chapter 5 Flashcards
Young adulthood (20-35)
- sexual maturity
- max. Ht
- peak bone mass
3rd decade (20s)
- loss of bone density
- max. muscle mass, then decline
5 year after maxi. Ht
max. strength, endurance, agility
30s
- catabolic phase slighter higher anabolic unless PA
- ↓ muscle mass–> ↓ BMR–> ↓ calorie needs
Middle adulthood (50-69)
- catabolism > anabolism–> imbalance
- ↓ muscle mass–> ↓ BMR–> ↓ calorie needs
- average Wt ↑ till 7th (60s)
aging person fails to adjust cal. intake to energy expenditure
xs. body Wt+ fat–> accumulate in wastline
prevent by PA
PA
prevent/ slow down ↓ bone/ muscle mass
↑ waistline
↑↑↑ risk of HTN, diabetes, CVD, chronic heart disease
BMI > 25–> OBESITY
morbidity of obesity ↑ - Overwright > 25lb --> ↑ risk of CHD in female by 2-3X --> ↑LDL, ↓HDL , ↑LDL/HDL metabolic chronic disorder--> diabetes, CVD, HTN, liver disease, cancer (breast, colon, prostate)
shift in industrialization
- shift in natural composition of diet
- ↑intake of animal fat, ↓complex CHO+ fibre
- cancer, CHD, obesity, dental disease
fruit+ vegetable
protection
- > =5 serving–> ↓ premenopausal breast CA
- rich in Vit C/ β-carotene
Key aspect accelerate aging, ↑ chronic disease
- ↑ in sat.fat, alcohol, Na, sugar+ ↓ in fiber
- smoking, little exercise, high stress
educate health diet and exercise
- delay onset of aging and chronic disease
- ↑ optimal function for longer period
- ↑ quality of life
unified dietary guidelines
- eat a variety of foods
- plant source
- > =5 serving of fruit and vegetable daily
- > =6 bread, pasta, cereal grains
- ↓ high fat food, ↓ animal source
- minimum simple sugar
population ageing
occur when ↑ median age of a country/ region due to ↑ life expectancy and/ or ↓birth rate
aging, time dependent changes
↓ organ mass
↓ # of GI cell
↓ function of organ (kidney)
–> mortality and morbidity rate happen elderly
usual aging
- process accelerated by disease& lifestyle factor
- poor exercise habit and alcohol and tobacco abuse
successful ageing
- age- related change not due to disease& lifestyle
- have sound nutritional habits, exercise regularly, regular BP
- non-smoker, no Xs alcohol, no diabetes, no obesity
Nutritional factor effect ageing
- Vit E–>Influence immune function
- Multivitamin+ mineral–> ↓1/2 infection rate
- malnutrition
- age-related disease (cataract , dementia) inhibited by supplement
- green vegetable (Vit C/ E)
- folate supplement
- fish, fish oil
nutritional intervention
a practical approach for modulating immune function compared to pharmacological intervention
Immunosenescence
age-related alteration in immune response–> decline in T-cell
Vitamin E
immune enhancing effect
-bio. active form Alpha tocopherol, most effective
improve T-cell
–> inhibits prostaglandin E2 in macrophages
–>reverse altered cytokine profile of T-cell
–> - Th1 cytokin IL-1 and IFN-γ production, IL-2 receptor expression
Best predictor of total number of visit to hospital or physician
Malnutrition
green vegetable (Vit C/ E)
- boost immune function
- ↓ incidence of cataract
- improve mental ability+ prevent some forms of dementia
folate supplement
- ↓ dementia, ↑ mental function
- deficiency–> 3X risk of dementia
- early dementia–> Wt loss–> folate metabolism
fish, fish oil
- ↑ cognitive perforce
- ↓ dementia
Body composition of elderly
skinny fat
obesity
- ↓ LBM+ ↑ fat (↓ cell mass, ↓ bone mineral)–> ↑ Wt
- due to ↓ PA+ hormonal change - ↓ growth hormone
