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NUFS 356 > Lecture 3 - Nutrition Status and Reproduction, Nutrition Prior to Pregnancy > Flashcards

Lecture 3 - Nutrition Status and Reproduction, Nutrition Prior to Pregnancy Flashcards

1
Q

Explain the reproductive systems for females?

A
  • Born with immature ova (eggs). About 7 million ova but only about 300,000 at puberty
  • Starting at puberty - ova mature about every 28 days (ovulation)
  • Ova mature within follicles in the ovaries
  • Decades of exposure (think when you have a girl she is carrying the potential for your grandkids too)
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2
Q

Explain the reproductive systems of males

A
  • Born with sperm-producing systems
  • Start producing sperm at puberty - ongoing not cyclic
  • More susceptible to shorter exposures (unlike females)
  • Response to testosterone is 70-80 days
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3
Q

What are endocrine organs associated with reproduction and what hormones do they release?

A
  • Hypothalamus - releases gonadotropin releasing hormone (GnRH)
  • Pituitary - releases follicle-stimulating hormone (FSH) and luteinizing hormone (LH)
  • Ovaries and placenta from adrenal glands, adipocytes - releases estrogen and progesterone (testosterone)
  • Testes (adrenal glands) - releases testosterone
  • happens in both males and females
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4
Q

Explain the hypothalamus-anterior pituitary-gonadal axis for men

A
  • Hypothalamus sends GnRH to the anterior pituitary which releases LH and FSH.
    This stimulates the testes (ovaries in women) they then release testosterone (estrogen).
  • Release of testosterone causes a negative feedback to hypothalamus and the anterior pituitary
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5
Q

Explain how hormone levels change during the menstrual cycle

A
  • Days 1-7 (Follicular phase): FSH and LH stay level, growth of the follicle, estrogen increasing until day 12, progesterone stays level
  • Day 12-14: LH increase triggering ovulation , FSH increase, estrogen drops, progesterone starts to increase
  • Day 14-28 (Luteal phase): thickening of ednometrial lining lining, progesterone levels increase and estrogen levels stay the same, LH and FSH levels are lower
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6
Q

What effect does obesity have on fertility?

A
  • Associated with infertility or subfertility in both females and males
  • Excess adipose tissue, particularly excess visceral adipose tissue, alters hormones involved in reproduction
  • Result of overnutrition which is common in today’s society
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7
Q

Explain how hormones impact the male reproductive system?

A
  • GnRH levels fluctuate&raquo_space;> LH and FSH release&raquo_space;> Testosterone release from testes
  • Testosterone and other androgens stimulate the maturation of sperm (70-80 days to mature)
  • Mature sperm stored in the epididymis until released (released in semen which contains fluid and nutrients)
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8
Q

Explain how undernutrition impacts fertility in males and females

A
  • Females: hypothalamic amenorrhea (e.g. female athlete triad)
  • Males: impaired sperm number, viability, and motility, decreased sexual drive
  • Caused by negative energy balance, weight loss, low body fat, (can be from intense physical exercise)
  • Nutritional status impacts the status of hormones thus causing the above impacts
  • In women, body senses that organs are not capable of hosting an embryo so it is protecting the host
  • Acute malnutrition has a larger impact than chronic malnutrition because we are able to adapt (growth can still be disrupted)
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9
Q

Why was there a reduction in births during the Dutch Famine (44/45)

A
  • Malnutrition due to rationing
  • Men away to war
  • High stress situations
  • Other reasons, not solely due to nutrition
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10
Q

What effects do micronutrients have on fertility? Give examples of micronutrients

A
  • Antioxidants have role in protection of ovum/corpus luteum and sperm from reactive oxygen molecules
  • Vitamin C, Vitamin E, beta-carotene, selenium
  • Lower intake of antioxidants associated with infertility
  • Zinc has a role in testosterone synthesis and sperm maturation
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11
Q

How do BMI and waist circumference impact health risk?

A
  • Underweight and overweight have increased health risk
  • Obese 1 = high
  • Obese 2 = very high
  • Obese 3 = Extremely high
  • Waist circumference of >102cm for males and >88cm for females (indicates central adiposity) can also indicate health risk
  • You can have a healthy BMI but a large waist circumference that will lead you to health risk
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12
Q

How can obesity specifically impact females and their fertility?

