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Electronic Theses, Treatises and Dissertations The Graduate School

2013

A Descriptive Study of Body Composition

Abnormalities and Health Risks in Patients
with Obesity
Jingjie Xiao

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 THE FLORIDA STATE UNIVERSITY

COLLEGE OF HUMAN SCIENCES

A DESCRIPTIVE STUDY OF BODY COMPOSITION ABNORMALITIES AND HEALTH

RISKS IN PATIENTS WITH OBESITY

By

JINGJIE XIAO

A Thesis submitted to the

Department of Nutrition, Food and Exercise Sciences
in partial fulfillment of the
requirements for the degree of
Master of Science

Degree Awarded:
Summer Semester, 2013
Jingjie Xiao defended this thesis on June 12th, 2013.

The members of the supervisory committee were:

Carla Prado

Professor Directing Thesis

Michael Ormsbee

Committee Member

Robert J. Contreras

Committee Member

The Graduate School has verified and approved the above-named committee members, and
certifies that the thesis has been approved in accordance with university requirements.

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 ACKNOWLEDGEMENTS

I dedicate this thesis to my parents, Jianli Xiao and Xianfeng Yang, and my major professor Dr.
Carla Prado. Mom and Dad, you both have been an incredible influence in my life and without
your support I could not have the opportunity to study abroad. You have always been
encouraging me to overcome the difficulties in all parts of life and trusting me on my abilities to
pursue my dream. Dr. Prado, you have guided me throughout the whole project and persuaded
me to become the best I can be. Thank you for all you have done for me, with all my love!

I also would like to thank Dr. Michael Ormsbee and Dr. Robert J. Contreras for being on my
thesis committee and improving my writing techniques. Additionally, I would like to thank
Tallahassee Memorial Bariatric Center for offering me the opportunity to conduct this project.

Lastly, I would like to express my gratitude to my lab colleagues, Sarah Purcell and Katelyn
Willbur for their advice on my writing.

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 TABLE OF CONTENTS

List of Tables ................................................................................................................................. vi

List of Figures ............................................................................................................................... vii
List of Abbreviations ................................................................................................................... viii
Definition of Terms..........................................................................................................................x
Abstract .......................................................................................................................................... xi
1. INTRODUCTION ...................................................................................................................1
1.1 Background ....................................................................................................................1
1.2 Purpose of Study ...........................................................................................................2
1.3 Research Hypotheses .....................................................................................................2
1.3.1 Hypothesis 1........................................................................................................2
1.3.2 Hypothesis 2 .......................................................................................................2
2. LITERATURE REVIEW .......................................................................................................4
2.1 Definition of Sarcopenia .................................................................................................4
2.1.1 Prevalence of Sarcopenia .....................................................................................5
2.1.2 Mechanisms of Sarcopenia ..................................................................................5
2.1.3 Health Consequences of Sarcopenia ....................................................................7
2.2 Definition of Obesity ......................................................................................................8
2.2.1 Prevalence of Obesity ..........................................................................................8
2.2.2 Mechanisms of Obesity........................................................................................9
2.2.3 Health Consequences of Obesity .......................................................................10
2.3 Definition of Sarcopenic Obesity..................................................................................11
2.3.1 Prevalence of Sarcopenic Obesity .....................................................................11
2.3.2 Etiology of Sarcopenic Obesity .........................................................................12
2.3.3 Health Consequences of Sarcopenic Obesity ....................................................13
2.4 Body Composition Methodologies ...............................................................................14
3. MATERIALS AND METHODS ...........................................................................................18
3.1 Study Population ...........................................................................................................18
3.2 Data Collection ............................................................................................................18
3.2.1 Demographic Characteristics .............................................................................19
3.2.2 Anthropometrics / Body Composition Assessments..........................................19
3.2.3 Metabolic Profile ...............................................................................................20
3.2.4 Health Status: Comorbidities, Functional Outcomes, and Physical Activities ..21
3.3 Statistical Analysis ........................................................................................................22
4. RESULTS ..............................................................................................................................23
4.1 Demographic Characteristics ........................................................................................23
4.2 Anthropometric and Body Composition Characteristics ..............................................23
4.2.1 Sarcopenic Obesity ............................................................................................24
4.3 Metabolic Profile by Body Composition Phenotype ....................................................24

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 4.4 Health Status: Comorbidities, Functional Outcomes, and Physical Activities by Body
Composition Phenotype ................................................................................................25
5. DISCUSSION ........................................................................................................................34
5.1 Review of Hypotheses and Conclusions .......................................................................34
5.2 Summary .......................................................................................................................34
5.3 Discussion of Results ....................................................................................................35
5.3.1 The FMI/FFMI Ratio .........................................................................................35
5.3.2 Gender- and Age-related Variations in Body Composition ...............................36
5.3.3 Metabolic Abnormalities ...................................................................................37
5.3.4 Comorbidities / Functional Limitations / Physical Activities ............................38
5.4 Limitation and Future Research ....................................................................................40
APPENDICES ...............................................................................................................................42

A. APPROVALS ........................................................................................................................42

B. DATA COLLECTION FORM..............................................................................................47

REFERENCES ..............................................................................................................................56

BIOGRAPHICAL SKETCH .........................................................................................................67

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 LIST OF TABLES

2.1 Summary of body composition measurement by BIA .......................................................15

4.1 Overall characteristics of study patients ............................................................................26

4.2 Comparison of body composition characteristics between sarcopenic obese and non-
sarcopenic patients by gender ........................................................................................................28

4.3 Overall metabolic, comorbid, medical and functional characteristics of sarcopenic obese
and non-sarcopenic obese patients .................................................................................................29
4.4 Odds ratio and 95% CIs for the univariate effect of variables on low back pain ..............30
4.5 Comparison of daily activities between sarcopenic obese and non-sarcopenic obese
groups .............................................................................................................................................30

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 LIST OF FIGURES

3.1 Scheme of the relationship between fat mass index (FMI, depicted by larger grey circles)
and fat-free mass index (FFMI, black circles) portraying different body composition types .......20

4.1 Relationship between body weight (kg) and Fat mass index/Fat-free mass index ratio
(kg/m2) ...........................................................................................................................................31

4.2 Relationship between age (years) and A) Fat mass index (FMI, kg.m2); B) Fat mass
index/Fat-free mass index ratio (FMI/FFMI ratio, kg/m2); and C) Fat-free mass index (FFMI,
kg/m2) ............................................................................................................................................32

4.3 A) Fat-free mass index (FFMI, kg/m2); B) Fat mass index (FMI, kg/m2) and C) Percent
body fat (%BF) distribution between sarcopenic obese and non-sarcopenic obese patients by
gender ............................................................................................................................................33

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 LIST OF ABBREVIATIONS

ASM: Appendicular Skeletal Muscle

BIA: Bioeletrical Impedance Analysis

BMI: Body Mass Index

BCM: Body Cell Mass

CRP: C-Reactive Protein

CT: Computerized Tomography

CV: Coefficient of Variance

DXA: Dual Energy X-Ray Absorptiometry

FFM: Fat-Free Mass

FFMI: Fat-Free Mass Index

FM: Fat Mass

FMI: Fat Mass Index

GH: Growth Hormone

HR: Hazard Ratio

IGF-1: Insulin-Like Growth Factor 1

IL: Interleukin

LBM: Lean Body Mass

LST: Lean Soft Tissue

MRI: Magnetic Resonance Imaging

NHANES: National Health and Nutrition Examination Survey

REE: Resting Energy Expenditure

SMI: Skeletal Muscle Index

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TNF-α: Tumor Necrosis Factor

WHO: World Health Organization

ix
 DEFINITION OF TERMS

Adipose Tissue: A connective tissue formed by adipocytes, collagenous and elastic fibers,
fibroblasts and capillaries. There are four types of adipose tissue: subcutaneous, visceral,
interstitial and yellow marrow.

Appendicular Skeletal Muscle Mass (ASM) Index: The sum of skeletal muscle mass from
arms and legs adjusted by height in meters squared (kg/m2).

Body Cell Mass (BCM): Body composition compartment consisting of all intracellular
components, including intracellular water.

Fat-Free Mass (FFM): The sum of lean tissues of the body including bone mineral content,
therefore it includes: total body water, total body protein, carbohydrate, non-fat lipid, soft tissue
minerals and bone mineral content.

Lean Body Mass (LBM) or Lean Soft Tissue (LST): the sum of lean compartments of the
body (excluding bone mineral content), it includes: total body water, total body protein,
carbohydrate, non-fat lipid and soft tissue minerals.

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 ABSTRACT

Background: Body composition abnormalities are independent predictors of health outcomes in

a variety of disease states. The simultaneous condition of low muscle mass and high fat mass,
termed sarcopenic obesity, is an abnormal body composition phenotype associated with
metabolic abnormalities and comorbidities.
Objectives: The purpose of this study was to investigate the overall body composition variability
among obese patients, and to compare health characteristics between sarcopenic obese and non-
sarcopenic obese patients.
Methods: In this retrospective, chart review study, patients ( ≥18 years old) seeking weight loss
treatment at a local center in Tallahassee, FL and with available baseline bioelectrical impedance
analysis (BIA) data were included in this study. The ratio between fat mass index [FMI, defined
as fat mass (kg)/height (m)2] and fat free mass index [FFMI, defined as fat free mass (kg)/height
(m)2] were used to define sarcopenic obesity. Medical records were further reviewed for
information on metabolic profile and health status.
Results: Ninety-one obese patients with a mean age of 57 ± 11 years were included in this study.
Body mass index (BMI) ranged from 31.6 to 68.7 kg/m2. Eighty-one percent were morbidly
obese. The FMI/FFMI ratio was variable ranging from 0.35 to 2.46 kg/m2, independent of body
weight. A gender-specific FMI/FFMI ratio above the median was used to depict the sarcopenic
obesity phenotype. This corresponded to: FMI/FFMI ≥ 1.05 kg/m2 in women and FMI/FFMI ≥
0.78 kg/m2 in men. As expected, men presented with higher body weight, height, waist
circumference and FFMI, compared to women. On the contrary, women presented with higher
percent body fat and FMI/FFMI ratio. No gender differences were observed for body mass index
(BMI), fat mass and FMI. Plasma albumin concentration was lower in sarcopenic obese patients
compared to non-sarcopenic obese patients (P=0.032). Sarcopenic obese patients reported a
higher prevalence of low back pain compared to their counterparts. In fact, sarcopenic obesity
was the strongest predictor of low back pain, with an odds ratio of 2.3 (95% CI=1.01-5.41,
P=0.048). Similarly, the prevalence of alcoholism and sexual dysfunction were significantly
greater among sarcopenic obese patients compared to non-sarcopenic obese patients (P=0.026
and P=0.030, respectively).

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Conclusion: A wide variability in body composition was observed in this cohort of patients,
illustrating how the proportions of fat to fat-free tissues may differ among patients with similar
BMI. We suggest the use of the FMI/FFMI ratio as a potential approach for the assessment of
sarcopenic obesity in patients with severe obesity. Using this approach, patients with a
sarcopenic obesity phenotype presented with higher risk of certain metabolic abnormalities and
comorbidities.

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 CHAPTER ONE
INTRODUCTION

1.1 Background
Body composition refers to the amounts/proportions of fat and lean tissues in the body.
New in vivo technologies to assess human body composition have rapidly developed in the past
decades, such as bioelectrical impedance analysis (BIA), dual X-ray absorptiometry (DXA), and
computerized-tomography (CT) image analysis. These techniques have allowed for the
identification of abnormal body composition phenotypes, which are associated with increasing
health risks, such as physical frailty (1), functional limitations (2) and mortality (3). Abnormal
body composition phenotypes include sarcopenia (deficiency of muscle mass and/or strength),
obesity (excess adipose tissue) and sarcopenic obesity, which is defined as being sarcopenic and
obese simultaneously (4).
Of particular interest is sarcopenic obesity, which is difficult to detect since BMI (body
mass index = body weight/ height2) only provides an assessment of the patient’s overall body
weight rather than the composition of that body weight (i.e. body composition) (5). Although
obesity is commonly assessed body weight and BMI, more sophisticated tools are needed to
assess the presence of sarcopenia. Sarcopenia is a common age-related disease, which is
characterized by gradual loss of muscle mass and decline of muscle function (6-8). One of the
most commonly accepted definitions of sarcopenia is a level of skeletal muscle mass lower than
2 standard deviations (SD) below the mean of a young reference population (9). The National
Institutes of Health and the World Health Organization (WHO) defines obesity as having a BMI
of 30 kg/m2 or higher (10).
The prevalence of sarcopenic obesity has been reported to range from 2% among elderly
individuals aged 60 to 69 years (4) to up to 90% among women aged 18 to 87 years (11).
Nonetheless, the prevalence of sarcopenic obesity has not been well characterized for several
reasons such as different definitions, different populations and reference groups being studied,
and various measurements of health outcomes. However, the prevalence of sarcopenic obesity is
rising because our population has continued to get older and more obese (12).

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 At present, the pathogenesis of sarcopenic obesity is not clearly understood. Possible
factors may include a combination of aging, hormone changes, pro-inflammatory factors and
reduced dietary intake, especially protein intake (13). Roubenoff (14) has proposed a schema,
identifying possible cyclic metabolic behaviors: the accumulation of adipose tissue leads to loss
of muscle mass by increasing circulating pro-inflammatory cytokines and insulin resistance; and
in turn, muscle loss reinforces fat gain by impairing the ability of physical activity.
Various published studies suggest that sarcopenic obesity is the worst-case scenario for
health risks and has been associated with poorer functional status and health outcomes compared
with sarcopenia or obesity alone (9, 15). Sarcopenic obesity has been associated with physical
disability (16, 17), functional impairment (18), increased cardiovascular disease risk (19), and
reduced survival (5).

1.2 Purpose of Study

The purpose of the present study was two-fold: to investigate the overall body
composition variability among obese patients seeking treatment at the Tallahassee Memorial
Bariatric Health Center (TMBC) and to compare the demographic and clinical characteristics
between sarcopenic obese and non-sarcopenic obese patients.

1.3 Research Hypotheses

1.3.1 Hypothesis 1

The distribution of FMI/FFMI ratio will present with a degree of variability greater than
two folds.

1.3.2 Hypothesis 2

Compared to non-sarcopenic obese patients, sarcopenic obese patients:

a) will present with higher rates of metabolic abnormalities and co-morbidities, as
assessed by the TMBC New Patient Questionnaire:
- higher prevalence of metabolic syndrome.

2
 - lower levels of albumin, creatinine, total protein, vitamin D, TSH, T3, T4, AST
and ALT.
- higher prevalence of co-morbidities (acid reflux, arthritis, asthma, alcoholism,
cancer, diabetes, diminished hygiene, fatigue, gout, heart disease, joint pain,
nausea, osteoporosis, sexual dysfunction, shortness of breath, sleep apnea,
thyroid disease, and weakness).
- higher prevalence of immobility and low back pain.
b) will report lower physical activity readiness and levels:
- at least one impediment to becoming physically active on the PAR-Q & YOU
Questionnaire.
- lower frequency of physical activities as reported by the Exercise History and
Attitude Questionnaire.

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 CHAPTER TWO
LITERATURE REVIEW

2.1 Definition of Sarcopenia

The concept of sarcopenia was originally proposed by Rosenberg in 1989 (8). Sarcopenia
was characterized by an involuntary age-related decline in lean body mass (8). More recently, the
European Working Group on Sarcopenia in Older People suggested including reduced muscle
strength in the definition of sarcopenia rather than considering low muscle mass alone (6). To
date, most studies of sarcopenia were conducted among elderly populations. Considering the
increased lifespan and progressive muscle atrophy with aging, a remarkable number of studies
have been focusing on the prevalence of this syndrome and its associations with health.
However, there has not been a standard diagnostic criterion to define sarcopenia due to different
populations, reference groups, and measurement methods being used (6).
The most commonly used definition of sarcopenia was developed by Baumgartner et al.
(9) based on data from the New Mexico Elderly Health Survey, conducted from 1993 to 1995.
The investigators defined sarcopenic individuals as those having a height-adjusted appendicular
skeletal muscle mass (ASM, the sum of lean tissues from arms and legs assessed by DXA) lower
than 2SD below the mean of young reference adults (9). Yet, this definition has been criticized
for not taking body fat into consideration, which leads to an underestimation of sarcopenia
among obese subjects (20). In order to control for body fat, Newman et al. (20) used ASM
adjusted for height and body fat mass to define sarcopenia. To estimate the prevalence of
sarcopenia, Janssen et al. (18) developed a similar approach based on BIA-derived skeletal
muscle mass. Muscle mass was then divided by body weight and expressed as a percentage of
skeletal muscle index (SMI= skeletal muscle/body weight × 100). Two levels of sarcopenia were
identified: Class I (if SMI was between one and two SD below the young reference mean value)
and Class II (if SMI was lower than 2SD below the young reference mean value). Class I and
class II sarcopenia were identified as follows: men 37% to 31%, and less than 31%; women 28%
to 22%, and less than 22% (18). Later on, Janssen and colleagues identified two levels of
sarcopenia cutoff values in older individuals based on the association between sarcopenia and
physical disability risk. The height-normalized skeletal muscle mass (SM/height2) cutoffs within

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5.76 to 6.75 kg/m2 or within 8.51 to10.75 kg/m2 were selected to define moderate risk physical
disability in women and men respectively, whereas cutoffs lower than 5.75 kg/m2 or 8.50 kg/m2
were selected to define high risk physical disability in women and men respectively (17).

