G&D Final Part 2

  1. What contributes to lower than desired vit D in children and adolescents? 4
    1. Ability of skin to synthesize vitamin D (intensity of UVB exposure, skin type, surface area exposed)

    2. Inadequate nutritional practices

    3. Children with little/no outdoor activities, always wear sunscreen, avoid sunlight exposure, spend most of their time playing inside

    4. Obese children (bc excess body fat is associated with low 25(OH)D concentrations
  2. 1. What is metabolic syndrome? 5

    2. How can obesity-related inflammation be measured? (6)

    3. Define insulin resistance. What is it caused by? (4) What does it cause?
    1. Cluster of CV factors, including central obesity (waist circumference), hypertension, increased fasting blood glucose, high TGs, low HDL. Potential screening tool for risk in adolescents but not widely used clinically bc requires cutoff values in 3 out of 5 components and not good for other races. 

    2. C-reactive protein which activates phagocytotic cells. High-sensitivty CRP is more accurate. Low adiponectin levels indicate high insulin resistance and other inflammatory markers (TNFa, ILs, RBP4)

    3. The inability of physiological insulin levels to produce movement of glucose into cell

    Caused by genetics, high visceral obesity, low adiponectin, and high FFAs. Causes oxidative stress to tissues
  3. 1. Is hsCRp a good test to assess CVD risk in adolescents? (6)

    2. Pros? (5)

    3. Cons? (5)
    1. HsCRP levels are associated with increased waist circumference, adiposity, insulin resistance, body mass, atherosclerotic plaque formation, and metabolic syndrome, but not enough conclusive evidence has been shown in adolescents. 

    2. (1) Ease of use, (2) no racial bias, (3) appear stable in individuals over course of several years, (4) stable as measurements of BP and cholesterol, (5) can discriminate between healthy obese and those at risk for CVD.

    3. (1) Lack of prospective data linking hsCRP levels in adolescents to any clinical outcome, (2) unlikely to see data anytime son, (3) no cut-off levels of hsCRP identified for higher risk, (4) no long-term data regarding how clinical interventions targeting lifestyle change modifies these levels, (5) stability is more thoroughly studied in adults.
  4. 1. What are other tools that author mentions that may be able to identify obese adolescents at higher risk of CVD and T2D?
    • 1. Fasting insulin
    • 2. Adiponectin
    • 3. RBP-4
    • 4. Diagnosis of MetS
  5. 1. What is the female athlete triad? What 3 factors characterize the triad?

    2. How does bone impairment occur? (3)

    3. What is energy availability?

    4. What is amenorrhea? (primary vs. secondary)
    1. Unhealthy condition of athletes who exercise for a long time without properly compensating in diet. 

    Low energy availability (reduces amount of energy for cellular maintenance, thermoregulation, growth, reproduction)--> amenorrhea --> low bone mineral density. 

    • 2. . Impairs
    • bone health and development indirectly by (1) inducing amenorrhea and (2) removing
    • estrogen’s restraint on bone resorption, and (3) directly by suppressing the
    • hormones that promote bone formation. 

    3 Energy availability - dietary energy intake - exercise energy expenditure ---> amount of dietary energy remaining for other body functions after exercise. 

    4. Lack of period for 3 months. Primary - delay in onset of menarche. Secondary - amenorrhea beginning after menarche.
  6. 1. What does a woman's BMD reflect cumulative history of? (4)

    2. What are some health consequences of E availbility, amenorrhea, and low BMD?
    - Psychological (3)
    - Complications (7)

    3. Which athlete are at greatest risk for low-energy availability? (4)

    4. When should screening for the triad be done?

    5. Prevention and treatment recommendations
    1. Optimal/peak BMD in childhood adolescence, as well as energy availability, menstrual status, and exposure to other envr/genetic factors. 

    2. Psychological - low self-esteem, depression, anxiety, eating disorders

    CV, endocrine, reproductive (infertility), GI, skeletal (stress fractures), renal, CNS complications

    3. Those who restrict dietary intake, exercise for prolonged periods, vegetarian, thin-build sports

    4. Pre-participation physical exam/annual check ups and when other symptoms occur

    5. Multidisciplinary treatment - physician, RD, psychologist, athletic trainers. 

    Emphasize optimizing energy availability. 

    Treatment: increasing energy intake or reducing energy expenditure, resistance training, calcium, vitaminD

    Estrogen therapy, bisphosphonates, leptin,
  7. 1. What are the ages
    puberty normally starts in boys and girls? How does the growth spurt differ
    between the sexes?

