Revision 638000584 of "Zerona" on enwiki

'''Zerona''' is a low-level laser device developed by Erchonia Corp. for non-invasive body slimming of the waist, hips, and thighs. It has been shown to disrupt [[adipocyte]], or fat cell, membranes causing the release of stored [[lipids]] and fatty material, in turn, promoting adipocyte collapse. The device was first introduced to the market in 2008 as an [[off-label use]] device for slimming, but later was cleared as a [[Medical device#Class II: General controls with special controls|Class II medical device]] by the [[Food and Drug Administration]] in 2010 indicated for use as a non-invasive dermatological aesthetic treatment for the reduction of circumference of hips, waist, and thighs. Zerona was the first aesthetic device to receive this indication by the FDA following the completion of a [[placebo-controlled]], randomized, [[double-blind]], multi-centered [[clinical trial]].  Clinical study participants randomly assigned to receive “active” or real treatment displayed an average loss of {{Convert|3.5|in|cm|abbr=on}} across the waist, hips, and thighs in two weeks.  This was compared to study participants randomly assigned to the “sham” or [[placebo]] group who exhibited a reduction of {{Convert|0.68|in|cm|abbr=on}} after two weeks.<ref name=pmid20014253>{{cite journal |pmid=20014253 |first1=Robert F. |last1=Jackson |first2=Doug D. |last2=Dedo |first3=Greg C. |last3=Roche |first4=David I. |last4=Turok |first5=Ryan J. |last5=Maloney |year=2009 |url=http://www.erchonia.com/files/uploads/1/file/Jackson_3LT%20Non-Invasive%20Approach%20for%20Body%20Contouring%20Randomized%20Controlled%20Study_LISM_12_09.pdf |title=Low-Level Laser Therapy as a Non-Invasive Approach for Body Contouring: A Randomized, Controlled Study |journal=Lasers in Surgery and Medicine |volume=41 |issue=10 |pages=799–809 |doi=10.1002/lsm.20855}}</ref>

== Device ==
Zerona is a Class II low-level laser medical device. [[Low level laser therapy]] (LLLT) represents a division of [[photomedicine]] utilizing defined parameters of laser light for the treatment of a specific medical ailment.  The efficacy and safety of this subtle therapeutic approach is dependent on the [[wavelength]], [[Absorbed dose|dosage]], pulsation, and [[Intensity (physics)|intensity]] being applied. For instance, laser therapy has exhibited a biphasic dose response revealing that too much applied energy could hamper or prevent the desired clinical outcome from transpiring.<ref name=pmc2790317>{{cite journal |pages=358–83 |doi=10.2203/dose-response.09-027.Hamblin |pmc=2790317 |title=Biphasic Dose Response in Low Level Lightherapy |year=2009 |last1=Hamblin |first1=Michael R. |last2=Carroll |first2=James D. |last3=Chen |first3=Aaron C.-H. |last4=Huang |first4=Ying-Ying |journal=Dose-Response |volume=7 |issue=4 |pmid=20011653}}</ref> The development of Zerona required significant clinical investigation to determine the ideal output parameters to ensure optimal efficacy and safety.  Studies evaluated Zerona’s interaction with individual to several million fat cells in order to determine the precise slimming setting. Zerona is a [[monochromatic]] semiconductor diode laser that emits 5 independent 635&nbsp;nm divergent beams.

== History ==
Initial trials for Zerona began back in late 1998 in Cali, Colombia, by Dr. Rodrigo Neira and his wife Dr. Clara Neira at the [[Universidad Nacional de Colombia]].  They first applied the device as an adjunct to [[liposuction]] to reduce pain and inflammation commonly experienced after the invasive surgical procedure. In hopes of achieving better pain reduction they began applying LLLT prior to aspiration and surprisingly found that the subcutaneous fat appeared softer and easier to extract. Fascinated with this finding, the Neiras started performing histological investigations to determine why laser had its biological influence on fat tissue. Using [[scanning electron microscopy]] and [[transmission electron microscopy]], they observed the formation of transitory pores or openings in the protective membranes of adipocytes which enabled stored intracellular lipids to be released from enlarged fat cells. The term emulsification was applied to describe the laser-induced liberation of the stored lipids. The initial findings were later confirmed by three individual sites including the [[University of Singapore]], [[University of Mexico]], and the [[University of Chicago]]. These findings prompted the development of a device, the EML Laser, to assist in the surgical procedure, liposuction, with the intent to emulsify the fat thereby softening the area prior to aspiration.  A placebo-controlled, randomized, double-blind, multi-centered clinical study was performed to evaluate the clinical utility of this application as an adjunct to liposuction and found that laser therapy decreased operating room times, increased the volume of fat extracted, less force was required by the physician to breakup fat, and the recovery for patients was significantly improved.<ref name=pmc2790317/> Based on the findings of this study the FDA cleared the EML device in 2001 for use as an adjunctive therapy to liposuction.<ref>{{cite web|last=Karu|first=Tiina I.|title=Critical Review Multiple Roles of Cytochrome c Oxidase in Mammalian Cells Under Action of Red and IR-A Radiation|url=http://www.isan.troitsk.ru/dls/publ3/344.pdf|work=isan.troitsk.ru|publisher=nstitute of Laser and Information Technologies, Russian Academy of Sciences, Troitsk, Moscow Region, Russian Federation|accessdate=17 February 2014}}</ref>