2.1.1 Prevalence of Sarcopenia

The variation in diagnostic criteria leads to different prevalence rates of this disordered
body composition phenotype (21). Nevertheless, there is consensus that the occurrence of
sarcopenia is increasing with age and usually associated with reduced muscle strength (6).
Baumgartner et al. (9) reported that more than 50% elderly individuals (≥80 years) were
sarcopenic in the New Mexico Aging Process Study. Janssen et al. (18) analyzed a population-
based data set from the Third National Health and Nutrition Examination Survey (NHANES III)
and reported a prevalence of sarcopenia of approximately 59% in women and 47% in men, aged
60 to 69 years. Additionally, prevalence rates increased from the 3th to the 6th decade of life.
More recently, the prevalence of sarcopenia has also been reported among different ethnicities.
Masanes and colleagues examined a cohort of healthy community-dwelling elderly in Spain and
reported sarcopenia prevalence rates of 33% in women and 10% in men, aged 70 to 80 years
(22). Using data from communities in Taipei, China, Chien and colleagues reported sarcopenia
prevalence rates of 18.6% and 23.6% in elderly women and men respectively (23). The
prevalence of sarcopenia was estimated at 23.21% among an elderly women cohort (≥60 years)
in Brazil (24). Although in most cases sarcopenia has been defined as a decline in muscle mass
for epidemiologic purposes, reduction in muscle strength and muscle efficiency (muscle strength
per unit of muscle mass) have also been characteristic features of sarcopenia (25).

2.1.2 Mechanisms of Sarcopenia

A number of underlying mechanisms have been proposed to cause this loss of muscle
mass/strength, including changes in muscle structure and composition, metabolism and lifestyle
factors. Muscle contributes approximately 40% of the total body mass and 75% of the body’s
cell mass (BCM, body composition compartment consisting of all intracellular components,
including intracellular water), which is the metabolic active compartment of the body (26).

5
Muscle changes associated with aging include a disproportionate loss of fast myosin heavy-chain
(MHC) and actin, which are key contractile proteins (25-27). The ability to synthesize muscle
contractile proteins is directly associated with muscle strength (28). Progressive loss of motor
neurons, which stimulates muscle contraction; and losses of motor neurons from the spinal cord
may play a role in the development of sarcopenia (29). Oxidative stress and molecular
inflammation also play important roles in age-related muscle protein breakdown, modulating
transcription factors and kinases, and contributing to sarcopenia (30).
Furthermore, several studies have confirmed an age-related decline in muscle fiber size
and number, especially pointing towards fast-twitch type II fibers which are predictive of muscle
strength and power (31, 32). “The motor unit remodeling” can also be interpreted as a process
that the surviving neurons adopt muscle fibers as a compensation for dropout of motor neurons
(33). Considering motor unit remodeling, older adults were reported to have larger motor units
than young adults; nevertheless, the remodeled motor units are less efficient in stimulating fiber
function and in extreme cases can cause tremor or weakness (34). In addition to changes of
muscle mass and structure, alterations in muscle composition also contribute to the loss of
muscular strength. With the use of CT, an increase in connective tissue and fat tissue within the
muscle has been observed among sarcopenic subjects (35).
There is evidence that endocrine function deterioration with aging is associated with the
loss of muscle mass and quality. Many hormones are involved in the regulation of protein
metabolism throughout lifetime, such as testosterone, estrogen, growth hormone (GH) and
insulin-like growth factor-1 (IGF-1). As people age, testosterone production reduces, speeding
up the loss of muscle mass (36). As an anabolic hormone, testosterone treatments have been
associated with increased muscle mass, even though the effects on muscle strength are
contradictory (37). IGF-1 and GH have an anabolic effect on muscle protein synthesis (38).
Notably, circulating IGF-1 level is correlated with MHC synthesis rate (28). Therefore, the
decrease of these hormones with aging contributes to muscle loss or lack of maintenance (39).
The increase of inflammatory cytokines among elderly individuals is another complicating factor
that impetuses muscle atrophy. A high level of interleukin-1 (IL-1), interleukin-6 (IL-6), and
tumor necrosis factor-a (TNF-α) is correlated with increased muscle catabolism (13).
Malnutrition is also a crucial risk factor in the development of sarcopenia in elderly
populations. Reduced energy intake leads to muscle atrophy with reduced muscle contraction

6
and metabolism (40). A lack of adequate amino acids intake will inhibit protein synthesis
affecting muscle anabolism and muscle strength increments (41). It is well established that
Vitamin D deficiency is also associated with low muscle mass and strength (40). Physical
inactivity plays an important role in the decline of muscle quantity and quality (33). In addition,
increased physical activity has multifactorial benefits on muscle function and performance.
Exercise training exerts a direct effect on several signaling pathways which improves anabolic
activities (42). It is suggested that exercise training is associated with improvements in insulin
sensitivity and increased lipid oxidation (43). Resistant training has been demonstrated to
increase muscle strength and size in older adults and aerobic exercise may also has an anabolic
effect on skeletal muscle (44).

2.1.3 Health Consequences of Sarcopenia

Sarcopenia was reported to be associated with impaired physical function, physical

disability, low quality of life and increased mortality rate in numerous studies. In 1998,
Baumgartner et al. investigated the health problems associated with sarcopenia. In this study,
sarcopenia was an independent predictor of self-reported physical disability, after controlling for
age, ethnicity, income, comorbidity, physical activity, alcohol intake and smoking (9). Visser et
al. (45) conducted a prospective study to examine whether low muscle mass and strength were
predictive of incident mobility limitation in persons aged 70 to 79 years. After 2.5 years follow
up, males and females in the lowest quintile of mid-thigh muscle cross-sectional area were
respectively 90% and 68% more likely to develop mobility limitations compared to the highest
muscle size quintile. In addition, the risk of developing mobility limitations in the lowest quintile
of muscle strength was 2.64 and 2.15 times greater for males and females, respectively (45).
Along with these findings, Janssen (46) investigated the influence of sarcopenia on the
development of physical disability among elderly individuals at both cross sectional and
longitudinal levels. Muscle mass was categorized into normal, moderate sarcopenia, and severe
sarcopenia in this study. At baseline, 71.5% of males had moderate sarcopenia and 15.8% had
severe sarcopenia, while the prevalence of moderate and severe sarcopenia were of 44.1% and
9.3% among females respectively. Those in the severe sarcopenia groups were found to have the
greatest likelihood of disability with stronger associations observed in males compared to

7
females (46). However, when compared to the longitudinal analysis, the influence of sarcopenia
on disability was considerably stronger in the cross-sectional analysis (46). Sarcopenia has also
been associated with increased risk of overall death. Recently, Landi et al. (1) analyzed the
relationship between sarcopenia and mortality using data from the Aging and Longevity Study, a
prospective cohort study conducted among people over 80 years old. Sarcopenic patients had a
greater risk of death for all causes than non-sarcopenic subjects (HR =2.32, CI =1.01 to 5.43) (1).
In addition to clinical problems, sarcopenia has also been associated with increased
public health expenditures. The estimated healthcare cost attributable to sarcopenia in the United
State in 2000 was $ 18.5 billion, which represented about 1.5% of total healthcare expenditures
for that year (47).

2.2 Definition of Obesity

According to the WHO, BMI can be categorized into five strata of height-adjusted body
weights: ≤18.5 kg/m2 for underweight , 18.5-24.9 kg/m2 normal weight, 25.0-29.9 kg/m2
overweight, ≥30.0 kg/m2 class I obesity, 35.0-39.9 kg/m2 class II obesity, and ≥40.0 kg/m2
morbid obesity (10). Therefore, obesity is defined as BMI equal or greater than 30 kg/m2. Body
fat percentage has also been used to define obesity and several studies have reported a high
correlation between BMI and percent body fat (48, 49). “Healthy” ranges of percent body fat are
approximately 12% to 20% for men and 20% to 30% for women (50). The WHO defines obesity
as having percent body fat greater than 25% in males or 35% in females. These values were
established based on a BMI value of 30 kg/m2 (51). Adipose tissue distribution also has a great
impact on health outcomes. Particularly, abdominal or upper-body obesity has been associated
with a number of metabolic abnormalities and diseases, such as increased blood pressure, and
insulin resistance (52, 53).

2.2.1 Prevalence of Obesity

The prevalence of obesity has been dramatically rising in the United State in the last three
decades. According to NHANES data, the prevalence of obesity showed a large increase
between NHANES II and NHANES III (NHANES I, 14.1%; NHANES II, 14.5% and NHANES
III 22.5%) (54). Approximately 36% of American adults were obese in 2009 to 2010, and the

8
prevalence significantly increased with age among women but not men (55). Likewise, a high
prevalence of obesity is observed among elderly individuals (aged 60 or older) (56). More than
one-third of older adults aged 65 and over were obese in 2007–2010 (57). By using values
greater than the median percent body fat for each sex (> 27% in men and > 38% in women), ,
Baumgartner et al. (4) reported a prevalence of obesity of 43.5% among elderly individuals (≥ 60
years old).

2.2.2 Mechanisms of Obesity

The etiology of obesity is multifactorial. Several factors have contributed to this

syndrome, such as demographic, social economic status, lifestyle and biological factors. Among
them, metabolic factors, diet and physical inactivity are believed to play a major role in the
development of obesity (58). However, ultimately, excess adipose tissue is caused by an
imbalance between energy intake and energy expenditure (59).
Both genetic and environmental factors are involved in the pathophysiology of excess
body fat storage. Heredity accounts for 30% to 40% of the variations in BMI while environment
contributes 60% to 70% (53). People with “obese genes” are only inherited with a tendency to be
obese but not destined to be obese. Evidence comes from a research conducted among obese
individuals, in collaboration with their family members, indicating that genes explained 25% to
40% of the individual differences in BMI (60). However, genetic predisposition itself cannot
explain why the tendency of obesity is more prevalent today than it was 30 years ago. Lifestyle
changes including adaptation to increased energy-dense food intake and sedentariness, and lack
of drive for physical activity are all thought to interact with genes and contribute to the dramatic
increase in the prevalence of obesity in the past two decades (61). Nevertheless, the influence of
energy intake on obesity rates seems paradoxical. Evidence from the U.S. Department of
Agriculture National Wide Food Consumption Survey demonstrated a decrease in average fat
and energy intake in both men and women, regardless of the increase in obesity rate between the
years of 1977 and 1988 (62). Schoeller and Buchholz hypothesized that this paradox may be
explained by the increased emphasis on carbohydrate intake which might not have a metabolic
advantage (63).

9
 In addition to the consumption of extra calories, reduced physical activity, and other
lifestyle related misbehaviors, social economic status and cultural diversity are factors leading to
positive energy balance. Several studies have demonstrated that low incomes, low levels of
education and poverty are highly associated with obesity (64, 65). However, the correlation
between social economic status and obesity varies among different ethnicities and gender (63).
Overweight and obesity are strongly related with higher circulating levels of
inflammatory markers, such as C-reactive protein (CRP), IL-6 or TNF-a (56). Low-grade
inflammation has been recognized as a potential mechanism in increasing adipose tissue storage
(66). Alteration in endocrine function also affect fat storage, and several hormones are believed
to play a role, including ghrelin, leptin, growth hormone, androgens, and IGF-1(67, 68). In
addition, hypothyroidism and hypercortisolism are potential contributors to obesity (69).

2.2.3 Health Consequences of Obesity

The economic costs for obesity are incremental. Additionally, the health care costs
associated with obesity include direct medical costs and indirect costs, such as medical care,
surgery, absenteeism and decreasing productivity (70, 71).
Obesity is closely associated to several metabolic abnormalities, such as insulin
resistance, hyperinsulinemia, and glucose intolerance; and the associations were independent of
genetic factors (72). The metabolic changes can further develop into a cascade of syndromes,
including diabetes, dyslipidemia, and even heart failure (53). In a 12-year prospective study,
adipocyte fatty acid binding protein, which is one of the most abundant circulating adipokines,
was reported to be predictive of the development of cardiovascular disease (73).
Excess body fat and high BMI influence the overall quality of life of obese individuals.
Based on the NHANES III study conducted from 1988 to1994, elderly individuals (aged 70 and
older) in the highest quintile for body fat had higher likelihood to report functional limitations
and the risk was higher for women (74).

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 2.3 Definition of Sarcopenic Obesity
Sarcopenic obesity is a simultaneous occurrence of low skeletal muscle mass (6) and
excess adipose tissue (52). Like sarcopenia and obesity, the definition of sarcopenic obesity
remains debatable.
Using DXA measurements, Baumgartner et al. (16) defined sarcopenic obese individuals
as those who presented with an ASM index below two SD and a percent body fat above the 60th
percentile of an age-matched population. Accordingly, males with sarcopenic obesity had an
ASM index lower than 7.26 kg/m2 and a body fat percentage above 28%; females with
sarcopenic obesity had an ASM index lower than 5.45kg/m2 and a body fat percentage above
40% (16). Chung et al. developed a modified method to define sarcopenic obesity among an
Asian population by using ASM/Weight (ASM/Wt) and BMI. Using a cross-sectional survey of
elderly individuals aged 60 years or older, these researchers classified patients as sarcopenic
obese if their ASM/Wt was lower than one SD below the mean of young healthy reference adults
and their BMI was equal or greater than 25kg/m2 (75). Using prediction equations developed by
previous studies (9, 76), Davison and colleagues defined sarcopenic obese as a body fat
percentage in the upper two quintiles and a level of muscle mass in the lower two quintiles (74).
There were also attempts to define sarcopenic obesity based on fat-free mass (FFM) and fat mass
(FM). Schutz et al. (77) defined reference values of FFMI (FFM/height2) and FMI (FM/ height2)
for sarcopenic obesity. Additionally, residuals of the regression equation of FFM relative to FM
have also been used as cutoffs and shown to be associated with reduced muscle strength and
reduced aerobic fitness among postmenopausal women (78).

2.3.1 Prevalence of Sarcopenic Obesity

In the combined New Mexico Elder Health Survey and New Mexico Aging Process
Study, the prevalence of sarcopenic obesity increased from 2% in individuals aged 60 - 69 years
to up to 10% in individuals above 80 years of age (4). In a cross-sectional study of 1526 women
and 1391 men participants from NHANES III, Davison et al. (74) reported the prevalence of
sarcopenic obesity to be 7.4% in women and 9.6% in men aged 70 years and older. Zoico et al.
(79) reported a prevalence of sarcopenic obesity of 12.4% in a sample of 167 healthy women
aged 67-78 years old.

11
2.3.2 Etiology of Sarcopenic Obesity

Sarcopenic obesity is the confluence of two epidemics: aging and obesity (12).
Roubenoff (14) has contextualized sarcopenic obesity as a cyclical pattern. The increase in
adipocytes induces elevated secretion of leptin, tumor necrosis factors (TNFs) and other pro-
inflammatory factors. These metabolic changes interfere with muscle protein metabolism and
insulin sensitivity. Additionally, altered amino acid metabolism and impaired insulin sensitivity
further promote fat mass gain. The loss of LBM is also related with the loss of the metabolically
active BCM, which results in reduced resting energy expenditure. Ultimately, the cumulative
result of these metabolic changes leads to fat gain. Concurrently, muscle loss affects physical
activity level, which is also a contributor to fat mass accumulation, which in turn, reinforces
muscle loss (14). Therefore, this cyclical pattern of multifactorial processes, eventually lead to
muscle loss and fat gain. Excess adipose tissue causes increased production of certain hormone-
like cytokines, particularly leptin, TNF-α as well as IL-6, promoting protein degradation and
insulin resistance, enforcing muscle loss and fat gain (16). There is also evidence that altered
endocrinal functions, such as age-related hormone changes, are involved in the development of
sarcopenic obesity, including alterations of insulin, GH, IGF-1, corticosteroids and testosterone.
It has been well established that insulin acts as an inhibitor in muscle protein breakdown and
promotes skeletal muscle protein synthesis (80). Excess weight gain impairs the anabolic action
of insulin, leading to a decrease in muscle synthesis (41). GH and IGF-1 are anabolic factors
involved in protein anabolism and activation of satellite cell proliferation and differentiation
(41). Waters et al. investigated the relationships between hormonal alterations and body
composition among elderly individuals. Forty-five healthy participants were divided into normal
lean, sarcopenic, obese, and sarcopenic-obese groups. A decreased secretion of GH was reported
in obese and sarcopenic-obese individuals and this decrease was unresponsive to glucocorticoid
suppression in those with sarcopenic obesity, indicating a distinguished regulatory mechanism of
GH secretion in these individuals. In addition, no differences in cortisol concentrations were
found among all groups, although leptin levels were higher in obese and sarcopenic-obese groups
compared to the other two groups (81).
With advancing age, serum concentration of pro-inflammatory cytokines, such as TNF-α,
IL-1β, IL-6, elevates as a result of the imbalance between catabolic and anabolic hormones (82).