- ↓ estrogen+ testosterone–> BMD
- ↓ testosterone –> ↓ muscle mass–> inability to maintain protein store
- ↓ LBM before ↓ BMD ↓ BMR
indicator of true fat mass and hence obesity of elderly
- fat mass, not BMI–>BMI cannot distinguish between fat mass and muscle mass
- Perfect body fat (male> 30 PBF, female> 40)
- Wast circumference> 40inch male, >30 women–> T2DM& heart disease (cannot discriminate visceral vs. subcutaneous fat)
HTGW (hypertriglyceridemic waist)+ visceral fat+ TG–> CVD - visceral fat–> fat liver–> ↑TG by liver–> insulin resistance
decline in resilience of hypothalamus-pituitary-adrenal (HPA) axis
↑ intramyocellular fat mass
↑ insulin resistance
key to sustain muscle mass
adequate caloric/ protein+ PA
cytokine
↑ adipose tissue–> ↑ cytokine–> ↑ low grade inflammation–> ↓ muscle protein meta.+ func.–> ↑ protein degradation in myofibrillar–> ↓ protein syn. –> muscle wasting
sarcopenia
age-related loss of muscle mass+ function
loss capacity for myofibrillar to contract
prevent by resistance training
Chronic disease
- CVD (due to heart condition/ HTN)
- Cancer (leading cause of death)
- diabetes
- hypertension
- high blood cholesterol
- obesity
- visual impairment
- dementia
- osteoporosis (arthritis)
use of drugs–> influence nutrient requirement, absorption, utilization, excretion
frail elderly
> =3
- muscle weekness
- slow walking speed
- exhaustion
- low physical activity levels
- unintentional weight loss
- -> risk of fall, hospital admission, death in several years
theories of ageing
↓ caloric intake–> ↓ accumulation of FR–> better ability to handle oxidative damage–> ↑ lifespan–> conferring protection to chronic disease
- cellular mutations
- ↓ hormonal recreation
- cross-linking
- free radicals
- immune system deterioration （immunosenescence）
- pre-programmed ageing under genetic control
- cellular mutations
- drugs, UV light, mutagens, radiation–> DNA damage, ↓DNA repair activity–> error in DNA replication, transcription, translation–> error of RNA & protein synthesis, ↓ function of cell
- environmental stressor–> damage & kill cells, apoptosis
- DNA methylation+ methyl group on cytosine nucleotide–> predator of mortality, biological age, epigenetic clock
- difference between (+)DNA methylation predicted age and (-)chronological age–> heritable trait, associated with ↑ risk of mortality
- ↓ hormonal recreation
- ↓ growth hormone–> ↑ adipose tissue–> ↓ LBM
- ↓ testosterone–> ↓ ability to maintain protein store& bone mass
- ↓ estrogen–> ↓ ability to maintain protein store
- insulin
- cross-linking
- glycated protein –> crossing-linking
- glucose molecule attach to another molecule–> advanced glycation end product (AGE)–> intracellular damage+ apoptosis
- free radicals
environmental exposure via radiation, natural body process
macromolecular damage
↓ caloric intake= ↓ FR accumulation
- immune system deterioration （immunosenescence）
- ↓ immune competence–>↓ T& B cell function
- autoimmune disorder+ chronic inflammatory disease
- thymic involution–> ↓ thymocytes mature to T cell–> ↓ T cell
- ↓ cell-mediated immunity/ immune competence/ immune dysregulation
- pre-programmed ageing under genetic control
- natural limit to cell division
- death gene P53
- age–> protective function of telomere fail–> DNA repair machinery/proliferation (require P53 to stop)–> apoptosis for rapid turnover cell (blood cell) –>cell senescent