== Mechanism of action ==
The exact mechanism of action for Zerona is not fully understood. As a low-level laser device the theory of action is defined as bioorganic [[photochemistry]], a discipline that explores the interaction between [[photons]] and biochemical pathways within cells.  Like many other science principles, bioorganic photochemistry is defined by laws, and the first law of [[photochemistry]] states that a photoabsorbing structure must be present to yield a clinical outcome. [[Cytochrome c oxidase]], a terminal enzyme found within the [[electron transport chain]] of the [[mitochondria]], has been reported by Karu et al. (2010) to function as a photoabsorbing complex within eukaryotic cells ([[eukaryote]]).<ref>{{cite web|url=http://www.accessdata.fda.gov/cdrh_docs/pdf7/K072206.pdf|publisher=Erchonia Medical Inc.|title=Erchonia EML Laser|accessdate=17 February 2014|date=April 28, 2008}}</ref> This enzyme is responsible for facilitating the transport of electrons across the [[inner mitochondrial membrane]] to reduce oxygen and generate a proton [[electrochemical gradient]]. Cytochrome c oxidase serves an important role in the metabolic process known as [[oxidative phosphorylation]], which is the production of the high energy molecule [[adenosine triphosphate]] (ATP).<ref>{{cite book |first1=Reginald |last1=Garrett |first2=Charles M. |last2=Grisham |chapter=Electron Transport and Oxidative Phosphorylation |title=Biochemistry |edition=3rd |year=2005 |pages=640–73 |isbn=978-0-534-49033-1}}</ref><ref name=pmid6479342>{{cite journal |pages=95–9 |doi=10.1016/0014-5793(84)80577-3 |title=Increase of proton electrochemical potential and ATP synthesis in rat liver mitochondria irradiated in vitro by helium-neon laser |year=1984 |last1=Passarella |first1=S. |last2=Casamassima |first2=E. |last3=Molinari |first3=S. |last4=Pastore |first4=D. |last5=Quagliariello |first5=E. |last6=Catalano |first6=I.M. |last7=Cingolani |first7=A. |journal=FEBS Letters |volume=175 |pmid=6479342 |issue=1}}</ref><ref name=pmid2476986>{{cite journal |pages=1428–34 |doi=10.1016/0006-291X(89)91138-8 |title=Increase in RNA and protein synthesis by mitochondria irradiated with Helium-Neon laser |year=1989 |last1=Greco |first1=M |journal=Biochemical and Biophysical Research Communications |volume=163 |issue=3 |pmid=2476986 |last2=Guida |first2=G |last3=Perlino |first3=E |last4=Marra |first4=E |last5=Quagliariello |first5=E}}</ref> Stimulation of cytochrome c oxidase with a well-defined monochromatic low-level laser instrument modulates cellular metabolism and secondary biological cascades which can affect cell function and behavior giving rise to the positive clinical outcomes that have been reported.<ref name=pmc2790317/> Subsequent to laser stimulation the mitochondrial membrane potential and proton gradient increases, prompting changes in mitochondria optical properties and increasing the rate of ADP/ATP exchange.<ref>{{cite journal |pages=355–61 |doi=10.1089/pho.2005.23.355 |title=Exact Action Spectra for Cellular Responses Relevant to Phototherapy |year=2005 |last1=Karu |first1=T.I. |last2=Kolyakov |first2=S.F. |journal=Photomedicine and Laser Surgery |volume=23 |issue=4 |pmid=16144476}}</ref><ref>{{cite book |first1=Aleksandr Nikolaevich |last1=Terenin |year=1954 |title=Photochemistry of dyes and related organic compounds |oclc=32060439}}{{Page needed|date=July 2011}}</ref><ref>{{cite journal |pages=265–322 |doi=10.1016/0304-4173(85)90014-X |title=Electron transfers in chemistry and biology |year=1985 |last1=Marcus |first1=R |last2=Sutin |first2=Norman |journal=Biochimica et Biophysica Acta |volume=811 |issue=3}}</ref> It is suggested that laser irradiation increases the rate at which cytochrome c oxidase transfers electrons from cytochrome c to dioxygen.<ref name="pmid6479342" /><ref name="pmid2476986" /><ref>{{cite journal |pmid=10379650 |year=1998 |last1=Konev |first1=SV |last2=Beljanovich |first2=LM |last3=Rudenok |first3=AN |title=Photoreactivation of the cytochrome oxidase complex with cyanide: the reaction of heme a3 photoreduction |volume=12 |issue=5 |pages=743–54 |journal=Membrane & cell biology}}</ref> Moreover, it has been proposed that laser irradiation reduces the catalytic center of cytochrome c oxidase, making more electrons available for the reduction of dioxygen.<ref>{{cite journal |pages=324–36 |doi=10.1016/j.jinorgbio.2004.10.011 |title=Cytochrome  oxidase, ligands and electrons |year=2005 |last1=Brunori |first1=M |last2=Giuffre |first2=A |last3=Sarti |first3=P |journal=Journal of Inorganic Biochemistry |volume=99 |pmid=15598510 |issue=1}}</ref><ref>{{cite journal |pages=46–54 |doi=10.1002/lsm.20589 |title=Low-energy laser irradiation increases endothelial cell proliferation, migration, and eNOS gene expression possibly via PI3K signal pathway |year=2008 |last1=Chen |first1=Chung-Huang |last2=Hung |first2=Huey-Shan |last3=Hsu |first3=Shan-hui |journal=Lasers in Surgery and Medicine |volume=40 |pmid=18220263 |issue=1}}</ref><ref>{{cite journal |pmid=1053185 |year=1975 |last1=Mester |first1=E |last2=Korényi-Both |first2=A |last3=Spiry |first3=T |last4=Tisza |first4=S |title=The effect of laser irradiation on the regeneration of muscle fibers (preliminary report) |volume=8 |issue=4 |pages=258–62 |journal=Zeitschrift fur experimentelle Chirurgie}}</ref> In turn, an increase in electron and proton transfer increases the quantity of ATP that is synthesized which can directly affect numerous intracellular proteins.

