Basic Nutrition Note - Lecture notes 4 PDF

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15.BASIC NUTRITION1. NUTRITIONWhy do we need to eat? A. Maintenance of the body i. repair ii. growth iii. function B. Need a mix of nutrients in the right proportion. C. Imbalances may result in disease and deficiency disorders D. Need a supply of nutrients that cannot be made by the body.2. NUTRITI...

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15.02.2019

BASIC NUTRITION 1. NUTRITION Why do we need to eat? A. Maintenance of the body i.

repair

ii.

growth

iii.

function

B. Need a mix of nutrients in the right proportion. C. Imbalances may result in disease and deficiency disorders D. Need a supply of nutrients that cannot be made by the body.

2. NUTRITION: MICRONUTRIENT REQUIREMENTS A. Vitamins: Organic elements i.

A, D, E, K, (fat soluble)

ii.

B1, B2, B6, B12, Niacin, Pantothenic Acid,

iii.

Folic Acid, Biotin, C (water soluble)

B.

Minerals: Inorganic elements i.

Calcium, Phosphorus, Potassium

ii.

Sulphur, Chloride, Magnesium, Iron,

iii.

Iodide, Manganese Copper,

iv.

Cobalt, Zinc, Fluoride, Selenium, Chromium

3. VITAMINS A. Required as co-enzymes to facilitate metabolism B. Involved in protein synthesis C. Blood cell production and clotting D. RNA and DNA production E. Antioxidants F.

Growth of bones and teeth (regulation of cells and Ca++ absorption)

G. Wound healing H. Cell growth

4. FAT SOLUBLE VITAMINS

5. WATER SOLUBLE VITAMINS

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6. METABOLISM A. Metabolism: chemical reaction taking place within the body. B. All reactions are either CATABOLIC or ANABOLIC i.

Catabolism- breakdown of complex molecules to release energy (exergonic)

ii.

Anabolism- building of complex molecules, requires energy (endergonic)

7. METABOLISM: ENERGY TRANSFER A. Adenosine triphosphate (ATP) transfers energy to enable reactions i.

Anabolic: ATP into ADP + P + energy

ii.

Catabolic: ADP + P into ATP + heat

8. METABOLISM: CARBOHYDRATES I A. Glucose is used in several different ways in the body: i.

As an immediate energy source - either aerobic or anaerobic metabolism.

ii.

Synthesis of amino acids (many cell types)

iii.

Synthesis of glycogen (mainly hepatocytes and muscle cells)

iv.

Formation of triglycerides (formed in hepatocytes, stored in adipose tissue.

v.

Endurance training can increase the glycogen storage capacity to an extent.

9. METABOLISM CARBOHYDRATES II A. Although several different types of monosaccharide are absorbed from the small intestine, they are converted to glucose in the hepatocytes (liver cells). They then undergo the following reactions in the mitochondria: aerobic and anaerobic will both produce energy: different amounts. Feeds the electron transport chain B. This diagram gives an overview of aerobic cellular respiration; as the bonds in the glucose molecule are broken down, energy is released and some of it is used to create bonds between ADP and phosphate to form ATP, which can then be used in anabolic reactions elsewhere in the body. Some of the electrons are transferred to NAD and FAD and can then be used in the electron transport chain: as the electrons are passed from one 3

transporter molecule to the next, energy is released which is used to create bonds between ADP and phosphate to form ATP. The remaining hydrogen atoms then combine with oxygen to form water.

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METABOLISM:

CARBOHYDRATES III Glycogenesis and glycogenolysis A. Glycogen can also be broken down into glucose in the absence of insulin (and presence of glucagon) to increase blood glucose level B. Insulin stimulates hepatocytes and skeletal muscle cells to convert glucose into glycogen.

11.

METABOLISM: CARBOHYDRATES IV. GLUCONEOGENESIS A. Glucose production from protein or fat in a large-scale production:

12.

i.

Starvation

ii.

Low carb diet

iii.

Endocrine disorder e.g. hyperthyroidism

iv.

Endurance exercise

METABOLISM: CARBOHYDRATES V. GLUCONEOGENESIS A. Driven by cortisol and pancreatic glucagon

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i.

Hepatocytes convert triglycerides, lactic acid and amino acids to glucose

ii.

Lactic acid produced by exercise is slowly converted back to glucose

iii.

Endurance training can increase the glycogen storage capacity to an extent.

13.

METABOLISM: LIPIDS A. Diffuse across cell membranes into the lymphatic system B. Oxidised to produce ATP C. Used as structural or to synthesis other molecules e.g. lipoproteins D. If not used immediately, stored in adipose tissue. E. Triglycerides stored more readily than glycogen

14.

LIPIDS AND THEIR FUNCTIONS

15.

METABOLISM: LIPIDS - CATABOLISM A. Lipolysis: triglycerides break down into fatty acids and glycerol

16.

i.

Fatty acids produce more ATP than glycerol by entering the Kreb’s cycle following beta-oxidation

ii.

Glycerol is converted to glucose or pyruvic acid depending on ATP level.

METABOLISM: LIPIS - ANABOLISM A. Lipogenesis: excess carbohydrates, proteins and fats are stored as triglycerides

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i.

E.g. αα to acetyl Co-A into fatty acids then triglycerides

ii.

Fatty acids from glucose and protein can also be turned into lipoproteins, phospholipids and cholesterol

17.

METABOLISM: LIPIDS - CATABOLISM AND ANABOLISM A. Triglycerides are broken down into glycerol and fatty acids B. They enter the catabolic process at different points, and are broken down to form ATP (lipolysis) C. Lipolysis is increased as a result of increased levels of hormones adrenalin, noradrenalin and cortisol D. Lipogenesis can also happen – essentially the same reactions in reverse, increased when blood levels of insulin increase. i.

