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Nutrition through life > 4.1 Embryology and Teratology > Flashcards

4.1 Embryology and Teratology Flashcards

1
Q
  • what is teratogenesis?
  • define malformations. –> could be (3)
A
  • teratogenesis = production of birth defects
  • malformations = non-reversible morphological defects present at birth –> could be exterior or internally located (ie heart defect) or only microscopically visible
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2
Q

what is the leading cause of infant mortality in Canada in 2020?

A

congenital malformations, deformations and chromosomal abnormalities (389)
- followed by disorders related to short gestation and low birth weight, not elsewhere classified (174)
- followed by newborn affected by maternal complications of pregnancy

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3
Q

7 causes of developmental defects in humans

A
  1. known genetic causes (20%)
  2. chromosomal aberrations (3-5%) –> can be seen at birth)
  3. metabolic (1-2%) –> diabetes, obesity
  4. radiation (<1%)
  5. infection (2-3%) –> ie in 1st trimester, bacteria can cross cause no barrier in placenta
  6. drug/chemical (4-5%) –> social drug or medication that mother is using
  7. unknown causes (65-70%)
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4
Q

which protein/antioxidant can bind to metals quite avidly = metal detoxification BUT can also bind to key microminerals like zinc and block its flow into placenta/fetus?

A

metallothionein

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5
Q

6 (negative) human pregnancy outcomes
*what can prevent?

A
  • postimplantation loss (loss of fertilized egg): 31%
  • major birth defects: 4%
  • minor birth defects: 14%
  • low birth weight: 7%
  • infant mortality: 1.4%
  • abnormal neurological function: 16%
  • nutrition pre and during pregnancy!
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6
Q

*schéma!
FIRST TRIMESTER:
- physiological processes?
- 2 teratogenic exposure outcomes: explain + examples
SECOND/THIRD TRIMESTER:
- physiological processes?
- 3 teratogenic exposure outcomes: explain + examples

A

FIRST TRIMESTER:
- at first: fertilization, cleavage, blastulation, implantation –> gastrulation –> primary morphogenesis (structure of organs are build)
- miscarriage + major structural defects like neural tube defects, gastroschisis, single outflow tract, phocomelia
SECOND/THIRD TRIMESTER:
- organogenesis! + birth
- abnormal organ differentiation, growth and function (these 3 can also sometimes happen in first trimester)

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7
Q

organogenic period = critical period:
- 4 things take place
- what can affect this period?

A

cell organization, cell division, cell differentiation and organogenesis (formation of organs)
- poor diet!

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8
Q

what are the 3 steps of growth during pregnancy ish? + RISK?
1. day 17 to week 8
2. (mix of 1 and 3)
3. after 8 weeks gestation

A
  1. hyperplasia! = increase in cell number
    - time of maximum vulnerability for teratogenic effects
    - day 17 to week 8 after fertilization
  2. hypertrophy AND hyperplasia –> increase in cell size + cellular division
  3. hypertrophy
    - hyperplasia ceases
    - risk for development of organ or biochemical malfunctions
    - around 8 weeks gestion
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9
Q

how many cells?
- fertilization (hour 0 ish)
- 36 hours
- 48 hours
- 3 days
- 4 days: number of cells –> NAME? 2 parts

A
  • 0h: 1 cell
  • 36h: 2 cells
  • 48h: 4 cells
  • 3 days: 16-32 cells
  • 4 days: a hollow ball of 64-128 cells = blastocyst = outer region (trophoblast) + inner cell mass
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10
Q
  • how many days after fertilization is blastocyst implanted in endometrium?
  • when is blastocyst most susceptible to toxins?
  • how can blastocyst get nutrition before placenta is formed?
A
  • 8-14 days
  • once blastocyst is implanted and placenta is established! –> when fetus has access to maternal blood supply = increased susceptibility to toxins
  • trophoblast cells release proteolytic enzymes to destroy and digest maternal cells to get histriotrophic nutrition
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11
Q

Pre-implantation
- 2 names for the cell thingy
- time frame?
- increase in cell _______ but no increase in cell _______
- exposure to toxicants?
- fate of cells determined?

A
  • zygote, blastocyst
  • < 1 week
  • increase in cell number (hyperplasia) but no increase in cell size (no hypertrophy)
  • no effect to exposure to toxicants, slight decrease in growth or lethality –> low susceptibility to teratogens and few developmental abnormalities
  • fate of cells not determined –> great restorative capacity
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12
Q

what is the neural groove?
- when does it appear?