12
The relationship between higher cytokine (IL-6 and TNF-α) levels and low muscle strength was
evident among elderly populations (83). In addition, obesity promotes inflammation status. IL-1β
is produced mainly by macrophages, endothelial cells and astrocytes. The pro-inflammatory role
of IL-1β is played through the activation of T-helper cells, the production of prostaglandin E2,
and self-induction effect. TNF-α, produced by macrophages and adipocytes, is a contributor to
cachexia syndrome, cardiovascular disease and osteoporosis. It works closely with IL-1β in the
regulation of IL-6 production. IL-6, released mainly from macrophages, myocytes, and T
lymphocytes, stimulates a pro-inflammatory process in the body, leading to muscle loss and bone
catabolism (84). As such, TNF-α, IL-1β, and IL-6 have been indicated as pathogenic factors
contributing to an imbalance between protein synthesis and breakdown (38). Cesari et al. (85)
evaluated the relation between body composition and biomarkers of inflammation, reporting that
both CRP and IL-6 had a strong and positive relation with total body fat mass. However, the
considered biomarkers were inversely correlated with ASM after adjustment of fat mass,
indicating that pro-inflammatory cytokines are major contributors in the vicious cycle between
fat gain and muscle loss.

2.3.3 Health Consequences of Sarcopenic Obesity

The health outcomes of sarcopenic obesity involve the impact of both sarcopenia and
obesity. Evidence suggests that sarcopenic obese individuals have a greater risk of interrelated
health outcomes compared to those who have the onset of either body composition type alone.
Sarcopenic obesity has been associated with several clinical outcomes, such as impaired physical
function and quality of life (4, 86). By analysis of data from the New Mexico Aging Process
Study and the New Mexico Elder Health Survey, Baumgartner et al. (9) reported that sarcopenic
obesity was the strongest predictor of risk of falls and physical disabilities. The associations
remained significant after controlling for age, ethnic status, smoking and comorbidity. In an 8-
year follow up study, Baumgartner et al. (16) evaluated changes in self-reported disability,
assessed by the Instrumental Activities of Daily Living (IADL) questionnaire among 451
community-dwelling elderly individuals. Sarcopenic obese individuals presented with a 2.5 to
3.0 times higher likelihood to report IADL disability compared to other body composition
phenotypes (nonsarcopenic-obese, sarcopenic-nonobese or nonsarcopenic-nonobese) individuals.

13
Additionally, sarcopenic obese individuals presented with the greatest drop in IADL scores
during the 8-year follow-up (16). Although sarcopenic obesity was not directly assessed,
Sternfeld et al. (2) reported negative associations between fat mass and physical performance
(assessed by walking speed and grip strength) and positive associations between LBM and
muscle quality (assessed by grip strength). Sarcopenic obesity has also been associated with knee
osteoarthritis. In a large cross-sectional study, the prevalence of knee osteoarthritis was higher in
sarcopenic obese individuals compared to those with sarcopenia or obesity along (87).
Sarcopenic obesity has also been associated with poor health outcomes in clinical populations. In
end-stage renal disease patients, Honda et al. (88) showed that the prevalence of cardiovascular
disease and diabetes were higher among those with sarcopenic obese. Sarcopenic obesity has
also been predictive of shorter survival in patients with solid tumors of respiratory and
gastrointestinal tracts (5).

2.4 Body Composition Methodologies

As described previously, body composition abnormalities are associated with several
clinical implications; therefore, body composition assessment allows for the identification of
chronic under or over nutrition, and the evaluation of the effectiveness of nutritional intervention
on body composition changes (89). As discussed in Chapter One, conventional techniques, such
as body weight and BMI are incapable to detect body composition abnormalities in that they
cannot offer information on the distribution of different compartments and its predictive
prognostic value (90). For example, at the same BMI, females have more adiposity than males
and elderly individuals tend to have lower amounts of LBM compared to adults (91).
Several body composition techniques have been developed in the past few decades
including: BIA, DXA, magnetic resonance imaging (MRI), and air displacement
phethysmography (BOD POD®). However, DXA, MRI and BOD POD® measurements are
cost-sensitive and require highly trained operators. Compared to these techniques, BIA has
relative advantages; it is low-cost, portable, non-invasive, and convenient to operate (92). For
these merits, BIA has been largely used in field and epidemiologic studies (93).
Bioelectrical impedance analysis measurement is based on the principle that alternating
electric current passes through different body part at different rates. Impedance is defined as the
frequency-dependent opposition of a conductor to the alternating electric current (94). It is

14
derived from resistance (R) and reactance (Xc), representing the pure opposition of the conductor
and the dieletric component of impedance respectivly (94). Since the alternating current flows
through the body tissues at different rates, the current is partitioned into different body
components. BIA measures the conductivity of water content in human bodies which is the
electrolyte-rich fluid (94). FFM is an electrolyte-rich tissue and muscle mass is the major
component of FFM. Therefore, most current passes through muscle mass; whereras adipose
tissue, bone and organ restrain the flow of current and rarely allow it to pass through (76). In
summary, FFM is negatively associated with impedance and non-lean mass plays a minor role in
influencing impedance. The principle of BIA measurement is that different body components of
a conductor have different oppositions to the alternating current.
Bioelectrical impedance analysis is a commonly used technique in the assessment of
sarcopenic obesity. A summary of studies investigating the prevalence and clinical impact of
sarcopenic obesity (assessed by BIA) is presented in Table 2.1.

Table 2.1. Summary of body composition measurement by BIA*

Author, Year Purposes Indexes used to Major results
define SO

Sternfeld et al., To relate physical Relative measure of Total FM was inversely related to physical
2002 (2) function (self-reported body composition, the performance and functioning. Compared to
and measured) with body lean-to-fat ratio, lower muscle mass, excess FM was more
composition and to defined by dividing predictive of poor physical performance,
investigate the influence lean by fat mass functional limitation, and subsequent
of lean to fat mass ratio disability and mortality. Muscle strength
(absolute vs. relative) on was associated with lean mass but the
physical performance and magnitude of the association decreased as
functional limitation FM increased.

Davison et al., To investigate the Body fat% from Prevalence of SO was 7.3%. High% FM
2002 (74) associations between Baumgartner’s and BMI associated with functional
body composition and predictive equation. limitations with women but with a less
functional limitations Muscle mass from clear pattern in men. SO was not associated
Janssen’s predictive with greater likelihood of functional
equation. Upper two limitations.
quintiles for fat and
lower two quintiles for
relative muscle mass

15
Table 2.1. – continued
Author, Year Purposes Indexes used to Major results
define SO

Stenholm et To study the relationship OB: % FM and WC: Persons with SO had higher prevalence of
al., 2008 (86) of OB with walking sex-specific quartiles walking limitation compared with those
limitation and to examine with OB or SC. %FM, CRP and handgrip
the role CRP and BMI: WHO cut-offs. strength were associated with walking
handgrip strength in that limitation.
association Muscle strength: sex-
specific quartiles

Monteiro et To establish a reference Skeletal muscle mass The ratio between visceral fat and thigh
al., 2010 (95) dataset for temporal index from Janssen et muscle area was significantly increased in
parameters during al. (17). OB: BMI ≥ subjects with metabolic syndrome.
walking and to explore 25.5 kg/m2
the effect of OB and SO
on the same parameters

Siervo et al., To assess the prevalence SC: skeletal muscle Prevalence of SO ranged from 0 to 67% in
2011 (11) of SC or SO and to index Janssen’s those younger than 60 years of age and
determine the change in method (17) from 49 to 90% in those≥60 years.
prevalence using different
adiposity indexes OB: BMI ≥ 30kg/m2 ;
WC> 88cm; FM% ≥
35%; FM index ≥
9.5kg/m2

Visser et al., To assess the impact of SC: defined as FFM Prevalence of SO was 2.1%. Low FFM
2012 (96) SO and FM and FFM index. 14.5 kg/m2 for was associated with postoperative
independently on adverse women , and 15.7 infections while FM was not. SO was
outcome and its relation kg/m2 for men associated with lower muscle function.
with muscle function in
patients undergoing OB: FM index. 11.8
cardiac surgery kg/m2 for women, and
8.3 kg/m2 for men.

Lu et al., 2012 To explore the SC was defined by the SO is a major independent risk factor for
(97) relationship between SO percentage of total metabolic syndrome with a 12-fold higher
and metabolic syndrome skeletal mass (total risk compared to those without SC and
skeletal muscle obesity.
mass/weight ×100).
Cutoffs were
established at <37% in
men and < 27.6% in
women.

OB: BMI ≥ 25.5

kg/m2

Barbat-Artigas To test whether low SC: skeletal muscle Muscle quality increased as skeletal
et al., 2012 muscle mass is associated mass index by Janssen muscle and skeletal muscle index
(98) with better muscle quality et al. (17). decreased. Muscle quality was also related
in obese individuals OB: FM ≥ 40%. to functional capacity.
Muscle quality:
handgrip strength

16
*Adapted from Prado et al. (99). Abbreviations: BIA: Bioelectrical Impedance Analysis, SO: Sarcopenic Obesity,
FM: Fat Mass, FFM: Fat Free Mass, OB: Obesity, WC: Waist Circumference, CRP: C-Reactive Protein, SC:
Sarcopenia, BMI: Body Mass Index, WHO: the World Health Organization

Numerous studies have developed predictive equations for estimating LBM/muscle mass
from BIA measurements. These BIA-derived equations have been useful in estimating the
prevalence of sarcopenic obesity (74, 86), public health costs (76) and clinical outcomes (100).
However, the accuracy and validity of this technique is still under discussion. Several factors
have been identified that might influence the accuracy of BIA measurement and should be
controlled in clinical settings.
Food and beverage consumed prior to BIA measurement might affect impedance. Slinde
et al. (101) reported a decrease of impedance lasted two to four hours after ingestion of a
standard meal. Nevertheless, no significant change in body composition measurement after fluid
consumption has been reported (102). In order to control for any variations, the recommended
standard technique is an overnight fasting before impedance measurement (103).
Recent exercise is another factor contributing to the variation in BIA measurement. The
hypothesized mechanisms are increased cardiac output, blood flow to skeletal muscle, heat
dissipation and dehydration after exercise (104).
Variations in body composition is extremely variable by ethnicity, ethnic-specific
predictive equations should be used for accurate BIA measurements. As the majority of BIA
predictive equations have been developed on Caucasian populations. Biological differences, such
as height, weight, fat distribution, and body density lead to major differences in body
composition (92). Therefore, predictive equations should be validated for specific populations. In
addition, medical conditions (edema), individual differences (menopause), posture of the subject
and environment factors (temperature) may also play a role in altering body composition
assessed by BIA measurement.

17
 CHAPTER THREE
MATERIALS AND METHODS

3.1 Study Population

This study was based on data obtained from patients receiving treatment at the
Tallahassee Memorial Bariatric Center and has been approved by The Florida State University
Human Subjects Committee and the Institutional Review Board at Tallahassee Memorial
HealthCare, Inc.
From 2011 onwards, BIA measurements were incorporated as part of patient’s initial
assessment (first consultation) and were included in their medical records. Caucasian patients
with available BIA measurements, aged ≥ 18 years and with a BMI ≥ 30 kg/m2 were eligible to
participate in this study. Ineligible patients included those with severe diseases such as stroke,
class II heart failure, inflammatory digestive disease, lipodystrophy, and those who were on oral
steroid therapy.

3.2 Data Collection

As part of the TMBC standard of practice for newly admitted patients, a thorough health
examination was conducted which includes information on demographics, BIA body
composition measurements, weight change history, medical/surgical histories, psychiatric
disorders, laboratory results, and medications. Additional information on physical function
[Physical Activity Readiness (PAR-Q & YOU) Questionnaire] and physical activity (Exercise
and Attitude Questionnaire) were also available. From the available information, relevant data
was selected and presented in Appendix A. This data collection form was converted to Microsoft
Access (Microsoft Office 2010). A subset of information included in the data collection form
(Appendix B) was used to answer the specific hypothesis discussed in this Thesis, as described
below.

18
3.2.1 Demographic Characteristics

Marital status was divided into three categories: single, married/partner, or

divorced/widow/widower. Educational level was categorized as grade school, high school,
college or post-graduate. Self-reported income was used as proxy for socioeconomic status.
Annual income was classified into five categories: 0 – 30,000, 30,000 – 50,000, 50,000 –
75,000, 75,000 – 100,000, and >100,000.

3.2.2 Anthropometrics / Body Composition Assessments

Body weight, FFM, FM, %BF, and TBW were the variables collected using a Tanita
Body Composition Analyzer, Model: TBF -310 (Tanita Corporation of America, Inc., Arlington
Heights, IL, USA). Measurements involving weight were rounded to the nearest 0.1 pound.
Height was measured to the nearest 0.1 inch by Accustat Ross Stadiometer. Body mass index
was calculated as the ratio of weight (kg)/height squared (m2) and classified according to WHO
categories (Class I Obesity, 30.0-34.9 kg/m2; Class II Obesity, 35.0-39.9 kg/m2; Class III Obesity,
≥40 kg/m2). Waist circumference (WC) was measured at a graduation length of 1/8 inch at the
narrowest point between the lower border of the rib cage and the iliac crest by SECA 201
Ergonomic Circumference Measuring Tape.
In view of the lack of a consensus definition on sarcopenic obesity (99), the fact that our
population was relatively younger (age ≥ 18 years) than elderly populations in which sarcopenic
obesity has been commonly studied, and presented with a high prevalence of extreme cases of
obesity (81.3% morbidly obese), the ratio of FMI/FFMI was used to categorize our cohort into
those with sarcopenia and those without sarcopenia. As proposed by Prado et al. (99), weight
gain normally occurs alongside a variable rate of accretion of FFM which can potentially give
origin to either an obese (normal FFM accretion) or to a sarcopenic obese (low FFM accretion)
phenotype. Since the proposed ratio includes both FMI and FFMI, we are able to account for
proportional differences in these body composition compartments.
Figure 3.1 illustrates the concept of the FMI/FFMI ratio. Because of our relatively small
sample size, we dichotomized the FMI/FFMI ratio using the gender-specific median. Therefore,

19
FMI/FFMI ratios below the gender-specific median were classified as non-sarcopenic obese and
ratios above median were classified as sarcopenic obese.

Normal Non-sarcopenic Obese Sarcopenic Obese

Figure 3.1. Scheme of the relationship between fat mass index (FMI, depicted by larger grey circles) and fat-free
mass index (FFMI, black circles) portraying different body composition types. Adapted from: Prado et al. Anti Canc
Agents Med Chem. Ahead of print (105)

3.2.3 Metabolic Profile

Current smoking status was categorized as ‘No’, ‘Yes-occasionally’ and ‘Yes-everyday’.

Alcohol consumption was categorized into ‘occasional’, ‘every day’ and ‘none’. Blood pressure
was measured in the right arm by large adult blood pressure cuff and two-tube bladder (Welch
Allyn Diagnostics). Both systolic and diastolic blood pressure readings were recorded.
Biochemical parameters were obtained in several local laboratories in the Tallahassee region
within three months of BIA measurement collection. However, not all patients had blood tests on
file and only laboratorial tests taken within three months of BIA measurement were collected.
When available, data on fasting plasma glucose, lipid profile (total cholesterol, triglyceride, and
high-density lipoprotein (HDL)-cholesterol levels), liver and kidney functions, and vitamin D
were collected for this study.
Laboratorial and anthropometric results were further explored to investigate the presence
of metabolic syndrome as per the United States National Cholesterol Education Program Adult
Treatment Panel III Guidelines (106). Metabolic syndrome was defined by the presence of at
least three of the following risk factors: central obesity (WC ≥ 88 cm or 35 inches for women
and ≥102 cm or 40 inches for men); systolic blood pressure ≥ 130 mmHg and/or diastolic blood
pressure ≥ 85 mmHg; fasting plasma glucose level ≥ 100 mg/dL; triglyceride levels ≥ 150 mg/dL;
and low HDL- cholesterols (< 40 mg/dL for men and < 50 mg/dL for women).

