Obesity Flashcards
Normal BMI
18.5-25
Overweight BMI
25-30
Obese class 1 BMI
30-35
Obese class 2 BMI
35-40
Obese class 3 BMI
40+
Prevalence of obesity/overweight in adults
71.6%
The Cost of Obesity
21% of annual medical costs in the United States. Around $149 billion a year
Contributing Factors to obesity
Genetic, epigenetic, and societal/environmental factors, Early childhood food experiences, social network
Genetic factors to obesity
Several genes have been identified and there are several genetic syndromes associated with obesity
How impairments in executive function affects obesity
the ability to engage in goal‐oriented behaviors, self‐regulation, and working memory are common in obesity.
Early childhood experiences and obesity
influence preferences towards food choices and eating habits/behaviors.
These preferences for foods may even develop in utero (“Prenatal and Postnatal Flavor Learning”) and during breast feeding as breast milk is flavored by maternal dietary intake.
Parental eating behaviors influence those of their children.
Activity habits also tend to develop in adolescence.
Social network and obesity
A person’s chances of becoming obese increase by 57% if they had another friend
become obese and 40% if a spouse became obese.
Peer groups even as early as childhood tend to organize around people with similar activity patterns and people tend to model our activity around our least fit friend
Social economic status and obesity
Higher rates of obesity observed in patients of lower SES
Financial burden of lifestyle interventions may be a significant factor influencing adherence for many patients (Travel, co-payments, equipment, gym memberships)
Lower access to green recreational spaces and team sports in childhood.
School programs for health/physical education and athletics have been cut.
White adipose tissue
Lipid storage and undergoes pathological expansion during obesity
Brown adipose tissue
Thermogenic, large amounts of mitchondria, dissipate large amounts of chemical energy as heat, defends core body temperature in cold weather
Contributes to energy expenditure
adipose tissue in Visceral/Intra-abdominal
Produce more pro-inflamatory cytokines; tumor necrosis factor-alpha (TNF-α) and
interleukin-6 (IL-6) and less adiponectin
Increased sympathetic activity
Strongly lined to cardiovascular disease, type 2 diabetes and various other condition
Adipose tissue is a type of \_\_\_\_ cell A. autocrine B. paracrine C. endocrine D. All of the above
D
Adipose tissue produces
Produces adipose-derived cytokines Adipokines
Also produces ANG-2 and ROS, changes to
Leptin sensitivity and signaling
Adipokines
some are beneficial (adiponectin) while some are pathogenic and induce atherogenesis, insulin resistance, inflammation and endothelial dysfunction
Obesity and affects of adipokines and adiponectin
abnormal production of pro-inflammatory adipokines and reduction in adiponectin
ET-1 is a vasodilator or vasoconstrictor?
Vasoconstrictor
Nitric oxide is a vasodilator or vasoconstrictor?
vasodilator
adiponectin function
increases NO bioavailability
Perivascular Adipose Tissue (PVAT)
Vascular homeostasis is maintained by the opposite action of endothelium-derived relaxing and contracting factors, mainly nitric oxide (NO) and endothelin (ET)-1.
Obesity and PVAT
Obese patients also have lower levels of adiponectin compared to healthy and greater production or pro-inflammatory adipokines (TNF-α, IL-6 etc)
TNF-α reduces NO bio-availability in obese patients and thus NO’s effect on ET-1
May also increase ROS and Angiontensin-2 production in obesity
Coronary PVAT
Altered contractile effects of obese coronary PVAT are related to differences in smooth muscle responsiveness between obese and lean coronary arteries. They have primary effects of increased vascular tone and impaired relaxation
Atherosclerotic plaques
have been shown to occur predominantly in epicardial coronary arteries that are encased in PVAT
myosteatosis
which is the presence of intermuscular and intramuscular adipose tissue
Myosteatosis induces pathological changes to skeletal muscle structure and insulin signaling pathways into the muscle
Myosteastosis is induced with obesity.
Implications of Obesity on Muscle
Reduction in anabolic hormones such as insulin-like growth factor-1 (IGF-1) and Testosterone
Obesity results in an increased secretion and expression of Myostatin.
The Obesity Paradox
Although obesity is a cardiovascular risk factor in epidemiological studies, an “obesity paradox” exists in which obese patients are associated with more favorable prognosis compared to lean patients among cohorts of cardiac patients.
BMI and CVD
BMI may be a less accurate reflection of CVD risk within individuals.
Cardiorespiratory fitness
more closely linked to mortality risk in populations exhibiting an obesity paradox
CRF “neutralizes” the obesity paradox
Clinical implications on obesity paradox
Strategies to reduce mortality risk in such populations should emphasize preserving or increasing CRF and LM more than weight loss alone
More Reliable Way to Measure Obesity
waist and hip measurement
Waist circumference measurement for increased risks
Men: >94cm (37inches)
Women: >80cm (31 inches)
Waist to hip ratio for increased risks
Men: 0.9
Women: 0.85
Bariatric Surgery
Indicated for individuals BMI >40 kg/m2
Weight loss often more dramatic and sustained than medical management. Reduces comorbidities like diabetes, hyperlipidemia and hypertension
Obesity significantly associated with more functional difficulty:
Moderate-Vigorous activities Lifting/Carrying groceries Walking 1 or more flights of stairs Bending/kneeling Walking 1 or more blocks Bathing or dressing Increased Fall Risk
Realistic goal for weight loss in obese patients
5%–15%. Even a 5% reduction in body weight, and weight loss takes time (4-6 months for most programs)
moderate intensity aerobic exercise training (AET)
Strong evidence to support this mode for weight loss. Goal is around 225–300 minutes per week.
