Obesity and Malnutrition Flashcards
OBESITY
● State of excess of adipose tissue mass ● Not just the fact that you are heavy ○ Excess fat cells add to your weight ■ Can cause additional problems inside your body ● Body mass index (BMI) ○ Most widely used method ○ BMI = weight/height2 (in kg/m2) ○ ≥30 kg/m2 defines obesity ○ 25.0 to 29.9 is termed overweight
ADIPOSOPATHY
Fat itself is causing an increase in morbidity and mortality by inducing other complications that cause the other condition
EPIDEMIOLOGY
● Obesity is very common nowadays because of the
increased production of food. There is an increased
availability of food that wasn’t available in the past.
● TODAY: Tendency to become more sedentary -
classes online, can eat and drink while listening, less
time to burn off fats
PREVALENCE
● Prevalence of medically significant obesity is increasing worldwide. ● Estimates of prevalence in U.S. adults >20 years of age ○ Overweight / Obese : 70% ○ Extreme obesity (BMI >40 25 kg/m2): 5.7% ● Sex ○ More common among women (38%) ■ Maybe because of genetics ■ May accumulate fat more easily ● Socioeconomic status ○ More common among poorer populations ○ In industrial societies, obesity is more common among poor women ■ Choices for food is limited ■ Forced to take in non-healthy food ● Age ○ Prevalence is increasing in children.
BODY WEIGHT
● Regulated by both endocrine and neural
components
● Easier to gain weight than to lose it
● A complex interplay that try to maintain weight
○ Alterations:
■ Weight loss: inc.appetite, decrease energy
expenditures
■ Overfeeding: decrease appetite, increase
energy expenditures
LEPTIN
● Major regulator
● Secreted by adipose cells
● Acts through brain circuits in the hypothalamus
● Influences appetite, energy expenditures and
neuroendocrine function
● Influences how we eat, how we burn what we eat
and how the body reacts
● Obesity = Increase in leptin
○ To increase metabolism and decrease appetite
● Fasted state = Decrease in leptin
APPETITE
● Neural afferents (vagal) - secondary to distention
↑ Ghrelin
appetite is statied, you lose your
appetite
↓ Glucose
your appetite is stimulated
Leptin, Insulin, Cortisol
stimulates appetite
Cultural factors
Other cultures want more plump women/men
Psychological factors
Bulimia, Anorexia - can control appetite
Neuropeptide Y, MCH, AgRP, Orexin,
Endocannabinoid
increases appetite
𝛂-MSH (melanocyte-stimulating hormone) -
induces satiety
Serotonin
decreases your appetite depending on
the various factors that stimulate it
Resting or basal metabolic rate
○ Energy being spent just by doing nothing
○ Accounts for 70% of daily energy expenditures
○ If you want to lose weight you should eat less
than your BMR
○ The bigger you are, the higher the BMR
because the body needs more calories to
function better
2. Energy cost of metabolizing and storing food
Thermic effect of exercise
5-10% - even if you exercise for half the day
Adaptive thermogenesis
○ Mostly seen among infants
○ Occurs in brown adipose tissues (BAT)
○ Expends stored energy as heat - they induce
heat formation
○ Leptin stimulates physiologic action of BA
○ Adults - less BAT, mostly white adipose tissue
(store fat for energy)
ADIPOSE TISSUE
● Lipid storing adipose cell ● Stromal/vascular component containing preadipocyte and macrophages ● Mass increases by lipid deposition and increase in adipocyte number
ADIPOCYTE
● Storage depot of fat ● Endocrine cell ● Leptin is stored in the adipocytes ○ ↑ adipocyte ↑ leptin ↓ appetite ○ ↓adipocyte ↓ leptin ↑ appetite
Factors released by adipocyte
Complement factors- Adipisin leptin, adiponectin, Resistin TNF-a, IL6 FFA, Glycerol Aromatase PAI-1, Angiotensinogen, RBP4
ETIOLOGY
● Obesity has a multifactorial etiology
○ Genetic influences
■ If your mother is on the plus size, your
tendency will still be on the plus size
■ Monozygotic twins - almost the same BMI
■ Dizygotic twins - it would depend on the
environment
○ Environmental Influences
○ Cultural factor
○ Diet
ENVIRONMENTAL INFLUENCES
● Availability and high caloric composition of the diet
● Sedentary lifestyle
● Sleep deprivation
● Recent increase in the prevalence of obesity
worldwide is largely due to lifestyle factors (changes
in diet, physical act)
● Physiologically, obesity results from an imbalance
between energy intake and energy expenditure.
○ Increased energy intake
○ Decreased energy expenditure
○ Combination of the 2 factors
● If there is a mutation in the leptin receptor
even if
you produce the leptin you will still feel that you are
starving because you don’t receive the signal from
the leptin, because the receptor is mutated.
POMC
stimulates the
feeling of satiety. If you have a mutation here then
again it’s very similar
TrkB
if there is a mutation, there is an increase of appetite. It doesn’t deliver satiety but it increases
appetite.
Prader-Willi syndrome
“FLK”- funny looking kid, you
dont look normal.
● Cohens- no medium size
DISEASES ASSOCIATED WITH OBESITY
● Cushing’s syndrome
● Hypothyroidism
● Insulinoma
○ Secondary to the feeling of hypoglycemia.
They tend to eat in order to relieve the feeling
of being hypoglycemic
● Craniopharyngioma and other disorders involving
the hypothalamus
GENETIC SYNDROMES ASSOCIATED WITH OBESITY
● Präder–Willi syndrome ● Laurence-Moon-Biedl syndrome ● Ahlström syndrome ● Cohen syndrome ● Carpenter syndrome ● Fragile X syndrome ● Wilson–Turner syndrome ● Albright’s hereditary osteodystrophy
Cohen & Carpenter
- least noticeable
Ahlstrom & Cohen
mental retardation is normal
PATHOLOGIC CONSEQUENCE OF OBESITY
● Insulin Resistance and T2DM ● Reproductive disorders ● Cardiovascular disease ● Pulmonary disease ● Hepatobiliary disease ● Cancer ● Bone, joint and cutaneous disease
METABOLIC MANIFESTATIONS OF ADIPOSOPATHY
● High blood glucose (prediabetes mellitus, type 2
diabetes mellitus)
● High blood pressure
● Metabolic syndrome
● Adiposopathic dyslipidema
● Insulin resistance
● Hepatosteatosis (fatty liver)
● Hyperuricemia and gout
● Cholelithiasis
● Acanthosis Nigricans
● Nephrolithiasis
● Glomerulopathy
● Pro-thrombotic predisposition
● Neuropsychiatric diseases (such as worsening
depression or loss of gray matter due to
adiposopathic immune and endocrine responses)
● Asthma (due to adiposopathic immune and endocrine responses)
● Worsening of other inflammatory diseases (osteoarthritis, atherosclerosis, etc.)
WOMEN
● Hyperandrogenemia ● Hirsutism ● Acne ● Polycystic ovarian syndrome ● Menstrual disorders ● Infertility ● Gestational diabetes mellitus ● Preeclampsia ● Thrombosis
MEN
● Hypoandrogenemia ● Hyperestrogenemia ● Erectile dysfunction ● Low sperm count ● Infertility
GENITOURINARY
● Urinary stress incontinence
● Pelvic prolapse (e.g. cystocele, rectocele, uterine
prolapse, vault prolapse)
REPRODUCTIVE PRE PREGNANCY Men
● Buried or hidden penis
● Erectile dysfunction
● Psychological barriers to sexual behavior
● Infertility
