UNIT NAME: CLINICAL DIAGNOSIS AND MANAGEMENT 7
UNIT CODE HHD 5187
Subject: Nutrition and Diet 1
Lecturer: Dr Catherine Sicurella
Week Week of LECTURE TOPIC Content Readings; Activities Additional information
Nutritional Assessment Background Lecture notes to be purchased.
1 2nd Mar (Australian dietary guidelines discussed) knowledge quiz Assignment 1 distributed
Digestion & Absorption Tutorial: Nutritional assessment
2 9th Mar Gastrointestinal Nutrition skills applied. Dietary variety
Drug/Nutrient interactions discussed.
Energy Tutorial: Gastro nutrition case study
3 16th Mar Clinical focus: Obesity Herbs in nutrition.
Fats Tutorial: Obesity case study
4 23rd Mar Clinical focus: Arthritis & omega 3s Label reading. Dieting aids.
Cardiovascular disease & dietary Is your saturated fat Tutorial: Healthy eating case study
5 recommendations. intake in line with NHF resources & pick the tick
30th Mar NHF guidelines?
Assignment 1 due
6 6th April
Carbohydrates Tutorial: CVD case study
7 27th April Clinical focus: fibre & health, Diabetes Lower your cholesterol with
Mellitus lifestyle changes
GI and probiotics
Protein Tutorial: Diabetes case study.
8 4th May Clinical focus: vegetarianism; high protein diets Prevention of diabetes by lifestyle
Fat soluble vitamins Does vitamin C Tutorial: vegetarian case study
9 11th May Clinical focus: vitamin deficiency diseases prevent colds? “Health foods” & organic foods
Water soluble vitamins Tutorial::vitamin deficiency case
10 18th May Clinical focus: vitamin deficiency diseases study. New research into vitamins.
Minerals: (Na, K, Ca, P) Tutorial: vitamin deficiency case
11 25th May Clinical focus: hypertension, osteoporosis study. Foods that fight disease.
Minerals: (Fe, Selenium, Zn, Iodine, Mg) Tutorial: osteoporosis case study
12 1st Jume Clinical focus: anaemia Eating for exams.
Week 1: NUTRITIONAL ASSESSMENT
Nutritional status = amount physiological needs for nutrients are being met. It is
influenced by many factors that may change as we age:
Nutrient intake Nutrient requirements
Development of Malnutrition
Well Inadequate dietary intake Diet History
nourished Impaired absorption
Increased nutrient loss
Depletion of tissue levels and body stores Biochemical
At risk changes
Altered physiological function
Deterioration in capacity of cells to function normally
Clinical signs and
Malnourished Clinical Symptoms symptoms
Diagnosing risk of malnutrition
A. Nutritional screening
Used to discover if a client is at risk of a nutrient imbalance.
“ Are you following a special diet?” “Do you drink about 8 glasses of fluid/day?” ;
“Have you lost or gained any weight recently?”; “Have you had a recent change in
appetite?”; “Are you taking supplements?”; “What foods are you allergic to?”
Using either informal or validated screen, decision is made whether patient at
risk of not having an optimal nutritional status.
Next step is a nutritional assessment to determine what nutritional intervention
Optimal nutritional status is our aim for each client
This is achieved by balancing nutrient intake with nutrient requirement. When
this doesn‟t happen eventually malnutrition will occur.
The first stage of malnutrition is poor diet, then abnormal biochemistry, then
Nutritional screening should detect clients at risk of sub optimal nutrition
Nutritional assessment determines what nutritional intervention is appropriate
B. Nutritional Assessment
Measures several parameters & compares each with a standard.
Collect height, current weight, weight history.
Calculate Body Mass Index (weight in kg/ [height in m]2 ) and compare with
Body Mass Index Standards
<16 severe thinness
<17 moderate thinness
17-18.5 mild thinness
18.5-25 normal weight range (this becomes 23-28 for elderly)
>40 morbid obesity
These BMI measures are not suitable for Aboriginal and Torres Strait Islander
peoples, whose healthy BMI range may be lower than that for Australians of
European descent. This is due to their ancestry as traditional hunter-gatherers who
were lean and physically fit.
Similarly, for Asian people cut-off points for health risks appear to be lower than for
Weight history: Unintentional weight change of +/-5kg or more over 6 months is
significant and should be investigated.
Blood plasma, serum & urine often sampled for nutrient concentrations but
generally reflect recent intake, not longer term nutritional status.
Tissues indicate nutrient storage status but cannot be sampled routinely
Interpretation can be confounded by: presence of disease; failure in sampling;
incorrect test choice; other factors (recent transfusion, altered fluid balance,
recent vitamin/mineral supplement etc)
EG Low Albumin = Poor protein intake/malnutrition OR impaired digestion/liver
High albumin = dehydration
Urea & Electrolytes:
Low Sodium = 90% of time due to diuretic
High Sodium = almost always due to dehydration
Low Potassium = almost always due to increased K loss (vomiting, diarrhoea,
High Potassium = almost always due to decreased K loss (eg acute renal
Urea & creatinine = elevated in renal failure (normal creatinine levels rise as we age
because our kidney function decreases during ageing).
3. Clinical signs & symptoms of malnutrition
Potential risk factors for poor nutrition: anorexia, difficulties chewing & swallowing,
nausea, vomiting, constipation
Examples of clinical signs of malnutrition:
Overnutrition Ascorbic Acid
Excess body weight Thiamin deficiency deficiency
Excess fat under skin Confusion Spongy bleeding gums
Muscle weakness Bleeding under skin
Protein Energy Muscle tenderness Enlarged end of bones
malnutrition Sensory loss
Hair & skin changes Loss of reflexes Iron deficiency
Loss of fat & muscle Enlarged heart Pale eye membranes
Enlarged liver Bleeding under skin
Apathy Spoon shaped nails
Oedema Vitamin A deficiency
Dry eye membranes
Dull soft cornea
4. Diet history.
Establish WHAT and HOW MUCH the patient usually eats. Ask about what eaten in
past 24 hours, then go through a checklist of common foods and ask how often these
are eaten. Note: we all under report!
Standards for comparison:
The quantitative standard is the recommended dietary intakes (RDIs) set for
The qualitative standard is Australian dietary guidelines
Recommended Dietary Intakes (RDIs)
“RDIs are the levels of intakes of essential nutrients, considered in the judgement of
the NH & MRC, on the basis of available scientific knowledge, to be adequate to
meet the known nutritional needs of practically all healthy persons”
RDIs include a large safety margin to account for individual variations in absorption
& metabolism (should cover 97.5%).
RDIs most useful at a population level. Recent national diet surveys showed the
Consumes above the RDI for protein, total & saturated fat, refined
Consumes below the RDI for fibre, zinc, magnesium, folate, iron (women
only), calcium (women only)
This is a reflection of low intakes of fruit, vegetables, legumes, nuts and fish, and a
high intake of animal products.
RDIs were replaced by “Nutrient Reference Values” in May 2006
EAR (Estimated average requirement): the daily nutrient intake level estimated to
meet the requirement of half the healthy individuals in a life stage / gender group.
This is used to plan diets for GROUPS not individuals.
RDI (Recommended Dietary Intake): The average daily intake that is sufficient to
meet the nutrient requirements of nearly all (97-98%) healthy individuals in a life
stage/gender group. These are calculated using the EAR plus 2 standard deviations.
AI (adequate intake): used instead of an RDI when the RDI cannot be determined.
UIL (upper intake limit): highest intake of a nutrient on a daily basis likely to pose
no adverse health outcome to almost all individuals.
Suggested Dietary Targets (SDTs) for disease prevention: These are a new set of
nutrient intake recommendations. They are set higher that the RDI and aim to help
prevent chronic diseases such as heart disease or some cancers. They correspond to
what high consumers of a given nutrient already eat. For example, vitamin C‟s RDI is
45mg, but the SDT is 220mg for men, 190mg for women. They apply to healthy
adults only, not children.
Major changes to RDIs in the 2006 review:
RDI for folate has doubled to 400micrograms for women and men of all age
RDI for calcium has increased both men and women to 1000 –1300mg which
means 4-5 serves of dairy a day.
The iron range for women is broader at 8-18mg compared to 12-16mg
previously. The RDI for men has increased by 1mg, to 8mg.
The zinc RDI for men has increased by 2mg, from 12mg to 14mg. The zinc
RDI for women has decreased from 12mg to 8mg.
Sodium’s range of intake has been reduced. The upper limit is now 920mg,
down from 2300mg. (Average sodium intake is over 4000mg!)
RDIs would be used on individuals as a quantitative standard when doing a
computer dietary analysis.
Example of a practical application of RDIs:
For weight maintenance:
Female = 7000-9000 kJ per day
Male = 10 000-13 000 kJ per day
Protein Women = 45g/day
Men = 55g/day
Carb 45-60% of total energy (230-310g per
Fat 30% of total energy (70g per day)
Saturated fat Less than 10% of total energy (<23g per
Iron 12-16mg if female under 54, 7mg for
over 54 females & men
Calcium 800mg women under 54, 1000mg women
over 54 & men
The qualitative standard we use when examining diet is the Australian dietary
To help educate the public on how to make healthy food choices these guidelines
were first prepared by the NH & MRC in 1992. They summarise current knowledge
regarding diet & disease in Australian adults and the nutrients in our food supply.
They provide a means of comparing a patient‟s diet to the recommended dietary
The NHMRC Dietary Guidelines for Australian Adults 2003
Enjoy a wide variety of nutritious foods:
Eat plenty of vegetables, legumes and fruits
Eat plenty of cereals (including breads, rice, pasta, noodles), preferably
Include lean meat, fish, poultry and/or alternatives such as legumes and nuts
Include milks, yoghurts, cheese and/or alternatives
Drink plenty of water
And take care to:
Limit saturated fat and moderate total fat intake
Choose foods low in salt
Limit your alcohol intake if you choose to drink
Consume only moderate amounts of sugars and foods containing added sugars
Prevent weight gain: be physically active and eat according to your energy needs
Care for your food: prepare and store it safely
Encourage and support breast feeding
(A 2004 Melbourne study found that of 10,500 women surveyed, only 2 met all these
5. Physical activity Need to know to estimate energy requirements. Bed rest =
1.2xBMR light activity = 1.3xBMR moderate activity=1.4xBMR heavy
6. Social situation: to evaluate social barriers to good nutrition
7. Medications: to evaluate drug/nutrient interactions
Nutritional screen alerts you to patients at risk of suboptimal nutritional status
Nutritional assessments then done on these patients to define what dietary
intervention is appropriate
Nutritional assessments involve collating information on anthropometry,
biochemistry, clinical data, diet data, social details, physical activity &
This information is compared with standards to determine what goals should
be set to attain the patient‟s optimal nutritional status.
Setting Nutritional Management Goals
Goals should be clear, realistic, achievable and negotiated with patient
Should have a measurable outcome (eg to reduce bodyweight by 5kg over 12
Interventions are how the patient will achieve the nutritional mx goals
Interventions should reflect patient tastes, culture & lifestyle (eg increase fruit
& veg in your diet, change to fat reduced products, increase your fish intake
to 2 meals/week).To help negotiate goals with clients or explain interventions,
there are many educational tools – see below.
Australian Guide to Healthy Eating
Developed 1998 by the Commonwealth Department of Health & Ageing to help
Australians develop the “skills and knowledge necessary to choose a healthy diet”.
12345+ Food & Nutrition Plan
12345+ Food & Nutrition Plan
Developed by CSIRO in 1991
It uses the old pyramid model for a healthy diet
1 serve should come from meat & meat alternatives, 2 serves from milk &
milk products, 3 serves from fruit, 4 serves from vegetables and at least 5
serves from breads and cereals
We are moving from a “nutrient” based approach, towards a “food” based
approach. Food contains about 12000 components beyond nutrients.
These phytochemicals appear to play a role in protecting the body from CVD,
cancer, promote longevity. Therefore it makes sense to have as much variety
Some overseas dietary guidelines are already using this approach eg Japanese
guidelines suggest eating 30 or more different foods each day.
Summary of Australian & International dietary guidelines
1. Include at least 2 varied fish meals/week
2. Include several varied lean red meat meals/week; vegetarians need legumes or
nuts daily with wholegrain cereals to ensure adequate iron and zinc
3. Include lean poultry or pork about once a week
4. Include at least 1-2 varied legume meals/week
5. Include a handful of nuts several times/week, preferably in vegetable dishes
6. Include eggs & egg dishes weekly
7. Include several portions of reduced fat/high calcium milk and milk products or
calcium fortified soy milk/tofu daily
8. Try to have several cups of a variety of vegetables daily, especially onion,
garlic and herbs
9. Try to have 2 pieces of fruit/day
10. Try to have mainly wholegrain, reduced salt cereals (about 5 serves/day)
11. Choose lean meat and reduced fat dairy products
12. Prefer unrefined natural fat in nuts, seeds, soy, olives, avocado as the fat is
accompanied by other phytochemicals
13. Prefer cold pressed monounsaturated oils for cooking
14. Increase water and tea intake, avoid soft drinks and limit juices to 1/day,
alcohol to 2 standard drinks/day
15. Limit indulgences to 2/day
Practice Exam Question
Fiona is a 30-year-old administrative assistant being treated for wrist pain. Fiona‟s
weight is 60kg (slowly increased from 52kg over past 10 years), height is 155cm. No
recent biochemistry/pathology results available. She reports a good appetite, mild
chronic constipation. Lives alone and has a sedentary lifestyle. Her usual diet consists
of 4 slices white toast with butter and jam for breakfast, a packet soup or ham
sandwich for lunch, chocolate biscuits and coffee during the afternoon and for dinner
she has takeaway noodles, pizza or just toasted cheese sandwiches if she has worked
late. Drinks water, cordial or tea (with milk and sugar). Fiona is considering taking a
multivitamin as “insurance.”
1. Do a nutritional assessment. (6 marks)
2. Using this assessment, suggest 3 nutritional goals. (3 marks)
3. Should Fiona be taking a multivitamin as a form of “insurance”? (3 marks)
4. What are 3 interventions to assist with Fiona‟s constipation? (3 marks)
When are supplements needed?
Special Needs Group Supplement
Before Conception Folic Acid (500ug)
During Pregnancy Iron, folic acid, calcium, omega 3 fats
Breastfeeding Calcium, omega 3s, water
Vegans B12, Iron, zinc, calcium, omega 3s
Alcoholics B groups vitamins, especially thiamin and
Elderly Calcium, vitamin D. B12 may be poorly
During illness or surgery Protein, vitamin C
Dietary analysis ( worth 40%)
DUE DATE: 18 March 2008
The aims of this project are
To gain a better understanding of the nutrient content of food
To learn how to follow the recommended nutrient intake for Australians
To appreciate the difficulties associated with dietary change
1. Keep a food diary for 3 days, recording everything that you ate and
drank. Don‟t forget to include the quantity eaten, as well as the item.
2. Download Foodworks from www.xyris.com.au onto your computer
(go to “downloads” on the top menu bar of the home page, choose
“foodworks professional 2007” & follow the instructions – requires
12MB of free space.)
3. Create a new food record in Foodworks. Enter your age, sex, weight,
height, activity status (open “help” menu, choose “terms and
definitions” in content, then choose “physical activity levels
explained”). Record your BMI and estimated energy expenditure. Then
enter day 1‟s intake (under “Foods”). Repeat this with a new day‟s
intake on the same food record.
Set the right hand “analysis” column to “AvgDay” ; with “All
components” listed below that and comment on:
– how close your average kJ intake over 3 days was to your average
“estimated energy expenditure” . If there is a large discrepancy, is this
supported by recent weight loss or gain? Or were there inaccuracies in
the food diary or in estimating energy expenditure?
- which nutrients, if any, were on average consumed below the RDI
(use “NRV - all” option on RHS of page). Remember to allow for any
dietary supplements you take regularly.
- the % energy derived from carbohydrate, fats and protein and the
proportions of saturated, monounsaturated and polyunsaturated fats
eaten. If possible, comment on the glycemic index of your diet.
Note: if you want to look at a single day individually, right mouse
button click on that day‟s foods, choose “select” then choose “day”.
This information can help you write up your results or plan a new
4. Use “Foodworks” to help you plan a daily menu for yourself that
follows the recommended composition of 50-60% carbohydrate, <30%
fat (including <10% saturated fat & <10% polyunsaturated fat), 10-
20% protein, at least 30g fibre & meets all RDIs. (To get the fat ratio
correct, first adjust your diet so total fat is under 30%, then alter the
polyunsaturated/monounsaturated/saturated fat ratios to be 25-33%
polyunsaturated/33-50% monounsaturated/ 25-33% saturated.) Note
you can click on individual nutrients displayed in the right hand side
(eg “saturated fat”) to see which food items are responsible for the
greatest or least amounts of this nutrient in your diet.
5. Submit this menu as the second part of your results.
6. Follow this 1 day diet plan.
Discuss the differences between your usual diet and the “ideal” diet you have planned.
Discuss any difficulties you encountered when changing your diet. What advice
would you give patients to assist them in making changes to their diet?
Week 2: DRUG-NUTRIENT INTERACTIONS & GASTROINTESTINAL
Short term: Acute toxic reactions may occur b/t food & drugs
Long term: Changes in appetite, nutrient absorption, metabolism & nutrient
High risk patient groups for interactions
1.Elderly: Drug-nutrient interactions occur most commonly during long term
treatment of chronic disease, so elderly most vulnerable group. They tend to take
more drugs, absorb nutrients less well, and more likely to have a poor diet.
2. Developing fetus, infants & pregnant women have elevated nutrient requirements
so at greater risk.
3. Malnourished patients are vulnerable to drug-nutrient interactions as protein losses
and changes in body composition alter protein binding and the volume of distribution.
4. Specific nutrient deficiencies can alter the mixed function oxidase system and
hence drug transformation. EG iron deficiency increases activity, magnesium
deficiency decreases activity.
5. High % body fat: obese & elderly have increased distribution of fat soluble drugs as
greater proportion of adipose tissue.
Drugs that affect appetite
Decrease appetite: most drugs of abuse (amphetamines, cocaine, methadone),
Ritalin (may see “catch up growth” when discontinue), cytotoxic agents,
Increase appetite/cause weight gain: see handout
Drugs that affect absorption
Laxatives – can cause steatorrhea & faster transit so losses of calcium &
Aspirin – chronic use damages mucosa & affects iron & calcium absorption
Antacids – raised stomach pH means decreased absorption of calcium, iron,
Colchicine (anti inflam. treats gout) impairs B12 absorption
Neomycin – alters gut mucosa so malabsorption of fat, protein, Na, K, Ca.
Folic acid antagonist: Methotrexate – used in cancer treatment & RA. Folic
acid is displaced from dihydrofolate reductase by methotrexate, so instead
excreted. DNA synthesis inhibited so rapidly dividing cells die
Vitamin B6 antagonists – penicillamine, Ldopa
Vitamin K antagonists – warfarin
Monoamine Oxidase Inhibitors
2 classes of biologically active amine – psychoactive amines (neurotransmitters eg
noradrenalin & dopamine) and vasoactive amines (pressor amines eg tyramine,
serotonin, histamine). This second class present in some foods but usually deactivated
by monoamine and diamine oxidases. However if on monoamine oxidase inhibitors
(some antidepressants) must avoid foods containing these vasoactive amines (mainly
tyramine). They could cause restriction of blood vessels & elevated BP (cheese,
smoked fish, wine, beer, preserved meat, broad beans, meat/yeast extracts).
Phenytoin (anti convulsant) - chronic treatment causes folate depletion hence
OCP – Originally thought that women on pill needed more vitamin B6 but not
generally the case. Some women do have lower serum & rbc levels of folate but
supplementation is not justified. Women coming off the pill with the intention of
getting pregnant should however be very conscious of taking adequate folate
Glucocorticoids: long term can cause osteoporosis in 50% of patients as calcium
absorption is reduced and calcium excretion is increased. Also decreased glucose
Should take lowest possible dose, adequate calcium, vitamin D, physical activity &
Antihypertensives – if on diuretics at risk of K and Mg depletion & calcium & zinc. If
on B- blocker then increased TG and decreased HDL may be seen & glucose
Effect of food on drug absorption & metabolism
Presence of food can reduce therapeutic dose by slowing so reducing absorption.
Stomach & intestinal pH, rate of gastric emptying can influence drug absorption.
Most drugs are absorbed by passive diffusion across the GIT epithelium into the
bloodstream so pH is critical as ionization status of drug must be correct to allow
diffusion to occur. Thus hypochlorhydria in the elderly significant.
High protein diets can accelerate drug metabolism by increasing MFOS activity.
Food or Beverage Drug Effect
Caffeine-containing drinks Theophylline Increased intake may
enhance drug side effects
Grapefruit juice Drugs known to be Excess intake can increase
affected by grapefruit blood levels of drug
include those taken for
anxiety, depression, high
irregular heart rhythms,
high cholesterol and
Bran Digoxin May reduce drug
Food in general propanolol Increases drug absorption
aspirin May decrease absorption
Antimicrobial agents May reduce drug
High protein diet L-dopa Amino acids from diet
inhibit absorption of drug
Licorice Antihypertensive agents & Large amounts tend to
diuretics induce hypokalemia and
Milk & milk products tetracyclin Calcium inhibits drug
Salt lithium Low salt diets may
enhance drug activity, high
salt inhibit activity
Vegetables (onions, warfarin Vitamin K rich foods can
broccoli, lettuce ) inhibit action
Drugs that cause weight gain – see handout
Nutrition & Gastrointestinal Disease
Function of Gastrointestinal Tract
Chewing assists with digestion by breaking foods into smaller pieces. Saliva contains
amylase which begins to breakdown starch. A bolus of food of formed which is
swallowed under voluntary control. Peristalsis moves food into stomach.
storage of food (in upper portion of stomach – up to 1.5L can be stored)
secretion of enzymes (eg pepsin)
secretion of acid. Gastric acid secretion is stimulated by gastrin, which is
triggered by distention of stomach, impulses from vagus nerve (eg sight &
smell of food) or presence of food in stomach.
mixing before release to SI in form of chyme. This allows easier digestion &
absorption in the SI.
Stomach empties in 1- 4 hrs. CHO, protein exit more rapidly than fat, liquids more
rapidly than solids, small particles more quickly than large particles and isotonic food
more quickly than hypertonic foods.
Most of the digestive process is completed in duodenum
Remaining small intestine used for absorption of nutrients
The stomach acidifies the chyme to a pH of about 2. This is neutralized by
secretion of bicarbonate secreted in bile from liver and pancreatic secretions.
The pancreas secretes digestive enzymes directly into the SI as well as
SI surface is covered in villi, which consist of epithelial enterocytes which
The villi capillary blood supply carries the nutrients via the portal vein to the
Some of the pancreatic enzymes:
Enzyme Type Substrate Product
Amylase Starch Maltose
Trypsin Protein Peptides
Chymotrypsin Protein Peptides
Elastase Elastin Peptides
Carboxypeptidase Peptides Amino acids
Aminopeptidase peptides Amino acids
Lipase Triglyderides Fatty acid + 2 monoglycerides
A major portion of nutrients are stored or metabolised in the liver. Sugars are
stored as glycogen, amino acids built into protein or metabolized. Some
vitamins & minerals are stored in liver.
Glucose taken up by many tissues in body eg brain, heart, muscles, kidneys.
Calcium mainly taken up by bone, iron by bone marrow etc.
Carbohydrate Digestion Summary
Site Digestive action
Mouth Alpha amylase begins starch digestion
Stomach Acidification & mixing but no significant breakdown of
Liver-bile secretion Pancreas enzyme secretion
SI Pancreatic amylases:
Starch - maltose
Maltase – maltose to glucose
Sucrase – sucrose to glucose & fructose
Lactase – lactose to glucose & galactose
LI Some fermentation of fibre to SCFA; absorption of Na,
SCFA & water
Summary of protein digestion
Site Digestive action
Stomach HCl & pepsin begin protein digestion
Liver-bile secretion Pancreas-enzyme secretion of inactive protease
SI Activation of pancreatic proteases: trypsin,
Amino/carboxypeptidase: protein to peptides or amino
Peptides to AA
Summary of fat digestion
Site Digestive action
Stomach Gastric lipase: only minor fat digestion
Liver-bile secretion Pancreas-enzyme secretion
SI Bile salts
facilitate emulsification of fat to micelles
Lipase = TG fat to monoglycerides + glycerol + free
Absorbed FFA resynthesised to TG and secreted into
The body‟s ability to digest meals is very adaptable and pancreatic secretions can
easily be altered to suit high protein vs high carbohydrate diets, 6 meals vs 1 meal etc.
Principle function is to extract remaining Na, K, water from chyme that enters
Microorganisms (mainly bacteria) gain their energy by fermenting dietary
fibre (the food residues that cannot be broken down by pancreatic enzymes).
End product of fermentation includes short chain fatty acids (acetic, propionic,
butyric acids). These act as an energy source for colonic epithelial cells and
butyrate may be protective against cancer as promotes differentiation.
Principle causes: neuromuscular disorders (eg CVA, head injury, Parkinson‟s disease,
multiple sclerosis); physical obstruction (stricture), infection
Stages of dysphagia
1. Some swallow reflex:
Thickened liquid diet, pureed diet, minced diet or soft diet required depending on
strength of swallow & cough reflex.
2. No swallow reflex:
Nil orally, enterally fed
Swallow status determined by speech pathologist
Symptoms of dysphagia:
Marked slowness in eating, fatigue/drooling during meals, frequently clearing throat,
complaint of food sticking in throat, unexplained respiratory symptoms/infections
Nutritional consequences of dysphagia:
1. Weight loss. Due to reduced food intake (fatigue during meal) or nutrient
2. Constipation. Due to reduced fibre intake
3. Dehydration. Reduced intake of thickened fluids
1. Oesophageal neuromuscular disorders affecting LES pressure
2. Abdominal obesity/pregnancy increasing back pressure in stomach
3. Excessive consumption of foods which lower LES pressure (fat, alcohol,
4. Smoking lowers LES pressure
1. Weight reduction (if obese)
2. Avoidance of large meals
3. Avoidance of food or drink 3 hours before bed
4. Avoidance of poorly tolerated foods by individual (fatty foods, acid foods,
very hot/cold foods)
5. Avoidance of bending, stooping after eating and eating upright. Elevation of
bed head by 15cm/use of pillows
Gastric & Duodenal Ulcer
Symptoms include severe abdominal discomfort (related to meals), vomiting,
heartburn, nausea, weight loss.
Reduction of mucosal resistance to stomach acid through Helicobacter pylori
infection primary cause.
1. Avoid foods that cause pain and discomfort (eg alcohol, spicy food, excess
2. Avoid large meals & chew well to minimize stomach distension
3. Avoid fried foods if pain is acute.
Irritable Bowel Syndrome
Medically defined as abdominal discomfort or pain (>12 weeks) in past 12 months:
Relief with defecation &/or
Change in frequency of stools
Change in appearance of stools
Abnormal stool frequency or form
Straining passage of mucus
Very prevalent condition (15% of Australians, 75% of patients female)
Must be diagnosed by symptoms
Can be triggered by abnormal intestinal motility, inflammation/post
infection, brain-gut interactions, stress
Reassurance, dietary change and stress management can help
Common food triggers:
Wheat, Fructose…avoid apple, pear, honey, fruit juice (eg juice bars), dried fruit.
Lactose (due to lactose intolerance), Polyols (sensitive to laxative effect)…avoid
sugar free gums and lollies, Fat (enhanced gastrocolonic response), Caffeine
(stimulates colonic motor activity)…avoid caffeine
Common condition predominantly occurring in the sigmoid colon. Small pouch-
like protrusions develop in the bowel wall. Occurs in about 30% of over-65‟s.
Cause unknown, linked to diets low in fibre hence increased bowel pressure.
More common in meat eaters. Inflammation = diverticulitis.
1. Softening of stools to allow easier expulsion. Diets high in wheat fibre best.
Wheat bran needs to be introduced slowly to prevent abdominal gas.
2. Adequate fluid (>2L/day) & exercise will assist.
3. Chew food well and avoid nuts, seeds, spices during acute attacks.
Lining of intestine is damaged by gluten (an immune reaction causes inflammation &
villous atrophy). Gluten is in wheat, oats, rye, barley.
Adult clinical symptoms – diarrhoea, anemia, weight loss, fatigue, abdominal
discomfort. Less common – infertility, dermatitis herpetiformis, bone & joint pains.
Child clinical symptoms – bulky, foul stools; diarrhoea or constipation; poor weight
gain; anemia; retarded growth; abdominal discomfort.
Diagnosed only by duodenal biopsy, followed by histological improvement 6 months
after gluten withdrawal.
Gluten found in many products containing derivatives of wheat, oats, rye & barley.
Nutrition assessment checklist:
Usual nutritional assessment PLUS
Has patient had diagnosis confirmed by small bowel biopsy?
Symptoms & weight loss?