A
  • where central nervous system starts to develop
  • axis of the embryo
  • 16 days post-ovulation ish
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13
Q

Gastrulation
- time frame?
- cell migration through what?
- formation of how many germ layers? describe
- susceptibility to teratogens?

A
  • 2-3 weeks
  • cell migration through primitive streak (a midline structure)
  • formation of 3 germ layers:
    1. ectoderm (brain, CNS, skin)
    2. mesoderm (voluntary muscles, CV and excretory systems)
    3. endoderm (digestive and respiratory systems, glandular organs)
  • VERY susceptible to teratogens bc this is when organs are starting to grow
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14
Q

when does the neural tube have to be closed?

A

by day 27! if there’s impediment in growth, might not get to optimal size –> problematic!
- any part that remains open gets exposed to amniotic fluid –> causes neural tube damage

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15
Q

what does the embryo look like at days 27-29 post-ovulation?

A

general structure of embryo is fully formed (head, arms legs, body ish)

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16
Q

organogenesis
- time frame?
- ____ and ______ structures established
- 4 physiological things about cells
- susceptibility to teratogenesis?

A
  • 3-8 weeks
  • organs and body structures established
  • cell proliferation, cell migration, cell-cell interactions and tissue remodeling
  • EXTREMELY susceptible to teratogenesis –> periods of maximum susceptibility for each forming structure
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17
Q

8th week of gestation –> are most organs developed already?
- no longer a _______, now a ________

A

yes! –> now time for maturation
- no longer an embryo, now a fetus

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18
Q

fetal/neonatal
- time frame?
- what happens (3)
- what happens if toxic exposure (2)
- which part of body is particular susceptible to defects in 3rd trimester –> (3 examples)

A
  • 8 weeks to birth
  • tissue differentiation, growth and physical maturation
  • drug OR toxicity from deficiency/excess –> effects on growth and functional maturation
  • BRAIN! CNS and reproductive abnormalities, behavioral and motor deficits
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19
Q

BIG FIGURE:
- when is the zygote not susceptible to teratogens? 3 things happen then
- when is embryo susceptible to major morphological/ structural abnormalities? in which parts of body?
- when is embryo susceptible to functional defects and minor morphological abnormalities? in which parts of body?
*exception ish?

A
  • 1-2 weeks! Dividing zygote, implantation and gastruation
  • 3 weeks to 8 weeks –> CNS, heart, upper limbs, lower limbs, ear, eyes, teeth, palate, external genitalia
  • 8 weeks to birth –> same body parts ish but mostly CNS, eyes, teeth, palate, external genitalia, ear
    *heart, upper and lower limb functional effects can be seen from weeks 7-8
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20
Q

what are 3 classes of teratogens + examples?

A
  1. MEDICATIONS
    - seizure medications, accutane, thalidomide, lithium, chemotherapy drugs
  2. SOCIAL DRUGS
    - alcohol, cocaine, cigarettes –> epigenetic effect!
  3. ENVIRONMENTAL AGENTS
    - organic solvents, heavy metals, pesticides, PCBs –> from higher exposure ie from workplace, water spill…
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21
Q

4 things that can cause teratogenic effects? (excluding the 3 big classes of teratogens)

A
  1. high temp (sauna) or fever
  2. infectious diseases: rubella, cytomegalovirus, toxoplasmosis
  3. chronic diseases: diabetes, severe overweight –> hormonal milieu: high glucose, high ketone levels…
  4. nutrient deficiencies and excesses
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22
Q

what are 5 medications that could cause which defects?

A
  1. dilantin (anticonvulsant) –> fetal hydrantoin syndrome (10% risk)
  2. thalidomide (morning sickness) –> limb and ear abnormalities (20%) (high genetic susceptibility)
  3. antineoplastic drugs (cancer drugs) –> congenital abnormalities
  4. diethylstillbestrol (prevent pregnancy complications) –> uterine and cervical defects (22-53%)
  5. dextromethorphan (cougn suppressant) –> CNS abnormalities
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23
Q

excess of which 4 nutrients can cause which disabilities for the fetus?