20
3.2.4 Health Status: Comorbidities, Functional Outcomes, and Physical Activities

Medical and surgical history information was collected to further investigate the
occurrence of certain conditions, including arthritis, asthma, gout, osteoporosis, cancer, heart
disease and sleep apnea. Information on comorbidity problems was also collected and those
related to body composition were selected: acid reflux, alcoholism, diminished hygiene, fatigue,
immobility, joint pain, low back pain, nausea, shortness of breath, sexual dysfunction, thyroid
disease and weakness. The PAR-Q & YOU questionnaire, adopted from American College of
Sports Medicine Standards and Guidelines for Health and Fitness Facilities (107), was used for a
pre-evaluation of patients’ physical activity readiness. Seven questions were asked with answer
options of either ‘Yes’ or ‘No’ to each: 1)“Has your doctor ever said that you have a heart
condition and that you should only do physical activity recommended by a doctor?”; 2)“Do you
feel pain in your chest when you do physical activity?”; 3) “In the past month, have you had
chest pain when you were not doing physical activity?”; 4) “Do you lose your balance because of
dizziness or do you ever lose consciousness?”; 5) “Do you have a bone or joint problem (for ex:
back, knee or hip) that could be made worse by a change in your physical activity?”; 6) “Is your
doctor currently prescribing drugs (for ex: water pills) for your blood pressure of heart
condition?”; 7) “Do you know of any other reason why you should not do physical activity?”.
Patients were further divided into two groups: ‘Yes’ to one or more of the above
questions and ‘No’ to all questions. These variables were further dichotomized into ‘No’ to
depict no problems and ‘Yes’ for the presence of at least 1/7 items and a comparison between
sarcopenic obese and non-sarcopenic obese patients was conducted. Relevant data were selected
from the Exercise and Attitude Questionnaire to investigate patients’ physical activity levels;
questionnaire items explored variables associated with daily activities: “How many hours do you
spend watching TV per day?”; “How many hours do you spend using your computer?”; “How
much of your work day is spent at a desk?”; “How much of your work day is spent walking
around?”; and “How much of your day is spent standing in one spot?”; “At least once/week do
you participate in regular activity like brisk walking, jogging, biking, swimming, etc. long
enough to work up a sweat? (‘Yes’ or ‘No’)”.

21
 3.3 Statistical Analysis
In this descriptive, retrospective study, the total number of charts reviewed was estimated
to provide a small margin of error and a tight confidence interval. Although this is an ongoing
study, our current sample size of 91patients provides us an estimated margin of error of 0.1 =
0.98/√91. Such a small margin of error gives a tight confidence interval and high power.
Continuous data are presented as mean ± standard deviation (SD) and range. The
Pearson’s correlation coefficient was used to measure the strength of association between
continuous variables. Assumptions concerning normal distribution of residuals and constant SD
were checked. Comparisons between sarcopenic obese and non-sarcopenic obese groups were
assessed by independent samples t-Test or Mann-Whitney independent samples test for
continuous variables, as appropriate. Categorical variables are presented as percentages and
compared using Chi-square (χ²) test or Fisher’s exact test, as appropriate.
Binary logistic regression was used to obtain the odds ratio (OR) and 95% CIs for
outcome prediction, with multivariate analysis pursued for variables in the model reaching a
level of significance of ≤ 0.100. All tests were two-sided and statistical significance was reported
at the P≤0.05 level. All analyses were conducted using SPSS Statistics (version 21.0, IBM
Corporation, Armonk, NY).

22
 CHAPTER FOUR
RESULTS

4.1 Demographic Characteristics

To date, data on 132 patients have been collected as part of this ongoing study. Three
individuals were overweight (BMI <30 kg/m2) and 38 were non-Caucasians and were therefore
not included in this analysis. Therefore, 91 individuals (67 women and 24 men) were included.
No differences were observed for marital status, education level, self-reported household
income, and tobacco/drug use between sarcopenic obese and non-sarcopenic obese patients.
Overall, 14.8% of the patients were single, 59.3% were married or had a partner, and 25.9% were
divorced or widows/widowers. Education levels were as follows: 1.3% grade school, 35.4% high
school, 44.3% college and 19.0% post-graduate. Approximately 24.0% of the patients had an
annual household income lower than $ 30,000, 36.1% between $50,000 and $75,000, 12.5%
between $75,000 and $ 100,000, and 5.6% had an income above $100,000. In regards to drug
and tobacco use, 2 patients (out of 82 with available data) reported history of drug use; 3.7%
reported occasional tobacco use and 4.9% reported daily tobacco use.

4.2 Anthropometric and Body Composition Characteristics

Table 4.1 shows the characteristics of study participants. The majority of patients were
women (~74%) with a mean age of 57 ± 11 (range 27 – 79 years). Men presented with higher
body weight, height, WC, FFM, FFMI and TBW compared to women. On the contrary, women
presented with higher %BF and FMI/FFMI ratio. No gender differences were found for BMI,
FM and FMI. The FMI/FFM ratio was extremely variable ranging from 0.35 to 2.46 kg/m2. This
variability was independent of body weight, Figure 4.1. As exemplified in this figure, a person
with approximately 113 kg may have a FMI/FFMI ratio anywhere between 0.54 and 1.23 kg/m2.
Fat mass index was inversely correlated with age (r=-0.26, P=0.014) while no significant
association was observed between age and FFMI or FMI/FFMI ratio (r=-0.02, P=0.848 and
r=-0.19, P=0.077, respectively) Figure 4.2 A, B, and C.

23
4.2.1 Sarcopenic Obesity

The median FMI/FFMI ratio was 1.05 kg/m2 for women and 0.78 kg/m2 for men,
therefore, sarcopenic obesity was defined as a FMI/FFMI ≥ 1.05 kg/m2 or ≥ 0.78 kg/m2 for
women and men, respectively. Therefore, a total of 46 sarcopenic obese patients (74% women)
were identified, Table 4.2.
No age differences were observed among sarcopenic obese and non-sarcopenic obese
patients, although sarcopenic obese women tended to be older compared to their counterparts
(P=0.077), Table 4.2. The distribution of FFMI, FMI and %BF between sarcopenic obese and
non-sarcopenic obese patients for men and women is shown in Figure 4.3 A, B and C. In both
genders, body weight, %BF, FM, FMI and FMI/FFMI ratio were significantly greater in the
sarcopenic obese group, Table 4.2. Although FFM and FFMI were higher in non-sarcopenic
obese men compared to sarcopenic obese men, no differences were observed among women,
Table 4.2. Sarcopenic obese women had significantly greater BMI compared to non-sarcopenic
obese women, with no differences observed in men, Table 4.2.
No differences were found among BMI categories (obese classes I, II and III) by gender
(P=0.196, data not shown) but the prevalence of sarcopenic obesity was significantly higher in
morbidly obese patients. The prevalence of sarcopenic obesity among BMI categories was 0%,
33.3% and 56.8% for classes I, II and III obesity respectively, compared to 100.0%, 66.7% and
43.2% for non-sarcopenic obesity (P=0.022).
In order to investigate the prevalence of sarcopenic obesity among women receiving or
not receiving HRT, women were divided by age (< 50 or ≥ 50 years). Among women ≥ 50 years
(n = 55), 18.2% reported taking HRT. A greater proportion of women taking HRT were non-
sarcopenic obese although this difference was not statistically significant (80.0% vs. 20.0%
sarcopenic obese, P=0.078).

4.3 Metabolic Profile by Body Composition Phenotype

The overall metabolic characteristics of sarcopenic obese and non-sarcopenic obese
patients are presented in Table 4.3. Not all patients had laboratorial tests on file (sample size is
depicted with data presentation in Table 4.3). With the exception of albumin levels, no
differences were observed between sarcopenic obese and non-sarcopenic obese groups for any of

24
the assessed metabolic parameters. Albumin plasma concentration was significantly lower in
sarcopenic obese patients compared to non-sarcopenic obese patients (P=0.035). Although not
statistically significant, the prevalence of metabolic syndrome was greater among sarcopenic
obese patients. Approximately 63.0% of the sarcopenic obese patients and 44.4% of the non-
sarcopenic obese patients reported metabolic syndrome (P=0.075), Table 4.3. All patients
presented with central obesity.
Only 2 patients were taking thyroid medication (levothyroxine). The prevalence of
thyroid diseases was not different between sarcopenic obese and non-sarcopenic obese patients
(P=0.080), Table 4.3.

4.4 Health Status: Comorbidities, Functional Outcomes, and Physical Activities by Body
Composition Phenotype
As presented in Table 4.3, all patients reporting alcohol abuse were sarcopenic obese
(P=0.026). Compared to non-sarcopenic obese patients, the prevalence of sexual dysfunction was
also significantly greater among sarcopenic obese patients versus non-sarcopenic obese patients
(17.4% vs. 2.2%, P=0.030). Although not statistically significant, the prevalence of asthma was
higher among sarcopenic obese individuals compared to their counterparts (23.9% versus 8.9%,
respectively, P=0.088). Likewise, the prevalence of nausea was higher in sarcopenic obese
individuals, but only with a trend towards significance (P=0.059).
In regards to functional outcomes, the prevalence of mobility problems tended to be
higher among sarcopenic obese patients compared to their counterparts (17.4% vs. 4.4%
respectively, P=0.090), Table 4.3. A greater proportion of sarcopenic obese patients presented
with low back pain compared to non-sarcopenic obese patients (60.9% vs. 40.0% respectively,
P=0.046).
In order to further explore the association between sarcopenic obesity and low back pain,
a univariate model was used including body composition variables, as well as variables known to
predict low back pain (psychological distress/ depression, age, and gender) (108), Table 4.4. A
multivariate analysis was not pursed for all body composition variables due to multicollinearity
(2), Table 4.4 Sarcopenic obesity was the strongest predictor of lower back pain; patients
presenting with sarcopenic obesity were 2.3 times more likely to present with lower back pain
compared to non-sarcopenic obesity patients, Table 4.4.

25
 Selected daily activities from the Exercise and Attitude Questionnaire are shown in Table
4.5. No significant differences were observed between sarcopenic obese and non-sarcopenic
obese groups for any of the reported activities. Overall, 23.8% of patients (n=80) reported being
involved in regular physical activity at least once/week; the mean FMI/FFMI ratio was not
different between patients participating (0.95 kg/m2) or not (0.99 kg/m2) in regular physical
activity (P=0.124, data not shown). No differences of physical activity readiness assessed by
PAR-Q & YOU Questionnaire were observed between sarcopenic obese and non-sarcopenic
obese patients, Table 4.5.

Table 4.1. Overall characteristics of study patients

Women (N = 67) Men (N = 24)

Variables Total (N = 91) Mean ± SD Mean ± SD P-valuea

(Range) (Range)
Age (yr) 57.0 ± 11.0 56.6 ± 11.9 58.0 ± 8.3 0.596
(27.0-79.0) (27.0-79.0) (35.0-73.0)
Weight (kg) 128.3 ± 24.1 122.2 ± 21.0 145.3 ± 24.5 <0.0001
(78.3-191.4) (78.3-181.6) (114.0-191.4)
Height (cm) 166.1 ± 8.9 162.5 ± 6.9 176.1 ± 5.7 <0.0001
(148.6-190.5) (148.6-182.9) (166.7-190.5)
WC (cm)(23M)b 134.7 ± 16.0 132.3 ± 15.7 141.8 ± 14.9 0.013
(97.8-170.2) (97.8-167.6) (119.4-170.2)
BMI (kg/m2) 46.4 ± 7.6 46.2 ±7.3 47.0 ± 8.5 0.685
(31.6-68.7) (31.6-68.7) (36.0-65.6)
BF (%) 49.1 ± 7.1 51.0 ± 4.3 43.8 ± 10.2 0.002
(25.6-71.0) (42.0-58.8) (25.6-71.0)
FM (kg) 63.4 ± 17.2 62.9 ± 14.5 65.0 ± 23.6 0.678
(29.7-113.9) (34.0-95.0) (29.7-113.9)
2
FMI (kg/m ) 23.0 ± 6.0 23.8 ± 5.0 21.0 ± 7.9 0.129
(9.4-36.7) (13.7-32.8) (9.4-36.7)
FFM (kg) 64.5 ± 13.6 59.3 ± 8.6 79.0 ± 14.6 <0.0001
(43.8-113.9) (43.8-95.9) (46.4-113.9)
2
FFMI (kg/m ) 23.3 ± 3.9 22.5 ± 3.2 25.5 ± 4.8 0.001
(14.5-36.3) (16.4-36.3) (14.5-34.5)

26
 Table 4.1. - Continued
Women (N = 67) Men (N = 24)
Variables Total (N = 91) Mean ± SD Mean ± SD P-valuea
(Range) (Range)
FMI/FFMI (kg/m2) 1.00 ± 0.29 1.06 ± 0.18 0.87 ± 0.44 0.005
(0.35-2.46) (0.73-1.43) (0.35-2.46)
TBW (kg) 47.5 ± 10.0 43.4 ± 6.3 58.7 ± 10.0 <0.0001
(32.0-83.4) (32.0-70.2) (33.9-83.4)
Data are expressed as mean ± SD and range.
a
Independent samples t-test, women vs. men.
b
N that differ from the whole group are shown.
WC = Waist Circumference; BMI = Body Mass Index; BF = Body Fat; FM = Fat Mass; FMI = Fat Mass Index; FFM = Fat Free Mass; FFMI = Fat Free Mass
Index; TBW = Total Body Water.

27
Table 4.2. Comparison of body composition characteristics between sarcopenic obese and non-sarcopenic patients by gender
Women (N = 67) Men (N = 24)
Sarcopenic Obese Non-sarcopenic Sarcopenic Obese Non-sarcopenic
Variables (N = 34) Obese (N = 33) P-valuea (N = 12) Obese (N = 12) P-valuea
Age (yr) 54.1 ± 11.8 59.2 ± 11.5 0.077 56.1 ± 7.6 60.0 ± 8.8 0.255
(27.0-73.0) (28.0-79.0) (35.0-67.0) (41.0-73.0)
Weight (kg) 132.7 ± 17.9 111.3 ± 18.3 <0.0001 156.2 ± 27.1 134.5 ± 16.3 0.029
(109.1-169.6) (78.3-181.6) (118.7-191.6) (114.0-162.3)
Height (cm) 163.5 ± 7.2 161.5 ± 6.6 0.239 176.6 ± 7.1 175.7 ± 4.3 0.719
(152.4-182.9) (148.6-180.3) (166.7-190.5) (168.9-181.6)
WC (cm)
(23M)b 140.3 ± 11.7 124.1 ± 15.3 <0.0001 143.8 ± 18.0 139.5 ± 11.0 0.497
(112.4 – 160.0) (97.8 – 167.6) (119.4 – 170.2 ) (124.5 – 153.0)
BMI (kg/m2) 49.6 ± 5.4 42.8 ± 7.4 <0.0001 50.4 ± 10.2 43.5 ± 4.8 0.143
(39.4-58.8) (31.6-68.7) (36.0-65.6) (36.6-49.2)
BF (%) 54.6 ± 2.3 47.4 ± 2.4 <0.0001 50.7 ± 9.0 43.5 ± 4.8 <0.0001
(51.3-58.8) (42.0-51.1) (37.4-71.0) (25.6-43.6)
FM (kg) 72.7 ± 11.5 52.8 ± 9.4 <0.0001 80.1 ± 23.3 49.9 ± 11.2 0.001
(57.1-95.0) (34.1-85.7) (51.1-113.9) (29.7-63.6)
2
FMI (kg/m ) 27.1 ± 3.6 20.3 ± 3.6 <0.0001 25.9 ± 8.1 16.2 ± 3.8 0.002
(20.5-32.8) (13.7-32.4) (14.9-36.7) (9.4-21.0)
FFM (kg) 60.0 ± 7.4 58.5 ± 9.7 0.366 73.4 ± 15.8 84.5 ± 11.4 0.045
(50.2-77.0) (43.8-95.9) (46.4-100.5) (69.1-113.9)
2
FFMI (kg/m ) 22.4 ± 2.2 22.5 ± 4.0 0.711 23.7 ± 5.7 27.3 ± 2.8 0.052
(18.4-28.5) (16.4-36.3) (14.5-34.1) (22.8-34.5)
FMI/FFMI 1.21 ± 0.11 0.90 ± 0.08 <0.0001 1.14 ± 0.48 0.60 ± 0.15 <0.0001
(1.05-1.43) (0.73-1.04) (0.78-2.46) (0.35-0.77)
Data are expressed as mean ± SD, range.
a
Independent samples t-test or Mann-Whitney independent samples test.
WC = Waist Circumference; BMI = Body Mass Index; BF = Body Fat; FM = Fat Mass; FMI = Fat Mass Index; FFM = Fat Free Mass; FFMI = Fat Free Mass
Index; TBW = Total Body Water.