Biochem of Fe, Folate, B12 done?
Diet history – esp iron, calcium, fibre
Lactose intolerance present/suspected?
Fat intolerance present/suspected?
Nutritional Intervention Checklist:
Patient understands disease & its effects
Strict gluten free diet for life
Educated re: food labels (gluten in wheat & barley derivatives eg malt extract,
yeast extract, starches, thickeners, maltodextrin)
Nutritionally adequate diet
?Need for micronutrient supplements
?Bone densitometry test
Medications checked for gluten
Joined Coeliac Society
Relatives screened (10% +ve)
Inflammatory Bowel Disease: Crohn‟s disease & Ulcerative Colitis
IBD can affect people at any age, most common age group is 15 to 30 years. About
23,000 Australians affected.
Characterised by periods of active flare ups followed by remission.
UC = Inflammation of the mucuous membrane or superficial lining of the large
Crohn‟s = Inflammation of the full thickness of the intestinal wall, can involve any
part of the GIT.
In active flare ups:
Individual treatment plans may include high energy/protein supplements drinks to
meet increased nutrient needs and replace lost protein.
Low residue diets may be recommended if the flare up affects the large bowel or
terminal ileum, to help reduce irritation to the bowel. Breads and cereals may be
limited to white bread, white rice, pasta, cornflakes and vegetables to potatoes,
Enteral (tube) feeding using elemental formulae may also be used to rest the bowel
and produce remission.
Eat a well balanced diet and aim to replace nutrients lost during previous flare ups.
Exclusion of whole food groups is not recommended unless under medical advice.
Prebiotics and probiotics may help improve the health of the gut to maintain
remission. They stimulate the growth/activity of bacteria in the bowel which produce
short chain fatty acids, which are important for maintaining colonocyte integrity. This
is an area undergoing further research.
Fish oil seems to have an anti inflammatory effect in IBD (some trials have shown it
helps achieve and maintain remission; the Japanese have a high intake of fish and low
rates of IBD). Amounts used in clinical trials were 6-10 fish oil tablets (2-3gm of
EPA/DHA) a day. Having oily fish regularly should also be of benefit.
Drug-nutrient interactions may mean vitamin or mineral supplements are needed eg
folic acid, vitamin D, calcium.
John is a 45-year-old administrative assistant being treated for wrist pain. His weight
is 100kg, waist circumference is 120cm, height is 180cm. No recent
biochemistry/pathology results available. He reports having symptoms of gastro-
oesophageal reflux most days. Lives alone and has a sedentary lifestyle. His usual diet
consists of 6 slices white toast with butter and jam for breakfast, 4 cheese or ham
sandwiches for lunch, several chocolate biscuits during the afternoon and for dinner
he has takeaway noodles, pizza or fish and chips. Has recently switched to diet soft
drinks as his main beverage.
1. Do a nutritional assessment. (6 marks)
2. What are 3 common causes of gastro-oesophageal reflux? (3 marks)
3. What are 6 lifestyle interventions that could assist with management of John‟s
reflux? (6 marks)
Herbs and Herbal Supplements
Herbs & Safety
1. Take herbs only for minor illness. If taken in conjuction with other
medication, inform your GP.
2. Buy reputable brands with guaranteed concentrations of active ingredients
3. Be aware contaminants (eg pesticide residue) may be present
4. Remember side effects can still occur (natural does not equal safe)
5. Don‟t take herbs if pregnant or breastfeeding
6. Get advice from a qualified herbalist
Weight for weight, herbs and spices generally contain more antioxidants than fruits
and vegetables. This may help them protect us from cardiovascular disease and
cancer. They also add variety and flavour without extra salt or fat.
Used for nausea & morning sickness. Shown more effective than standard anti nausea
drugs in some studies, no effect in others. Safe & may be effective. A small trial
found it modestly effective in arthritic knee pain relief (Osteoarthritis Cartilage 2000;
Evening Primrose oil
Used for PMS. Some studies support its use, but final proof is lacking. Check quantity
of GLA per tablet as each brand varies – more is better. It increases clotting time so
avoid if taking an anticoagulant.
Promoted as immune booster and has been shown to stimulate activation of T cells
hence stimulating immune system action. It does have anti viral and anti bacterial
properties. Should not be taken for long periods due to its effect on the immune
Can slow growth of bacteria, yeasts, fungi so act as broad spectrum antibiotic. Only
fresh garlic, not supplements, act in this way. Consuming 1 clove/day may reduce
total cholesterol by 9% (JAMA 1994; 271:1660-61). It may reduce blood pressure
slightly and lower clotting (J Hypertens 1994; 12:463) Garlic also contains a variety
of antioxidants. Again fresh garlic best choice, or buy a supplement high in allicin &
avoid odourless garlic tablets as they are ineffective.
Appears to have a wide range of effects (stimulant, immune booster, BP normaliser)
but most studies done in animals. Buy only from a reputable herbalist & expect to pay
for high quality ginseng. 4 recent studies of ginseng supplements suggest it may
reduce glycemia but bigger trials on diabetics needed (Diabetes Care 2004; 27:839)
Ref: Saxelby “Nutrition for life” 2002 Hardie Grant Books, Victoria
1. Why is it important to monitor drug/nutrient interactions?
2. What drug/nutrient interactions would you be concerned about if a patient was
3. Which drug/nutrient interaction would you be concerned about if a patient was
4. What advice would you give a woman who has been on the OCP about to try
to become pregnant ?
5. Which nutrient does warfarin interact with?
6. What dietary restrictions are necessary if taking monoamine oxidase inhibitors
7. What are the 4 major functions of the stomach?
8. What are the 3 main classes of pancreatic exocrine enzymes?
9. What are 3 nutritional consequences of dysphagia?
10. Which lifestyle interventions are appropriate for managing irritable bowel
11. Which 2 sugars do IBS clients sometimes malabsorb?
12. What are the 4 main classes of grain that a person with Coeliac disease must
13. What are 3 co-morbidities associated with untreated or poorly managed
Week 3: ENERGY
The energy equation: energy in = energy out
1. ENERGY IN
Fuels for energy
The body can oxidise carbohydrate, protein, fat or alcohol for energy production.
C6H12O6 + O2 = H2O + CO2 + Energy
Energy + ADP + Pi = ATP. ATP is used to provide energy to contract a muscle.
The amount of energy available to the body from a food can be calculated by igniting
the sample of food inside a bomb calorimeter and measuring the heat released. In
reality digestion & absorption are not 100% efficient processes (some nutrients are
lost in the faeces). This is especially true for bulky vegetarian diets which are less
accessible to digestive enzymes.
Taking these losses into account the following energy values are accepted:
Macronutrient Net energy
carbohydrate 16 kJ/g
fat 37 kJ/g
protein 17 kJ/g
alcohol 27 kJ/g
water 0 kJ/g
Fat is the most energy dense nutrient, followed by alcohol, so generally
recommended reducing fat and alcohol in the diet to lose weight - can eat twice as
much CHO than fat and still eat the same number of kJ!
The fat content and the water content have the largest impact on the kJ content of any
A knowledge of macronutrient net energy values & a knowledge of the macronutrient
composition of foods allows you to calculate your daily energy intake.
EG 100g milk = 3g protein, 4g fat, 9g CHO, 84g water = 200kJ
Easy in theory, hard in practice as if you weigh your food to record what you are
eating, you will probably alter your usual intake. If you recall what you ate instead
this is less accurate.
2. ENERGY OUT
There are 3 components of energy expenditure: the resting metabolic rate, the
thermogenic effect of food and physical activity.
Resting Metabolic Rate (RMR)
When measured after at least 8 hours rest & 10 hours since last meal, this is called the
basal metabolic rate, otherwise it is the RMR – the energy needed for the mechanical
processes to sustain life (respiration, circulation etc).
Nervous tissue generally responsible for about half of the RMR, the liver consumes
29% as it metabolises nutrients, muscles at rest about 20%.
Determinants of BMR:
Body size: larger people have more metabolising tissues so a higher BMR
Sex: Females are smaller so have a lower BMR than males
Bodyfat: Fat tissue has a lower metabolic rate as it is primarily a storage tissue, unlike
muscle which is an active tissue
Hormonal & nervous controls: metabolic rate is influenced by hormones eg
thyroxine, adrenalin, growth hormone & insulin can also influence metabolic rate.
Infection or illness: severe infection, illness or injury increases BMR so sick are more
prone to weight loss.
Fasting Reduces BMR by 15%.
Drugs: Caffeine, nicotine will raise metabolic rate about 10%
Menstrual cycle: BMR is highest just before menstruation, and lowest 1 week before
ovulation. Average of extra 630kJ/day required in second half of cycle
Pregnancy: BMR increased by increased cardiac work & growth
Growth: children have a higher BMR as have a greater surface area in relation to
volume so lose heat more rapidly, so BMR set higher to maintain heat. Also must
meet demands of growth. After maturity our BMR falls about 10% each year partly
due to loss of muscle mass.
Thermogenic effect of food (TEF)
Metabolic rate rises after eating, due to the additional energy expended in peristalsis,
synthesis & secretion of digestive acids, active transport of nutrients into cells,
excretory processes. Proteins cause the greatest rise and fats the least. Thermogenic
effect of food adds 10% to total energy expenditure (unless diet is high in protein,
which adds 15% to total energy expenditure).
Energy Expenditure in Physical Activity
Component of energy expenditure that varies the most between individuals (eg energy
expended at rest is about 1.2 x BMR; heavy activity is about 5 x BMR). Energy
expended will vary according to body size and fitness level.
Calculating total energy expenditure via Schofield Equation
Step 1. Calculate BMR:
Males 10-18 years = 0.074 x weight +2.754
18-30 years = 0.063 x weight + 2.896
30-60 years = 0.048 x weight +3.653
over 60 = 0.049 x weight +2.459
Females 10-18 years = 0.056 x weight +2.898
18-30 years = 0.062 x weight +2.036
30-60 years = 0.034 x weight + 3.538
over 60 = 0.038 x weight +2.755
Answer is in MJ/day. Gives an estimate of BMR that is reasonably accurate for 2/3 of
Step 2. Multiple BMR by appropriate activity factor (1.2 = bedrest, 1.5 = light, 2.0 =
heavy activity) to get estimate of energy expenditure (MJ/day).
Calculate energy intake by nutrient composition consumed
Calculate total energy expenditure by estimating BMR and multiple by
average activity factor. This should equal total energy eaten if weight is stable.
Faecal energy losses
Net energy value
Energy used to maintain BMR
Energy used for activity
Energy used for production of maternal
Retained energy (energy stored as fat, glycogen, used to build protein)
3. ENERGY BALANCE
Mechanisms governing energy intake to match energy expenditure are
complex and not fully understood
Yet we are able (without conscious effort) to maintain our weight over long
periods of time.
Energy intake is influenced by appetite and satiety. Appetite stimulates us to
begin eating, satiety signals we have consumed enough.
Short term control of appetite & satiety signals appears to be via the vagus nerve and
several hormones. Presence of protein or especially fat in the intestine stimulates
cholecystokinin release, which acts as a satiety hormone via its receptor. Stretching
the stomach beyond 400ml also appears to stimulate release of satiety hormones in the
gut which act on the hypothalamus to decrease appetite.
Long term control of our energy intake also exists, as demonstrated by the many
people who lose large amounts of weight then gradually regain the weight to return to
their original weight.
Leptin is one of the hormones though to influence long term energy intake. It is
produced by adipocytes. As adipocytes grow larger they produce more leptin, which
acts on the hypothalamus to suppress appetite. Deficiencies in leptin production or
leptin receptors can result in morbid obesity.
4. ENERGY IMBALANCE: OVERWEIGHT & OBESITY
Key features of overweight & obesity:
It is a complex, multifactorial, chronic disease
It has genetic and environmental components
It is linked to substantial co-morbidity
It requires long term management
Prevalence of overweight/obesity in Australia
Australians are getting larger
By 50, approximately 75% of Australian males and 60% of Australian females
are overweight or obese
Rates of obesity doubled 1980 – 1995
35% of Australian report gaining weight in past 12 months
Australian gaining 1gm/day per person on average.
Obesity increasing worldwide
“ there is an escalating epidemic of excess weight gain and obesity…affecting all
ages…in all regions of the world” (WHO, 1997)
Defining overweight and obesity
Occurs when energy intake exceeds energy expenditure over a sustained
period of time
Energy is dynamically balanced in free living organisms
Can use Body Mass Index
Body Mass Index (BMI)
Bodyweight doesn‟t give an indication of body composition
BMI devised in an attempt to related weight to height
BMI = Weight/Height 2 (kg/m2)
BMI gives an indirect measure of adiposity
Is not relevant for the extremely muscular or children
Underweight BMI <18.5
Note: These BMI measures are not suitable for Aboriginal and Torres Strait Islander
peoples, whose healthy BMI range may be lower than that for Australians of
European descent. This is due to their ancestry as traditional hunter-gatherers who
were lean and physically fit. Similarly, for Asian people cut-off points for health risks
appear to be lower than for other Australians. Overweight range = 26-31.0; obese
range = >32 for Maori and Pacific Islanders.
Measures the fat distribution pattern of the individual
Central adiposity is associated with an increased risk for CVD and NIDDM
WHR= waist (cm)/hip (cm)
WHR > 1.0 in men and >0.85 in women = increased health risk
Indicator of health risk
Optimal for men of European descent = > 94cm, higher risk > 102cm
Optimal for women of European descent = > 80cm, higher risk> 88cm
These targets may be 10cm lower in Asian and Indian populations
For women, hip size is an independent predictor of good health – bigger is
Bodyweight, morbidity and mortality
Obesity & mortality
Impact on health influenced by
Extent of obesity
Location of the body fat
The magnitude of weight gain during adulthood
Wt gain in early adulthood
Obesity often occurs with smoking, excess alcohol consumption, hypertension and
insulin resistance so is it an independent risk factor for mortality?
Obesity & morbidity
Associated with NIDDM, CHD, hypertension, gall bladder disease, certain cancers,
osteoarthritis, psychosocial disturbances. Most improve with weight loss.
Obesity & NIDDM
Strongly linked in all populations studied
Risk of NIDDM increases as BMI increases
Nurses study – obese 40 x increased risk of NIDDM
Components of obesity most associated with development of NIDDM are obesity
during childhood and adolescence, progressive weight gain from 18 years and
Obesity & Osteoarthritis
Mechanical stress, metabolic changes or diet causative?
Obesity & CHD
Moderate risk factor eg Framingham study
Found occurrence and death from CHD predicted by amount of
overweight at study entry
Link independent of age, cholesterol, smoking, BP and glucose tolerance
Obesity & Psychosocial problems
Complete fewer yrs schooling
Less likely to enter prestigious professions, reduced income
Obesity & Children
Poor parental knowledge of nutrition
Using food as reward or a substitute for attention
Grandparents are often guilty
Families eat together less often
Lack of physical activity also impacts –less walking, more sedentary
(MJA 2006 184:64) Watching more than 2 hours/day of TV assoc. with 1
or more serves/day of high energy drinks; 1 or more serves/day or high
energy snacks; less than 2 serves/day of fruit; less likely to do organized
Obese children have a 25-50% chance of becoming obese adults, and suffer
social discrimination, poor self esteem, depression
Weight maintenance is encouraged
All the family to change their pattern of eating and activity
Foods high in nutrients but low in energy encouraged
The family needs to become more active together.
Children are more likely to eat healthy meals if
* they have been involved in the preparation of the meal eg shopping
* helped with the cooking
* they are allowed to serve themselves
* presentation is VERY important, as is the influence of peers
A healthy child will not let themselves starve
Parental responsibility to provide a nutritious meal, but it is the child‟s
responsibility to eat it.
Limit meal times to 20 minutes
New foods need to be introduced to children up to 10 times
Aetiology of Obesity
Weight loss is difficult
Body opposes changes in weight
Initial weight loss is rapid because
1. Water is lost with glycogen
2. Dieters are more rigid
3. Metabolism has not slowed
Diet don‟t work for 3 major reasons:
Weight loss causes the metabolic rate to fall (as lean tissue is also lost)
Weight loss causes hunger & appetite to increase
Weight loss causes fat to be preferentially stored not burned
Result: weight loss very rarely continues beyond 4 or 6 months. Weight then
regained at same rate it was lost as body fights to return to its natural
Most commercial weight loss programs “weight cycle” people. Their failure
rate is about 95%.
Weight cycling is more dangerous to health than being obese but at a stable
weight (eg Framingham study, American Journal of Epidemiology
Weight loss is associated with higher overall mortality (Framingham, MRFIT,
Harvard Alumni). Could be because of the loss of organ, muscle and bone
Factors influencing body fat levels
Things that can be changed: Things that can’t be changed:
Food: fat/sugar/alcohol Genes
Drink: soft drinks/fruit juice Age
Movement: work/leisure/recreation Gender
Age & sex
Australians gain weight as they age (25–40 M, 50+ F)
Men more likely to become overweight
Women more likely to become obese
several genes involved evidence: lean parent/child , twin studies
weight gain has a genetic basis 25-70% of bw determined genetically.
Recent increase cannot be due to genetic change – environment is allowing us
to meet our genetic tendency to obesity
Test your genes (by Garry Egger)
1. Were either or both parents obese (BMI >30) or very obese (BMI>40) for most
of their lives?
Obese Very Obese
No 0 0
Yes, 1 parent 7 14
Yes, both parents 14 28
2. Do you have any first degree relatives who have been obese for most of their
Score 2 points for every immediate family member up to a maximum of 10 points.
3. How would you describe the average BMI of your siblings?
Not obese=0; obese= 6; very obese= 12
4. When did you first become overweight or obese?
Never 0 0
Before age 10 20 30
Before age 20 10 20
Before age 30 5 10
<20 = Your weight problem is not significantly genetically related, so means lifestyle
is the main cause which is relatively easy to address.
20-50 = Moderate hereditary component to your weight problem, which makes it
slightly harder to lose weight.
30-100 = Significant hereditary component to your weight problem, so close attention
from a dietitian is needed with a long term plan to get results.
Focus on kJ to lose weight
Fat stores come mainly from dietary fat (CHO not converted to fat)
Fat = 37kJ/gm, costs 3-5% of this to store it
CHO =17 kJ/gm, costs 25% of this to store it
Body prefers to burn CHO and to store fat
Fat is slow to produce satiety
Fat is a flavour carrier
Decreasing fat intake may be effective ( kJ) & achievable ( more acceptable
Nutrition knowledge and education
No link for females
Some link for males
Men prefer group wt loss programs BUT alcohol must be allowed!
Not solely to blame as sedentary lifestyle is norm
Less opportunities for activity today
TV & childhood obesity link? (displaces activity, reduces metabolism and
50% of Australians do no activity for health
Higher weight gain in pregnancy, gaining more weight early in pregnancy & stopping
smoking increases risk of obesity .Women retain 86% of weight gained in first 20
weeks (Int J Ob 1996;20:526-32)
Major source of energy in the diet (27kJ/g).
Alcoholic drinks also high in sugar, further increasing kJ
Body burns alcohol & spares fat for storage
Alcohol promotes abdominal fat deposition
Fat cell metabolism
LPL promotes fat storage in adipose and muscle cells.
More active in breast, hips, thighs in women, abdomen in men.
LPL activity increases after weight loss, most dramatically in those heaviest prior to
Energy expenditure also decreases, which promotes weight regain.
Management of obesity
Long term weight loss requires a combination of behavioral changes, activity changes
and diet changes
1. Change negative feelings, particularly depression & anxiety
2. Focus on overcoming the pressure of social situations, such as traveling and
3. Self monitor your behaviour to see what triggers overeating
4. Increase your internal motivation
5. Build a network of social support
6. Carry out regular physical activity
7. Set goals at very gradual increments
8. Set realistic goals
1. Don‟t confuse using exercise to increase fitness with exercise for fat loss. To
increase fitness high intensity exercise 3-4 times/week is needed; to lose fat
physical movement everyday is required.
2. All movement contributes to energy expenditure! Aim to walk for at least 30
minutes. It is the distance you cover that is important for weight loss, not
whether you ran or walked that distance.
3. Irregular exercise classes will do little to contribute to fat loss, especially if
you relax more than usual after the class.
4. Physical activity needs to increase as weight comes off, to counteract the
slowing in metabolism or weight loss will not be maintained. Either type,
duration or intensity need to change as weight is lost to continue weight loss.
5. Swimming is not as effective for weight loss as other weight bearing activity.
6. Exercise before breakfast as you blood sugar & glycogen stores are lowest, so
a greater proportion of fat is accessed for the fuel mix.
7. Don‟t eat immediately after exercise so circulating blood fats can be used by
muscles and not returned to adipose cells.
8. Spot reduction of fat does not work as fat is mobilised from all over the body.
Step 1: Decrease fat & increase fibre Increase variety
Increase the proportion of protein
Step 2: Decrease glycemic index & energy density
Step 3: Decrease portion size
If this doesn‟t work:
Step 4:Reduce alcohol and
Step 5:Measure kJs in food and reduce total intake by 2100kJ/day
You are helping with a health promotion project at the local primary school. The
project aims to address childhood obesity, by introducing nutrition into its
curriculum and revamping the canteen. The canteen used to offer a range of pies,
sausage rolls, vegemite or cheese sandwiches, fruit juice drinks, muesli bars, fruit
roll ups and savoury biscuits. It is now introducing some salads, fruit and healthy
wraps. It is also adding an extra hour per week of physical education into the
2a) What is the percentage of Australian children estimated to be overweight or
obese? (1 mark)
2b) Why is important to prevent or treat childhood obesity? (4 marks)
2c) Comment on the canteen‟s old menu in relation to childhood obesity (4
2d) How could you encourage the children to try the new canteen items? (2
Dieting Aids (Ref Saxelby Nutrition for life)
Sold as powders, granules or tablets, made from psyllium, cellulose, guar gum or
citrus fibre. Taken with water before a meal to swell in the stomach and create a
feeling of satiety. Can be helpful if people have trouble stopping eating when full.
Not so good for binge eaters. Cheaper, healthier option is increase fruit and
vegetable content of meals.
Chitin or Chitosan
Chitin is found in the shells of crustaceans. Sold as a “fat binder” which “soaks up
dietary fat” and then excretes it in the stool. It does attract fat in the stomach
through its ionic charge, so works in theory. In practice 1 teaspoon binds 8g of fat,
which won‟t make a lot of difference to the typical 70-100g/fat eaten each day.
Therefore a low fat diet essential to see any results. Avoid if allergic to shellfish.
Regarded as a ”slimming” food, but has no special slimming powers.
Sweetner Used in Comments
Saccharin Tablets for tea, coffee Unpopular as potentially
linked to cancer but
Cyclamate Tablets for tea, coffee Banned in USA as very
large doses in rats cause
Aspartame (Nutrasweet, Diet soft drinks, gum Not suitable for
Acesulfame-K (Sunnette) Diet yoghurt Long term safety
Flavoured milk established
Sucralose (Splenda) Sugar substitute Non toxic, non
other sweetners can be
used in cooking
Sorbitol/Xylitol/Mannitol Used in sugar free lollies Laxative in high doses
Claimed to lowers blood sugar & insulin levels, so prevents fat storage.
Chromium needed for metabolism of CHO, protein, fat & helps insulin in glucose
transport. Picolinate said to increase chromium absorption. No proof it works.
Chinese Slimming teas
Generally contain diuretics or laxatives, hence their “slimming” ability!
Ephedra/Ma Huang & Guarana
Herbal extracts that “eliminate wastes and toxins” so “trapped cellulite can be
released” or digestive system cleansed are very popular. Ephedra used in Chinese
medicine for asthma, but also sold for weight loss. Can increase BP and heart rate
so dangerous if have heart disease, diabetes, HT. Guarana also sold as a weight
loss aid as increases metabolic rate – also dangerous if have high BP or heart
disease, or pregnant.
Increases metabolism & mobilizes free fatty acids to increase fat burning
Increases metabolism through the action of capsaicin
Claimed to prevent the conversion of carbohydrate to fat in the body, however this
does not occur in the body under normal circumstances. Claimed to reduce
Reading Food Labels
What’s low in fat?
Aim for <3g fat/100g serve on nutrition information panel
Look for Skim
“lite” can mean the food is low in fat, low sugar, low salt or light in colour (eg olive
oil) so has little meaning.
“low cholesterol” does not mean low fat! Eg vegetable oils have no cholesterol but
are high in fat
“Baked NOT fried” does not mean there is less fat than the same product in the fried
Foods labeled creamed, toasted or roasted will generally be high fat foods
What’s low in sugar?
Look for low calorie
“Unsweetened” or “no added sugar” foods can still contain naturally occurring sugar.
Sugar can be listed as sugar, maltose, lactose, sucrose, fructose, glucose, dextrose,
syrup, honey, fruit juice concentrate
“Carbohydrate modified” products still often high in fat
What’s low in salt?
Look for No added salt
What’s high in fibre?
Ingredient list: Ingredients are listed in order of quantity. If fat is one of the first 3
ingredients the food is not a good choice. Fat can appear as vegetable oil, copha,
coconut, shortening, cream, lard, dripping, mono or diglycerides.
Some examples of what to look for:
Cereal: Sugar: <30g per 100g serve
Fibre: > 10g per 100g serve
Sodium:< 300mg per 100g serve
Dry biscuits: Fat:<10g per 100g serve
Fibre: >7g per 100g serve
When trying to lose weight, aim to keep meals to less than 1200kJ, snacks less than
600kJ. Energy dense products contain more than 1000kJ per 100gm so should be
consumed with caution!
1. With weight loss, fat cells:
a. decrese in size only
b. decrease in number only
c. decrease in both number and size
d. decrease in number, but increase in size
2. Obesity is caused by:
c. defective genes
d. multiple factors
3. The biggest problem associated with use of drugs in treating obesity is
b. chronic dosage
d. adverse side effects
4. A realistic weight loss goal is to reduce body weight to
a. Your weight at 25
b. BMI in 20-25 range
c. By 10% over 6 months
d. By 15& over 3 months
5. Successweight loss depends on
a. avoiding fat and increasing water intake
b. taking supplements and drinking 8 glasses/day
c. increasing protein and reducing carbs
d. reducing kJ intake and increasing physical activity
1. A male athlete is 25 years old and weight 85kg. What is his estimated energy
requirement (assume he averages light activity) ?
2. A training diet should consist of at least 60% carbohydrate. If his energy
intake is equal to his energy expenditure, how many gm of CHO does he
3. What is a bomb calorimeter used for/?
4. Which nutrients contribute the most energy to our diet?
5. What are some of the determinants of our BMR?
6. How much of our total energy expenditure is taken up by the process of
digestion & absorption?
7. Which hormone regulates our weight in the long term?
8. What % of the Aus population is obese?
9. How much weight is the average Australian gaining per person per day?
10. Which aspects of obesity are linked with increased mortality?
11. What are some comorbidities linked to obesity?
12. Which are the danger ages for weight gain in males and females?
13. Why is dietary fat thought responsible for most weight gain?
14. Why are low birthweight babies thought to be at higher risk of obesity?
15. Why do most people lose weight quickly when they first start a diet?
Week 4: LIPIDS
Simple lipids include fatty acids and their esters with glycerol (triglycerides or
Straight chain hydrocarbons containing a methyl group at one end and a carboxyl on
Most fatty acids consumed by us have 4- 22 carbons; 16 and 18 carbon chains are the
Fatty acids are classified by:
no. of carbons
the position of the 1 st double bond (counting from methyl end the 1 st double
bond is termed “”or “n”)
the number of double bonds.
EG Linoleic acid is C18:2 n-6 (or C18:2
Saturated fatty acids (SFAs)
No double bonds in the carbon backbone. Prevalent in meat, dairy and palm &
coconut oils. In general the more saturated an oil is, the firmer it is at room
Monounsaturated fatty acids (MUFAs)
Only 1 double bond. Oleic acid (found in high levels in olive oil) is the most prevalent
in food. Canola, avocado, peanuts & almonds are rich in monounsaturated fatty acids.
Polyunsaturated fatty acids (PUFAs)
Contain 2 or more double bonds. Most prevalent PUFA in diet is linoleic acid – found
in vegetable seed oils.
PUFAs are especially vulnerable to rancidity as O 2 attacks the double bonds to form
peroxides, which produce off flavours and smells. Vitamin E protects against
rancidity as it is preferentially oxidised. Most foods high in PUFAs are also high in
vitamin E. Manufacturers protect high fat foods from O 2 as much as possible, eg
adding antioxidants or packing in N2 .
There are 2 families of PUFAs – omega 3 (n-3) and omega 6 (n-6). They are not
interconvertible and have very different roles in the body.
Essential fatty acids (EFAs)
Linoleic acid (n-6) and alpha linolenic acid (n-3) cannot be synthesised by the
body so must be provided by diet.
