EVALUATION OF LOW LEVEL LASER THERAPY ON BODY CONSTITUTION AND LEPTIN HORMONE BY RADIOIMMUNOASSAY A Thesis Submitted in Partial Fulfillment for the Requirements of Master Degree in Physical Therapy
By Sara Said Youssef Ali B.Sc. in Physical Therapy Cairo University 2006
SUPERVISORS Prof. Dr. Zahra Mohamed Hassan Serry Professor of Physical Therapy for Cardiovascular/ Respiratory Disorder and Geriatrics Faculty of physical therapy Cairo University Dr. Fatma Aboel magd M. Hamid Dr. Einas Shafie Salem Lecturer of physical therapy for Lecturer of Rheumatology and Rehabilitation Cardiovascular /Respiratory National Centre for Radiation Research Disorder and Geriatrics and Technology (NCRRT) Faculty of physical therapy Atomic Energy Authority Cairo University (AEA) Faculty of Physical Therapy Cairo University 2012
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Acknowledgement
First of all and above of all I would like to kneel thanking Allah who provided me with power and patience for completion of this work. It is an honor for me to express my deepest gratitude and deep thanks to Prof. Dr. Zahra Mohamed Hassan Serry , Professor of Physical Therapy for Cardiovascular/ Respiratory Disorder and Geriatrics, faculty of physical therapy Cairo University. For being an outstanding advisor and excellent professor. Her constant encouragement, support and valuable scientific suggestions made this work successful. I am grateful for Dr. Fatma Aboel magd M. Hamid Lecturer of physical therapy for Cardiovascular /Respiratory Disorder and Geriatrics, Faculty of physical therapy Cairo University for her great help, supervision and guidance throughout the procedures of the study. My deepest thanks for Dr. Einas Shafie Salem Lecturer of Rheumatology and Rehabilitation National Centre for Radiation Research and Technology (NCRRT) Atomic Energy Authority (AEA) for suggesting the subject of the study, providing facilities, keen supervision and reading the manuscript. I would like to thank Dr. Mohamed M. Saeed Lecturer of Internal medicine, National Centre for Radiation Research and Technology (NCRRT), Atomic Energy Authority (AEA) for his advice in choosing the topic of the study and great interest. Special mention and warmest thanks to my dear parents, brother and sister for their support through my entire life and especially to accomplish this study. Last but certainly not least; Special thanks are due to my patients and colleges for their active participation in this work. Sara Said Youssef Ali (2012)
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Evaluation of Low level laser therapy on body constitution and leptin hormone by radioimmunoassay/ Sara Said Youssef Ali; Supervisors: Prof. Dr. Zahra Mohamed Hassan serry, Dr. Fatma Abo el magd M. Hamid Department for Cardiovascular/ Respiratory Disorder and Geriatrics, Faculty of Physical Therapy, Cairo University and Dr. Einas Shafie Salem; Lecturer of Rheumatology and Rehabilitation, National Centre for Radiation Research and Technology, Atomic Energy Authority, Master Thesis 2012. Abstract Background: Asymmetric fat distribution with excessive fat accumulation in particular areas often affects a person's self image, self esteem, and overall quality of life. Purpose of the study: to investigate the efficacy of the low level laser therapy (LLLT) on body constitution and leptin hormone by radioimmunoassay. Methods: Twenty women were included in this study. Their ages ranged from 30 40 years. They were divided into two groups of equal number. Procedures: Group A (Overweight group): included 10 women with BMI ≥ 25 29.9 Group B (Obese group): included 10 women with BMI ≥ 30.both groups received LLLT , for 30 minutes, 2 times per week for 8 weeks as a total period of treatment . BMI, WC, HC, WHR, serum Leptin, cholesterol and triglyceride level were measured before and after finishing the study. Results: There was significant improvement in anthropometric measurements( on both abdomen and thigh fats) of both groups treated with low level laser therapy, decrease in serum leptin level in over weight group and increase in triglyceride serum level in both groups within normal level Conclusion: low level laser therapy is effective as a non invasive & safe method of body contouring . Key words : low level laser therapy, leptin, obesity, adipose tissue and Radioimmunoassay.
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LIST OF ABBREVIATIONS AgRP : agouti related peptide ATP : Adenosine Tri phosphate BAT : brown adipose tissue BBB: blood brain barrier BMI : body mass index Cm: centimetre CNS : central nervous system CRP : C reactive protein CVD : cerebro vascular disease dSAT : deep subcutaneous adipose tissue EAT : Epicardial adipose tissue FFAs : free fatty acids Ga Al : gallium aluminum Ga As : gallium arsenide H.C. : Hip circumference HDL : high density lipoprotein He Ne : helium neon IL 1: Interleukin 1 IL 6: Interleukin 6 IMAT : Intermuscular adipose tissue Kg : kilogram LDL: low density lipoprotein LEDs : Light emitting diodes LLLT : Low Level Laser Therapy LPL : lipoprotein lipase NPY : neuropeptide Y RIA : Radio immune assay RNA: Ribonucleic acid. SAT: Subcutaneous adipose tissue SLIPs : serum leptin interacting proteins sSAT :superficial subcutaneous adipose tissue T2DM : type 2 diabetes mellitus TG : triglycerides
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TNF α: Tumour Necrosis Factor α VAT: Visceral adipose tissue VLDL: very low density lipoproteins WAT : White adipose tissue WC : waist circumference WHO : world health organization WHR : waist to hip ratio α MSH : α melanocyte stimulating hormone
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LIST OF TABLES
Table No. Title Page (1) The International Classification of adult underweight, overweight and obesity according to BMI ……... 8 (2) Adipose Tissue as an Endocrine Organ……………. 14 (3) Main endogenous chromophores present in mammalian cells / tissues……………………………. 31 (4) Common types of low energy lasers……………...... 33 (5) Physical characteristics of patients in both groups (A&B)………………………………………………... 52 (6) Mean ±SD, t and P values of Body Weight pre and post treatment of group (A)……………………. 55 (7) Mean ±SD, t and P values of Body Weight pre and post treatment of group (B)…………………… 56 (8) Independent t test between groups A and B for Body Weight pre and post treatment……………………… 57 (9) Mean ±SD, t and P values of BMI pre and post treatment of group (A)……………………………. 59 (10) Mean ±SD, t and P values of BMI pre and post treatment of group (B)……………………………… 60 (11) Independent t test between groups A and B for BMI pre and post treatment…………………………….. … 61 (12) Mean ±SD, t and P values of Waist circumference pre and post treatment of group (A) ...... … 62 (13) Mean ±SD, t and P values of Waist circumfe rence pre and post treatment of group (B)… 63 (14) Independent t test between groups A and B for Waist circumference pre and post treatment……………… 64 (15) Mean ±SD, t and P values of Hip circumference pre and post treatment of group (A). …………..………. 65 (16) Mean ±SD, t and P values of Hip circumference pre and post treatment of group (B)………………….... 66 (17) Independent t test between groups A and B for Hip circumference pre and post treatment …………….. 67 (18) Mean ±SD, t and P values of Waist hip ratio pre and post treatment of group (A)……………………..…. 68 (19) Mean ±SD, t and P values of Waist hip ratio pre and post treatment of group (B)………………………… 69 (20) Independent t test between groups A and B for Waist hip ratio pre and post treatment ……………………. 70
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Table No. Title Page (21) Mean ±SD, t and P values of Leptin level pre and post treatment of group (A)………………………… 71 (22) Mean ±SD, t and P values of Leptin level pre and post treatment of group (B)………………………… 72 (23) Independent t test between groups A and B for Leptin level pre and post treatment.……………………….. 73 (24) Mean ±SD, t and P values of Cholesterol level pre and post treatment of group (A)……………….. 74 (25) Mean ±SD, t and P values of Cholesterol level pre and post treatment of group (B)………………… 75 (26) Independent t test between groups A and B for Cholesterol level pre and post treatment.………….. 76 (27) Mean ±SD, t and P values of Triglycerides level pre and post treatment of group (A)………………..….. 77 (28) Mean ±SD, t and P values of Triglycerides level pre and post treatment of group (B)……………….…… 78 (29) Independent t test between groups A and B for Triglycerides level pre and post treatment.………….. 79 (30) Correlation Analysis between the Waist circumference and Leptin level …………………….. 80 (31) Correlation Analysis between the Waist circumference and Triglycerides level ……………… 81 (32) Correlation Analysis between the Hip circumference and Leptin level …………………………………….. 82 (33) Correlation Analysis between the Hip circumference and Triglycerides level ……………………………… 83
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LIST OF FIGURES
Figure Title Page No. (1) Structure of white and brown adipose tissue ...... 12 (2) Leptin……………………………………………….…….. 20 (3) Arndt Chaltz Law…………………………………………. 35 (4) Radioimmunoassay test ...... 38 (5) Standard weight and height scale ...... 42 (6) The Gamma Counter device ………………………………. 43 (7) Spectrophotometer ...... 44 (8) Low level LASER device ………………………………..... 45 (9) Head and digital screen of the laser device.……...………... 45 (10) Protective goggles. ……………………………...…………. 46 (11) Measurement of Body Weight ……..…………………….. 47 (12) Mean ±SD of the age for groups (A, B)…………………… 53 (13) Mean ±SD of the weight for groups (A, B)…………..….. 53 (14) Mean ±SD of the height for groups (A, B)………………. 54 (15) Mean ±SD of the BMI for groups (A, B)………………... 54 (16) Mean ±SD of Body Weight pre and post treatment of group (A)……………………………………………………….… 56 (17) Mean ±SD of Body Weight pre and post treatment of group 57 (B)………………………………………………………….. (18) Mean ±SD of Body Weight pre and post treatment of 58 groups (A, B)………………………………………………. (19) Mean ±SD of BMI pre and post treatment of group (A). ..... 60 (20) Mean ±SD of BMI pre and post treatment of group (B). ..... 61 (21) Mean ±SD of BMI pre and post treatment of groups (A, B)………………………………………...... 62 (22) Mean ±SD of Waist circumference pre and post treatment of group (A). ...... 63 (23) Mean ±SD of Waist circumference pre and post treatment of group (B). ...... 64
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Figure Title Page No. (24) Mean ±SD of Waist circumference pre and post treatment of groups (A,B) ...... 65 (25) Mean ±SD of Hip circumference pre and post treatment of group (A)………………………………………………..… 66 (26) Mean ±SD of Hip circumference pre and post treatment of group (B)………………………………………………..... 67 (27) Mean ±SD of Hip circumference pre and post treatment of groups (A, B). ...... 68 (28) Mean ±SD of Waist hip ratio pre and post treatment of group (A). ……………………………….……………….. 69 (29) Mean ±SD of Waist hip ratio pre and post treatment of group (B)………………………………………………… ... 70 (30) Mean ±SD of Waist hip ratio pre and post treatment of groups (A, B). ...... 71 (31) Mean ±SD of Leptin level pre and post treatment of group (A)………………………………………………………...... 72 (32) Mean ±SD of Leptin level pre and post treatment of group (B)……………………………………………………… 73 (33) Mean ±SD of Leptin level pre and post treatment of groups (A, B). ………………………………………….………… 74 (34) Mean ±SD of Cholesterol level pre and post treatment of group (A). ……….….………………...... 75 (35) Mean ±SD of Cholesterol level pre and post treatment of group (B)………………………………………………...... 76 (36) Mean and ±SD of Cholesterol level pre and post treatment of groups (A, B)……………………………...…………...... 77 (37) Mean ±SD of Triglycerides level pre and post treatment of group (A)………………………………………………..... 78 (38) Mean ±SD of Triglycerides level pre and post treatment of group (B)………………………………………………..... 79 (39) Mean ±SD of Triglycerides level pre and post treatment of groups (A, B)……………………………………………..... 80 (40) Correlation between Waist circumference and Leptin level. 81
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Figure Title Page No. (41) Correlation between Waist circumference and Triglycerides level…………………………….…...... 82 (42) Correlation between Hip circumference and Leptin level………...... 83 (43) Correlation between Hip circumference and Triglycerides level ……………………………...... 84
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CONTENTS Page Acknowledgment Abstract List of abbreviations i List of tables iii List of figures v Chapter (І): INTRODUCTION ………………………………………………… 1 Statement of the problem …………………………………... 2 Purpose of the study………………………………………… 2 Significance of the study………………………………...... 2 Basic Assumptions …………………………………………. 3 Hypothesis…………………………………………………... 3 Definition of terms ………………...……………………….. 4 Chapter II REVIEW OF THE LITERATURE ...... 6 Obesity………………………………….. …………………. 6 Classification of obesity………………………………… 6 Adipose tissue ………………………………………..….. 10 Structure of adipose tissue …………………………... 10 Adipose tissue as endocrine organ…………………… 12 Classification of body fat…………………………….. 15 Gender differences in adipose organ function………... 18 Leptin…………………………………………………...... 20 Factors affecting blood level of leptin……..………… 21 Role of leptin in body weight regulation…………... 23 Leptin resistance…………………………………… 24 Leptin deficiency ………………………………………. 25 Leptin replacement……………………………………… 25 Laser………...... 26 Definition………………………………………………. 26 laser Physics …………………………………...... 26 Properties of laser light……………………………… 26 Principle components of laser system…………...... 27 Types of laser………………………………………... 28 Safety classification of lasers……………………...... 29 Dangers and contraindications of laser……………... 30 Laser tissue interaction……………………………… 30 Classification of lasers……………………………….. 32 Low level laser therapy…………………………….. 34 Radioimmunoassay……………………………….………. 37
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Radioimmunoassay principle.………...……………... 37 General procedure of Radioimmunoassay…………. 39 Chapter III SUBJECTS AND METHODS ………………………………… 40 Subjects………………………………………………….. 40 Design of the study………………………………………. 41 Equipments and tools…………………………………….. 42 Measuring equipments ……………………………... 42 Therapeutic equipment…………...…………………... 44 Procedures………………………………………….……... 46 Measurement procedures…………..….…...………… 46 Treatment procedures………………….…..………… 50 Statistical procedures………………………………..… 51 Chapter IV Results ……………………………………………………………. 52 Chapter V Discussion ……………………………………………………...... 85 Chapter VI Summary and Conclusion ...... 91 Recommendation s...... 93 References ……………………………………………………...... 94 Appendices ……………………………………………………….. 107 Arabic Summary …………………………………………………..
