel RP, Dwyer RM, Meeker CA, Lask G, Kelly AP, Uitto J. Laser treatment of
    keloids: a clinical trial and an in vitro study with Nd:YAG laser. Lasers Surg Med 1984;
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    9. Shields TD, O'Kane S, Leckey D, Allen JM, Gilmore WS. The effect of laser irradiation
    upon human mononuelear leukoeytes in vitro (abstract). Lasers Surg Med 1992;
    4(Suppl): 11.

    10. Agaiby A, Dyson M. The efiect of fight on t﷓lymphocytes proliferation in vitro (abstract).
    Lasers Surg Med 1992: 4(Suppl): 12.

    11. van Breugel HHFI, Sodaar P, Bar PR. Low energy He﷓Ne laser irradiation effects on
    proliferation and laminin production of rat schwann cells in vitro (abstract). Lasers Surg
    Med 1991; 3(Suppl); 10.

    12. Mulligan K, Woolery S, Anders JJ. The effect of low energy He﷓Ne laser irradiation on
    neurite elongation in vitro (abstract). Lasers Surg Med 1991; 3(Suppl): 10.

    13. Steinlechner CWB, Dyson M. The effects of low level laser therapy on the proliferation
    of keratinocytes in vitro (abstract). Lasers Surg Med 1990; 2(Suppl): 12.

    14. Young S, Bolton P, Dyson M, Harvey W, Diamantopoulos C. Macrophage
    responsiveness to light therapy. Lasers Surg Med 1989; 9: 497﷓505.

    15. Manteifel V, Karu T. Ultrastructural changes in human lymphocytes under He﷓Ne laser
    radiation (abstract). Lasers Surg Med 1992; 4(Suppl): 10.

    16. Sato 11, Landthaler M, Haina D, Schill WB. The effects of laser light on sperm motility
    and velocity in vitro. Andrologia 1984; 16: 23.

    17. Trelles MA, Mayayo E, Miro L, Rigau J, Baudin G. Are mast cells implicated in the
    interaction of low﷓power﷓laser and tissue? American Society for Laser Medicine and
    Surgery Abstracts. Lasers Surg Med 1988; 8: 174.

    18. Yu W, Nairn JO, Lanzafame RJ. The effects of photo irradiation on the secretion of TGF
    and PDGF from fibroblasts in vitro. LasersSurg Med 1994; Suppl 6: 8.

    19. Passarella S, Casamassima E, Molinari S, et al. Increase of proton electrochemical
    potential and ATP synthesis in rat liver mitochondria irradiated in vitro by helium﷓neon
    laser. FEBS Lett 1984; 175: 95.

    20. Kubasova T, Kovacs L, Somosy Z, Unk P, Kokai A. Biological effect of He﷓Ne laser:
    investigations of functional and inicromorphological alterations of cell membranes, in
    vitro. Lasers Surg Med 1984; 4: 3 8 1.

    21. Passarella S, Casamassirna E, Quagliariello E, Caretto G, Jirillo E. Quantitative analysis
    of lymphocyte﷓Salmonega interaction and effect of lymphocyte irradiation by helium﷓neon
    laser. Biochem Biophys Res Comm 1985; 130: 546.

    22 Fork RL. Laser stimulation of nerve cells in aplysia. Science 1971; 171: 907﷓908.

    23. Baxter GD, Walsh DM, Allen JM, Lowe AS, Bell AJ. Effects of low intensity infrared
    laser irradiation upon conduction in the human median nerve in vivo. Exp Physiol 1994;
    79(2): 227﷓234.

    24. Lowe AS, Baxter GD, Walsh DM, Allen JM. Effect of low intensity laser (830nm)
    irradiation on skin temperature and antidromic conduction latencies in the human median
    nerve: relevance of radiant exposure. Lasers Surg Med 1994; 14(l): 40﷓46.

    25. Karti TI, Ryabykh TP, Fedoseyeva GE, Puchkova NI. Helium﷓Neon laser﷓induced
    respiratory burst of phagocytic cells. Lasers Surg Med 1989; 9: 585﷓588.

    26. Agaiby A, Dyson M. The effect of light on t﷓lymphocytes proliferation in vitro (abstract).
    Lasers Surg Med 1992; 4(Suppl): 12.

    27. Mester R, Toth N, Mester A. The biostimulative effect of laser beam. Laser Basic
    Biomedical Research 1982; 22: 4.

    28. Mester E, Jaszsagi﷓Nagi E. The effect of laser radiation on wound healing and collagen
    synthesis. Studia Biophysica 1973; 35: 227﷓230.

