Final Section 1: Food Insecurity and Alcohol Flashcards
2016 mortality from malnutrition stats
5,600,000 children under 5 died
90,000,000 undernourished and underweight worldwide
particularly in African, India, Asia, and South America
Severe Acute Malnutrition
SAM
WHO says weight for height -2 is wasting, +2 overweight from median Child Growth Standards for children under 5
-3 STD is severe wasting
any degree of wasting has elevated risk of death
top causes of death for children due to SAM
neonatal (following birth), pneumonia, diarrhea, malaria, measles, HIV/AIDS, injuries, other
PEU acute and chronic effects
acute: stunting, low weight for height
chronic: stunting, low weight for height and low height for age
definition of stunting
compromised growth in length/height and growth of vital organs
classes of PEU
1°: malnutrition due to inadequate intake, poverty, low food supply, poor quality food
linked with armed conflicts, political turbulence and natural disasters
2°: malnutrition due to disease state, decreased intake, decreased absorption/utilization, increased losses, increased requirement
Marasmus
“successful” adaptation to PEM, inadequate general nutrition
under 2 years of age, under 60% weight for age
skin and bones appearance
due to severe deprivation or impaired absorption
develops slowly
severe weight loss, muscle wasting, including heart
anxiety and apathy
good appetite sometimes
Kwashiorkor
“unsuccessful adaptation”, due to inadequate protein intake/absorption due to infection
presents with additional health issue: edema, fatty liver
loss of appetite
60-80% weight for age
rapid onset, earlier onset during weaning period (age 1-3), earlier than marasmus
why does kwashiorkor lead to loss of appetite and fatty liver?
fluid retention leads to loss of appetite
no proteins to transport fats from the liver can lead to fatty liver
edema explanation
plasma proteins leave leaky blood vessels and go into tissues, which attracts water
pressure leaves indentation in skin
long term PEU consequences
decreased development of all kinds, productivity in adulthood, reproduction, potential of society as a whole
infections due to PEU
lack of antibodies, anemia due to hemoglobin not synthesized, dysentery, fever, fluid imbalance, heart failure
infections common: diarrhea, pneumonia, UTI, measles, tuberculosis, parasitic infections (Fe and vitamin A deficiency)
how to rehabilitate someone with PEU
restore fluid and electrolyte imbalances
slow increase of protein (meal replacement shake)
treat infections
involve locals
malnutrition in socioeconomically transitioning countries
double burden of under and over nutrition (mortality vs. chronic diseases)
ex. Indonesia
34% of health care burden is childhood PEU
- also iron, vit A, and iodine deficiency
11% overweight/obesity and growing, largest % type II
food security definition
all people at all times have access to sufficient, safe, and nutritious food and clean water to maintain a healthy active life
how does food insecurity lead to under and over nutrition
poverty –> food insecurity/hunger –> inadequate intake –> malnutrition
poverty –> food insecurity –> excess intake of energy, fat and sugar –> obesity
food insecurity in canada
1 in 6 children in Canada
most affordable foods are unhealthy
old Canada alcohol recommendations
moderation, max 4
males - 1-2 drinks/day
females - 1 drink/day
with food
avoid if pregnant, operating machinery, or can’t control intake
new Canada alcohol recommendations
max 2 drinks per week males and females
3-6 drinks per week increases breast and colon cancer risk
>7 drinks per week increases risk of heart disease and stroke
1 drink =
1/2 oz pure ethanol
5 oz wine
12 oz beer
1.5 oz shooter
10 oz wine cooler
alcohol effect on the brain
narcotic sedative and depressant
brain cells cannot regenerate, liver can regenerate to a point
.05% - judgement and reasoning
0.1% - vision and speech
0.15% - coordination of voluntary muscles
0.3% - stupor, confusion
0.4% - respiration and heart action
alcohol metabolism pathway ADH
absorbed quickly through stomach/SI, passes directly into blood
non-inducible system, enzyme is always produced, 70% metabolism
1. ethanol (by alcohol dehydrogenase) –> NADH + H+
2. acetaldehyde + coA (by acetaldehyde dehydrogenase) –> NADH + H+
3. acetyl coA
located in liver and stomach of men
alcohol metabolism pathway MEOS
Microsomal Ethanol Oxidizing System, mitochondria of liver
absorbed quickly through stomach/SI
inducible system
20% of metabolism
1. Ethanol, NADPH + H+, 1/2 O2 (microsomal ethanol oxidizing system) –> NADP + H2O
2. Acetaldehyde + NAD+ (acetaldehyde dehydrogenase) –> NADH + H+
3. acetyl CoA
what does it mean that MEOS is inducible?