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Chapter1 Introduction
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INTRODUCTION
Obesity is a chronic disease that concerns over a billion adult people throughout the world. It is estimated that the number of those affected by the disease will double by the year 2030. Consequently, obesity can be considered epidemic which is going to become the biggest health problem of the century. Along with the number of those suffering from obesity, the prevalence of complications resulting from the excess of adipose tissue is also growing (Gnacińska et al., 2010). Obesity is associated with increased basal lipolysis in adipose tissue, elevated circulating free fatty acids (FFAs) and is accompanied by abnormalities in both glucose and lipid metabolism (Singla et al., 2010). Leptin is a peptidic hormone secreted by the fat tissue and plays an important role in body fat distribution. Previous studies suggest a relationship between leptin level, body mass index (BMI) and fat distribution (Barrios Ospino et al., 2010). Low Level Laser Therapy (LLLT) is used to promote tissue regeneration and this type of therapy is based on the stimulatory effects induced by the absorption of a specific wavelength of light by the functioning photo acceptor molecules (chromophores) (Karu, 2010).
LLLT was reported to liquefy or release stored fat in adipocytes by the opening of specialized yet not identified cell membrane associated pores after a brief treatment (Brown et al., 2004). Reduction of subcutaneous fat in the thigh of normal women using LLLT was reported by Lach, (2008) . Diode laser was successfully used for body contouring of the waist, hip and thighs (Jackson et al., 2009) and (Caruso Davis et al., 2011).
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Statement of the Problem: Is low level laser therapy has effect on body contouring & leptin level in blood in overweight and obese females? Purposes of the study: The objective of this study was to evaluate the effectiveness of diode laser system as a non invasive body contouring intervention method as well as a therapeutic modality for weight reduction. Significance of the study:
Obesity is a major public health issue, with a rapidly increasing prevalence. Obese people, defined on the basis of high BMI, have a much greater risk of developing myocardial infarction and stroke than subjects with normal levels of total body fatness ( Sikorski et al.,2011).
It was shown that not only the quantity of the fat mass but also the fat tissue deposition at visceral level as measured by waist circumference(WC) is an important recognized risk factor for cardiovascular diseases associated with obesity (Pataky et al., 2009).
The applicability and reliability of anthropometric measures like WC, BMI besides cross referencing measurements including WHR as useful measures in the prognosis of metabolic syndromes, cardiovascular diseases and cancers were suggested by Yang et al., (2011).
This study was designed to investigate the effectiveness of LLLT in weight reduction and body contouring of the waist and thigh of women ages 30 to 40 years. Results were assessed clinically by weight reduction, body mass index (BMI), waist circumference (WC), Hip circumference (H.C.) and waist to hip ratio (WHR) as well as, in vitro assessment by Radio immune assay (RIA) of serum leptin level. The relationship between abdominal adiposity as measured by WHR, BMI, waist
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circumference , hip circumference and serum blood level of leptin hormone was studied pre and post treatment with diode laser. Therefore the results of this study will increase the understanding of the relationship between abdominal obesity and serum level of leptin hormone in obese and overweight adult women.
Basic Assumptions: It was assumed that:
• All information taken from the patients were correct. • All patients did not receive any drugs that could affect the results of the study. • All patients did not receive any other weight reduction method. • All patients of experimental group received equal time of treatment. • All patients had no endocrine, metabolic, cardiovascular problems or cancer. • Both evaluation & therapeutic equipment were valid. • All patients took 2 3 liters of water per day to ensure rapid elimination of waste product. • All patients will follow the instructions during treatment. • All subjects will continue in the study. • Physiological & psychological variations will not affect the study. • All patients were nonsmokers. • The results will be obtained from this study will be of value to physical therapist. Hypothesis:
It was hypothesized that Low level laser therapy may not affect leptin hormone levels or body contouring in obese women.
Definition of Terms:
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Adipose tissue:
It is a specialized connective tissue that functions as the major storage site for fat in the form of triglycerides. Adipose tissue is found in mammals in two different forms: white adipose tissue and brown adipose tissue. The presence, amount and distribution of each vary depending upon the species. Most adipose tissue is white (Hauguel de Mouzon et al., 2006).
LASER:
Laser is acronym for light amplification by stimulated emission of radiation. (Karu, 2002) .
Low Level Laser Therapy LLLT (photobiomodulation):
It is a phototherapy which involves the application of red to near infra red light over injuries or lesions to stimulate healing and control acute and chronic pain (Hawkins and Abrahamse, 2005).
Leptin: important role in body fat distribution. Leptin & leptin receptors is an important factor in regulation of both appetite and energy expenditure, this hormone acts on hypothalamus to increase food intake and decrease energy expenditure, to reach its central site of action, circulating leptin must across the blood brain barrier and stimulate hypothalamic leptin receptors (Brennan and Mantzoros ,2007)
Radioimmunoassay (RIA):
Radioimmunoassay is based on the antigen antibody reaction in which a trace amount of the radiolabeled antigen competes with endogenous antigen for limited binding sites of the specific antibody against this antigen. The accuracy of RIA is based on the reasonable
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assumption that the radiolabeled antigen and the native antigen have similar affinities for the specific antibody (Lagarde et al., 2003).
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Chapter II Review of Literature
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REVIEW OF LITERATURES
Obesity
The world health organization (WHO) recognized obesity as a worldwide disease that poses a serious threat to public health. Persons who are overweight or obese have substantially increased risk for morbidity from numerous chronic disorders (Ross et al., 2000). Obesity as a disease is a complex interplay of genetic, socioeconomic, and psychological factors. The results of which is a prolonged positive energy balance instead of normal homeostasis (Tawadrous, 2001).
Obesity is one of the most common forms of disturbed nutrition among population, resulting in a surplus of energy which converted to fat and stored as adipose tissue (Abu Raia, 2001).
Obesity is associated with an increased number of adipocytes. A lean adult has about 35 billion adipocytes, each containing about 0.4 to 0.6 лg of triglyceride. An extremely obese adult can have four times as many adipocytes (125 billion), each containing twice as much lipid (0.8 to 1.2 лg) of triglyceride (Larsen et al., 2002).
Classification of obesity:
a) According to body mass index (BMI);
The most commonly used method for classifying an individual as overweight or obese is based on BMI, a value that is determined by dividing weight (in kilograms) by the square of height (in meters). In adult overweight is defined by a BMI of >25.0 kg/m 2, and obesity is defined by a BMI of >30 kg/m 2 (Racette et al., 2003).
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The WHO (2004), classified the degrees of obesity(table 1) beginning with overweight, defined by BMI between 25.0 and 29.9 kg/m 2, through class I obesity (BMI 30.0 to 34.9 kg/m 2), class II obesity (BMI, 35.0 to 39.9 kg/m 2) and class III or extreme obesity (BMI >40kg/m 2). b) According to waist circumference:
Waist circumference is an important measure of obesity risk. A high risk waist circumference is accepted to be 35 inches or greater for women and 40 inches or greater for men (Aronne, 2002) .
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Table (1): The International Classification of adult underweight, overweight and obesity according to BMI (WHO, 2004)
BMI(kg/m 2) Classification Principal cut off points Additional cut off points Underweight < 18.50 < 18.50 Severe thinness < 16.00 < 16.00 Moderate thinness 16.00 16.99 16.00 16.99 Mild thinness 17.00 18.49 17.00 18.49 18.50 22.99 Normal range 18.50 24.99 23.00 24.99 Overweight ≥ 25.00 ≥ 25.00 25.00 27.49 Pre obese 25.00 29.99 27.50 29.99 Obese ≥ 30.00 ≥ 30.00 30.00 32.49 Obese class I 30.00 34.99 32.50 34.99 35.00 37.49 Obese class II 35.00 39.99 37.50 39.99 Obese class III ≥ 40.00 ≥ 40.00 C) According to body fat distribution: Obesity can be classified according to body fat distribution. The way in which the fat is distributed falls into two categories. Fat is either deposited on hips and legs with excess gluteofemoral fat (gynacoid type), (pear shape), (pear shaped peripheral obesity) or deposited centrally around the abdomen with excess subcutaneous abdominal fat (android), (apple shaped central obesity) (Barker, 2002). Data have shown that waist circumference is the most reliable estimates of visceral fat; waist circumference alone is as good as the ratio of waist circumference to the hip circumference (Ronti et al., 2006). Subjects in the desirable range (20 25 kg/m 2) have a lower mortality and risk of diseases than those above the range.
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The mean BMI taken from the metropolitan tables is 22.4 kg/m 2 for the women. Studies showed that BMI actually is a measure of body fat related to height rather than percent of the body fat and that is a better measure of obesity than percentage of body fat. The BMI gradually increase with age of both genders with no consistent difference between men and women (WHO, 2000).
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Adipose tissue Adipose tissue is a complex, essential, and highly active metabolic and endocrine organ. Adipose tissue not only responds to afferent signals from traditional hormone systems and the central nervous system but also expresses and secretes factors with important endocrine functions. These factors include leptin, other cytokines, adiponectin, complement components, plasminogen activator inhibitor 1, proteins of the renin angiotensin system, and resistin (Rokling Andersen et al., 2007). Adipose tissue is also a major site for metabolism of sex steroids and glucocorticoids. The important endocrine function of both adipose tissues is emphasized by the adverse metabolic consequences of both adipose tissue excess and deficiency. A better understanding of the endocrine function of adipose tissue will likely lead to more rational therapy for these increasingly prevalent disorders (Kershaw and Flier, 2004) . Structure of adipose tissue: Fig. (1) In humans, adipose tissue is located beneath the skin, around internal organs, in bone marrow and in breast tissue. Adipose tissue contains several cell types, with the highest percentage of cells being adipocytes, which contain fat droplets. Other cell types include fibroblasts, macrophages, and endothelial cells. Adipose tissue contains many small blood vessels. In the skin, it accumulates in the subcutaneous layer, providing insulation from heat and cold. Around organs, it provides protective padding (Schaffler et al., 2006).
The two forms of adipose tissue are white and brown adipose tissue. Brown adipose is found in newborns (2 5 % of the body weight)
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and can be used to dissipate stored energy as heat (thermogenesis), while adults have mainly white adipose (Fantuzzi, 2005).
The structure of white and brown adipose tissue is also different. White fat is composed mainly of globular cells containing large lipid vacuoles, with the few mitochondria and the nucleus of the cell being found near the edge of the cell while brown adipose cells are smaller than white fat cells, and contain smaller lipid vacuoles as well as many more mitochondria. The presence of numerous mitochondria causes the brown coloring of these adipocytes, which also receive more capillary blood flow than their white counterparts (Hauguel de Mouzon et al., 2006).
White adipose tissue (WAT) does not consist simply of mature adipocytes, which store triacylglycerols; there are a variety of other cells (e.g. fibroblasts, endothelial cells, macrophages) which constitute around 50% of the total cellular content (Cannon and Nedergaard, 2008).
Fig. (1): Structure of white and brown adipose tissue (Cannon and Nedergaard, 2008)
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Adipose tissue as an endocrine organ: table (2) Adipose tissue has many important physiological functions. Energy storage is one of its primary roles. In addition, it also has a role to play in maintaining normal glucose levels, in thermal insulation/thermo regulation , lubrication (primarily in the pericardium) and protecting visceral organs from physical damage (Hutley and Prins, 2005).
WAT has been recognised as a dynamic endocrine organ involved in a wide range of physiological systems and metabolic processes, with extensive cross talk with other tissues and organs. White adipocytes are recognised to secrete several major hormones additional to leptin, as adiponectin, together with a range of other protein signals and factors termed ‘adipokines’ (or adipocytokines) (Singh et al., 2012).
The adipokines, are highly diverse in terms of structure and function, and include proteins involved in lipid metabolism, insulin sensitivity, vascular function and blood pressure regulation. Importantly, a number of adipokines are directly linked to immunity and the inflammatory response; these include cytokines, chemokines and acute phase proteins, as well as other inflammation related proteins (Schaffler et al., 2006).
Some of the adipokines are mainly produced by the adipose tissue like leptin and resistin, while others are also synthesized in other tissues like tumour necrosis factor alpha (TNF α), interleukins 6 (IL 6), and interleukin 1 (IL 1). Because all of these factors can act in an autocrine, paracrine or endocrine manner in the organisms, adipokines are thought to serve as mediators linking obesity, metabolic syndrome, diabetes, inflammation, immunity and other obesity related diseases (Rokling Andersen et al., 2007).
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The adipokines contribute to the regulation of other physiological pathways, including the cardiovascular and reproductive systems. Further, a number of adipokines participate in maintenance of energy balance, enabling adipose tissue to contribute to its own regulation. Control of adipose endocrine function is tightly intertwined with energy storage, to the extent that both excess gain and loss of adipose tissue mass disrupt normal adipokine profiles and in turn negatively impact reproduction, immune function and other systems regulated by adipokines (Ronti et al., 2006).
Table (2): Adipose Tissue as an Endocrine Organ (Kershaw and Flier, 2004): Cytokines and cytokine related Leptin proteins TNFα IL 6 Other immune related proteins MCP 1 Proteins involved in the fibrinolytic system Tissue factor Complement and complement related Adipsin (complement factor D) proteins Complement factor B Adiponectin Lipids and proteins for lipid Lipoprotein lipase (LPL) metabolism or transport Cholesterol ester transfer protein (CETP) Apolipoprotein E Enzymes involved in steroid Cytochrome P450 dependent metabolism aromatase Proteins of the RAS AGT Other proteins Resistin TNFα: Tumour Necrosis Factor Alpha., IL 6: Interleukin 6.
