Nutrition and Aging Flashcards
Rate of aging -> age related diseases -> death
3 factors contribute -> genetics (senescence genes, genes coding for components of biomolecules defense systems), lifestyle factors (diet, housing, exercise), environment (exposure to chemicals, disease causing organisms)
Xenobiotic detoxification systems
activity of these enzymes declines with age
Disability threshold
Functional capacity of individual’s tissues and organs (lungs and kidney) may develop and decline at different rates -> below this point there is a functional disability -> different people reach this at different stages
Total dysfunction of the lung
normally occurs at 130-140 years old, this number is lowered by ROS, smoking, COPD (lungs reach maturity at 18-25 years)
Frailty
ability to withstand challenges -> in between senility and death
Programmed aging
aging theory that says that limited number of cell divisions and neuroendocrine and brain function decrease
Inefficient DNA repair
aging theory that says over a lifetime -> proportion of cells carrying abnormal DNA increases
Free radical damage
aging theory that says there is a decreased efficiency of free radical scavenging systems as we age
Summation of cumulative damage to life systems sustained throughout lifetime
aging theory that says accumulation of damaged cell lipids and proteins and raised levels of oxidant and inflammatory stress (increase in CRP)
Programmed cellular aging
majority of our cells initially contain telomeres of a certain length -> with each cell division this length is diminished by a fixed amount
Cardiovascular changes with aging
atherosclerosis, hypertension
Central nervous system changes with aging
reduced cognitive function
Musculoskeletal changes with aging
skeletal muscle atrophy, osteoporosis
Respiratory changes with aging
reduced lung volume, obstructive pulmonary disease
Endocrine changes with aging
non-insulin dependent diabetes, hypercortisolemia
Immune changes with aging
generally decline in function -> especially T cells
Factors leading to increased morbidity and mortality in the elderly
sarcopenia, malnutrition and frailty (all inter-related)
Frailty
clinical syndrome characterized by at least 3 of the following criteria -> weight loss, self reported exhaustion, weakness (fall in hand grip strength), slow walking speed, low physical activity
Sarcopenia
excessive loss of skeletal muscle -> impairment in activities of daily living, loss of strength, increased incidence of falls, increased incidence of hip factors, calf circumference < 31cm
Conditions leading to sarcopenia
age related (sex hormones, apoptosis, mitochondrial dysfunction), cachexia, starvation and malabsorption, endocrine (corticosteroids, GH, IGF-1, thyroid, insulin resistance), Disuse (immobility, physical inactivity, zero gravity), neurodegenerative diseases (motor neuron loss)
Aging
associated with loss of lean body mass -> particularly skeletal muscle
Malnutrition
weight loss >5% in 3 months or 10% in 6 months, BMI < 20, serum albumin <3.5 g/dL
Increase in signs of inflammatory and oxidative stress
increased cytokine production, loss of muscle and bone, increased blood lipids, increased amount of disease with an inflammatory components in its cause -> shown by an increase in plasma triglycerides and CRP as people age
IL-6
level of protein synthesis (myosin heavy chain in this study) is decreased as this marker of inflammation increases
Aging process
increases production of proinflammatory cytokines -> inhibits function of T cells and B cells -> antioxidants can prevent this (NFkB)
Chronic activation of inflammatory signaling pathways
causes immuno-senescence (dysfunction of T and B cells, monocytes, NK cells, neutrophils, thymic shrinkage, altered Th1/Th2 profile, genetics), metabolic dysregulation and poor aging outcomes (infections, cancer, CVD, metabolic syndrome, frailty) -> need to prevent this in order to improve aging (no smoking, no obesity)
CRP and IL-6
when you have both increased in your blood it significantly increases your risk of dying than just one by itself
Proteins and other cell components
become damaged by cross-linking carboxylation, glycation, etc and are removed by tissue degradation -> protein degradation slows with aging and damaged proteins and other molecules accumulate in all tissues exerting a pro-inflammatory influence
Glycation (furosine) and glycoxidation (pentosidine)
biochemical relationship between these markers -> Ne-carboxymethyl-lysine (CML) can also potentially originate from lipid peroxidation and pentosidine from ascorbate
Foods rich in AGEs/ALE’s (advanced glycation end products)
dairy products, grains, meat, (increases from boiling to oven frying), egg yolk powder, lecithin powder, Chinese soy products, coffee, tea, alcohol and beer
Increased accumulation of the glycoxidation product
CML was reported to be significantly increased in old adults and even more significantly in diabetic patients
Increased AGE
intake in diabetic patients triggers changes in markers of inflammation -> linked to diabetes and vascular dysfunction -> high serum levels predict increased CHD in non-diabetic men but not non-diabetic women
Vitamin B6, E and selenium
improvement in immune function if deficient
Vitamins B6, 12 and folate
protection against lung cancer in non-smokers
Carotenoids, vitamins C and E
adequate lifetime amounts may produce decline in cognitive function
Omega 3 PUFA
prevention or reversal of atherosclerosis, improvement in immune function
IL10 (1082 polymorphism)
anti-inflammatory -> if you have the genotype to be a high producer you have a good chance of being over 100 (GG)
IL-1 pro-inflammatory SNP
Men live longer without this
TNF alpha pro inflammatory SNPs
Women live longer with this (counter intuitive)
Who have higher inflammation (CRP) and more fatty and less stable plaques
Men
Increased EPA (fish oil)
has more of an effect on older subjects and inhibits inflammation more successfully (more inflammation going on in older people)
fish oil is more affective in this group (not related to age)
TNF-a-308 AA allele causes increased inflammation
can increase the lifespan (seen in Rhesus monkeys), prolong disease onset (more animals free of symptoms)
Low calorie diet (calorie restriction)
survive longer (BMR is set at a lower rate)
Lower body temperature
people with low fasting insulin, people with higher levels of DHEA
Live longer
study looking at reduced calorie diet decreases systolic blood pressure
Biosphere 2
study looking at calorie restricted/calorie restricted + exercise -> led to significant weight decrease and decrease in body core temperature
CALERIE
prevent inflammatory stress from becoming worse -> reduce the likelihood of immunosuppression
Healthy aging