A
  • Can cause menstrual irregularities due to:
    1) Increased androgens (testosterone)
    2) Increased leptin (made by adipose. Increased adipose = increased leptin. Triggers first menses in women) and estrogen
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13
Q

Explain what PCOS is and what occurs with this syndrome

A
  • Polycystic ovarian syndrome
  • Related to obesity leading to infertility
  • Hyperandrogenism (elevated testosterone)
  • Impaired ovarian folliculogenesis (due to hyperinsulinemia) - insulin resistant
  • Associated with android fat distribution
  • Overall creates a hard layer around ovaries which disrupts the cycle within the ovary (not undergoing ovulation)
  • Some researchers say it is the female manifestation of metabolic syndrome
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14
Q

In PCOS what comes first, insulin resistance or hyperandrogenemia?

A
  • Genetic programming, central obesity, and diet can lead to IR or Ovarian steroidogenesis (hyperandrogenemia) these then can lead to the other
  • Ultimately culminates in PCOS which will cause dyslipidemia, cvd, diabetes risk, and higher bp
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15
Q

How can obesity impact male fertility? How does this occur?

A
  • Males: decreased sperm count and motility, increased risk of erectile dysfunction
  • Decreased testosterone
  • Leptin, estrogen
  • Increased scrotal temperature (sperm need optimal temperature, otherwise proteins denature)
  • J shaped curve for BMI and risks (underweight will also have these risks which is the same for women)
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16
Q

What other nutritional factors are associated with infertility for males and females?

A
  • Females:
  • Vegetarian/vegan if not doing it properly
  • Iron status (important in fertility cycle)
  • Alcohol
    -Males:
  • Vitamin D
  • Alcohol
  • Heavy metals, chemicals (occupational exposure rather than day to day (atypical exposure))
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17
Q

What are the 3 critical periods of fetal development for organ and tissue development?

A

1) Hyperplasia (increased cell multiplication)
2) Hyperplasia and hypertrophy
3) Hypertrophy (Increased cell size)
- hyperplasia requires an environment that is optimal. If not there can be an insult or change that is irreversible

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18
Q

What does critical period mean in fetal development?

A

Point of time when environment should be optimal. If it is not there can be no reversing changes

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19
Q

When can major congenital anomalies occur vs functional defects and more minor anomalies?

A
  • major congenital anomalies occur in highly sensitive periods of growth in the first 8 weeks of pregnancy
  • Less sensitive periods begin later, dependent on what you are looking at
  • CNS has the longest sensitive period lasting until 16 weeks
  • During highly sensitive periods exposures/illness/nutrient deficiencies can have impacts that cannot be reversed
  • If exposures occur in less sensitive periods it is possible that they may be reversed
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20
Q

Why is nutritional status prior to pregnancy important?

A
  • Some critical periods of fetal development occur before women know they are pregnant
  • If nutrients unavailable during critical period, can not ‘catch-up’ later (effects not reversible)
  • Teratogens (toxins) need period of time to clear circulation
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21
Q

What are neural tube defects (NTDs) and when do they occur?

A
  • Failure of closure of the neural tube during early development
  • Week 3 and 4 (women wouldn’t know they are pregnant, as a result is the most common defect)
  • Various presentations and degrees of severity
  • Mechanisms are unclear but link to folic acid
22
Q

What are the two phases of female reproduction?

A

Follicular and luteal

23
Q

What occurs during the follicular phase?

A
  • Day 1 to 14
  • Low estrogen and progesterone&raquo_space; release of GnRH&raquo_space; release of FSH and LH
  • Growth and maturation of follicles and ova
  • Release of estrogen (and progesterone)
  • Thickening of outer uterine wall (endometrium)
  • Peak LH levels stimulate ovulation (day ~14)
24
Q

What occurs during the luteal phase?