28
Table 4.3. Overall metabolic, comorbid, medical and functional characteristics of
sarcopenic obese and non-sarcopenic obese patients
Sarcopenic Obese Non-sarcopenic
Variables (N = 46) Obese (N = 45)
Mean ± SD Mean ± SD P-valuea
Metabolic Variables
Systolic BP (mmHg)(44SO,43OO)b 133.7 ± 17.0 135.5 ± 16.1 0.452
b
Diastolic BP (mmHg)(44SO,43OO) 76.7 ± 11.1 79.2 ± 17.2 0.652
Total Cholesterol (mg/dl)(30SO,26OO)b 187.0 ± 45.4 178.0 ± 36.6 0.628
b
LDL (mg/dl)(29SO,25OO) 105.1 ± 27.9 98.2 ± 33.8 0.362
b
HDL (mg/dl)(29SO,26OO) 53.4 ± 22.3 48.2 ± 13.8 0.637
Fasting Glucose (mg/dl)(32SO,27OO)b 111.2 ± 27.0 105.3 ± 32.4 0.152
b
Triglycerides (mg/dl)(29SO,26OO) 153.0 ± 79.0 170.0 ±104.5 0.637
b
Albumin (g/dl)(33SO,26OO) 4.0 ± 0.3 4.2 ± 0.3 0.035
Creatinine (mg/dl)(34SO,30OO)b 0.9 ± 0.50 0.9 ± 0.29 0.244
b
Total Protein (g/dl)(32SO,26OO) 7.0 ± 0.55 6.9 ± 0.3 0.637
b
Vitamin D (ng/ml)(21SO,21OO) 29.1 ± 12.6 34.2 ± 13.4 0.170
TSH (mIU/L)(23SO,21OO)b 2.3 ± 1.7 1.8 ± 1.3 0.452
b
T3 (pg/ml)(11SO,6OO) 5.1 ± 7.0 7.7 ± 11.4 0.404
b
T4 (ng/dl)(18SO,21OO) 1.9 ± 2.2 1.7 ± 1.8 0.530
b
AST (U/L)(32SO,30OO) 22.8 ± 9.8 21.7 ± 5.4 0.657
ALT (U/L)(31SO,28OO)b 27.2 ± 18.7 25.2 ± 10.3 0.903
Comorbidities / Medical Symptoms
MetSc (29SO,22O)b 29 (63.0%) 20 (44.4%) 0.075
Acid Reflux 21 (45.7%) 14 (31.1%) 0.154
Arthritis 26 (56.5%) 23 (51.1%) 0.605
Asthma 11 (23.9%) 4 (8.9%) 0.088
Alcoholism 6 (13.0%) 0 (0.0%) 0.026
Cancer 4 (8.7%) 9 (20.0%) 0.145
Diabetes 12 (26.1%) 17 (37.8%) 0.231
Diminished Hygiene 4 (8.7%) 1 (2.2%) 0.361
Fatigue 23 (50.0%) 19 (42.2%) 0.457
Gout 7 (15.2%) 2 (4.4%) 0.158
Heart Disease 2 (4.3%) 3 (6.7%) 0.677
Joint Pain 31 (67.4%) 27 (60.0%) 0.463
Nausea 7 (15.2%) 1 (2.2%) 0.059
Osteoporosis 3 (6.5%) 3 (6.7%) 1.000
Sexual Dysfunction 8 (17.4%) 1 (2.2%) 0.030

29
 Table 4.3. - Continued
Sarcopenic Obese Non-sarcopenic
Variables
(N = 46) Obese (N = 45)
Mean ± SD Mean ± SD P-valuea
Shortness of Breath 17 (37.0%) 18 (40.0%) 0.765
Sleep Apnea 23 (50.0%) 25 (55.6%) 0.596
Thyroid Disease 8 (17.4%) 15 (33.3%) 0.080
Weakness 11 (23.9%) 8 (17.8%) 0.472
Functional Outcomes
Immobility 8 (17.4%) 2 (4.4%) 0.090
Low Back Pain 28 (60.9%) 18 (40.0%) 0.046
Data are expressed as mean ± SD or number (percentage).
a
Mann-Whitney independent sample test for continuous variables and Fisher’s exact test or Chi-Square test for
categorical variables.
b
N that differ from the whole group are shown. cMetS (prevalence was reported as having three or more of the
following conditions: WC ≥ 88 cm or 35 inches for women and ≥102 cm or 40 inches for men; systolic blood
pressure ≥ 130 mmHg or diastolic blood pressure ≥ 85 mmHg; fasting plasma glucose level ≥ 100 mg/dL;
triglyceride levels ≥ 150 mg/dL; and HDL- cholesterols < 40 mg/dL for men and < 50 mg/dL for women).
BP = Blood Pressure; MetS = Metabolic Syndrome.

Table 4.4. Odds ratio and 95% CIs for the univariate effect of variables on low back pain
Coefficient (SE) Odds Ratio (95%CI) P-value
1
Sarcopenic Obese 0.85 (0.43) 2.3 (1.01-5.41) 0.048
FMI (kg/m2) 0.11 (0.04) 1.1 (1.03 – 1.20) 0.007
FFMI (kg/m2) 0.04 (0.06) 1.0 (0.93 – 1.16) 0.484
BMI (kg/m2) 0.07 (0.03) 1.1 (1.01-1.15) 0.017
Age (yr) -0.09 (0.01) 0.1 (0.95-1.03) 0.626
Gender2 0.30(0.48) 1.0 (0.41-2.62) 0.950
1 2
Versus non-sarcopenic obese patients (defined as the gender-specific median FMI/FFMI). Versus men

30
Table 4.5. Comparison of daily activities between sarcopenic obese and non-sarcopenic
obese groups
Sarcopenic Obese Non-sarcopenic
Activities P-valuea
(N = 46) Obese (N = 45)
Watching TV (hours/day) (39SO,39OO)b 3.0 ± 2.5 2.9 ± 1.9 0.705
b
Computer Use (hours/day) (28SO,39OO) 4.1 ± 3.6 3.8 ± 3.2 0.914
Work At Desk (hours/day) (36SO,40OO)b 5.2 ± 3.4 3.8 ± 3.6 0.132
Walking Around (hours/day)
1.5 ± 2.0 2.1 ± 2.2 0.107
(36SO,37OO)b
Standing One Spot (hours/day)
0.6 ± 1.3 0.7 ± 1.2 0.500
(33SO,37OO)b
PAR-Q & YOUc(40SO,38O)b 40 (87.0%) 45 (84.4%) 0.732
Data are expressed as mean ± SD or percentage.
a
Mann-Whitney independent samples test for continuous variables and Chi-square test for categorical variables.
b
N that differ from the whole group are shown.
c
Prevalence reported as having at least one out of seven PAR-Q & YOU questions checked as ‘Yes’.

Figure 4.1. Relationship between body weight (kg) and Fat mass index/Fat-free mass index
ratio (kg/m2)
Ratio ranges from 0.54 to 1.23 kg/m2 for a person at ~113kg. FMI = Fat Mass Index; FFMI = Fat Free Mass Index

31
 A B
r = -0.26, P=0.014 r = -0.19, P=0.077

C
r = -0.02, P = 0.848

Figure 4.2. Relationship between age (years) and A) Fat mass index (FMI, kg/m2); B) Fat
mass index/Fat-free mass index ratio (FMI/FFMI ratio, kg/m2); C) Fat-free mass index
(FFMI, kg/m2)

32
 A B

Figure 4.3. A) Fat-free mass index (FFMI, kg/m2); B) Fat mass index (FMI, kg/m2) and C)
Percent body fat (%BF) distribution of sarcopenic obese and non-sarcopenic obese patients
by gender

33
 CHAPTER FIVE
DISCUSSION

5.1 Review of Hypotheses and Conclusions

Hypothesis 1: The distribution of FMI/FFMI ratio will present with a degree of variability
greater than two folds (Chapter One).
Hypothesis 1 was accepted as the distribution of FMI/FFMI ratio ranged from 0.35
kg/m2 to 2.46 kg/m2 in the patient participants.
Hypothesis 2: Compared to non-sarcopenic obese patients, sarcopenic obese patients will:
a) present with higher rates of metabolic abnormalities and comorbidities, as assessed by the
TMBC New Patient Questionnaire (Chapter One);
b) report lower physical activity readiness and levels, as assessed by the PAR&Q
Questionnaire and Exercise History and Attitude Questionnaire (Chapter One).
Hypothesis 2a was partially accepted as a lower plasma albumin concentration (P=0.035)
and a higher prevalence of low back pain (60.9%), alcoholism (13.0%) and sexual dysfunction
(17.4%) were reported among sarcopenic obese patients, compared to non-sarcopenic obese
patients. No other differences were observed for the other variables collected between the two
body composition groups. Hypothesis 2b was rejected because no differences on physical
activities were observed between sarcopenic obese and non-sarcopenic obese patients.

5.2 Summary
The major findings of this thesis demonstrated a wide variability in body composition as
assessed by the FMI/FFMI ratio in this cohort of obese patients illustrating how variable the
proportions of fat to fat-free tissues may differ even in patients with similar BMI. Furthermore,
sarcopenic obesity was associated with higher risk of certain metabolic abnormalities and
comorbidities. The findings reported here highlight the potential use of the FMI/FFMI ratio as an
index for the assessment of abnormal body composition phenotypes in patients with severe
obesity.

34
 5.3 Discussion of Results
As reported in Chapter One, this study sought to describe the variability in body
composition, as well as the relationship between abnormal body composition (defined as a high
FMI/FFMI ratio) and overall health of obese patients. Overall heath was defined using metabolic,
functional and physical activity characteristics of the study population.

5.3.1 The FMI/FFM Ratio

In this study, we used the FMI/FFMI ratio to categorize patients into sarcopenic obese or
non-sarcopenic obese, which is an index that considers the potential inter-relationship between
these body composition compartments, rather than the absolute amount of each component (99).
As expected, the ratio was strongly correlated with FM, %BF and FFM, as well as BMI. Fat
mass was significantly higher in the sarcopenic obese group, compared to the non-sarcopenic
obese group in both genders; however, a difference in FFMI was only observed among men
(lower in the sarcopenic obese group). The inconsistency in FFM findings between genders may
be reflective of differences in adiposity, since women had a significantly higher %BF than men.
Moreover, the results of a study on a large cohort of healthy elderly individuals reported lower
rates of skeletal muscle depletion in women, compared to men (FFM was 1.0 kg/decade lower in
men and 0.4 kg/decade lower in women aged 60 years and older) (109). Therefore, FM
contributed the most to the FMI/FFMI ratio difference observed between the two body
composition groups in women and the concept of FMI/FFMI ratio may be particularly useful for
clinical evaluation of sarcopenic obesity in men.
Compared to body composition indexes of separate FM or FFM measurements (and its
derivatives), the FMI/FFMI ratio may be a more reliable prognostic index for the effect of body
composition on health (99). Using data from a convenient clinical sample of 560 obese women
(18 – 80 years old) with a BMI between 30 and 40 kg/m2, Prado et al. (99) reported an age-
related curvilinear relationship and a progressive narrowing of FM/FFM ratio with increased age,
suggesting that the ratio accurately depict body composition changes expected with aging (4). In
a similar approach, Sternfeld et al. (2) reported that a higher lean-to-fat ratio was related to faster
walking speed and less likelihood of functional limitation among elderly individuals ( ≥ 55

35
years). The association of adiposity to muscle ratio and physical limitation was also
demonstrated in a large community-dwelling elderly adult population ( >65 years) (110). The
above results suggested that the use of the lean-to-fat ratio considers the joint effects of lean
mass (a protective factor) and fat mass (a risk factor), and hence was a better predictor of
functional outcomes (2).

5.3.2 Gender- and Age-related Variations in Body Composition

The results of the present study indicate that both gender and age have an impact on the
variability of body composition components. Although BMI was not different by gender, men
presented with more FFM while women had a higher %BF, again confirming the variability in
body composition independent of BMI. These gender differences in body composition were
expected, as men have greater amounts of FFM than women, and women have greater %BF than
men at any age (39). In a cohort of morbidly obese patients, Lafortuna et al. (111) reported that a
unit increase in body weight was accounted for by an almost equal increase in FM and FFM in
men, whereas female bodily weight gain consisted of nearly triple the amount of FM compared
to FFM.
In this present study, we showed that FMI decreased with age. Previous studies have
described contradictory results. A longitudinal cohort study of elderly individuals, reported a
significant increase in FM with increasing age in men (112). Many cross-sectional studies
indicate that FM increases with age in both men and women. Kyle et al. (109) have shown that
FM increased with age in both genders in a large cohort of individuals aged 18 to 60 years and
decreased from 60 to 94 years of age. Zhu et al. (113) reported a curvilinear pattern
between %BF and age, that %BF reached a peak at the age of 50-59 in blacks and 60-90 in
whites and decreased afterwards. Similar results were reported by Mott et al., (114) a
deceleration in the rate of increase in fat mass with age was observed in both genders among
almost all ethnicities (Asians, Blacks, and Whites), with exception of Puerto Rican men. The
discrepancy between our observations and previous studies may be due to differences in the
population studied, study design (cross sectional versus longitudinal) and body composition
measurements used. Moreover, our study sample size was relatively small which might also
confound the correlation between age and FM. Although a negative relationship was observed

36
between FMI/FFM ratio and age, this difference was only trending towards significance
(P=0.077), and likely driven due to differences in FM.
It is of interest that in the present study, age was not strongly associated with a decrease
in FFMI, even though FMI decreased with aging. Although a parallel change in both
compartments is expected, specific direction of FMI and FFMI changes remains controversial
(115). Additionally, the high prevalence of morbidly obese patients in our study (81.3%) may
help explain these conflicting results. We can speculate that in morbidly obese patients, FM
decreases with age but not enough to induce significant losses of FFM, suggestive that FFM or
even a slight increase in FFM is needed to support the heavy load of excess adiposity.

5.3.3 Metabolic Abnormalities

Although the prevalence of metabolic syndrome was not statistically higher in sarcopenic
obese patients (63.0%) compared to non-sarcopenic obese (44.4%) patients, a trend towards
significance was observed (P=0.075). The association between sarcopenic obesity and metabolic
syndrome has been contradictory. Barbat-Artigas et al. (98) reported that sarcopenic obese
postmenopausal women were metabolically healthy. Baumgartner et al. (16) showed that the
prevalence of metabolic syndrome was highest in the group of non-sarcopenic obese subjects
among healthy elderly individuals. In contrast, Kim et al. (116) used ASM to visceral fat area
ratio (muscle/fat ratio) in a large cohort of healthy Korean adults to examine the association
between sarcopenic obesity and metabolic syndrome. The authors reported that subjects with
metabolic syndrome had significantly lower muscle/fat ratio (116). It has also been suggested
that the increased prevalence of cardio-vascular diseases among sarcopenic obese individuals
would be predicted by a high prevalence of metabolic syndrome among these individuals (117).
Unfortunately, the precise relationship between FFM and FM and the incidence of metabolic
complications is unclear (118).
In the present study, plasma albumin concentrations were lower for sarcopenic obese
patients. Lower albumin concentration has been linked as a risk factor for muscle catabolism
(119). Likewise, a recent study in elderly individuals showed that low albumin concentration was
significantly associated with mortality and frailty (P<0.001) (120). Hemelrijck et al. (121)
showed a combination of CRP, albumin, gamma-glutamyl transferase, and HDL as predictive

37
factors for mortality in individuals aged 50 years or over. Although information on mortality and
frailty was not available in this study, our finding sheds light on the use of clinical biomarkers
that recognize people potentially at risk for sarcopenic obesity, which could in turn be associated
with these outcomes.