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Classification of body fat: 1. Visceral Fat: Visceral fat depots, including omental and mesenteric adipose tissue, represent a risk factor for the development of cerebro vascular disease (CVD) and type 2 diabetes mellitus (T2DM). Visceral adipose tissue mass correlates with development of insulin resistance, while total or subcutaneous tissue mass does not (Wajchenberg, 2000) . It has been thoroughly confirmed that the adipocytes of visceral fat tissue are more lipolytically active than subcutaneous adipocytes and thus contribute more to the plasma free fatty acid levels (Hajer et al., 2008) . This was found in particular in diabetic obese individuals, where it was linked to a significant up regulation of leptin and down regulation of adiponectin gene expression in mesenteric visceral adipose tissue (VAT ) compared to subcutaneous adipose tissue (SAT) and omental VAT (Yang et al., 2008). The metabolic activity of a cell is dependent on its mitochondrial content. Thus, the level of mitochondrial uncoupling and energy efficiency may have an effect on obesity in WAT as well as brown adipose tissue (BAT) (Virtanen et al., 2002). 2. Subcutaneous Fat: As SAT is less metabolically active than VAT, it may have better short term and long term storage capacity. Thus, this depot is important to accumulate triglycerides (TG) in periods of excess energy intake and supply the organism with FFAs in periods of fasting, starvation, or exercise. Another suggested role of SAT is to be a buffer during intake of dietary lipids, thus protecting other tissues from lipotoxic effects (Frayn, 2002). In humans, SAT is anatomically divided by a stromal fascia (fascia superficialis) into superficial subcutaneous adipose tissue (sSAT) and
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deep subcutaneous adipose tissue (dSAT), with distinct histological features. While sSAT has not been linked to risk for T2DM, the size of dSAT depots is significantly linked to the fasting insulin level and insulin stimulated glucose utilization, as is total fat and VAT (Kelley et al., 2000) . The association between dSAT and insulin resistance is particularly seen in male obese patients (Smith et al., 2001) . When studying the expression and secretion of hormones and cytokines in lean subjects, dSAT was found to be more similar to VAT than sSAT (Walker et al., 2007) . Interestingly, SAT seem to have an exclusive role in leptin secretion, since it correlates with plasma leptin levels (in contrast to plasma insulin levels which correlate with inter abdominal fat (Cnop et al., 2002). 3. Gluteofemoral Fat: The subcutaneous gluteofemoral fat tissue is measured by hip or thigh circumference, or leg adipose tissue mass. Accumulation of fat in this depot is believed to have a protective role against diabetes and cardiovascular disease (Manolopoulos et al., 2010). Indeed, low amount of this tissue has been associated with an unfavorable lipid and glucose profile (Snijder et al., 2005). An increase in gluteofemoral tissue size has been connected to increase in HDL cholesterol and decrease in total and LDL cholesterol levels in several studies . Gluteofemoral fat is also positively associated with adiponectin and leptin serum levels (Buemann et al., 2006). Tracing of specific lipid fraction in blood samples from veins draining femoral or abdominal fat showed that there was a lower metabolic flux from femoral fat and that femoral fat had a preference for uptake of FFA and very low density lipoprotin (VLDL) TG compared to
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chylomicron TG, thus accumulating recycled fat rather than dietary fat (McQuaid et al., 2010). The gluteofemoral fat tissue may thus provide protection from ectopic deposition of excess fat. While the abdominal subcutaneous adipose tissue has a role as buffer during daily fatty acid intake .The gluteofemoral fat tissue may have an important role in TG storage. Since it shows less metabolic activity and is more lipolytically inert than upper body adipose depots, it seems to be involved in the long term sequestering of fatty acids (Frayn, 2002). 4. Intermuscular Fat: Few studies have focused on intermuscular adipose tissue (IMAT), and little is known about its specific metabolic activities. However, due to its increased level in T2DM patients, IMAT has been suggested be a risk factor along with VAT for the development of obesity related diseases (Gallagher et al., 2009). The amount of IMAT seems to be associated with age and lack of activity (Marcus et al., 2010). 5. Epicardial Fat: Epicardial adipose tissue (EAT) is the visceral fat layer located around the heart and is believed to be important for the buffering of the coronary arteries, and in providing fatty acids as a source of energy for the cardiac muscle. The release of adiponectin and adrenomedullin could have a protective effect on the heart during metabolic or mechanical insults (Iacobellis and Barbaro, 2008) . On the other hand, other studies shown that EAT will locally influence heart and vasculature through the secretion of pro inflammatory cytokines and will contribute to coronary atherosclerosis (Rabkin, 2007) .
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Studies indicate that the amount of EAT can be related to carotid artery stiffness in obese patients with hypertension, while waist circumference shows no statistically significant link (Natale et al., 2009) . 6. Brown adipose tissue: In humans, small areas of BAT are found in the thorax region (supraclavicular), and in the chest and abdomen (Van Marken Lichtenbelt et al ., 2009). There are indications that the non shivering heat generation is important for the development of obesity (Mattson, 2010). It seems that reduced amount and thermogenic capacity of BAT may contribute to a life long predisposition for obesity. Although adult humans possess only a small percentage of BAT compared to WAT, the possibility to pharmacologically increase BAT amount or activity would be a potential treatment for obesity (Kajimura et al., 2009).
Gender differences in adipose organ function:
Gender exerts profound effects on metabolism and endocrine function of the adipose organ. Women have a higher percentage of body fat than men and tend to store adipose tissue preferentially in the gluteal femoral region as opposed to the classic male pattern obesity concentrated in the visceral and abdominal depots (Sumner et al., 2002).
The increased gluteal femoral adiposity in women is associated with larger fat cell size, increased stimulated lipolysis, and increased triglyceride synthesis in these depots (Karastergiou et al., 2012).
In contrast, increases in abdominal adipose tissue in men are associated with decreased stimulated lipolysis, decreased triglyceride synthesis, and increased LPL activity in these depots (Blaak 2001).
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Interestingly, the difference in visceral adipocyte metabolism between genders disappears with menopause and may be the cause of weight gain in the abdominal region with menopause. Together, these findings suggest that female sex hormones play a significant role in these gender depot differences, leading to differences in adipocyte metabolism. Estrogen is an obvious candidate and may mediate several of these differences in adipocyte metabolism (D’Eon et al., 2005).
However, estrogen also increases adipocyte expression of perilipin and α2A adrenergic receptors which are two proteins with antilipolytic properties (Pedersen et al., 2004)
Therefore, estrogen may mediate the gender differences in depot specific LPL activity leading to increases in adipose tissue deposition in the gluteal femoral region of females (Hensley et al., 2003).
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Leptin
Fig. (2): leptin (Considine, 2011)
Leptin (Greek leptos meaning thin) is a signaling factor encoded by the obese gene, located on chromosome 7 in humans, in adipose tissue. Human leptin is a protein of 167 amino acids. Leptin is a four helix bundle with one very short strand segment and two relatively long interconnected loops. This is consistent with a classification as a cytokine four helix bundle (Brennan and Mantzoros, 2007).
Leptin is expressed predominantly in adipose tissue, in correlation with the amount of fat present in adipocytes. It has been shown to have a key role in a range of processes including the regulation of appetite and energy expenditure, glucose homeostasis, bone formation, regulation of puberty and reproduction, immunity, inflammation and metabolism (Hutley and Prins, 2005).
Leptin is secreted from adipose tissue; it circulates in the blood, probably bound to a family of binding proteins, and acts on central neural networks that regulate ingestive behavior and energy balance. Leptin provides a communication link from fat tissue and the brain. Leptin is
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mainly expressed by adipocytes but low levels are produced in the stomach, intestine, mammary epithelium, placenta, skeletal muscle, and possibly the brain (Rasouli and Kern, 2008).
Factors affecting blood level of leptin:
The concentrations of leptin in adipose tissue and plasma closely parallel the mass of adipose tissue and adipocyte size and triglyceride content. Its production is strongly influenced by nutritional state .Thus, leptin increases in obesity and falls with weight loss .These changes are dependent on insulin and glucose (Jo et al., 2005). Overeating increases serum leptin concentrations by nearly 40 percent within 12 hours, long before any changes in body fat stores. Conversely, in both normal weight and obese subjects, fasting reduces serum leptin concentrations by 60 to 70 percent in 48 hours (Mak et al., 2006) . Singla et al., (2010) stated that; the concentrations are similar in normal subjects and patients with type 2 diabetes mellitus of the same weight. Thus, chronic endogenous hyperinsulinemia does not increase leptin secretion, although infusion of insulin and glucose for two days does. They added that leptin is increased by chronic glucocorticoid exposure and inflammatory cytokines. In contrast, cold exposure and adrenergic stimulation decrease leptin. The concentrations are higher in women than in men, decrease with age in both women and men. Higher serum leptin concentrations are associated with an earlier onset of puberty. Serum leptin concentrations are similar in black and white children of similar body composition. Leptin is also higher in women, partly due to higher production by SAT, stimulation by estrogens, and inhibition by androgens. Pregnant women have higher serum leptin concentrations than nonpregnant women.
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Breastfeeding may reduce the risk of child obesity, as leptin is produced in the breast and is present in milk. (Considine, 2011)
There is a diurnal rhythm of serum leptin concentrations, the values being 20 to 40 percent higher in the middle of the night as compared with daytime. The peak shifts in parallel with shifts in the timing of meals. (Ruhl et al., 2007). Leptin is the primary signal through which the hypothalamus senses nutritional state and modulates food intake and energy balance . Leptin is transported widely throughout the central nervous system (CNS), but the most intensive region of uptake is at the arcuate nucleus. The leptin transporter is also not static but modulated in several conditions. The rate at which leptin is transported across the blood brain barrier (BBB) is decreased in obesity and with starvation but increased with short term fasting. All of these effects can be explained, at least partially, by the ability of triglycerides to inhibit leptin transport across the BBB (Banks et al., 2004).
Jackson and Ahima, (2006) stated that there are at least five forms of the leptin receptors .The heterogeneous distribution of leptin receptors in extra hypothalamic brain regions, like cerebellum, cerebral cortex, substantia nigra and hippocampus, suggests that leptin probably modulates neural pathways distinct from those related to body weight regulation .
The kidneys play a significant role in the plasma removal of leptin. Given its size (16,000 Daltons), leptin is freely filtered by the glomerulus. However, while leptin is freely filtered, little or no leptin cleared by the kidneys appears in the urine. It was calculated that renal leptin uptake accounted for approximately 80 percent of all leptin removed from plasma. Lung, liver, or muscle tissues could play a role in
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leptin metabolism, as these tissues also express leptin receptor messenger RNA (Briley and Szcech, 2006).
Role of leptin in body weight regulation: a) Effects on the central nervous system:
Leptin is present in circulation and cerebrospinal fluid. It crosses the BBB and binds to receptors in the hypothalamus. Leptin has been shown to alter the regulation of hormones in the hypothalamus pituitary adrenal axis and affects growth hormone. Leptin works by down regulating (inhibiting) the activity of orexigenic (appetite stimulating) neurons that contain neuropeptide Y (NPY) and agouti related peptide (AgRP), and by increasing the activity of anorexigenic (appetite reducing) neurons expressing α melanocyte stimulating hormone (α MSH). The NPY neurons are a key element in the regulation of appetite; small doses of NPY injected into the brains of experimental animals stimulates feeding, while selective destruction of the NPY neurons in mice causes them to become anorexic (Kelesidis et al., 2010). The melanocortin system includes both agonist α MSH and antagonist peptides (AgRP). Increased melanocortin receptor stimulation following leptin administration plays an important role in leptin induced hypophagia and increased sympathetic nervous system activity and is partly responsible for leptin induced weight loss (Mak et al., 2006) .
b) Effects on other body systems: (Gandhi et al., 2009).
Leptin has an important role in the secretion of gonadotropin releasing hormone . Women who are very thin from limited food intake or intense physical training may cease to menstruate because of their lack of leptin secreting fat cells. Treating them with recombinant human leptin can sometimes restore normal menstruation.
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Leptin stimulates the sympathetic nervous system to modulate the balance between the formation and breakdown of bone.
leptin acts directly on the cells of the liver and skeletal muscle where it stimulates the oxidation of fatty acids in the mitochondria. This reduces the storage of fat in those tissues (but not in adipose tissue).
Leptin resistance:
The high sustained concentrations of leptin from the enlarged adipose stores in obese people, results in leptin desensitization. The pathway of leptin control in these people might be flawed at some point so the body doesnot adequately receive the satiety feeling subsequent to eating (Kelesidis et al., 2010).
The mechanisms underlying leptin resistance are still being undefined. Several serum leptin interacting proteins (SLIPs) isolated by leptin affinity chromatography and identified by mass spectrometry and immunochemical analysis. It was confirmed that one of the major SLIPs is C reactive protein (CRP). In vitro, human CRP directly inhibits the binding of leptin to its receptors and blocks its ability to signal in cultured cells. C reactive protein was identified as a circulating factor that binds to leptin, impairs its signaling, and attenuates its physiologic effects. Recently, human CRP has been correlated with increased adiposity and plasma leptin. Data suggest that leptin enters the brain by a saturable transport system. The capacity of leptin transport is lower in obese individuals, and may provide a mechanism for leptin resistance (Gandhi et al., 2009).
Leptin uptake into the brain is facilitated by leptin receptors expressed by endothelial cells in the blood brain barrier that function as
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leptin transporters. Impaired leptin transport across endothelial cells of the BBB is one potential mechanism leading to leptin resistance (Singla et al., 2010).
Leptin deficiency :
Congenital leptin deficiency due to a mutation in the leptin gene or receptors produces massive obesity. Early onset obesity and profound hyperphagia are characteristic of these individuals, as are hyperinsulinemia and advanced bone age (Jackson and Ahima, 2006).
Other characteristics of affected patients included: (Mantzoros, 2009)
• Alterations in immune function (decrease in the absolute CD4+ T cell count with compensatory increase in the CD19+ B cell count). • Normal linear growth, but reduced adult height as adults (due to lack of pubertal growth spurt). • Delayed puberty due to hypogonadotropic hypogonadism. • Increased serum leptin concentrations (consistent with their elevated fat mass).
Leptin replacement:
Leptin treatment is ineffective in the majority of obese patients because human obesity is associated with leptin resistance . Leptin administration for the relative leptin deficiency in women with functional hypothalamic amenorrhea (due to weight loss, excessive exercise, or an eating disorder) may improve function of the reproductive axis (increased serum luteinizing hormone concentrations and pulsatility) as well as the thyroid and growth hormone axes (Welt et al., 2004).
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LASER
Definition of laser:
The word laser is an acronym for light amplification by stimulated emission of radiation. It refers to the production of a beam of a radiation which differs from the ordinary light in several ways (Karu, 2002).
Laser Physics:
Light is a form of electromagnetic energy that has wavelengths between 100 100,000 nanometers (nm=10 9 m) in electromagnetic spectrum. Light energy is transmitted through space as waves that contain photons. Each photon contains a definite amount of energy depending on its wavelength. Color is a frequency within the visible spectrum from violet at 400nanometers (higher energy photon) through red at 780 nanometers (lower energy photon). Beyond the red portion of the visual range is the infra red region and below the violet end are ultraviolet ray region (Webb and Dyson, 2003).
Properties of laser light: Laser light has the following characteristics (Kolyakov et al., 2001): 1 A high degree of monochromaticity: The light produced by a laser is single colored. The majority of the radiation emitted by the treatment device is clustered around a single wavelength with a very narrow bandwidth. In contrast, light generated by other sources comprises a wide variety of wavelengths ranging from the ultraviolet to the infrared. Wavelength is a factor in determining the therapeutic effects produced by laser treatment as this parameter determines which specific bimocular absorb the incident radiation and
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thus the specific photobiological interaction underlying any given treatment effect. 2 A high degree of collimation: In laser the rays of light or photons produced by the laser device for all practical purposes are parallel with almost no divergence of the emitted radiation over distance .This property keeps the optical power of the device bundled into a relatively small area over considerable distances. 3 A high degree of coherency: The light emitted by laser devices is not only of the same wavelength but also in phase so in conjunction with the two unique properties already outlined above the thoughts and peaks of the emitted waves match perfectly in time (temporal coherence) and in space (spatial coherence) as they are all travelling in the same direction. The distance over which the wavelengths stay in phase is called coherence length. It varies from less than a millimeter to hundreds of meters coherence. Principle components of laser system: The components of the laser system for the production of a laser radiation can be described as the following (Karu, 2003) : 1 Lasing medium: The material which is capable of producing laser is known as lasing medium. It can absorb energy from the external source and then gives off its excess energy as photons of light. Lasing medium could be solid crystal or semiconductor, liquid or gas. The lasing medium in low intensity laser or cold laser is either helium neon (He Ne) or semiconductor, i.e. gallium arsenide (Ga As). 2 Resonating chamber: The resonating chamber contains the lasing medium which is surrounded by two parallel mirrors at either ends. One of the mirrors has 100% reflectance while the other has slightly less
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reflectance. The mirror with slightly less reflectance serves as an output device which allows some of the photons to escape through it. 3 Energy source: A flashgun is used to excite the electrons of the lasing medium. The source of flashgun is usually current electricity.