    29 Abergel R, Meeker C, Lam T, Dwyer R, Lesavoy M, Uitto J. Control of connective
    tissue metabolism by lasers. Recent developments and future prospects. .J Am Acad
    Dermatology 1984; 11: 1142﷓1150.

    30. Saperia D, Glassbery E, Lyons R, Abergel P, Baneux P, Castel J, Dwyer R' Uitto J.
    Demonstration of elevated type 1 and type ill procollagen mRNA levels in cutaneous
    wounds treated with hellum﷓neon laser. Blochem Biophys Res Comm 1986; 138: 1123 ﷓

    3.1. Massey V. Activation of molecular oxygen by flavins and flavoproteins. J Biol Chem
    1994; 269: 22459﷓22462.

    32. Schreck R, Rieber P, Baeuerle PA. Reactive oxygen intermediates as widely used
    messengers in the activation of the NfkB transcription factor and HIV﷓1. EMBO J1991;
    10: 2247﷓2258.

    33. Stein B, Argel P, van Dam H. Ultraviolet﷓radiation﷓ induced c﷓jun gene transcription:
    Two AP﷓1 like binding sites mediate the response. Photochem Photobiol 1992; 55: 409

    34. Good PA, Claxson A, Morris CJ, Blake DR. A model for Desferrioxamine﷓induced
    retinopathy using the albino rat. Ophthalmologica 1990; 201: 32﷓36.

    35. Logan ID, McKenna PG, Barrett YA. An investigation of the cytotoxic and mutagenic
    potential of low intensity laser irradiation in Friend erythroleurnaemia cells. Mutation Res
    1995; 347: 67﷓71.

    36. Barbe MF, Tytell M, Gower DJ, Welch WJ, Hyperthermia protects against light damage
    in the rat retina. Science 1988; 241: 1817﷓1820.

    37. Keyse SM, Tyrrell RM. Heme oxygenase is the major 32 KDa stress protein induced in
    human skin fibroblasts by UVA radiation, hydrogen peroxide and sodium assenite. Proc
    Natl Acad Sci (USA) 1989; 86: 99﷓103.

    38. Vile GF, Basu﷓Modak S, Waltner C, Tyrrell RM. Heme oxygenase 1 mediates an
    adaptive response to oxidative stress in human skin fibroblasts. Proc Natl Acad Sci
    (USA) 1994; 91: 2607﷓2610.

    39. Wieman TJ, Fingar VH, Photodynamic therapy. Surg Clin North Am 1992; 72: 609

    40. Self CH, Thompson S. Light activatable antibodies: models for remotely activatable
    proteins. Nature (Med) 1996: 2: 817﷓820.

    Document 2:

    Phototherapy: a guide to the pitfalls of terminology

    Non-medical systems made for beauty and other peripheral uses can suffer from ‘specmanship’ that owes more to the marketing department than to the actuality of the device. This short guide is designed to help you make more sense of the advertising blurb.

    Light is that part of electromagnetic radiation that the human eye can see-. It lies between 400 and 700 nanometers. All the units for measuring and defining light are based on the Candela, which is the unit defining the luminous intensity from a small source, in a particular direction. The Candela was originally based on the light emission from a flame (originally a tallow candle hence the name)

    The graph below shows the relative response of the eye the scotopic curve is at night and the photopic is during the day. It is based on a constant power from the light source. If we consider the Photopic curve which has its peak at 555nm (yellow green) the eye sees 510nm (blue green) and 610nm (orange red) as being half as bright as the 555nm reference. So to achieve the same brightness as 555nm the 510nm and 610nm would require twice as much actual power.

    Similarly, if you had a 660nm source and a 630nm source of identical power the 630nm would look much brighter than the 660nm.

    It is obvious from the above that luminosity based data, while they are perfect for a lighting engineer and a marketing man seeking to make their phototherapy unit appear more powerful, are totally unsuitable for defining power for treatment purposes.

    The most common source of light for home use phototherapy units is the Light Emitting Diode (LED) An LED is a semiconductor device encapsulated in a plastic or epoxy module which, on activation by a current passing through it, produces photons (light). The material and structure of the semiconductor determines the wavelength (colour) produced. These devices are long lasting, very efficient and produce little heat. LEDs come in all shapes and sizes and their output is specified in Candela as they are designed for illumination. The light output is divergent varying from about 6o to 120o As you will see later, the type used for phototherapy are generally the narrow angle types.