The [[Downregulation and upregulation|upregulation]] of ATP induced by laser therapy is also responsible for the increased production of a natural byproduct known as [[reactive oxygen species]] (ROS).<ref name=pmid16248161>{{cite journal |pmid=16248161 |year=2005 |last1=Klebanov |first1=GI |last2=Chichuk |first2=TV |last3=Osipov |first3=AN |last4=Vladimirov |first4=IuA |script-title=ru:Роль продуктов перекисного окисления липидов в механизме действия лазерного облучения на лейкоциты крови человека |language=Russian |trans_title=The role of lipid peroxidation products in the effect of He-Ne laser on human blood leukocytes |volume=50 |issue=5 |pages=862–6 |journal=Biofizika |url=http://elibrary.ru/item.asp?id=9144231}}</ref><ref>{{cite journal |pmid=15129632 |year=2004 |last1=Vladimirov |first1=IuA |last2=Klebanov |first2=GI |last3=Borisenko |first3=GG |last4=Osipov |first4=AN |script-title=ru:Молекулярно-клеточные механизмы действия низкоинтенсивного лазерного излучения |language=Russian |trans_title=Molecular and cellular mechanisms of the low intensity laser radiation effect |volume=49 |issue=2 |pages=339–50 |journal=Biofizika}}</ref><ref name=pmid8570716>{{cite journal |pages=580–7 |doi=10.1111/j.1751-1097.1995.tb02388.x |title=Photodynamically generated 3-β-hydroxy-5α-cholest-6-ene-5- hydroperoxide: toxic reactivity in membranes and susceptibility to enzymatic detoxification |year=1995 |last1=Geiger |first1=Peter G. |last2=Korytowski |first2=Witold |last3=Girotti |first3=Albert W. |journal=Photochemistry and Photobiology |volume=62 |issue=3 |pmid=8570716}}</ref> This highly reactive oxygen molecule participates in numerous pathways within a cell. However, as the concentration of ROS elevates a process known as [[lipid peroxidation]] can occur where ROS reacts with lipids found within cell membranes temporarily damaging them.<ref name=pmid16248161/><ref name=pmid8570716/> It has been hypothesized that Zerona, as a low-level laser device, modulates cell metabolism resulting in a transient rise of ROS which temporarily degrades the membrane creating transitory pores or openings.