3 ways of cell senescent
- telomere shortening (replicative senescent)
- over-exposure to oncogene (over reactive–> cancer)
- DNA damaging
senescent cell–> biochemical detrimental to normal function neighbouring cell
Malnutrition in older adult
- ↓ body function
- chronic disease
- multiple medication
- need assistance with self-care
- tooth loss or oral pain
- eating poorly
- economic hardship
- reduced social contact
- -> progressive undernutrition
changes in organ function
- ↓ # and function of taste buds
- ↓ salivary secretion–> xerostomia
- ↓ esophageal function
- ↓ gastric function/ emptying
- ↓ liver/ biliary function (↓ drug metabolism–> overdose )
- ↓ pancreatic secretion
- change in intestinal morphology
- change in renal morphology (glomerulonephritis)
Antivitamin drugs
- inhibit vitamin absorption
- bind to them, unavailable to body
- ↑ catabolism
- ↑ excretion
- inhibit forming active form
drugs side effect
↓or ↑ appetite, taste change
polypharmacy
strong predictor of malnutrition
movement of drugs
absorption
distribution
metabolism (liver-cytochrome p450)
excretion
grape/ fruit juice
inhibit intestinal metabolism (cytochrome p450 3A4 enzyme)
Ca channel blocker, HMG-CoA inhibitors, anti-anxiety agents–> ↑ risk of toxicity–> 72hr, no fruit
warfarin (anti-coagulate) vs. Vit K
- warfarin prevent Vit k to active form
2. Vit K–> more coagulating factor–> drug less effective
Methotrexate (cancer drug) vs. pyrimethamine (for malaria)
folic acid antagonists–> reduced form–> folanic acid–> folic acid deficiency
-folanic acid not require to form active form, not require dihydrofolate reductase to active
alcohol
gastric irritant with NSAID–> GI bleed
alcohol cannot consume with hepatotoxic drug
cholesterol lowering drug–> bile acid sequestrant
- cholestyramine–> antihyperlipidemic bile acid sequestrant–> adsorb vitADEK+ folic acid
- X reabsorption of bile salt–> ↓ fat soluble vit. absrp.
- require supple.
Drugs damage to GI tract
- drug-nutrient interaction
- food- drug interaction
- ↓ nutrition absorption from antibiotic drug (neomycin)
- destroy intestinal mucosa, villi, microvilli, inhibit brush border enzyme
chemotherapeutic agents, NSAID, antibody
- alter ability to absorb mineral, Fe+ Ca
- damage gut mucosa
drug effect intestinal transport–> gochisin, anti-inflammatory agent
anti-inflammatory drugs
- inhibit lactase
2. damage on gut–> ↓fat+ micronutrient absorption
laxatives contain emollients, mineral oil
- keep water in stool and intestine
- -> dissolve fat+ fat soluble vit. –> excrete, not absorption
- -> ↓ transit time–> ↓ absorption of nutrient, Ca+ K loss
- higher fiber–> ↓ absorption of tricyclic anti-depressant
anti-ulcer drug (cimetidine)
- ↓ HCL product–> ↑ pH–> X absorb Ca, Fe, Zn, folic acid, β-carotene
- ↓ amount of B12 from food
- ↓ B12 available for binding intrinsic factor for absorption
- ↓intrinsic factor secretion
loop diuretics for bp (furosemide)
- ↑ renal excretion of thiamine –> cardiac abnormality
- inhibit co-transporter Na-K-Cl on kidney
- ↑ excretion of K, Mg, Na, Cl, Ca
- needs supple. electrolytes
diuretics (thiazide)+ corticosteroid
- ↑ K, Mg excretion, ↓ Ca excretion–> hyperclacemia–> vasodilation –> risk of cardiac arrhythmia
- corticosteroid–> ↓ Na excretion, ↑K, Ca excretion–> supplement of Ca+ Vit D–> ↓ risk of osteoporosis
aspirin increase folate excretion
- bind folate binding site in plasma protein