    2. What are the proposed reasons for current earlier onset of puberty compared to the past?
    1. Girls 8-13, menarche by 16; boys 9-14. Growth spurt occurs at 14 years at tanner 4 and girls - 12 years 3-3.5 tanner

    2. More established reason in girls - obesity & endocrine disrupters

    Boys (less established) obese and endocrine receptors - estrogen --> later puberty.

    Also UNHEALTHY CONDITIONS - exposure to chemicals, changes in diet, less physical activity.
  8. 1. How does puberty begin?

    2. Do newborns have mini-puberty?

    3. How does pubertal onset differ by ethnicity and gender?

    4. How has onset of menarche changed?

    5. How does fat mass and lean mass accrual differ bt races?
    1. Kisspeptin receptor releases GPR54 to hypothalamus --> GnRH released to pituitary --> Pituitary releases FSH and LH --> Puberty

    2. yes

    3. Girls: First AAs --> Hispanic Americans --> Whites

    Boys: Same pattern

    4. Now, it's a lot earlier. Used to be 16-17 years old. 

    5. Vastly different bt races for both males and females, but lean mass accrual is similar.
  9. 1. What are the differences in body composition
    between boys and girls after puberty.

    2. know the difference between a gynoid and
    android fat distribution 

    3. Describe the process of bone remodeling. Why is it important for adolescents to have enough calcium? What are the 2011
    recommendations for calcium intake for age 9-18?
    1. Puberty boys have 1.5x lean mass, 1.5x skeletal mass and 0.5x fat mass (males - 13% body fat, girls - 25%)

    2. Gynoid - mostly hips and thighs. Android - mostly visceral. 

    3. Bone remodeling = bone resorption (osteoclast) followed by bone formation (osteoblast). Enough calcium bc most of peak bone mass accrual occurs in adolescence and predicts long-term protective advantage into adulthood.

    1300 mg/day.
  10. 1. Difference between modeling and remodeling? 

    2. When do fracture rates peak in adolescence?

    3. What is calcium used for? (7)
    1. Modeling - increased bone mass and modifies bone shape - predominates during growth with new bone formation

    While remodeling is tightly coupled processes of breakdown and formation - vital for microdamage repair and maintenance of skeletal integrity. 

    2. 11-15 bc of 8 monthl ag between peak growth velocity and peak bone mineral accrual. 

    3. Bone formation, activation of blood clotting, muscle contraction, IC signaling, nervous system (membrane potential), endocrine system (exocytosis hormone secretion), cardiovascular system (membrane potential and contraction of muscle cells
  11. What is the current recommended daily intake of phosphorus, magnesium, and vitamin D for adolescents?
    • Phosphorus- 1250 mg/day (9-18
    • years)


    • 9-13 years female- 240 mg;
    • 14-18 years female- 310 (note: pregnant- 400 mg; lactating- 360 mg)

     8-13 years males- 240 mg; 14-18 years males- 410 mg

    Vitamin D- 600 IU (1-50 years)
  12. 1. Functions of magnesium? (8)

    2. What happens when you have a deficit of phosphate? (3)

    3. What are the most effective strategies in preventing nutrition related conditions as we age?

    4. What conditions contribute most to disability as we age? (7)

    5. What dietary changes help prevent coronary artery disease?
    1. Maintains normal muscle & nerve, bone, immune health, regulates blood sugar level, energy metabolism, protein synthesis, and prevents arrythmias. 

    2. Decreased mineralization and rickets, nerve conduction slowing, hemolytic anemia due to decrease in RBCs ATP production. 

    3. Change diet and exercise patterns (most effective early in life)

    4. Heart disease, cancer, stroke, fracture, pneumonia, osteoarthritis, and cataracts.

    5. Total cholesterol: HDL --> <3.5
  13. 1. What are the 3 major actions of vitamin D? 

    2. What are the organs required?

    3. What is 1 MED (minimal erythema dose) equal to?
    1. Major transcriptional regulator of bone matrix proteins; stimulates osteoclast bone resorption; stimulates intestinal absorption of calcium and phosphate

    2. Skin, liver, kidney, parathyroid gland

    3. 10,000-20,000 IU vitamin D (daily intake rec 600 IU)
  14. 1. Is obesity more of a risk factor for NCDs in middle or older age?

    2.Is there substantive evidence on how to promote health in the elderly?