They are precursors for other fatty acids and give rise to different classes of
eicosanoids (prostaglandins, thromboxanes, leukotrienes) which are hormone
like compounds that assist in the regulation of BP, heart rate, vascular dilation,
blood clotting, immune response & lipid metabolism.
Deficiency of linoleic acid=dermatitis, poor growth in infants. Deficiency of
alpha linolenic acid = neurological symptoms, learning & vision problems.
Long chain omega 3s are EPA are DHA, and these are most important for
maintaining good health. These are found in oily fish.
ALA is another omega 3 fat which is found in some plant foods eg flaxseed
ALA can be converted into EPA and DHA in the body but a high intake of
omega 6s will suppress this conversion. A typical western diet with a lot of
fried and processed foods will be very high in omega 6s.
Omega 6 fatty acids: Omega 3 fatty acids:
Linoleic acid Alpha linolenic acid
Sunflower oil, safflower oil, Green leafy veg, broccoli, legumes
vegetable & seed oils
Gamma linoleic acid Eicosapentaenoic acid
Early brain development? Fish oils
linolenic acid primrose
oil, blackcurrant seed oil
Retinal function, brain dev
Early brain dev; dermatitis
Prostanoid 2 series Prostanoid 1 series Prostanoid 3 series
Pro-aggregation, Anti-aggregatory, vasodilator
Trans fatty acids
In nature most unsaturated double bonds are in the cis form. In processing liquid oils
are hydrogenated to solidify them which produces trans fatty acids. Margarines and
high fat baked goods can have trans fatty acids; check label of margarines for
“contains virtually no trans fatty acids”
2 reasons why undesirable:
1. Inhibit conversion of linoleic and linolenic fatty acids to other EFAs so fetal
development in the pregnant woman make be compromised
2. Increase serum cholesterol levels
Used by manufacturers as extends the shelf life, since trans fat is more stable.
Contain 1 molecule of glycerol and 3 fatty acids. Because of their high energy density
are the major storage form of energy in the body (yield 2.5 x more ATP post
oxidation than glycogen). Also has structural, protective and insulating roles in the
body, and required for absorption & transport of fat soluble vitamins.
H C OOC R1
H C OOC R2
H C OOC R3
Medium Chain Triglycerides
Synthetic lipids that are digested in the GIT then absorbed directly into the portal
bloodstream, unlike other fatty acids which enter the lymph. Used clinically for
patients that are malabsorbing fat.
Essential component of structural membrane of cells, esp brain and nerve cells.
Required for synthesis of bile acids and steroids. Only found in animal foods. Can be
synthesised by the body. Precursor of vitamin D.
Plant sterols (phytosterols) resemble cholesterol, hence interfere with absorption of
cholesterol from the intestine.
Phospholipids – 2 fatty acids linked by a phosphorous containing substance.
All cell membranes consist of an impermeable bilayer of phospholipids which allows
proteins to move within it and accommodates exocytosis, endocytosis. Its degree of
fluidity is dependent on the length and degree of saturation of the fatty acids in the
bilayer (longer, more saturated fatty acids = less fluid & permeable membrane). The
fatty acid composition of the bilayer is a direct reflection of dietary fatty acids. Hence
the function of the bilayer is affected by diet.
Proteins within the bilayer need it to be flexible to allow them to function properly, eg
to allow substrate docking into a receptor or to endocytose. EG insulin resistance in
animals can be engineered by feeding them a highly saturated fatty acid diet, which
prevents the insulin receptor functioning normally. This is probably the underlying
mechanism of insulin resistance in humans.
Type of phospholipid. Assists with the transport & utilisation of cholesterol, but can
be synthesised by the body so supplements are unnecessary.
Fat substitutes contain fatty acids with chemical bonds that cannot be digested by the
body eg Olestra. Fat mimetics are starch, cellulose or protein based compounds that
have the same mouthfeel as fat but fewer kJ.
Lipid Transport & Storage
Dietary lipids are absorbed into the lymphatic system, and carried in the lymph as
chylomicrons (large particles of TG, cholesterol & phospholipids). Chylomicrons
enter the plasma, and encounter lipoprotein lipase on the endothelial cells lining the
capillaries. The TGs are cleaved to free fatty acids & glycerol, which enter the cell
and are re-esterified to TGs.
Most tissues can use FFA for energy (not brain, blood cells, skin). Glycerol is
oxidised for energy in the liver. The liver is responsible for regulating lipid levels in
the body. It synthesises TG from fatty acids, CHO or protein, it synthesises
cholesterol & phospholipids, it catabolises TG for energy production.
If fatty acids are needed for energy then TGs in the adipose tissue ares hydrolysed to
FFA and glycerol. FFA is bound to albumin for transport in the blood to the liver. FAs
in the liver are metabolised by oxidation. Final product of oxidation is acteyl CoA,
which enters the citric acid cycle with oxaloacetic acid from carbohydrate
metabolism. Glycerol returns to the liver for oxidation or formation into new TGs.
Excess acetyl CoA is converted in the liver to acetoacetic acid which is carried to
peripheral tissues for conversion back to acetyl CoA. When the body is relying almost
entirely on stored fat for energy (eg very high protein diet, prolonged fast, diabetes)
the amount of acetoacetic acid produced exceeds the ability of peripheral tissues to
oxidise it to acetyl CoA. Some of the acetoacetic acid becomes hydroxy butyric acid,
acetone (ketone bodies). Ketone bodies not used by skeletal muscle or heart for
energy need to be excreted in urine coupled to a base. This depletes the body of bases,
which eventually lowers the pH of body fluids (ketoacidosis) and can lead to coma,
The body can store unlimited amounts of fat, which is used for energy. About 60% of
the body‟s energy during rest comes from fat. The liver can convert excess CHO and
protein to fat. Without carbohydratesm fats break down to ketone bodies. After the
prolonged absence of glucose the brain and nerve cells develop the ability to obtain
about 2/3 of their minimum energy needs from ketone bodies. However this is not
enough to sustain life in the long term, and even people with high body fat levels will
die after prolonged fasts. Ketosis also induces a loss of appetite. Lean muscle
(protein) is converted to glucose and metabolism slows so much that the loss of fat
eventually becomes less than would be seen on a low KJdiet.
Recommended dietary intakes
Australian fat intakes = 12.5% SFA, 11.5% MUFA, 4.5% PUFA
Epidemiological evidence suggests the “ideal” fat intake is similar to 7% SFA, 15%
MUFA, 7% PUFA with a n-6:n-3 ratio between 5-1 and 10-1.
When looking at food labels, check the per 100gm column. Anything with less than
10gm of fat and 5gm of saturated fat is good.
FATS THROUGH THE LIFECYCLE
Pregnancy & the first year
High birthweights, rarity of pre-term deliveries in populations that eat large
amounts of fish led to suggestion EFAs from fish could delay spontaneous
delivery and increase birthweight. Mechanism: EPA/DHA are altering
eicosanoid/cytokine balance to delay the initiation of labour & cervical
10 trials have examined the ability of fish oil supplementation in pregnancy to
prolong gestation. A small positive effect is seen, particularly in women at
highest risk of preterm birth (no effect for twin pregnancies). No beneficial or
harmful effects on the fetus as a result of supplementation were measured.
All these trials used fish oils, which have much more EPA than DHA.
DHA is required for cerebral cortex and retinal development. The fetus and
newborn require a good supply of DHA via the placenta or breastmilk.
Preterm infants are the most vulnerable to DHA deficiency if they are denied
the placenta and breast milk. 12 trials have shown preterm infant formula
supplemented with DHA improves visual acuity, and possibly psychomotor &
language development. Therefore preterm formulas are supplemented with
DHA and AA.
Breast fed babies: receive DHA & AA from breast milk. This may explain the
5 point increase in adult IQ seen in 1 recent study of breast fed vs formula fed
babies. The level of DHA will vary with the mother‟s diet (eg vegan women
who consume no animal products have least, regular fish eaters most).
Formula fed babies: Trials of DHA-supplemented formula on full term babies
have shown either small positive or neutral effects on developmental outcome,
so WHO recommendation all formulas be supplemented.
Weaning diets are generally low in fat, especially DHA. Omega 3 enriched
eggs (“Veggs”, “Omegga”) are one way of significantly increasing DHA
intake during weaning. Whether this influences development is unknown.
Toddlers to Preschoolers
Need for nutrients is very high in this age group, and appetite & capacity can be
High fat foods valuable as they are energy dense, but should also provide many other
nutrients to support growth and tissue development. Total fat requirements recently
drafted as 30% energy, with not more than 10% saturated.
Reduced fat milks are not suitable for children under 2 as milk is a key food & energy
source for this group, and fat is needed to absorb the fat soluble vitamins .
To date there is no evidence linking deficiencies in EFAs and ADHD. Currently
studies underway to investigate whether exposure to n-3 fatty acids in utero or
postnatally influences immunological development and hence asthma and allergy risk.
So far no evidence that asthma sufferers should modify their n-3 intake to improve
Primary school children
Influence of family eating patterns very strong. Fat intake levels from early childhood
tend to track into adulthood, so important to establish good patterns. Children under 5
are not influenced by serving size, but over 5 children will begin to eat more if
serving sizes are increased. Draft guidelines suggest 30% of energy from fat, with
10% as saturated fat.
Early primary years =a high risk period for onset of obesity, and this has been linked
to fat & energy intake. Offer lower fat foods (eg sandwiches not pastries, fruit based
desserts not ice cream) and use mono or polyunsaturated spreads. Encourage healthy
snacks, fish intake & fruit and veg. Long chain omega 3‟s may help with childhood
asthma but evidence for this is not conclusive.
Another danger period for obesity onset due to reduced physical activity. Obese
teenagers more likely to be obese adults than obese children are. Amount of dietary
fat important in maintaining energy balance. Type of fat important for reducing heart
disease risk. Low fat foods are suitable, should also avoid hidden fats in baked
products & fats foods and include mono and polyunsaturated fats. 30% energy from
Long chain omega 3s are associated with:
Lower BP, lower TG levels, prevention of heart arrhythmias
Possibly protecting against Crohn‟s disease, rheumatoid arthritis (see
below) and psoriasis
Reducing risk of Alzheimer‟s
Reducing risk or severity of post-natal depression
Reducing risk of macular degeneration
The proportion of omega 3 to omega 6 fats in the diet seems to be very important, as
omega 6 fats will suppress the action of omega 3s.
A typical Australian diet is high in vegetable cooking oil, fried and processed foods so
many people have a ratio of omega 6: omega 3 fat of 20:1. Ideally it should be 4:1 or
Switching to a monounsaturated cooking oil and having more oily fish, whilst also
reducing saturated fat intake helps restore the ratio.
The new Australian SDTs for long chain omega 3s are 430mg/day for women,
610mg/day for men.
Lipids responsible for symptoms of inflammation in RA are mainly omega 6‟s: these
allow the formation of prostaglandins and leukotrienes (series 2). Studies have shown
omega 3 fatty acids, esp fish oil, are able to inhibit the production of these
prostaglandins, leukotrienes and also cytokines.
Epidemiological evidence for the effect of fish oil in RA: Japanese prevalence of RA
is 0.4% vs Australia‟s 1%, even though there is a large occurrence of a genotype
linked with increased susceptibility to RA. Thought to be because the Japanese
consume much greater amounts of seafood
A 1996 case control study found that women who ate more seafood were less likely to
develop RA – if >1.6g omega 3 fat eaten daily then risk of RA was decreased by
Intervention studies have supported this finding. 13 double blind placebo controlled
studies all found benefits for patients with RA when supplemented with fish oil, with
the most common improvement being in tender joint pain. 12 weeks was the
MINIMUM time to effect. The median intake of omega 3 fatty acids was large (3.3g),
but these patients had long standing disease.
Appears: Fish intake is useful in prevention of RA
Fish oil intake can have a role in treatment.
Also RA patients are at higher risk of CVD, so fish intake should also be encouraged
from this point of view (omega-3s reduce blood clotting)
See CVD lecture
Key points for all patients:
Fat is an essential nutrient – our bodies need some fat
Reduce the saturated fats which Australians overconsume
Choose mono or polyunsaturated fats from oils, spreads, avocados, nuts, seeds
Consume some omega – 3 fats
Low fat diets appear safe after 2 years of age for children at high risk of
Key points for infants & under 2‟s:
Babies need fat to fulfill their energy requirements for growth
Encourage breastfeeding for at least 6 months
Low fat diets are not appropriate for children under 2
From 6 months of age fat can be obtained from foods such as vegetable oils,
spreads, eggs, full fat milk and meat
Tips for patients
How to reduce saturated fat
Limit intake of obvious sources of saturated fat such as butter, cream, sour
cream, marscapone, coconut cream/milk, fat selvage on meat, skin on chicken
Limit intake of foods with hidden saturated fats, such as sausages, bacon,
devon, salami & other deli meats, meat pies, sausage rolls, potato crisps, corn
chips, hamburgers, pizza, fried fast food, gravy, rich sauces, full fat dairy
products (milk, cheese, yoghurt) cakes, muffins, pastries, doughnuts, biscuits,
Check labels for saturated fat
How to increase mono and polyunsaturates in diet
Use a variety of oils for cooking
Swap butter for a margarine
Consider alternative spreads eg avocado, hommus, peanut butter
Replace potato chips with nuts as a snack
Sprinkle lecithin or wheatgerm on cereal
How to increase omega-3 polyunsaturated fats
Eat fish twice a week (frozen, fresh or canned)
Choose vegetable oils that are a good source of omega-3 fats (flaxseed and
Choose plant sources of omega 3
Sources of omega-3 fats (in descending order of magnitude)
Oily fresh fish Atlantic salmon (600mg per 100g), smoked salmon, trevally,
yellowtail, mackerel, tuna
Canned fish Salmon, sardines, tuna* see table below
Eggs Omega-3 enriched eggs eg “Veggs”
White fresh fish Snapper, perch, gemfish, flounder, whiting, John Dory, flathead,
Seafood Oysters, prawns, mussels, scallops, squid, crab, octopus
Oils Flaxseed, canola, wheatgerm, soybean
Seeds Linseeds (ie flaxseeds), soy and linseed bread
Nuts Walnuts, pecans
Legumes Soybeans, tofu, soymilk, other beans and lentils
Wholegrains Wheatgerm, rye, barley, brans
Vegetables Most green leafy vegetables
Type of Canned fish Brand Amount of LC-omega 3
Sardines John West Scottish 2500mg
King Oscar Sardines 2000mg
Salmon John West pink salmon 1560mg
Paramount pink salmon 1450mg
Ally pink salmon 1300mg
Tuna Greenseas sandwich tuna 260mg
Solemare tuna 108mg
Sirena tuna 135mg
Rosemary is a 33 year old woman who has been referred to you. She has had
rheumatoid arthritis for the past year. She weighs 50kg. She lost 5kg prior to
diagnosis with RA but is now responding well to a new medication regime and slowly
regaining the weight. Her usual eating pattern consists of vegemite on toast with
polyunsaturated margarine for breakfast, a fruit bun for morning tea, a cheese
sandwich on wholemeal bread spread with margarine and a piece of fruit for lunch,
yoghurt or rice crackers as an afternoon snack and beef, lamb or chicken in a stirfry or
pasta sauce with vegetables for dinner. Beverages include fruit juice and water. Her
doctor has suggested that boosting her intake of omega 3 fats may help her manage
the rheumatoid arthritis.
6a) Why are long chain omega 3s sometimes recommended to RA patients? (4
6b) Name 2 marine long chain omega 3 fats (abbreviations are fine). (2 marks)
6c) Suggest 4 dietary changes to improve Rosemary‟s intake of long chain omega 3s.
6d) Rosemary‟s SDT for omega 3s is 430mg. What does “SDT” mean and what is the
role of SDTs in public health? How do SDTs differ from EARs? (5 marks)
Big Fat Myths (MJA pS123 vol176, 2002)
1. I don‟t need to eat any fat
2. Fats don‟t give us anything except calories
3. I must eliminate all fat from my diet to lose weight
4. Canola is the same as rapeseed
5. Canola oil is toxic/ contains a poison
6. Olive oil is the best to use
7. Light oils reduce your fat intake
8. I can‟t eat red meat because I have high cholesterol
Omega-3 supplemented products
Bread, margarine, milk, eggs, fish, small goods, baby formula
Pick the Tick Campaign
The "Tick" is the Heart Foundation's guide to help people make healthy food
choices quickly and easily. It also encourages food manufacturers to develop
or modify food products that support the Heart Foundation's Guidelines for
Tick Approval. In general, "approved" foods are relatively lower in saturated
fat, sodium and added sugar, and higher in dietary fibre.
A healthier choice
Tick approved products represent a healthier choice within a particular food
category. For example, the Tick Program approves some meat pies, as they
are lower in total fat and sodium than their regular counterpart. Pastries
(sweet and savoury) are currently the third highest source of saturated fat in
the Australian diet1.
High fat foods included
The Tick can appear on foods that are high in fat, like margarines, oils and
nuts. This is because the type of fat in these products have less saturated fats
and a greater proportion of unsaturated fats. The Tick is also found on dairy
foods, like cheese and ice cream, to help people choose the ones that are
lower in total fat, saturated fat and sodium when compared to standard foods
in these categories
Earning the Tick
All foods, without exception, must meet the Heart Foundation's Guidelines for
Tick Approval. Food companies must have their products independently (from
the manufacturer) chemically analysed, and meet the nutrient criteria before
they can use the Tick on their products. If a product fails to meet the
Guidelines, the Heart Foundation may work with the food manufacturer to
improve the nutritional profile of that product.
Changing the food supply
Many products have been intentionally formulated or reformulated to meet the
nutrient criteria. Tracking data shows that the Tick Program significantly
reduces the amount of saturated fat and sodium in the food supply each year.
Freedom to choose
As the Tick Program is a voluntary program, companies can choose whether
or not to have their products tested. Some companies choose not to
participate, even though their products would qualify for the Tick. Others
simply don't meet the nutrition guidelines or companies prefer to position their
product in a different market niche.
Food companies pay a royalty fee
Fee based on wholesales turnover of their Tick product As a non-profit, non-
government organisation, the Heart Foundation needs these fees to run the
Week 5: NUTRITION & CARDIOVASCULAR DISEASE
Check how well your diet matches the National Heart Foundation guidelines by
ticking the areas you could improve:
Do you: Could be
Use margarine spreads instead of butter or dairy blends
Use a variety of oils for cooking – some suitable choices include
canola, sunflower, soybean, olive and peanut oils.
Use salad dressings and mayonnaise made from oils such as canola,
sunflower, soybean and olive oils.
Choose low or reduced fat milk and yoghurt or „added calcium‟ soy
Try to limit cheese and ice-cream to twice a week
Have fish (any type of fresh or canned) at least twice a week.
Select lean meat (meat trimmed of fat and chicken without skin).
Try to limit fatty meats including sausages and delicatessen meats
such as salami
Snack on plain, unsalted nuts and fresh fruit.
Incorporate dried peas (e.g. split peas), dried beans (e.g. haricot
beans, kidney beans), canned beans (e.g. baked beans, three bean
mix) or lentils into two meals a week.
Make vegetables, and grain based foods such as breakfast cereals,
bread, pasta, noodles and rice the major part of each meal.
Try to limit takeaway foods to once a week, takeaway foods include
pastries, pies, pizza, hamburgers and creamy pasta dishes.
Try to limit snack foods such as potato crisps and corn crisps to once
Try to limit cakes, pastries and chocolate or creamy biscuits to once a
Try to limit cholesterol-rich foods such as egg yolks and offal e.g..
liver, kidney and brains.
Australian Statistics for Cardiovascular Disease
Is the leading cause of death in Australia
Accounts for 40% of all deaths
One Australian dies every 10 minutes of CVD
More than 80% of the adult population has at least one of the following preventable
cardiovascular risk factors: tobacco smoking, physical inactivity, high blood pressure,
22% Australians aged 14 years and over smoke on a regular basis.
43% Australians do little or no meaningful physical activity
Over seven million adult Australians are overweight; 2 million are obese
Three million Australians have high blood pressure. High blood pressure
increases the risk of cardiovascular disease by two to four times.
Six million Australians have hypercholesterolaemia
CVD death rates falling in industrialized countries, increasing in newly
Aboriginal and Torres Strait Islanders die from CVD at twice the rate of other
CHD is the most common form of CVD
At 40 years, CHD risk = 1 in 2 (M); 1 in 3 (F)
Lipid Transport in the body
Because lipids are hydrophobic they must be bound to a transport molecule to
circulate in the blood (lipoproteins).
Receptor activity =
+ PUFA, soy protein
60% LDL is taken up via receptors on liver, adrenals etc
Some of remainder may be oxidized by free radicals or glycosylated if diabetic
1. Initial injury to endothelium of vessel wall occurs. Can be physical damage
(blood flow), chemical damage (oxidized/glycosylated LDL), interaction with
activated cells eg platelet
2. Macrophages attach to injured endothelium, enter the sub-endothelial space &
accumulate cholesterol ester from oxidized LDL to become foam cells ---
lesion = fatty streak
3. Smooth muscle cells migrate to lesion and proliferate to form a connective
tissue matrix. There is accumulation of lipid and cholesterol in the matrix to
form a raised fibrous plaque (atheroma).
Platelet aggregation at this site can lead to thrombus formation and occlusion of artery
coronary heart disease, stroke
Epidemiology & CVD
Seven countries study (1980)
1st linking serum cholesterol level to CHD
Measured Greeks, Finns, Italians, Japanese, Dutch, Yugoslavs, Americans
Compared with national incidence of CHD
Linear relationship -graph
Migration of Japanese to USA shows variation not due to genetics
? due to diet
% dietary fat vs coronary death – some correlation
Ratio SFA and PUFA vs serum cholesterol – good correlation
Multiple Risk Factor Intervention Trial (MRFIT, 1986)
351,000 men / 6 year period
Serum cholesterol coronary heart disease mortality is strong and
continuous from cholesterol levels of 4.7mmol/l
There is no threshold concentration of serum cholesterol at which risk
Cholesterol lowering interventions
Simvastatin (1994), Pravastatin (1998)
Oslo trial (1981) – dietary intervention
1% reduction in mortality for each 1% reduction in total cholesterol
1% increase in LDL cholesterol may cause a 2-3% increase in CHD risk.
Every 0.25mmol/l increase in HDL decreases CHD risk by 2-3%
Recommended serum lipid levels:
National Heart Foundation recommendations for serum lipid levels have been revised:
Normal High Risk
Total cholesterol <5.5 mmol/l <4.0 mmol/l
LDL cholesterol <3.5 mmol/l <2.5 mmol/l
HDL cholesterol >1.0 mmol/l >1.0 mmol/l
Triglycerides <2.0 mmol/l <2.0 mmol/l
High risk patients are those which have:
Existing cardiovascular disease
Chronic renal failure/transplantation
Aboriginal or Torres Strait Islander Ethnicity
Total cholesterol >6.0 or LDL cholesterol >4.0 AND 2 or more of the risk
factors here: HDL cholesterol <1.0, significant family history, HT,
overweight/obesity, smoking, impaired glucose tolerance, renal impairment,
age >45 years.
Low HDL concentrations seem to be a more significant risk factor in women
Over 6 million Australian adults have a total cholesterol over 5.5.
OTHER RISK FACTORS FOR CVD
CVD occurs as a result of 2 processes: atherosclerosis and thrombosis.
Accelerants of either are a risk factor for CVD
These risk factors can be divided into modifiable and non modifiable.
Causes more than 1/5 of deaths from CVD
Seems to increase the levels of fibrinogen, tendency of blood to clot
Smoking decreases HDL levels
Low HDL, high LDL accelerates atherosclerosis
Ratio of LDL:HDL cholesterol = CVD risk
Elevated TG levels occur with lowered HDL
(Central) obesity increases risk of diabetes & HT, which both accelerate
Continuous relationship between BMI, total and LDL cholesterol
Obesity increases production of VLDL (as endogenous TG increased) and
Major risk factor for stroke
HT is itself increased by obesity and excess alcohol intake and possibly salt.
Physical activity will help reduce weight and BP, it has also been shown to
improve lipid profiles.
Poorly controlled diabetes
Diabetics are at increased risk of developing CHD
Insulin resistance / HT / increased tendency for thrombosis / dyslipidemia are
common in diabetics
Sensitivity to the effects of dietary cholesterol
Can effect levels of homocysteine too, although deficiencies in folate, B6 and
B12 will also cause this
High levels activate platelets and cause damage to the endothelial lining of the
Hypertension = increased risk
As atherosclerosis develops over many years
Pre-menopausal women have higher levels of HDL – decreased CHD
LDL-C less significant than HDL-C levels in pre-menopausal women.
HRT reduces risk of CHD for post menopausal women, by increasing HDL
and decreasing LDL and total cholesterol levels (oestrogen upregulates the
HRT increases risk of other morbidities
DIET AND CARDIOVASCULAR DISEASE
Saturated fatty acids
Sources in diet: Animal derived (meat, dairy products).
Plant sources = coconut oil, palm oil
Effect on lipids: (ie atherogenic effect)
The Seven Countries study - saturated fat NOT total fat = serum cholesterol levels.
EG Greeks = high fat intake, but mostly MUFA so low CHD mortality.
Mechanism: suppress LDL cholesterol receptor activity, although the exact
mechanism is unknown.
Effect on thrombosis:Long chain saturated fatty acids increase the tendency of blood
to clot as they stimulate the aggregation of platelets, so are thrombogenic.
NHF recommendation: saturated and trans fatty acid intakes together do not exceed
8% of total energy in the diet.
Trans fatty acids
Unsaturated fatty acids generally occur in nature in the cis form. Small amounts occur
naturally in dairy products. Trans form produced in food processing when oil is
hydrogenated to solidify it
Sources in diet: Some margarines
Effect on lipids: Compared with unsaturated fatty acids, trans fatty acids significantly
increase total and LDL cholesterol, and lower HDL cholesterol, although less potently
than some saturated fatty acids.
NHF recommendation: saturated and trans fatty acid intakes together do not exceed
8% of total energy in the diet
Monounsaturated fatty acids
Sources in diet: Olive oil, canola, avocado, nuts
Effects on lipids: Neutral effect on LDL cholesterol, slightly increase HDL
cholesterol, so will lower the LDL/HDL ratio
No effect on thrombosis. Substituting MUFA for SFA will decrease LDL cholesterol
and total cholesterol, and increase HDL cholesterol. Monounsaturated fatty acids are
the predominate fatty acid eaten in the Mediterranean area, and CHD incidence is
fairly low. However other protective factors could be involved.
NHF recommendation: a proportion of dietary saturated fatty acids should be replaced
by mono-unsaturated fatty acids as a strategy for reducing the intake of saturated fatty
Polyunsaturated fatty acids
Sources in diet: margarines and oils (sunflower, safflower, corn, soya bean); walnuts,
brazil nuts, pumpkin seeds, sesame seeds, sunflower seeds
Effect on blood lipids: Lowers total and LDL cholesterol, as increases activity of LDL
receptor and raises HDL cholesterol. No effect on thrombosis or BP.
NHF recommendation: n-6 polyunsaturated fatty acids contribute 8 to 10% of total
Eskimos - high fat diet but CHD death rate low, partly attributed to their high intake
of n-3 PUFAs. Also bruise and bleed very easily due to high intake?
Sources in diet: Polyunsaturated margarines, linseed, oily fish (herring, salmon, tuna,
makeral, sardines, gemfish)
Effect on blood lipids:
Little on LDL, HDL or total cholesterol
Potent effect on triglycerides – 3gm in diet can reduce TGs by 30%.
Mechanism- eicosapentaenoic acid and docosahexanoic acid effect the synthesis and
clearance of VLDL cholesterol and chylomicrons (the TG rich lipoproteins) hence
decreasing TG levels.
Effect on thrombosis: Decreases thrombosis, by 2 mechanisms:
1. Via thrombocytopenia
2. Via reduced platelet aggregation
3-series thromboxanes 2-series thromboxanes
3-series prostacyclin 2-series prostacyclin
NHF recommendation: At least two fish (preferably oily fish) meals per week are
consumed; both plant and marine n-3 polyunsaturated fatty acids are consumed since
it is possible that -linolenic acid and marine n-3 polyunsaturated fatty acids protect
against CHD by different mechanisms; and plant n-3 polyunsaturated fatty acid
intakes be at least 2g per day
Sources in diet: Only found in animal products. Eggs, offal, prawns rich sources
Effect on blood lipids: Varies b/t individuals. IF sensitive, LDL and HDL cholesterol
will increase, with the LDL fraction more affected
NHF recommendation: people at low coronary risk can reasonably eat moderate
quantities of cholesterol-rich foods; and people with plasma cholesterol levels greater
than 5.0mmol/L or with other risk factors should restrict the intake of cholesterol-rich
Sources in diet: insoluble fibre (found in wholegrains, brown rice, fruit and veg).
Soluble fibre = bran, wholegrains, legumes, fruit and veg.