A
  1. iodides –> congenital goitre (similar effect of iodine deficiency) + mental/physical disabilities
  2. fluoride –> spina bifida occulta (invisible)
  3. vitamin D –> facial abnormalities + mental disabilities
  4. vitamin A –> CNS abnormalities (like neural tube defect)
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24
Q

% of birth defects based on daily retinol intake (supplement):
- 0-5000 IU
- 5001-8000 IU
- 8001-10 000 IU
- > 10 0001 IU
*during which trimester specifically?

A
  • 0-5000 IU: 1.3%
  • 5001-8000 IU: 1.6%
  • 8001-10 000 IU: 1.7%
  • > 10 0001 IU: 3.2! –> almost 3x increase in risk!
  • during 1st trimester bc that’s when there’s neurodevelopment
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25
Q

which 4 vitamin deficiencies can have which effect on the fetus?

A
  1. vitamin A: eye abnormalities + microcephaly
  2. vitamin D: fetal rickets
  3. vitamin E (linked to excessive smoking –> can deplete vit E content) –> congenital abnormalities
  4. vitamin K: coumadin syndrome (coumadin interferes with vit K function –> causes birth defects)
26
Q

which 5 nutrient (excluding the 4 vitamins) deficiencies can cause which deficiencies in the fetus?

A
  1. protein (PEM) –> microcephaly
  2. folate –> neural tube defects (50-75% of neural tube defects linked with low folate status, also other factors are also linked)
  3. iodine –> cretinism (physical growth retardation, growth stunting
  4. copper (usually from inborne error of metabolism. =poor utilization of copper) –> connective tissue defects + brain and bone abnormalities
  5. zinc (even small periods of deficiency in mother) –> neural tube defects
27
Q

name the 3 drug-induced nutrient deficiencies that can cause tertogenesis

A
  1. folate antagonists (methotrexate –> treats inflammation and cancer) –> folate is not utilized by fetus = 30% risk of NTD
  2. vit K antagonists (coumadin) –> coumadin syndrome (7% risk of congenital heart disease
  3. anticonvulsant-induced folate and zinc deficiencies –> causes abnormal absorption and metabolism of folate and zinc
28
Q

what are 3 characteristics of fetal alcohol syndrome?

A
  1. craniofacial dimorphism:
    small head size, narrow receding forehead, receding chin, drooping eyelids, uneven ear placement and size, absence of groove in upper lip…
  2. growth retardation: head circumference, weight, height < 10th percentile
  3. retarded psychomotor and intellectual development
29
Q

fetal alcohol syndrome
- ____-______ relationship: explain
- increased risk with what?

A
  • dose-response relationship
  • 1 oz absolute alcohol consumed in late pregnancy = 160g decrease in birth weight
  • high risk: 3 oz alcohol/day OR 4 drinks/day
  • increased risk with binge drinking
30
Q

what are 3 adverse developmental effects of alcohol? (aside from fetal alcohol syndrom)

A
  1. partial fetal alcohol effects –> some but not all the physiological symptoms of FAS
  2. alcohol related birth defects (ARBD) –> microcephaly + heart, bone, kidney and lung malformations + minor physical abnormalities
  3. alcohol-related neurodevelopmental disorder (ARND) –> no facial deformities but have symptoms of CNS damage –> decreased attention span, decreased IQ, hyperactivity
31
Q

physiology of fetal alcohol syndrome:
- 95% of alcohol is metabolized by which enzyme
- does alcohol cross placenta freely?
- does mother and fetus have same level of alcohol?
- half life of alcohol in mother vs embryo/fetus
- detoxification and clearance of alcohol in mother vs embryo/fetus

A
  • alcohol dehydrogenase! (females have less active alcohol dehydrogenase)
  • NO placenta barrier –> alcohol crosses freely
  • mother may not experience alcohol-related symptoms while embryo/fetus may be affected adversely –> fetus gets more alcohol relative to weight/size
  • 1/2 life of alcohol is increased in embryo/fetus
  • detoxification and clearance is less developed in embryo/fetus
32
Q

mechanisms of developmental toxicity of alcohol
- calories?
- effect on which nutrient metbolism (2)
- toxicity from (2)
- excessive what in sensitive cell populations
- key organ damaged?
- alcohol metabolism also uses _______ –> consequence?

