PUBLIC HEALTH NUTRITION
LECTURE 1 FOLATE
RDI = 300 µg/d
Pregnancy 400 µg/d 4 weeks before and 8 weeks after conception
Functions folate
1. DNA metabolism
2. Amino acid metabolism
Folate metabolism
- Folate diet → THF (active form)
- THF → one carbon transfer for DNA, RNA and amino acid synthesis. So folate =
crucial for genetic stability
- Folate provides methyl groups for methylation reactions, impacting gene expression
- Folate helps convert homocysteine into methionine
Folate deficiency → DNA synthesis impaired → disrupted cell division
- RBC’s → larger immature blood cells
Folate and NTD
- Embryo development → rapid cell division
- Neural tube develops from day 21-27
- Inadequate folate → Lower cell division → NTD
NTD forms: Spina bifida & Anencephaly
Estimated lifetime expenditures:
1. Total lifetime cost of care → medical expenses
2. Emotional costs
Women with NTD pregnancies → higher levels of urinary formiminoglutamic acid
(FIGLU), suggesting a folate deficiency. FIGLU is elevated when folate metabolism is
impaired
Strategies to optimize folate status:
1. Diet → major changes needed & not good bioavailability
2. Supplements → not effective on population level
3. Fortification → population wide impact & consistent and controlled intake of folate
Limitations folic acid fortification
1. Possible other health effects
2. Safety concerns for groups who do not need more folic acid
- Possible B12 deficiency masking
,Folic acid & CVD
Methionine ←→ Homocysteine
- High levels of homocysteine are associated with an increased risk of CVD
- Folic acid can lead to a reduction in homocysteine levels because it helps to convert
homocysteine into methionine
- B12 further contributes to this reduction → combined B12 + folic acid = effective
reduction risk CVD (heart disease, stroke)
- Intermediate endpoints → changes in homocysteine levels
Clinical outcomes → incidence in heart attacks/strokes
- Individual trials may lack statistical power (small sample size & low homocysteine
reductions) so need to pool the results
- Limited evidence that confirms that homocysteine lowering interventions can prevent
myocardial infarction/stroke/reduce mortality
Mendelian randomization → genetic variation
Genetic variations are randomly assigned at birth → confounders equal between groups
Health issues with fortification and colorectal cancer (CRC)
- Higher folate possibly associated with reduced colorectal cancer risk
- But excessive folate may promote tumor progression
- Mixed study evidence
Concerns folic acid fortification
1. Presence PteGLU (unmetabolized folic acid) in blood → photo catalysis of this
associated with genotoxicity
2. Vit B12 deficiency masking
3. Role in CRC development
4. Association with twin births and insulin resistance of offspring
Recommendation folic acid fortification
- Monitoring high risk groups
- Conducting focused research
LECTURE 2 VITAMIN D
Vitamin D → Bone health, immune function, cell growth
- D2 via diet
- D3 produced in skin when exposed to sunlight
Both forms are converted into 25 hydroxyvitamin D (25-OH Vit.D), this is the major
circulating form and used to measure vitamin D status.
25-OH vitD can be converted into:
1. Active form → 1.25-(OH)2 Vit.D
2. Inactive form → 24.25-(OH)2 Vit.D
The kidneys convert it into the active form, and the liver can metabolize the active form into
the inactive form (metabolites) that are excreted through bile
, Active form functions
1. Increasing calcium absorption
2. Promoting bone growth & mineralization
3. Regulating the immune system
4. Inhibiting cell growth
Low calcium levels → Parathyroid gland releases PTH which stimulates kidneys to
convert VitD into the active form, which then aids in increasing calcium absorption. As
calcium levels normalize, the production of PTH is decreased, showcasing a classic example
of a negative feedback mechanism in the human body.
Vitamin D = calciferol
Vitamin D2 = ergocalciferol
Vitamin D3 = cholecalciferol
25-hydroxyvitamin D (25(OH)D) = calcidiol
1,25-dihydroxyvitamin D (1,25(OH)2D) = calcitriol
- Median intake 51-69 = 3-4 µg/d, but RDI = 10 µg/d → feasible if you add 6-7 µg/d
from sunlight exposure
- Median intake 70+ = 3-4 µg/d, but RDI = 20 µg/d → still not feasible
Therefore older persons should eat more dietary vitD and use supplements
1 μg = 40 IU
Serum: 1 ng/l = 2.5 nmol/l
Serum 25(OH)D levels < 50
nmol/l = deficient
With age the serum levels
decreas.