5.3.4 Comorbidities / Functional Limitations / Physical Activities

In this study, all alcohol-dependent subjects were sarcopenic obese. Previous studies have
demonstrated that protein degradation rate exceeded the rate of protein synthesis among alcohol
abusers, leading to impaired muscle function (alcoholic myopathy) (122). In a review study of
the pathology of alcoholic myopathy, muscle atrophy caused by alcohol abuse might be selective
of losing Type II fibers (123). Although the precise mechanism underlying the effect of alcohol
intake on muscle decline is uncertain, potential factors have been proposed. Fernandez-Sola et al.
(124) reported that apoptosis was present in the skeletal muscle of high-dose alcohol consumers
suggesting apoptosis might be involved in the pathogenesis of skeletal myopathy among alcohol
abusers by impairing cellular structures. Animal studies showed vitamin D deficiency could play
a role in alcoholic muscle fiber atrophy (125). The association of low vitamin D level with
muscle atrophy has been documented in human studies even though few studies reported this
association among alcoholic abusers (126). Likewise, no differences in vitamin D levels were
observed between alcoholic abusers and non-alcoholic patients (data not shown) or on vitamin D
levels between sarcopenic obese and non-sarcopenic obese patients in our study.
Alcohol abuse has also been associated with a lower body weight and FM because of
alcoholism-induced malnutrition though whether malnutrition is caused by alcohol itself or
alcohol-related organ dysfunction remains unknown (127). Addolorato et al. (128) showed a
low %BF and constant LBM in patients suffering from alcohol abuse and suggested that as
alcohol cannot be utilized as an energy source, fat oxidation and water content of FFM both
increase. This is contradictory to our results likely due to the lack of information on the duration
and dosage of alcohol consumed by our patients since the authors suggested that three months
are required to restore nutritional status of alcoholics (128).
In our study, the prevalence of sexual dysfunction was significantly different between
sarcopenic obese and non-sarcopenic obese patients (P=0.030). Seidman et al. (129) suggested

38
that testosterone deficiency was most consistently associated with sexual dysfunction and could
be reversed by testosterone replacement therapy in aging men. In a study attempting to determine
the relationship between testosterone, inflammation and symptom burden among male cancer
patients, testosterone levels were predictive of erectile function in these patients and testosterone
measures were potential markers of increased symptom burden, including sexual dysfunction
(130). It is intriguing that grip strength was also predicted by testosterone levels, in addition,
testosterone level was predicted by C-reactive protein levels, suggesting low testosterone level
and high inflammatory cytokines might affect muscle mass and sexual function differently (130).
Our finding is consistent with a recent report of lower muscle mass and higher fat mass in male
patients with late-onset hypogonadism (131) and is also consistent with a previous report of the
concurrent high prevalence of sexual dysfunction (64.1%) and muscle/joint problems (86.3%) in
postmenopausal women (132). Unfortunately, the mechanisms involving sexual dysfunction and
sarcopenic obesity are unknown, but we hypothesize that the high prevalence of sexual
dysfunction among our sarcopenic obese patients could be related to hormone deficiency and
increased inflammation.
Low back pain emerged as a significant condition associate with sarcopenic obesity. The
prevalence of low back pain is estimated at 15% to 20% among American adults and 50% to 80%
experience at least one episode of low back pain during lifetime (133). People with low back
pain often experience a vicious cycle of pain and disuse, suffering from impaired physical
function and reduced quality of life caused by little strength, endurance and flexibility in their
lower back (134). In addition, low back pain accounts for one-third of total compensation costs
and leads to approximately 40% of absenteeism from work (134).The present study asserts that
FMI/FFMI ratio was a better predictor of back pain compared to conventional anthropometric
parameters. Sarcopenic obese patients presented with a greater prevalence of low back pain
compared to their counterparts. To the best of our knowledge, no previous studies have examined
the relationship between the FMI/FFMI ratio and low back pain and most studies have relied on
anthropometric measures reporting conflicting findings. A systematic literature review reported
that body weight or BMI were not strongly associated with low back pain (135). In contrast,
Urquhart et al. (136) reported BMI was related to higher levels of back pain intensity.
Furthermore, by using dual radiograph absorptiometry, the researchers also reported that
individuals with high total body and lower limb fat mass were at higher risk for suffering from

39
low back pain, independent of LBM (136). On the contrary, a study sample from the Health,
Aging and Body Composition (Health ABC) study suggested that the onset of low back pain
may be caused by poor trunk muscle composition, assessed by CT (137). Additionally, Monteiro
et al. (95) reported a pressure increase in different foot areas among sarcopenic obese
postmenopausal women, suggesting that high levels of FM loaded on the lower extremity placed
the patients at higher risk of functional impairment. Other possible mechanism includes an
increased fat load per muscle unit, or a pro-inflammatory milieu leading to muscle atrophy and
eventually low back pain (138).
No differences were observed in self-reported physical activities levels between
sarcopenic obese and non-sarcopenic obese patients. Previous studies have reported conflicting
results. Two studies concluded that sarcopenia and sarcopenic obesity were not associated with
reduced physical capacity when compared to non-sarcopenic obese or normal groups in older
men and women (74, 139) . On the contrary, Baumgartner et al. (16) showed that low muscle
mass was predictive of decreased daily living activities and that sarcopenic obese individuals
were 2.6 times more likely to develop physical incapacity than other groups (sarcopenic, obese
or normal individuals) in a longitudinal cohort (16). Additionally, the authors reported that
sarcopenic obesity was associated with a lower physical capacity compared to other body
composition phenotypes (4). Unfortunately, we were unable to use validated and comparable
measures of physical activity and were therefore unable to make meaningful assumptions and
comparisons with our results.

5.4 Limitations and Future Research

The use of the gender-specific median of FMI/FFMI ratio to classify sarcopenic obese
and non-sarcopenic obese patients was a limitation. Patients above the ratio median are not
necessarily sarcopenic obese as this may be a fairly inclusive rather than exclusive cutpoint.
Unfortunately, we were unable to explore other cutpoints such as quantiles of FMI/FMMI due to
our relatively small sample size. It is likely that using a less inclusive cutpoint would
significantly affect the association of the FMI/FFM ratio with the variables hereby studied,
nonetheless, we were still able to report interesting results such as the association of a higher
FMI/FFMI ratio (depicting a sarcopenic obese phenotype) with low back pain. Previous studies
have also demonstrated the potential use of body composition ratios. Auyeung et al. reported that

40
adiposity to muscle ratio was predictive of physical limitation in a large cohort of older adults
(110). Sternfeld et al. (24) showed a higher lean mass/fat mass ratio was associated with faster
walking speed and less limitation. Likewise, the ratio of FFM/ body surface area has been
suggested to be a better index than BMI alone in clinical oncology (24).
As mentioned above, the use of the median as a cutpoint may underestimate the
occurrence and significance of sarcopenic obesity, especially in women who presented with a
less variable FFM than men. Furthermore, the use of the FMI/FFMI ratio does not account for
differences in muscle quality, which may be a more sensitive marker of sarcopenic obesity (140).
Another limitation of our study included the retrospective, cross-sectional design and the
relatively small sample size, with a smaller proportion of men. In addition, the health status
information was self-reported, introducing the problem of interpretation/definition of each
individual comorbidity, as well as mis-reporting the severity of the health problem (e.g.
exaggeration or under-reporting of physical function and physical activity). All these factors may
have affected the significant of sarcopenic obesity as a predictor of health in this patient
population. Likewise, no cause-effect relationships between the FMI/FFMI ratio and health
outcomes can be inferred.
We were also not able to collect potential confounder variables such as dietary intake and
menopausal status, which may substantially impact body composition (141). Last but not least,
patients were not fasting for BIA measurements and as mentioned in Chapter Two, food and
beverage consumed prior to BIA measurement might affect impedance but to which extent
remains unclear (92). Likewise, the use of BIA as a two compartment method (FM and FFM) is
also limited as the FFM compartment includes both LBM and bone mineral mass.
Our study is however the first to investigate the prevalence of abnormal body
composition among a relative young cohort of morbidly obese individuals. As this is an ongoing
study, we anticipate that further associations will emerge as our sample size increases.
Future studies should prioritize establishing a consensus definition and diagnostic criteria
for sarcopenic obesity and its related impact on metabolic abnormalities and health outcomes.
The use of state-of-the-art tools to assess body composition in morbidly obese patients (e.g.
DXA) is also recommended for a more in depth investigation of the biological validity of
sarcopenic obesity. The further understanding of this condition should ultimately lead to
appropriate strategies to prevent/ treat sarcopenic obesity.

41
APPENDIX A
APPROVALS

42
1 1. Project Title and Identification

1.1 Project Title

Prevalence and Characteristics of Sarcopenic Obesity in a Bariatric Population

Project is: Thesis

1.2 Principal Investigator (PI)

Name(Last name, First name MI): Highest Earned Degree:

Prado, Carla M. M. Doctorate

Mailing Address: Phone Number:

412 Sandels Building, 120 Convocation Way POBox 3061493 Campus 6451522
Code: 1493
Fax:

University Department: Email:

NUTRITION FOOD AND EXERCISE SCIENCES [email protected]

The training and education completed in the protection of human Occupational Position:
subjects or human subjects records: Faculty
NIH

1.3 Co-Investigators/Research Staff

Name(Last name, First name MI): Highest Earned Degree:

Ormsbee, Michael ; Co-Investigator Doctorate

Mailing Address: Phone Number:

430 Sandels Building Tallahassee, FL (850) 644-4793

Fax:
(850) 645-5000

University Department: Email:

NUTRITION FOOD AND EXERCISE SCIENCES [email protected]

The training and education completed in the protection of human Occupational Position:
subjects or human subjects records: Faculty
FSU Training Module

Name(Last name, First name MI): Highest Earned Degree:

43
Cain, Angelina ; Co-Investigator Bachelor's Degree

Mailing Address: Phone Number:

1981 Capital Circle NE Tallahassee, FL 850 431-5404

Fax:

University Department: Email:

NON-FSU DEPARTMENT [email protected]

The training and education completed in the protection of human Occupational Position:
subjects or human subjects records: Other
Other

Name(Last name, First name MI): Highest Earned Degree:

Thornberry, Robert ; Co-Investigator Bachelor's Degree

Mailing Address: Phone Number:

3334 Capital Medical Blvd. Suite 400 Tallahassee, FL 850.877.8174

Fax:
850.877.5636

University Department: Email:

NON-FSU DEPARTMENT [email protected]

The training and education completed in the protection of human Occupational Position:
subjects or human subjects records: Other
Other

Name(Last name, First name MI): Highest Earned Degree:

Xiao, Jingjie ; Research Staff Bachelor's Degree

Mailing Address: Phone Number:

901 West Jefferson St apt B2 Tallahassee, FL 850 5913559

Fax:

University Department: Email:

NUTRITION FOOD AND EXERCISE SCIENCES [email protected]

The training and education completed in the protection of human Occupational Position:
subjects or human subjects records: Student
None

44
45
46
 APPENDIX B
DATA COLLECTION FORM
Sarcopenic Obesity in Bariatric Patients

TMH Chart Number: FSU STUDY ID:

Date of Baseline Visit (initial consultation) ____/____/_______

mm dd yyyy

Date of BIA Scan ____/____/_______

mm dd yyyy

Demographics

Date of Birth ____/____/_______ Age______ Sex: Male Female

mm dd yyyy
Ethnicity_________
Household Income

0 - 30,000 30,000 – 50,000 50,000 – 75,000

75,000 – 10,000 Un >100,000

Current Highest Level of Education

Grade School High School College

Post-graduate

Body Composition Measurements

Lab Test Lab Value Unit of Collection

HEIGHT Cm
WEIGHT Lb
BMI
BMR Kj

47
IMPEDANCE Ω
FAT %
FAT MASS Lb
FFM Lb
TBW Lb

Waist circumference = ________inches

Weight History

Weight gain: Gradual Rapid

Onset: Childhood Puberty Pregnancy Adult Menopausal

Associated with life changes: College Career Marriage

Divorce Death Stress

Weight loss attempts: Yes No

Eating Disorder: Yes No

Physical/Lifestyle assessment

Blood Pressure ______/______mmHg

syst. diast.

Medical and Surgical History

Acid Reflux/Heartburn Diabetes Kidney Disease

Anemia DVT Liver Disease

Anxiety Gout Lung Disease

Asthma Glaucoma Osteoporosis

48
Arthritis Gallbladder Disorder Polycystic Ovaries

Cancer (Type__) Heart Attack Pulmonary Embolism

Carotid Disease Heart Disease Rheumatic/Scarlet Fever

Chest Pain Heart Murmur Sleep Apnea

Clotting Disorder High Blood Pressure Stroke

COPD High Cholesterol Thyroid Disease

Depression Irregular Menstrual Cycle Vascular Disease

Other:_________________________________________________________
Surgery:_____________ Location:___________ Date:_________
Surgery:_____________ Location:___________ Date:_________
Surgery:_____________ Location:___________ Date:_________
Surgery:_____________ Location:___________ Date:_________
Surgery:_____________ Location:___________ Date:_________
Surgery:_____________ Location:___________ Date:_________

Psychiatric History

Anxiety Alcoholism Anorexia

Depression Drug Addiction Binge Eating
Bipolar Disorder Schizophrenia Bulimia
Panic Attacks Nervous Breakdown Stress

Review of Systems: Please check any problems you have had over the last month.

Chest Pain Frequent Urination Headache

Leg Pain/Swelling Increased Hunger Dry Skin
Varicose Veins Increased Thirst Weakness
Acid reflux Numbness or Tingling Joint Pain
Abdominal Pain Incontinence Hemorrhoids
Nausea Sexual Dysfunction Hair loss
Vomiting Snoring Fatigue
Hernia Fever Low Back pain

49
Shortness of Breath Cough Irregular Heartbeats
Arm Pain Chills Brittle Hair/Nails
Cold Intolerance Constipation Dumping Syndrome
Heat Intolerance Diarrhea Immobility
Menstrual Changes Dizziness Diminished Hygiene
Infertility Blurred Vision Nose Bleeds

Social History

Single Divorced Married

Partner Widow/Widower
Tobacco Yes No How often? ____________
Drugs Yes No How often? ____________
Alcohol Yes No How often? ____________

Gynecologic History (For women only)

History of: Gestational Diabetes No Yes

Menstrual Periods: Hysterectomy No Yes
Hormone replacement No Yes

Laboratory Results

Lab Test Lab Value Unit of Collection Reference

Range
Cholesterol, Total mg/dL 125-200 mg/dL
HDL- Cholesterol mg/dL > OR=46 mg/dL
Triglycerides mg/dL <150 mg/dL
LDL-Cholesterol mg/dL <130 mg/dl(calc)
Chol/HDLC Ratio < OR=5.0 (calc)
Non-HDL Cholesterol mg/dL mg/dl(calc)
Glucose mg/dL 65-99 mg/dL
Urea Nitrogen (BUN) mg/dL 7-25 mg/dL
Creatinine mg/dL 0.50-1.05 mg/dL
eGFR Non-AFR. American Ml/min/1.73m2 > OR=60
Ml/min/1.73m2
eGFR AFR. American Ml/min/1.73m2 > OR=60

50
 Ml/min/1.73m2
BUN/Creatinine Ratio 6-22 (calc)
Sodium 135-146 nmol/L
Potassium 3.5-5.3 nmol/L
Chloride 98-110 nmol/L
Carbon Dioxide 21-33 nmol/L
Calcium 8.6-10.4 mg/ dL
Protein, Total 6.2-8.3 g/ dL
Albumin 3.6-5.1 g/ dL
Globulin 2.2-3.9 g/ dL
(calc)
Albumin/Globulin Ratio 1.0-2.1 (calc)
Bilirubin, Total 0.2-1.2 mg/ dL
Alkaline Phosphatase 33-130 U/L
AST 10-35 U/L
ALT 6-40 U/L
Vitamin D, 25-OH, Total 30-100 ng/mL
Vitamin D, 25-OH, D3 ng/mL
Vitamin D, 25-OH, D2 ng/mL
TSH mIU/L > OR=20 Years
0.40-4.50 mIU/L
T4, Free ng/dL 0.8-1.8 ng/ dL
T3, Free pg/mL 2.3-4.2 pg/mL
White Blood Cell Count Thousand/uL 3.8-10.8
Thousand/uL
Red Blood Cell Count Million/uL 3.80-5.10
Million/uL
Hemoglobin g/dL 11.7-15.5 g/dL
Hematocrit 35.0-45.0%
MCV fL 80.0-100.0 fL
MCH pg 27.0-33.0 pg
MCHC g/dL 32.0-36.0 g/dL
RDW 11.0-15.0%
Platelet Count Thousand/uL 140-400
Thousand/uL

51
 PATIENT MEDICATION LIST
Medication name Dose Taken by: Frequency Medication
(times per used for…
day)
By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

By mouth Injection
Inhaled ____

52
 Tallahassee Memorial Bariatric Center
Bariatric Nutrition Initial Assessment Form
Weight History
How many years have you been overweight? __ _
How many times have you tried to lose weight? __ __
What is your maximum adult weight (non-pregnant) and when? ____ _______
When did you start to gain excess weight and why? _______ _________

PAR-Q & YOU

YES NO 1.Has your doctor ever said that you have a heart condition and that you
should only do physical activity recommended by a doctor?

YES NO 2. Do you feel pain in your chest when you do physical activity?

YES NO 3. In the past month, have you had chest pain when you were not doing physical
activity?

YES NO 4. Do you lose your balance because of dizziness or do you ever lose
consciousness?

YES NO 5. Do you have a bone or joint problem (for ex: back, knee, or hip) that could be
made worse by a change in your physical activity?

YES NO 6. Is your doctor currently prescribing drugs (for ex: water pills) for your blood
pressure of heart condition?