Types of laser: Lasers are classified according to the nature of the material placed between the two reflecting surfaces. There are potentially thousands of different types of lasers each with specific wavelength and unique characteristics depending on the utilized medium (Karu and Kolyakov, 2005).
The lasing mediums used to create lasers include the following categories: crystal (solid state), gas, semiconductor, liquid and chemical (Tanzi et al., 2003).
1) Crystal Laser (Ruby Laser): it is called ruby laser because it contains the synthetic ruby (aluminium oxide and chromium) as a lasing medium. Synthetic rather than natural materials are used to ensure purity of the medium which is necessary for the physical characteristics of the laser to occur
2) Gas Lasers: These lasers developed in 1961, shortly after ruby laser. The gas lasers include the Helium Neon (He Ne), argon and carbon
dioxide (Co 2) laser along with numerous others
3) Diode Laser (Semiconductor Laser): Gallium and arsenide are used as a diode or semiconductor to produce an infrared invisible laser with a wavelength of 904 nm. By varying the ratio of gallium to aluminium, desired specific wavelengths are obtained. The advantage
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of semiconductor laser diode is that these can either emit a continous or a pulsed output
4) Liquid Lasers: Are also known as dye lasers because they use organic dyes as the lasing medium. By varying the mixture of the dyes, the wavelengths of the lasers can be varied .
5) Chemical Lasers: Are extremely powered and frequently used for military purposes, they are also called hot lasers and they are used in surgical cutting and coagulation as in ophthalmology and dermatology
Safety Classification of lasers: Laser can be classified into four groups according to their potential danger on the skin and the eyes (Sun and Tunѐr, 2004). Class 1 (Low power laser): This includes low power laser devices operating in the visible portion of the electromagnetic spectrum. The exceptionally low radiant power output of these units is (< 0.5 mW).That means they are suitable for therapeutic applications
Class 2 (visible low power laser): This classification is limited to low power laser in the visible range which is safe for extended period of irradiation over unprotected skin. He Ne with radiant power output up to 1 m W is class 2. Class 3 (visible and nonvisible mid power laser): Commercially therapeutic lasers fall within this category and pose ocular hazards. Radiant power output of such classes is extended from 1 mW to 500 mW. Class 4 (high power laser): This class includes lasers which are much hazardous than those included in class 3 especially to unprotected skin and the eyes. Units
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falling within this category are unsuitable as a therapeutic laser.
Example for such class is Argon and CO 2 lasers.
Dangers and contraindications:
Protective goggles, specific for the wavelength, must be used for the patient and the therapist. Although there are no contraindications reported for dental therapeutic lasers, some side effects exist. Suspected malignancies should never be treated by anyone but by the specialist. Because laser light affects several rheologic factors, patients with coagulation disorders need special attention (Siposan and Lukacs, 2001).
Laser tissue interaction: The interaction between light and tissue has three levels, firstly, the atomic, secondly the molecular and finally the macromolecular level. The atomic level of interaction is predominant in the X and Gamma ray bond of electromagnetic spectrum. The 2 nd level of light tissue interaction is the molecular level which can be described in simple terms as: excitation of the electron bonds within biomolecules, excitation of atoms to higher modes of oscillation relative to each other and as well as rotation of the whole biomolecules or parts of the whole molecules by the external electromagnetic field created by the incident light. Finally the 3 rd level of interaction is at the macromolecular and microstructural level. These interactions result in scattering (change in direction) of light as it propagate in tissues (Prahl et al., 2000).
The two most important modes of light interaction with tissue during laser treatment procedures are absorption and scattering. Laser absorption is primary in the infrared spectrum for wavelength longer than 1200 nm and in the ultraviolet spectrum for wavelengths shorter than 200 nm
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where the organic molecules responsible for light absorption can be divided into two groups. The first of these contains amino acids and nucleic acid bases and the other group is called chromophores (Whelan et al., 2001). Table (3): Main endogenous chromophores present in mammalian cells/tissues (Kolyakov et al., 2001) Chromophores Light absorption range
H2O Far UV (< 200 nm) and infrared (1000 1700 nm) DNA, RNA UV B (max. 260 nm) Proteins UV B (max. 270 280 nm) Urocanic acid UV B (max. 240 280 nm) Porphyrins, Blue (max. ca. 400 nm) with less intense bands in Hemoproteins the green (500 560 nm) and red (620 650 nm) and very weak bands at ca. 780 and 900 nm. Flavins Blue (420 440 nm) Carotenes Blue green (460 500) Bilirubin Blue green (460 500) Melanin All UV/visible spectrum, steadily decreasing with increasing wavelength
The absorption properties of tissue are determined by amino acids in the mid and far ultra violet. Scattering may be defined as a change in the direction of propagation of light. Measurements in human skin irradiated with a He Ne laser (632.8) have shown that 90% of the He Ne radiation is scattered parallel to the incident beam and only 10% is scattered sideways, the relative degree of absorption and scattering that occurs in particular situation is dependent upon the type of tissue through which the
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light is passing as well as the wavelength of the incident light ( Kolyakov et al., 2001).
Classification of lasers:
Lasers can be categorized either as high or low power depending on the intensity of energy they deliver (Karu and Kolyakov, 2005).
High power lasers also known as (Hot) lasers because of the thermal responses they generate. They are used in the medical realms in numerous areas including surgical cutting and coagulation, ophthalmology, dermatology, oncology and vascular surgery
Low power lasers also known as (cold or soft) lasers are used for wound healing and pain management. Low power lasers are relatively new area of application in medicine . These lasers produce a maximal output of less than 1 milli watt (1 mW = 1/1000 W) causing photochemical rather than thermal effects
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Table (4): common types of low energy lasers (Tanzi et al., 2003): Laser Wavelength Argon (AR) 488 514 nm Carbon dioxide (CO2) 10,600 nm Dye Variable Gallium arsenide (GaAs) 904 nm Or infrared(IR) Gallium aluminum arsenide(Ga Al 830 nm As) Helium Neon (He Ne) 623,8 nm Neodymium: Yttrium 1,064 nm Aluminum garnet (Nd:YAG) Ruby 694 nm
The names to identify and differentiate therapeutic lasers from surgical lasers include soft, cold, low intensity laser therapy, and LLLT. Therapeutic lasers are classified as class III medical devices, and surgical lasers are classified as class ІV. Some phrases and phenomena describing the biologic effects of the therapeutic lasers are laser photobiostimulation, or biostimulation. In addition to the stimulating effects, the cellular effects and the bioinhibition which can increase or decrease the physiologic functions to reach normalization. A more appropriate designation of the phenomenon might be laser photobiomodulation or laser bioactivation. The phrase “therapeutic laser” has also been used to suggest the purpose and intent of the treatment (Sun and Tun'r, 2004).
LLLT or “cold” lasers use radiation intensities so low so it is thought that any biological effects occur are due to the direct effects of radiation rather than the result of heating. Energies delivered are typically
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about 10 joules per cm 2 and using laser operating at powers of 50mW or less. LLLT devices have been advocated for relief of pain, healing of soft tissue disorders and treatment of peripheral neuropathies, and there is a number of low intensity lasers used clinically. The two most commonly used types are Helium Neon (He Ne) laser and The Gallium Arsenide (Ga As) laser. He Ne laser is a continuous wave with an averaged power output of 1mW. It has a depth of penetration (5 to 10 mm) depending on its wavelength (632.8 nm). It was the first laser available and it is reported to have beneficial effects in wound healing. It has the advantage that it emits red light, which is visible and therefore, the blink reflex protects the eye from it (Schindle et al., 2003) .
Exposure to lasers as well as light emitting diode (LED) light is currently applied in therapy. The most effective irradiation is that in the red and near Infrared range of the spectrum. The most commonly used sources are the He Ne laser (radiation at 632.8nm),Ga Al (630 685), The helium neon arsenate laser (780 870) and the (Ga As) laser (904nm), as well as light emitting diodes whose emission band lies in a wide region of the spectrum(670 to 950nm). The main reason for using the sources radiating in the red and near infrared spectral region is the fact that hemoglobin does not absorb light in this region and can penetrate deep into living tissues (karu, 2003). Low Level Laser Therapy (LLLT):
LLLT is also known as biostimulation or photobiostimulation this form of phototherapy involves the application of red to near infra red light over injuries or lesions to stimulate healing and control acute and chronic pain (Hawkins and Abrahamse, 2005).
Low energy photon irradiation by light in the infra red to near
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infra–red spectral range with low level lasers or light emitting diode (LED) arrays has been found to modulate various biological processes in cell culture and animal models (Karu and Kolyakov, 2005).
A biphasic dose response has been frequently observed where low levels of light have a much better effect on stimulating and repairing tissues than higher levels of light. The so called Arndt Schulz curve is frequently used to describe this biphasic dose response (Huang et al., 2011). Fig. (3)
Arndt Chaltz Law "Fig. (3)"
This law has been proposed as a suitable model for providing theoretical basis for the variable laser light effects upon tissues.
(c) (b)
Biological response (a) Intensity of stimulation Fig. (3): Arndt Chaltz Law (Huang et al., 2009) (a) Prethreshold (no biological response) (b) Biostimulation (c) Bioinhibition.
LLLT has been shown to increase the speed, quality and tensile strength of tissue repair, resolve inflammation and provide pain relief. Lasers are already used in a variety of medical and surgical fields, including dentistry, chiropractice, osteopathy, physiotherapy, pain attenuation, wound healing and acupuncture (Reddy et al., 2001).
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LLLT increases metabolism at cellular level, causing accelerated ATP production and protein synthesis. New blood vessels are formed and collagen synthesis is enhanced. Vascular relaxation and increased skin microcirculation are noted following administration of LLLT (Karu, 2003).
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Radioimmunoassay (RIA)
A serum leptin concentration is measured by radioimmunoassay on a morning fasting venous blood sample. Using recombinant human leptin, a sensitive RIA for this protein was developed that proved to be specific, precise, accurate, and robust. Its sensitivity is higher by an order of magnitude compared with currently commercially available assays, which allowed the precise measurement of low leptin levels especially in lean young children and male adolescents. The investigation of the stability of immunoreactive leptin demonstrated that serum leptin is a comparatively stable protein, which makes sample handling unproblematic. Recently, it was reported that leptin is partially bound to specific binding proteins in the circulation. Therefore, it was important to examine whether the assay detects only free or total leptin. From systematic studies of human sera from lean and obese subjects by exclusion chromatography, it became clear that the RIA detects primarily total leptin and that leptin binding proteins do not interfere in the assay, most probably because of the high affinity of the antibody. Serum leptin concentrations correlated with body mass index and were significantly higher in women than in men, except for obese patients (Lagarde et al., 2003).
Radioimmunoassay Principle: The principal of RIA involves competitive binding of radio labeled antigen and unlabeled antigen to a high affinity antibody. The labeled antigen is mixed with antibody at a concentration that saturates the antigen – binding sites of the antibody. Then the test samples of unlabeled antigen of unknown concentration are added in progressively larger amounts. The antibody does distinguish labeled from unlabeled antigen. So the two kinds of antigen compete for available binding sites
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on the antibody. As the concentration of unlabeled antigen increases, more labeled antigen will displaced from the binding sites. The decrease in the amount of radio labeled antigen bound to specific antibody in the presence of the test sample is measured in order to determine the amount of antigen present in the test sample. RIA measures the effect of varying concentration of compound in biological fluid on an in vitro system containing radioactive standards of the compound and a specific antibody. In fact RIA is a heterogeneous, limited reagent and competitive assay (Mayer, 2010).
Fig. (4): Radioimmunoassay test (Mayer 2010).
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General procedure for RIA:
A known quantity of an antigen is made radioactive, frequently by labeling it with gamma radioactive isotopes of iodine attached to tyrosine. This radio labeled antigen is then mixed with a known amount of antibody for that antigen, and as a result, the two chemically bind to one another. Then a sample of serum from a patient containing an unknown quantity of that same antigen is added. This causes the unlabeled (cold) antigen from the serum to compete with the radio labeled antigen for antibody binding sites, as the concentration of cold antigen is increased , more of the binds to the antibody , displacing the radio labeled variant , and reducing the ratio of antibody – bound radio labeled antigen to free radio labeled antigen (Mayer, 2010).
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Chapter III Subjects and Methods
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SUBJECTS AND METHODS Subjects:
Twenty women with abnormal body contouring & fat distribution at thigh &abdominal areas participated in the study. Their age ranged from 30 to 40 years. They were selected from the poly clinic of National Center for Radiation Research & Technology (Atomic Energy Authority). They were free from any other health problems that may affect the results of the study such as pregnancy, metabolic & cardiovascular diseases, local diseases of the skin, cancer or receive chemotherapy. All of them were weighted on the same weight scale. Their weights ranged from 70 120 kg.
The subjects were selected according to the following criteria:
Inclusive criteria:
Criteria of selecting the patients included the following:
• Their ages were ranged from 30 to 40 years. • Their BMI ranged from 26 – 40 kg /m2. • All women were non pregnant women. • Women were able to follow instructions. • Women were free from any pathological condition that may interfere with the treatment results. • All patients were conscious & cooperative. • None of them has been engaged in any organized slimming program.
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Exclusion criteria:
Any patient with any of the following was excluded from the study:
• women who follow simultaneous weight reduction methods. • Pregnant & lactating women and women with high blood prolactin level. • Diseases of the skin. • Thrombosis or post thrombosis syndrome. • Cancer or chemotherapy. • Cortisone Therapy. • Known metabolic disorders (i.e., diabetes mellitus, hypercholesterinemia etc.). • Open wounds, ulcers. • Inflammation within treatment area. • Endocrinal causes e.g. (hyperthyroidism, Cushing disease). • Any severe medical disorders, such as renal, neurological, psychological, obstructive and restrictive chest diseases. • Alcoholic addicted, drug addicted, smokers. • Patients receiving diuretics.