2. gastric bleeding
low albumin
- make drugs more potent by increasing availability to tissue
- low albumin–> low dosage
Body composition–drug
↑ adipose tissue–> fat soluble drugs accumulate–> ↑ toxicity
alendronate (fosamax)–> anti-osteoporosis
must sit upright for 30 mins after taking–> avoid esophagitis
drug induced diarrhea
diarrhea= >=3 unformed bowel action in 24hours
- Acute: episode of diarrhea lasting < 2 weeks
- Chronic: diarrhea for at least 3-6 weeks
- frequency and severity of dehydration & electrolyte loss–> sever nutrient deficiency
- ageing affect immune/ non immune defense
drug associated diarrhea contributing factor
- polypharmacy, self-medication, noncompliance regarding to usage
- inappropriate drug prescribing
drug associated diarrhea
- antibiotics (alter colonic bacteria)
- osmotic agent–> antacid (Mg trisillicate, Mg hydroxide)
- antineoplastic–> damage immature epithelial cell
- antimetabolites
- laxative
Bone remodelling
- replacement of old bone with newly synthesized bone tissue
- osteoblasts synthesize bone matrix
- osteoclasts dissolve bone mineral with acids and digest bone matrix+ recruitment of phagocytes to remove protein
regulated and coordinated cycle of removal of old bones followed by compensation of the new bone done by osteoblasts, in response to micro-damage in many mechanical loading
women menopause
rapid bone mass loss 3-5%/yr for 6-8yrs–> new set point
- ↓ serum 17b-estradiol, serum estrone
main determinant of peak bone mass 30yr
Ca intake
max rate of accretion of bone mass
pubertal growth spurt
low Ca intake
deplete bone calcium to maintain blood Ca level
factor increase osteoporosis
- men: larger skeleton, bone loss starts later and slower, no rapid hormonal change
- aging: older, lager risk, ↓ GH from anterior pituitary gland–> ↓ hepatic IGF1/ ↑ IGF2–> ↓growth factor bing proteins
- body size: smaller thin bone female higher risk
- family history
- ↓ estrogen
- low Ca, malnutrition
- amenorrhea (loss menstrual period)
- anorexia nervosa
- glucocorticoids–> steroid hormone–> inhibit osteoblast, IGF1 synthesis–> loss bone mass
- ↓ testosterone in men
- ↓ PA
- Cigarette
- Alcohol
- caucasian, asian
Type 1 osteoporosis
trabecular bone loss (skeleton)
- ↑ osteoclast–> rapid bone loss
- female ↓ estrogen, male ↓ testosterone
- PTH mobiliza Ca from bone to blood–>↑ osteoclast osteoclast
- female: male= 6:1
- 50-70
- rapid
estrogen
- ↑ osteoclast precursor cell apoptosis, ↓ differentiation
- transforming growth factor beta induce osteoclast apoptosis, bone structure
- formation TGF-beta
- suppress production of bone-resorbing cytokine and prostaglandins
Type 2 osteoporosis
cortical bone loss
- senile osteoporosis, age-related
- slow, steady
- 40yr
- osteoblast under activity
- female: male= 2:1
- accumulation of bone marrow fat at expense of osteoblast genesis
- adiposity inhibit osteoblast
- sacropenia
- estrogen deficiency
- ↑ PTH in men–> resorption–> ↑ osteoclast
- Ca& Vit D deficiency–> 2nd hyperparathyroidism–> ↑ osteoclast
- ↓ 25 (OH)D–> ↓1-25 (OH)2D and Ca absorption–> ↑NPTH–> ↓decrease intestinal Ca absorption and intake
Calcitriol
analogue alfacalcidol
- prevent osteoporosis
- goog for female BM with postmenopausal osteoporosis
- metabolically active form
exercise for women
- aerobic exercise 20min, 3times/week
- weight training
improve muscle strength and coordination
↓ risk of fall-related fracture