A
  • Day 15 to 28
  • Follicle becomes corpus luteum&raquo_space;> releases progesterone and some estrogen&raquo_space;> further endometrium development&raquo_space;> inhibit GnRH
  • If no fertilization: corpus luteum shrinks&raquo_space;> progesterone and estrogen levels decline
  • If fertilization: corpus luteum size increases&raquo_space;> continued release of progesterone and estrogen
25
Q

How is the Neural tube formed?

A
  • start with a neural plate
  • series of folds and involutions that form CNS
  • results in the formation of neural crest and spinal cord
  • all occurring within 4 weeks
26
Q

What is the prevalence of NTDs?

A
  • NTDs most common congenital anomaly in US and Canada
  • 1.0-1.6 per 1000 live births
  • Many suspected to be miscarried
  • long history of discovery
27
Q

What are the different types of NTDs?

A
  • Anencephaly: incomplete brain formation, absence of forebrain and skull. The neural tube not closed at all
  • Encephalay: protrusion of brain and membranes through skull (depends on length of exposure or what they are exposed to)
  • Spina bifida: incomplete spinal cord formation (severity depends on formation and defect)
28
Q

What are the clinical symptoms of spina bifida?

A
  • Lump formed that is made of nervous tissue, never normal
  • Control of muscles distal to (below) defect affected (often lower limbs, bladder, large intestine)
  • If defect is high in spinal cord, death may occur
  • Surgery in utero to fix
29
Q

What is the link between folate and NTDs?

A
  • women who give birth to babies with NTDs have lower serum folate and dietary intake of folate
  • epidemiological studies show regions with higher dietary folate intake have lower rates of NTDs
  • Women who take supplement containing folate before and during pregnancy have lower risk of having baby with NTDs
30
Q

What is folate and its forms?

A
  • It is a B vitamin so is water soluble and is able to donate a methyl group (Glutamate/glutamine)
  • Family of compounds:
  • Folate: polyglutamate
  • Folic acid: monoglutamate - more stable, what you would find in a supplement
  • Bioactive form: tetrahydrofolate
31
Q

Explain metabolism of folate

A
  • Folate in our circulation comes into cell with a carrier to become 5-MeTHF
  • 5MeTHF can be used for methylation reaction or nucleotide synthesis
  • Methylation pathway requires B12 and B6 and SAM (methyl donor) for conversion into homocysteine
  • Methylation of DNA for gene regulation, protein for structure and function, and lipid for synthesis
  • Other pathway is for formation of DNA and requires 5,10 Methylene THF reductase (known snp)
  • Pathways are regulating each other
32
Q

How does folate decrease NTDs?

A
  • Mechanism not completely understood
  • Methylation is likely the connection between folate and NTDs
  • Reduction in 5,10 Methylene THF will alter flux and reduce methylation pathway
33
Q

There are variations in MethyleneTHF Reductase gene. What are they and how do they impact NTDs?

A
  • Variance gene is associated with increased plasma homocysteine and risk of NTD
  • CC = normal MTHFR
  • CT = heterozygous variant (est 40% population) and increases risk of NTDs (OR 1.1 to 1.3)
  • TT = homozygous variant (est 10% population) and highest risk of NTDs (1.6 to 1.9)
34
Q

What two things influence folate metabolism and what can this result in?

A
  • Environment and genetics can alter folate metabolism
  • Causes a decrease in methylation of proteins, lipids or metabolites
  • Altered protein function and gene expression
  • Leads to NTDs
35
Q

How do DNA synthesis and methylation interact?

A
  • increased DNA synthesis and decreased methylation (TT)
  • Decreased DNA synthesis and increased methylation (CC)
  • Middle = CT
36
Q

What are the folate equivalents?

A
  • 1 Dietary Folate Equivalent (DFE):
    = 1 ug food folate
    = 0.6 ug synthetic folic acid (more bioavailable) with food
    =0.5ug synthetic folic acid from supplement on empty stomach
37
Q

What are the folate requirements?

A
  • RDA (adult females): 400ug/day
  • RDA (pregnancy): 600ug/day
  • UL (synthetic folic acid only): 1000 ug/day
38
Q

Should pregnant women supplement with folate?