Design of the study:
The study was conducted in The National Centre for Radiation Research and Technology(NCRRT) Atomic Energy Authority. It was conducted from 1/10/2011 to 25/10/2012. The study included two groups:
Group A (Overweight group): included 10 women with BMI ≥ 25 29.9 kg/m².
Group B (Obese group): included 10 women with BMI ≥ 30 kg/m².
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The treated groups received low level laser therapy (30 minutes per session, 2 times per week for 8weeks. Equipments and tools used:
The study equipment’s divided into measuring equipment and therapeutic equipment:
Measuring equipments and tools:
1 Standard weight and height scale:
TANITA body fat monitor/scale (TBF 611 Tanita Co operation Tokyo Japan) was used to measure weight and height for each subject before treatment and after 8weeks of treatment for both groups (A& B) to calculate BMI (Fig. 5).
Figure (5): standard weight and height scale.
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2 Tape Measurement: It was used to measure the waist and hip circumferences before and after the end of the treatment course for both groups A & B to calculate waist hip ratio.
3 Gamma counter device: Automatic Gamma Counter (Genesys TM , Genii TM gamma counters, LTI 1005, LTI Laboratory Technologies, INC., 43W900 Route 64 Maple Park, IL 60134, USA.) (Fig.6) that was in analysis of blood samples.
Figure (6): The Gamma Counter device.
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4 Spectrophotometer: was used to measure cholesterol, triglycerides for all patients before and after the study (Figure 7).
Fig. (7): Spectrophotometer.
Therapeutic equipment: • Low level laser scanner diode 808 nm wave length equipment (type Electronica PAGANI, Mod: HPL 1.6) (fig. 8&9). Mode: Continuous wave. Power: 1.6 watt Dose: 10 joule
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Fig. (8): low level LASER device.
Figure (9): head and digital screen of the laser device.
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• Protective goggles that was used for patients and therapist during application of laser therapy (fig.10).
Fig. (10): protective goggles. Measurement procedures:
Subjects were given information about measurement and treatment procedures, also about the laser device before beginning the treatment.
All women signed consent form of approval to participate in the study (Appendix I). The following procedures were followed for all subjects in both groups. a) Anthropometric measurements procedures: a – BMI calculation:
In order to calculate BMI for each patient, weight and height were measured for each patient by weight and height scale (fig.11).
Each subject was weighted in light clothes. The body mass index was calculated by a simple mathematical equation by dividing weight
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(kg)/ height (m 2) which was done before and after 8 weeks of treatment for both groups. calculating BMI according to the equation. BMI= weight (Kg) / height ² (m²) (WHO, 2004) .
Fig. (11) Measurement of body weight.
b WHR calculation: By using tape measurement and from standing position: The waist circumference was measured at the level of the umbilicus. Then the hip circumference was measured by passing posteriorly 5cm below the posterior superior iliac spines and anteriorly at the level of the upper border of symphesis pubis.
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BMI and WHR were performed three times by the candidate to insure reliability and accuracy and the mean of the results were reported. b) Laboratory measurements: Sampling procedures: Blood samples were taken from both groups, before and after two month of the experiment. This was done in Atomic Energy Authority .These samples were taken to measure: 1 leptin hormone . 2 Concentration of total cholesterol. 3 Concentration of triglycerides. Case preparation: Blood samples withdrawn from each patient after an overnight fasting of 12 14 hours. Each patient was well rested and seated for 5 10 minutes before blood collection. Sample requirement: About 5ml of venous blood was withdrawn then centrifuged at 10,000 rpm for 10 min., and then the supernatant serum was collected and kept frozen at 80ºC until biochemical analysis. The laboratory method: 1 Radioimmunoassay of leptin: (Ruhl et al., 2007) Assay principle: Samples should be handled as recommended in general: as fast as possible and chilled as soon as possible. In case there were be a longer period between the sample withdrawal and determination the undiluted
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samples were stored frozen at –20°C or below in tightly closable plastic tubes. Avoid on principal repeated freeze thaw cycles of serum/plasma, although Leptin levels were found to be unaffected by few cycles (5x). The high sensitivity of the assay allows measurement of human leptin in small sample volumes. Because of the wide effective range of this RIA kit a preparative sample dilution is generally not necessary. For most of the determinations (serum or plasma samples, and no extreme values expected). In case Leptin levels of more than 64 ng/ml are expected, e.g. Obese patients (BMI>35), the sample can be diluted, e.g. 1:10. Assay procedure . Standards or diluted samples (100 L; 1:3 to 1:10 in assay buffer) were pipetted into polystyrene tubes, and 100 L each of first antibody [1:10,000 in assay buffer, containing 150 g/mL rabbit gamma globulin (Sigma)] and radio iodinated leptin (150,000–200,000 c pm/mL in assay buffer) were added. After overnight incubation at room temperature, separation of free and bound tracer was achieved by adding 500 L of cold 4% (wt:vol) polyethylene glycol 6000 (Serva) containing a goat antirabbit IgG serum (DSL, Webster, MA; 1:150). After 30 min at 4 C, the bound tracer was precipitated by centrifugation (15 min × 2000 g) and the radioactivity was measured using a gamma counter spectrometer. 2) Serum Cholesterol and triglycerides levels: Both were estimated using the enzymatic colorimetric test .
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Treatment procedures:
In this study treatment protocol presented under the following headings
women treated as outpatients, each woman informed by the date and the time of her session. Measurement procedures were applied for each woman at the session 3 times by the therapist before the first session and at the end of the study. The women were instructed to wear goggles each time on laser irradiation to protect their eyes. Switch device on and adjust its arm to the area treated Cleaning area by alcohol to remove any resistance to laser absorption by the skin. The women were placed in a suitable comfortable position according To the area treated on a wooden plinth and in a suitable room for laser application as it free from any metals or mirrors to avoid any reflections. Supine lying position when applied to abdomen and prone lying when applied to buttocks and thighs and place the woman head at the plinth whole to keep in a comfortable position. When applied to abdomen the laser line limited between both anterior superior iliac spines. Laser dose 10 J. Treatment session was done 30 minutes, 2 sessions per weak for 8 weeks as a total period of treatment (Caruso Davis, 2011).
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Statistical procedures:
Data were collected for all patients and statistically analyzed using program (Graph Pad Instat 3).
Data are presented as mean, range, probability, standard deviation.
Paired (T) test: Was used to compare values between pre & post treatment within each group. Independent t test: Used to compare values between pre & post treatment within the two groups. The correlation coeffi5cient (r value): The correlation between the various parameters estimated in all groups was calculated using the correlation coefficient. The level of significance was determined as: P > 0.05 = Non significant. P < 0.05 = Significant. P < 0.001 = highly significant.
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Chapter IV Results
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RESULTS The purpose of this study was to investigate the effect of low level laser therapy on both anthropometric parameters and the serum leptin level in overweight and obese healthy females. General Characteristics of the Subjects: In this study, ten over weight and ten obese women were assigned. Table (5): Physical characteristics of women in both groups (A&B). Items Group A Group B Comparison (Over weight) (Obese) Mean ±SD Mean ±SD t value P value Age (years) 32.7 ±3.09 35.3 ±3.97 1.63 0.12 Weight (Kg) 77.85 ±5.39 99.9 ±15.21 4.32 0.0001** Height (cm) 164.35 ±6.94 161.1 ±9.02 0.9 0.37 BMI (Kg/m 2) 28.81 ±0.78 38.65 ±6.57 4.7 0.0001**
*SD: standard deviation, P: probability, : non significant, **: highly significant. Group (A) (Over weight group): Ten overweight women were included in this group. The data in table (5) and (Figure 12, 13, 14 and 15) illustrate their mean age 32.7±3.09 years, mean weight 77.85±5.39 kilograms (Kg), mean height 164.35±6.94 centimeters (cm), and mean BMI 28.81±0.78 (Kg/m 2). Group (B) (Obese group): Ten obese women were included in this group. The data in table (5) and (Figure12, 13, 14 and 15) declare their mean age 35.3±3.97 years, mean weight 99.9±15.21 kilograms (Kg), mean height 161.1±9.02 centimeters (cm), and mean BMI 38.65±6.57 (Kg/m 2). There were insignificant differences between both groups in their ages and heights where their t and P values were 1.63, 0.12 and 0.9, 0.37
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respectively, while there was a highly significant difference between both groups in their weight and BMI where their t and P values were 4.32, 0.0001and 4.7, 0.0001 respectively.
Group (A) Group (B)
50 40
30 35.3 32.7 20
Age (Years)
10 0 Fig. (12): Mean ±SD of the age for groups (A, B). Group (A) Group (B) 120 90 99.9 77.85 60
Weight(Kg) 30 0 Fig. (13): Mean ±SD of the weight for groups (A, B)
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.
Group (A) Group (B) 200 160 164.35 161.1 120
80 Height (Cm) 40 0 Fig. (14): Mean ±SD of the height for groups (A, B). Group (A) Group (B) 50 40 38.65 30 28.81 20 BMI (Kg/m2)BMI 10 0 Fig. (15): Mean ±SD of the BMI for groups (A, B).
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Anthropometric measurements: 1 Body Weight: i) Pre and post treatment results within subjects:
Group (A):
Table (6): Mean ±SD, t and P values of body weight pre and post treatment of group (A). Group A Body Weight (Over weight) Pre treatment Post treatment Mean 77.85 77.3 ±SD ±5.39 ±6.0 Mean difference 0.55 Percentage of improvement 0.7 % ↓ DF 9 t value 1.33 P value 0.21 *SD: standard deviation, P: probability, DF: degree of freedom
Table (6) & Figure (16) demonstrate the body weight pre and post treatment for group A. There was non significant difference in the paired t test between pre and post treatment body weight as the mean value of pretreatment body weight was 77.85 ± 5.39 while for post treatment it was 77.3±6.0 where the t value was 1.33 and P value was 0.21. The percentage of improvement (decrease) was 0.7 %.
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Pre treatment Post treatment 100 80
77.85 77.3 60 40
Weight (Kg) Body
20 0 Fig. (16): Mean ±SD of body weight pre and post treatment of group A. Group (B):
Table (7): Mean ±SD, t and P values of body weight pre and post treatment of group (B). Group B Body Weight (Obese) Pre treatment Post treatment Mean 99.9 97.25 ±SD ±15.21 ±14.83 Mean difference 2.65 Percentage of improvement 2.65 % ↓ DF 9 t value 3.83 P value 0.008* *SD: standard deviation, P: probability, *: significant, DF: degree of freedom
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Table (7) & Figure (17) show the body weight pre and post treatment for group (B). There was a significant difference in the paired t test between pre and post treatment body weight as the mean value of pretreatment body weight was 99.9± 15.21while it was 97.25±14.83 where the t value was 3.83 and P value was (0.008). The percentage of improvement (decrease) was 2.65 %. Pre treatment Post treatment 120 90 99.9 97.25 60
Weight Body (Kg) 30 0 Fig.(17): Mean ±SD of body weight pre and post treatment of group (B). ii)Comparison of the results between Groups: Table (8): Independent t test between groups A and B for body weight pre and post treatment. Independent t test Body Weight Pre Post Mean difference 22.05 19.95 t value 4.32 3.94 P value 0.0001** 0.001* *SD: standard deviation, P: probability, *: significant, **: highly significant.
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Table (8) & Figure (18) reveal the independent t test results for the body weight pre and post treatment between groups A and B. There was a highly significant difference in pretreatment values where the t value was 4.32 and p value was 0.0001 Also, there was a significant difference in the post treatment values where the t value was 3.94 and p value was 0.001.
Group (A) Group (B)
120 90 99.9 97.25 77.85 77.3 60
Body Body Weight (Kg) 30
0 Pre treatment Post treatment Fig.(18): Mean ±SD of body weight pre and post treatment of groups (A,B).
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2 BMI: i) Pre and post treatment results within Subjects:
Group (A):
Table (9): Mean ±SD, t and P values of BMI pre and post treatment of group (A). Group A BMI (Over weight) Pre treatment Post treatment Mean 28.81 28.58 ±SD ±0.78 ±0.45 Mean difference 0.22 Percentage of improvement 0.76 % ↓ DF 9 t value 1.49 P value 0.17
*SD: standard deviation, P: probability, NS: non significant, DF : degree of freedom. Table (9) & Figure (19) demonstrate the BMI pre and post treatment for group A. There was non significant difference in the paired t test between pre and post treatment BMI as the mean value of pretreatment BMI was 28.81 ± 0.78 while for post treatment it was 28.58±0.45 where the t value was 1.49 and P value was 0.17. The percentage of improvement (decrease) was 0.76 %.
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Pre treatment Post treatment 35 30 25 28.81 28.58
20 15 BMI (Kg/m2) 10 5
0 Fig.(19): Mean ±SD of BMI pre and post treatment of group (A). Group (B):
Table (10): Mean ±SD, t and P values of BMI pre and post treatment of group (B). Group B BMI (Obese) Pre treatment Post treatment Mean 38.65 37.64 ±SD ±10.67 ±6.57 Mean difference 1.01 Percentage of improvement 2.61 % ↓ DF 9 t value 3.17 P value 0.01* *SD: standard deviation, P: probability, *: significant, DF: degree of freedom
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Table (10) & Figure (20) indicate the BMI pre and post treatment for group (B). There was a significant difference in the paired t test between pre and post treatment BMI as the mean value of pretreatment BMI was 38.65 ± 10.67 and for post treatment it was 37.64±6.57 where the t value was 3.17 and P value was (0.01). The percentage of improvement (decrease) was 2.61 %. Pre treatment Post treatment 60 50 40 38.65 30 37.64 BMI (Kg/m2) 20 10 0 Fig.(20): Mean ±SD of BMI pre and post treatment of group (B). ii) Comparison of the results between Groups: Table (11): Independent t test between groups A and B for BMI pre and post treatment. Independent t test BMI Pre Post Mean difference 9.83 9.05 t value 4.7 4.47 P value 0.0001** 0.0001** *SD: standard deviation, P: probability, **: highly significance. Table (11) & Figure (21) depicts the independent t test results for the BMI pre and post treatment between groups A and B. There was a highly significant difference in pretreatment values where the t value was 4.7 and p value was 0.0001 and also, there was a significant difference in
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the post treatment values where the t value was 4.47 and p value was 0.0001.
Group (A) Group (B) 60 50
40 38.65 30 37.64 28.81 28.58
BMI (Kg/m2) 20
10 0 Pre treatment Post treatment Fig.(21): Mean ±SD of BMI pre and post treatment of groups (A,B). 3 Waist circumference: i) Pre and post treatment results within subjects:
Group (A):
Table (12): Mean ±SD, t and P values of waist circumference pre and post treatment of group (A). Group A Waist circumference (Overweight) Pre treatment Post treatment Mean 98.45 88.7 ±SD ±6.86 ±6.35 Mean difference 9.75 Percentage of improvement 9.9 % ↓ DF 9 t value 5.62 P value 0.0001**
*SD: standard deviation, P: probability, **: highly significance, DF : degree of freedom.