A
  • alcohol has caloric value –> replaces calories from other nutritious foods –> can lead to nutrient deficiency
  • alcohol increases excretion of zinc and folic acid –> effect on their metabolism
  • accumulation of alcohol (free radical) and acetaldehyde (byproduct of alcohol metabolism) = FR toxicity
  • excessive cell death (apoptosis) in sensitive cell populations
  • placental toxicity –> damaged form alcohol exposure –> placental won’t be able to deliver nutrients and oxygen to fetus
  • alcohol metabolism uses oxygen –> can lead to fetal hypoxia
33
Q
  • define neural tube defects
  • (2) develop from the neural tube and NTD cause various ____ disorders
A
  • congenital abnormalities of the fetal spine and CNS –> include defects of the neural tube
  • brain and spinal cord develop from the neural tube –> NTD cause various CNS disorders
34
Q

what are the 2 common NTDs? describe and explain

A
  1. ANENCEPHALY:
    - when head end of neural tube fails to close, resulting in absence of major portion of the brain, skull, scalp
    - babies with anencephaly are either stillborn or die shorly after birth
  2. SPINA BIFIDA (“split spine”):
    - incomplete closure of the embryonic neural tube results in an incompletely formed spinal cord during the first month of pregnancy (forms a bump ish on back)
    - there is usually nerve damage that causes at least some paralysis of the legs
    - depends on severity –> could be fixed by surgery (although neurological damage might stay( or results in paralysis
35
Q

what are 12 etiologies/risk factors of NTDs?

A
  1. multifactorial inheritance (12% of NTD have a genetic element)
  2. single gene disorder (autosomal recessive)
  3. chromosomal aneuploidy (trisomy 13)
  4. teratogens (valproic acid (leads to seizures), thalidomide)
  5. maternal insulin dependant diabetes metillus (IDDM)
  6. severe overweight (> 110kg)
  7. family history or prior NTD-affected pregnancy
  8. hot tub use or fever in early pregnancy
  9. folate deficiency or inborn error of folate metabolism = strongest link in population studies
  10. agricultural pesticides, chemicals, cleaning solvents, disinfectants
  11. lead, tobacco smoke, anesthetic agents
  12. radiation
36
Q

folates ingested with diet mainly exist as ________, which must be hydrolyzed to __________ to be transported across intestinal mucosa
- diet folate –> how much % absorption ish

A
  • polyglutamates –> monoglutamates
  • around 50% from food forms
37
Q

unlike natural dietary folate, folic acid must be metabolized to coenzymatic ____________ derivatives to be biologically active
- by which enzyme?
- bioavailable?

A
  • tetrahydrofolate
  • dihydroreductase enzyme
  • highly bioavailable! no limitation of being linked to polyglutamates
38
Q

MRC study: # of NTD and % of NTD
- folic acid w/o multi-vitamin
- folic acid and multi-vitamin
- no folic acid and no multi-vitamin
- only multivitamin
- conclusion?

A
  • ONLY folic acid = 2 NTD (0.6%)
  • both = 4 NTD
  • NOTHING/control = 13 (3.6%)
  • ONLY multivitamin = 8
  • CONCLUSION: multivitamins have no effect –> so prefound results that they had to stop the trial bc unethical to give nothing to placebo group
39
Q

when did health canada start folate fortification and why?
- reduction in provinces/geographical differences?

A
  • after study, health canada gave folate reqs but were not followed –> mandatory fortification took place in 1996 –> 46% reduction
  • magnitude of decrease was proportional to the prefortification baseline rate in each province and geographical differences almost disappeared after fortification began
40
Q

what are the current folic acid reqs for pregnant women/planning pregnancy?
- what about for women at high risk?

A
  • women planning pregnancy are advised to take 0.4 mg folic acid per day at least 1 month before conception AND during first trimester of pregnancy
  • women who are at high risk bc of previous NTD-affected pregnancy are advised to take 4 mg folic acid daily in periconceptional period
41
Q

there is evidence that folate deficiency can also induce pregnancy complications (5)
- how can it be minimized?

A
  1. gestational diabetes mellitus
  2. pregnancy-induced hypertension
  3. spontaneous abortion
  4. premature birth
  5. congenital heart disease
    - by folate supplements/fortification
42
Q

what is the key role of folate?
- synthesis of (2)
- metabolism of (4)
- formation of ____A_____ agents required for (2)
- hypo_____A________tion can alter (2)

A
  • one-carbon metabolism by facilitating transfer of 1-carbon units for
  • synthesis of purine and pyrimidine precursors of nucleic acids
  • metabolism of methionine, serine, glycine and histidine
  • formation of methylating agents required for normal metabolism and gene regulation
  • hypomethylation can alter cell proliferation and differentiation (bc methylation is needed for gene regulation/expression)
43
Q

how does folic acid work in reactions?