    In passing, I should mention Infrared emitters (usually 800nm upwards) which can be packaged in a similar manor to the LED or in metal cans with windows these have similar characteristics to LEDs but the output is invisible.

    The only true measurement of power is the Watt, or in the case of phototherapy the milliwatt (mW) so the power output of LEDs have to be measured by the phototherapy equipment manufacturers. The measurement of power alone is meaningless unless we describe the area that the light is covering.
    For instance a Light Emitting Diode (LED) shining on the skin will irradiate an area that varies with the distance that it is above the surface (as mentioned above all LED emitters are divergent) The further away the bigger the area so the area treated increases. The LED however is giving a constant power so the power per unit area is decreasing with distance.
    It follows that not only does the power have to be specified but the area being irradiated has to be specified and so we get to mw per square cm (mW/cm2) This is usually referred to as the Intensity. Ideally, a distance from the surface should be specified for the Intensity. This particularly applies to a single LED as the intensity at the tip when touching the skin is much higher than from 1cm away.

    The other important factor in any treatment is dosage. You would not take pills without knowing how many or how often to take them. In light therapy the accepted measure for dosage is the Joule which in Physics is the quantity of energy.

    1 Joule is 1 Watt for 1 Second or 1mW for 1000 Seconds

    It is obvious from the above that a Joule on its own does not tell the whole story as 1W for one second will have a different effect than 1mW for 1000 second.

    So to get a realistic view of the dosage it is no good just specifying Joules without specifying the Intensity (mW/cm2) or the length of time for 1 Joule.

    The other factor that has an effect on dosage is modulation. Modulation in the digital era is turning the emitting device on and off at various rates. If the light is modulated at 1 second on and 1 second off on a regular basis (1:1 mark space ratio) it is obvious that the Intensity is only on for half the time so the effective intensity is halved and so the dose is halved. That is only part of the story because it may be that the light is on for 1second and off for 10seconds (1:10 mark space ratio) so the effective intensity is one tenth and so is the dose.”But I would see that you all say.” Yes you would but if it was switching on and off at more than 25 times a second (25Hz) you would not see it. Therapy systems can have modulation up to 100,000 times a second (100KHz) particularly Laser systems. High frequency modulation rates in tissue do not have much support but there is considerable evidence that frequencies around 15Hz stimulate one of the bodies ‘messenger’ routes the Calcium channel.

    The interest in light therapy stems from the work of the late Prof. Endre Mester a Hungarian surgeon at Semmelwei’s Medical University, Budapest in the early 70s. Whilst studying the effects of low level Helium Neon Laser (638nm) light on mice he observed a biostimulatory effect. Encouraged by the idea of immune system biostimulation via light stimuli, Mester and his co-workers studied the light effect on various biological systems.

    For the next 30 years work with light therapy has continued and it has been demonstrated that it stimulates fibroblast proliferation and collagen production by fibroblasts, due to the induction of growth factor release from macrophages and other cells following light adsorption.

    It is obvious from the above that its main thrust has been in the field of tissue repair.

    Other areas have been researched, particularly, the treatment of Acne Vulgaris. It was discovered in the 70s by some scientists trying to find a way of counting the number of bugs on surface tissue that, the bugs fluoresced when irradiated with 420nm light. The reason for this reaction was the ‘bugs’ use of a porphyrin as part of its respiratory chain. The bug does not like too much oxygen and the fluorescing was the porphyrin producing it, so the bugs died.

    Various other wavelengths have this same effect on the porphyrin but to greater and lesser degrees.
    420nm is probably the most effective on the surface but unfortunately the adsorption of light into the skin is not linear. The adsorption of light at 420 nm (close to UV) is much less than the longer wavelengths like the red end of the spectrum. This is easily demonstrated in life. The reason that we get sunburnt is that all the energy at the UV end of the spectrum is adsorbed in the first fractions of millimeters of the skin so all the energy dissipating in that very thin layer burns the skin. At the infared end the light penetrates much further and gets adsorbed by the water and warms the tissue.

    So the argument is if 660nm also kills the bug and penetrates much further, reaching the bugs trapped in the sebaceous ducts which is the most effective? The red also has an anti inflammatory property calming down the infected area. I think that the argument as to the difference between 620nm – 680nm is invalid because the body is fairly easy to stimulate and on the healing side it is probably the same mechanisms that are stimulated by other electromedical products like ultrasound, galvanic currents or whatever is the flavour of the month.