Effect on lipids: Insoluble fibre – none. Soluble fibre - lowers total cholesterol and
LDL cholesterol around 3-5% if 15gm/day eaten.
It binds bile acids in the gut which means an increased fecal excretion of bile acid and
possible alters hepatic cholesterol synthesis.
Fibre also tends to reduce fat and cholesterol in the diet as high soluble fibre foods
are low in these nutrients.
NHF recommendations: The consumption of dietary fibre, especially cereal fibre, is
associated with a lower risk of CHD.
1. Foods rich in soluble fibre reduce the level of plasma cholesterol.
2. Although insoluble fibre such as wheat bran does not lower plasma cholesterol
levels, the epidemiological data do not distinguish between the two forms of
fibre and fibre-rich foods.
3. A target of 30g fibre daily for Australian adults is to be encouraged.
These include vitamin C, E, beta carotene, carotenoids (lycopene), flavonoids
Source in diet: Vegetables, fruit, vegetable seed oils, nuts, soybeans, tea, red wine
Effect: Populations that eat diets rich in antioxidants have lower rates of CHD. Does
not prove it is the antioxidants, could be that these diets are rich in fruit and
Studies where a vitamin E supplement was given showed reduced CHD mortality.
Mechanism: ?prevent the oxidation of LDL-cholesterol. ?reduce platelet adhesion and
inhibit smooth muscle cell proliferation
1. Foods rich in vitamin E and flavonoids are recommended components of a
healthy diet. These foods include vegetables, fruits, vegetable seed oils, nuts
and probably soybeans, tea and grape products.
2. Possible benefits of supplemental antioxidants are limited to vitamin E on
current evidence, although even in this case there are still no intervention trials
showing unequivocal benefit.
Linked to HT for over 50 years
No clear association as some more sensitive to Na than others
Sources in diet: bread, cheese, margarine, soups, sauces, processed foods NOT added
in cooking or at table
Effect on BP: The largest scale study of salt intake and BP included 10,000 people /32
countries. Found reduction of sodium intake of 100mmol/day will reduce BP by
Meta analysis = reduction by 3gm salt/day in the 50-59 age group would lower BP
5/2.5mmHg and reduce the incidence of stroke by 26% in the western world
NHF Recommendation: weight loss and sodium, alcohol restriction is best for
Evidence = vegetarians have a decreased LDL-C, BP so risk of CHD compared to
Possible mechanisms: Vegetarian diets are generally lower in total and saturated fat,
higher in fibre and antioxidants, and have a higher potassium:sodium ratio
NHF recommendations: The benefits of a vegetarian diet are not unique. An omnivore
diet that is low in total and saturated fat and contains plenty of fruits, vegetables and
wholegrain cereals may be just as effective as a vegetarian diet in terms of reducing
Sources in diet: Meat, egg, dark green leafy veg, wholegrains
Effect: Promotes LDL oxidation reactions so may accelerate CHD
1. NHF recommendations: The evidence for or against a role of iron in the
development of CHD is extremely limited at present.
2. Iron deficiency is a significant problem in our society, especially in infants,
premenopausal women and the elderly. Limiting the iron intake in such groups
is not recommended.
3. Further research is required to establish whether or not there is a relationship
between iron and CHD.
Effect: Any level of consumption will raise blood pressure.
High energy nutrient so contributes to obesity.
It also raises TG levels by stimulating hepatic synthesis.
Moderate intake does not increase mortality - ? due to increased HDL levels,
antiaggregatory effects of ethanol or antioxidants in wine.
.NHF recommendation: On cardiovascular and other health grounds, there is no
justification for recommending that non-drinkers of alcohol should take up the habit
or that any drinkers should increase their intake.
On those same grounds, there are strong reasons for all people who drink alcohol to
limit intake to moderate levels.
Those whose blood pressure or blood cholesterol levels are high, or who are
overweight, have additional reasons for moderating or avoiding use. Alcohol
consumers on medication to lower their blood pressure, should either stop drinking or
restrict their intake to one or two drinks per day at most, with the hope of reducing the
need for such medication.
Soy & CVD
1995 meta analysis found soy protein lowers LDL cholesterol by up to 12.9%
Whole soybean products preferable to soy protein isolates as they also contain
fibre, vitamin E, omega 3 fatty acids, phytoestrogens.
Therefore: antioxidant properties; an anti inflammatory effect in blood vessels
so minimise plaque formation; reduces blood clotting
USA food manufacturers may claim “25g of soy protein a day as part of a diet
low in saturated fat and cholesterol may reduce the risk of heart disease”
Aim for 3-4 serves/day: soy milk, soy yoghurt, soy beans, tofu, soy breakfast
cereal, soy & linseed bread
How much is a serve of soy?
One serve is:
1cup of soy milk
1 tub of soy yoghurt
1 carton of soy smoothie
1/3 cup soy beans, canned and drained
2 slices soy and linseed bread
60g hard tofu
45g soy breakfast cereal
3 or 4 serves/day will give 25gm of soy protein.
Wholegrains & CVD
4 large scale studies in the late 1990s have shown as consumption of
wholegrains (NOT refined cereal) increases, CHD incidence declines.
Appears due to combination of soluble fibre, folate and antioxidants &
phytoestrogens present in grains.
Oat bran, whole oat flour and rolled oats have been shown to modestly reduce
total and LDL cholesterol due to soluble fibre. Wheat fibre has no effect.
2005 CSIRO study found 20-40% reduction in CVD risk if having
USA food manufacturers allowed to use the health claim “Diets rich in
wholegrain foods and other plant foods and low in total, saturated fat and
cholesterol may reduce the risk of heart disease and some cancers”
Plant sterols & CVD
Plant sterols (sitosterol & campesterol) found at high levels in unrefined vegetable
An LDL-cholesterol reduction of at least 10% is seen in 90% of people when 1.6-2.4g
of sterol/day eaten. This effect is additive to reductions from statins that inhibit
A 2005 study ( Nutr Med Cardiovas Dis 2005 15: 337) found that lowering total and
saturated fat int the diet reduces LDL-cholesterol by about 12%, but adding a plant
sterol to this diet further lowered LDL-C by 20%.
Foods to ask CVD clients about when evaluating their diet:
Saturated fat (meat, dairy
products, commercial cakes,
Fruit & Veg intake
Reduce SFA fat in diet (cheese & icecream 2/week, takeaways, cake, chips
Substitute MUFA, PUFA (olive oil, canola, avocado, fish) for SFA (meat, full
cream dairy, butter & lard)
Have 2+ fish meals/week
Increase fruit, veg, wholegrain intake
Have 2+ legume meals/week
Try soy products
Decrease alcohol if TG elevated
Increase physical activity
Plant sterol spreads if on statins
Reduce cholesterol (<2eggs/week, occ. offal, shellfish)
Reduce salt if HT
When to refer to dietitian
Recent AMI/CVA/HT and not seen
Interventions not working
Not consuming balanced diet
Jenny is a 59 year old client who recently had her total cholesterol measured during a
check up and was told it is 6.0 mmol/l. Her weight is 82kg, height 170cm. She is a
busy senior manager so has no time for cooking and eats takeaway pasta, curries, fish
and chips or pizza most nights. Breakfast is usually skipped, and lunch is often a
quick sandwich or roll filled with ham or cheese and salad. She doesn‟t do any regular
exercise, does not smoke or drink.
3a) Do a nutritional assessment of Jenny (5 marks)
3b) What are 4 lifestyle interventions you could suggest to help Jenny lower her
cholesterol? (4 marks)
3c) What should her total cholesterol ideally be? What should her HDL cholesterol
be? (2 marks)
3d) Jenny has been reading about foods that can help lower cholesterol. Describe 3 of
the foods that can lower your cholesterol and the mechanism by which they do this. (6
3e) Why is a moderate alcohol intake thought to be protective against CVD? (2
8 foods that can lower cholesterol
1.Fruit and Vegetables
Those who consume a lot of fruit and veg have a lower risk of CVD. No longer
attributed to the antioxidants vitamin E, C and beta carotene. Many other antioxidants
being researched: carotenoids in green and orange veggies, catechins in tea,
anthocyanins in berries, rosemary and oregano, flavonoids in leafy green veg. Also
increases fibre & folate in diet which decreases homocysteine.
2. Red wine
“French paradox” is that the French eat large amounts of saturated fat but have low
rates of CVD. Thought to be because they have red wine with meals. Moderate
amounts of red wine can cause a decrease in LDL-C levels, but not white wine.
Polyphenols in red wine may act as antioxidants, and alcohol intake does increase
0.9g garlic appears to lower total (12%) and LDL-C (14%). Combining garlic with
fish oil tablets will also lower TGs (34%). (Am J Clin Nutr Brown et al1997)
Contain mainly monounsaturated and polyunsaturated fats. Study of 30,000 7 th Day
Adventists found people who eat nuts more than 4 times/week have 50% fewer heart
attacks than those who rarely eat nuts. Nuts also contain vitamin E, fibre and arginine.
Arginine is converted to NO which causes smooth muscle to relax.
Omega-3‟s reduce TG levels, prevent platelets clumping & clotting, reduce platelet
number so enhance blood viscosity, minimise cardiac arrhythmias. Oily fish highest
in omega 3‟s.
Green and black tea both contain flavonoids which act as antioxidants. High tea
consumption has been linked to reduced heart disease. Green tea is very rich in
antioxidants so suggested as the reason for little CVD in Japan and China. Adding
milk to tea does not affect absorption of the antioxidants.
25 gm soy protein/day (eg 1 L of soy milk) can reduce total cholesterol by 9%, LDL-
C by 12.9%, TG by 10% if hypercholesterolaemic. No effect if normal cholesterol.
Additional benefits from eating who soy beans, not protein isolate.
8. Oats and Psyllium
Oat bran, barley and rice bran contain soluble fibre so can bind to bile acids and
sterols and prevent their reabsorption from the bowel. Need about 1 heaped cup/day
of oat bran to see a benefit, less of psyllium as contains more soluble fibre. Rye bread
(>6 slices/day) can also slightly lower cholesterol in men (Rye bread decreases serum
total and LDL cholesterol in men with moderately elevated serum cholesterol.
J Nutr. 2000 Feb;130(2):164-70)..
Used to lower cholesterol by Prof.David Jenkins – reduced LDL by 35%
1.Soy protein – 40g/day – soy milk, yoghurt & tofu
2.Plant sterol cholesterol lowering margarine
3.Oat based breakfast
4.10-15 raw almonds/day
5.Increase in consumption of fruit & veg
Multiple choice questions:
1. Modifiable risk factors in coronary heart disease are:
a. age, lowered LDL cholesterol, obesity, hypertension
b. android obesity, diabetes, smoking, family history
c. high plasma triglycerides, diabetes, male sex, elevated cholesterol
d. diabetes, android obesity, hypertension, lowered LDL cholesterol
2. Antioxidants are thought to be protective against cardiovascular disease
a. They prevent oxidation of LDL cholesterol by joining with free
b. They are found in fruits and vegetables and wholegrains so increase
the fibre content of the diet
c. They form free radicals to help oxidize LDL-cholesterol
d. They form vitamin E, C and beta carotene, which have beneficial
3. In regard to the function of trans fatty acid, which is incorrect:
a. they have similar effects on the body to saturated fatty acids
b. they are found naturally in ruminant fats
c. are found in large amounts in Australian margarines
d. are formed during the hydrogenation of oil
4. The most effective way of reducing a person‟s cholesterol is to
a. Change the type of oil they use to a vegetable oil eg palm oil
b. Reduce organ meats, shellfish, eggs in diet
c. Reduce fatty meats and full cream dairy products in diet
d. Increase fish consumption to twice a week
e. Increase consumption of wheat bran and wholegrains
5.Weight reduction is beneficial in cardiovascular disease as
1. the body has less fat to contribute to the blood lipid profile
2. there is a fall in LDL-cholesterol and triglycerides
3. there is less oxidation of LDL-cholesterol
4. HDL-cholesterol levels are maintained while LDL-cholesterol levels
6. Hypertension control is best achieved by
a. reducing salt intake
b. decreasing LDL-cholesterol
c. weight reduction if overweight and exercise
d. increasing potassium in diet
Week 6: CARBOHYDRATES
Recommended that CHOs contribute >55% energy for optimal nutritional
Hunter-gatherer ancestors ate 25-40% energy from CHOs
Many traditional societies consume >55% of energy from CHOs. Food
sources high in CHOs generally also good sources of fibre, moderate sources
of protein and contain B group vitamins, vitamin E, Fe, Zn, Mg, P.
Diet high in CHO can be preventative against CHD, obesity & some cancers.
Generally store well, are relatively cheap and make best use of the world‟s
resources (few input resources compared to nutrient output)
CHO provides the largest source of energy to most Australians (about 45% of
energy – 200gm/day for women, 300gm/day for men).
Physiological functions of carbohydrates:
Provision of energy
Effects on satiety
Effects blood glucose
Fermentation – production of
hydrogen, methane and short chain fatty acids
Control of colonic epithelial cell function
Effects on bowel habit, laxation
Effects on large bowel microflora
CHO formula is C n H2nO n. Only CHOs containing 6 or 5 carbons and their polymers
are significant for human nutrition.
These are synthesised in plants via photosynthesis through the combining of CO 2 and
Types of carbohydrate:
Carbohydrate Food Sources End products of digestion
Glucose Fruit, honey glucose
Fructose Fruit, honey fructose/glucose
Sucrose Sugar, maple syrup glucose + fructose
Lactose Milk & dairy products glucose + galactose
Maltose Small amounts in some cereals glucose
Cellulose & Vegetable stalks, leaves & seed coats H2, CH4, CO2 & SCFA
Pectins Fruits As above
Gums and mucilages Plant secretions & seeds As above
Inulin Artichoke, garlic, onion, mushroom fructose (digestion incomplete)
Raffinose & stachyose Lentils & beans glucose, fructose, galatose
Starches & dextrins Grains, tubers, legumes glucose
Glycogen Meat & seafood glucose
Single sugars eg glucose, fructose.
Glucose is oxidised in human cells to produce energy and stored as glycogen
(chains of glucose) in liver and muscles. CNS can only use glucose as its
½ sweetness of sucrose so used in drinks if ill
Fructose is the sweetest of the sugars & cheap to produce from corn starch, so
often used commercially
Metabolism of monosaccharides:
Cells receive most of their CHO as glucose, since fructose is converted to
glucose in the liver.
Much glucose is oxidised to meet energy requirements, but some is converted
to other essential CHOs eg ribose, deoxyribose, glucosamine, and to the
carbon skeletons needed for production of non essential amino acids.
Excess CHO can be stored as glycogen or converted to fatty acids
The cellular entry of fructose is not insulin dependent, however it can still
eventually cause a rise in BGL if it converted to glucose, especially if person
is insulin impaired/deficient.
Glucose levels are regulated biochemically in the body by:
1. Liver breaking down its glycogen stores to glucose (glycogenolysis)
2. Muscle glycogen is broken down into lactic acid, which liver converts to
glucose or glycogen (Cori cycle)
3. If adequate glucose not available, amino acids are converted to glucose
Glucose levels are controlled hormonally by:
1. Insulin – released in response to high BGL. Increases rate of glucose
oxidation, glycogenesis, lipogenesis. Facilitates entry of glucose to muscle,
adipose cells, storage of glucose in liver & muscle, conversion to fat
2. Glucagon – stimulates glycogenolysis & gluconeogenesis.
3. Adrenalin – provides extra glucose for fight/flight response by promoting
glycogenolysis & inhibiting insulin release.
Sucrose (sugar) =glucose + fructose.
Maltose =glucose + glucose. Created during digestion of starch either in our
body or when a cereal grain sprouts starch breakdown occurs in the plant.
Lactose =glucose + galactose. Milk sugar, 1/6 sweetness of sucrose. Most
adults lack lactase so can only digest small amounts of lactose. Large
quantities cause osmotic diarrhoea & abdominal upset. Surgery to the GIT
often results in short term lactose intolerance.
Trehalose = glucose + glucose. Source = mushrooms, insects. Humans still
Include sorbitol, mannitol, xylitol.
Less sweet than the sugars, but more slowly absorbed so do not increase BGLs
Xylitol used in sugarless gums as it is not a substrate for cariogenic bacteria.
Created from nectar, which consists of sucrose & water. Most honey (except
“organic”) has been heated to prevent crystallization & yeast fermentation
during storage. This does not destroy botulinum spores so infantile botulism
can occur through honey ingestion. Honey is not recommended for children
Honey has no nutritional advantage over sugar. Slightly fewer kJ than sugar as
contains water & does contain some vitamins and minerals not in sugar but in
“Eat moderate amounts of sugar and foods containing added sugar”
Australians obtain about 15-20% of their energy from sugar. Overall this is
compatible with a healthy diet, but at higher intakes sugar begins to displace more
nutritious foods from the diet.
Adolescents get about 25% of their energy from snacks, adults about 20%, and
it is snacks that tend to be higher in sugar than meals (eg tea with sugar,
Sugar can add extra energy to the diet. Although in general there is no
relationship between high carbohydrate diets and obesity, a high consumption
of soft drinks by children was correlated with risk of obesity.
Evidence for the role of sugar in the development of dental caries is strong,
but otherwise there are no diseases linked with sugar consumption. Daily
consumption of xylitol in sugar free gum by children has been shown to
prevent the formation of dental caries, possibly by stimulating saliva
production. Cheese also appears to have a natural anticariogenic effect.
No evidence sugar causes hyperactivity in children
Where‟s the sugar in food?
Food Sugar (%) Food Sugar (%)
Sugar 100 Chocolate biscuits 41
Honey 82 Fruit cake 40
Sultanas 76 Nutrigrain cereal 35
Golden syrup 75 Liqueurs 30
Boiled sweets 74 Ice cream 22
Jam 67 Biscuits, sweet 22
Dates 66 Bananas 16
Milk chocolate 56 Grapes, white 15
Dried apricots 41 apples 12
Where‟s the sugar in drinks?
Drink Serve size Teaspoons of sugar
Soft drinks 1 can (375ml) 10
Cordial (made up) 1 glass (250 ml) 5.5
Fruit juice 100% orange 1 glass (250 ml) 4.5
Fruit juice drink, orange 1 glass (250 ml) 7
Flavoured milk 1 carton (300 ml) 7
Milkshake 350ml 10
MacDonald thickshake 340 ml 9
Port /sherry 60ml 1.5
The major polysaccharides in nutrition are generally polymers of glucose (eg starch,
glycogen & cellulose).
Found in plants and occurs in the amylose (straight chains of glucose) and the
amylopectin (branched) forms.
Amylopectin is more easily digested than amylose.
Ratio of amylose: amylopectin that gives each plant starch its properties - eg
Arborio vs long grain rice.
Starch granules are encased in cellulose. Cooking causes the starch granule to
swell and gelatinise eg porridge.
Where‟s the starch?
Food Starch (%) Food Starch (%)
Flour, white 73 Rice, white, cooked 28
Rice bubbles, corn 71-76 Pasta, cooked 25
Flour, wholemeal 52 Sweet corn 17
Scone, plain 51 Potatoes, boiled 13
Biscuit, sweet 49 Baked beans, 11
Bread, white 45 Rolled oats, cooked 9
Bread, wholemeal 38 Bananas 3-7
Crumpet 38 Pumpkin, boiled 3
Fruit loaf 36 Plain cake 22-34
Product of hydrolysis of starch. As starch molecules become smaller, their sweetness
and solubility increases, so dextrin often used as a sweetener in commercial foods.
Storage form of CHO in humans. Has branched chains of glucose polymers.
Polysaccharides- indigestible (Dietary fibre)
Chemically defined as “non starch polysaccharides” as same chemical structure as a
polysaccharide but is different to starch. It can be further divided into insoluble and
Fibre covers all dietary components not digested and absorbed in the small intestine.
These may be fermented by bacteria in the large intestine.
Adults should have 25-30g/day of fibre. Children need (age of child + 5)g.
Food gm Fibre per serve
Bran cereal 1 cup 7.2
Baked beans ½ cup 6.6
Rolled Oats 1 cup 3.4
Weetbix, 2 biscuits 3.2
Banana 1 medium 3.1
Carrots ½ cup 2.4
Peanuts ¼ cup 2.4
Orange 1 medium 2.4
Bread wholemeal 1 slice 2
Pasta white ½ cup 1.6
Rice brown ½ cup 1.5
Tomato 1 medium 1.5
Rice white ½ cup 0.8
Bread white 1 slice 0.8
Makes up structure of plant walls, and consists of glucose molecules that are linked
by enzyme-resistant bonds. Wholegrains, dried fruit, bran good sources. Insoluble but
capable of taking up water and swelling so will contribute to bulkier, softer stools
Wide variety of compounds that also contribute to plant cell wall structure. Insoluble
but also has high water binding capacity.
A woody non-CHO substance in bran and some vegetables, that is resistant to
fermentation so completely undigested.
Pectin is a non cellulose plant polysaccharide made of units of galactose derivatives.
Absorbs water and forms a gel so is used in jams. Forms gel in SI so slows
absorption, which assists BGL control and cholesterol absorption.
Gums and Mucilages
Gums are similar to pectin but include other sugars with the galactose units. Psyllium
= mucilage. Algal polysaccharides in seaweed and algae used for processing eg
carageenan used to thicken and stabilize many processed foods.
Insoluble & Soluble fibre
Insoluble: mainly cellulose, lignin, hemicelluloses. Aids bowel function by increasing
stool bulk & speeding transit. Also has potential to act as “prebiotic”
Cellulose Hemicellulose Lignin
Wholemeal flour Bran Mature veg
Bran Wholegrains Wheat
Vegetables Fruit with edible seeds
Soluble: Can hold water, form a gel & is a substrate for fermentation by bacteria. Can
remove cholesterol from body by binding bile acids & preventing reabsorption. Also
slows the rate of digestion of nutrients so assists with diabetes.
Legumes Citrus fruits
Physiological effects of fibre:
Stimulate chewing so saliva and gastric acid secretion
Fill stomach so provide sense of satiety
Increases fecal bulk so decreases luminal pressure
Normalises intestinal transit time
Becomes a substrate for colonic fermentation
Soluble fibre delays gastric emptying and slows rate of digestion & absorption
Soluble fibre lowers serum cholesterol
Alters gut epithelium, possibly increasing cellular proliferation
Prebiotics & Probiotics
Prebiotics: Non digestible food ingredients that selectively stimulate the growth or
activity of 1 or a limited number of bacteria in the colon, thereby improving health.
EG oligosaccharides inulin, raffinose & stachyose. These have been shown to
stimulate growth of bifidobacteria in the colon. Role for prebiotics in prevention of
inflammatory bowel disease recurrences & bowel cancer under investigation.
Probiotics: Strains of bacteria added to food that are capable of surviving digestion &
exerting beneficial effects on their host. EG L. Acidophilus. Lactose intolerance &
antibiotic associated diarrhoea can benefit from certain probiotics. Research into
preventative role in irritable bowel syndrome, dental caries & bowel cancer is
Fibre & disease
Because dietary fibre is not absorbed during its transit through the GIT, it has the
opportunity to interact with the intestinal surface & the products of digestion to assist
in the maintenance of good bowel health.
Constipation - adequate dietary cellulose is an important factor in preventing
constipation as is insoluble so increases faecal bulk. Sufficient water needs to be
consumed with cellulose to prevent dry stools.
Soluble fibre absorbs water which also increases faecal bulk & softens stool. This
speeds the transit of the stool through the intestine. Gas produced during fermentation
of soluble fibre also assists stool passage.
Insoluble fibre tends to “normalise” intestinal transit times – hastens it if constipated,
slows it during diarrhoea.
Foods known as laxatives: prunes, prune juice, pear juice, dried figs, raisins, liquorice.
2. Colon cancer
Burkitt, 1974: Observed Africans who eat a very bulky high fibre diet
do not have the same rates of colon cancer as seen in Western society.
Hypothesised that dietary fibre prevents colon cancer by reducing the
time the colon is exposed to mutagens by increasing transit time, and
by increasing bulk hence diluting mutagen concentration.
Also fermentation of fibre produces short chain fatty acids (propionate,
acetate, butyrate). This makes the bowel more acidic. Butyric acid
promotes the differentation of immature colonocytes & inhibits growth
of cancerous cells.
High fibre foods generally high in antioxidants, phenols and indoles,
all of which can lower the risk of colon cancer by destroying free
Folate has also recently been implicated as protective against colon
Wholegrains also contain phytate, which has the capacity to bind non
heme iron or copper (pro oxidants), phenolics (antioxidants), lignans
(weak phytoestrogen). European consensus: “a diet rich in high fibre
cereal foods is associated with a reduced risk of colorectal cancer”.
Some large scale epidemiology studies have found dietary fibre does
prevent colorectal cancer (Health Professionals Follow Up Study)
whilst others have found no protective effect (eg USA nurses study but
in this study little fibre was consumed even by the highest intake
Intervention studies in which fibre was given to prevent polyp
recurrence have also often failed to show a protective effect eg
Australian polyp prevention trial gave 25g wheat bran/day over 4 years
to patients who had a history of polyp removal, but no power in study
as very low rates of polyp recurrence in the control group.
Fibre supplement possibly ineffective as fibre is generally consumed as
part of plant food which contributes other protective agents.
Soluble fibres tend to slow gastric emptying, shorten intestinal transit, reduce
glucose absorption so reduce rises in BGLs and demand for insulin. Studies of
diabetics given large doses of soluble fibre allowed them to normalise their
BGLs and reduce medication in the short term.
High fibre foods also requires more chewing and increase satiety, which can
reduce intake and aid in weight loss in diabetics, which improves BGLs.
Classifying Carbohydrates: The Glycemic Index
The glycemic index is a method of assessing the blood glucose response to
Foods that give a slower, flatter blood glucose profile after digestion and
absorption assist in blood glucose control.
How Glycemic Index is measured
1. An amount of test food containing 50g of CHO is given to a volunteer to eat.
EG To test spaghetti, 200gm would be eaten as this contains 50g of CHO.
2. Blood sugar measurements are then taken every 15-30 minutes over the next 2
3. The blood sugar level is plotted and the area under the curve calculated.
4. The person‟s response to spaghetti is compared to their response to 50g of
glucose or white bread containing 50g/glucose
[Incremental blood glucose area after test food (50gm of CHO)
Corresponding area after equicarbohydrate portion of standard CHO food ] x 100.
The substance which produces the greatest rise in blood sugar is glucose, so this is
given the arbitrary value of 100, and all other foods are given a value from 0 -100.
High GI foods > 70; low GI foods < 55.
The higher the GI factor, the higher the blood sugar levels after consumption of the
The incorporation of low GI foods into diets has shown improvements in blood
glucose control, lipid profile and satiety.
Factors which influence the GI of a food will affect the rate of digestion or absorption.
Factor Mechanism Examples
Low degree of starch The less gelatinized Spaghetti, porridge
gelatinisation (swollen) the starch, the
slower the rate of
Swollen (cooked) starch
granules are easier to
digest as larger surface
area for SI enzymes
Intact grains (except rice) Fibrous outer coat prevent Legumes
enzymes breaking down
High amylose:amylopectin The more amylose a food Basmati rice
ratio contains, the slower its
rate of digestion
Fibre Soluble fibre increases the Rolled oats, apples
viscosity of intestinal
contents so slows
Fat Fat slows down the rate of Potato crisps have a lower
stomach emptying hence GI than baked potato
Anti-nutrients Some foods contain Soybeans
substances that inhibit
digestion of starch eg
LOW MEDIUM HIGH
AllBran, Fruit „n oats, natural Special K, natural muesli, Bran Sugared cereals, puffed
muesli, rolled oats, porridge, Buds, Just Right, Mini Wheats, rice creals* Cornflakes*,
Guardian, oat bran, Komplete Vitabrits, Nutrigrain, Sustain, Sultana Bran, Branflakes,
oven baked muesli, oat/rice Weetbix, Honey Smacks, Cocopops,
bran shredded wheat
all breads which are both light rye bread, sourdough wholemeal bread*, white
wholemeal and wholegrain (e.g, white*, pita bread, crumpet, bread*,
Helga's Classic Grain, hamburger bun, pizza*.