A

folic acid is converted to its active coenzyme form, tetrahydrofolate, which behaves as a donor or receiver of a one carbon entity in different oxidation states (formyl, methylene or methyl)

44
Q
  • which form of folate is distributed to all body tissues?
  • what is the major storage form/circulating form of folate in body? 50% in which organ
  • this form is highly bound to what?
A
  • tetrahydrofolate (THF) and its derivatives
  • 5-methyl-THF –> 50% in liver
  • albumin
45
Q

5-methyl-tetrahydrofolate:
- acts as a _______ donor in many metabolic reactions
- conversion of _________ to ___________
- biosynthesis of ______ from _______ and of what?

A
  • methyl donor
  • homocysteine into methionine
  • glycine from serine AND of DNA precursor molecules
46
Q

explain the loop of homocysteine to ________ to ________ to ________ back to homocysteine

A
  1. Homocysteine –> Methionine
    - needs B12 and methionine synthase (which converts 5-Me-TH4-folate to TH4-folate)
    - folate donates methyl group to B12, B12 donates methyl group to methionine (?)
  2. Methionine –> S-Adenosyl-mehionine (SAM)
    - key methylating compound –> methylates protein, lipids and DNA
    - low SAM = hypomethylationof DNA = improper gene expression
  3. SAM –> S-adenosyl-homocysteine (SAH)
    - through methyltransferase
  4. SAH –> Homocysteine
    - homocysteine accumulates if folate deficiency
47
Q

describe the loop of 5-me-TH4-folate to _______ to _______ back to 5-Me-TH4-folate

A
  1. 5-Me-TH4-Folate –> TH4-folate
    - through B12 and methionine synthase
    - also converts homocysteine to methionine
  2. TH4-folate to 5-methylene-TH4-folate
  3. 5-methylene-TH4-folate –> 5-Me-TH4-Folate
    - thorugh 5-methylene tetrahydrofolate reductase
    - this rxn activates folate
48
Q

what happens if there’s a SNP on 5-methylene-tetrahydrofolate reductase enzyme?

A

enzyme is less active –> higher risk of NTD and birth defects bc low 5-Me-TH4-folate = no conversion of Homocysteine to methionine

49
Q

Homocysteine can be methylated ish to become methionine. what is the other pathway for homocysteine?

A
  1. homocysteine –> cystathionine using B6 as cofactor
  2. cystathionine to cysteine using cystathionase enzyme and B6 cofactor
50
Q

why can low folate or low B12 lead to anemia?

A
  • low folate = less 5-me-TH4-folate –> megaloblastic anemia
  • low B12 (= methyl trap) = less TH4-folate –> megaloblastic anemia
51
Q

why would folic acid supplementation mask B12 deficiency?

A

bc folic acid can generate 5-Me-THF-folate –> continues to make nucleic acids necessary for RBC
- usually, without folic acid supplements, there won’t be enough 5-Me-TH4-folate bc 5-Me-TH4 folate won’t be converted back to TH4-Folate by B12 (TH4-folate is needed to make 5-me-TH4-folate)
- but since folic acid is taken as a supplement, there will always be en exogenous source of TH4-folate –> so 5-Me-TH4-F will be formed and RBC will be normal
- B12 deficiency will not be seen –> bad thing bc lack of B12 can cause irreversible brain damage (from increased level of homocysteine)

52
Q

increase in homocysteine from B12 or folate deficiency can lead to
- 2° accumulation of what? –> consequence
- ______ ______ –> damage to (4) + decrease in functional activity of what?