== Clinical trial ==
In 2008, a [[clinical trial]] to investigate the efficacy of Zerona was conducted. The trial enrolled 67 subjects, 35 of which were randomly assigned to receive active treatment with 32 randomly assigned to the control group. Patients received treatment every-other day for two weeks receiving a total of 6 treatments. Patients' waist, hips, and thighs were treated concurrently for 40 total minutes each treatment, including 20 minutes of anterior or front treatment and 20 minutes of posterior or back treatment. Measurements were taken at baseline, weeks one and two, and a two-week post-procedure follow-up measurement. After two weeks the active treatment group averaged a cumulative reduction of 3.54&nbsp;inches compared to the control group which averaged a cumulative reduction of just 0.68&nbsp;inches. At the two-week post-procedure follow-up, active group participants did not exhibit a significant gain in their measurements. No adverse events or side-effects were reported during the clinical trial.<ref name=pmid20014253/>

== Ongoing research ==
{{Off-topic|date=July 2014}}
The adipocyte or fat cell is described as an endocrine organ cell responsible for the synthesis of bioactive peptides which participate in autocrine, paracrine, and endocrine pathways.  The physical adaptability of the adipocyte is extraordinary, enabling it to expand nearly 1,000 fold in volume and 10 fold in diameter in order to store excessive fuel as triglycerides.<ref>{{cite journal |pmid=9843879 |year=1998 |last1=Marques |first1=BG |last2=Hausman |first2=DB |last3=Martin |first3=RJ |title=Association of fat cell size and paracrine growth factors in development of hyperplastic obesity |volume=275 |issue=6 Pt 2 |pages=R1898–908 |journal=The American journal of physiology}}</ref> During periods of limited food intake fat tissue rapidly transitions to an abundant provider of non-esterfied free fatty acids which upon their release into the circulatory system can undergo beta-oxidation to supply energy.  The storage capacity of adipocytes remains a key component of its function but has been shown to modulate the synthesis of bioactive peptides, specifically adipose-derived hormones.<ref name="pmid19948207"/><ref name="pmid18334583"/>

Studies have revealed a correlation between deregulated adipose tissue function and excessive fat mass having deleterious effects on the endocrine and immune systems.<ref name=pmid19948207>{{cite journal |pages=69–78 |doi=10.1016/j.mce.2009.11.011 |title=The autocrine and paracrine roles of adipokines |year=2010 |last1=Karastergiou |first1=Kalypso |last2=Mohamed-Ali |first2=Vidya |journal=Molecular and Cellular Endocrinology |volume=318 |pmid=19948207 |issue=1–2}}</ref><ref name=pmid18334583>{{cite journal |pages=2255–62 |doi=10.1210/jc.2007-2188 |title=Adipokine Protein Expression Pattern in Growth Hormone Deficiency Predisposes to the Increased Fat Cell Size and the Whole Body Metabolic Derangements |year=2008 |last1=Ukropec |first1=J. |last2=Penesova |first2=A. |last3=Skopkova |first3=M. |last4=Pura |first4=M. |last5=Vlcek |first5=M. |last6=Radikova |first6=Z. |last7=Imrich |first7=R. |last8=Ukropcova |first8=B. |last9=Tajtakova |first9=M. |last10=Koška |first10=Juraj |last11=Zórad |first11=Štefan |last12=Belan |first12=Vítazoslav |last13=Vaňuga |first13=Peter |last14=Payer |first14=Juraj |last15=Eckel |first15=Juergen |last16=Klimeš |first16=Iwar |last17=Gašperíková |first17=Daniela |journal=Journal of Clinical Endocrinology & Metabolism |volume=93 |issue=6|display-authors=8 }}</ref><ref name=pmid18037457>{{cite journal |pages=206–18 |doi=10.1016/j.physbeh.2007.10.010 |title=The role of adipose tissue dysfunction in the pathogenesis of obesity-related insulin resistance |year=2008 |last1=Goossens |first1=Gijs H. |journal=Physiology & Behavior |volume=94 |issue=2}}</ref><ref name=pmid20107860>{{cite journal |pages=1277–92 |doi=10.1007/s00018-010-0263-4 |title=Adipocyte extracellular matrix composition, dynamics and role in obesity |year=2010 |last1=Mariman |first1=Edwin C. M. |last2=Wang |first2=Ping |journal=Cellular and Molecular Life Sciences |volume=67 |issue=8 |pmid=20107860 |pmc=2839497}}</ref><ref name=pmid19192421>{{cite journal |pages=26–32 |doi=10.1007/s11892-009-0006-9 |title=Impact of increased adipose tissue mass on inflammation, insulin resistance, and dyslipidemia |year=2009 |last1=Gutierrez |first1=Dario A. |last2=Puglisi |first2=Michael J. |last3=Hasty |first3=Alyssa H. |journal=Current Diabetes Reports |volume=9 |pmid=19192421 |issue=1 |pmc=2735041}}</ref> Excessive body fat results in adipocyte hypertrophy or acquired [[lipodystrophy]].  Significant adipocyte expansion is believed to interrupt the interplay of transcriptional factors and other intracellular components yielding pathological consequences.<ref name=pmid19948207/><ref name=pmid18334583/><ref name=pmid18037457/><ref name=pmid20107860/><ref name=pmid19192421/>