Performax, Burgen, 9 grain
mutigrain, fruit loaf,
pumpernickel, dark rye,
Wheat pasta*, egg fettucine*, long grain white rice*, Sunbrown quick rice*,
Chinese vermicelli*, meat Buckwheat, taco shells, Calrose shortgrain rice*,
ravioli, macaroni*, tortellini, gnocchi, couscous, maize pre-cooked rice, tapioca,
spaghetti*, brown rice, cornmeal, semolina Corn chips, millet, rice
Doongara/clever rice*, Basmati pasta*, noodles*,
rice*, parboiled ricepearl barley, popcorn*.
buckwheat, bulgur, cracked
Soya beans, kidney beans, Green gram dahl, green pea Broad beans, lima
lentils, butter beans, chick soup, split pea soup. beans, pinto beans.
peas, haricot beans, lentils,
baked beans, bengal gram,
Green peas, sweet corn (not New canned potatoes, new cooked carrots, French
super sweet), sweet potato, potatoes, beetroot, potatoes fries, baked/boiled/
raw carrots, eggplant, boiled in their skins mashed potatoes*
brocolli, cauliflower, (especially pontiac,
cabbage, mushrooms, sebago, desiree,
capsicum, tomatoes, lettuce, instant), parsnip,
green beans supersweet corn,
Cherries, plums, grapefruit, Mango, paw paw, sultanas*, watermelon*, very ripe
peaches, apples, pears, fig, bananas (just ripe), raisins*, “medium fruits”*.
dried/fresh apricots, grapes*, canned fruit in syrup. dates, pineapple,
kiwi fruit, oranges, jam, cantaloupe
canned fruit (no syrup).
Whole milk, skim milk, Icecream (full fat). Tofu frozen dessert
chocolate milk, full fat Vitari frozen fruit, gelati,
yoghurt, low fat flavoured low fat icecream
sweetened yoghurt, custard,
Fructose (fruit sugar). Lactose (milk sugar), jam sugar, Glucose,
Nutella, dark chocolate, Glucodin, jellybeans,
sorbet lifesavers, honey,
Apple juice*, grapefruit juice, Cordial, orange juice* all soft drinks*,
Sustagen. Lucozade*, Gatorade*,
(from The GI Factor, Brand-Miller)
Clinical uses for glycemic index:
1. Low GI diets reduce risk of heart attack (Harvard nurses study)
2. Low GI diets reduce risk of developing diabetes (Harvard nurses study)
3. Low GI diets can increase HDL levels (British study on 1400 subjects)
4. High GI diets encourage overeating
5. High GI foods after sport rapidly replenish glycogen levels
6. ? High GI diets linked to myopia
GL is a measurement of both the amount of CHO in a serve of food AND its GI. By
measuring both parameters a better estimate of the food‟s effect on BSL can be made.
Glycemic load is calculated as no. of grams of CHO in the serve x GI/100.
High GI food x large portion = high GL
High GI food x small portion = med or low GL
Low GI food x large portion = med or high GL
This means some foods with a high GI but that contain little CHO in a normal serve
will end up with a low GL (eg watermelon). Other foods with a low GI but a lot of
CHO in a normal serve will have a medium GL (eg spaghetti).
Low GL = less than 10
Medium GL = 11-19
High GL = 20 or more – these foods will raise BSLs most.
How to reduce the glycemic load of your diet
1. Bread: Choose wholegrain breads (eg BurgenTM, pumpernickel, sourdough,
2. Rice & pasta: Choose Basmati rice or rice noodles. Most pasta is low GI
3. Potato: choose sweet potatoes
4. Breakfast cereal: choose wheatbran, psyllium or oat based cereals
5. Use more beans (including soy), peas, lentils, nuts instead of rice, potato, pasta
Phyllis is 75 years old and recently had a polyp removed from her bowel. Her doctor
has advised her to follow a high fibre diet but she isn‟t certain what this means. Her
weight is 65kg (stable for past year) and height is 150cm.She is taking captopril for
her BP – currently 130/100. Sedentary lifestyle & supportive husband Reports good
appetite and yesterday ate: Orange juice, white toast and Rice Bubbles for breakfast;
sweet biscuit for morning tea, cheese sandwich on white bread for lunch, plain cake
for afternoon tea, roast chicken with white rice, green beans, grilled tomato for dinner,
ice cream for dessert, fruit juice for supper.
1. Do a nutritional assessment of Phyllis
2. What interventions might you suggest to meet the nutritional goal of
increasing fibre intake?
3. Phyllis has a list of questions for you about fibre:
A. Which bran is best: wheat oat, barley or rice?
B. Is a high fibre diet OK for my daughter (she has IBS)?
C. Is wheat germ as good as bran?
D. Will a high fibre diet help me lose weight?
Example of increasing fibre in the diet:
Low fibre High fibre
Breakfast Fibre (g) Breakfast Fibre (g)
Orange juice 0 Whole orange 2.0
Rice Bubbles 1.0 Weet Bix 4.1
Milk 0 Milk 0
Toast, white 0.7 Wholemeal toast 2.1
Morning Tea Morning Tea
Sweet biscuit 0.7 Fruit cake 1.4
Cheese sandwich, 1.3 Cheese and salad 4.7
white bread sandwich,
Afternoon Tea Afternoon Tea
Plain cake 0.3 Apple or pear 3.4
Roast chicken 0 Roast chicken 0
Rice, white 0.8 Baked jacket 2.1
Green beans 2.0 Green peas 6.7
Grilled tomatoes 1.4 Corn on the cob 4.0
Ice cream 0 Fresh fruit salad 3.0
Fruit juice 0 Fresh fruit 3.0
TOTAL 9.0g TOTAL 36.5
Some tips for increasing fibre intake:
Eat whole fruits instead of drinking fruit juices
Substitute white rice, bread, pasta with brown and whole wheat versions
Incorporate whole grain cereals for breakfast
Snack on raw vegetables instead of chips, crackers or chocolate bars
Substitute legumes for meat 2 to 3 times per week in chili and soups,
Experiment with international dishes (such as Indian, middle-eastern) which
use whole grains and legumes as part of the main meal (Indian dahls) or as
part of salads (tabouli).
Prebiotics & Probiotics
Probiotics: Live microbes which can help restore the microbial balance in the intestine
and also induce beneficial effects (eg reduction of diarrhoea, boosting of immunity,
reduction of lactose intolerance, anti cancer activity). Consumed in fermented foods
or as freeze-dried supplements.
Probiotic = Lactobacillus casei Shirota. Been used as a probiotic since 1955 and has
been shown to survive digestion and reach the large bowel intact. Most studies done
in animals. Promising for: diarrhoea prevention, stimulation of immune system,
prevention of listeria monocytogenes infection. Contains as much sugar as a small
apple to feed culture.
Probiotic = Lactobacillus acidophilus johnsonii (sold as LC1). Effective for
gastroenteritis prevention, antibiotic associated diarrhoea, possibly reduces activity of
Probiotic = Lactobacillus GG, L.acidophilus, Bifidobacterium. LGG is best studied &
appears most effective probiotic so far identified. Shown to decrease rate of dental
caries in children (inhibits growth of mutans Streptococci) and reduce GI and
respiratory infection in children. Most consistent probiotic in preventing
Prebiotics: Selectively stimulate the growth or activity of one of the microbes in the
colon, therby improving health.
Prebiotic: Inulin. Oligosaccharide that is fermented to SCFA. This lowers the colonic
pH and has been shown to increase the solubility and hence absorption of calcium and
magnesium. Also stimulate growth of probiotics such as bifidobacteria. Currently
being researched for potential to reduce cholesterol levels.
Burgen‟s Rye for digestive balance
Prebiotic:Hi-Maize. Form of starch that is resistant to digestion. Instead fermented to
See June 2001 American Journal of Clinical Nutrition for review of Probiotics.
What % of energy should CHO contribute to the diet?
What % of energy do most Australians get from CHO?
What are the 3 major classes of carbohydrates?
Is honey nutritionally superior to sugar?
Justify the dietary guideline “ Eat moderate amounts of sugar and foods containing
What is cellulose made of?
What are some of the physiological effects of fibre?
What are 3 diseases/conditions that a high fibre intake can assist?
Week 7: NUTRITION & DIABETES MELLITUS
Diabetes is the disease state caused by impaired carbohydrate metabolism. Can be due
1. Insulin deficiency (Type I/ juvenile/ IDDM)
2. Increased insulin resistance at the cellular level (Type II/ mature onset/
Other types include Gestational Diabetes Mellitus, drug induced diabetes and
malnutrition related diabetes.
Insulin - is both anticatabolic and anabolic
- facilitates cellular transport
- has the opposite effect to the counteregulatory hormones
(glucagon, growth hormone, cortisol, adrenalin, noradrenalin)
The Effect of Insulin Deficiency
Reduced entry of glucose to muscle cells for glycogen synthesis and usage
Reduced entry of glucose to adipose cells for synthesis of triglyceride fat
Reduced activation of enzymes of glucose metabolism in hepatic cells
Glucagon and adrenalin stimulate the liver to release glucose by converting
glycogen to glucose
Loss of stimulation of fatty acid synthesis
Increased mobilization of fatty acids from triglyceride
Rise in plasma lipids as lipoprotein lipase not activated
Reduced transport of amino acids into cells
Reduced aggregation of ribosomes so decreased protein synthesis
Increased gluconeogenic enzymes
Insulin/glucagon ratio falls, so increased gluconeogenesis
Decreased rate of entry of K into cells
Rates of diabetes in Australia are increasing:
Approximately 4% of the Australian population has diabetes
For every diagnosed case there is thought to be one undiagnosed case.
Why are there so many cases of undiagnosed diabetes?
The normal blood glucose levels are 3.5 – 8 mmol/L. Symptoms only appear if blood
glucose is consistently above 15mmol/L.
Symptoms of high blood glucose levels:
1. Polyuria, polydipsia and glucosuria
a) At BSLs >10mmol/l renal tubules no longer resorb glucose so glucose
enters the urine
b) Glucose is an osmotic diuretic so promotes the excretion of larger
volumes of water and salts
c) This excessive diuresis can cause dehydration and hence triggers the
symptom of thirst.
2. Blurred vision
a) High BSLs will cause fluid shifts in the chamber of the eye
b) This affects the accommodating capacity of the lens
c) Vision improves when BSLs decrease.
3. Fatigue and Hunger
Lack of glucose in the cells = decrease in available energy for the body = fatigue
Hunger = ? caused by the lack of glucose transport to the hypothalamus
4. Increased risk of infection
High BSLs have a toxic effect on leukocytes so lower the body‟s resistance to
5. Weight loss, ketonuria and ketoacidosis
a) Glucose is no longer an adequate energy source for the body in states of
b) Fat stores are mobilized so weight loss occurs.
c) Ketone bodies are excreted by the kidneys as by-product of fat metabolism
d) Ketone bodies must be excreted in the urine coupled to a base, so bases are
lost from the body and pH of tissues falls, acidosis develops.
e) Untreated acidosis coupled with dehydration and electrolyte imbalances
(caused by the osmotic diuretic effect of excess glucose) will lead to a coma and
In the presence of symptoms diabetes can be diagnosed as a fasting plasma glucose
>7mmol/L OR a random blood glucose > 11mmol/L.
In the absence of symptoms a glucose tolerance test should be done and should show
a fasting plasma glucose >7mmol/L, 1 hour plasma glucose > 11mmol/L and 2 hour
plasma glucose > 11 mmol/L.
Ideal blood glucose control
Ideal Intermediate Poor
Preprandial BG <6 <8 >10
Postprandial BG <8 <11 >13
Urinary glucose 0 0 +
HbA1c <7.0% 7.1-9.0% >9.0%
HbA1c - is the proportion of glucose – linked Hb
- indicates the average blood glucose level over the previous 2
- measures long term control of BSLs.
- Two large intervention trials found the risk of diabetic
complications decreases as HbA1c falls.
Classes of diabetes
Type 1 Diabetes (IDDM)
Beta cell destruction
Severe insulin deficiency
Hyperglycemia & mobilization of fat stores
Production of Ketoacids
The typical characteristics of Type 1 diabetes are:
- Ketonuria or ketoacidosis present
- Rapid onset before 30 years
- Moderate to severe symptoms
- Significant weight loss
- Immune markers of beta cell destruction eg GAD (glutamic acid
decarboxylase on surface of beta cells) autoantigen and GAD
These patients are dependent on insulin for survival.
Type 2 diabetes (NIDDM)
Affects about 90% of Australian diabetics
Genetics may predispose to the condition - certain populations (eg
Aborigines, southern Europeans, Indians) more susceptible
Lifestyle factors are also important as diabetes rates increase in traditional
societies that change to a Western lifestyle of high fat food and little exercise.
Beta cells are not destroyed and insulin continues to be produced.
The key factor is insulin resistance.
If body weight is reduced, symptoms improve
1. A reduction in available insulin receptor sites (common in obese
2. A reduction in insulin binding to its receptor site
3. Impaired glucose transport following attachment of insulin to receptor
4. These cause peripheral insulin resistance & reduced glucose uptake
5. Hyperglycemia evident
6. Increased insulin secretion
7. “Beta cell exhaustion” eventually occurs
8. Impaired insulin secretion
9. This causes increased FFA & glucose production
A state of complete insulin absence does not occur and hence Type 2s are not
dependent on insulin for survival. However diabetes inevitably progresses and may
eventually require insulin.
Characteristics of Type 2 diabetics
Later onset of symptoms
Central obesity (about 80% of cases have this)
Approximately half the people diagnosed are asymptomatic and may be undiagnosed
for up to 6 or 7 years before long term complications will emerge and result in
Syndrome X (the “metabolic syndrome” or “insulin resistance syndrome” )
At least 1 in 4 Australians has Syndrome X
It is characterized by:
High insulin levels
Excess fat around the abdomen
High blood TGs
Low HDL cholesterol levels
Obesity is thought to be the cause of these symptoms:
1. Adipose cells in the abdomen are more metabolically active, so release more
TGs into the circulation. The TGs interfere with the activity of the insulin
receptor, pushing insulin levels up. High insulin levels prevent adipose cells
from efficiently extracting and storing TGs from chylomicrons and VLDL,
further boosting TG levels.
2. Obesity can also directly cause a rise in insulin levels. Adipose tissue in
obesity produces less adiponectin (which increases insulin sensitivity) and
more resistin (which decreases insulin sensitivity). Central adiposity is the best
clinical marker of insulin resistance.
3. Insulin resistance interferes with the normal dilation of blood vessels. High
insulin levels promote sodium resorption, causing fluid retention and an
increased blood volume. All these factors can promote high blood pressure.
Syndrome X can lead to type 2 diabetes and CVD.
Impaired Glucose Tolerance
IGT - blood glucose levels outside the normal range but it is not elevated
enough to meet the criteria for diabetes.
Often coupled with other components of the metabolic syndrome such as HT,
obesity and dyslipidemia.
10 year follow up studies have found that 1/3 of IGT patients will progress to
type 2 diabetes, 1/3 will return to normal and 1/3 will remain IGT.
Gestational Diabetes Mellitus
Defines glucose intolerance that first occurs during pregnancy
Onset is during the 2 nd or 3rd trimester
Presents as marked insulin resistance
Appears to be mainly due to the hormones human placental lactogen, human
chorionic gonadotropin, progesterone and glucocorticoids.
These have an anti-insulin action, thus preventing the uptake of glucose by
Maternal age, adiposity and inactivity can also contribute
Occurs in about 3% of pregnancies in Westernised countries but up to 20% in
populations with high rates of diabetes. At greater risk if relative has diabetes.
Risks of Gestational Diabetes
Glucose crosses the placenta so high maternal glucose levels can trigger the release of
insulin in the fetus, which stimulates growth. Fetal macrosomia is defined as a birth
weight above 4.5kg which increases risk of fetal death in utero, birth trauma,
respiratory distress syndrome, rebound hypoglycemia and jaundice.
2.Future risk of diabetes
About 50% of women who had GDM will develop Type 2 diabetes over the next 10
Complications of Diabetes Mellitus
A. LONG TERM COMPLICATIONS
Occur as a result of damage to the capillary wall.
Non insulin dependent tissues accumulate glucose during hyperglycemia.
Rising intracellular levels of glucose leads to accelerated protein
Microangiopathy is the result of the accumulation of glycosylated collagenous
protein in the basement membrane of capillaries which thickens it and reduces
its permeability to oxygen.
Causes about 25% of blindness in Australia
Result of microangiopathy in the retina. This encourages the formation of new
capillaries which tend to burst with consequent retina haemmorhage.
Yearly eye checks are advised for diabetics.
Diabetic nephropathy causes about 25% of all renal failure in Australia.
This is also caused by thickening of the basement membrane of the capillaries
and will lead to microalbuminuria, then proteinuria and finally renal
Control of hypertension delays progression.
Peripheral and autonomic neuropathy can result from the damage to the
myelin sheath by elevated blood glucose levels. Peripheral neuropathy
commonly leads to loss of sensation to the feet and toes which can cause
injuries to go unnoticed/untreated.
Healing of injuries is slowed by poor blood supply and infections are common
in states of hyperglycemia.
This increases the risk of gangrene and amputation.
Autonomic neuropathy can result in postural hypotension, delayed gastric
emptying and nausea, intermittent diarrhoea, bladder atony and impotence.
Main vessels affected are coronary, cerebral & peripheral arteries so increased
risk of AMI, stroke, peripheral vascular disease.
Dyslipidemia will further increase the risk of CVD.
Large studies in the UK and USA have shown that good control of BGLs is effective
at reducing risk of long term complications.
B. SHORT TERM COMPLICATIONS
This is a BGL above 10mmol/l. The causes can include:
medications which increase blood glucose (eg steroids)
other illnesses and infections
missed or insufficient insulin or OHA
not enough exercise or changes to the eating pattern
This is a BSL below 3.5mmol/L. Only people treated with insulin or sulphonylureas
are at risk of hypos. The causes include:
insufficient food or delayed meals
physical activity without sufficient food
excess insulin or sulphonylureas
excess alcohol without food
Lack of glucose to the nervous system causes double vision, headache, tremor,
confusion and the sympathetic nervous response increases pulse, sweating and anxiety
Hypoglycemic unawareness can occur in people with long standing diabetes or
repeated episodes of hypos.
1. If possible take a blood test to confirm hypoglycemia
2. Take about 15 g of a fast acting carbohydrate (preferably glucose)
Eg 150 ml lucozade, 3 glucose tablets, 5 jelly beans or 150mls of lemonade. Repeat
after 5 minutes if symptoms not improving
3. Take a slow acting carbohydrate to stabilize blood glucose eg piece of fruit or
If consciousness lost, intramuscular glucagon is required.
Management of Diabetes
This is instigated immediately for Type 1 patients and when diet and lifestyle
changes have not improved BSLs of Type 2 diabetes patients.
Oral Hypoglycemic Agents:
Are used on Type 2 patients to stimulate the pancreas to release insulin
(sulphonylurea group eg gliclazide) or improve insulin action at the cellular level
(biguanide group eg metformin).
As diabetes progresses control of BGLs worsens and eventually Type 2 patient may
Type 1 patients depend on insulin. A typical regime may be 3 injections of rapid
acting insulin before each meal and 1 injection before bed of slow acting insulin. This
approximates physiological insulin production.
1. Physical activity
Strongly encouraged for people with Type 1 and especially Type 2 diabetes as
Increased energy expenditure
Improved insulin sensitivity
Reduced hepatic glucose production
Changes in lipid levels
Lowering of BP
Improved well being.
Get medical check up first & start slowly
Improved insulin sensitivity decreases after 48 hours so regular exercise is
Blood glucose monitoring pre and post exercise allows the individual to adjust
insulin or carbohydrate intakes.
Type 1 diabetics should not exercise if BSL >15mmol/L
Moderate exercise of <30 minutes rarely needs additional CHO or decreased
insulin, but a snack is recommended if BSL is <6mmol/L
1 hour of exercise requires an additional 15g of CHO (eg piece of fruit or
sandwich either before or after exercise)
Strenuous exercise requires an additional 30gm of CHO and a small decrease
in the insulin dose for that time period
Diabetic athletes should keep training diaries to monitor BSLs before, during and
after exercise, food and fluid consumed, duration & intensity of exercise, insulin
2. Weight loss
Weight loss is the first line of treatment for Type 2 diabetics
Weight loss is associated with improved insulin sensitivity Small weight
losses of only 4-5 kgs can still improve insulin sensitivity and improve lipid
profiles and hypertension
Clients should be reassured that improvements in diet and exercise will still be
beneficial in reducing their risk of complications, even if they do not manage
to lose weight.
Type 1 diabetics also should avoid becoming overweight because of the
increased tendency of hyperlipidemia, hypertension and increased risk of
High carbohydrate, low fat diets
Diets low in fat (<30% of energy), high in fibre (>30gm/day) and carbohydrate
decrease fasting and average BSLs, increase insulin sensitivity, increase satiety and
maintain or reduce lipid levels. This type of diet is not easy to follow. Aimed at
reducing weight & chol but often pushes up TGs
High monounsaturated fat diets
Epidemiology studies have shown Mediterranean diets decrease post prandial BG,
decrease mean BG, increase insulin sensitivity, decrease fasting and postprandial
TGs, maintain HDL cholesterol, decrease BP, reduce weight and abdominal weight
and are easier to comply with.
A Mediterranean diet includes:
Red meat 1-2 times/month
Sweets, eggs, poultry, fish a few times/week
Cheese, yoghurt, olive oil, fruit, legumes, vegetables, breads, rice, pasta,
polenta or couscous / everyday
Good choice if not overweight or similar to usual diet
High carb, low fat diet Mediterranean diet
Total fat 20-30% 40-50%
Saturated fat 10% or less 10% or less
Polyunsaturated fat 10% or less 10% or less
Monounsaturated fat 10% or less 20-30%
Carbohydrate 50-60% 30-40%
Protein 10-20% 10-20%
It is recommended that diabetics have at least 0.8 g/kg bodyweight and protein
contribute 10-20% of their energy intake.
Limiting fat intake is important for 2 reasons:
1. The most common complication of diabetes is CVD, and saturated fat in particular
has been linked to the progression of CVD.
2. A high fat intake is associated with increased weight, and excess weight decreases
Saturated fat intake should be less than 10% of energy intake as it is associated with
increased total and LDL cholesterol and triglycerides.
Polyunsaturated fats should also make up less than 10% of energy intake.
Same recommendations as CVD.
Fish intake recommended as shown to reduce clotting tendency and reduce risk of
CVD. Omega 3‟s can help insulin resistance.
How to maximize omega 3‟s:
1. Eat oily fish (tuna, salmon, sardines, trout) regularly. White fish has about ¼
the omega 3 content so still of some benefit
2. Use canola or flaxseed oil for cooking
3. Use canola margarine as a spread instead of saturated fat in butter, cream,
4. Also minimise omega 6 polyunsaturates (use less safflower, sunflower, corn
oil, polyunsaturated margarine)
5. Eat dark green leafy veg each day, as part of 5 serves of fruit and veg
6. Include soy foods, omega enriched eggs, walnuts, pecans, linseeds, all of
which are high in omega 3‟s.
Sucrose is no longer a focus for management as it does not provoke a large
rise in blood sugars in moderation.
Recommended sucrose contribute <10% of overall energy
Preferably eaten in nutrient dense foods (small quantity of jam on wholemeal
bread) rather than lollies or soft drinks.
“Non nutritive” sweetners recommended
They provide very little extra energy, don‟t affect BSLs.
Include saccharin, cyclamate (these no good for cooking) aspartame,
sucralose, alitame, acesulfame K.
“Nutritive” sweetners can affect BSLs, so not recommended. Include sorbitol,
mannitol, xylitol, isomalt, polydextrose, fructose, lactose.
Starchy carbohydrates (eg porridge, bread, rice, pasta, potato, legumes) - should
be included in each meal
- should make up at least ¼ of that meal
- should be spread evenly throughout the day.
Therefore regular meals are important for diabetics.
They also must have a bedtime snack if taking insulin to avoid hypos in the night.
Timing of meals and activity can be varied but the insulin regime must also be varied.
Practical advice: Include 1 low GI food in each meal, but remember fat lowers the GI
of foods, and foods high in fat are not recommended for diabetics. Also each person
responds individually to various foods so the GI value is only a guide.
? soluble fibre slows the rate of digestion and absorption of carbohydrate and
hence assists with BGL control and improves lipid profiles.
Fibre increases satiety without a large increase in energy intake, which assists
with weight loss
Recommended: At least 30g fibre/day. Wholegrains, fruit and vegetables, high
fibre breakfast cereals etc promoted.
Alcohol causes hypoglycemia in people taking insulin or sulphonylureas. This
is because alcohol inhibits gluconeogenesis and augments the action of
insulin. Hypoglycemia is more likely if alcohol is consumed without CHO or
Recommended: A limit of 1-2 standard drinks/day with 2 alcohol free days a
week. Consumption of CHO with alcohol, preferably as a meal but if no other
sources of CHO are available chips, corn chips or regular soft drinks can be
used as a source of CHO. Alcohol should be avoided when diabetes is
NIDDM can initially be managed by a healthy diet (low in fat, high fibre,
regular CHO) & exercise, without needing medication.
Newly diagnosed diabetics need to see a dietitian or can do a Diabetes
Education course (see local hospital or community health centre).
Timing of meals important: aim for 3 meals and 3 snacks spread evenly
throughout the day so carbohydrate intake even.
Weight loss will improve blood glucose and may reduce medication needed.
Regular daily exercise is essential to help reduce abdominal fat and insulin
resistance of muscle tissue.
Steven has come in for a consultation and his medical history shows that he is being
treated for the metabolic syndrome by his GP. His waist measurement is 120cm, his
weight is 125kg, height 190cm. His usual diet consists of skipping breakfast, coffee
and cake for morning tea, a takeaway from the local Indian restaurant for lunch, a
large portion of red or white meat for dinner with a salad, 3 or 4 glasses of wine with
dessert and chocolate in the evenings. He does no organised physical activity.
4a) Besides abdominal obesity and raised triglycerides, list 3 other symptoms of the
metabolic syndrome? (3 marks)
4b) Explain how obesity can contribute to the metabolic syndrome. (9 marks)
4c) What is a specific dietary change that may lower TG levels? (1 mark)
4d) Why is it important to identify and treat the metabolic syndrome? (2 marks)
What is Glycemic Index and Glycemic Load?
GI is a way of classifying foods containing carbohydrate. Since
there is no rate limiting step in the conversion of polysaccharides
into glucose, foods high in polysaccharides (“complex
carbohydrates” or “starchy” foods) can be capable of increasing
blood glucose levels to the same extent as simple sugars.
GI is formally defined as the incremental area under the blood
glucose curve after consumption of 50g of CHO from a test food
divided by the area under the curve after eating a control food
containing 50g of CHO. Therefore GI is a meaure of how quickly a
food is digested and absorbed. High GI foods cause a rapid rise in
blood sugar levels, and a corresponding large release of insulin.
In general, refined grain products have a high GI, legumes and
unprocessed grains have a moderate GI and nonstarchy fruits and
vegetables have a low GI.
Glycemic load is the GI x carbohydrate content, which takes into
account some foods may have a high GI but contain little CHO (eg
carrots), hence have little effect on BSL.
Evidence supporting consumption of low glycemic load diets:
High glycemic load diets consumed long term shown to increase
risk of developing type 2 diabetes & CVD (Harvard Nurses study);
increase HbA1c in type 1 diabetics (European study)
Low GI diets linked to higher HDL cholesterol measures.
High GI diets associated with low HDL, high TG,
hypercoagulation, colon cancer, breast cancer.
Diabetics shown to improve HbA1c on low GI diets, CVD patients
improve lipids on low GI diets.
Arguments against use of GI:
Mainly a political stance in USA – because most GI research was
done in Canada & Australia, Americans dismissed it.
Also some concerns that high fat foods have low GI values so
might seem to promote these.
No very long term prospective trials done on GI yet as relatively
new area of research.
GI is used in Australia to help diabetics, athletes, CVD patients,
obesity patients with weight loss, but not supported by American
Diabetes Association or American Heart Foundation.
GI needs to be used to compare food choices within the same food group (in the same
manner as the Healthy Heart Tick).
1.What are the acute physiological problems of a patient who has just developed type
2. What are the possible long term complications which may develop over a
period of years in the patient with poorly controlled diabetes?
3. What are the signs and symptoms of hypoglycemia?
4. What are the causes of hypos?
5. How would you treat hypoglycemia?
6. How would you decide if the BSL control of your client was satisfactory?
7. Why is fat an important macronutrient in diabetes management?
8. Why is weight control the central plank of T2 diabetes management?
9. Should sucrose be consumed by diabetics?
10. Should artificial sweetners be used by diabetics?
11. What are the risks associated with gestational diabetes?
12. What are some exercise guidelines for diabetics?
13. Which diet is better for diabetics – high CHO, low fat or high MUFA,
14. Your client wants to take fish oil supplements to help his RA. Given he is also
diabetic, what advice would you give him?
15. How is GI calculated?
16. What are some of the factors that influence GI values?
1. Insulin acts to: (Choose the false answer)
a. Increase gluconeogenesis
b. Increase glucose entry into the cell
c. Increase amino acid uptake by the cell
d. Increase fat metabolism
2. Information required to help differentiate the diagnosis of Type 1 and Type 2
a. age at diagnosis, weight at diagnosis, blood glucose levels
b. blood glucose level, age at diagnosis, presence of ketones
c. age at diagnosis, weight at diagnosis, presence of ketones
d. urine glucose level, insulin levels, presence of weight loss
3. The initial treatment plan for an obese person with Type 2 diabetes should be the
a. An oral hypoglycemic agent
b. A weight reduction program
c. Both a and b
d. A controlled CHO intake
4. In all cases of Type 1 diabetes it is important to monitor blood glucose
a. Serum potassium
b. Serum cholesterol & triglycerides
c. Pancreatic amylase
d. Urinary ketones
e. Both b and c
f. Both b and d
5. Choose the true statement:
a. GI is a method of measuring an individual glucose and insulin response to a
CHO containing food
b. GI is an alternative way to measure CHO intake
c. A high GI food should give a slower, flatter response than a low GI food
d. GI research shows that equivalent amounts of CHO from different foods elicit
different glycemic responses.