A
  • 2° accumulation of SAH (bc increase in homocysteine) –> inhibition of DNA methyltransferase rxns + DNA hypomethylation + altered gene expression
  • Oxidative stress –> damage to mitochondrial and nuclear DNA’ protein structure and fct, membrane lipids and signal transduction pathways + decrease in functional activity of methionine synthase through limiting the availability of vit B12
53
Q

which enzyme is needed to convert 5-methylene-TH4-folate to 5-methyl-TH4-folate?
- what are 2 most common SNPs?
- heterozygosity for these variants associated with (3)
- what can “cure” the symptoms caused by these genetic polymorphisms

A
  • methylene-tetrahydrofolate reductase
  • 677C3T and 1298A4C substitutions
  • associated with 50-60% reduction in enzyme activity, reduced folate concentrations and hyperhomocysteinemia
  • folic acid supplementation!
54
Q
  • which 2 physiological changes (decrease in ______ and increase in ______) in mothers with NTD infants –> leads to defects in what pathway?
  • families with NTDs tend to have what?
  • how can folic acid supplementation help (2)
A
  • mothers with NTD infants –> decrease plasma folate + increase homocysteine levels –> leads to defects in folate-dependent homocysteine pathway
  • families with NTDs tend to have in-born errors of metabolism (shortage of methyltetrahydrofolate reductase)
  • normalizes RBC [folate] and decreases blood homocysteine
55
Q
  • elevated/lowered homocysteine = risks factor for pregnancy complications –> 3 examples
  • plasma [homocysteine] are 30-60% higher/lower in pregnancy
  • folic supplementation will decrease/increases maternal and fetal [homocysteine]
A
  • ELEVATED –> risk factor for preeclampsia, spontaneous abortion, recurrent early miscarriages
  • lower in pregnancy! (driven by supplementation + body accommodates: upregulates homocysteine pathway to support growth! good if enough folate in diet)
  • decrease maternal and fetal homocysteine concentration
56
Q
  • maternal homocysteine at preconception, at 8 weeks and at birth –> inversely related to what?
  • can preconceptional homocysteine predict homocysteine associated pregnancy complications?
A
  • inversely related to birth weight –> high homocysteine = low birth weight
  • possibility that it can! –> there is a strong correlation btw preconceptional homocysteine and homocysteine during pregnancy
57
Q
  • what is a good biomarker for folate? vs a “bad” one
  • what is the best: dietary folate, folic acid supplementation or fortified foods –> in order to change folate status?
A
  • RBC folate = representative of stores! vs blood folate –> more reflective of recent changes (ie a meal high in folate)
  • folic acid supplements > fortified foods > dietary folate > dietary advice > control
58
Q

is it enough for women to consume enriched cereal grain product as their only source of folate?

A
  • no! lower RBC folate status –> higher predicted NTD prevalence than women receiving supplemental folic acid
    *20% of canadian women of childbearing age do not reach RBC folate values (906 nmol/L) for maximal reduction of NTD risk
  • typical non-pregnant women: 230 ug dietary folate intake –> fortification only increases by 100 ug –> only 10% take in 400 ug/day
    *often, healthy diet = decrease processed foods = decrease foods containing fortification of folate (bc whole grain products are not fortified)
59
Q
  • meeting optimal RBC folate concentration for NTD risk reduction requires a daily intake of _______ ug dietary folate equivalent (_____ ug of folic acid supplement)
A
  • 600 ug of dietary folate = 400 ug Folic acid supplement
  • can only be achieved if consuming FA-containing supplements in addition to fortified foods
60
Q

what are the possible adverse effects of folic acid (FA) fortification? (4)

A
  1. folic acid requires reduction via dihydrofolate reductase (DHFR) (converts folic acid to tetrahydrofolate)
    - rate limiting step: DHFR has very weak activity in humans –> high doses of FA saturate DHFR = accumulation of unmetabolized FA
  2. high doses (> 5000 ug/day) during first period of pregnancy –> more likely to have shorter telomeres at age 4 + lower psychomotor development of infants at 1 year of age
  3. masking of B12 deficiency –> neurological damage
  4. folic acid and 5-methyl-TH4-folate compete to get into cells!
61
Q

what is an alternative supplement to folic acid?
- benefits? (3)
- limitation?

A
  • 5-methyl-tetrahydrofolate
    *natural folate represents 98% of all plasma folates
    1. does not need DHFR to become active –> doesn’t induce unmetabolized folic acid
    2. similarly effective in maintaining erythrocyte and serum folate in pregnancy and after delivery
    3. efficient in reducing homocysteine levels in healthy women including carriers of the MTHFR 677C3T
  • LIMITATION: no large-scale clinical studies have been performed yet on NTDs

Nutrition through life (13 decks)

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