Macronutrients Flashcards

1
Q

What are the average fat consumed?
What is the reccomendation?

A

Average UK diet: 88g fat - 40% of total energy intake
Triacylglycerols (TAGS) - small amount of cholesterol (0.5-1.0 g)
UK DoH recommendation 2-5 g /day
UK diet 8-15g /day
deficiency very rare

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2
Q

Why are dietary fats neccasary?

A

WE NEED Essential fatty acids

major constituents of membrane phospholipids
precursors of eicosanoids (prostaglandins, thromboxanes, prostacyclins

linoleic acid (C18:2 ω6) - 18 carbons, 2 double bonds, 1st double bond is at 6th carbon from methyl length
linolenic acid (C18:3 ω3)

We cannot synthesise these fatty acids as we cant introduce double bonds before 6 - omega 6 and omedga 3 double bond cant be synthesised

high intakes of the ω3 series may additionally provide protection against CV disease (fish oils)
* . also for developing brain

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3
Q

Risk factors of cardiovascular disease?

A

Risk factors:
* genetic susceptibility
* smoking
* sedentary life style
* high blood pressure (hypotention)
* high serum cholesterol (Low Density Lipoprotein)
* Obesity
* Diabetes
* Trans fat intake?

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4
Q

How is cholesterol increased and decreased?

A

Increase in saturated fatty acids leads to increase in LDL (low density level) and total cholesterol
* Also decrease HDL
* Reduce Trans fat intake to lower cholesterol

blood cholesterol can be lowered to some extent by increasing polyunsaturated fatty acids in the diet
effect of mono-unsaturated fatty acids less clear

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5
Q

What are the different types of fat and what’s the diffrence in the structures?

A

trans - looks more like a saturated fatty acid
reduced kink from double bond

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6
Q

What is Carbohydrates?
How much of our diet does it make up?

A
  • 40% of total energy of diet in affluent societies
  • 80-90% in poor populations
  • Starch
  • non starch polysaccharides (fibre)
  • sugars, mainly sucrose
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7
Q

Where does carbohydrate originate ?
Is Carbohydrate neccessary?

A
  • mainly plant origin except lactose and v.small amount glycogen

Not in theory needed
* has protein-sparing effect - means we dont have to get as much energy from protein
* low CHO diets lead to fat utilisation and ketosis

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8
Q

What Monosaccharides do we consume?
Where can we find this?

A

Glucose - small amounts in fruit
fructose – small amounts in fruit
sorbitol – commercially prepared mainly in foods for diabetics - doesn’t raise blood glucose
inositol – in fibre as hexaphosphate (phytic acid) - negatively charged interferes with absorption of iron and calcium due to thier postive charge

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9
Q

What Disaccharides do we consume?
Where can we find this?

A

Sucrose is most common
* less than 60g/day no dental caries
* UK consumption 105 g/day

lactose (milk)
* no known adverse effects on health
* but many non European populations
* cannot tolerate lactose - don’t have the enzyme to split lactose

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10
Q

Polysaccharides

A

Starch – Most common
* crystalline and insoluble

**Non-starch (NSP) **term replaces ‘fibre’
* from cereals, vegetables and fruit
* NSP rich foods are low in energy and high in bulk (for proper function of gut)
* low intakes related to constipation, diverticular disease, appendicitis, cancer of the colon

Children need more protein not fibre

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11
Q

Protein diet averages vs reccomendations?

A

Usually = 10-15% of total energy of diet.
US/UK = 14%
developing countries = 10%

UK recommendations:
* 0.75g/kg body weight for adults and no more than 1.5g/kg/day
* 55g/day for men and 44g/day for women

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12
Q

Why do we need protein?

A

‘Essential’ amino acids needed for:

  • synthesising new protein
  • catecholamines
  • thyroid hormones
  • neurotransmitters
  • haem
  • glutathione
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13
Q

Why is the quality of protein important?

A

proteins of animal origin more effective in supporting growth of lab animals than those from plants because Amino acid pattern nearer that of body protein

  • ‘high quality’ proteins higher utilisation and less waste.
  • low quality proteins (usually plants) deficient in certain amino acids

Mixtures of ‘low quality’ proteins can complement deficit. e.g. wheat and pulses (Each defficinet in one AA and together they make up for it)
* important in poor countries where diet mainly vegetarian

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14
Q

What are the recomendations for babies based on?

A

infants: based on milk intake of breast fed infants showing satisfactory growth

for pregnancy: compatible with protein deposition for 3.3 kg infant

for lactation: based on protein content of human milk

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15
Q

What could happen with Protein – Energy Malnutrition?

A

Excessive intake may lead to bone demineralisation or deterioration of renal function in patients with renal disease

Lack of Protien
* Growth Failure
* Marasmus
* Kwashiorkor
* Marasmic kwashiorkor

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16
Q

Consequences of Childhood malnutrition?

A
  1. Stunting of growth
    normal weight for height
  2. Growth Failure
    low height for age
17
Q

What is severe PEM?

A

BMI Classification
Normal - 18.5-25
Under this - 17 is severe PEM (Protein energy Malutrition)

18
Q

What are Extreme forms of PEM?

A

Marasmus
Kwashiorkor
Marasmic kwashiorkor

  • General lack of food as opposed to specific deficiencies of vitamins or minerals
  • Kwashiorkor was thought to be a specific deficiency of protein
19
Q

What contributies to childhood PEM?

A
  1. poverty
  2. poor sanitation
  3. infection
20
Q

How does Classification of PEM in chidren occur?

A

oedema = Fluid retention (oedema) occurs when fluid isn’t removed from the body tissues, including the skin … a feeling of stiffness or aching and weight fluctuations.

21
Q

Why does Marasmus occur?

A

Any age of vulnerable groups in a population developed as well as developing countries

**developing countries: **
chronic shortage of food or acute famine or both (usually seen in first year of life)

**developed countries: **
socially and economically disadvantaged groups
disorders of appetite and nutrient absorption disease e.g cancer, AIDS

22
Q

Symptoms of Marasmus?

A
  • extreme emaciation
  • loss of body’s fat reserves
  • muscle wasting
  • loss of protein from vital organs
  • impaired immune response
  • loss of intestinal mucosa and so impaired absorption
  • diarrhoea
  • apathy - Does not respond to pain or comfort
23
Q

Kwashiorkor symtoms? What differs?

A

With oedema = swelling

Features additional to marasmus:
* severe oedema (painless, pitting)
* liver enlargement and fat infiltration
* changes in colour and texture of hair
* dermatitis
* if very severe can lead to permanent mental retardation

24
Q

What are the causes of kwashiorkor?

A
  • infection often precipitates kwashiorkor
  • not specifically a protein deficiency with adequate energy as previously thought

most likely cause:
* general food deficiency with added deficiency of antioxidant nutrients not being able to cope with added oxidative stress of infection
* infection increases protein requirement

25
Q

What is Marasmic Kwashiorkor?

A

Mixture of the two conditions

  • not clear what determines which form.
  • sometimes both can be found in one family - child can switch from one to the other
26
Q

What is the Treatment of PEM?

A

Success depends on duration and severity
* Fluid and electrolyte balance first
* ORS - simplest 8 tsp sugar, 1 tsp salt in 1 litre boiled water - if not available
* dextrose solution
* dilute milk
* normal food when tolerated