Week 8: PROTEIN
Proteins consist of amino acids linked by peptide bonds.
The primary structure of a protein is the amino acid sequence. Secondary
structure refers to helices, coils or pleats that form as they fold up.
The overall structure is its tertiary structure.
“Simple” proteins consist only of amino acids.
“Conjugated” proteins: a non protein component is attached to help facilitate
its function eg iron in haemoglobin, lipid in lipoproteins.
Used for anabolic process of building/maintaining tissues; as an energy source
(17kJ/g); formation of enzymes and hormones; as antibodies; in transportation eg
lipoproteins, albumin; maintain normal osmotic relations in body fluids (eg low
albumin will cause oedema).
Essential and Non Essential amino acids
Essential Conditionally Essential Non Essential
Arginine Proline Glutamate
Leucine Serine Alanine
Isoleucine Tyrosine Aspartate
Valine Cysteine Glutamine
Essential = body synthesis inadequate to meet metabolic needs. Deficiency causes
weight loss, impaired growth, and amino acid specific symptoms.
Non essential = can be synthesized from essential amino acids or from other
Conditionally essential = Essential under some clinical conditions eg taurine, cysteine
for preterm babies.
Special functions of amino acids
Tryptophan = precursor of niacin and serotonin
Methionine = required for synthesis of choline and carnitine
Phenylalanine = precursor of tyrosine, thyroxine, adrenalin
Tyrosine = precursor for melanin
Glycine = combines with toxic substances to convert them before excretion
Histidine = precursor of histamine
Hormonal regulation of protein levels
Growth hormone stimulates protein synthesis
Insulin stimulates protein synthesis by accelerating amino acid transport
across cell membranes
Testosterone stimulates protein synthesis during growth periods
Glucocorticoids stimulate gluconeogenesis & ketogenesis from proteins
Thyroxine increases rate of metabolism of all cells, so protein metabolism is
Food proteins Synthesis Tissue proteins,
of non hormones,
essential aa enzymes etc
Amino Acid pool
Renal excretion conversion
Excess nitrogenous tissue
amino acids constituents
Glucose, ketone Urea
Acetyl CoA, citric
Animal protein sources (meat, egg, milk, fish) are of very high quality (a small
amount in the diet will provide adequate levels of all amino acids).
For vegetarians the issue of protein quality is more important. Plant sources of
protein tend to contain a limiting amino acid, the amino acid present in the
Eating a combination of protein sources reduces the risk of deficiency in an
essential amino acid.
EG cereal protein is low in lysine, rice is low in threonine, whilst legume
protein is limited in methionine, so by combining grains with legumes
adequate protein is consumed.
This is known as the complementary protein principle.
Recommended dietary intakes
Based on nitrogen balance studies done pre-1985.
0.75g/kg of high quality protein was felt sufficient to meet the needs of 97.5% of the
adult population (includes large safety margin).
Unethical to do such studies on children so their requirements RDIs based on
measured intake of protein.
Infants under 6 months = 2.0g/kg ideal bodyweight/day
7-12 months = 1.6g/kg day, 1-3 years=1.2g/kg,
4-18 years= 1.0g/kg.
Athletes may need higher protein intakes – up to 2.5g/kg day if increasing muscle
mass. Easily obtained by diet.
During illness or injury a hypercatabolic state can occur, which causes an increase in
metabolic rate and an accelerated loss of body protein. There is increased production
of stress hormones, cytokines, eicosanoid hormones, and increased production of
acute phase proteins.
Coupled with a poor food intake, a deficiency in energy intake and protein can occur
& inhibit recovery.
Therefore patients with injury/mild trauma require 1.0-1.5g /kg bodyweight/day;
severe stress/trauma 1.5-2.0g/kg bw/day; surgery/fractures/growth period/pregnant
Food sources of protein
Animal: milk, eggs, meat, fish
Legume: peanut, soybean, beans, peas, lentils
Cereals: rice, wheat
Fruits & vegetables: small amounts
Conditions of low protein intake
1.Kwashiorkor (word from Ghana)
Not be seen in Australia but is the classic disease of protein deficiency.
Age of onset typically 1-4 years.
Caused by diets low in protein, which is of poor quality. Extreme protein deficiency
leads to hypoalbuminaemia, oedema, enlarged fatty liver. Muscle wasting that occurs
is often masked by the oedema.
Often occurs in conjunction with energy deficiency, in which case called Protein
Part of several religious faiths or philosophical movements (Seventh Day Adventists,
Buddhists, Catholic Trappist monks, Hare Krishnas). Also chosen for ecological
beliefs, health reasons, economic reasons or opposition to animal cruelty.
In general, vegetarians have lower LDL cholesterol, are less likely to suffer heart
disease, breast, bowel and lung cancer, have lower BP, weigh less and have a lower
risk of type 2 diabetes.
Reasons: ?higher intake of fibre ?lower intake of fat ?lower intake of high GI foods
?more antioxidants ?less likely to smoke ?drink less alcohol & caffeine ?less stressed
Types of vegetarian diets:
Vegans – avoid all food of animal origin. Diet based on grains, nuts, legumes, fruit
and vegetables. May also avoid products made from or tested on animals.
Lacto vegetarians – avoid meat and eggs but include dairy foods
Lacto ovo vegetarians – avoid meat, but include eggs and dairy foods. Best choice for
vegetarians who are pregnant, breast feeding, or still growing as easiest to meet
Semi vegetarian – Has occasional fish or chicken in diet.
Fruitarian – Eats only fruits and nuts. Real risk of nutrient deficiencies.
Macrobiotic – Excludes all animal foods, dairy products, eggs. Uses only
unprocessed, unrefined, organic cereals, grains, fruits and vegetables.
Potential nutrient deficiencies in a vegetarian diet:
Most vegetarians have sufficient protein to easily meet the RDI, especially if they
include eggs or dairy products. Vegans may be potentially at risk of protein
deficiency, especially if pregnant, breastfeeding, a baby, child, teenager or an athlete.
Important 2 different plant protein sources are eaten in combination to complement
each other, as each will be limiting in a different amino acid. Mixed proteins sources
should provide a sufficient quality & quantity of amino acids. Legumes should
probably comprise about 15% of dietary energy as they are a good quality source of
protein & complement cereal by providing lysine. A mixture of 70:30 cereals to
legumes has been suggested as ideal. Nuts and seeds are also a good source of protein
to include. Examples of good protein combinations: pea soup with bread, pasta with
bean and vegetable sauce, Lebanese bread dipped in hommous, Indian lentil dhal with
rice or chappati.
Key message is have a variety each day of protein foods. Child vegans need energy,
protein dense foods – nuts, cereals, legumes, with less emphasis on fruit and
2. Vitamin B12
Found in milk cheese, yoghurt and eggs, vegans especially at risk of
deficiency, many vegetarians low.
Frank deficiency causes pernicious anemia and nervous system
degeneration. Mild deficiency can elevate homocysteine levels and hence CVD
3-5 year‟s supply stored in the liver, so deficiency rare in adults, but
can occur in breast fed babies of vegan mothers. Pregnancy will deplete her
stores, and result in B12 deficient breast milk.
Vegans need B12 fortified soy milk or a supplement (2
micrograms/day sufficient). Vitamin B12 in supplements is derived from
Fallacy that mushrooms are “meat for vegetarians” and contain
adequate amounts of B12 due to bacterial contamination present on them.
Mushrooms, tempeh, seaweed, Guinness, spirolina etc are not reliable sources of
vitamin B12. No vitamin B12 in vegemite.
Vegetarian diets usually high in vitamin C, helps with the absorption of non
haem iron, although those with high iron needs (menstruating women,
pregnant women, young children) may need a supplement.
Vegans may struggle to obtain adequate iron and calcium, so a fortified soy
milk should be chosen.
Vegetarian iron sources: iron enriched breakfast cereals, dark green leafy
vegetables, beans, lentils, dried fruit, cocoa powder.
Non dairy calcium sources: fortified soy milk, green leafy veggies, tahini, almonds,
Brazil nuts, hazelnuts, tofu, dried figs.
Vegetarian zinc sources: wholemeal and grain breads, bran, wholegrain cereals, zinc
fortified breakfast cereals (eg CocoPops, Sultana Bran), pulses, nuts.
Vegan diets can be used by children, but adequate supplies of B12, protein, energy,
iron, zinc, calcium need to be given – most vegan children are at the low end of
normal for growth. Use small meals and frequent snacks to help children meet their
requirements. Include full cream soy milk & chop or grind nuts and seeds to aid their
digestion. Emphasise grains, nuts, legumes over fruit & veg.
Example of adequate diet for Vegans
Food group Serving number for adults (add 1 extra
serve in each group if pregnant)
Breads preferably wholegrain (1 slice = 1 5
Cereals:wheat flakes, flour, bulgur,
wheatgerm, rice, oatmeal, pasta, breakfast
cereal (1 serve = 100g when cooked)
Citrus fruits (including juices) (1 serve= 1
120g fruit or 120ml juice)
Dark green or deep orange veg (broccoli, 1
kale, dried apricots, carrots etc) (1 serve
= 100g cooked)
Other fruits and veg (apple, potato, 5
tomato, banana, raisin, sweetcorn,
avocado) (1 serve= 100g cooked or raw)
Pulses:lentils, soya, beans, split peas, 2
tofu, tempeh, peanuts (1 serve =100g)
Nuts and seeds: sunflower, sesame,
pumpkin seeds, tahini (1 serve=30g)
Fortified soya milk (1 serve = 250ml) 2
Vegetable oils and spreads: soya, olive, 3
canola (1 serve = 1 teaspoon)
B12 vitamin supplement 1
High protein diets (based on work of Dr Neil Mann, RMIT)
A true high protein diet consisting almost solely of protein will kill you. American
early settlers who ate only wild rabbit suffered nausea, diarrhoea, death due to
hyperammonemia & hyperaminoacidemia.
Many so called “high protein diets” are really low carb or high fat or low energy,
combined with a moderate protein intake.
EG Atkins diet = 27% protein, 5% carb, 68% fat
Zone diet = 34% protein, 36% carb, 29% fat
Sugar Busters = 27% protein, 52% carb, 21% fat
Paleolithic diet (est.) = 37% protein, 41% carb, 22% fat
Some interesting facts:
1. During 2002 recognition that “high fat diets cause heart disease” has no good
scientific evidence to support it. Furthermore it ignores other dietary factors
and the importance of genetics in CVD.
Saturated fat causes an increase in cholesterol, and this increases the risk of
cholesterol contributing to atheroma formation and hence heart disease, but there
is no evidence that a diet high in saturated fat by a person not already at high risk
of CVD will shorten their lifespan.
2. High protein, controlled fat diets reduce cholesterol levels
3. High CHO diets increase the proportions of small dense atherogenic LDL, increase
TGs and decrease HDL.
4. Prospective cohort study of 80,000 women found that replacing high GI
carbohydrate choices with protein foods reduces IHD.
All these facts support a shift away from promoting low fat diets, and towards
promoting a diet more similar to that which we evolved on (low GI foods, moderately
high in meat & protein, low in saturated fat, relatively high in omega 3 fats, low salt).
Our ancestors also had a low stress, smoke free, active lifestyle which also decreased
their risk of Syndrome X conditions (obesity, diabetes, HT) prevalent in industrialised
Diets in human evolution:
Primitive stage (2 million years): low saturated fat, mod. high protein, low GI diet (no
grains, legumes or dairy)
Agriculture (10,000 years) : high unrefined CHO, low fat, low GI diet (wholegrains,
some meat & dairy)
Industrial revolution (200 years): high refined CHO, high GI
Fast food revolution (40 years): high refined CHO, high saturated fat
Modern hunter gatherers: Have a high reliance on animal foods plus high fibre wild
plant foods. Similar macronutrient content to Paleolithic diet.
Almost all modern hunter gatherers experience Type 2 diabetes if follow a Western
diet (ie shift from moderately high protein to high CHO diet).
Hypothesised this is because they are prone to insulin resistance. During feast/famine
cycles it is a survival advantage to be insulin resistant as this means excess energy is
more easily stored as fat. Also redirects glucose to brain and fetus instead of muscle
This suggests we are genetically unsuited to a Western style diet. Example of „modern
Half cantaloupe, 2 lean pork chops, broccoli, salad
200g salmon Dessert
Lunch Fresh blueberries & almonds
Shrimp (7) & vegetable salad
Nuts, fruits and cold lean chicken
Nutrient Daily Intake %Energy
Protein 170g 32
Carb 142g 27
Fat 100g 40
Saturated fat 17g 7
MUFA 50g 20
PUFA 33g 13
thiamin 4.6g 417
riboflavin 3.6g 281
Vit C 559g 932
Vit D 0 0
Vit A 6860 RE 850
Vit E 26.5mg 330
calcium 890mg 110
iron 21.5mg 143
zinc 19.8mg 165
Potential concerns with a high protein intake:
Safety of protein intakes above 2.5g/kg bodyweight is unknown
High protein metabolism results in increased urinary urea load and increased
potential renal acid load hence subsequent calcium loss in urine is possible. A
high intake of fruit and vegetables will make urine more alkaline to prevent Ca
loss. Mineral waters high in bicarbonate (eg Evian) will also counteract acid
Does high protein intakes increase homocysteine levels - untrue
Does high meat intake means high saturated fat intake as meat is fatty –
Australian meat is lean
Is a state of ketosis is dangerous? – ketosis is a normal state for humans in
response to a food shortage. Ketone bodies are a more efficient fuel for the
CNS & heart than glucose. It is ketoacidosis which is dangerous.
High protein diets and weight loss
Fat loss requires lipolysis and oxidation
For lipolysis of fat stores to occur, need low levels of insulin
High GI CHOs most effective at increasing insulin levels
As a result CHOs are oxidized in preference to lipids.
Lipids are oxidized most efficiently when blood glucose and glycogen stores
are low, hence insulin is low
This can be achieved by fasting, exercise and/or limiting CHO intake
(especially high GI carbohydrate)
Paleolithic diets had low GI
Remember, a “diet” will probably cause weight to yoyo. Instead need to
commit to a lifestyle change of eliminating refined CHO and replacing with
fruit, veg, nuts, fish and meat
Julia is 13 years old and has decided to become a lacto ovo vegetarian. Her mother
has brought her to see you, as she is very concerned Julia won‟t be meeting all her
nutrient requirements if she cuts meat & fish out of her diet. Her weight is 45kg,
height 155cm. She eats a yoghurt and 1 slice of toast with Vegemite for breakfast, has
biscuits with milk for morning tea, lunch is a cheese & salad sandwich, after school
snacks are fruit & muesli bars, and for dinner she has been eating the family meals but
avoiding the meat. She participates in school sports for an hour twice a week.
1a) Which nutrients are vegetarians at higher risk of deficiency? Suggest a good
food source of each nutrient that would be acceptable to a lacto ovo vegetarian. (5
1b) Explain the complementary protein principle, and how Julia could apply it to
her evening meals. (3 marks)
1c) How can she ensure an adequate iron intake as a vegetarian? What are 2
components in food that can inhibit iron absorption? (4 marks)
1d) What are 3 diseases that vegetarians are at lower risk of developing? (3 marks)
Endurance type athletes tend to become vegetarian to meet high CHO
requirements or help with weight control.
Be aware some female athletes use vegetarianism as an excuse to mask an
Encourage a wide intake of foods high in protein and CHO in each meal.
1.Why an athlete has become vegetarian (may have erroneous dietary beliefs). Moral
or religious beliefs need to be respected.
2. Style of vegetarianism athlete follows. Vegan diets should be closely checked for
Nutrients of concern
If recent vegetarian, may struggle to maintain energy intake as vegetarian diets
generally less nutrient dense. Ask if been maintaining weight on vegetarian diet.
Energy dense, low bulk foods include tofu, TVP, fruit juices, dried fruit & nuts, nut
spreads, honey and jam.
Tends to be lowest for lunch. Athletes have limited cooking time, so baked beans,
tahini or peanut butter sandwiches, luncheon meat substitutes made from wheat gluten
are quick, high protein lunch choices.
Recommend fortified soy milks, yoghurts & custards, fortified breakfast cereals,
broccoli, kale, bok choy.
Fortified soy milk or a supplement required.
FBE (Hb, transferrin, ferritin) should be checked for all vegetarian athletes. Fortified
breakfast cereals, some breads, gluten based meat substitutes, dried fruit, dark green
leafy veg. Consume with vitamin C.
More information: www.sanitarium.com.au.
Generally understood to be foods which are grown organically, processed as little as
possible and contain no added preservatives, artificial colours or flavours.
All foods could be regarded as “health” foods if part of a balanced diet - a food
legally cannot use the word “health” as part of its brand name for this reason
Most Health Food shops also sell a wide range of vitamins, minerals and other dietary
How Health foods are marketed:
Labelled “natural” “wholesome” “pure”
Claimed our soils are depleted of nutrients (untrue)
Claimed vitamin & food supplements needed because our food supply is
deficient in nutrients (untrue)
Claimed our food supply contains chemicals which are poisons
Use of testimonials from customers
Use of celebrities/sportspeople for endorsements
Supported by books by health food gurus
Types of “Health” Food:
Are allowed to be presented as alternatives to Western medicines & can make
The strength of the claim on label must match the supporting evidence eg
strong claim = randomised clinical trial.
Must have AUST-R or AUST-L number on label.
AUST-R = registered medicine: pre market safety, quality & EFFICACY
AUST-L = listed medicine: pre market safety & quality established
If AUST number not on label, AVOID as safety & quality unproven.
Method of farming that is sustainable and environmentally sensitive.
Food is pesticide free (independent yearly surveys show non organic food
contains either zero or trace quantities of pesticides)
No difference in nutrient composition to non organic food
Dried yeast is the richest source of 7 B group vitamins
However it doesn‟t match our vitamin B requirements perfectly – eg 1tbsp
bakers yeast has 20% of our biotin RDI but 400% of folate RDI
Cheaper sources of B group vitamins are wheatgerm and unprocessed bran
Secretion from the salivary glands of bees
Used as rejuvenator. Severe allergic reactions can occur & can take 2 or 3
exposures before they occur
A plankton, claimed to be a rich source of vitamin B12.
Actually high in vitamin B12 analogues which are of no value to humans
Rich in iodine, claimed to help slimmers burn fat (no evidence). Occasionally batches
withdrawn due to high levels of arsenic.
From dried pods of the Middle Eastern carob tree.
Carob powder has less fat then cocoa powder & no caffeine or theobromine
(stimulants in cocoa).
Carob chocolate bars have as much fat and kJ as chocolate.
Made from roasted barley or chicory. Useful if sensitive to caffeine.
More fibre, vitamins & minerals than chocolate bars
Honey, glucose & other sugars usually make up about 50% of bar by weight
Made from guarana seeds. Contains caffeine like substances which have same effect
on body, so can decrease perception of fatigue, increase heart rate.
Extract of apricot kernels, also known as amygdalin or vitamin B17. Has been
claimed to cure cancer. Can be metabolized to cyanide so dangerous to humans.
Known to be beneficial externally, but benefit of eating it as general tonic unproven.
Week 9: FAT SOLUBLE VITAMINS
Vitamins (“vital amines” 1912): organic compounds found in small amounts
in food. Each has a specific & essential function in the body.
Vitamins (except D) cannot be synthesised by the body, so a dietary
deficiency will cause a vitamin deficiency disease.
Frank vitamin deficiencies are very rare in Australia, however the extent of
subclinical deficiency is very hard to define and hence determine. This
subpopulation is at nutritional risk in that they are consuming suboptimal
doses of vitamins – whether this is having a functional effect is hard to
Deficiency in one vitamin can interfere with the function of another, whilst
excessive intake of a vitamin can have toxic effects.
In the Asia Pacific region, people with frank deficiencies in vitamin A, B1, B2
and folate can be still be found.
Individuals with hypervitaminosis also exist.
Ideally should obtain vitamins from food as they are provided in conjunction
with other complementary nutrients & there is little chance of overdosing.
Vitamin pills are consumed regularly in Australia by about 25% men, 35%
o May feel food supply is nutrient depleted
o May feel their diet is inadequate
o May believe benefits come from higher doses
o Appeal to both “natural medicine” and “evidence based medicine”
So many contradictory studies can pick and choose those you like to support vitamin
supplement use, and be reassured that what are taking is “natural” so must be good for
Classified by their solubility in water – fat soluble (ADEK) and water soluble
Could also classify by function: B complex vitamins tend to be involved in the
metabolism of nutrients for energy release, vitamins B12 and folate are
required for synthesis of DNA; vitamins AEC are antioxidants.
Fat Soluble Vitamins
These are digested and absorbed in the same manner as fat, so any conditions
of fat malabsorption will limit absorption of these vitamins.
Can be stored in the body (generally in the liver) so deficiency states take
longer to set in than for water soluble vitamins. However this also means large
doses are more likely to produce toxic outcomes as they are stored not
Also tend to be more robust in cooking and are not lost in cooking water.
Is present in 2 forms in food – as the preformed vitamin itself (known as
retinol) and in the provitamin form, the carotenoids. Most common carotenoid
is beta carotene.
Retinol is found almost exclusively in animal foods containing fat, such as
dairy products and especially liver.
Provitamin A is found in deep yellow and green plants as carotenoids. Beta
carotene is the most abundant and has the highest vitamin A activity, being
equal to about 1/6 the activity of retinol. It is less efficiently used than retinol
in the body as less well absorbed.
Vitamin A activity is quoted as “retinol equivalents” to take into account
absorption and degree of conversion to vitamin A.
The liver produces a retinol binding protein which carries retinol to tissues, so
liver dysfunction from PEM or liver disease can affect vitamin A status. About
90% of vitamin A in the body is stored in the liver.
Vitamin A roles: in vision, growth, reproduction, immunity, epithelial tissue
maintainence. Particularly important during periods of rapid cellular
Deficiency causes keratinisation of mucous membranes eg skin & eyes. Major
cause of blindness in the 3 rd world.
Each form of vitamin A has a different role:
Retinol – supports reproduction and is major transport/storage form
Retinal – reduced form, intermediate in conversion of retinol to retinoic acid.
Used in vision
Retinoic acid – intracellular hormone and transcription factor so influences
cellular differentiation, growth, embryonic development – thus excessive
amounts are teratogenic.
Beta carotene – antioxidant. Role in vision is as a component rhodopsin which
is used for dim light vision. “Night blindness” is therefore a symptom of
vitamin A deficiency, although zinc deficiency can also cause this (as zinc
needed for RBP production).
Vitamin A deficiency very rare in Australia, more common in Asia, where it causes
blindness by xerophthalmia.
“Liver cleansing diets” do not mean the person needs additional vitamin A
High levels of vitamin A as retinol are toxic. A single large dose (ie 100 x RDI
for adults, 20 x for children) can cause acute toxicity (nausea, vomiting,
dizziness, headache) whilst much more common is daily large doses of 10 x
RDI can cause chronic toxicity (headache, hairloss, joint pain, dry itchy skin,
Pregnant women must avoid taking more than 2400ug/day (from food,
fortified food and supplements) as linked with spontaneous abortion, gross
fetal abnormalities or severe learning disabilities. All multivitamins containing
vitamin A must carry a warning on the label re: pregnancy.
OCP users have higher vitamin A levels in their blood so should not take
vitamin A supplements.
A recent study of 72,000 American women found that over an 18 year period
those with the highest intake of retinol (from supplements or fortified milk &
breakfast cereal) had double the risk of hip fracture due to osteoporosis. Long
term vitamin A toxicity causes thinning of bones.
2 case studies from the Royal Children‟s Hospital on vitamin A toxicity
published 2001. Featured a 2 year old girl and a 4 year old boy. Both were
being treated with preparations from naturopaths which were very high in
vitamin A for leg pain & lack of appetite. Once the supplements were
discontinued the inflammation of the bone resolved in the girl but the boy was
left with permanent vision loss from vitamin A toxicity.
High levels of beta carotene in food are not harmful (but will cause yellowing
of skin). High intakes of beta carotene supplements are linked with an increase
in lung cancer (Finnish male smoker trial) and bowel polyps in those at high
risk. Choose a beta carotene supplement made from D.Salina (natural form).
VITAMIN A SUMMARY:
Food sources: high = cod liver oil, palm oil, liver; medium = carrot, spinach, sweet
potato, egg yolk, milk
RDI = 750ug RE for adults in Australia.
1. Vision. Essential component of rhodopsin in the retina which is used for
vision in dim light
2. Epithelial surfaces. Essential for maintenance of specialised epithelial cells in
3. Bone growth. Essential for normal bone formation, needed for bone cell
Deficiency symptoms (primary):
1. Night blindness – usually first symptom
2. Keratinisation of epithelial surfaces – when occurs in cornea of eye leads to
xerophthalmia and blindness
3. Poor dental health (needed for development of enamel forming epithelial
Deficiency of vitamin A rare in Australia but may occur secondary to:
1. Malabsorption of fat eg coeliac disease, cystic fibrosis
2. Severe liver disease so loss of stores
3.Zinc deficiency which reduces transport of vitamin A to tissues
In developing countries up to 5 million children are affected, with resultant
respiratory disease & diarrhoea.
1. May reduce risk of breast, lung, colon, prostate, cervical cancer
2. May reduce risk of heart disease and stroke (AO function)
3. May retard macular degeneration (AO function)
Toxicity (in XS of 1000ug/kg bodyweight for adults, less for children)
1. 1 study on smokers found lung cancer rates markedly INCREASED when
given beta carotene in high doses. Will also cause yellowing of skin
2. Loss of appetite, headache, blurred vision, irritability, hair loss, dry skin, bony
growths, haemorrhages, bone fractures, liver damage, death
3. Congenital abnormalities can occur if excessive amounts taken in pregnancy.
Discovered when searching for a cure for rickets that cod liver oil will
prevent it. In 1920s found a substance in the skin produced after exposure to UV
light also gave protection.
As long as have access to sunlight there is no dietary requirement.
Suggested exposure: hands, arms, face for 5-10 minutes, 3 times/week (without
The darker your skin, the longer you need to spend in the sun to attain
adequate vitamin D. Solariums that produce UVB rays are efficient at triggering
vitamin D production. Exposure to UVA rays from solariums will destroy B
vitamins such as folate so dangerous for pregnant women.
2 major forms in nature – vitamin D-2 (ergocalciferol, found in yeast
and fungi) and vitamin D-3 (cholecalciferol, animal origin).
In humans, provitamin D-3 is synthesised in the liver from cholesterol
and carried to the skin. The action of UV light converts it to 25-hydroxy
cholecalciferol (calcidiol). This enters the circulation and is converted to active
vitamin D (1, 25 hydroxy cholecalciferol or calcitriol) in the kidney.
Small amounts of vitamin D are found in fatty fish, butter, eggs, and
fortified margarine (the major dietary source of vitamin D).
Sufficient exposure to sunlight negates the need for dietary vitamin D.
Amount of vitamin D synthesised in skin depends on length & intensity of
sunlight. Also destroyed by sunlight.
Those at risk of vitamin D deficiency are infants in cold climates,
Islamic women, elderly & institutionalised. In adults this manifests as
osteomalacia, in children as rickets
Vitamin D works with PTH to increase Ca and P levels in the blood by
stimulating absorption of Ca and P from the small intestine, resorption in the
kidney and withdrawal from bones.
Formation of the active form of vitamin D is therefore strictly
controlled. This is via the existing levels of calcitriol itself, and blood levels of
PTH, calcium, phosphorus.
Most cells have a nuclear vitamin D receptor, which raises the question
as to vitamin D‟s general role in cells. EG children with rickets are more
susceptible to infection, so is vitamin D needed for immune function? Also now
suggested that vitamin D required for insulin and prolactin secretion, stress
responses and cell differentiation.
Vitamin D deficiency in Australia
One Melbourne study in 2000 found 46% of elderly people in nursing homes were
vitamin D deficient. Another study (Glover et al, 2001) noted that 80% of veiled, dark
skinned pregnant women attending a Melbourne ante-natal clinic were vitamin D
deficient. The main sources of vitamin D are sunlight, margarine (provides 55% of
dietary intake), fish and eggs. Margarine consumption has fallen by 25% in the last 10
years as we try to cut the amount of fat in our diet, and we are constantly warned to
limit our exposure to sunlight to avoid skin cancer. The overall result has been a
decrease in vitamin D intake, which is a concern for the elderly. Low vitamin D status
in the elderly has been linked with increased risk of falling and fracture. Some elderly
are potentially being misdiagnosed with fibromyalgia, when they actually have
osteomalacia from vitamin D deficiency.