Risk groups vitamin D
deficiency
1. No UV exposure
2. Dark skin
3. Suntan lotion
4. Obesity
5. Old age
Obesity risk group
- Low serum D levels → higher body fat
- High BMI → low response to whole body irradiation
- Supplementation worked better on people with low BMI’s
- Weight loss helped in increasing vitamin D levels
But, no need to supplement all obese persons:
1. Vit D is stored in fat cells
2. Obese persons have no higher risk for vitD related outcomes (falls, fractures,
osteoporosis)
LECTURE 1 FOLATE
RDI = 300 µg/d
Pregnancy 400 µg/d 4 weeks before and 8 weeks after conception
Functions folate
1. DNA metabolism
2. Amino acid metabolism
Folate metabolism
- Folate diet → THF (active form)
- THF → one carbon transfer for DNA, RNA and amino acid synthesis. So folate =
crucial for genetic stability
- Folate provides methyl groups for methylation reactions, impacting gene expression
- Folate helps convert homocysteine into methionine
Folate deficiency → DNA synthesis impaired → disrupted cell division
- RBC’s → larger immature blood cells
Folate and NTD
- Embryo development → rapid cell division
- Neural tube develops from day 21-27
- Inadequate folate → Lower cell division → NTD
NTD forms: Spina bifida & Anencephaly
Estimated lifetime expenditures:
1. Total lifetime cost of care → medical expenses
2. Emotional costs
Women with NTD pregnancies → higher levels of urinary formiminoglutamic acid
(FIGLU), suggesting a folate deficiency. FIGLU is elevated when folate metabolism is
impaired
Strategies to optimize folate status:
1. Diet → major changes needed & not good bioavailability
2. Supplements → not effective on population level
3. Fortification → population wide impact & consistent and controlled intake of folate
Limitations folic acid fortification
1. Possible other health effects
2. Safety concerns for groups who do not need more folic acid
- Possible B12 deficiency masking
,Folic acid & CVD
Methionine ←→ Homocysteine
- High levels of homocysteine are associated with an increased risk of CVD
- Folic acid can lead to a reduction in homocysteine levels because it helps to convert
homocysteine into methionine
- B12 further contributes to this reduction → combined B12 + folic acid = effective
reduction risk CVD (heart disease, stroke)
- Intermediate endpoints → changes in homocysteine levels
Clinical outcomes → incidence in heart attacks/strokes
- Individual trials may lack statistical power (small sample size & low homocysteine
reductions) so need to pool the results
- Limited evidence that confirms that homocysteine lowering interventions can prevent
myocardial infarction/stroke/reduce mortality
Mendelian randomization → genetic variation
Genetic variations are randomly assigned at birth → confounders equal between groups
Health issues with fortification and colorectal cancer (CRC)
- Higher folate possibly associated with reduced colorectal cancer risk
- But excessive folate may promote tumor progression
- Mixed study evidence
Concerns folic acid fortification
1. Presence PteGLU (unmetabolized folic acid) in blood → photo catalysis of this
associated with genotoxicity
2. Vit B12 deficiency masking
3. Role in CRC development
4. Association with twin births and insulin resistance of offspring
Recommendation folic acid fortification
- Monitoring high risk groups
- Conducting focused research
LECTURE 2 VITAMIN D
Vitamin D → Bone health, immune function, cell growth
- D2 via diet
- D3 produced in skin when exposed to sunlight
Both forms are converted into 25 hydroxyvitamin D (25-OH Vit.D), this is the major
circulating form and used to measure vitamin D status.
25-OH vitD can be converted into:
1. Active form → 1.25-(OH)2 Vit.D
2. Inactive form → 24.25-(OH)2 Vit.D
The kidneys convert it into the active form, and the liver can metabolize the active form into
the inactive form (metabolites) that are excreted through bile
, Active form functions
1. Increasing calcium absorption
2. Promoting bone growth & mineralization
3. Regulating the immune system
4. Inhibiting cell growth
Low calcium levels → Parathyroid gland releases PTH which stimulates kidneys to
convert VitD into the active form, which then aids in increasing calcium absorption. As
calcium levels normalize, the production of PTH is decreased, showcasing a classic example
of a negative feedback mechanism in the human body.
Vitamin D = calciferol
Vitamin D2 = ergocalciferol
Vitamin D3 = cholecalciferol
25-hydroxyvitamin D (25(OH)D) = calcidiol
1,25-dihydroxyvitamin D (1,25(OH)2D) = calcitriol
- Median intake 51-69 = 3-4 µg/d, but RDI = 10 µg/d → feasible if you add 6-7 µg/d
from sunlight exposure
- Median intake 70+ = 3-4 µg/d, but RDI = 20 µg/d → still not feasible
Therefore older persons should eat more dietary vitD and use supplements
1 μg = 40 IU
Serum: 1 ng/l = 2.5 nmol/l
Serum 25(OH)D levels < 50
nmol/l = deficient
With age the serum levels
decreas.
Risk groups vitamin D
deficiency
1. No UV exposure
2. Dark skin
3. Suntan lotion
4. Obesity
5. Old age
Obesity risk group
- Low serum D levels → higher body fat
- High BMI → low response to whole body irradiation
- Supplementation worked better on people with low BMI’s
- Weight loss helped in increasing vitamin D levels
But, no need to supplement all obese persons:
1. Vit D is stored in fat cells
2. Obese persons have no higher risk for vitD related outcomes (falls, fractures,
osteoporosis)