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Table (12) & Figure (22) signify the waist circumference of the pre and post treatment of group A. There was a highly significant difference in the paired t test between pre and post treatment as the mean value of pretreatment waist circumference was 98.45 ± 6.86 and for post treatment it was 88.7±6.35 where the t value was e5.62 and P value was 0.0001 the percentage of improvement (decrease) was 9.9%. Pre treatment Post treatment 120 90 98.45 88.7 60
30 (Cm) Circumference Waist
0 Fig.(22): Mean ±SD of waist circumference pre and post treatment of group (A). Group (B):
Table (13): Mean ±SD, t and P values of waist circumference pre and post treatment of group (B). Group B Waist circumference (Obese) Pre treatment Post treatment Mean 111.3 100.3 ±SD ±12.43 ±9.1 Mean difference 11.0 Percentage of improvement 9.88 % ↓ DF 9 t value 5.69 P value 0.0001** *SD: standard deviation, P: probability, **: highly significance, DF: degree of freedom
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Table (13) &figure (23) demonstrate the waist circumference of the pre and post treatment of group B. There was a highly significant difference in the paired t test between pre and post treatment as the mean value of pretreatment waist circumference was 111.3± 12.43 and for post treatment it was 100.3±9.1 where the t value was 5.69 and P value was 0.0001 the percentage of improvement (decrease) was 9.88%.
Pre treatment Post treatment 140
120 100 111.3 100.3 80 60 40 Waist Circumference (Cm) Circumference Waist 20 0 Fig.(23): Mean ±SD of waist circumference pre and post treatment of group (B). ii) Comparison of the results between Groups: Table (14): Independent t test between groups A and B for waist circumference pre and post treatment. Independent t test Waist circumference Pre Post Mean difference 12.85 11.6 t value 2.86 3.3 P value 0.01* 0.004* *SD: standard deviation, P: probability, *: significance. Table (14) & Figure (24) demonstrate the independent t test results for the waist circumference of the pre and post treatment between groups A and B. There was a significant difference in pretreatment values where
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the t value was 2.86 and p value was 0.01 Also, there was a significant difference in the post treatment values where the t value was 3.3 and p value was 0.004.
Group (A) Group (B) 150 120 111.3 90 98.45 100.3 88.7 60
30 Waist Circumference (Cm) Circumference Waist 0 Pre treatment Post treatment Fig.(24): Mean ±SD of waist circumference pre and post treatment of groups (A,B). 4 Hip circumference: i) Pre and post treatment results within subjects:
Group (A):
Table (15): Mean ±SD, t and P values of hip circumference pre and post treatment of group (A). Group A Hip circumference (Overweight) Pre treatment Post treatment Mean 110.95 108.05 ±SD ±3.98 ±4.54 Percentage of improvement 2.61 %↓ DF 9 t value 4.94 P value 0.001* *SD: standard deviation, P: probability, *: significant, DF: degree of freedom
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Table (15) & Figure (25) show the hip circumference of the pre and post treatment of group A. There was a significant difference in the paired t test between pre and post treatment hip circumference as the mean value of pretreatment Hip circumference was 110.95± 3.98 and for post treatment hip circumference was 108.05±4.54 where the t value was 4.94 and P value was 0.001 the percentage of improvement (decrease) was 2.61 %. Pre treatment Post treatment 140 120
100 110.95 108.05 80 60 40
Hip(Cm) Circumference
20 0 Fig.(25): Mean ±SD of hip circumference pre and post treatment of group (A). Group (B):
Table (16): Mean ±SD, t and P values of hip circumference pre and post treatment of group (B). Group B Hip circumference (Obese) Pre treatment Post treatment Mean 127.8 121.6 ±SD ±11.32 ±10.67 Mean difference 6.2 Percentage of improvement 4.85 %↓ DF 9 t value 6.92 P value 0.0001** *SD: standard deviation, P: probability, **: highly significance, DF: degree of freedom.
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Table (16) & Figure (26) declares the hip circumference of the pre and post treatment of group B. There was a highly significant difference in the paired t test between pre and post treatment hip circumference as the mean value of pretreatment hip circumference was 127.8± 11.32 and for post treatment it was 121.63±10.67 where the t value was 6.92 and P value was 0.0001 the percentage of improvement (decrease) was 4.85 %.
Pre treatment Post treatment 150
120 127.8 121.6 90
60 Hip Circumference Hip (Cm) Circumference 30
0 Fig. (26): Mean ±SD of hip circumference pre and post treatment of group (B). ii)Comparison of the results between Groups: Table (17): Independent t test between groups A and B for hip circumference of the pre and post treatment. Independent t test Hip circumference Pre Post Mean difference 16.85 13.55 t value 4.43 3.69 P value 0.0001** 0.002* SD: standard deviation, P: probability, **: highly significant, *: significant. Table (17) & Figure (27) indicates the independent t test results for the hip circumference of the pre and post treatment between groups A and B. There was a highly significant difference in the pretreatment values where the t value was 4.43 and p value was 0.0001 and also, there was a
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significant difference in the post treatment values where the t value was 3.69 and p value was 0.002. Group (A) Group (B)
150 120 127.8 121.6 110.95 90 108.05 60
30
Hip Circumference Hip (Cm) Circumference 0 Pre treatment Post treatment Fig.(27): Mean ±SD of hip circumference pre and post treatment of groups (A,B). 5 Waist hip ratio: i) Pre and post treatment results within Subjects:
Group (A):
Table (18): Mean ±SD, t and P values of waist hip ratio of the pre and post treated group (A). Group A Waist hip ratio (Overweight) Pre treatment Post treatment Mean 0.88 0.83 ±SD ±0.06 ±0.06 Mean difference 0.05 Percentage of improvement 5.68 %↓ DF 9 t value 7.03 P value 0.0001** *SD: standard deviation, P: probability, **: highly significance, DF: degree of freedom.
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Table (18) & Figure (28) demonstrate the waist hip ratio pre and post treatment for group A. There was a highly significant difference (paired t test) between pre and post treatment Waist hip ratio. The mean value of the pretreatment waist hip ratio was 0.88± 0.06 and for post treatment waist hip ratio was 0.83±0.06 where the t value was 7.03 and P value was 0.0001. The percentage of improvement (decrease) was 5.68 %.
Pre treatment Post treatment 1 0.8 0.88 0.83 0.6 0.4 hipWaist ratio
0.2
0 Fig. (28): Mean ±SD of waist hip ratio pre and post treatment of group (A). Group (B):
Table (19): Mean ±SD, t and P values of waist hip ratio of the pre and post treatment of group (B). Group B waist hip ratio (Obese) Pre treatment Post treatment Mean 0.87 0.83 ±SD ±0.06 ±0.06 Mean difference 0.05 Percentage of improvement 5.05 %↓ DF 9 t value 3.09 P value 0.01* *SD: standard deviation, P: probability, *: significant, DF: degree of freedom
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Table (19) & Figure (29) declares the waist hip ratio of the pre and post treatment for group B. There was a significant difference in the waist hip ratio in the paired t test between pre and post treated group B. The mean value of pretreatment waist hip ratio was 0.87 ± 0.06 and for the post treatment it was 0.83±0.06 where the t value was 3.09 and P value was 0.01. The percentage of improvement (decrease) was 5.05 %. Pre treatment Post treatment 1 0.8 0.871 0.826 0.6 0.4 hipWaist ratio
0.2 0 Fig. (29): Mean ±SD of waist hip ratio of the pre and post treated group (B). ii) Comparison in the results between Groups: Table (20): Independent t test between groups A and B for waist hip ratio pre and post treatment. Independent t test waist hip ratio Pre Post Mean difference 0.02 0.01 t value 0.56 0.18 P value 0.58 0.85 *SD: standard deviation, P: probability. Table (20) & Figure (30) indicate the independent t test results for the waist hip ratio of the pre and post treatment (between group A and B). There was a non significant difference in pretreatment values where the t value was 0.56 and p value was 0.58. Also, there was a non significant
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difference in the post treatment values where the t value was 0.18 and p value was 0.85. Group (A) Group (B)
1
0.8 0.88 0.871 0.83 0.826 0.6 0.4 Waist hipWaist ratio 0.2
0 Pre treatment Post treatment Fig. (30): Mean ±SD of waist hip ratio of the pre and post treated groups (A, B). Laboratory measurements: 1 Leptin level: i) Pre and post treatment results within subjects:
Group (A):
Table (21): Mean ±SD, t and P values of leptin level of the pre and post treated group (A). Group A leptin level (Overweight) Pre treatment Post treatment Mean 28.68 17.62 ±SD ±4.16 ±6.79
Mean difference 11.06 Percentage of improvement 38.56 %↓ DF 9 t value 5.95 P value 0.0001** *SD: standard deviation, P: probability, **: highly significance, DF: degree of freedom`
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Table (21) & Figure (31) demonstrate the leptin level of the pre and post treated group A. There was a highly significant difference in the paired t test in leptin level between the pre and post treated group A. The mean value of pretreated group leptin level was (28.68± 4.16) and for post treatment it was 17.62±6.79 where the t value was5.95) and P value was 0.0001. The percentage of improvement (decrease) was 38.56 %.
Pre treatment Post treatment 35 30 25 28.68
20 15 Leptinl level 17.62 10 5 0 Fig. (31): Mean ±SD of leptin level pre and post treatment of the group (A). Group (B):
Table (22): Mean ±SD, t and P values of leptin level of the pre and post treated group (B). Group B Leptin level (Obese) Pre treatment Post treatment Mean 29.28 19.86 ±SD ±4.98 ±5.42 Mean difference 9.42 Percentage of improvement 32.17 %↓ DF 9 t value 8.95 P value 0.0001** *SD: standard deviation, P: probability, **: highly significance, DF: degree of freedom
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Table (22) & Figure (32) illustrates the leptin level of the pre and post treated group B. There was a highly significant difference in leptin level (paired t test) between pre and post treatment leptin level. The mean value of the pretreatment stage of leptin value was 29.28 ± 4.98 while, it was (19.86±5.42) for the post treatment period. The t value was 8.95 and P value was 0.0001. The percentage of improvement (decrease) was 32.17 %.
Pre treatment Post treatment 35 30 25 29.28 20
15 19.86 Leptinl level
10 5 0 Fig. (32): Mean ±SD of leptin level of pre and post treated group (B). ii)Comparison of the results between Groups: Table (23): Independent t test between groups (A and B) of leptin level pre and post treatment. Independent t test Leptin level Pre Post Mean difference 0.6 2.24 t value 0.29 0.81 P value 0.77 0.42 *SD: standard deviation, P: probability, S: significance, NS: no significant. Table (23) & Figure (33) show the independent t test results for the leptin level of the pre and post treated groups (A and B). There was a non significant difference in pretreatment values where the t value was 0.29 and p value was 0.77 Also, there was a non significant difference in
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the post treatment values where the t value was 0.81 and p value was 0.42. Group (A) Group (B) 35 30 25 28.68 29.28 20 19.86 15 17.62
Leptin level 10 5 0 Pre treatment Post treatment Fig.(33): Mean ±SD of leptin level pre and post treatment of groups (A,B). 2 Cholesterol level: i) Pre and post treatment results within Subjects: Group (A): Table (24): Mean ±SD, t and P values of cholesterol level pre and post treatment of group (A). Group A Cholesterol level (Overweight) Pre treatment Post treatment Mean 168.26 177.33 ±SD ±16.43 ±14.63
Percentage of improvement 5.38 %↑ DF 9 t value 0.99 P value 0.34 *SD: standard deviation, P: probability, DF: degree of freedom Table (24) & Figure (34) indicate the cholesterol level of the pre and post treated group A. There was a non significant difference in the cholesterol level in the paired t test between pre and post treated group A. as the mean value of cholesterol level pretreated was 168.26± 16.43 and it
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was 177.33±14.63in the post treated group A. Where the t value was 0.99 and P value was 0.34. The percentage of increase was 5.38 %. Pre treatment Post treatment 200
160 168.26 177.33 120 80 Cholesterol level 40
0 Fig. (34): Mean ±SD of cholesterol level pre and post treatment of group (A). Group (B): Table (25): Mean ±SD, t and P values of cholesterol level of the pre and post treated group (B). Group B Cholesterol level (Obese) Pre treatment Post treatment Mean 154.22 182.39 ±SD ±23.43 ±22.94 Percentage of improvement 18.26 %↑ DF 9 t value 3.89 P value 0.004* *SD: standard deviation, P: probability, *: significant, DF: degree of freedom Table (25) & Figure (35) demonstrated the cholesterol level pre and post treatment for group (B). There was a significant difference in the paired t test between pre and post treatment cholesterol level as the mean value of pretreatment cholesterol level was (154.22± 23.43) and for post
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treatment cholesterol level was (182.39±22.94) where the t value was (3.89) and P value was (0.004). The percentage of increase was 18.26 %. Pre treatment Post treatment 240 200
160 182.39 154.22 120 Cholesterol level 80
40 0 Fig. (35): Mean ±SD of cholesterol level of the pre and post treated group (B). ii)Comparison of the results Between Groups: Table (26): Independent t test between groups A and B for cholesterol level pre and post treatment. Independent t test Cholesterol level Pre Post Mean difference 14.03 5.06 t value 1.55 0.58 P value 0.13 0.56 *SD: standard deviation, P: probability. Table (26) & Figure (36) reveal the independent t test results for the Cholesterol level of the pre and post treatment between groups A and B. There was no significant difference in pretreatment values where the t value was (1.55) and p value was (0.13), and also, there was no significant difference in the post treatment values where the t value was (0.58) and p value was (0.56).