Solutions? Vitamin D supplements for elderly? Fortify milk?
Should only be taken if blood levels of vitamin D shown to be low eg as in
hypothryroidism or some kidney diseases. Much better to expose skin to
sunlight for short periods as vitamin D lives longer in the body if made in the
skin rather than taken orally.
Most toxic of all vitamins – even 5 x RDI can give symptoms. Causes too
much calcium to be absorbed, so some is deposited in soft tissues & kidneys.
Supplements in elderly appear to reduce osteoporosis fractures. Safe upper
VITAMIN D SUMMARY
Food sources: high = cod liver oil; medium = fatty fish, margarine, egg yolk, butter
RDI = 5ug for children and adults under 50.
1. Absorption of calcium and phosphorous
2. Increases rate calcium and phosphorus form and maintain bone, with vitamin
A and C.
3. Reduces excessive cellular division, so promotes differentiation
4. Modulates immune function.
Clinical signs: Rickets in children, osteomalacia in adults. Due to impaired
mineralisation of bone matrix and defective collagen synthesis.
Deficiency can occur secondary to:
Diseases of liver & kidney
At risk populations: dark skinned, veiled women, elderly, “skin cancer aware”
1 May help prevent osteoporosis
2 May reduce cancer risk and enhance immunity
Excessive intake in children can lead to loss of appetite, headache, nausea, vomiting,
intense thirst and polyuria, calcification of soft tissues, bone disease, death. Large
doses of cod liver oil can cause toxic levels of vitamin D.
Is an antioxidant. Exists in at least 8 different forms in nature, with
tocopherol being the most abundant.
Richest dietary source is commercial vegetable oil, in which vitamin E
protects the PUFAs from breakdown.
Nuts next best source, and all vegetables and meats contain some vitamin E.
The requirement for vitamin E by the body increases according to intake of
PUFAs. Since foods high in PUFAs are also good sources of vitamin E, it is
very hard to become deficient in this vitamin.
Potentially over-refining oils could lead to reduction of vitamin E levels so
this should not be encouraged.
Evidence of vitamin E deficiency is sometimes seen in intestinal
malabsorption syndromes and in low birthweight infants. Otherwise
supplementation does not appear necessary in a normal diet.
Recent evidence suggests vitamin E may protect against atherosclerosis by
protecting LDL from oxidation (oxidized LDL taken up more readily by
macrophages to form foam cells so fatty streaks).
Some intervention studies have found a reduction in risk from CHD if taking a
100mg vitamin E supplement, others have not.
Vitamin E & disease:
Cancer: Vitamin E is present in the membranes around every cell to help prevent
oxidation of PUFAs and possibly proteins in membrane. Possibly prevents damage to
RNA and DNA (hence anticancer activity). To date 5 large trials looking at
supplements and colon and lung cancer have not shown a preventative effect.
CVD: Vitamin E thought to prevent LDL oxidation hence atherosclerosis . In tissue
culture vitamin E appears to prevent LDL accumulating in foam cells.
Epidemiological studies have shown that populations with a higher intake of vitamin
E have a lower incidence of CHD. The 2 biggest studies were the Health
Professionals study (39910 men) and Nurses Health Study (87245 women). Both
showed reduced risk of CHD (40% and 34% respectively) in groups with highest
blood levels of vitamin E. The European MONICA study also showed that groups
who ate food high in vitamin E had lower risk of CHD. However intervention studies
to determine which dose of vitamin E reduces LDL oxidation have produced unclear
results. Indeed at least one study of Iowa women has shown that those taking high
level supplements had a 25% increased risk of death from CHD.
The concern is (inconsistent) effects are seen at doses much higher than would be
obtainable from food, so vitamin E is probably acting in a role outside its usual
Alzheimer’s: Two recent trials have shown diets rich in vitamin E and C (but not
supps) have been linked to a reduction in Alzheimer‟s, (one in Netherlands, one in
US) which suggests the antioxidant action of the nutrients is preventing oxidative
damage (causing lesions) to the brain.
Vitamin E supplements sell very well as widely credited with many roles and
people seem unaware of food sources.
Despite some positive trials in reducing CVD incidence with a supplement,
there are other trials that do not support this conclusion. Beneficial dose is still
to be agreed on too. Therefore safest bet is to have a diet high in vitamin E, or
stick to a low dose supplement. Safe upper dose =130-270mg or 200-400 IU
of d alpha tocopherol (avoid dl alpha tocopherol supplements)
Check if taking fish oil tablets vitamin E has been added.
Linseed oil potentially risky source as the PUFAs in it are so unstable and
oxidise so quickly the vitamin E may be rapidly used up mopping up the
oxidative products that form after pressing. Eating linseeds is a better choice
as the seeds stick to the bowel wall for up to 10 days whilst bacteria break
them down and release the PUFAs.
Athletes AT HIGH ALTITUTES on 800mg vitamin E supplements had lower
lactic acid in their blood. Possibly there is greater breakdown of the fats in the
membrane around the rbc in low oxygen environments which is counteracted
by vitamin E antioxidant action. At normal altitudes no benefit seen.
VITAMIN E SUMMARY
Food sources: polyunsaturated vegetable oils (high); peanut oil, olive oil, nuts, seeds,
RDI: 7-10mg/day for everyone over 8 years.
1. As an antioxidant to protect the lipid membranes of cells, integrity of red
blood cells from oxidative damage. Also protects beta carotene and
unsaturated fatty acids from oxidative breakdown.
2. May be involved in haemoglobin formation
3. In food prevents the breakdown and oxidation of PUFAs.
Not reported in Australian adults. May occur in low birthweight infants given formula
low in vitamin E, causing haemolytic anemia.
Theoretical risk of deficiency in malabsorption syndromes eg cystic fibrosis
May reduce risk of heart attack and angina
May slow macular degeneration
May prevent spinal cord damage in CF patients
Relatively non toxic. 300mg/day may cause severe influenza, malaise, fatigue, gut
disturbances. Imbalance between vitamin E and K can impair blood clotting.
2 naturally occurring forms: vitamin K-1 (phylloquinone, in green plants) and vitamin
K-2 (menoquinone, synthesised by intestinal bacteria). Approx ½ our vitamin K needs
are met by bacterial production in our gut, the rest comes from diet. Vitamin K is
found in green leafy veg, soybeans, wheatgerm, but fruit and animal products contain
VITAMIN K SUMMARY:
Food Source: broccoli, spinach, soybeans, cabbage (high); wheatbran, green beans
AI: men = 70ug, women = 60ug
1. Involved in synthesis of clotting factors II, VII, IX and X
2. Through the action of these clotting factors may influence calcium metabolism
Hemorrhage occurs as clotting time is delayed
Prophylactic dose given to all newborns to reduce risk of hemorrhage. This is
because of poor placental transfer of vitamin K and absence of vitamin K
producing bacteria in newborn gut. Newborns to be breastfed have higher risk of
vitamin K deficiency as less vitamin K in breast milk than formula and intestinal
flora slower to develop.
Malabsorption syndromes may prevent adequate absorption
Liver diseases may reduce synthesis of clotting factors
Warfarin can cause a bleeding tendency if vitamin K intake is poor.
May be important in prevention of osteoporosis
?role in cancer prevention
Regulation of bone metabolism
Toxic if given over long periods. Safe upper dose = 30mg
Janette works the night shift and sleeps during the day while her husband cares for her
child. She is 30 years old, with a BMI of 22. She is lactose intolerant so avoids dairy
products, and is also allergic to seafood. She recently fractured a bone in her wrist
while lifting a box.
1. Which nutrient could Janette be deficient in?
2. How could she correct this deficiency?
3. What are the key roles of vitamin D in the body?
4. Are any foods fortified with vitamin D?
Fat soluble vitamins: Multiple Choice
1. Which foods are rich sources of vitamin E
a. liver, eggs, butter
b. fatty fish, egg yolk, margarine
c. wheat germ oil, almonds, vegetable oils
d. broccoli, cabbage, spinach
2. Which of the options below best describes the absorption of fat soluble
a. requires emulsifications by bile and micelle formation for maximal
b. requires the action of amylase
c. requires the action of proteolytic enzymes
d. all of the above
3. The main function attributed to vitamin K is
a. The visual cycle
b. Blood clotting
c. Antioxidant activity
d. Maintenance of bone integrity
4. Which factors contribute to haemorrhagic disease of the newborn?
a. low capacity for synthesis of prothrombin in neonatal liver
b. poor placental transfer of lipids and low content of vitamin K in breast
c. absence of bacteria in neonatal intestine
d. all of the above
5. Which of the following groups are at risk of vitamin D deficiency?
a. elderly confined to nursing homes with no access to sunlight
b. children and women who inadvertently avoid sunlight for religious or
c. people with chronic renal failure
d. all of the above
6. Which of the following statements about supplementation with fat soluble
vitamins is correct?
a. supplementation with any fat soluble vitamin at doses greater than the
RDI poses a health risk because they are not excreted in the urine
b. vitamin E supplements equivalent to 10 x RDI have no demonstrated
c. vitamin A supplements have no side effects and can be recommended
for any age group
d. fat-soluble vitamins are readily metabolized by the liver and excreted
in the faeces.
Extra salad, hold the egg, cheese, bacon. Avoid the big ones – Big Macs, Whoppers.
If making own burgers, rinsing with warm water after cooking reduces fat content.
Serve with salad to give better balance to meal. Easy to over consume – avoid by
ordering a small or thin/crispy crust.
Woodfired pizza toppings often lower in fat than regular toppings
Olives, anchovies, ham, cheese, salami all add a lot of salt to pizzas
Go for BBQed or rotisserie over fried
Balance KFC with corn cob, coleslaw, bean salad or mashed potato & gravy
Lebanese Doner Kebab
Generally healthy, although meat is sometimes coated in fat to keep it moist during
cooking. Shish kebab is better choice.
Very high in saturated fat & salt
Ask for no salt & grilled not fried fish
Avoid sweet & sour, deep fried & lemon sauce dishes – high fat
Get steamed not fried rice
Avoid adding extra soy sauce as already high in salt
Choose dishes based on beans and salad.
Meat pies, sausage rolls
Go for meat & vegetable pies as lower in fat. If kept warm for a long time will have
lost some B vitamins.
Best & worst takeaway choices
Worst Choice: Big Mac (24g fat) with large fries (28g fat)
Best choice: Filet –o-Fish (16g fat) or Junior burger (8g fat) with salad
Worst choice: 2 pieces chicken (29g fat), chips (20g fat)
Best choice: Tender roast chicken(16g fat), mashed potato & gravy (1.8g fat
Worst choice: super supreme pan pizza (30g fat/2 slices)
Best choice: thin & crispy vegetarian (18g fat/2 slcies)
Worst choice: chicken & chips (47g fat)
Best choice: ¼ chicken, no skin, no stuffing (9g fat)
Worst choice: Whopper with cheese (46g fat)
Best choice: Aussie burger (32g fat); Vegie burger (32g fat)
Worst choice: 6‟‟ meat ball sub (13g fat)
Best choice: 6‟‟ turkey breast sub (4g fat)
(Nutrition for life, Saxelby 2002)
Week 10: WATER SOLUBLE VITAMINS
Thiamin (vitamin B1)
Function: Co-enzyme in many enzyme systems mainly involved in releasing energy
from CHO, protein and fat.
Deficiency: Frank deficiency causes beri beri. Only seen in chronic alcoholics.
a. GI = loss of appetite, indigestion
b. Nervous system = impaired sensation, loss of reflexes, difficulty moving (dry beri
beri). If oedema also present = wet beri beri. If brain involved = Wernicke‟s
encephalopathy (involuntary eye movement, muscular uncoordination). Progresses to
Korsakoffs pyschosis if untreated (memory defect & confabulation).
c. Cadiovascular symptoms = cardiac failure
0.1mg/1000kJ for all ages. The more CHO and alcohol you have, the more thiamin
you need so RDI is quoted in terms of energy intake.
Good food sources
Vegemite, pork, wholegrains, fortified cereals, bread, legumes, seeds, salmon
Effect of cooking
Heat and water destroy thiamin so moist heat is very destructive. Typically
about 25% lost during cooking.
Refining of cereal products also causes losses so bread, cereal often fortified.
Essential for recovery from chronic alcoholism. Otherwise unnecessary in a balanced
The body doesn‟t store much thiamin so a constant supply from the diet is needed.
Thiamin as an occasional supplement is not well absorbed. Often included at high
doses in multivitamins because it is so cheap and not toxic at high doses.
Riboflavin (vitamin B2)
Function: Part of a group of enzymes (flavoproteins) which are involved in cell
respiration & release of energy from CHO, fat, protein.
Deficiency: No evidence of deficiency in Australia. Symptoms = cracking of lips and
corners of mouth; smooth tongue; visual disturbances; conjunctivitis.
Good food sources: vegemite, cornflakes, milk, cheese
RDI: 0.12mg/1000kJ for all ages. Linked to energy requirements as used to help
release energy from food. Physical activity may increase riboflavin needs, but few
athletes would be at risk of deficiency. Less riboflavin needed during sleep so people
getting less sleep may have higher requirements.
Effect of cooking
Causes some losses. If vinegar or lemon juice present losses are high, so should be
added just before serving. Milk exposed to light for 2 hours loses about ½ its
Chronically high alcohol intake causes a need for riboflavin supplements. Otherwise
the rapid appearance of it in the urine (turns a bright greenish yellow) demonstrates
most amounts taken are far in excess of what the body needs. Aftertaste of
multivitamins is due to riboflavin. Some research suggests it may help prevent
migraines, traditionally prescribed in combination with magnesium & feverfew.
Niacin (vitamin B3)
Function: Part of the coenzyme nicotinamide adenine dinucleotide (NAD)& is
involved in cell respiration & metabolism of CHO, protein, fat
Deficiency: Frank deficiency causes pellagra
Symptoms: dermatitis, diarrhoea, dementia.
Good food sources: vegemite, wheatbran, ovaltine, peanut butter, beef
RDI: 1.6mg niacin equivalents/1000kJ for all ages. In practice about half our niacin
intake comes from food, half is made in the body from tryptophan. 60mg tryptophan
can be converted to 1mg niacin, hence use of niacin equivalents
Effect of cooking
Up to 75% may be lost during cooking. Niacin in traditional varieties of corn is bound
in an unusable form, so was traditionally soaked in lime juice to make tortillas and
hence release the niacin.
Niacin supplements have been made popular as a means of increasing HDL
cholesterol levels, and at pharmaceutical doses they are effective at doing this.
However there are a number of side effects at this dosage (flushing, GI disturbances).
During pregnancy tryptophan conversion to niacin increases 3 fold, due to the
influence of oestrogen increasing the enzyme used for conversion. That is why
women on the pill should not take niacin supplements.
Pantothenic acid (vitamin B5)
Function: Part of the acetyl carrier co-enzyme A & involved in many chemical
reactions in the body eg energy release via metabolism of CHO, fat, protein; synthesis
of amino acids, fatty acids, sterols, vitamin D.
Deficiency: Only able to be induced under experimental conditions.
RDI: Unknown as so abundant in the food supply would be deficient in many other
vitamins too if excluded B5 from diet.
Food sources: egg yolk, broad beans, apricot, beef, milk all good sources. Can be lost
from grains during milling.
Often promoted as being in royal jelly, but no evidence to support claims. Some
sports studies have reported improvements with supplements, others have not.
Pyridoxine (vitamin B6)
Function: Required by over 100 enzymes in the body. Required for synthesis &
metabolism of serotonin; synthesis of niacin from tryptophan; formation & growth of
rbc, release of energy from CHO and fat.
B6 can also bind to steroid receptors, so displace oestrogen. OCP users did need extra
B6 but no longer required in the lower dose format.
Deficiency: Non specific symptoms eg irritability, depression, dermatitis.
Good food sources: vegemite, walnuts, bananas, egg yolk, chicken, potatoes
Large doses have sometimes been prescribed for PMS, leading to peripheral neuritis.
Max safe dose is only 10mg/day, some people take up to 50mg or more.
Some women find relief from morning sickness with B6 supplements, others do not.
Because of B6‟s role in production of glucose, some athletes take B6 supplements.
Many researchers have now concluded athletes should not take B6 supplements
because they cause glycogen muscle stores to be broken down more quickly during
exercise – obviously undesirable. Also B6 lowers circulating fatty acids during
exercise which may be used as fuel – again undesirable.
Family of more than 30 compounds. Folate is the form found in food, folic acid is the
form used in supplements or fortified foods, folacin is the provitamin converted to
folic acid in the body.
CVD: Folate acts with B12 and B6 to convert homocysteine (risk factor for CVD) to
cysteine and methionine. Many studies have shown that when our levels of B6, B12
or folate are low, homocysteine levels are high so risk of CVD increases.
Neural tube defects: Early 1980s showed 200-400ug folate supplement lowered
incidence of neural tube defects. Must be taken before the 6 th week of pregnancy
when the neural tube closes. Mechanism unsure – folate required in conjuction with
B12 to deliver methionine to fetus. Also environment appears to play a role – much
higher rates of spina bifida in Australia than the US or UK. Mexican women have
high rates but only if they are pregnant in Mexico, not in the USA. Farming families
seem more commonly affected in 1 study. One UK study (Lancet) found for every
1000 women on folate there were 10 fewer birth defects but twice as many
miscarriages as usual.
Cancer: Folate required for synthesis of DNA so methotrexate, the folate antagonist,
is an anticancer drug. Good evidence that high intake of folate prevents colon cancer
was gathered by the US Nurses study – 3 fold higher incidence in women with lowest
intake of folate from foods. Replicated in animal studies.
Deficiency: Causes macrocytic anemia. Rapidly dividing cells also affected. Most
common vitamin deficiency in Australia. Seen in institutionalised elderly, chronic
alcoholics, pregnant women.
RDI: 200ug/day for adults; 400ug/day for pregnant women
Good food sources: green leafy veggies, peanuts, peas, egg yolk, oranges, wholemeal
bread, fortified cereal
Effect of cooking
V. unstable vitamin. Destroyed by heat and oxidation over 100C. Raw veggies least
losses, but steaming causes fewer losses than boiling.
For prevention of neural tube defect: Clear evidence of benefit of supplement for all
women with potential to become pregnant, as supps important so early in preg.
400ug/day is recommended, which can be achieved by a diet high in fresh fruit, veg,
wholegrains, nuts, legumes, fortified cereal. If a supplement is prescribed it should be
specifically for pregnancy and have 500ug of folic acid in it (some multivitamins have
very low folate levels). If the woman has an affected child or a family history of
neural tube defect, supplements of 5mg/day recommended.
Folate supplements not recommended in elderly as can mask symptoms of pernicious
anemia (due to B12 deficiency).
For high homocysteine levels: One study showed a reduction if 200ug/day taken, but
this increase can easily be done by altering diet.
For osteoarthritis: One study gave 6400ug folic acid and 20ug B12 supps to
osteoarthritis patients. They reported improved grip strength and hand tenderness over
group taking NSAIDS.
Function: If B12 is absent the body cannot use folate. B12 assists folate in production
of DNA. Also needed for production of rbc with folate – if lacking folate bone
marrow cells become megaloblasts. On its own B12 used for production of myelin.
To be absorbed from the SI, B12 must first be bound to intrinsic factor produced in
B12 and vegans: Plant sources of B12 only contain B12 as a result of microbial
contamination. For example mushrooms may have some contaminating B12 from
their compost, but it is far less than the required amount. Spirulina and comfrey
contain forms of B12 than are inaccessible to humans. Best source is fortified soy
drinks or supplement. If pregnant vegan woman should definitely take a supplement
so baby‟s nervous system can develop normally. Even vegetarians who eat milk &
eggs tend to have fairly low levels of B12, so supplementation during pregnancy &
lactation may be advisable. Vegetarians usually have diets high in folate so this masks
deficiency until nerve damage apparent.
Deficiency: Pernicious anemia, neurological disturbances. Vegans , newborns of
vegans, gastectomy patients at greatest risk.
Drugs: Of note: cochicine (used in gout & joint inflammation) & biguanides (used in
diabetes) may warrant an occasional B12 injection if taken long term. Metformin also
inhibits B12 absorption but if taken with milk or calcium carbonate tablets this is
Good food sources: sardines, oysters, egg yolk, beef, fish, cheese
RDI: Much larger intakes of B12 recommended than needed to allow for low
absorption and for the fact body stores tend to increase over lifespan possibly to
compensate for low absorption by elderly. RDI for adults = 2.0ug/day.
Unnecessary if consume animal products. Supplements may be needed if a vegan and
not having fortified products, and especially if still growing. Pregnant vegans and
vegetarians should take supps, especially if not eating large amounts of fortified soy
Elderly can become deficient as insufficient intrinsic factor made in the stomach for
absorption, or poor absorption as lack of gastric acid and pepsin (acid + pepsin act to
free B12 from food), in which case oral supplements are useless and injections
No data to support B12 supplementation of athletes – placebo effect only!
Function: Cofactor for 8 enzymes in body. 3 involved in collagen production; 2
involved in carnitine production (used to make energy in muscle cells); 1 in making
norepinephrine and 1 to make serotonin from tryptophan.
Converts non heme iron from Fe3+ to Fe2+ so it can be absorbed.
Acts as an antioxidant
The common cold: Taking megadoses of vitamin C to ward off or treat colds was
popularised by Linus Pauling in the 1970s. He won a Nobel prize in chemistry in
1954 and one for peace in 1962. He somehow managed to calculate that if early man
ate a diet high in vitamin rich plant food he would eat 2300-12000mg/day. Today it is
agreed the amount is more like 350-400mg. He felt he developed fewer colds on
megadoses of vitamin C. More than 60 trials have failed to show any benefit in
reducing incidence, although some do show a reduction in duration (eg by 19% in 1
Australian trial with identical twins). Vitamin C manufacturers still use this angle to
promote their product.
Cancer: Vitamin C was claimed to assist the treatment of cancer by Pauling in
conjuction with a physician. However they used a cohort labeled “untreatable” much
earlier in their disease than is usual. The Mayo clinic ran a trial giving patients
10000mg/day, and found no benefit. It is true that vitamin C prevents the conversion
of nitrites to nitrosamine so vitamin C containing foods such as tomato should be
eaten with preserved meats to prevent stomach cancer. Fruit & veg are protective
against cancer, but it is not single vitamins within them responsible, but the array of
phyotchemicals interacting together.
Antioxidants: Although has capacity to work as an antioxidant, uncertain under which
conditions it does in the body. EG does not appear to reduce LDL oxidation. Large
doses of antioxidants can cause these substances to act as pro oxidants eg 1 UK trial
showed doses of 500mg.day caused people to have an increase in DNA damage
compared with the placebo. This could predispose to cancer, CVD, RA.
Deficiency: Frank deficiency causes scurvy (defective collagen synthesis, bruise &
bleed easily, delayed wound healing, susceptibility to infection, anemia, fatigue).
Uncommon in Australia. Most vulnerable groups = newborns of mothers taking
megadoses, institutionalised elderly, chronic alcoholics, women who smoke & take
RDI: Some dispute as to how much is needed. Australian RDIs (men 40mg/day,
women 30mg/day) reflect the quantity needed to prevent scurvy plus a large safety
margin to allow for people like smokers who require greater amounts. When intake
exceeds 130mg/day the tissues are saturated and unmetabolised vitamin C appears in
the urine. If we ate the recommended amount of fruit and veg we would have
200mg/day, so some argue this should be the recommended intake.
Good food sources: blackcurrants, capsicum, oranges & lemons.
Effect of cooking: rapidly destroyed by heat, light, oxygen so losses during cooking
inevitable. Least losses by microwaving, greatest when boiled for long periods. Even
greater losses in alkaline conditions eg adding bicarb to veg.
Supplements: No evidence to support high doses of vitamin C for anyone, so should
avoid supplements >500mg. Depending on individual tolerance, diarrhoea will occur
after consuming 1000-10 000mg. Because the excess is excreted, little toxicity.
Possibly could increase kidney stone development as oxalate is metabolic by product
of vitamin C metabolism.
? high doses may increase absorption of mercury and a few reports of mothers taking
megadoses of vitamin C during pregnancy then baby developing scurvy soon after
birth as they had become dependent on high doses of vitamin C.
A supplement of 500mg taken at the first sign of a cold may reduce duration slightly.
No performance benefit seen for athletes compared with placebo except for athletes
with low levels of vitamin C.
If you suffer from haemochromatosis (population rate =1/300, common if of Irish
descent) large doses are hazardous as promote iron absorption. Many unaware they
have the condition – seen in men, as women lose blood regularly.
Function: Coenzyme, needed for synthesis & breakdown of fatty acids and amino
Deficiency: The only susceptible group are people who eat large amounts of raw
eggs as the avidin in egg white binds to biotin and prevents its absorption. Cooking
alters the shape of avidin so it no longer binds biotin. Body builders who take skim
milkshakes with 6 or more raw egg whites added to increase their protein intake over
several months are at high risk of deficiency. An oral supplement won‟t help as it
will not be absorbed – an injection is needed. Breast feeding women should also avoid
raw egg white as well. Symptoms include lethargy, loss of appetite, nausea, vomiting
Good food sources: yeast, egg yolk, soy beans
RDI: None in Australia. 100ug/day estimated to be safe and adequate.
Kate is 30 years old and referred for mild neck pain (no significant past medical
history). She weighs 58kg and is 160cm tall. She reports a good appetite and generally
eats a fruit salad & yoghurt for breakfast, a fruit smoothie for morning tea, salad or
sushi for lunch, a piece of fruit & some wholewheat crackers with cheese for
afternoon tea, a salad or cooked vegetables with fish or meat for dinner, and a fruit
based dessert. She drinks water, tea or juices. She works at a computer terminal all
day but does a circuit class 3 days/week and a yoga class once/week. Kate lives alone
and does all her own cooking & shopping. She takes 2x500mg vitamin C tablets/day
“for health maintenance”.
1. Do a nutritional assessment of Kate. (6 marks)
2. What are 3 roles of vitamin C in the body? (3 marks)
3. What are 2 risks associated with very high doses of vitamin C? (2 marks)
4. Give an example of when a vitamin C supplement is justified. (1 mark)
Ideally not used BUT there are some special needs groups:
Special needs groups Supplement needed
Before conception 400ug can protect against birth defects
During pregnancy Extra iron, folate, calcium, omega-3s
Breast feeding Extra calcium & omega-3s
Vegans B12, iron, zinc, calcium
Smokers (& passive smokers) Doubles vitamin C requirement CO
destroys circ vit c & may need more
Alcoholics B group vitamins (especially thiamin),
zinc, potassium, vitamin E
Athletes May need extra vitamin C & E, iron
Elderly Absorption generally declines but
requirements for B12, B6, calcium &
vitamin D increase
During illness or after surgery/burns Vitamin C and protein for tissue synthesis
Side effects of high supplement doses:
Vitamin or Mineral Side effect of high doses
Vitamin A >2400ug/day can be teratogenic. Can also
cause nausea, liver damage, hair loss,
Vitamin D >50ug causes vomiting, nausea, liver
damage. Causes calcium to be deposited
in soft tissues
Vitamin C >2000mg/day cause upset stomach,
diarrhoea, cramps. Increases risk of iron
Vitamin B6 >2000mg/day may cause numbness or
tingling in hands and feet
Niacin Can cause mild flushing reaction at over
Beta carotene Turns skin yellow
Iron May cause constipation or GI upset
May interfere with absorption of zinc
Keep away from toddlers – can kill!
Selenium Hair & nail loss, irritability, nerve
calcium Can interfere with iron absorption
Food…an alternative to supplements
People with a high intake of broccoli & related vegetables (cabbage, cauliflower,
brussel sprouts) have a reduced risk of several cancers (esp prostate & colon). The
indoles and isothyacynates are thought to activate tumour suppressors and block
carcinogen uptake from foods. Also good source of vitamin C, beta carotene, folate.
Garlic & chilli
Populations (mainly Asian) with high garlic & chilli consumption have low rates of
obesity, even after allowing for higher levels of physical activity & lower calorie
intakes. Chilli is thought to increase metabolic rate by increasing heat production –
same as caffeine. Garlic seems to reduce fat & CHO intake.
Source of lycopene, which is a powerful antioxidant and gives tomatoes their red
colour. 1995 study by Harvard Medical school looked at 48,000 men & found that
those with a high intake of lycopene has a much lower risk of prostate cancer.
Tomatoes, tomato sauce & pizza were the main sources of tomato eaten. Having 10 or
more serves/week of tomato based foods was associated with a 35% reduction in
prostate cancer risk, having 4-7 serves/week of tomato based food was associated
with a 22% reduction in prostate cancer risk. Lycopene is fat soluble so best to cook
tomatoes in olive oil.