Adipocyte [[hypertrophy]] has been shown to directly disrupt [[angiogenesis]], [[adipogenesis]], extracellular matrix dissolution and reformation, lipogenesis, growth factor production, glucose metabolism, lipid metabolism, enzyme production, immune response, and hormone production.<ref name=pmid17021375>{{cite journal |pages=242S–9S |doi=10.1038/oby.2006.317 |title=Adipose Tissue as an Endocrine Organ |year=2006 |last1=Ahima |first1=Rexford S. |journal=Obesity |volume=14 |pmid=17021375}}</ref> Furthermore, studies have illustrated an alteration in [[gene expression]] recording an upregulation in [[proinflammatory]] factors including classic [[cytokines]] and [[complement factors]].<ref name=pmid17021375/><ref name=pmid18473870>{{cite journal |pmid=18473870 |year=2008 |last1=Heilbronn |first1=LK |last2=Campbell |first2=LV |title=Adipose tissue macrophages, low grade inflammation and insulin resistance in human obesity |volume=14 |issue=12 |pages=1225–30 |journal=Current pharmaceutical design |doi=10.2174/138161208784246153}}</ref><ref name=pmid17505154>{{cite journal |pmid=17505154 |year=2007 |last1=Bahceci |first1=M |last2=Gokalp |first2=D |last3=Bahceci |first3=S |last4=Tuzcu |first4=A |last5=Atmaca |first5=S |last6=Arikan |first6=S |title=The correlation between adiposity and adiponectin, tumor necrosis factor alpha, interleukin-6 and high sensitivity C-reactive protein levels. Is adipocyte size associated with inflammation in adults? |volume=30 |issue=3 |pages=210–4 |journal=Journal of endocrinological investigation}}</ref> A rise in pro-inflammatory [[adipokines]] coupled with cytokine production may promote the onset of metabolic disorders like [[atherosclerosis]].<ref name=pmid19723556>{{cite journal |pmid=19723556 |year=2010 |last1=Galic |first1=S|last2=Oakhill |first2=JS |title=Adipose tissue as an endocrine organ |volume=316 |issue=2 |pages=129–39 |journal=Molecule Cell Endocrinology |doi=10.1016/j.mce.2009.0.018|doi_brokendate=2014-03-23 }}
</ref>

Positively correlated with increased adipose tissue size are pro-inflammatory factors: [[tumor necrosis factor-α]] (TNF-α), [[interleukin-6]] (IL-6), and [[C-reactive protein]]. Participating in [[paracrine]] and [[autocrine]] signaling, adipocyte impairment may account for metabolic dysfunction as adipose tissue communicates with multiple body systems including nervous, immune, skeletal, cardiovascular, and gastrointestinal.<ref name=pmid17021375/> Positive caloric intake can result in adipocyte [[hypertrophy]] modulating adipose tissue function and increasing a patient’s risk of developing serious metabolic disorders.

