Final study guide Flashcards
What are DRIs? What references do DRIs include?
DRIs are new references for planning and assessing nutrient intakes, developed by scientific review committees. They include the EAR, RDA, AI, and UL.
What is the EAR? How is it determined? What is its purpose?
The Estimated Average Requirement (EAR) is the usual intake level that is estimated to meet the requirement of half (50%) of the healthy individuals in a life stage and gender group. The EAR is a suitable method for determining adequate intakes within groups. EARs are determined from a specific criterion of adequacy and are the foundation for setting the RDA.
What is the RDA? How is it determined? What is its purpose?
The Recommended Dietary Allowance (RDA) is determined from the addition of two standard deviations to the EAR, representing the intake level that is estimated to meet the requirement of 97.5% of the healthy individuals in a life stage and gender group. RDAs are intended to be met through average daily intake over a period of days (intakes are averaged). They are developed to prevent the occurrence of chronic diseases, maintain good health, and avoid deficiency. The RDA is a suitable method for determining adequate intake for an individual and is considered a REQUIREMENT.
What is the AI? How is it determined? What is its purpose?
The Adequate Intake (AI) is used instead of an RDA when an EAR cannot be calculated due to insufficient information and lack of evidence. Both the RDA and AI may be used as goals for individual intake. The AI is based on the observed nutrient intake by a group of healthy people that are assumed to be adequate. The AI is an INTAKE (NOT a requirement) likely to exceed the actual (but unknown) requirements of almost all healthy individuals.
What is the UL? How is it determined? What is its purpose?
The Tolerable Upper Intake Level (UL) is the highest average daily nutrient intake level likely to pose no risk of adverse health effects for almost all individuals in the general population. The UL is NOT intended to be a recommended intake, as there are no established benefits of intake above the RDA or AI. The UL refers to total intake from food, fortified food, nutritional supplements, and water intake (i.e. hard water). For certain nutrients, the UL solely refers to intake from supplements.
What is the overall structure of the standing committee for the DRIs?
The Standing Committee on the Scientific Evaluation of Dietary Reference Intakes oversees and coordinates the recommendations from the nutrient panels and the two subcommittees. The Nutrient Expert Panels develop a series of DRI reports, in conjunction with the two subcommittees. A total of 7 reports from 7 individual subcommittees are submitted, dealing with 7 areas of nutrient requirements. The Upper Reference Level Subcommittee derives the tolerable upper intake levels for all nutrients, while the DRIs Subcommittee helps the population interpret and apply the information they receive.
What are the factors taken into consideration to establish the DRIs?
DRIs focus on chronic disease prevention, but this has been taken further by incorporating:
Looking at the RDA values for micronutrients, as research has suggested their importance in the development of chronic diseases;
Recommendations are set for deficiency, disease prevention, and chronic disease prevention;
A UL is established due to the common use of food and nutritional supplements;
Non-essential food components, such as phytochemicals, are being considered for chronic disease prevention
What are conceptual similarities between DRIs and the former RDAs and RNIs?
They must account for:
Individual variability in a population (i.e. coefficient of variability of the population);
If the population’s requirement is highly variable, producing a flatter curve with a high standard deviation, the RDA would be much higher than the EAR.
Bioavailability;
Sex and age differences;
Physiological state (e.g. pregnancy and lactation).
What are conceptual differences between DRIs and the former RDAs and RNIs?
When possible, the reduction in the risk of chronic degenerative disease is included in the formulation of the RDA.
Concepts of probability and risk explicitly underpin the determination of the DRIs, and applications.
Upper levels of intake are established.
Food components that may not meet the traditional concept of a nutrient are considered.
The main criticism of the former RDAs and RNIs were that the indices of nutritional adequacies that were used were based on insufficient information, as there were no metabolic studies to estimate their recommendations. The mean intakes of the healthy population, lacking signs of deficiencies, were used as the standard for nutrient adequacies and recommendations, which may not reflect the actual requirement or a person or a group of people.
What are the four criteria of adequacy?
Biomarkers of exposure
Blood levels, balance studies, pool saturation (e.g. hemoglobin saturation)
Biomarkers of mechanisms or functional outcome
Enzyme saturation or enzyme activity (e.g. transketolase activity)
Biomarkers of effect
Analysis of the efficacy outcome, which indicates if there is an increased risk for a clinical outcome (e.g. bone mineral density, LDL levels)
Biomarkers of a clinical outcome
Symptomatic state (e.g. osteoporosis, dental caries)
What differentiates the current RDA from former RDAs and RNIs?
The RDA is determined QUANTITATIVELY through the EAR (by adding two standard deviations), rather than through a judgment-based safety factor, which differentiates it from the former RDAs and RNIs.
How does the determination of energy requirements differ from other nutrients? Why?
Energy requirements are estimated on an INDIVIDUAL basis using sex, age, height, weight, and the physical activity level to estimate total energy expenditure. RDAs are not used for energy, as setting higher intakes increases the risk of overconsumption of energy, and consequently, obesity.
What can you conclude if the intake is below the AI? What can you conclude if the AI is above the AI?