A 1994 CSIRO study showed almonds significantly lower blood cholesterol BUT
they were eaten instead of spreads and fatty foods, not as an extra. High in vitamin E,
fibre, arginine & calcium.
So far, five large prospective cohort studies (the Adventist Health Study, the Iowa
Women Health Study, the Nurses' Health Study, the Physicians' Health Study, and the
CARE Study) have examined the relation between nut consumption and the risk of
CHD and all have found an inverse association. In addition, several clinical studies
have observed beneficial effects of diets high in nuts (including walnuts, peanuts,
almonds, and other nuts) on blood lipids. The beneficial effects of nut consumption
observed in clinical and epidemiologic studies underscore the importance of
distinguishing different types of fat. Most fats in nuts are mono- and polyunsaturated
fats that lower low-density lipoprotein cholesterol level. Based on the data from the
Nurses' Health Study, we estimated that substitution of the fat from 1 ounce of nuts
for equivalent energy from carbohydrate in an average diet was associated with a 30%
reduction in CHD risk and the substitution of nut fat for saturated fat was associated
with 45% reduction in risk.
Recent trial comparing women taking probiotic LGG and cranberry juice for 6
months. Found cranberry juice but not LGG prevented urinary tract infections by
inhibiting the attachment of E coli to the bladder wall.
Water…how much do we need?
August 2002 American Journal of Physiology issue has review on water needs.
“Drink 8 glasses/day” probably stems from muddled interpretation of a 1945 Food
and Nutrition Board report. That report said the body needs about 1 milliliter of water
for each calorie consumed - almost 8 cups for a typical 2,000-calorie diet - but most
of this quantity is contained in prepared foods. No research done that shows the
average person needs to drink 8 glasses/day.
“If you feel thirsty you are already dehydrated” Only true for elderly with diminished
thirst sensation & serious athletes. Otherwise the advice “drink when thirsty” is a
good guide to fluid needs.
“Water blocks dieters' hunger”. Studies show water with food can help you feel full
faster, but that just drinking water between meals has little effect.
“ Coffee, tea, cola don‟t count toward fluid intake as they are diuretics” A University
of Nebraska study that found coffee, tea and sodas are hydrating for people used to
caffeine and thus should count toward their daily fluid total.
American Institute of Medicine currently researching water requirements for normal
people. People with kidney stones & athletes have higher fluid requirements.
Otherwise urine colour is good guide to hydration status.
Week 11 and 12: MINERALS
Minerals make up 4-5% of our bodyweight (1/2 of this is calcium).
Macrominerals: calcium, phosphorous, magnesium, sodium, chloride, potassium &
Micro or trace minerals: iron, zinc, copper, iodide, manganese, fluoride, molybdenum,
cobalt, selenium, chromium, tin, nickel, vanadium, silicon.
Functions of Iron:
Iron is a very reactive mineral so must be bound to proteins to prevent undesirable
reactions occurring in the body.
Our bodies contain about 3g of iron, mainly in the form of haemoglobin. Iron
is required by haemoglobin for its structure and function. The heme portion of
the molecule contains iron which combines with oxygen in lungs or CO 2 in
Myoglobin also contains a heme group to help it store oxygen in the muscles.
Production of ATP in the mitochondria requires iron –dependent
oxidation/reduction reactions to occur.
Cytochrome P450 (which converts water insoluble drugs to water soluble
drugs for excretion) contains iron.
Iron also influences immune system – an excess of iron will increase risk of
bacterial infection, as bacteria require iron for growth. A deficiency reduces
concentrations of circulating T lymphocytes and NK cell activity. Transferrin
and lactoferrin may protect from infection by withholding iron from access by
bacteria.The immune response of healthy elderly was enhanced with iron
supps in one study.
Iron is essential for brain function at all ages – required for function and
synthesis of neurotransmitters, myelin.
Effect of iron deficiency in children delays development significantly. Eg
delayed sensory motor skills, attention, learning, memory.
Types of iron
Haem iron: found in animal foods (chicken, beef, fish and offal). Generally
only about 5-10% of dietary iron, but absorption can be up to 25%. Absorption
is enhanced by the animal proteins present in these foods, but mechanism is
unknown. Gastric acid is required for the absorption of iron as it enhances its
solubility. Iron in breast milk is more readily absorbed than iron in formula,
mechanism again uncertain.
Non haem iron is found in plant food (legumes, wholegrains, green leafy veg,
eggs). Makes up most of our dietary iron but only about 5% may be absorbed.
Improved by up to 50% by eating the non haem iron with vitamin C. Non
haem iron needs to be solubilised to be absorbed. It is reduced in the acid of
the stomach to Fe2+ then solubilised by binding to substances such as vitamin
C or sugars. It is then absorbed by mucosal cells.
Other factors that assist in non haem iron absorption include malic acid and
citric acid, both are found in vegetables so are more reason to eat varied meals.
Vitamin A and beta carotene also have been shown to improve absorption of
iron from rice, wheat and corn.
States of iron deficiency, pregnancy and growth also increase iron absorption.
Absorption appears to be inhibited by phytates (found in high fibre foods),
tannins (in tea – if anemic don‟t have tea with meals), phosphate (in egg),
oxalate (in some veg), polyphenols (in red wine). These can combine with iron
and inhibit absorption.
Calcium rich foods or supplements may inhibit absorption of haem and non
haem iron (eg young children given too much cow‟s milk).
Excretion of iron
Lost only by bleeding and in small amounts via sweat, faeces (mainly unabsorbed
dietary iron), skin. Normally about 1mg iron lost/day. During menstruation losses can
be additional 0.5 to 1.4mg/day.
RDI for Iron
Pregnant women 22-36
Breast feeding women 12-16
Post menopause women 5-7
0-6 months breast fed 0.5
0-6 months bottle fed 3
7-12 months 9
1-11 years 6-8
12-18 years 10-13
Sources of Iron
Food Iron (mg)
Red meat 100g 3.7
Fortified breakfast cereal (1 bowl) 3.0
Lentils 2/3 cup cooked 2.5
Cashews 25 nuts 2.5
Wholegrain bread 1 slice 1.6
Dried apricots 10 halves 1.6
Baked beans 100g 1.6
Fish 100g 1.2
Rolled oats 30g 1.1
Almonds 25 nuts 1.0
Eggs 50g 1.0
Broccoli 100g 1.0
Chicken 80g 0.6
White bread 1 slice 0.3
Iron deficiency is the most common nutritional deficiency in the world. Symptoms =
weakness, tiredness, inability to maintain a constant body temperature (causing chills
and hot flushes), impaired immune system. Eventually hypochromic microcytic
anemia will arise. Diagnosed as low Hb, high transferrin, low ferritin and pathology
of blood. This means less O2 to tissues.
At risk groups: menstruating females, pregnant women, infants, preschoolers,
adolescents, long distance runners, vegetarians on inadequate diets.
Deficiency in children will hinder development and behaviour, whilst deficiency in
pregnancy will increase risk of pre term delivery and low birthweight babies.
Haemochromatosis affects about 1/300 Caucasian people. Genetic condition of iron
absorption causing a build up of iron in the liver, pancreas and heart, which can lead
to cirrhosis, diabetes, CVD or arthritis. Treatment is phlebotomy to reduce iron levels.
Iron supplements, vit C supplements and high intakes of red meat should be avoided.
Iron may act as a pro oxidant to increase risk of CVD, but whether this is a
confounding effect is uncertain.
Most abundant mineral in the body. Can be subdivided into skeletal calcium
and serum calcium. Skeletal calcium is further broken down into exchangeable
(available for short term calcium homeostasis) and non exchangeable calcium
Bone is constantly being synthesised and resorbed, with the person‟s age
determining which process predominates. Peak bone mass is achieved in our
20s, but inadequate calcium intake during childhood may prevent us attaining
this. Bone loss commences in our 50s, with females losing bone more quickly
as oestrogen levels suddenly drop.
Bone loss after menopause seems to be genetically determined to a large
extent, and calcium intake alone will not influence rate of bone loss. Other
factors that influence progression of osteoporosis include consuming adequate
calcium as a child and teenager to support bone growth, consuming sufficient
calcium during adult life, regular exercise and HRT in the 5 years post
Roles of calcium include assisting transmission of ions across membranes,
releasing neurotransmitters at synapses, function of protein hormones,
activation of enzymes. Ionised calcium initiates the formation of a blood clot
by stimulating thromboplastin release from platetlets & converting
prothrombin to thrombin. Also used with Na, K, Mg to regulate heart beat and
Serum calcium is maintained at homeostasis by parathyroid hormone and
calcitonin and vitamin D.
When calcium levels in blood drop, PTH promotes release of calcium from
bone, renal tubular resorption and indirectly stimulates absorption in intestine.
If levels too high calcitonin inhibits bone resorption. Resorption also triggered
by falls in oestrogen and inhibited by testosterone.
Most absorbed in ileum. Usually 20-30% absorbed, sometimes as little as
10%. Absorbed by 2 methods. One is by active transport and controlled by
vitamin D. Vitamin D stimulates calcium uptake of the intestinal mucosal cell
by promoting the production of a calcium binding protein. The second method
is by passive diffusion along the length of the SI.
Calcium absorption increased by: calcium deficiency, growth, pregnancy,
lactation, high impact exercise that stimulates bone density.
Sufficient vitamin D and an acid environment needed for absorption. Lactose
enhances calcium absorption.
Calcium absorption decreased by: lack of vitamin D, oxalic acid (in rhubarb,
spinach), phytates (in cereals), fibre, medications that interfere with calcium
absorption (glucocorticoids inhibit both active and passive absorption; iron
Excess is excreted in the faeces and urine in roughly equal amounts. A high urinary
excretion is triggered by a high salt or protein diet and low calcium & phosphorus
intakes. Caffeine may increase calcium excretion (eg 1994 study showed a low
calcium diet plus 2-3 cups brewed coffee increased bone loss in post menopausal
women) but a glass of milk may offset this risk.
RDI for Calcium
Pre menopausal women 800
Pregnant women 1100
Breast feeding women 1200
Post menopause women 1000
0-6 months breast fed 300
0-6 months bottle fed 500
7-12 months 550
1-11 years 800
12-18 years (boys) 1200-1000
12-18 years (girls) 1000-800
Sources of Calcium
Food Calcium mg
Milk 1 glass 290
Fortified low fat milk 1 glass 400-500
Yoghurt 200g 305
Cheese 30g 260
Cottage cheese 100g 75
Almonds 50g 125
Sesame seeds 20g 200
Salmon 100g 185
Tuna 100g 10
Soya beans 1 cup 130
Fortified soy milk 1 cup 290
Broccoli 100g 125
Baked beans ¼ cup 50
Most cereals per 20g serve 15
3 major conditions:
1. Bone deformities. Abnormalities in bone structure occur in osteoporosis (bone
density reduced), osteomalacia (usually occurs with vitamin D deficiency and
imbalance in calcium:phosphorous ratio) and rickets (can occur in presence or
absence of vitamin D – 2 different forms) .
2. Tetany. Very low levels of calcium in the blood may increase irritability of
nerve fibres, causing spasms and cramps in the legs.
3. Hypertension. An inverse relationship between low calcium intake and high
BP has been highlighted by studies such as the DASH study (see sodium
Reducing risk of osteoporosis
1. Diets high in salt & protein accelerate bone loss, as they promote excretion of
calcium in the urine
2. Excessive caffeine also promotes loss of calcium
3. Aluminum inhibits calcium absorption, so avoid overuse of antacids
4. Vitamin D is required for calcium absorption – housebound elderly may be at
5. Consume adequate calcium (3 serves dairy/day) during growth & before
menopause as peak bone mass reached in 20s, and bone becomes less capable
of storing calcium as it ages.
6. Weight bearing exercise encourages good bone density
7. Avoid excess alcohol and smoking, which accelerate bone loss
Calcium citrate not calcium carbonate better for elderly as more soluble (elderly lack
acid to solubilise carbonate). High calcium intakes can inhibit iron absorption and
zinc absorption so these supplements should be taken at different times. See lecture 2
for discussion of calcium supplements.
About 80% found as calcium phosphate in teeth and bones. Remainder found as
DNA/RNA, ATP, cyclic AMP (2 nd messenger), phospholipids, phosphoproteins,
phosphosugars. Also phosphorylation reactions important for activating enzymes by
Generally about 65% of dietary phosphate is absorbed. It is absorbed along the
length of the GIT but mainly in the SI where active transport and passive
diffusion are used.
Absorption is promoted by vitamin D but inhibited by the insoluble complexes
it forms with phytates and calcium. Large amounts of dietary calcium can also
repress vitamin D levels so further decrease absorption.
What are the ideal proportions of calcium to phosphorous to maximise
absorption of both minerals? The high levels of phosphates in cows milk
inhibit calcium absorption, but the lower levels of phosphate in human milk
facilitate calcium absorption.
Primarily renal. Excretion regulated by dietary intake, amount absorbed, plasma
phosphate concentrations. Reduction in urinary excretion caused by low dietary
intake, increases in plasma insulin, thyroid hormone, growth hormone,
1000mg. Safe upper limit = 4500mg.
Generally good sources of protein are sources of phosphate eg meat, poultry, fish,
eggs very high in phosphate. Dairy products, nuts, cereals, legumes, grains are good
Found in such a variety of foods that a deficiency is only seen in cases of starvation.
Very serious outcome of deficiency – neuromuscular, skeletal, hematological and
renal abnormalities due to its wide range of functions.
Refeeding starved patients without providing sufficient phosphate, alcoholism or
premature babies fed unfortified human milk can cause clinical phosphate deficiency.
About 60% of Mg is in bone, 26% in muscle, rest in soft tissue & body fluids. Is an
intracellular cation. Stabilises the structure of ATP in the ATP-dependent enzyme
reactions. Mg is a cofactor for many enzymes used in metabolism of macronutrients
and synthesis eg synthesis of fatty acids and protein, phosphorylation of glucose
Important for nerve transmission & neuromuscular activity (calcium generally acts to
cause muscle contraction, Mg causes muscle relaxation).
Excess Mg inhibits bone calcification, and causes CNS depression, anaesthesia,
Generally 35-45% of Mg is absorbed in the SI. Facilitated diffusion occurs at low
concentrations, whilst simple diffusion occurs at high concs. Amount absorbed
depends on the Mg level of the person, amount of Mg in the diet, and the composition
of the diet. Levels of Mg kept constant in the serum by alterations in excretion and
absorption. The kidney conserves Mg if intake is low, whilst promoting urinary
excretion if intake is high. Lactating women tend to excrete less Mg to meet their
270mg (women); 320mg (men). Safe upper limit = 350mg
Most young people easily meet their requirements; elderly may be at slight risk of
deficiency according to 1995 NNS.
Good sources are seeds, nuts, legumes, wholegrains, dark green veg. Fish, meat, milk
are poor sources. Lost during refining of grains and flour.
Widely distributed so deficiency is rare. Clinical deficiency can be caused when there
is a shift in electrolyte balance eg due to renal disease, diuretics, malabsorption,
diabetes, post surgical stress.
Jane is 27 years old and a new patient. During your initial assessment she mentions
that her mother was recently diagnosed with osteoporosis and Jane is keen to reduce
her risk of developing it. Her weight is 59kg (stable over past 3 years) and height is
162cm. No recent biochemistry/pathology results available. She used to enjoy netball
but has not played recently due to the long hours she works as an account manager.
According to her diet history she often has coffee, cereal, whole milk & fruit for
breakfast. Morning tea may be coffee & a muffin. Noodles or sushi with Diet Cola
may be eaten for lunch. Dinner is often eaten in restaurants with work colleagues, and
she will usually have at least one glass of wine. She smokes about 5 cigarettes/day.
She also takes a calcium supplement everyday.
5a) Do a nutritional assessment of Jane. (6 marks)
5b) What are some dietary or lifestyle interventions you can suggest to help Jane
minimise the likelihood of osteoporosis? (7 marks)
5c) What advice would you offer about the formulation and time of day she takes her
calcium supplement? (2 marks)
Should I aim to get calcium from food or a supplement?
Calcium from food:
Safest, cheapest and best absorbed source of calcium. Calcium is better
absorbed in the presence of lactose in dairy products but the exact reason is
Even more calcium in reduced fat/high calcium milks eg PhysiCAL so better
choice than whole milk to increase calcium intake
Soy milk with added calcium also good choice as phytoestrogens are present –
these can mimic action of oestrogen which assists in preventing bone
Calcium in sesame seeds, nuts, prawns, dark green veggies and figs not as well
absorbed as dairy calcium as phytates (in bran and wholegrains) and oxalates
(in vegetables) inhibit calcium absorption.
Calcium from supplements:
Check label for amount of elemental calcium in tablets (<200mg elemental
calcium is a waste of money) (eg Blackmore‟s Bio-calcium = 360mg
Ca/tablet; Blackmore‟s Total Calcium = 64mg Ca/tablet)
Take before bed as calcium uptake by bone peaks during the night
A supplement containing vitamin D is helpful if elderly or bedridden
If allergic to seafood avoid supplements made from oyster shell
If you are also taking an iron supplement, take it at a different time as they
interfere with each other
Do not exceed recommended doses
Calcium citrate not calcium carbonate better for elderly as more soluble
(elderly lack acid to solubilise carbonate).
High calcium intakes can inhibit iron absorption and zinc absorption so these
supplements should be taken at different times.
Calcium supplements taken over several years can slow bone loss in
osteoporosis IF combined with HRT and physical activity, but cannot replace
Eating for Exams
1. Eat regular meals
Try to have healthy regular meals, even if feeling too stressed to be hungry
2. Get plenty of iron and zinc
These will improve memory and concentration- needed for function of
neurotransmitters. Lean meat, fish, nuts, brown rice, wholegrains all good sources.
3. Top up omega-3 fats
Required for production of serotonin and dopamine. Need adequate amounts to
increase ability to deal with stress & concentrate. Also high intake of omega 3‟s will
reduce cortisol production, which inhibits short term memory. Use canned tuna,
salmon, omega-3 enriched bread, eggs, spreads or fish oil capsules (check vitamin E
present in capsule).
4. Get plenty of B vitamins
Vegetables, legumes, vegemite, cereals good sources. Adequate amounts needed for
peak mental performance.
5. Eat plenty of nutritious snacks
Small snacks fuel the brain with glucose. EG Yoghurt, nuts & dried fruit, milk &
cereal, raisin toast, rice cakes with peanut butter or cheese.
6. Stay well hydrated
7. Try to maintain your usual sleep routine so the night before the exam you are
more likely to sleep well.
8. Limit the caffeine
Too much will leave you irritable, anxious and unable to sleep. Keep to 3-4 cups of
instant coffee or 2 cups of percolated coffee. Save it for the time of day you have least
enthusiasm for study, and don‟t drink it after 6pm if it keeps you awake.
9. Get some moderate exercise everyday
Moderate exercise increases blood flow to the brain. Strenuous exercise causes the
production of cortisol, hence inhibition of short term memory.
Meditation for 20 minutes before bed will assist in sleeping & stress management
For the EXAM
Before the exam, have a meal that includes carbohydrate and protein – carbs
provide fuel for the brain, whilst protein will sustain your energy levels longer.
EG cereal & milk, cheese on toast, etc.
Try to stick with old favourites.
Don‟t have a large, high carbohydrate meal before an afternoon exam or you
will feel sleepy, stick with a light lunch.
If you are too nervous to eat before an exam, have a milk shake or smoothie.
Function: found in extracellular body fluids.
Involved in maintaining volume & osmotic balance of body
fluids; needed for electrical activity of muscles & nerves; transport of amino acids &
Kidneys regulate sodium levels by excreting excess. High intakes of sodium cause
fluid retention, and can add up to 1kg to body weight. This extra fluid can increase
Sources: 90% of sodium in the diet comes from salt (sodium chloride). Other sources
include monosodium glutamate (MSG), baking powder (sodium bicarbonate),
effervescent tablets (Asproclear, Eno, Berocca) and some soda waters.
Recommended salt consumption:
Sodium (mg) Sodium (mmol) Salt (g)
Body requirement 200 8.5 0.5
RDI 920-2300 40-100 2.3-6
Average intake 2300-4600 100-200 6-12
High salt consumption:
Risk of stroke & CVD increases continuously with increased BP, as shown by 9 large
prospective cohort studies. Sodium reduction has been shown by many trials to reduce
BP. A reduction of 3g/day of salt intake would result in an average decrease of
5mmHg (systolic)/2.5 mmHg (diastolic) for those over 50 years, and reduce age
specific stroke mortality by about 22%. Excess sodium intake also increases risk of
gastric cancer, heart failure, oedema, osteoporosis (as promotes excretion of calcium).
A high salt diet is thought to increase arterial blood pressure in susceptible
individuals. In about 70% of cases of hypertension an extremely low salt diet will
improve BP. A meta analysis has noted the full effect of a low salt diet on BP is not
seen for at least 5 weeks. Populations who habitually consume a low salt diet do not
record increased BP as they age.
Most patients with hypertension have an underlying genetic predisposition. Their
hypertension is then triggered by:
1. Being overweight
2. Heavy alcohol intake
4. Sedentary lifestyle
5. High salt diet
Smoking will aggravate established hypertension.
Treating hypertension by lifestyle changes
Lowering of systolic BP by 5mmHg can be achieved by each of the following:
1. Weight loss of 5kg if overweight (greatest contributor to hypertension)
2. Reduce alcohol intake from 4-5 drinks to 1-2
3. Exercise (40 min, 3-4 x week)
4. Reducing salt intake from 12g to 6g/day
5. DASH diet
Preferable to treat hypertension by lifestyle changes as they can minimise or alleviate
use of medication. They also have benefits beyond BP reduction, such reduction of
risk of diabetes & CVD.
DASH diet (Dietary Approaches to Stop Hypertension)
Resulted in an average reduction of 11.5mmHg (systolic blood pressure).
DASH diet promotes a balanced intake of protein, fat, CHO. Low in sodium, high in
magnesium, potassium, calcium because magnesium works with calcium, potassium,
sodium to regulate heart beat, muscle contraction & bone building. Calcium has been
shown to lower blood pressure in human trials & shown to counteract the increase in
BP that occurs in a high sodium diet. Potassium complements sodium & is important
for normalising BP. Diet includes omega-3s as they are able to lower BP, and reduce
blood clotting. In food terms the diet is rich in fruit & vegetables, fish, nuts, legumes,
low fat dairy & monounsaturated fats. It limits sweets & sugary drinks. Best results
were seen when sodium intake was restricted.
How to limit salt intake:
High salt foods (use sparingly or buy salt reduced)
Bread, hard cheeses, margarine/butter, processed meat, sauces, gravy powders,
vegemite, some breakfast cereals (see below), canned soup, takeaways, potato crisps,
Low salt foods (use freely)
Some breakfast cereals (see below), rice, pasta, fruit & veg, milk, soy, meat, fish,
Sodium content of breakfast cereals:
Low sodium (<120mg) Sodium (mg/100g)
Mini Wheats 3
Puffed Wheat 3
Rolled Oats 10
Honey Smacks 17
Just Right 49
Natural Muesli 30-100
Medium sodium (120-400mg)
Good Start 350
All Bran 380
Sports Plus 395
Bran Flakes 397
Vita Brits 400
High sodium (>400mg)
Froot Loops 469
Special K 536
Coco Pops 564
Rice Bubbles 720
Corn Flakes 800
Salt substitutes such as potassium chloride not recommended as they perpetuate the
taste for salty food & they can be dangerous for people taking potassium-sparing
diuretics or ACE inhibitors, and renal patients.
Do not add salt to baby food, and be careful about introducing solids that might be
high in salt (eg gravy). A baby‟s kidneys are too immature to cope with high salt
High sodium on blood biochemistry: dehydrated
Function: Found in intracellular fluids. Controls water balance via interactions with
sodium and chloride ions. Also involved in the stimulation of muscles & nerves.
Absorbed in SI, excretion controlled by kidneys.
RDI = 50-140mmol/day for everyone over 8 years. Safe upper limit: no firm data but
>10g in 1 dose can cause cardiac arrest
Rich dietary sources are fruit, vegetables, legumes, nuts, lean meat. As food is
processed the potassium content falls & the sodium content rises. Read labels & aim
for 1:1 ratio of sodium to potassium in product, as potassium counteracts the effect of
sodium on BP.
Low potassium on blood biochemistry: generally due to diarrhoea, vomiting, diuretics
High potassium on blood biochemistry: acute renal failure or hyperaldosteronism
(usually drug induced)
Function: part of many metalloenzymes involved in various metabolic processes such
as CHO metabolism, DNA synthesis, protein synthesis, bone metabolism (required
for osteoblast activity & calcification), synthesis of neurotransmitters.
Also required for wound healing; essential for normal taste, smell, sight; needed for
sexual maturation & reproduction.
Rich food sources: lean meat, chicken, seafood, milk, wholegrains, legumes, nuts.
RDI: 12mg (adults). Safe upper limit = 40mg.
Absorption of zinc requires the acidity of the stomach to solubilise the zinc salts in
food, and allow their absorption in the SI. Like iron, several factors affect the
bioavailability of zinc:
Low zinc status High phytate content of food
Low dietary zinc Dietary fibre
Animal protein Iron & calcium supplements
Fermentation/germination of cereals
Zinc deficiency: Rare in Australia. Mild deficiency may occur in 3 rd world countries,
particularly if eating little meat & a lot of fibre (so vegetarian children at higher risk
of zinc deficiency). Symptoms = impaired growth, delayed sexual maturation,
increased susceptibility to infection, impaired neurophysiological function.
Zinc deficiency often occurs in conjunction with iron deficiency, so young women,
pregnant women & breastfeeding women tend to be affected.
Trials of zinc supplements to treat colds & flu have been conducted for a decade but
results are inconclusive.
Function: part of the antioxidant enzyme glutathione peroxidase, which neutralizes
free radicals. Therefore being studied for a role in cancer & CVD prevention. Can
protect against heavy metal poisoning from cadmium, mercury & silver.
Rich food sources: nuts (especially Brazil), seafood, lean meat, eggs, mushroom,
garlic, grains. Levels of selenium in food reflect the amount of selenium in the soil.
Deficiency: In the Keshan region of China selenium levels are low in the soil and
locals develop Keshan disease (cardiomyopathy associated with low plasma selenium
RDI = 70ug (women) or 85 ug (men). Safe upper limit = 400ug
Function: most iodine in body is concentrated in the thyroid gland, where it is used to
manufacture thyroxine (T4) and triiodothyronine (T3), which control growth,
thermogenesis & metabolism of all tissues.
Rich dietary sources: iodine is very soluble so easily lost from soil eg mountainous
areas usually low in iodine, so foods grown in these soil are low in iodine. Sea is
iodine reservoir, so seafood is a good source. Other sources of iodine in our diet are
iodine fortified salt & food products from animals given iodine supplemented feed.
Iodised salt was used to counteract iodine deficiency, which was common in Australia
in the past. As we reduce our salt intake iodine deficiency is again emerging.
Absorption: in SI, excreted in urine. Goitrogens in food inhibit the uptake of iodine by
the thyroid gland. Brassica vegetables (cabbage, brussel sprouts) contain goitrogens
which are metabolized to thiocyanate, which interferes with iodine uptake by the
Deficiency of iodine: iodine deficiency disorders include symptoms of abortion, still
birth, infant mortality, congenital abnormalities, cretinism, goiter, hypothyroidism
RDI: 120mg (women); 150mg (men). Safe Upper limit: 1000mg
Functions: Component of several enzymes involved in energy production, collagen
synthesis, manufacture of neurotransmitters. Partners iron in erythropoiesis, aids in
Rich food sources: oyster, crab, lobster, mussels, nuts, cocoa powder, wholegrains
RDI: 0.9mg/day suggested, upper safe limit 10mg
Deficiency: a dietary deficiency has not been clearly identified in otherwise healthy
people. In specific disease states copper deficiency can occur, resulting in anemia,
neutropenia and abnormal bone formation & vascular abnormalities.
Functions: required for normal growth. Also forms part of the Glucose Tolerance
Factor which enhances the action of insulin so helps regulate blood glucose
Rich food sources: yeast & yeast extract, egg yolk, lean meat, wholegrains, cheese,
RDI: 25ug (women); 35ug (men). Safe upper limit = 1000ug
Deficiency: will result in insulin resistance. Does not mean all cases of insulin
resistance are due to chromium deficiency.
Functions: its incorporation into bone & teeth increases the crystallinity of these
tissues. Adequate fluorine hardens and increases resistance of tooth enamel to decay.
Under investigation for a role in prevention of osteoporosis.
Rich food sources: fluoridated drinking water, small amounts in fish & tea.
Fluoridated drinking water is associated with reduced incidence of childhood dental
caries. High intakes of fluoride can cause a mottling of tooth enamel.
RDI: 3mg (women), 4mg (men). Safe upper limit = 10mg.