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Group (A) Group (B)
240
200 160 177.33 182.39 168.26 154.22 120 80 Cholesterol level Cholesterol 40 0 Pre treatment Post treatment Fig.(36): Mean ±SD of cholesterol level of the pre and post treated groups (A,B). 3 Triglycerides level: i) Pre and post treatment results within Subjects:
Group (A):
Table (27): Mean ±SD, t and P values of triglycerides level of the pre and post treatment of group (A). Group A Triglycerides level (Overweight) Pre treatment Post treatment Mean 71.58 102.51 ±SD ±15.72 ±20.41
Percentage of improvement 43.21 %↑ DF 9 t value 5.48 P value 0.0001**
*SD: standard deviation, P: probability, **: highly significance, DF : degree of freedom
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Table (27) & Figure (37) demonstrate the triglycerides level pre and post treatment for group (A). There was a significant difference in the paired t test between pre and post treatment triglycerides level. The mean value of pretreatment triglycerides level was 71.58± 15.72 and for post treatment triglycerides level was 102.51±20.41 where the t value was 5.48 and P value was 0.0001. The percentage of increase was 43.21 %. Pre treatment Post treatment 150 120 90 102.51 60 71.58 Triglycerides level
30 0 Fig. (37): Mean ±SD of triglycerides level pre and post treatment of group (A). Group (B):
Table (28): Mean ±SD, t and P values of triglycerides level of the pre and post treated group (B). Group B Triglycerides level (Obese) Pre treatment Post treatment Mean 60.65 94.9 ±SD ±9.42 ±26.1 Percentage of improvement 56.47 %↑ DF 9 t value 3.46 P value 0.007* *SD: standard deviation, P: probability, *: significant, DF: degree of freedom
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Table (28) & Figure (38) demonstrate the triglycerides level pre and post treatment for group (B). There was a significant difference in the paired t test between pre and post treatment triglycerides level as the mean value of pretreatment triglycerides level was 60.65± 9.42 and for post treatment Triglycerides level it was 94.9±26.1 .The t value was 3.46 and P value was 0.007. The percentage of increase was 56.47%.
Pre treatment Post treatment 150 120 90 94.9 60
Triglycerides level 60.65 30
0 Fig.(38): Mean ±SD of triglycerides level pre and post treatment of group (B). ii)Comparison of the results between Groups: Table (29): Independent t test between groups A and B for triglycerides level pre and post treatment. Independent t test Triglycerides level Pre Post Mean difference 10.93 7.61 t value 1.88 0.72 P value 0.07 0.47 *SD: standard deviation, P: probability. Table (29) & Figure (39) point out the independent t test results for the triglycerides level (pre and post treatment between groups A and B). There was non significant difference in the pretreatment values where the t value was 1.88 and p value was 0.07. Also, there was a non
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significant difference in the post treatment values where the t value was 0.72 and p value was 0.47. Group (A) Group (B)
150 120
90 102.51 94.9
60 71.58 60.65
Triglycerides level 30
0 Pre treatment Post treatment Fig.(39): Mean ±SD of triglycerides level pre and post treatment of groups (A,B). Correlative data: Correlation (r) between waist circumference and leptin level: Table (30): Correlation analysis between the waist circumference and leptin level. correlation coefficient r value +0.53 P value 0.001* *r value: correlation coefficient, P value: probability, *: significant.
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As shown in table (30) & Figure (40), the correlation analysis between waist circumference and leptin level revealed that there was a positive correlation between waist circumference and leptin level where the r value (+0.52) and had an associated probability value of 0.001. Fig (40): Correlation between waist circumference and leptin level Correlation between waist circumference and triglycerides level: Table (31): Correlation (r) analysis between the waist circumference and triglycerides level. correlation coefficient r value 0.64 P value 0.0001** *R value: correlation coefficient, P value: probability, **: highly significance. As shown in table (31) & Figure (41), the correlation analysis between waist circumference and triglycerides level revealed that there was negative correlation (r )between waist circumference and
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triglycerides level where the r value equals ( 0.64) and had an associated probability value of (0.0001). Fig (41): Correlation between waist circumference and triglycerides level Correlation between hip circumference and leptin level: Table (32): Correlation analysis between the hip circumference and leptin level. correlation coefficient r value +0.43 P value 0.005* *R value: correlation coefficient, P value: probability, *: significant. As shown in table (32)& Figure (42), the correlation analysis between hip circumference and leptin level revealed that there was significant positive correlation between hip circumference and leptin level where the r value equals +0.43 and had an associated probability value of 0.005.
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Fig. (42): Correlation between hip circumference and leptin level Correlation between hip circumference and triglycerides level: Table (33): Correlation Analysis between the hip circumference and triglycerides level. correlation coefficient r value 0.41 P value 0.008* r value: correlation coefficient, P value: probability, *: significant. As shown in table (33) & Figure (43), the correlation analysis between hip circumference and triglycerides level revealed that there was significant negative correlation between hip circumference and triglycerides level where the r value equals 0.41 and had an associated probability value of 0.008.
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Fig (43): Correlation between hip circumference and triglycerides level
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Chapter V Discussion
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DISCUSSION The rising global trends in generalized obesity, defined using body mass index (BMI) have been well described. It has been argued that waist circumference (WC) is as good, or even better, as a measure of excess adiposity than BMI . Abdominal fat deposition is a key component of obesity. Some, but not all, studies have shown that WC may be a better predictor for the risk of myocardial infarction , type 2 diabetes , metabolic syndrome , medical care costs , and all cause mortality than BMI. WC is a simple and convenient way of measuring abdominal or central obesity and is a major determinant of the National Cholesterol Education Program Adult Treatment Panel III and International Diabetes Federation criteria for the definition and diagnosis of metabolic syndrome. WC has been proposed to be routinely used as part of clinical cardiovascular risk assessments and interpretation of obesity related health risks (Howel, 2012).
The effects of LLLT appear to be limited to a specified set of wavelengths of laser (Bjordal et al., 2008). And though more research is required to determine the ideal wavelengths, durations of treatment, dose and location of treatment (Brosseau et al., 2005) . Administering LLLT below the dose range does not appear to be effective (Bjordal et al., 2003). The factors of wavelength, effective dose, dose rate effects, beam penetration, the role of coherence, and pulses (peak power and repetition rates) are still poorly understood in the clinical setting. The typical laser average power is in the range of 1 500 m W; some high peak power, short pulse width devices are in the range of 1 100 W with typical pulse widths of 200 ns. The typical average beam irradiance then is 10mW/cm 2 5 W/cm 2. The typical wavelength is in the range 600 1000 nm (red to
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near infrared), but some research has been done and products outside of this range are available (Huang et al., 2009).
The objective of this study was to evaluate the effectiveness of diode laser system as a non invasive body contouring intervention method as well as a therapeutic modality for weight reduction. Therefore the current study was conducted to evaluate the efficacy of the low level laser therapy (LLLT) on body constitution and leptin hormone by radioimmunoassay.
Twenty women were included in this study. Their ages ranged from 30 40 years. They were divided into two groups of equal number. Group A (Overweight group) included 10 females with BMI ≥ 25 29.9 kg/m², Group B (Obese group) included 10 females with BMI ≥ 30 kg/m² .Both groups received LLLT , for 30 minutes, 2 times per week for 8 weeks as a total period of treatment . BMI, WC, HC, WHR, serum leptin, cholesterol and triglyceride level were measured before and after finishing the study.
Analysis of the results showed that:
• The anthropometric measurements (BMI, WC, HC, WHR) decreased significantly after completion of the study within each group, except the body weight and BMI in overweight group , which showed no change. • Regarding the leptin level a significant reduction in the leptin level with each group from pre to post treatment values although there was non significant change when comparing both groups. • The cholesterol level showed non significant change within overweight group from pre to post treatment measurements while it
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is increased in obese group significantly from pre to post treatment measurements within normal range. While comparison of both groups showed non significant difference either pre or post treatment. • The triglycerides level showed a significant increase from pre to post treatment measurements within each group and a non significant change was found when comparing both groups. • Another important finding of this study is the presence of positive correlation between leptin level and waist and hip circumference and a negative correlation between the waist and hip circumference and triglycerides level.
Among those who completed the study 80% responded to treatment. Individuals reported looser fitting clothing and satisfaction with the procedures and results and change in clothes sizes. Collateral advantages included improvement of constipation and regulation of menstruation. Adverse effects were limited to occasional increase in menstruation and urinary frequency.
LLLT in the current study was performed using diode laser which is a cheap, easy to handle and does not produce heat as it depends on the chemical effect and not thermal effect, On the other hand both conventional liposuction and laser assisted lipolysis used by many authors( Dudelzak et al.,2009 and Dibernardo et al., 2009 and Fakhouri et al., 2012) depend on internal application of laser energy to adipose tissue to induce selective thermal lipolysis, are more complicated procedures and may be associated with epidermal and dermal thermal injuries ( McBean and Katz,2011) .
Knowledge of the penetration depth of laser radiation in human skin is an essential prerequisite to identify its method of action. Mathematical
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simulations and estimates from the literature suggest that the depth of penetration of laser radiation using wavelengths from 630nm up to 1100nm may be up to 50mm (Esnouf et al., 2007).
The results of the current study can be attributed to that low level laser therapy with wave length 808 nm fall in near infrared area which has a penetration power till the subcutaneous fat and has a lipolytic effect on fat cells which in consequence has an effect on body contours and also on leptin level in body as it secreted from adipose tissue and its value positively correlate with amount of body fats.
The results of the current study agree with Jackson et al., 2009 and Jackson et al., 2012 who reported significant reduction in the circumferential measurements across waist, hips and thighs. They used diode laser with wavelength 635nm. Transmission electron microscopic images have demonstrated the formation of transitory specialized cell membrane associated pores in adipocytes followed by collapse of adipose cells after brief treatment with LLL.
The results of Caruso Davis et al., 2011 came in accordance with the current results as they reported significant reduction in the circumferential measurements across waist, hips and thighs through use of laser treatment which increases fat loss from adipocytes by release of triglycerides, without inducing lipolysis or cell lysis. The fat loss was probably a consequence of the laser creating temporary pores in the fat cells through which triglycerides were leaked.
Gold et al., 2011 investigated the efficacy of LLLT in reducing thigh circumference as it increases collagen production, reduce edema, increases membrane permeability and relives pain inflammation, all
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without destroying fat cells. And showed a significant reduction in thigh circumference statistically and by MRI proven fat reduction.
Singla et al., 2010 mentioned that in response to fasting leptin level fall rapidly before and out of proportion to any changes in fat mass, triggering the neuroendocrine response to acute energy deprivation. In human this response includes decreasing reproductive hormone levels which prevents pregnancy, decrease thyroid hormone that slow metabolic rate
Lach (2008) used LLL to reduce the subcutaneous fat thickness in the thigh of normal women, through using the infrared laser light that preferentially absorbed in lipids liquefying fat, allowing it to be mobilized into interstitial space then moved towards and into the lymphatic system.
Friedman (2011) reported that the majority of obese subjects are leptin resistant. The high sustained concentrations of leptin from the enlarged adipose stores result in leptin desensitization, which establishes that obesity is a resultant of hormone resistance rather than hormone deficiency. A key issue for future studies will be to elucidate the molecular mechanisms responsible for leptin resistance.
On the other hand the results of the current study contradict the results of a studies done by Elm et al., (2011) and McBean and Katz, (2011)
Elm et al., (2011) evaluated the efficacy of diode laser for body contouring and circumference measurements revealed no statistically significant reduction at either 7days or 1 month post treatment. The authors came into conclusion that there is a need for more evidence to
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show clinical circumferential reduction before LLLT can be recommended as an effective therapeutic option, but the difference between this study and the results of the current study may be due to different duration of treatment.
McBean and Katz (2011) reported that while an increasing number of studies evaluated the effects of LLLT as a save modality for removal of unwanted fatty tissue, Controversy remains regarding the efficacy of this treatment at a clinical level .
In conclusion, there was significant decrease in anthropometric measurements (on both abdomen and thigh fats) of both groups treated with low level laser therapy, decrease in serum leptin level and increase in triglyceride serum level within normal level in both groups after application of low level laser on abdomen and thighs for 30 minutes 2 times/week for 8weeks in over weight and obese females so LLLT can be recommended as a safe modality for body contouring.
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Chapter VI Summary, Conclusion and Recommendations
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SUMMARY AND CONCLUSIONS
Balanced body fat distribution is very important for an individual's physical attractiveness and body image. Asymmetric fat distribution with excessive fat accumulation in particular areas often affects a person's self image, self esteem, and overall quality of life. Studies have shown that women with 'normal' body contours are viewed as more healthy likeable, successful, and virile; whereas people with inconsistent body shape are viewed as older and less desirable.
In the present study, the effects of low level laser therapy on body constitution and leptin hormone were investigated.
The study was carried out on 20 women suffered from abnormal body fat distribution. Their age ranged from 30 to 40 years, they were not involved in any other weight reduction method or regimen and they were free from any other health problems that could affect the results of the study. Patients were randomly chosen from the poly clinic of the National Center for Radiation Research & Technology (Atomic Energy Authority) in Egypt.
Patients were divided into two groups of equal number : Group A (Overweight group): included 10 women with BMI ≥ 25 29.9 Group B (Obese group): included 10 women with BMI ≥ 30.both groups received LLLT on abdomen and/or thighs , for 30 minutes, 2 times per week for 8 weeks as a total period of treatment .
Anthropometric measurements included (BMI, W.C., H.C., and W.H.R.) were done before treatment and at the end of the study.
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As regard laboratory measurements (leptin, cholesterol, and triglyceride) blood samples were taken before treatment and after 8 weeks.
Within the limitations of the present study, the notable results were: 1. There was reduction in body measurements of women received low level laser therapy on abdomen and buttocks and decrease in leptin hormone as evidenced by radioimmunoassay. 2. There was more noticeable decrease in body anthropometric measures in (group B) obese group treated with low level laser therapy than those of (group A) overweight group while there is a significant decrease in leptin hormone assay in overweight group more than obese. The results of this study were compatible with the expectations that low level laser therapy had positive results and significant effects on body reshaping and leptin hormone in women without any hazard effects of elevation of blood level cholesterol or triglycerides.
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RECOMMENDATIONS The results of the study had indicated a need to consider the following recommendations: (1) Further studies are needed to compare between male and females (sex factor), different ages of patients (age factor) and their effects on body fat distribution patterns. (2) Furthers investigations are needed to compare between different treatment parameters to detect the most beneficial duration, joules and wavelengths which can be used for this purpose.
(3) Low Level Laser can be used in conjunction with other physical therapy modalities and protocols to improve some deficient benefits not achieved during this study (weight reduction).
(4) Further researches should extend for a longer period than 8 weeks. (5) Further researches should be undertaken to include large number of subjects providing better statistical analysis of data. (6) Follow up after stopping treatment for a period of time is important in promising cases. (7) It was noticed that in most of the patients improvement of menstruation, constipation and urination were achieved. This point needs further investigations.
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Chapter VII References
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Appendices
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Appendix (I) Sample consent form I ………………………….freely and voluntary consent to participate in
a research program under the direction of Sara Said Youssef Ali .
A through description of the procedure has been explained and I
understand that I may withdraw without prejudice to me.
Date: Participant:
…………… ……………………….