    A word about Acne Rosacea: As far as I am aware there has not been any controlled clinical trials done using red light with rosacea. However, some people have been using all red versions of the DermaLux with some success and there is one person using a wound healing red LED cluster on the condition. There are various schools of thought on the causes of Rosacea one of which is that it is the same bug (p.acnes) that causes Acne Vulgaris but working a different way. If this is the case then red light should have a beneficial effect because it can kill the ‘bug’. If it is not the case then the anti-inflammatory properties of red light should ‘calm down’ the enlarged capillaries whatever the cause.
    35 year-old male
    Erythmatotelangiectatic rosacea & Ocular
    20 + laser treatments.
    Toleraine Soothing Light Facial Fluid for moisturizer. I don't use a special cleanser. Clonidine daily; klonopin sometimes.
    BEST and CURRENT TREATMENT I use: Low-Level Red Light Therapy LED array.
    Please feel free to PM me with your low-level red light therapy (LLRLT) questions. I'm happy to help if I can.

  • #2
    Hello David

    Thanks for that. Very interesting and Adrian is always willing to help anybody who contacts him regarding light therapy.

    Must admit not sure that the "acne bug" is implicated with rosacea myself and I think that it is felt that it is more that red light demonstrates an anti-inflammatory effect rather than killing off the Propionibacterium acnes (P.acnes).

    The original acne trials were carried out with Dermalux red / blue fluorescent tube lamps and I actually bought one of the prototype lamps from them to try before the main retail units were released to the public. I know Tony Chu did try and get a rosacea clinical trial started with all red Dermalux units but it never got off the ground due to lack of funding, which was a shame. The trial that is suppose to start this year on rosacea is using an LED unit and involves volunteers visiting Hammersmith twice a week for 15 minute sessions with this unit. When I get a chance I will see if Tony will reveal to me more details of the trial so I can post something on the Forum. I know whenever I saw Tony and we talked about red light he always felt that LED would be more effective for rosacea but I always argued that infra red worked for me.




    • #3
      Yeah, I know that aestheticians and laser doctors are using that "Gentlewaves" unit for in-office sessions. Adrian mentioned that light circa 600-660nm is probably helpful to some degree for collagen production and its anti-inflammatory effects. The Gentlewaves is an LED array with 2,000 LEDs, I think, at 590nm (yellow light). My array is, from what I've read, the same thing as the Gentlewaves, but using red light rather than yellow, and, of course, I don't have to make mine look pretty. ;)

      I find it interesting that this machine is being used for in-office treatments. I think it's something like 30 minutes 8 times over a period of a couple of months. If you read the results of these treatments, they're fairly underwhelming in their efficacy. I would bet that if the Gentlewaves were used like you one uses the home phototherapy units--everyday for 15 minutes--that the yellow light would prove to be roughly analagous to red light units. Don't know on this one, though.

      I've started putting my face right at the edge of that half-moon curve that's pictured in my other thread; I used to sit about a foot or 16 inches away. But the LEDs are densely arrayed and the diffusion angle of 30 degrees gives me total coverage on my skin even at this close distance. I can actually feel the light as it's working on my skin--it leaves my skin feeling mildly "tingly" and "tight" and not prone to flushing.

      Given how my face has responded since I've been using my array more each day and using it at a shorter distance, I'm expecting to be doing a hell of a lot better in 6 months. If my progress continues along this trajectory, I should really only need some touch-up IPL to get some of the permanent redness/telangiectasia and the flushing will be taken care of the red light. Given the light penetractes ~ 8mm into the skin, that should affect most of the vasculature that's there, I'd think. And there does seem to be a direct correlation to how many LEDs you use, how long your exposure time is, and the level of flushing prevention and standing redness reduction that you get.

      I'm becoming more and more convinced that if people would start using a heavy-duty LED array early on, laser treatments might not be necessary, or, you'd only need a couple if you had some permanently dilated vessels to take care of. I just wish we could get more people trying this modality out and test it with some other subtypes. It's a one-time cost with LEDs, no drugs are involved--what's not to like?

      The only thing I'm concerned about now is, if I did decide to go on low-dose accutane to whiten up my eyes some, if I'd be able to use the light therapy or not. I'm thinking I could, as it's not UV, but, I'd need to look into this more.

      35 year-old male
      Erythmatotelangiectatic rosacea & Ocular
      20 + laser treatments.
      Toleraine Soothing Light Facial Fluid for moisturizer. I don't use a special cleanser. Clonidine daily; klonopin sometimes.
      BEST and CURRENT TREATMENT I use: Low-Level Red Light Therapy LED array.
      Please feel free to PM me with your low-level red light therapy (LLRLT) questions. I'm happy to help if I can.