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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 granted 510k market clearance 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 3.5 in (8.9 cm) 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 0.68 in (1.7 cm) after two weeks.[1]


Zerona is a class II low-level laser under 21 CFR 878.540. 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, dosage, pulsation, and 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.[2] 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 nm divergent beams.


Initial trials for the 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, Dr. Neira and his wife started performing histological investigations to determine why laser had this unique biological influence on fat tissue. Utilizing 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.[2] Based on the findings of this study the FDA cleared the EML device in 2001 for use as an adjunctive therapy to liposuction[3] .

Mechanism of action[edit]

The exact mechanism of action for the 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)[4] . 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).[5][6][7] 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.[2] 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.[8][9][10] It is suggested that laser irradiation increases the rate at which cytochrome c oxidase transfers electrons from cytochrome c to dioxygen.[6][7][11] 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.[12][13][14] 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 upregulation of ATP induced by laser therapy is also responsible for the increased production of a natural byproduct known as reactive oxygen species (ROS).[15][16][17] 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.[15][17] It has been hypothesized that the 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[edit]

In 2008, the clinical trial to investigate the efficacy of Zerona commenced. The trial enrolled 67 subjects, 35 of which were randomly assigned to receive active treatment with 32 randomly assigned to the control group. Both groups were asked to sign an affidavit stating that during the clinical trial they would make no changes to their lifestyle and would not participate in any other program or consume any supplements that would promote slimming. Furthermore, patients were asked to track their daily activities and caloric intake through the entire duration of the trial. This daily journal ensured that patients were not making any changes that could impact the outcome. 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 inches compared to the control group which averaged a cumulative reduction of just 0.68 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.[1]

Ongoing Research[edit]

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.[18] 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.[19][20]

Studies have revealed a correlation between deregulated adipose tissue function and excessive fat mass having deleterious effects on the endocrine and immune systems.[19][20][21][22][23] 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.[19][20][21][22][23]

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.[24] Furthermore, studies have illustrated an alteration in gene expression recording an upregulation in proinflammatory factors including classic cytokines and complement factors.[24][25][26] A rise in pro-inflammatory adipokines coupled with cytokine production may promote the onset of metabolic disorders like atherosclerosis.[27]

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.[24] 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.[28] 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.[28] 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.[24]

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.[29] 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. The 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.

An article published in the American Journal of Cosmetic Surgery in 2010 demonstrated a statistically significant reduction in both serum triglyceride and total cholesterol levels following a standard two-week, six treatment Zerona administration.[30]

External links[edit]


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  16. ^ Vladimirov, IuA; Klebanov, GI; Borisenko, GG; Osipov, AN (2004). "Молекулярно-клеточные механизмы действия низкоинтенсивного лазерного излучения" [Molecular and cellular mechanisms of the low intensity laser radiation effect]. Biofizika (in Russian) 49 (2): 339–50. PMID 15129632. 
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