If the intake is below the AI, there is no quantitative (or qualitative) estimate that can be made of the probability of nutrient adequacy, as the point where risk increases cannot be determined; conclusions cannot be made concerning whether the intake is adequate.
If the intake is above the AI, then the diet is almost certainly adequate (low prevalence of inadequate intake). However, the proportion of deficient individuals consuming above the AI in a group cannot be determined.
How is the RDA determined from the EAR?
The EAR represents the intake to meet half the requirement of half of the population (50%). If the standard deviation of the EAR is available (normal distribution curve), the RDA is calculated as the EAR + 2 SDEAR, allowing 97.5% of the population to reach their requirement. If the SD of the EAR is not available, the coefficient of variation is assumed to be 10%, and the RDA is calculated as the EAR x 1.2. If there is insufficient evidence to support an EAR (and, thus, an RDA), then the AI is used instead.
What are dietary guidelines? How do dietary guidelines differ from RDAs?
Dietary guidelines refer to optimal proportions of energy-yielding macronutrients and are a consequence of RDAs. They do not usually describe nutrients, but food components or food groups (i.e. cereals and grains) by providing semi-quantitative advice on consumption (e.g. percentages of total energy). Dietary guidelines serve as an educational device. Dietary guidelines target the intake of every man, women, and child, as opposed to RDAs, which separates numbers for males and females of different age categories. Dietary guidelines primarily examine macronutrients, relying more on epidemiological and food consumption data than the RDA does.
What was the focus on Canada’s Food Guide’s previous revision?
Nutrient targets
Energy levels
Food groups
Serving sizes
What is the recommendation for dietary fat intake? What are the issues with planning intake recommendations for fat within a group setting?
Essential fatty acids are required nutrients (possessing an AI), while fat is not. Currently, the recommendation of dietary fat intake is within the range of the AMDR (20 to 35% of energy intake, with a midpoint of around 30%). If the group mean is at 30% of fat intake, then a substantial PROPORTION of the group is consuming a higher intake of fat than required, increasing their risks of chronic disease. However, if the population intake was below 30%, then a substantial PROPORTION of the population would be at risk for essential fatty acid deficiency. A low-fat diet also implies shifts in the types of foods consumed (little animal protein), which may decrease consumption and bioavailability of iron, zinc, and calcium, as well as decrease the absorption of fat-soluble vitamins.
Describe the major events of the reproductive timeline, and the risks of adverse outcomes associated with them.
Pre-Implantation (1 week)
Exposure to toxins may lead to no effect, slight decrease in growth, or lethality, as the fate of the cells has not yet been determined, providing them with great restorative capacity. There is a LOW susceptibility to teratogens.
Gastrulation (2-3 weeks)
Gastrulation is characterized by cell migration through the primitive streak, giving rise to the three germ layers. Gastrulation is VERY susceptible to teratogens, as the neural tube must close during gastrulation (by day 27-28), or else neural tube defects (NTDs) occur.
Organogenesis (3 to 8 weeks)
The organogenic period is a period of maximal cell division and differentiation, giving rise to the major organs (weeks 3 to 8). Organogenesis is VERY susceptible to teratogens, and there are periods of maximum susceptibility associated with each structure.
Fetal and Neonatal (8 weeks to Birth)
Tissue differentiation, growth, and physical maturation of the fetus occur. There is little differentiation of organs (apart from external genitalia), and, thus, toxic exposure impacts growth and functional maturation, rather than morphological defects.
Describe 4 reasons that explain why the developing fetus is more susceptible to alcohol than the mother.
The half-life of alcohol is increased (clearance of alcohol is decreased) in the fetus due to the decreased alcohol-metabolizing ability of the fetus, given its organ immaturity.
The nervous system is more susceptible to alcohol toxicity since it is undergoing rapid development.
Increased alcohol dose on a body-weight basis in the fetus, relative to the mother.
The fetus has depressed antioxidant capacity to detoxify free radicals induced by alcohol metabolism.
Describe the pathways of homocysteine metabolism, including the nutrients involved in the mechanisms.
Methionine is converted to SAM by methionine adenosyl transferase. The additional methyl group of SAM may be transferred to a substrate (DNA, RNA, protein), which may alter cellular function.
The transfer of a methyl group to a substrate converts SAM to SAH, which is then hydrolyzed to homocysteine.
Homocysteine is metabolized via two pathways:
Homocysteine is metabolized to regenerate methionine, utilizing methionine synthase, vitamin B12, and folate.
Homocysteine is converted to cysteine via a transsulfuration pathway, utilizing cystathionase and vitamin B6.
How may impairment in folate metabolism lead to neural tube defects?
Mothers with NTD infants have lower plasma folate and elevated homocysteine levels, indicating defects in the folate-dependent homocysteine pathway.
A deficiency in folate results in the inability of methionine synthase to convert homocysteine to methionine. The conversion of homocysteine to methionine requires a methyl group, donated by 5-methylene-tetrahydrofolate.
The inability to regenerate methionine from homocysteine leads to an accumulation of homocysteine, and a secondary accumulation in SAH.
A SAH accumulation leads to the inhibition of DNA methyltransferase reactions, DNA hypo-methylation, and altered gene expression. Limiting gene expression during fetal development may cause issues.