YES NO 7. Do you know of any other reason why you should not do physical activity?

53
 Exercise History and Attitude Questionnaire

1. Please rate your exercise level on a scale of 1 to 5 (1= easy, 55= very strenuous) at each
age.
Age: 15-20 ____21-30_____31-40_____41-50______51-60______61+_____
2. Were you a high school and/or college athlete?
YES NO If yes, please explain: ___________
3. Rate yourself on a scale of 1 to 5 (1= least and 5= most)
Athletic Ability Competition Cardiovascular Capacity
1 1 1
2 2 2
3 3 3
4 4 4
5 5 5

Muscular Capacity Flexibility Capacity

1 1
2 2
3 3
4 4
5 5
4. When you start an exercise program
I stick with it until I accomplish my goal.
I stick with it most of the time.
I’m good for a month and then miss a month and then back on again repeatedly.
I usually don’t stick with it very long and then quit.
5. How much time are you willing to devote to an exercise program?
______minutes per day _______days per week
6. Do you currently do cardiovascular exercise?
Type(s):_______________ __________minutes per day ______days per week
7. Rate your perception of exertion during your cardiovascular exercise.
Light Fairly Light Somewhat Hard Hard
8. How long have you been exercising regularly?
_________months ____________years

9. What other exercise, sport or active recreational activities have you participated in?
In the past 6 months? ______
In the past 5 years? ______
10. Can you exercise during your work day? Yes No
11. What types of exercise interest you?
Walking Cycling Stair Climbing Jogging Group Exercise Yoga/Pilates
Elliptical Swimming Strength Training Racquet Sports Rock Climbing

54
 Other______________
12. What do you want exercise to do for you? ______________________________
13. Rate each goal separately: 1 Not Important 2 Somewhat Important 3Extremely
Important
a. Improve cardiovascular fitness ___
b. Lose weight ___
c. Lose body fat ___
d. Reshape my body ___
e. Improve performance for sports or other activity___
f. Improve my ability to cope with stress___
g. Improve flexibility____
h. Increase strength___
i. Improve balance___
j. Increase energy level___
k. Feel better___
l. Prevent/treat a medical condition___
14. How many pounds would you like to lose? ____ pounds
15. What is your usual pace of walking?
a. _____casual or strolling(less than 2 mph)
b. _____average or normal (2-3mph)
c. _____fairly brisk (3-4 mph)
d. _____brisk or striding (>4mph)
16. How many flights of stairs do you climb each day? _____flights/day
17. How many hours do you spend watching TV per day? ____hours/day
18. How many hours do you spend using your computer? ____hours/day
19. How much of your work day is spent at a desk? ___hours/day
20. How much of your work day is spent waking around? ___hours/day
21. How much of your day is spent standing in one spot? ____hours/day
22. At least once/week do you participate in regular activity like brisk walking, jogging, biking,
swimming, etc. long enough to work up a sweat?
No Yes How many times/week? ________ Activity________

Completed by: _________________

Date: ____/____/_______
mm dd yyyy

55
 REFERENCES

1. Landi F, Cruz-Jentoft AJ, Liperoti R, Russo A, Giovannini S, Tosato M, Capoluongo E,

et al. Sarcopenia and mortality risk in frail older persons aged 80 years and older: results from
ilSIRENTE study. Age Ageing 2013;42:203-209.

2. Sternfeld B, Ngo L, Satariano WA, Tager IB. Associations of body composition with
physical performance and self-reported functional limitation in elderly men and women. Am J
Epidemiol 2002;156:110-121.

3. Villareal DT, Banks M, Siener C, Sinacore DR, Klein S. Physical frailty and body
composition in obese elderly men and women. Obes Res 2004;12:913-920.

4. Baumgartner RN. Body composition in healthy aging. Ann N Y Acad Sci 2000;904:437-
448.

5. Prado CM, Lieffers JR, McCargar LJ, Reiman T, Sawyer MB, Martin L, Baracos VE.
Prevalence and clinical implications of sarcopenic obesity in patients with solid tumours of the
respiratory and gastrointestinal tracts: a population-based study. Lancet Oncol 2008;9:629-635.

6. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, Boirie Y, Cederholm T, Landi F, Martin FC, et
al. Sarcopenia: European consensus on definition and diagnosis: Report of the European
Working Group on Sarcopenia in Older People. Age Ageing 2010;39:412-423.

7. Delmonico MJ, Harris TB, Lee JS, Visser M, Nevitt M, Kritchevsky SB, Tylavsky FA, et
al. Alternative definitions of sarcopenia, lower extremity performance, and functional
impairment with aging in older men and women. J Am Geriatr Soc 2007;55:769-774.

8. Rosenberg IH. Summary comments. The American Journal of Clinical Nutrition

1989;50:1231-1233.

9. Baumgartner RN, Koehler KM, Gallagher D, Romero L, Heymsfield SB, Ross RR, Garry
PJ, et al. Epidemiology of sarcopenia among the elderly in New Mexico. Am J Epidemiol
1998;147:755-763.

10. Consultation WHO. Obesity: preventing and managing the global epidemic. World
Health Organization technical report series 2000:894.

11. Siervo M, Stephan, B. C. M., Nasti, G., & Colantuoni, A. Ageing, adiposity indexes and
low muscle mass in a clinical sample of overweight and obese women. Obesity Research &
Clinical Practice 2012;6:e63-e70.

56
12. Roubenoff R. Sarcopenic obesity: the confluence of two epidemics. Obes Res
2004;12:887-888.

13. Morley JE, Baumgartner RN, Roubenoff R, Mayer J, Nair KS. Sarcopenia. J Lab Clin
Med 2001;137:231-243.

14. Roubenoff R. Sarcopenic obesity: does muscle loss cause fat gain? Lessons from
rheumatoid arthritis and osteoarthritis. Ann N Y Acad Sci 2000;904:553-557.

15. Kyle UG, Pirlich M, Lochs H, Schuetz T, Pichard C. Increased length of hospital stay in
underweight and overweight patients at hospital admission: a controlled population study. Clin
Nutr 2005;24:133-142.

16. Baumgartner RN, Wayne SJ, Waters DL, Janssen I, Gallagher D, Morley JE. Sarcopenic
obesity predicts instrumental activities of daily living disability in the elderly. Obes Res
2004;12:1995-2004.

17. Janssen I, Baumgartner RN, Ross R, Rosenberg IH, Roubenoff R. Skeletal muscle
cutpoints associated with elevated physical disability risk in older men and women. Am J
Epidemiol 2004;159:413-421.

18. Janssen I, Heymsfield SB, Ross R. Low relative skeletal muscle mass (sarcopenia) in
older persons is associated with functional impairment and physical disability. J Am Geriatr Soc
2002;50:889-896.

19. Stephen WC, Janssen I. Sarcopenic-obesity and cardiovascular disease risk in the elderly.
J Nutr Health Aging 2009;13:460-466.

20. Newman AB, Kupelian V, Visser M, Simonsick E, Goodpaster B, Nevitt M, Kritchevsky

SB, et al. Sarcopenia: alternative definitions and associations with lower extremity function. J
Am Geriatr Soc 2003;51:1602-1609.

21. Bijlsma AY, Meskers CG, Ling CH, Narici M, Kurrle SE, Cameron ID, Westendorp RG,
et al. Defining sarcopenia: the impact of different diagnostic criteria on the prevalence of
sarcopenia in a large middle aged cohort. Age (Dordr) 2012;1-11.

22. Masanes F, Culla A, Navarro-Gonzalez M, Navarro-Lopez M, Sacanella E, Torres B,

Lopez-Soto A. Prevalence of sarcopenia in healthy community-dwelling elderly in an urban area
of Barcelona (Spain). J Nutr Health Aging 2012;16:184-187.

23. Chien MY, Huang TY, Wu YT. Prevalence of sarcopenia estimated using a bioelectrical
impedance analysis prediction equation in community-dwelling elderly people in Taiwan. J Am
Geriatr Soc 2008;56:1710-1715.

57
24. Silva AO, Karnikowski MG, Funghetto SS, Stival MM, Lima RM, de Souza JC, Navalta
JW, et al. Association of body composition with sarcopenic obesity in elderly women. Int J Gen
Med 2013;6:25-29.

25. Lindle RS, Metter EJ, Lynch NA, Fleg JL, Fozard JL, Tobin J, Roy TA, et al. Age and
gender comparisons of muscle strength in 654 women and men aged 20-93 yr. J Appl Physiol
1997;83:1581-1587.

26. Nair KS. Age-related changes in muscle. Mayo Clin Proc 2000;75 Suppl:S14-18.
27. Scott W, Stevens J, Binder-Macleod SA. Human skeletal muscle fiber type
classifications. Phys Ther 2001;81:1810-1816.

28. Balagopal P, Rooyackers OE, Adey DB, Ades PA, Nair KS. Effects of aging on in vivo
synthesis of skeletal muscle myosin heavy-chain and sarcoplasmic protein in humans. Am J
Physiol 1997;273:E790-800.

29. Roubenoff R. Sarcopenia and its implications for the elderly. Eur J Clin Nutr 2000;54
Suppl 3:S40-47.

30. Meng SJ, Yu LJ. Oxidative stress, molecular inflammation and sarcopenia. Int J Mol Sci
2010;11:1509-1526.

31. Lexell J. Human aging, muscle mass, and fiber type composition. J Gerontol A Biol Sci
Med Sci 1995;50 Spec No:11-16.

32. Verdijk LB, Snijders T, Beelen M, Savelberg HH, Meijer K, Kuipers H, Van Loon LJ.
Characteristics of muscle fiber type are predictive of skeletal muscle mass and strength in elderly
men. J Am Geriatr Soc 2010;58:2069-2075.

33. Roubenoff R. Origins and clinical relevance of sarcopenia. Can J Appl Physiol
2001;26:78-89.

34. Enoka RM. Neural strategies in the control of muscle force. Muscle Nerve Suppl
1997;5:S66-69.

35. Goodpaster BH, Thaete FL, Kelley DE. Composition of skeletal muscle evaluated with
computed tomography. Ann N Y Acad Sci 2000;904:18-24.

36. Burgos Pelaez R. Therapeutic approach to malnutrition and sarcopenia. Nestle Nutr Inst
Workshop Ser 2012;72:85-99.

37. Maggio M, Lauretani F, Ceda GP. Sex hormones and sarcopenia in older persons. Curr
Opin Clin Nutr Metab Care 2013;16:3-13.

38. Waters DL, Baumgartner RN, Garry PJ. Sarcopenia: current perspectives. J Nutr Health
Aging 2000;4:133-139.

58
39. Roubenoff R, Hughes VA. Sarcopenia: current concepts. J Gerontol A Biol Sci Med Sci
2000;55:M716-724.

40. Volkert D. The role of nutrition in the prevention of sarcopenia. Wien Med Wochenschr
2011;161:409-415.

41. Rolland Y, Czerwinski S, Abellan Van Kan G, Morley JE, Cesari M, Onder G, Woo J, et
al. Sarcopenia: its assessment, etiology, pathogenesis, consequences and future perspectives. J
Nutr Health Aging 2008;12:433-450.

42. Lenk K, Schuler G, Adams V. Skeletal muscle wasting in cachexia and sarcopenia:
molecular pathophysiology and impact of exercise training. J Cachexia Sarcopenia Muscle
2010;1:9-21.

43. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta
Physiol (Oxf) 2008;192:127-135.

44. Forbes SC, Little JP, Candow DG. Exercise and nutritional interventions for improving
aging muscle health. Endocrine 2012;42:29-38.

45. Visser M, Goodpaster BH, Kritchevsky SB, Newman AB, Nevitt M, Rubin SM,
Simonsick EM, et al. Muscle mass, muscle strength, and muscle fat infiltration as predictors of
incident mobility limitations in well-functioning older persons. J Gerontol A Biol Sci Med Sci
2005;60:324-333.

46. Janssen I. Influence of sarcopenia on the development of physical disability: the

Cardiovascular Health Study. J Am Geriatr Soc 2006;54:56-62.

47. Janssen I, Shepard DS, Katzmarzyk PT, Roubenoff R. The healthcare costs of sarcopenia
in the United States. J Am Geriatr Soc 2004;52:80-85.

48. Gallagher D, Visser M, Sepulveda D, Pierson RN, Harris T, Heymsfield SB. How useful
is body mass index for comparison of body fatness across age, sex, and ethnic groups? Am J
Epidemiol 1996;143:228-239.

49. Deurenberg P, Yap M, van Staveren WA. Body mass index and percent body fat: a meta
analysis among different ethnic groups. Int J Obes Relat Metab Disord 1998;22:1164-1171.

50. Abernathy RP, Black DR. Healthy body weights: an alternative perspective. Am J Clin
Nutr 1996;63:448S-451S.

51. Physical Status: the Use and Interpretation of Anthropometry. Report of a WHO Expert
Committee. World Health Organization technical report series 1995;854:1-452.
52. Jordan J, Engeli S, Redon J, Sharma AM, Luft FC, Narkiewicz K, Grassi G, et al.
European Society of Hypertension Working Group on Obesity: background, aims and
perspectives. J Hypertens 2007;25:897-900.

59
53. Pi-Sunyer FX. The obesity epidemic: pathophysiology and consequences of obesity.
Obes Res 2002;10 Suppl 2:97S-104S.

54. Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Overweight and obesity in the
United States: prevalence and trends, 1960-1994. Int J Obes Relat Metab Disord 1998;22:39-47.

55. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity in the United States,
2009-2010. NCHS Data Brief 2012:1-8.

56. Mathus-Vliegen EM. Obesity and the elderly. J Clin Gastroenterol 2012;46:533-544.

57. Fakhouri TH, Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity among
older adults in the United States, 2007-2010. NCHS Data Brief 2012:1-8.

58. Weinsier RL, Hunter GR, Heini AF, Goran MI, Sell SM. The etiology of obesity: relative
contribution of metabolic factors, diet, and physical activity. Am J Med 1998;105:145-150.

59. Pi-Sunyer X. A clinical view of the obesity problem. Science 2003;299:859-860.

60. Bouchard C. The genetics of obesity. CRC Pressl LIc. 1994.

61. Crowley VE. Overview of human obesity and central mechanisms regulating energy
homeostasis. Ann Clin Biochem 2008;45:245-255.

62. Heini AF, Weinsier RL. Divergent trends in obesity and fat intake patterns: the American
paradox. Am J Med 1997;102:259-264.

63. Schoeller DA, Buchholz AC. Energetics of obesity and weight control: does diet
composition matter? J Am Diet Assoc 2005;105:S24-28.

64. Drewnowski A. The economics of food choice behavior: why poverty and obesity are
linked. Nestle Nutr Inst Workshop Ser 2012;73:95-112.

65. Lantz PM, House JS, Lepkowski JM, Williams DR, Mero RP, Chen J. Socioeconomic
factors, health behaviors, and mortality: results from a nationally representative prospective
study of US adults. JAMA 1998;279:1703-1708.

66. Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol
2011;29:415-445.

67. Trayhurn P. Biology of leptin--its implications and consequences for the treatment of
obesity. Int J Obes Relat Metab Disord 2001;25 Suppl 1:S26-28.

68. Baudrand R, Carvajal CA, Riquelme A, Morales M, Solis N, Pizarro M, Escalona A, et

al. Overexpression of 11beta-hydroxysteroid dehydrogenase type 1 in hepatic and visceral

60
adipose tissue is associated with metabolic disorders in morbidly obese patients. Obes Surg
2010;20:77-83.

69. Weaver JU. Classical endocrine diseases causing obesity. Front Horm Res 2008;36:212-
228.

70. Moriarty JP, Branda ME, Olsen KD, Shah ND, Borah BJ, Wagie AE, Egginton JS, et al.
The effects of incremental costs of smoking and obesity on health care costs among adults: a 7-
year longitudinal study. J Occup Environ Med 2012;54:286-291.

71. Trogdon JG, Finkelstein EA, Hylands T, Dellea PS, Kamal-Bahl SJ. Indirect costs of
obesity: a review of the current literature. Obes Rev 2008;9:489-500.

72. Ronnemaa T, Koskenvuo M, Marniemi J, Koivunen T, Sajantila A, Rissanen A, Kaitsaari

M, et al. Glucose metabolism in identical twins discordant for obesity. The critical role of
visceral fat. J Clin Endocrinol Metab 1997;82:383-387.

73. Chow WS, Tso AW, Xu A, Yuen MM, Fong CH, Lam TH, Lo SV, et al. Elevated
circulating adipocyte-fatty acid binding protein levels predict incident cardiovascular events in a
community-based cohort: a 12-year prospective study. J Am Heart Assoc 2013;2:e004176.

