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Chronic Disease > Nutrition X Genes + Age Related Disease > Flashcards

Nutrition X Genes + Age Related Disease Flashcards

1
Q

What does gene x environment interactions target

A

Disease pathways and prevention pathways eg antioxidants or immune system

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2
Q

What are nutrients and the 2 types

A

Active chemicals in our diet
Macro- fat,carb,protein needed for energy and growth
Micro- vitamins and minerals for health

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3
Q

What is the first known example of how diet impacted genes

A

Lactase tolerance through adaptive mutations in the gene

Appeared in Turkish farming cultures whcih then migrated to Northern Europe 80% now tolerant

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4
Q

What dna repair mechanism seen to cause longevity so maybe is impaired during ageing

A

Parp

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5
Q

Does ageing have set genes

A

No dependant on accumulative damage

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6
Q

What is the free radical theory

A

Where rod builds up and accelerates senescence both by telomeric shortening and cellular senescence and also causes inflammation via nfkb and ap1 tf

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7
Q

How does inflammation relate ageing to disease

A

Inflammation a big basis for a lot of chronic age diseases eg cvd and ra

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8
Q

What does telomere shortening cause in return to further cause damage

A

Mt dysfunction through p53 activation which blocks pary coactivators

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9
Q

What is the term called where removal of correct proteins not done during ageing

A

Loss of proteostasis

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10
Q

How is ageing linked to the same common pathways of age related diseases

A

They show loss of mt function, loss of oxidative stress management , repair mechanisms, cellular maintenance and inflammatory problems

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11
Q

What % of inter individual variations made up by snps

A

90%

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12
Q

What 3 things do snps cause differences in

A

Variations in dietary requirements

Susceptibility to disease

Medication response

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13
Q

What else do snps need because of their low or

A

Environment

Eg pnpla3 and obesity for nafld

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14
Q

Explain how snps used to confer advantage now are detrimental

A

Different diets, pathogens etc

Used to have famine so developed snp for fat storage now detrimental

Some snps to fight pathogens now autoimmunity

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15
Q

What is the difference between nutrifenomics and genetics

A

Genomics is how nutrients affect gene exp/protein exp. Looked at via transcriptomics and proteomics

Genetics is how our genes affect our response to nutrients and their effects on us

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16
Q

Why are both looked at

A

For personalised nutritional advice

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17
Q

What is the main advantage of a candidate approach to study snps

A

Small population so can match them.

And because only certain functional snps in known genes looked at can have additional tests like snp x nutrition tests

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18
Q

What is the main disad

A

Only 1-20 snps looked at so missing out on viral info on other snp associations

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19
Q

Why does a larger popn needed in pathway approach

A

More snps tested both known functionality and unknown in target genes

Need to maintain statistical power

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20
Q

To reduce risk of false positives what needs to be done to the p value and why is this bad

A

Reduce the p value threshold, meaning it is hard to identify snps with small effects

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21
Q

Using what technique in pathway eradicates the need for this

A

Tagsnps

As you’re testing less snps

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22
Q

What sorts of tests can still be done in pathway but not in gwas

A

Snpxsnp and snpxnutrient interacfion

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23
Q

How many snps tested in gwas

A

5 million because testing all snps not just in certain pathways

24
Q

What does this allow for

A

Identifying new gene/snp associations and new pathways

25
Q

What can’t be done in gwas which is in candidate and pathway

A

Matched controls and further tests

26
Q

What is an issue with genotyping Plato forms in gwas

A

Very westernised so don’t necessarily portray the LD and allele freq in other ethnicities

27
Q

Which 2 pathways have been studied via candidate approach for snp x nutrient interactions

A

Lipid metabolism (apoa1 x pufa)

Bcmo1 x vit a/retinol

28
Q

What does apoa1 do

A

Lipid metabolism involvemnef

Efflux of hdlc and transport to liver

29
Q

What does increased hdlc reduce risk of

A

Cvd

30
Q

Do snps in apoa1 cause changes in hdlc conc alone

A

No they need influence of pufa intake (polyunsaturated fatty acids from diet)

31
Q

A allele carriers usually have lower apoa1 and hdlc conc. how was this reversed in women (study)

A

Higher conc of pufa intake

32
Q

What did higher conc of pufa cause in gg carriers

A

Lowered hdlc conc so increase cvd risk

33
Q

What did lower conc for gg do

A

Increase hdlc in gg

34
Q

What is b carotene

A

A pro vitamin carotenoid (from plant/veg)

Which is converted to vitamin A

35
Q

Which snp affects the availability of vitamin A in this pathway of conversion

A

Bcmo1

36
Q

Why is this an issue in vegans

A

Only source of vitamin a in diet is pro vit A carotenoids

37
Q

Why is vitamin A needed

A

Can cause night blindness and increased risk of infection as necessary for t lymphocyte proliferation

Also needed for cell growth and differentiation

38
Q

Why is this a Bcmo1 snp x snp interaction

A

Because a double mutant in females caused greater loss of enzymatic activity

39
Q

What does bcmo concert b carotene into which was found in lower ratio in mutant females

A

Retinal

40
Q

What is folate

A

Naturally occurring folic acid (vit b9)

41
Q

What is it converted to for activity by mthfr

A

5- methyl thf

42
Q

What things is folate major for

A

Dna / rna synthesis / repair via nucleotide synthesis

Methylation

Detoxification of homocysteine hcy (cvd risk factor)

43
Q

Which congenital defect means folate supplementation recommended

A

Ntd

44
Q

What sorts of chronic diseases could folate deficiencies or the snp in folate metabolism cause

A

Cancers, cvd

45
Q

What enzyme converts folate to active 5-methyl thf

A

Mthfr

46
Q

How is hcy detoxified

A

Uses 5-methyl thf to remethylate it into methionine which is used to form SAM methyl donor

47
Q

What snp is in the mthfr

A

C677t

48
Q

What does it do

A

Reduces the activity of mthfr in 37C (body temp) if T allele carried

49
Q

What would carrying TT and also low folate intake do

A

V high hcy levels and low plasma folate

= increased cvd risk

50
Q

How is it a diet x snp interaction

A

Folate intake will compensate and reduce levels of hcy in TT carriers

51
Q

What is the issue with higher folate

A

Can also cause cancer risks - eg maybe via methylation of tumour suppressors or by donating nucleotides for tumour cell growth

52
Q

Is there variations in snp frequency in diff populations

A

Yes, v low in african Americans but high in Asia and Hispanics

53
Q

Does TT impact on Ntd risk

A

Yes if mother is TT/has high hcy/low folate = Ntd risi

54
Q

Why is genotyping seen as important for therapy here and why is it difficult

A

TT carriers need highest supplementation of folate to return it back to normal levels

Difficult because of that cancer risk

55
Q

During folate deficiency, what is incorporated into dna instead of thymidine which causes dna strand breaks and malignancy

A

Uracil

56
Q

Why would snps in mthfr be protective of this

A

Because they increase available 5,10 methylene thf for thymidine synthesis

57
Q

Under normal folate arguments how does it reduce cancer

A

Methylation of protooncogenez

Purine and thymidine production for dna repair

Chronic Disease (16 decks)

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