how does this lead to tolerance of drugs and alcohol?
enzyme produced when alcohol is present in blood
when drugs are processed, decreased alcohol processing and vice versa (system is busy)
system kicks in later, when consistently triggered there is always enzymes available and increases metabolism of alcohol/drug leading to tolerance
percent alcohol released through breath and urine
10%
how does alcohol abuse lead to fatty liver?
the enzymes of MEOS are busy and cannot process all the alcohol
acetyl coA cannot enter TCA and instead is turned into fatty acids and then triglycerides
what causes fibrosis and then cirrhosis of the liver?
liver tissues damaged by prolonged presence of acetaldehyde, leading to decreased protein synthesis and cell damage, and then fibrosis
when liver tries to regenerate with fibrosis, it leads to cirrhosis (irreversible)
how does alcohol cause acidosis?
increase H+ production through metabolism pathway to acetyl coA including reduction of NAD+
acetyl coA produces fat and ketones which are acidic
decreased gluconeogenesis leads to ketosis
less NAD+ available and so pyruvate produces lactate rather than acetyl coA
alcohol effects on nutrition
empty calories, 7 kcal/g
compromises status of thiamine, folate, vit D, and B6
dehydration
increased FA synthesis, decreased AA synthesis and gluconeogenesis, increased AA catabolism
Wernicke-Korsakoff syndrome
thiamine destruction from alcohol intake
Anemia from alcohol
due to folate excretion
vitamin D consequences of alcohol
decreased vitamin D activation in liver
B6 consequences from alcohol
B6 loss from binding protein
fetal alcohol syndrome causes
irreversible brain damage, growth restriction, cognitive impairment, facial abnormalities, vision abnormalities
Health Canada and Pediatric Society recommendations for alcohol with pregnancy
stop drinking as soon as planning to get pregnant to avoid 1-9 out of 1000 fetal alcohol syndrome births
what is the French paradox?
low CVD despite high saturated fat intake
high red wine consumption, resveratrol helps protect against LDL oxidation
alcohol increases HDL levels
moderate alcohol consumption increases risk of:
hypertension, stroke, cirrhosis, cancers, ulcers, osteoporosis, depression, fetal alcohol syndrome, drunk driving, insomnia, alcoholism, 200$ billion per year in medical costs
personal strategies to reduce risk of alcohol
drink in moderation, drink slowly, drink with food, don’t drive, seek help if needed
1 drink can be metabolized in 1 hour (.5oz ethanol by ADH pathway)
CAGE
questions you’ve asked yourself which indicate a problem:
cut down?
annoyed by criticism?
guilty about drinking?
eye-opener?
treatment for alcoholism
2 years active treatment, AA, abstinence, medications like antabuse (blocks AcAld DH and gives hangover instantly) and reviva (decreases craving and high effect by blocking binding of opioid receptors)
cirrhosis definition
irreversible liver damage caused by alcohol, hepatitis B or C, or iron toxicity due to hematochromatosis
leads to carinoma
as the liver constantly repairs, accumulation of fibrosis tissue, scars and nodules and connective tissue leading to impaired function
steatosis
fatty accumulation in the liver due to cirrhosis
alcoholic hepatitis
inflammation of the liver due to cirrhosis
liver resection
removal of part of the liver as a treatment for cirrhosis instead of a transplant