High intensity interval training (HIT)
may be an effective alternative mode of exercise training for obese individuals
When compared to moderate intensity AET, HIT has similar outcomes, shorter training durations, and higher levels of enjoyment in obese individuals
Role of Physical Therapy
Education
Goal Setting
Exercise prescription either with or without bariatric surgery.
Addressing any barriers to movement and exercise
Assessments for exercise capacity
6MWT, 2 Min Step Test, incremental shuttle walking test (ISWT), or Cardiopulmonary Exercise Testing (CPET)
Assessments Strength and Mobility
Hand-held dynamometry, 30 sec chair rise test, 5 time sit to stand, TUG
Goals and intentions for treatment
Weight loss/Energy balance
Improving cardiorespiratory fitness
Improving functional mobility
Improving body composition (Lean/Fat-Free Mass)
Improving strength and mobility
How to keep patients going
Pick an activity or exercise that they enjoy!
Develop a Social Team
Add in activity to daily routine
Patient adherence and consistency
The primary factor that predicts a successful response to a weight loss program is patient adherence.
Pick something that moves you and healthy food you like to eat.
effect of diabetes on the body
Endothelial and vascular smooth muscle cell function propensity to
thrombosis
Contributes to atherosclerosis and its complications.
Hyperglycemia decreases endothelium-derived NO
Increased synthesis of vasoconstrictor prostanoids and endothelin-1
Increased activated platelets, increased coagulation factors (factor VII, vWF and tissue factor ) and inhibited pathways for fibrinolysis
Non-diabetic
At physiological levels, insulin regulates vascular homeostasis by maintaining the balance of endothelial derived NO and ET-1
Insulin resistance
In patients with insulin resistance, this relationship become paradoxical and P13K is selectively reduced allowing ET-1 production to be unopposed.
In addition to vasoconstriction ET-1 has other adverse effects on vascular health.
Advanced glycation end-products (AGE) Also known as “glycotoxins”
The formation of AGEs is a part of normal metabolism. But in Diabetic patients, AGEs is excessively high resulting in Increased ROS, increased arterial stiffness, impaired wound healing, increases
in diastolic pressure, retinopathy, neuropathy.
Signs and Symptoms of diabetes
Frequent Urination Excessive Thirst Extreme fatigue Vision Changes (Blurry) Feelings of hunger Cuts/bruises that are slow to heal Weight loss (DM 2) Polyneuropathy
Diabetic Polyneuropathy sensory
usually insidious in onset and showing a stocking-and-glove distribution in the distal extremities
Diabetic Polyneuropathy motor
Distal, proximal, or more focal weakness, sometimes occurring along with sensory neuropathy (i.e., sensorimotor neuropathy)
Diabetic Polyneuropathy autonomic
Neuropathy that may involve the cardiovascular, gastrointestinal, and genitourinary systems and the sweat glands
Primary risk factor for type II Diabetes. need 3/5
Large waist circumference/abdominal obesity Elevated triglycerides Low HDL Hypertension Elevated blood glucose level (fasting)
Increased level of C-reactive protein (CRP) causes
Increases risk of atherosclerosis and HTN
Type 1 Diabetes
Onset generally 6-13 y/o but can also occur in adults
Beta cells in Islets of Langerhans fail to produce sufficient insulin
Type 2 Diabetes
Onset generally >40 y/o
Hallmark: insulin resistance
Hypoglycemia
Glucose Levels ~ <70mg/dl for DM
Hypoglycemia early symptoms
Palpitations Fatigue Pale skin Shakiness and incoordination Anxiety Sweating Hunger Irritability Tingling sensation around the mouth Weakness
Hypoglycemia severe symptoms
Confusion, Abnormal behavior Inability to complete routine tasks Visual disturbances (blurred vision) Seizures Loss of consciousness
Hyperglycemia
Often Asymptomatic <200mg/dl
Hyperglycemia early symptoms
Frequent urination Increased thirst Blurred vision Fatigue Headache
Hyperglycemia Severe Symptoms
Nausea and vomiting Shortness of breath Dry mouth Weakness Confusion Coma Abdominal pain Fruity-smelling breath Presence of Ketones
Ketoacidosis
Caused by metabolism of fats and proteins which produce ketones
More common in DM1 than DM2
Ketoacidosis early symptoms
Increased Thirst
Dry mouth
Frequent or more frequent urination
Glucose Levels >240mg/dl
Ketoacidosis Severe Symptoms
Dry or flushed skin Nausea, vomiting, or abdominal pain Difficulty breathing Fruity odor on breath A hard time paying attention, or confusion May eventually lead to coma
Exercise for the Diabetic Patient benefits
Exercise increases glucose uptake during AND after exercise
Increased insulin- INDEPENDENT glucose uptake (1-3 hours)
Increased insulin SENSITIVITY lasts hours to days