18.

Notice also that ketone bodies are usually broken down as part of this process. This happens when you get a high level of beta-oxidation of fatty acids, which can happen during starvation, when there is little glucose available. People undergoing a diabetic hypo (so low blood glucose due to excess insulin usually) may suffer from ketosis; the ketones can be detected on the breath. Ketosis can cause the blood to become very acidic (ketoacidosis) and can ultimately cause death.

METABOLISM: PROTEIN A. Amino acids are transported from the GI by active transport B. Making new protein e.g. hormones, enzymes, muscle, collagen, antibodies C. Stimulated by IGFs, Thyroid Hormones, Insulin, Oestrogen, Testosterone D. 10 αα required from diet (essential αα)

19.

i.

Complete protein: meat, fish, eggs, milk

ii.

Incomplete: leafy veg, beans, grains

PROTEIN CATABOLISM A. Catabolism is stimulated by cortisol B. Proteins are catabolised (broken down) into αα used for growth and repair C. Can’t be stored so excess are used for ATP 6

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20.

METABOLISM: PROTEIN A. Deamination before entering the Kreb’s cycle (removal of NH2 group) B. Converted to glucose, triglycerides (lipogenesis) or ketone bodies (ketogenesis) i.

Ketosis- where energy comes from the breakdown of ketone bodies.

ii.

Sign of diabetes or low carb diet

iii.

Characterised by acidic breath

21.

DIET AND HEALTH RELATED PROBLEMS A. Pescatarianism i.

Varies depending on whether dairy and eggs are eaten

ii.

May have problems with Vitamin D, B12 and Iron levels

B.

Vegetarianism i.

Problems with maintaining protein and iron levels

ii.

Need essential amino acids lysine and methionine -

Lysine deficiency: consequences for infertility

-

Production of hormones and antibodies

-

Methionine involved in absorption of zinc

iii.

Complete protein sources include soybean for lysine and methionine

iv.

Grains (whole-wheat) and legumes for methionine. E.g. peanuts, oatmeal, and etc.

C. Veganism: i.

Protein replacement

ii.

Lack of vitamin B12

iii.

Anaemia

iv.

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-

Megaloblastic RBCs (lack of DNA production), hyper segmented neutrophils

-

Neurological symptoms (dizziness, tinnitus, lesions in cerebrum, peripheral neuropathy)

-

Folate deficiency

Can be avoided through the use of Dietary supplements: -

Fortified products

-

Synthetic supplements

22.

CAUSES OF NUTRITIONAL DEFICIENCIES Causes of malnutrition: A. Famine: i. B.

Poverty: i.

Education

ii.

Lack of food

iii.

Limited access to variety

C.

War: i.

Famine

ii.

Transport links

D.

Child/teenage pregnancy: i.

E.

23.

Starvation lack of food and variety

Removal of nutrients by the foetus Lack of variety

i.

Weight loss diet

ii.

Eating disorders / addiction / psychological

iii.

Poverty

DEFICIENCIES AND OBESITY A. Thiamine (B1)- cofactor for glucose and amino acid metabolism B. In glycolysis it is essential for the action of pyruvate dehydrogenase C. A deficiency decreases glucose metabolism leading to endothelial cell dysfunction. D. Severe thiamine deficiency can lead to beri beri. Neurological and heart symptoms e.g. Fast HR, numbness of hands and feet. E. Presence of vitamin D receptors on Pancreatic B cells F.

Low vitamin D is associated with B cell dysfunction

G. Presence of vit D in B cells increases insulin gene transcription H. 80-90% of obesity patients have vitamin D deficiency 9

I.

Link with obesity, vitamin D and glucose metabolism

24.

EFFECTS OF NUTRITIONAL DEFICIENCIES: PROTEIN Marasmus and Kwashiorkor: undernutrition caused by lack of protein or amino acids - poor growth, muscle wasting. A. Kwashiorkor: enough calories but lacking in protein (essential amino acids) i.

Leads to oedema, liver damage

B. Marasmus: too little protein and too few calories. Muscle wasting i.

25.

Muscle wasting

EFFECTS OF NUTRITIONAL DEFICIENCIES: PROTEIN A. Phenylketonuria: i. B.

Inability to break down phenylalanine to release essential amino acids (tyrosine). Detection:

i. C.

New-born spot test: results in nervous system damage, melanin production Treatment:

i.

Through diet - low protein and amino acid supplement, avoiding artificial sweeteners.

ii.

Tyrosine is involved in the Dopa pathway.

26.

EFFECTS OF NUTRITIONAL DEFICIENCIES: VITAMINS A. Vitamin K: i.

Affects clotting.

ii.

Neonatal injection at birth prevents Haemorrhagic Disease of the New-born (HNB) - intracranial and retroperitoneal bleeding.

iii.

Vitamin K injections at birth (voluntary)

B.

Vitamin C: i.

C.

Scurvy Vitamin D:

i.

Supplements required in Northern hemisphere. Especially after movement from sunnier countries.

ii.

Affects Ca absorption and bone development.

D. Hypervitaminosis: i.

Fat soluble vitamins can build up and cause problems.

ii.

e.g. Vitamin A stored in the liver.

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iii.

Polar explorers unwittingly died of excess vitamin A. Pregnant women must avoid liver products to protect the foetus.

E. Vitamin A is metabolised to Retinoic Acid.

27.

EFFECTS OF NUTRITIONAL DEFICIENCIES: MINERALS A. Iron: anaemia i. B.

Weak, tired, decreased cognitive ability in children Calcium: osteopenia

i.

Bone density decrease.

ii.

Fatigue, muscle cramp, heart arrhythmia.

iii.

Can be dietary, linked to medications or lack of vitamin D.

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