إ ار ا ا ر ا را ا أ ا ه :...... ا و ع ا ر ھ ا ا ا ا اف و ا / رة و ذ ل و و ح ط ا ج و أن أ أي و ون أي ر . ا : ا ر : 107
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Arabic Summary
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ﺘﻘﻴﻴم اﻝﻌﻼج ﺒﺎﻝﻠﻴزرﻤﻨﺨﻔض اﻝﺸدﻩ ﻋﻠﻰ ﺒﻨﻴﺔ اﻝﺠﺴم وﻫرﻤون اﻝﻠﻴﺒﺘﻴن ﺒواﺴطﺔ ﺘﻘﻨﻴﺎت اﻝﻤﻨﺎﻋﻪ اﻻﺸﻌﺎﻋﻴﻪ / ﺴﺎرة ﺴﻌﻴد ﻴوﺴف ﻋﻠﻰ ؛ ﺘﺤت اﺸراف: أ.د / زﻫرﻩ ﻤﺤﻤد ﺤﺴن ﺴرى، أﺴﺘﺎذ ﻤﺴﺎﻋد اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ﻻﻀطراﺒﺎت اﻝﺠﻬﺎز اﻝدورى اﻝﺘﻨﻔﺴﻰ وا ﻝﻤﺴﻨﻴن ، ﻜﻠﻴﺔ اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ، ﺠﺎﻤﻌﺔ اﻝﻘﺎﻫرة / د ، اﻴﻨﺎس ﺸﻔﻴﻊ ﺴﺎﻝم، ﻤدرس اﻝروﻤﺎﺘﻴزم واﻝﺘﺄﻫﻴل ، اﻝﻤرﻜز اﻝﻘوﻤﻰ ﻝﺒﺤوث وﺘﻜﻨوﻝوﺠﻴﺎ اﻻﺸﻌﺎع ، ﻫﻴﺌﺔ اﻝطﺎﻗﻪ اﻝذرﻴﻪ د/ ، ﻓﺎطﻤﻪ اﺒو اﻝﻤﺠد ﻤﺤﻤد ﺤﺎﻤد، ﻤدرس اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ، ﻗﺴم اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ﻻ ﻀطراﺒﺎت اﻝﺠﻬﺎز اﻝدورى اﻝﺘﻨﻔﺴﻰ و اﻝﻤﺴﻨﻴن ، ﻜﻠﻴﺔ اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ، ﺠﺎﻤﻌﺔ اﻝﻘﺎﻫرة . رﺴﺎﻝﺔ ﻤﺎﺠﺴﺘﻴر (٢٠١٢) . ا ا :ا ا ھ ه ى ا وو ا ان ا ا ا وا رداف ذات ا ا ن ا ا ث ان ا ا ( ا ا ) و اض ا و ا ا وا وا و ا ا ث ل ا ا ا ء ا و ا ا ء ا ا ام ا ر اء ھ ه ا و ذ ا ا ا و ا ا . ا ض ا را ا : ى ا ج ر ا ه ا وھ ن ا , و ا ءآ ا ت ا وا ات ا ھ ن ا ا ت ا ا . ط ا : ا ك ھ ه ا را 20 ه ا رھ اوح 30 40 و إ ا : ا ا و10 ات اوح ا 25 29.9 / و ا ا10 ات ا ا 30 / ، ا ج ر ا وا رداف ة 30 د ا ع ة 8 ا . ا ت ط ا و ت س ى ا ول وا ھ ن ا وھ ن ا ا ت ا ا و ا ج . ا : أظ ت ا وق ذات د إ و ا ا ج و ه ا و أ ا ا ا ا ا ج ر ت ا ط ا و ا و ا ض ھ ن ا ظ ھ وا ا ق ا ت و ا ج ام ت ا ا . ا ت ا ا : ا ر ا ه ، ھ ن ا و ت ا ا .
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اﻝﻤﻠﺨص اﻝﻌرﺒﻰ ﻋﻨوان اﻝﺒﺤث: ﺘﻘﻴﻴم اﻝﻌﻼج ﺒﺎﻝﻠﻴزر ﻤﻨﺨﻔض اﻝﺸدﻩ ﻋﻠﻰ ﺒﻨﻴﺔ اﻝﺠﺴم وﻫرﻤون اﻝﻠﻴﺒﺘﻴن ﺒواﺴطﺔ ﺘﻘﻨﻴﺎت اﻝﻤﻨﺎﻋﺔ اﻻﺸﻌﺎﻋﻴﺔ . ﻤﻘدﻤﺔ ﻋن اﻝﺒﺤث: اﻝﺴﻤﻨﻪ اﻝﻤوﻀﻌﻴﻪ ﻤﺸﻜﻠﻪ ذات اﻨﺘﺸﺎر واﺴﻊ ﻋﻠﻰ ﻤﺴﺘوى اﻝﻌﺎﻝم وﺘؤﺜر ﺘﺄﺜﻴر ﺴﻠﺒﻰ ﺼﺤﻴﺎ ﻋﻠﻰ اﻻﺸﺨﺎص ﻋﺎﻤﺔ وﻨﻔﺴﻴﺎ ﻋﻠﻰ اﻝﺴﻴدات ﺨﺎﺼﺔ وﺘﻠك اﻝﻤﺸﻜﻠﻪ ﺤﺘﻰ اﻻن ﻴﺼﻌب اﻝﺘوﺼل اﻝﻰ ﺤﻠﻬﺎ ﺒطرق اﻤﻨﻪ ووﺠد ان ﻫرﻤون اﻝﻠﻴﺒﺘﻴن ﻝﻪ ﻋﻼﻗﻪ وﺜﻴﻘﻪ ﺒﺎﻝﺴﻤﻨﻪ ﻓﻰ ﺘﻠك اﻻﻤﺎﻜن وﺒﻤﺎ ان اﻝﻠﻴزر اﺼﺒﺢ ﻤن ا ﻜﺜر اﻝﺘﻘﻨﻴﺎت اﻝﺤدﻴﺜﻪ اﻤﺎﻨﺎ وﻓﺎﻋﻠﻴﻪ واﻨﺘﺸﺎر ﻓﻰ ﺤل ﻜﺜﻴر ﻤن اﻝﻤﺸﻜﻼت اﻝﺼﺤﻴﻪ اﻝﺘﻰ ﻋﺠز ﻋن ﺤﻠﻬﺎ ﻜﺜﻴر ﻤن اﻝوﺴﺎﺌل اﻻﺨرى اﻝﻤﺴﺘﺨدﻤﻪ ﻓﻰ ﺘﻠك اﻻﻏراض واﻝذى ﺘم اﺨﺘﺒﺎرﻩ ﻤﻌﻤﻠﻴﺎ واﺜﺒت ﻨﺠﺎﺤﻪ . اﻝﻬدف ﻤن اﻝﺒﺤث: أ ﺠرى ﻫذا اﻝﺒﺤث ﻝﺘﻘﻴﻴم ﻓﻌﺎﻝﻴﺔ اﻝﻌﻼج ﺒﺎﻝﻠﻴزر ﻤﻨﺨﻔض اﻝﺸدﻩ ﻋﻠﻰ ﺒﻨﻴﺔ اﻝﺠﺴم وﻫرﻤون اﻝﻠﻴﺒﺘﻴن ﺒواﺴطﺔ ﺘﻘﻨﻴﺎت اﻝﻤﻨﺎﻋﺔ اﻻﺸﻌﺎﻋﻴﻪ. ﻤواد و اﺴﺎﻝﻴب اﻝﺒﺤث: أ ﺠرﻴت ﻫذﻩ اﻝدراﺴ ﺔ ﻋﻠﻰ ﻋﺸرون ﺴﻴدﻩ ﻴﻌﺎﻨون ﻤن ﻋدم ﺘﻨﺎﺴق ﺒﻤﻨﺎطق اﻝﺒطن او اﻻرداف و ﻗد ﺘراوﺤت اﻋﻤﺎرﻫن ﻤﺎ ﺒﻴن 30 - 40 ﺴﻨﻪ و ﻗد ﺘم ﺘﻘﺴﻴﻤﻬن إﻝﻰ ﻤﺠﻤوﻋﺘﻴن ﻤﺘﺴﺎوﻴﺘﻴن ﻓﻰ اﻝﻌدد : اﻝﻤﺠﻤوﻋﺔ اﻷ وﻝ ﻰ : ﺘﻜوﻨت ﻫذﻩ اﻝﻤﺠﻤوﻋ ﺔ ﻤن 10 ﺴﻴدات ﻴﺘراوح ﻤؤﺸر ﻜﺘﻠﺔ اﻝﺠﺴم ﺒﻴن -25 29.9 ﻜﺞ/ ﻤﺘر ﻤرﺒﻊ . اﻝﻤﺠﻤوﻋﺔ اﻝﺜﺎﻨﻴﺔ: واﻝﺘﻰ ﺘﻜوﻨت ﻤن10 ﺴﻴدات ﻴزﻴد ﻤؤﺸر ﻜﺘﻠﺔ اﻝﺠﺴم ﻋن 30 ﻜﺞ/ ﻤﺘر ﻤرﺒﻊ. ﺠﻤﻴﻌﻬن ﺘﻠﻘﻴن ﻋﻼج ﺒﺎﻝﻠﻴزر ﻝﻤدة 30 دﻗﻴﻘﻪ، ﻤرﺘﻴن اﺴﺒوﻋﻴﺎ ،ﻝﻤدة ﺜﻤﺎن اﺴﺎﺒﻴﻊ ﻋﻠﻰ ﻤﻨطﻘﺘﻰ اﻝ ﺒطن او اﻻرداف .
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وﻝﻘد اظﻬرت اﻝﻨﺘﺎﺌﺞ اﻨﻪ: ﻫﻨﺎك ﻤزﻴد ﻤن اﻝﺘﺤﺴن ﻓﻲ ﺘﻘﻠﻴل ﻗﻴﺎﺴﺎت اﻝﻤﻨﺎطق اﻝﻤﻌﺎﻝﺠﻪ ﻓﻰ ﻜﻼ اﻝﻤﺠﻤوﻋﺘﻴن وﻝﻜن اﻝﺘﺤﺴن ﻜﺎن ﻤﻠﺤوظ ﺎ اﻜﺜر ﻓﻰ اﻝﻤﺠﻤوﻋﻪ اﻝﺜﺎﻨﻴﻪ ﻤن ﺤﻴث اﻝﻘﻴﺎﺴﺎت وﻓﻰ اﻝﻤﺠﻤوﻋﻪ اﻻوﻝﻰ ﻤن ﺤﻴث ﻨﺴﺒﺔ ﻫرﻤون اﻝﻠﻴﺒﺘﻴن ﻓﻰ اﻝدم ﻓﻲ اﻝﺴﻴدات اﻝﻼﺘﻰ ﺘ م ﺘطﺒﻴق اﻝﻠﻴزر ﻋﻠﻴﻬن. وﻋﻠﻴﻪ ﻴﻤﻜن اﺴﺘﻨﺒﺎط اﻵ :ﻲﺘ اﻝﻌﻼج ﺒﺎﻝﻠﻴزر ذو ﻓﺎﻋﻠﻴﻪ و اﻤﺎﻨﺎ ﻓﻰ ﺘﻨﺴﻴق ﺸﻜل اﻝﺠﺴم وﺘﻘﻠﻴل ﻨﺴﺒﺔ ﻫرﻤون اﻝﻠﻴﺒﺘﻴن ﻓﻰ اﻝدم واﻝﻤﺴﺌول ﻋن اﻝﺸﻬﻴﻪ ﻝدى اﻝﺴﻴدات.
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ا ت
ء ا ا ٳ ج ا :
)1 ٳ اء ا ا را ت ر ا ات وا ل ، ا ر ا و ھ ا ط ز ا ھ ن .
)2 ٳ اء ا ا را ت ر ا ا ج ( ة ا ج – ا ة ا ل ا ) .
)3 ج ا ا ا ر ا ت ام أ ج اك ا ر ل ا ا ل ھ ه ا را .
)4 ٳ اء ا ا را ت ا أ ن ا .
)5 ٳ اء ا ا ث ام ت ا وذ ا ا و ا ت.
)6 ا ت ا ه ا ء ا را ذو اھ ه.
)7 ا ا ا ا ة وا ل ھ ه ا را وا ج ا ا و ا : ا م ا وره ا و ت ا ل وا ز ى ا ات ا ا ج ر.
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ﺘﻘﻴﻴم اﻝﻌﻼج ﺒﺎﻝﻠﻴزر ﻤﻨﺨﻔض اﻝﺸدﻩ ﻋﻠﻰ ﺒﻨﻴﺔ اﻝﺠﺴم وﻫرﻤو ن اﻝﻠﻴﺒﺘﻴن ﺒواﺴطﺔ ﺘﻘﻨﻴﺎت اﻝﻤﻨﺎﻋﺔ اﻻﺸﻌﺎﻋﻴﺔ ﺘوطﺌﺔ ﻝﻠﺤﺼول ﻋﻠﻰ درﺠﺔ اﻝﻤﺎﺠﺴﺘﻴر ﻲﻓ اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ﻤﻘدﻤ ﺔ :ﻤن ةﺴﺎر ﺴﻌﻴد ﻴوﺴف ﻋﻠﻰ ﺒﻜﺎﻝورﻴو س اﻝﻌﻼج اﻝطﺒﻴﻌﻲ (٢٠٠٦ ) ﺘﺤت إﺸراف أ. د / زﻫرﻩ ﻤﺤﻤد ﺤﺴن ﺴرى أﺴﺘﺎذ ﺒ ﻘﺴم ع .ط ﻻﻀطراﺒﺎت اﻝﺠﻬﺎز اﻝدورى اﻝﺘﻨﻔﺴﻰ واﻝﻤﺴﻨﻴن ﻜﻠﻴﺔ اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ﺠﺎﻤﻌﺔ اﻝﻘﺎﻫرة /د ﻓﺎطﻤﻪ اﺒو اﻝﻤﺠد ﻤﺤﻤد ﺤﺎﻤد /د أﻴﻨﺎس ﺸﻔﻴﻊ ﺴﺎﻝم ﻤدرس ﺒ ﻘﺴم ع. ط ﻻﻀطراﺒﺎت اﻝﺠﻬﺎز ﻤدرس اﻝروﻤﺎﺘﻴزم واﻝﺘﺄﻫﻴل اﻝدورى اﻝﺘﻨﻔﺴﻰ واﻝﻤﺴﻨﻴن ﺒ ﺎﻝﻤرﻜز اﻝﻘوﻤﻰ ﻝﺒﺤوث ﻜﻠﻴﺔ اﻝﻌﻼج اﻝطﺒ ﻴﻌﻲ وﺘﻜﻨوﻝوﺠﻴﺎ اﻻﺸﻌﺎع ﺠﺎﻤﻌﺔ اﻝﻘﺎﻫرة ﻫﻴﺌﺔ اﻝطﺎﻗﻪ اﻝذرﻴﻪ ﻜﻠﻴﺔ اﻝﻌﻼج اﻝطﺒﻴﻌﻲ ﺠﺎﻤﻌﺔ اﻝﻘﺎﻫرة ٢٠١٢
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