    3. What does AHA recommend?
    1. Middle age.

    2. No - most policy that addresses malnutrition and frailty. No recommendations for dietary interventions for older adults as a secondary measure!!

    3. Healthy body weight, recommended lipid/BP/glucose levels, exercise, avoid tobacco, consume diets rich in fruits and vegetables, whole grains, fat-free/low-fat dairy products, lean meats, oily fish 2x/week.
  15. 1. What are some current dietary patterns?

    2. What % do daily snacks account for?

    3. What is main driver of food choice?

    4. What are some limitations to dietary counseling?
    1. Not enough fiber, fruit, veggies; french fries were most common vegetable consumed; increased eating events, SSB, portion sizes, snacking, etc)

    2. 21-25% (up from 18% from before)

    3. Taste preference

    4.1) may not include an assessment of patient’s interest in making dietary change 2) primary care providers have a notoriously low estimate of self-efficacy with regard to nutrition counseling (doctors are insecure ☹) 3) providers are unwilling to confront patients with regard to weight issues 4) times constraint and restriction on reimbursement impose limitations on traditional medical office visits
  16. 1. Impact of high carb diet on lipid profiles?

    2. How much should total fat intake be?

    3. How does substituting carbs for fat affect HDL? What is a better predictor of CHD than total fat intake? (2)

    4. How does replacing carbs affect bp and blood lipid levels?

    5. Does fruit and vegetable consumption reduce cancer risk? CV risk?
    1. Adverse metabolic effects 

    2. 30% of energy or less. 

    3. Decreases HDL. HDL: total fat ratio OR HDL:SAT ratio.

    4. Improves. 

    5. No, Yes.
  17. 1. What effect does alcohol have on health? (4)

    2. What is sarcopenia?

    3. In general, what happens to people as they get older regarding weight, caloric intake, and metabolism

    4.What are the socioeconomic and psychosocial characteristics of young adulthood (20s-30s) and how does this affect nutrition

    5. What are key micronutrients in young adulthood?
    1. 1-2 drinks/day reduces risk of MI, reduces cognitive decline and lowers risk of diabetes, BUT HIGHER RISK OF BREAST CANCER

    2. Sarcopenia = decline in skeletal muscle mass and muscle strength. Increased body fat is associated with decreased skeletal tissue. 

    3. Basal metabolism slows down and calorie intake should be reduced. Sedentary lifestyle creates greater need for exercise. 

    4. Households esetablished, individuals become parents, changing work environment makes everything more difficult. Psychosocial -> positive development will build on personal relationships to self-fulfillment. 

    20-30s are more time-restricted so less time to be healthy .

    5. Calcium, iron, etc.
  18. 1.What are some of the physiological and psychosocial changes in older adults (60s and 70s) and how might they interact with nutrition?

    2. What are the 4 major non-communicable diseases? 

    3. What are the 4 cancers that are the most common cause of death?

    4. Risk factors for major non-comm diseases? (6)
    1. Retirement, recreation, struggle, struggle with family of death, disorientation/senility, nocturnia, shopping difficulties, inability for body to synthesize/process certain nutrients. 

    2. CV, cancer, diabetes, osteoporosis

    3. Lung, breast, colorectal, prostate

    4. Smoking, alcohol, high cholesterol, low physical activity, lack of access to care, poverty
  19. 1. Describe interaction of stunting and weight gain as a child and obesity as an adult?

    2. How does gaining height affect adult obesity?

    3. What is moderate alcohol consumption?

    4. Four lifestyle changes recommended for all adults? Also know details of diet

    5. AHA's recommended exercise?
    1. Wealthier people have declines in stunting and wealth is not necessarily correlated with obesity.

    2. gaining height doen't affect adult obesity

    3. 1 drink/woman; 2 drinks/guy

    4. Avoid tobacco use, pursue physical activity, avoid being overweight, consume a healthy diet

    Healthy types of fat, reducing trans/sat fat. Plenty of fruits and vegetables, replace refined grains with whole grains, liimt sugar intake, limit excessive caloric intake, limit sodium intake. 

    5. 150 min of moderate intense exercise/week or 75 minutes of vigorous exercise
  20. 1. What is the mechanism of aging?

    2. What influences rate and severity of aging?
    1. Decline in # of cells along with changes within the cells that damage cellular organelles and changes in the basic genetic material that affect cel replication

    2. Lifestyle choices, disease history, exposure to envr hazards/pollution --> act on genes --> affecting aging
Card Set
G&D Final Part 2
adolescent + adult