Oxidative stress, resulting from defects in the homocysteine pathway, may also affect development by damaging mitochondrial and nuclear DNA, protein structure and function, membrane lipids, and signal transduction pathways.
How would deficiencies or excesses in nutrients involved in homocysteine metabolism, apart from folate, cause impairments in folate metabolism?
A high intake of vitamin A suppresses 5-methylene tetrahydrofolate reductase, which is linked to the formation of NTDs, as there is a decreased capacity of re-generating methionine from homocysteine.
There is a decrease in the functional activity of methionine synthase by limiting the availability of vitamin B12 and by decreasing folate stores.
There is a decrease in the conversion of homocysteine to cysteine via the transsulfuration pathway and cystathionase, if there is a deficiency in vitamin B6.
What are the major roles of the placenta?
- Metabolism
The placenta synthesizes compounds used by the fetus, such as glycogen, lactate, and cholesterol. - Transport
The placental membrane acts as a barrier, preventing the passage of large compounds.
The placenta is highly permeable to a variety of substances, and thus offers limited protection against xenobiotics. - Endocrine
The placenta secretes hCG after implantation, allowing for the maintenance of the corpus luteum, which secretes estrogen and progesterone.
Placental lactogen is produced by the placenta in late gestation, and influences carbohydrate and fat metabolism.
At the 10th week of gestation, the placenta takes over the production of progesterone from the corpus luteum. Progesterone inhibits the secretion of LH and FSH (prevents ovulation), supports the endometrium, and suppresses contractility of uterine smooth muscle.
The placenta secretes estrogen maximally towards the end of gestation, which antagonizes myometrial-suppression by progesterone, eventually allowing parturition to take place. - Hormone catabolism
Glucocorticoids, insulin, and thyroxin access to fetal tissues are largely controlled by the placenta. - Protection against xenobiotics
- Nutrient storage
Differentiate sources of obligatory and non-obligatory weight gain occurring during pregnancy.
Fetal obligatory weight gain is characterized by the growing presence of the fetus, placenta, and amniotic fluid.
Maternal obligatory weight gain is characterized by the enlarged uterine and breast tissue, as well as the expanded blood volume.
Non-obligatory weight gain is characterized by a gain in adipose tissue, protein stores, and extracellular fluid.
What are the effects of maternal malnutrition on fetal growth retardation? What is the role of the placenta in assuring the proper growth of the fetus? Provide various examples as to how maternal malnutrition influences the placenta, and the fetus.
The fetal size is proportional to the placental size, as a superior circulation exists in a larger placenta, allowing for the optimal development of the fetus.
The placenta is responsible for carrying nutrients from the maternal circulatory system to the fetal circulatory system, assuring its growth. IUGR infants have microscopically less branching of the villi.
Maternal malnutrition (e.g. iron deficiency) may lead to a reduced blood volume expansion, which decreases cardiac output and placental blood flow, resulting in a decreased placental size, reduced nutrient transfer, and subsequently, fetal growth retardation.
Sodium, water, and protein are also vital to maintain an adequate blood volume during pregnancy.
Differentiate proportionate and disproportionate IUGR.
In proportionate IUGR, the length, weight, and head circumference of infants are proportional, occurring within the similar percentile (or, the head is small as compared to the body – microcephaly). Proportional IUGR is due to extreme fetal malnutrition, or decreased growth potential due to a congenital infection, genetic disorder, or environmental toxins.
In disproportionate IUGR, the weight is disproportionately small as compared to the length and head circumference. Disproportionate IUGR is due to uteroplacental insufficiency or maternal malnutrition.
Describe the physiological changes that occur during pregnancy, relating their impact on nutrient requirements.
kidney
An increase in GFR and decrease in tubular reabsorption capacity occurs, leading to an increased blood volume, to facilitate the increased excretion of fetal waste products.
This leads to an increase in renal losses of glucose, folate, iodine, and amino acids.
Describe the physiological changes that occur during pregnancy, relating their impact on nutrient requirements. - stomach
There is a depression of function due to a decreased secretion of pepsin and histamine, leading to an increased risk of heartburn due to the relaxation of the cardiac sphincter, causing a higher risk of regurgitation.
Describe the physiological changes that occur during pregnancy, relating their impact on nutrient requirements.- GI
There is a decrease in motility, mainly to slow down transit time, leading to an increased efficiency of absorption of certain nutrients, including vitamin B12, calcium, and iron.
However, the decrease in motility increases the risk of constipation, if it is combined with a lack of sufficient fluid intake.
Describe the physiological changes that occur during pregnancy, relating their impact on nutrient requirements.- heart
There is cardiac hypertrophy, which increases cardiac output to allow a larger blood volume to circulate, improving blood flow to the placenta and fetus.
Describe the physiological changes that occur during pregnancy, relating their impact on nutrient requirements.- lungs
There is increased ventilation to accommodate for increased oxygen demands by the fetus, placenta, and maternal tissues.
During pregnancy, BMR increases by 15 to 20% due to the increase in oxygen consumption. A week after the baby is born, the BMR returns to normal.