A
  • Health Canada recommends women who can become pregnant should take 400ug synthetic folic acid/day from multivitamin supplement
  • Premise - based on data collected over a long period of time, it appears that women don’t (generally) meet folic acid recommendations
39
Q

Give examples of food sources of folate

A
  • Naturally occurring folate:
  • Vegetables: peas, beans, asparagus, dark leafy greens
  • Fruits: oranges, orange juice, pineapple juice
  • Fortified foods: Bread and grain products
    -150 ug folic acid/100g flour
  • 200 ug folic acid/100g pasta
40
Q

Does folate fortification help reduce NTDs in Canada?

A
  • Prevalence of open NTDs in Ontario:
  • 1.13 per 1000 pregnancies before 1998 (prior to fortification)
  • 0.52 per 1000 pregnancies in 2000 (reduced prevalence by half)
  • Similar decreases in anencephaly and spinal bifida
  • Folic acid in excess on high fat diet showed offspring are gaining more weight than those who did not have excess folic acid
41
Q

What are teratogens and give examples of them

A
  • Substances that can produce or increase the incidence of an abnormality in embryonic or fetal development
  • Drugs (including alcohol), chemicals, infections, radiation
  • Vitamin A, lead, mercury
42
Q

Is Vitamin A toxicity a concern? Where does it result from?

A
  • In developed countries vitamin A toxicity is a greater concern than deficiency
  • In developing countries vitamin A deficiency is common
  • Vitamin A is a teratogen in mega doses
  • Toxic level not usually from food but a result of:
  • Mega dose supplements
  • Retinoid drugs (accutane)
43
Q

What can retinoid drugs do?

A
  • Retinoid drugs such as isotretinoin (e.g. Accutane)
  • Increased risk of spontaneous abortion and birth defects
  • Craniofacial defects, cleft palate, cardiovascular and CNS abnormalities
  • Neuropsychological impairment later in life
44
Q

What is the RDA and UL for Vitamin A?

A

RDA: 700 ug/d
UL: 3000 ug/d (pre-formed only)

45
Q

What should you do to avoid Vitamin A related defects?

A
  • Avoid megadose supplements: increased rate of birth defects with 3,000 ug/d
  • More than one form of birth control while taking retinoid drugs and stop use at least 6 months before pregnancy (store in fat so it stays in the body longer)
  • Beta carotene is okay
46
Q

What is methyl mercury, where do we get it, and what can it do?

A
  • Methyl mercury is a teratogen
  • Main food source of methyl mercury is contaminated fish
  • Diet high in mercury before and during pregnancy can cause CNS defects including cerebral atrophy, seizures, mental impairment, blindness
47
Q

Should women eat fish while pregnant?

A
  • Fish is a good source of long chain omega-3 fatty acids that are important for fetal brain development
  • Health Canada reports that most fish in Canada have very low mercury levels (exceptions are fresh or frozen tuna, shark, marlin, orange roughy, escolar, and canned albacore tuna)
  • Large predatory fish have larger amounts of mercury because it accumulates over food chain (algae-small fish-big fish)
  • Women who are planning to get pregnant or those who are currently pregnant are advised to have at least 150g of cooked, low mercury fish each week (2-3 servings of fish a week in CFG)
48
Q

Why should pregnant women not drink alcohol?

A
  • Alcohol is a teratogen and it crosses the placenta and the fetal liver can not metabolize
  • Most affected is CNS development (CNS is earliest and longest) as it is a critical period through-out pregnancy
  • Heavy alcohol intake causes increased risk of miscarriage, stillbirth and infant mortality
49
Q

What is FASD? What is it caused by and what are the symptoms?

A
  • Fetal alcohol spectrum disorder (mild to severe cases)
  • Growth impairment, neurological abnormalities, facial characteristics
  • Developmental delays, behavioural and learning disabilities (some of these don’t show until they are older)
  • Alcohol consumption during pregnancy is thought to be the most common cause of impaired mental functioning
  • Have a flat midface, short nose, indistinct philtrum, thin upper lip, short palpebral fissures
50
Q

How much alcohol should pregnant women consume?

A
  • Unknown if there is a safe level and likely varies between individuals
  • Alcohol should be completely avoided before and during pregnancy

NUFS 356 (5 decks)

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