74. Davison KK, Ford ES, Cogswell ME, Dietz WH. Percentage of body fat and body mass
index are associated with mobility limitations in people aged 70 and older from NHANES III. J
Am Geriatr Soc 2002;50:1802-1809.

75. Chung JY, Kang HT, Lee DC, Lee HR, Lee YJ. Body composition and its association
with cardiometabolic risk factors in the elderly: a focus on sarcopenic obesity. Arch Gerontol
Geriatr 2013;56:270-278.

76. Janssen I, Heymsfield SB, Baumgartner RN, Ross R. Estimation of skeletal muscle mass
by bioelectrical impedance analysis. J Appl Physiol 2000;89:465-471.

77. Schutz Y, Kyle UU, Pichard C. Fat-free mass index and fat mass index percentiles in
Caucasians aged 18-98 y. Int J Obes Relat Metab Disord 2002;26:953-960.

78. Oliveira RJ, Bottaro M, Junior JT, Farinatti PT, Bezerra LA, Lima RM. Identification of
sarcopenic obesity in postmenopausal women: a cutoff proposal. Braz J Med Biol Res
2011;44:1171-1176.

79. Zoico E, Di Francesco V, Guralnik JM, Mazzali G, Bortolani A, Guariento S, Sergi G, et

al. Physical disability and muscular strength in relation to obesity and different body composition
indexes in a sample of healthy elderly women. Int J Obes Relat Metab Disord 2004;28:234-241.

80. Balagopal P, Proctor D, Nair KS. Sarcopenia and hormonal changes. Endocrine
1997;7:57-60.

61
81. Waters DL, Qualls CR, Dorin RI, Veldhuis JD, Baumgartner RN. Altered growth
hormone, cortisol, and leptin secretion in healthy elderly persons with sarcopenia and mixed
body composition phenotypes. J Gerontol A Biol Sci Med Sci 2008;63:536-541.

82. Yeh SS, Schuster MW. Geriatric cachexia: the role of cytokines. Am J Clin Nutr
1999;70:183-197.

83. Visser M, Pahor M, Taaffe DR, Goodpaster BH, Simonsick EM, Newman AB, Nevitt M,
et al. Relationship of interleukin-6 and tumor necrosis factor-alpha with muscle mass and muscle
strength in elderly men and women: the Health ABC Study. J Gerontol A Biol Sci Med Sci
2002;57:M326-332.

84. Morley JE, Baumgartner RN. Cytokine-related aging process. J Gerontol A Biol Sci Med
Sci 2004;59:M924-929.

85. Cesari M, Kritchevsky SB, Baumgartner RN, Atkinson HH, Penninx BW, Lenchik L,
Palla SL, et al. Sarcopenia, obesity, and inflammation--results from the Trial of Angiotensin
Converting Enzyme Inhibition and Novel Cardiovascular Risk Factors study. Am J Clin Nutr
2005;82:428-434.

86. Stenholm S, Harris TB, Rantanen T, Visser M, Kritchevsky SB, Ferrucci L. Sarcopenic
obesity: definition, cause and consequences. Curr Opin Clin Nutr Metab Care 2008;11:693-700.

87. Lee S, Kim TN, Kim SH. Sarcopenic obesity is more closely associated with knee
osteoarthritis than is nonsarcopenic obesity: a cross-sectional study. Arthritis Rheum
2012;64:3947-3954.

88. Honda H, Qureshi AR, Axelsson J, Heimburger O, Suliman ME, Barany P, Stenvinkel P,
et al. Obese sarcopenia in patients with end-stage renal disease is associated with inflammation
and increased mortality. Am J Clin Nutr 2007;86:633-638.

89. Gibson RS. Anthropocentric assessment of body composition. Principles of nutritional

assessment. New York: Oxford University 1990:187-208.

90. Bohm A, Heitmann BL. The use of bioelectrical impedance analysis for body
composition in epidemiological studies. Eur J Clin Nutr 2013;67 Suppl 1:S79-85.

91. Shu H, Zheng YS, Li CL, Lu YH, Liu MY, He XH. [Body composition analysis among
adults with different body weights]. Zhonghua Yi Xue Za Zhi 2012;92:3412-3416.

92. Dehghan M, Merchant AT. Is bioelectrical impedance accurate for use in large
epidemiological studies? Nutr J 2008;7:7-26.

93. Karelis AD, Chamberland G, Aubertin-Leheudre M, Duval C, Ecological mobility in A,

Parkinson g. Validation of a portable bioelectrical impedance analyzer for the assessment of
body composition. Appl Physiol Nutr Metab 2013;38:27-32.

62
94. Heymsfield S. Human body composition. Human Kinetics 10% 2005;918.

95. Monteiro M, Gabriel R, Aranha J, Neves e Castro M, Sousa M, Moreira M. Influence of

obesity and sarcopenic obesity on plantar pressure of postmenopausal women. Clin Biomech
(Bristol, Avon) 2010;25:461-467.

96. Visser M, van Venrooij LM, Vulperhorst L, de Vos R, Wisselink W, van Leeuwen PA,
de Mol BA. Sarcopenic obesity is associated with adverse clinical outcome after cardiac surgery.
Nutr Metab Cardiovasc Dis 2012.

97. Lu C-W YK-C, Chang H-H, Lee L-T, Chen C-Y, Huang K-C. Sarcopenic obesity is
closely associated with metabolic syndrome. Obesity Research & Clinical Practice 2012.

98. Barbat-Artigas S, Filion ME, Plouffe S, Aubertin-Leheudre M. Muscle quality as a

potential explanation of the metabolically healthy but obese and sarcopenic obese paradoxes.
Metab Syndr Relat Disord 2012;10:117-122.

99. Prado CM, Wells JC, Smith SR, Stephan BC, Siervo M. Sarcopenic obesity: A Critical
appraisal of the current evidence. Clin Nutr 2012;31:583-601.

100. Heber D, Ingles S, Ashley JM, Maxwell MH, Lyons RF, Elashoff RM. Clinical detection
of sarcopenic obesity by bioelectrical impedance analysis. Am J Clin Nutr 1996;64:472S-477S.

101. Slinde F, Rossander-Hulthen L. Bioelectrical impedance: effect of 3 identical meals on

diurnal impedance variation and calculation of body composition. Am J Clin Nutr 2001;74:474-
478.

102. Evans WD, McClagish H, Trudgett C. Factors affecting the in vivo precision of
bioelectrical impedance analysis. Appl Radiat Isot 1998;49:485-487.

103. Fogelholm M, Sievanen H, Kukkonen-Harjula K, Oja P, Vuori I. Effects of meal and its
electrolytes on bioelectrical impedance. Basic Life Sci 1993;60:331-332.

104. Kushner RF, Gudivaka R, Schoeller DA. Clinical characteristics influencing bioelectrical
impedance analysis measurements. Am J Clin Nutr 1996;64:423S-427S.

105. Prado CM, Yara L. M. Maia, Michael Ormsbee. Michael B. Sawyer, Vickie E. Baracos.
Assessment of Nutritional Status in Cancer - The relationship between body composition and
pharmacokinetics. . Anti-Cancer Agents in Medicinal Chemistry Ahead of print.

106. Lorenzo C, Williams K, Hunt KJ, Haffner SM. The National Cholesterol Education
Program - Adult Treatment Panel III, International Diabetes Federation, and World Health
Organization definitions of the metabolic syndrome as predictors of incident cardiovascular
disease and diabetes. Diabetes Care 2007;30:8-13.

63
107. Tharrett SJ, & Peterson, J. A (Eds.). ACSM's health/fitness facility standards and
guidelines. . Human Kinetics 10% 2012.

108. Power C, Frank J, Hertzman C, Schierhout G, Li L. Predictors of low back pain onset in a
prospective British study. Am J Public Health 2001;91:1671-1678.

109. Kyle UG, Genton L, Hans D, Karsegard L, Slosman DO, Pichard C. Age-related
differences in fat-free mass, skeletal muscle, body cell mass and fat mass between 18 and 94
years. Eur J Clin Nutr 2001;55:663-672.

110. Auyeung TW, Lee JS, Leung J, Kwok T, Woo J. Adiposity to muscle ratio predicts
incident physical limitation in a cohort of 3,153 older adults-an alternative measurement of
sarcopenia and sarcopenic obesity. Age (Dordr) 2012.

111. Lafortuna CL, Maffiuletti NA, Agosti F, Sartorio A. Gender variations of body
composition, muscle strength and power output in morbid obesity. Int J Obes (Lond)
2005;29:833-841.

112. Gallagher D, Ruts E, Visser M, Heshka S, Baumgartner RN, Wang J, Pierson RN, et al.
Weight stability masks sarcopenia in elderly men and women. Am J Physiol Endocrinol Metab
2000;279:E366-375.

113. Zhu S, Wang Z, Shen W, Heymsfield SB, Heshka S. Percentage body fat ranges
associated with metabolic syndrome risk: results based on the third National Health and
Nutrition Examination Survey (1988-1994). Am J Clin Nutr 2003;78:228-235.

114. Mott JW, Wang J, Thornton JC, Allison DB, Heymsfield SB, Pierson RN, Jr. Relation
between body fat and age in 4 ethnic groups. Am J Clin Nutr 1999;69:1007-1013.

115. Schautz B, Later W, Heller M, Muller MJ, Bosy-Westphal A. Total and regional
relationship between lean and fat mass with increasing adiposity--impact for the diagnosis of
sarcopenic obesity. Eur J Clin Nutr 2012;66:1356-1361.

116. Kim TN, Park MS, Lim KI, Yang SJ, Yoo HJ, Kang HJ, Song W, et al. Skeletal muscle
mass to visceral fat area ratio is associated with metabolic syndrome and arterial stiffness: The
Korean Sarcopenic Obesity Study (KSOS). Diabetes Res Clin Pract 2011;93:285-291.

117. Lim S, Kim JH, Yoon JW, Kang SM, Choi SH, Park YJ, Kim KW, et al. Sarcopenic
obesity: prevalence and association with metabolic syndrome in the Korean Longitudinal Study
on Health and Aging (KLoSHA). Diabetes Care 2010;33:1652-1654.

118. Lim KI, Yang SJ, Kim TN, Yoo HJ, Kang HJ, Song W, Baik SH, et al. The association
between the ratio of visceral fat to thigh muscle area and metabolic syndrome: the Korean
Sarcopenic Obesity Study (KSOS). Clin Endocrinol (Oxf) 2010;73:588-594.

64
119. Bourdel-Marchasson I, Laksir H, Puget E. Interpreting routine biochemistry in those aged
over 65 years: a time for change. Maturitas 2010;66:39-45.

120. Fontana L, Addante F, Copetti M, Paroni G, Fontana A, Sancarlo D, Pellegrini F, et al.

Identification of a metabolic signature for multidimensional impairment and mortality risk in
hospitalized older patients. Aging Cell 2013;12:459-466.

121. Van Hemelrijck M, Harari D, Garmo H, Hammar N, Walldius G, Lambe M, Jungner I, et

al. Biomarker-based score to predict mortality in persons aged 50 years and older: a new
approach in the Swedish AMORIS study. Int J Mol Epidemiol Genet 2012;3:66-76.
122. Preedy VR, Peters TJ. Alcohol and skeletal muscle disease. Alcohol Alcohol
1990;25:177-187.

123. Preedy VR, Crabb DW, Farres J, Emery PW. Alcoholic myopathy and acetaldehyde.
Novartis Found Symp 2007;285:158-177; discussion 177-182, 198-159.

124. Fernandez-Sola J, Nicolas JM, Fatjo F, Garcia G, Sacanella E, Estruch R, Tobias E, et al.
Evidence of apoptosis in chronic alcoholic skeletal myopathy. Hum Pathol 2003;34:1247-1252.

125. Gonzalez-Reimers E, Duran-Castellon MC, Lopez-Lirola A, Santolaria-Fernandez F,

Abreu-Gonzalez P, Alvisa-Negrin J, Sanchez-Perez MJ. Alcoholic myopathy: vitamin D
deficiency is related to muscle fibre atrophy in a murine model. Alcohol Alcohol 2010;45:223-
230.

126. Kim MK, Baek KH, Song KH, Il Kang M, Park CY, Lee WY, Oh KW. Vitamin D
deficiency is associated with sarcopenia in older Koreans, regardless of obesity: the Fourth
Korea National Health and Nutrition Examination Surveys (KNHANES IV) 2009. J Clin
Endocrinol Metab 2011;96:3250-3256.

127. Addolorato G, Capristo E, Caputo F, Greco AV, Ceccanti M, Stefanini GF, Gasbarrini G.
Nutritional status and body fluid distribution in chronic alcoholics compared with controls.
Alcohol Clin Exp Res 1999;23:1232-1237.

128. Addolorato G, Capristo E, Marini M, Santini P, Scognamiglio U, Attilia ML, Messineo

D, et al. Body composition changes induced by chronic ethanol abuse: evaluation by dual energy
X-ray absorptiometry. Am J Gastroenterol 2000;95:2323-2327.

129. Seidman SN, Weiser M. Testosterone and mood in aging men. Psychiatr Clin North Am
2013;36:177-182.

130. Burney BO, Hayes TG, Smiechowska J, Cardwell G, Papusha V, Bhargava P, Konda B,
et al. Low testosterone levels and increased inflammatory markers in patients with cancer and
relationship with cachexia. J Clin Endocrinol Metab 2012;97:E700-709.

65
131. Tajar A, Huhtaniemi IT, O'Neill TW, Finn JD, Pye SR, Lee DM, Bartfai G, et al.
Characteristics of androgen deficiency in late-onset hypogonadism: results from the European
Male Aging Study (EMAS). J Clin Endocrinol Metab 2012;97:1508-1516.

132. Llaneza P, Fernandez-Inarrea JM, Arnott B, Garcia-Portilla MP, Chedraui P, Perez-

Lopez FR. Sexual function assessment in postmenopausal women with the 14-item changes in
sexual functioning questionnaire. J Sex Med 2011;8:2144-2151.

133. Goode AP, Carey TS, Jordan JM. Low back pain and lumbar spine osteoarthritis: how are
they related? Curr Rheumatol Rep 2013;15:1-8.

134. Winett RA, Carpinelli RN. Potential health-related benefits of resistance training. Prev
Med 2001;33:503-513.

135. Leboeuf-Yde C. Body weight and low back pain. A systematic literature review of 56
journal articles reporting on 65 epidemiologic studies. Spine (Phila Pa 1976) 2000;25:226-237.

136. Urquhart DM, Berry P, Wluka AE, Strauss BJ, Wang Y, Proietto J, Jones G, et al. 2011
Young Investigator Award winner: Increased fat mass is associated with high levels of low back
pain intensity and disability. Spine (Phila Pa 1976) 2011;36:1320-1325.

137. Hicks GE, Simonsick EM, Harris TB, Newman AB, Weiner DK, Nevitt MA, Tylavsky
FA. Cross-sectional associations between trunk muscle composition, back pain, and physical
function in the health, aging and body composition study. J Gerontol A Biol Sci Med Sci
2005;60:882-887.

138. Kim SK, Jung I, Kim JH. Exercise reduces C-reactive protein and improves physical
function in automotive workers with low back pain. J Occup Rehabil 2008;18:218-222.

139. Bouchard DR, Dionne IJ, Brochu M. Sarcopenic/obesity and physical capacity in older
men and women: data from the Nutrition as a Determinant of Successful Aging (NuAge)-the
Quebec longitudinal Study. Obesity (Silver Spring) 2009;17:2082-2088.

140. Bouchard DR, Janssen I. Dynapenic-obesity and physical function in older adults. J
Gerontol A Biol Sci Med Sci 2010;65:71-77.

141. Muller MJ, Lagerpusch M, Enderle J, Schautz B, Heller M, Bosy-Westphal A. Beyond

the body mass index: tracking body composition in the pathogenesis of obesity and the metabolic
syndrome. Obes Rev 2012;13 Suppl 2:6-13.

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 BIOGRAPHICAL SKETCH

JINGJIE XIAO

Jingjie was born in Gongyi, Henan, China to Jianli Xiao and Xianfeng Yang. She
attended high school at No. 2 High School in Gongyi. Jingjie majored in Food Quality and
Safety in Shandong Agricultural University for a bachelor’s degree in 2007. After she graduated
from college, she continued to pursue a master’s degree at the Florida State University in 2011;
and Jingjie switched majors to Nutrition Sciences. During her master’s study, Jingjie received
China linkage Scholarship for 2012-2013 term and she was also awarded the Pao-Sen Chi
Scholarship in 2012. During 2012-2013, Jingjie completed her master’s course work and started
working on her thesis project. She volunteered in the Youth Program in 2011 and later on
participated in the Understanding Nutrition Now (SUNN) as a peer health educator. Jingjie has
been dedicated with doing research and will continue to pursue a PhD degree under the guidance
of Dr. Carla Prado after her graduation.

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