Directly associated with enlarged fat mass is the chronic disease [[diabetes]]. [[Adiponectin]], a hormone solely produced by adipocytes, has demonstrated insulin sensitive effects promoting anti-diabetic characteristics.<ref name=pmid16642957>{{cite journal |pages=9S–15S |doi=10.1038/oby.2006.276 |title=Metabolic Actions of Adipocyte Hormones: Focus on Adiponectin |year=2006 |last1=Ahima |first1=Rexford S. |journal=Obesity |volume=14 |issue=2S}}</ref> As a plasma protein, adiponectin has been reported to regulate insulin sensitivity via the activation of AMPK and reduction of mTOR/S6 kinase activity consequentially reducing insulin receptor substrate 1 inhibitory serine phosphorylation in several tissues.<ref name=pmid16642957/> The synthesis of adiponectin is tightly coupled with adipose tissue fat mass, demonstrating a negative relationship with larger masses.  Individuals who are classified as obese display a lower plasma adiponectin concentration when compared to non-obese groups. Furthermore, a direct correlation between low adiponectin levels and the onset of type-2 diabetes has been reported. Adiponectin modulation is reflective of the deleterious outcome that manifests when the adipocyte accumulates tremendous volume.<ref name=pmid17021375/>

Studies have demonstrated the physiological importance of adipocytes.  [[Lipoatrophy]], a condition in which the total number of adipocytes are reduced, reveals an association with [[insulin resistance]], [[hyperglycemia]], and liver [[steatosis]].<ref>{{cite journal |pages=271–8 |doi=10.1172/JCI7901 |title=Surgical implantation of adipose tissue reverses diabetes in lipoatrophic mice |year=2000 |last1=Gavrilova |first1=Oksana |last2=Marcus-Samuels |first2=Bernice |last3=Graham |first3=David |last4=Kim |first4=Jason K. |last5=Shulman |first5=Gerald I. |last6=Castle |first6=Arthur L. |last7=Vinson |first7=Charles |last8=Eckhaus |first8=Michael |last9=Reitman |first9=Marc L. |journal=Journal of Clinical Investigation |volume=105 |issue=3 |pmid=10675352 |pmc=377444|display-authors=9 }}</ref> Therefore, preserving cell viability while restoring a lean state is an important strategy as adipocytes exert a protective action by releasing beneficial endocrine hormones. Zerona has been proven to restore a lean state adipocytes without inducing cell apoptosis. It is hypothesized that Zerona could serve as an adjunct to other dietary therapies to promote insulin sensitivity and reduce the risk of diabetes.  Zerona, based on histological evidence, has proven to reduce adipose tissue fat mass of the waist, hips, and thighs while preventing fat cell death. The formation of the transitory pore within the adipocyte membrane results in adipocyte cell collapse and its return to a lean state.  Reduced fat mass is associated with the synthesis of beneficial hormones like adiponectin which promotes insulin sensitivity within numerous tissues.

A 2010 article in the ''American Journal of Cosmetic Surgery'' demonstrated a statistically significant reduction in both serum triglyceride and total cholesterol levels following a standard two-week, six treatment Zerona administration.<ref>{{cite journal |first1=Robert F. |last1=Jackson |first2=Greg C. |last2=Roche |first3=Kevin |last3=Wisler |year=2010 |title=Reduction in Cholesterol and Triglyceride Serum Levels Following Low-Level Laser Irradiation: A Noncontrolled, Nonrandomized Pilot Study |journal=The American Journal of Cosmetic Surgery |volume=27 |issue=4 |pages=177–84 |url=http://www.erchonia.com/files/uploads/1/file/Jackson_Reduction%20in%20Cholesterol%20and%20Triglyceride%20Serum%20Levels%20Following%203LT_AJCS_2010.pdf}}</ref>

==Zerona Canada marketing controversy==
In January 2014 a broadcast story on Zerona Canada marketing fraud allegations was aired by the Canadian [[investigative journalism|investigative]] [[newsmagazine]] [[television program]] [[16:9 (TV series)|''16x9'']].<ref>{{cite web|author1=Alan Carter|author2=Krysia Collyer (Producer)|title=Full Story: Fat Zapping|url=http://globalnews.ca/video/1091434/full-story-fat-zapping|publisher=[[Global Television Network]]|date=January 18, 2014}}</ref>

== References ==
{{reflist|2}}

==External links==
* [http://www.erchonia.com/ Erchonia Corp., Official Website]

[[Category:Laser medicine]]
[[Category:Management of obesity]]